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Sample records for anthracnose disease caused

  1. Chilli anthracnose disease caused by Colletotrichum species.

    PubMed

    Than, Po Po; Prihastuti, Haryudian; Phoulivong, Sitthisack; Taylor, Paul W J; Hyde, Kevin D

    2008-10-01

    Anthracnose disease is one of the major economic constraints to chilli production worldwide, especially in tropical and subtropical regions. Accurate taxonomic information is necessary for effective disease control management. In the Colletotrichum patho-system, different Colletotrichum species can be associated with anthracnose of the same host. Little information is known concerning the interactions of the species associated with the chilli anthracnose although several Colletotrichum species have been reported as causal agents of chilli anthracnose disease worldwide. The ambiguous taxonomic status of Colletotrichum species has resulted in inaccurate identification which may cause practical problems in plant breeding and disease management. Although the management and control of anthracnose disease are still being extensively researched, commercial cultivars of Capsicum annuum that are resistant to the pathogens that cause chilli anthracnose have not yet been developed. This paper reviews the causal agents of chilli anthracnose, the disease cycle, conventional methods in identification of the pathogen and molecular approaches that have been used for the identification of Colletotrichum species. Pathogenetic variation and population structure of the causal agents of chilli anthracnose along with the current taxonomic status of Colletotrichum species are discussed. Future developments leading to the disease management strategies are suggested. PMID:18837103

  2. Chilli anthracnose disease caused by Colletotrichum species§

    PubMed Central

    Than, Po Po; Prihastuti, Haryudian; Phoulivong, Sitthisack; Taylor, Paul W.J.; Hyde, Kevin D.

    2008-01-01

    Anthracnose disease is one of the major economic constraints to chilli production worldwide, especially in tropical and subtropical regions. Accurate taxonomic information is necessary for effective disease control management. In the Colletotrichum patho-system, different Colletotrichum species can be associated with anthracnose of the same host. Little information is known concerning the interactions of the species associated with the chilli anthracnose although several Colletotrichum species have been reported as causal agents of chilli anthracnose disease worldwide. The ambiguous taxonomic status of Colletotrichum species has resulted in inaccurate identification which may cause practical problems in plant breeding and disease management. Although the management and control of anthracnose disease are still being extensively researched, commercial cultivars of Capsicum annuum that are resistant to the pathogens that cause chilli anthracnose have not yet been developed. This paper reviews the causal agents of chilli anthracnose, the disease cycle, conventional methods in identification of the pathogen and molecular approaches that have been used for the identification of Colletotrichum species. Pathogenetic variation and population structure of the causal agents of chilli anthracnose along with the current taxonomic status of Colletotrichum species are discussed. Future developments leading to the disease management strategies are suggested. PMID:18837103

  3. First report of Colletotrichum nigrum causing anthracnose disease on tomato fruit in New Jersey

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Anthracnose fruit rot is one of the most serious diseases affecting the production of tomato (Solanum lycopersicum L.) in the United States and is typically incited by Colletotrichum coccodes, C. gloeosporioides or C. dematium (Farr and Rossman 2016). During the summer of 2013, symptoms characteris...

  4. Anthracnose disease of centipedegrass turf caused by Colletotrichum eremochloae, a new fungal species closely related to Colletotrichum sublineola

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Colletotrichum is a cosmopolitan anamorphic fungal genus responsible for anthracnose disease in hundreds of plant species worldwide, including members of the grass family Poaceae. Anthracnose disease of the widely planted, non-native, warm-season lawn grass, Eremochloa ophiuroides (centipedegrass),...

  5. Occurrence of Anthracnose on Chinese Mallow Caused by Colletotrichum malvarum.

    PubMed

    Kim, Wan Gyu; Hong, Sung Kee; Kim, Jin Hee

    2008-06-01

    Anthracnose symptoms were frequently observed on leaves, petioles, and stems of Chinese mallow grown in Namyangju, Korea, during a disease survey performed in November, 2007. The disease incidence was as high as 30% in the 12 greenhouses investigated. A total of 38 isolates of the Colletotrichum species were obtained from the anthracnose symptoms, and all the isolates were identified as Colletotrichum malvarum based on their morphological and culture characteristics. Three isolates of the fungus caused anthracnose symptoms on leaves and stems following artificial inoculation, which were similar to those observed during the greenhouse survey. In this study, mycological and pathological characteristics of C. malvarum identified as causing anthracnose of Chinese mallow were clarified. PMID:23990748

  6. First report of Colletotrichum chlorophyti causing soybean anthracnose

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Anthracnose of soybean is caused by several Colletotrichum species. Petiole samples were collected from Alabama, Illinois, and Mississippi. Diseased tissues suspected of being caused by Colletotrichum species were cut into 1-2 cm in lengths, surface-disinfested, and placed on water agar. Pure cultur...

  7. Phyllosticta musarum Infection-Induced Defences Suppress Anthracnose Disease Caused by Colletotrichum musae in Banana Fruits cv ‘Embul’

    PubMed Central

    Abayasekara, C. L.; Adikaram, N. K. B.; Wanigasekara, U. W. N. P.; Bandara, B. M. R.

    2013-01-01

    Anthracnose development by Colletotrichum musae was observed to be significantly less in the fruits of the banana cultivar ‘Embul’ (Mysore, AAB) infected with Phyllosticta musarum than in fruits without such infections. Anthracnose disease originates from quiescent C. musae infections in the immature fruit. P. musarum incites minute, scattered spots, referred to as freckles, in the superficial tissues of immature banana peel which do not expand during maturation or ripening. P. musarum does not appear to have a direct suppressive effect on C. musae as conidia of C. musae germinate on both freckled and non-freckled fruit forming quiescent infections. Our investigations have shown that P. musarum infection induced several defence responses in fruit including the accumulation of five phytoalexins, upregulation of chitinase and β-1,3-glucanase, phenylalanine ammonia lyase (PAL) activity and cell wall lignification. 1H and 13C NMR spectral data of one purified phytoalexin compared closely with 4′-hydroxyanigorufone. Some of the P. musarum-induced defences that retained during ripening, restrict C. musae development at the ripe stage. This paper examines the potential of P. musarum-induced defences, in the control of anthracnose, the most destructive postharvest disease in banana. PMID:25288931

  8. Phyllosticta musarum Infection-Induced Defences Suppress Anthracnose Disease Caused by Colletotrichum musae in Banana Fruits cv 'Embul'.

    PubMed

    Abayasekara, C L; Adikaram, N K B; Wanigasekara, U W N P; Bandara, B M R

    2013-03-01

    Anthracnose development by Colletotrichum musae was observed to be significantly less in the fruits of the banana cultivar 'Embul' (Mysore, AAB) infected with Phyllosticta musarum than in fruits without such infections. Anthracnose disease originates from quiescent C. musae infections in the immature fruit. P. musarum incites minute, scattered spots, referred to as freckles, in the superficial tissues of immature banana peel which do not expand during maturation or ripening. P. musarum does not appear to have a direct suppressive effect on C. musae as conidia of C. musae germinate on both freckled and non-freckled fruit forming quiescent infections. Our investigations have shown that P. musarum infection induced several defence responses in fruit including the accumulation of five phytoalexins, upregulation of chitinase and β-1,3-glucanase, phenylalanine ammonia lyase (PAL) activity and cell wall lignification. (1)H and (13)C NMR spectral data of one purified phytoalexin compared closely with 4'-hydroxyanigorufone. Some of the P. musarum-induced defences that retained during ripening, restrict C. musae development at the ripe stage. This paper examines the potential of P. musarum-induced defences, in the control of anthracnose, the most destructive postharvest disease in banana. PMID:25288931

  9. Colletotrichum incanum sp. nov., a curved-conidial species causing soybean anthracnose in USA

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Soybean anthracnose is caused by a number of species of Colletotrichum that as a group represent an important disease that results in significant economic losses. In the present study, Colletotrichum species were isolated from soybean petioles and stems with anthracnose symptoms from soybean fields ...

  10. Leaf anthracnose, a new disease of swallow-worts caused by Colletotrichum lineola from Russia

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Black swallow-wort Vincetoxicum nigrum (L.) Moench and pale swallow-wort Vincetoxicum rossicum (Kleopow) Borhidi (family Apocynaceae subfamily Asclepiadoideae) are invasive plants and are the targets of biological control efforts to control their spread in the USA. In 2010, diseased leaves of a rela...

  11. Screening strawberry plants for anthracnose disease resistance using traditional and molecular techniques

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Anthracnose is one of the most destructive diseases of strawberry which may cause fruit rot, leaf and petiole lesions, crown rot, wilt, and death. Crop loss due to anthracnose diseases can reach into the millions of dollars. Three species of Colletotrichum are considered causative agents of anthr...

  12. Occurrence of Anthracnose on Highbush Blueberry Caused by Colletotrichum Species in Korea

    PubMed Central

    Hong, Sung Kee; Choi, Hyo Won; Lee, Young Kee

    2009-01-01

    A total of 82 isolates of Colletotrichum species were obtained from anthracnose symptoms of highbush blueberry trees grown in the Gochang area of Korea during a disease survey in 2008. Out of the isolates, 75 were identified as Colletotrichum gloeosporioides and the others as C. acutatum based on their morphological and cultural characteristics. Twenty six of C. gloeosporioides isolates produced their teleomorph Glomerella cingulata in PDA culture. Three isolates of each C. gloeosporioides and C. acutatum caused anthracnose symptoms on the leaves by artificial inoculation, which were similar to what was observed in the orchards. Previously in Korea, only C. gloeosporioides has been reported as causing anthracnose in blueberries. This is the first report that C. acutatum causes anthracnose in the highbush blueberry in Korea. PMID:23983555

  13. Sorghum pathology and biotechnology - A fungal disease perspective: Part II. Anthracnose, stalk rot, and downy mildew

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Foliar diseases and stalk rots are among the most damaging diseases of sorghum in terms of lost production potential, thus commanding considerable research time and expenditure. This review will focus on anthracnose, a fungal disease that causes both foliar symptoms and stalk rots along with the st...

  14. Genome Sequence and Annotation of Colletotrichum higginsianum, a Causal Agent of Crucifer Anthracnose Disease.

    PubMed

    Zampounis, Antonios; Pigné, Sandrine; Dallery, Jean-Félix; Wittenberg, Alexander H J; Zhou, Shiguo; Schwartz, David C; Thon, Michael R; O'Connell, Richard J

    2016-01-01

    Colletotrichum higginsianum is an ascomycete fungus causing anthracnose disease on numerous cultivated plants in the family Brassicaceae, as well as the model plant Arabidopsis thaliana We report an assembly of the nuclear genome and gene annotation of this pathogen, which was obtained using a combination of PacBio long-read sequencing and optical mapping. PMID:27540062

  15. Genome Sequence and Annotation of Colletotrichum higginsianum, a Causal Agent of Crucifer Anthracnose Disease

    PubMed Central

    Zampounis, Antonios; Pigné, Sandrine; Dallery, Jean-Félix; Wittenberg, Alexander H. J.; Zhou, Shiguo; Schwartz, David C.

    2016-01-01

    Colletotrichum higginsianum is an ascomycete fungus causing anthracnose disease on numerous cultivated plants in the family Brassicaceae, as well as the model plant Arabidopsis thaliana. We report an assembly of the nuclear genome and gene annotation of this pathogen, which was obtained using a combination of PacBio long-read sequencing and optical mapping. PMID:27540062

  16. BREEDING STRAWBERRIES (FRAGARIA X ANANASSA) FOR RESISTANCE TO ANTHRACNOSE CAUSED BY COLLETOTRICHUM ACUTATUM

    Technology Transfer Automated Retrieval System (TEKTRAN)

    In the United States, anthracnose fruit and crown rots of strawberry, incited by the fungal species Colletotrichum acutatum, C. fragariae, and C. gloeosporioides, were initially considered 'southeastern' diseases. These diseases are becoming significant problems in other strawberry production regio...

  17. Colletotrichum incanum sp. nov., a curved-conidial species causing soybean anthracnose in USA.

    PubMed

    Yang, Hui-Ching; Haudenshield, James S; Hartman, Glen L

    2014-01-01

    Soybean anthracnose is caused by a number of species of Colletotrichum that as a group represent an important disease that results in significant economic losses. In the current study, Colletotrichum species were isolated from soybean petioles and stems with anthracnose symptoms from soybean fields in Illinois. Multigene sequence phylogenic analysis, combining rDNA internal transcribed spacer, actin, β-tubulin, glyceraldehyde-3-phosphate dehydrogenase and histone H3 gene regions, revealed a group of isolates collected in this study to be distinct from other established Colletotrichum species. This new group was phylogenetically closer to C. liriopes, C. tofieldiae and C. verruculosum than to C. truncatum, another species with curved conidia commonly found on soybean. A representative isolate from this new group was used to examine its morphology, cultural characteristics and pathogenicity to soybean; it was found to differ from C. truncatum in colony culture characteristics and sizes of conidia and appressoria. As a result of the molecular phylogenetic, morphological and pathogenicity analyses, we named this species Colletotrichum incanum. Of the 84 Colletotrichum isolates collected from soybean petioles, 40 were C. incanum, indicating that this species may commonly occur. PMID:24603833

  18. Screening for anthracnose disease resistance in strawberry using a detached leaf assay

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Inoculation of detached strawberry leaves with Colletotrichum species may provide a rapid, non-destructive method of identifying anthracnose resistant germplasm. The reliability and validity of assessing disease severity is critical to disease management decisions. We inoculated detached strawberr...

  19. Characterization of Colletotrichum acutatum Causing Anthracnose of Anemone (Anemone coronaria L.)†

    PubMed Central

    Freeman, Stanley; Shabi, Ezra; Katan, Talma

    2000-01-01

    Anthracnose, or leaf-curl disease of anemone, caused by Colletotrichum sp., has been reported to occur in Australia, western Europe, and Japan. Symptoms include tissue necrosis, corm rot, leaf crinkles, and characteristic spiral twisting of floral peduncles. Three epidemics of the disease have been recorded in Israel: in 1978, in 1990 to 1993, and in 1996 to 1998. We characterized 92 Colletotrichum isolates associated with anthracnose of anemone (Anemone coronaria L.) for vegetative compatibility (72 isolates) and for molecular genotype (92 isolates) and virulence (4 isolates). Eighty-six of the isolates represented the three epidemics in Israel, one isolate was from Australia, and five isolates originated from western Europe. We divided these isolates into three vegetative-compatibility groups (VCGs). One VCG (ANE-A) included all 10 isolates from the first and second epidemics, and 13 of 62 examined isolates from the third epidemic in Israel, along with the isolate from Australia and 4 of 5 isolates from Europe. Another VCG (ANE-F) included most of the examined isolates (49 of the 62) from the third epidemic, as well as Colletotrichum acutatum from strawberry, in Israel. Based on PCR amplification with species-specific primers, all of the anemone isolates were identified as C. acutatum. Anemone and strawberry isolates of the two VCGs were genotypically similar and indistinguishable when compared by arbitrarily primed PCR of genomic DNA. Only isolate NL-12 from The Netherlands, confirmed as C. acutatum but not compatible with either VCG, had a distinct genotype; this isolate represents a third VCG of C. acutatum. Isolates from anemone and strawberry could infect both plant species in artificial inoculations. VCG ANE-F was recovered from natural infections of both anemone and strawberry, but VCG ANE-A was recovered only from anemone. This study of C. acutatum from anemone illustrates the potential of VCG analysis to reveal distinct subspecific groups within a

  20. Morphological, genetic, and pathogenic characterization of Colletotrichum acutatum, the cause of anthracnose of almond in Australia.

    PubMed

    McKay, Suzanne F; Freeman, Stanley; Minz, Dror; Maymon, Marcel; Sedgley, Margaret; Collins, Graham C; Scott, Eileen S

    2009-08-01

    Almond anthracnose was reported for the first time in Australia in 1998 and has since been observed in all of the major almond-growing regions. The organism causing anthracnose was confirmed as Colletotrichum acutatum using taxon-specific polymerase chain reaction (PCR). Three main morphotypes of C. acutatum from almond in Australia were identified (namely, pink, orange, and cream colony color) and the optimum temperature for mycelial growth of representative isolates was 25 degrees C. Australian isolates of C. acutatum were more similar morphologically to the pink subpopulation of C. acutatum from California than to the gray Californian subpopulation and the isolates of Colletotrichum from Israel. Inter-simple-sequence-repeat (ISSR) PCR analysis revealed that the majority of Australian isolates shared an identical banding pattern whereas Australian isolates of C. acutatum from almond were distinct from isolates of the pink and gray subpopulations of C. acutatum from almond in California and of Colletotrichum spp. from almond in Israel. Sequence analysis of the internally transcribed spacer (ITS1-2) ribosomal DNA region of representative isolates differed from the results of ISSR-PCR in that polymorphisms were revealed among isolates, indicating that some genetic variation may be present. Pathogenicity experiments on detached leaves and fruit revealed pathogenic variation among representative isolates of C. acutatum from almond in Australia, California, and Israel; however, all isolates tested caused disease. Distinct subgroups among Australian isolates of C. acutatum from almond were not supported on the basis of morphology, mycelial growth rates, ISSR-PCR, and pathogenicity. PMID:19594318

  1. Foliar Application of Extract from an Azalomycin-Producing Streptomyces malaysiensis Strain MJM1968 Suppresses Yam Anthracnose Caused by Colletotrichum gloeosporioides.

    PubMed

    Arunachalam Palaniyandi, Sasikumar; Yang, Seung Hwan; Suh, Joo-Woh

    2016-06-28

    Yam anthracnose caused by Colletotrichum gloeosporioides (C.g) is the most devastating disease of yam (Dioscorea sp.). In the present study, we evaluated the culture filtrate extract (CFE) of azalomycin-producing Streptomyces malaysiensis strain MJM1968 for the control of yam anthracnose. MJM1968 showed strong antagonistic activity against C.g in vitro. Furthermore, the MJM1968 CFE was tested for inhibition of spore germination in C.g, where it completely inhibited spore germination at a concentration of 50 μg/ml. To assess the in planta efficacy of the CFE and spores of MJM1968 against C.g, a detached leaf bioassay was conducted, which showed both the treatments suppressed anthracnose development on detached yam leaves. Furthermore, a greenhouse study was conducted to evaluate the CFE from MJM1968 as a fungicide for the control of yam anthracnose. The CFE non-treated plants showed a disease severity of >92% after 90 days of artificial inoculation with C.g, whereas the disease severity of CFE-treated and benomyl-treated yam plants was reduced to 26% and 15%, respectively, after 90 days. Analysis of the yam tubers from the CFE-treated and non-treated groups showed that tubers from the CFE-treated plants were larger than that of non-treated plants, which produced abnormal smaller tubers typical of anthracnose. This study demonstrated the utility of the CFE from S. malaysiensis strain MJM1968 as a biofungicide for the control of yam anthracnose. PMID:26975770

  2. Application of silver nanoparticles for the control of colletotrichum species in vitro and pepper anthracnose disease in field.

    PubMed

    Lamsal, Kabir; Kim, Sang Woo; Jung, Jin Hee; Kim, Yun Seok; Kim, Kyong Su; Lee, Youn Su

    2011-09-01

    Pepper anthracnose caused by Colletotrichum species is one of the most important limiting factors for pepper production in Korea, its management being strongly dependent on chemicals. The aim of this work was to evaluate the possibilities of using silver nanoparticles instead of commercial fungicides. In this study, we evaluated the effect of silver nanoparticles against pepper anthracnose under different culture conditions. Silver nanoparticles (WA-PR-WB13R) were applied at various concentrations to determine antifungal activities in vitro and in the field. The application of 100 ppm concentration of silver nanoparticles produced maximum inhibition of the growth of fungal hyphae as well as conidial germination in comparison to the control in vitro. In field trials, the inhibition of fungi was significantly high when silver nanoparticles were applied before disease outbreak on the plants. Scanning electron microscopy results indicated that the silver nanoparticles caused a detrimental effect on mycelial growth of Colletotrichum species. PMID:22783103

  3. Molecular and phenotypic characterization of Colletotrichum species associated with anthracnose disease in peppers from Sichuan Province, China

    PubMed Central

    Liu, Fangling; Tang, Guiting; Zheng, Xiaojuan; Li, Ying; Sun, Xiaofang; Qi, Xiaobo; Zhou, You; Xu, Jing; Chen, Huabao; Chang, Xiaoli; Zhang, Sirong; Gong, Guoshu

    2016-01-01

    The anthracnose caused by Colletotrichum species is an important disease that primarily causes fruit rot in pepper. Eighty-eight strains representing seven species of Colletotrichum were obtained from rotten pepper fruits in Sichuan Province, China, and characterized according to morphology and the glyceraldehyde-3-phosphate dehydrogenase (GAPDH) sequence. Fifty-two strains were chosen for identification by phylogenetic analyses of multi-locus sequences, including the nuclear ribosomal internal transcribed spacer (ITS) region and the β-tubulin (TUB2), actin (ACT), calmodulin (CAL) and GAPDH genes. Based on the combined datasets, the 88 strains were identified as Colletotrichum gloeosporioides, C. siamense, C. fructicola, C. truncatum, C. scovillei, and C. brevisporum, and one new species was detected, described as Colletotrichum sichuanensis. Notably, C. siamense and C. scovillei were recorded for the first time as the causes of anthracnose in peppers in China. In addition, with the exception of C. truncatum, this is the first report of all of the other Colletotrichum species studied in pepper from Sichuan. The fungal species were all non-host-specific, as the isolates were able to infect not only Capsicum spp. but also Pyrus pyrifolia in pathogenicity tests. These findings suggest that the fungal species associated with anthracnose in pepper may inoculate other hosts as initial inoculum. PMID:27609555

  4. Molecular and phenotypic characterization of Colletotrichum species associated with anthracnose disease in peppers from Sichuan Province, China.

    PubMed

    Liu, Fangling; Tang, Guiting; Zheng, Xiaojuan; Li, Ying; Sun, Xiaofang; Qi, Xiaobo; Zhou, You; Xu, Jing; Chen, Huabao; Chang, Xiaoli; Zhang, Sirong; Gong, Guoshu

    2016-01-01

    The anthracnose caused by Colletotrichum species is an important disease that primarily causes fruit rot in pepper. Eighty-eight strains representing seven species of Colletotrichum were obtained from rotten pepper fruits in Sichuan Province, China, and characterized according to morphology and the glyceraldehyde-3-phosphate dehydrogenase (GAPDH) sequence. Fifty-two strains were chosen for identification by phylogenetic analyses of multi-locus sequences, including the nuclear ribosomal internal transcribed spacer (ITS) region and the β-tubulin (TUB2), actin (ACT), calmodulin (CAL) and GAPDH genes. Based on the combined datasets, the 88 strains were identified as Colletotrichum gloeosporioides, C. siamense, C. fructicola, C. truncatum, C. scovillei, and C. brevisporum, and one new species was detected, described as Colletotrichum sichuanensis. Notably, C. siamense and C. scovillei were recorded for the first time as the causes of anthracnose in peppers in China. In addition, with the exception of C. truncatum, this is the first report of all of the other Colletotrichum species studied in pepper from Sichuan. The fungal species were all non-host-specific, as the isolates were able to infect not only Capsicum spp. but also Pyrus pyrifolia in pathogenicity tests. These findings suggest that the fungal species associated with anthracnose in pepper may inoculate other hosts as initial inoculum. PMID:27609555

  5. Screening strawberry (Fragria x ananassa) germplasm for anthracnose disease resistance using traditional techniques and molecular makers

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Anthracnose of strawberry may be caused by any of three Colletotrichum species: C. acutatum, C. gloeosporioides or C. fragariae. These destructive pathogens may infect the fruit, leaves, petioles, crowns or roots and may cause plant death. Traditional and molecular approaches were used to identify a...

  6. The potential of a fluorescent-based approach for bioassay of antifungal agents against chili anthracnose disease in Thailand.

    PubMed

    Chutrakul, Chanikul; Khaokhajorn, Pratoomporn; Auncharoen, Patchanee; Boonruengprapa, Tanapong; Mongkolporn, Orarat

    2013-01-01

    Severe chili anthracnose disease in Thailand is caused by Colletotrichum gloeosporioides and C. capsici. To discover anti-anthracnose substances we developed an efficient dual-fluorescent labeling bioassay based on a microdilution approach. Indicator strains used in the assay were constructed by integrating synthetic green fluorescent protein (sGFP) and Discosoma sp. red fluorescent protein (DsRedExp) genes into the genomes of C. gloeosporioides or C. capsici respectively. Survival of co-spore cultures in the presence of inhibitors was determined by the expression levels of these fluorescent proteins. This developed assay has high potential for utilization in the investigation of selective inhibition activity to either one of the pathogens as well as the broad-range inhibitory effect against both pathogens. The value of using the dual-fluorescent assay is rapid, reliable, and consistent identification of anti-anthracnose agents. Most of all, the assay enables the identification of specific inhibitors under the co-cultivation condition. PMID:23391904

  7. Identification of actinomycetes from plant rhizospheric soils with inhibitory activity against Colletotrichum spp., the causative agent of anthracnose disease

    PubMed Central

    2011-01-01

    Background Colletotrichum is one of the most widespread and important genus of plant pathogenic fungi worldwide. Various species of Colletotrichum are the causative agents of anthracnose disease in plants, which is a severe problem to agricultural crops particularly in Thailand. These phytopathogens are usually controlled using chemicals; however, the use of these agents can lead to environmental pollution. Potential non-chemical control strategies for anthracnose disease include the use of bacteria capable of producing anti-fungal compounds such as actinomycetes spp., that comprise a large group of filamentous, Gram positive bacteria from soil. The aim of this study was to isolate actinomycetes capable of inhibiting the growth of Colletotrichum spp, and to analyze the diversity of actinomycetes from plant rhizospheric soil. Results A total of 304 actinomycetes were isolated and tested for their inhibitory activity against Colletotrichum gloeosporioides strains DoA d0762 and DoA c1060 and Colletotrichum capsici strain DoA c1511 which cause anthracnose disease as well as the non-pathogenic Saccharomyces cerevisiae strain IFO 10217. Most isolates (222 out of 304, 73.0%) were active against at least one indicator fungus or yeast. Fifty four (17.8%) were active against three anthracnose fungi and 17 (5.6%) could inhibit the growth of all three fungi and S. cerevisiae used in the test. Detailed analysis on 30 selected isolates from an orchard at Chanthaburi using the comparison of 16S rRNA gene sequences revealed that most of the isolates (87%) belong to the genus Streptomyces sp., while one each belongs to Saccharopolyspora (strain SB-2) and Nocardiopsis (strain CM-2) and two to Nocardia (strains BP-3 and LK-1). Strains LC-1, LC-4, JF-1, SC-1 and MG-1 exerted high inhibitory activity against all three anthracnose fungi and yeast. In addition, the organic solvent extracts prepared from these five strains inhibited conidial growth of the three indicator fungi

  8. Diagnosis of centipedegrass anthracnose caused by Colletotrichum eremochloae sp. nov.

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Centipedegrass (Eremochloa ophiuroides) is a medium-textured, stoloniferous warm-season turfgrass used as home lawn and utility turf. It is well-adapted to a wide range of soil conditions but grows best in sandy, acidic soils of low fertility and can withstand some shade. Diseases arise when centip...

  9. Anthracnose of lucky bamboo Dracaena sanderiana caused by the fungus Colletotrichum dracaenophilum in Egypt.

    PubMed

    Morsy, Ahmed A; Elshahawy, Ibrahim E

    2016-05-01

    Dracaena sanderiana, of the family Liliaceae, is among the ornamental plants most frequently imported into Egypt. Typical anthracnose symptoms were observed on the stems of imported D. sanderiana samples. The pathogen was isolated, demonstrated to be pathogenic based on Koch's rule and identified as Colletotrichum dracaenophilum. The optimum temperature for its growth ranges from 25 to 30 °C, maintained for 8 days. Kemazed 50% wettable powder (WP) was the most effective fungicide against the pathogen, as no fungal growth was observed over 100 ppm. The biocontrol agents Trichoderma harzianum and Trichoderma viride followed by Bacillus subtilis and Bacillus pumilus caused the highest reduction in fungal growth. To the best of our knowledge, this report describes the first time that this pathogen was observed on D. sanderiana in Egypt. PMID:27222738

  10. Anthracnose of lucky bamboo Dracaena sanderiana caused by the fungus Colletotrichum dracaenophilum in Egypt

    PubMed Central

    Morsy, Ahmed A.; Elshahawy, Ibrahim E.

    2016-01-01

    Dracaena sanderiana, of the family Liliaceae, is among the ornamental plants most frequently imported into Egypt. Typical anthracnose symptoms were observed on the stems of imported D. sanderiana samples. The pathogen was isolated, demonstrated to be pathogenic based on Koch’s rule and identified as Colletotrichum dracaenophilum. The optimum temperature for its growth ranges from 25 to 30 °C, maintained for 8 days. Kemazed 50% wettable powder (WP) was the most effective fungicide against the pathogen, as no fungal growth was observed over 100 ppm. The biocontrol agents Trichoderma harzianum and Trichoderma viride followed by Bacillus subtilis and Bacillus pumilus caused the highest reduction in fungal growth. To the best of our knowledge, this report describes the first time that this pathogen was observed on D. sanderiana in Egypt. PMID:27222738

  11. Involvement of miR160/miR393 and their targets in cassava responses to anthracnose disease.

    PubMed

    Pinweha, Nattaya; Asvarak, Thipa; Viboonjun, Unchera; Narangajavana, Jarunya

    2015-02-01

    Cassava is a starchy root crop for food and industrial applications in many countries around the world. Among the factors that affect cassava production, diseases remain the major cause of yield loss. Cassava anthracnose disease is caused by the fungus Colletotrichum gloeosporioides. Severe anthracnose attacks can cause tip die-backs and stem cankers, which can affect the availability of planting materials especially in large-scale production systems. Recent studies indicate that plants over- or under-express certain microRNAs (miRNAs) to cope with various stresses. Understanding how a disease-resistant plant protects itself from pathogens should help to uncover the role of miRNAs in the plant immune system. In this study, the disease severity assay revealed different response to C. gloeosporioides infection in two cassava cultivars. Quantitative RT-PCR analysis uncovered the differential expression of the two miRNAs and their target genes in the two cassava cultivars that were subjected to fungal infection. The more resistant cultivar revealed the up-regulation of miR160 and miR393, and consequently led to low transcript levels in their targets, ARF10 and TIR1, respectively. The more susceptible cultivar exhibited the opposite pattern. The cis-regulatory elements relevant to defense and stress responsiveness, fungal elicitor responsiveness and hormonal responses were the most prevalent present in the miRNAs gene promoter regions. The possible dual role of these specific miRNAs and their target genes associated with cassava responses to C. gloeosporioides is discussed. This is the first study to address the molecular events by which miRNAs which might play a role in fungal-infected cassava. A better understanding of the functions of miRNAs target genes should greatly increase our knowledge of the mechanism underlying susceptibility and lead to new strategies to enhance disease tolerance in this economically important crop. PMID:25462963

  12. Sequencing of an Anthracnose-resistant sorghum genotype and mapping of a major QTL reveal strong candidate genes for Anthracnose resistance

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Anthracnose, caused by the fungal pathogen Colletotrichum sublineolum Henn. ex. Sacc. and Trotter 1913, is an economically damaging disease of sorghum [Sorghum bicolor (L.) Moench] in hot and humid production regions of the world. Control of anthracnose is almost exclusively through the use of genet...

  13. Anthracnose of centipedegrass turf

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Anthracnose is a destructive fungal disease of centipedegrass (Eremochloae ophiuroides) turf that occurs throughout the southern United States and China. In this diagnostic guide, we provide an overview of the causal pathogen, Colletotrichum eremochloae, along with disease symptoms and signs, host ...

  14. Colletotrichum species associated with jute (Corchorus capsularis L.) anthracnose in southeastern China

    PubMed Central

    Niu, Xiaoping; Gao, Hong; Qi, Jianmin; Chen, Miancai; Tao, Aifen; Xu, Jiantang; Dai, Zhigang; Su, Jianguang

    2016-01-01

    Anthracnose, caused by the Colletotrichum species of fungi, is one of the most serious diseases affecting jute in China. The disease causes chlorotic regions with black brown sunken necrotic pits on the surfaces of stems. In late stages of disease, plants undergo defoliation, dieback and blight, which make anthracnose a major threat to jute fiber production and quality in China. In this study, 7 strains of Colletotrichum fungi were isolated from diseased jute stems from Zhejiang, Fujian, Guangxi, and Henan plantations in China. Multi-locus sequence (ACT, TUB2, CAL, GS, GAPDH and ITS) analysis coupled with morphological assessment revealed that C. fructicola, C. siamense and C. corchorum-capsularis sp. nov. were associated with jute anthracnose in southeastern China. C. fructicola and C. siamense were previously not associated with jute anthracnose. C. corchorum-capsularis is a new species formally described here. Pathogenicity tests confirmed that all species can infect jute, causing anthracnose, however the virulence of the 3 species differed. This report is the first associating these three species with jute disease worldwide and is the first description of the pathogens responsible for jute anthracnose in China. PMID:27121760

  15. Colletotrichum species associated with jute (Corchorus capsularis L.) anthracnose in southeastern China.

    PubMed

    Niu, Xiaoping; Gao, Hong; Qi, Jianmin; Chen, Miancai; Tao, Aifen; Xu, Jiantang; Dai, Zhigang; Su, Jianguang

    2016-01-01

    Anthracnose, caused by the Colletotrichum species of fungi, is one of the most serious diseases affecting jute in China. The disease causes chlorotic regions with black brown sunken necrotic pits on the surfaces of stems. In late stages of disease, plants undergo defoliation, dieback and blight, which make anthracnose a major threat to jute fiber production and quality in China. In this study, 7 strains of Colletotrichum fungi were isolated from diseased jute stems from Zhejiang, Fujian, Guangxi, and Henan plantations in China. Multi-locus sequence (ACT, TUB2, CAL, GS, GAPDH and ITS) analysis coupled with morphological assessment revealed that C. fructicola, C. siamense and C. corchorum-capsularis sp. nov. were associated with jute anthracnose in southeastern China. C. fructicola and C. siamense were previously not associated with jute anthracnose. C. corchorum-capsularis is a new species formally described here. Pathogenicity tests confirmed that all species can infect jute, causing anthracnose, however the virulence of the 3 species differed. This report is the first associating these three species with jute disease worldwide and is the first description of the pathogens responsible for jute anthracnose in China. PMID:27121760

  16. Species of the Colletotrichum acutatum complex associated with anthracnose diseases of fruit in Brazil.

    PubMed

    Bragança, Carlos A D; Damm, Ulrike; Baroncelli, Riccardo; Massola Júnior, Nelson S; Crous, Pedro W

    2016-04-01

    Although Colletotrichum acutatum was recently investigated and shown to be a species complex comprising about 30 species, the name is still used in its broad sense for anthracnose pathogens of fruits in Brazil. In this study, a multilocus molecular analysis was carried out based on a dataset of ITS, HIS3, GAPDH, CHS-1, TUB2 and ACT sequences of Colletotrichum strains belonging to the C. acutatum species complex from fruits collected in different regions in Brazil combined with sequences of ex-type and other reference strains of species belonging to this complex. The strains were revealed to belong to Colletotrichum nymphaeae, Colletotrichum melonis, Colletotrichum abscissum and one new species, namely Colletotrichum paranaense, from apple and peach. Morphological descriptions of the new species and a strain closely related to but diverging from C. melonis are provided. From the data presently available, the most common species on apple fruits in Brazil is C. nymphaeae. In a pathogenicity test, strains of all four species caused lesions on detached apple, peach and guava fruits, except for strain CBS 134730 that did not infect guava fruits. PMID:27020156

  17. Nitrogen Fertilizer Affects the Severity of Anthracnose Crown Rot Disease of Greenhouse Grown Strawberries

    Technology Transfer Automated Retrieval System (TEKTRAN)

    The influence of nitrogen, phosphorus, and potassium on the severity of anthracnose crown rot was evaluated in three greenhouse studies. Strawberry plants were fertilized three times weekly with a modified Hoagland's Nutrient Solution containing the treatments and inoculated eight weeks after treat...

  18. Differential resistances to anthracnose in Capsicum baccatum as responding to two Colletotrichum pathotypes and inoculation methods

    PubMed Central

    Mahasuk, Pitchayapa; Chinthaisong, Jittima; Mongkolporn, Orarat

    2013-01-01

    Chili anthracnose, caused by Colletotrichum spp., is one of the major diseases to chili production in the tropics and subtropics worldwide. Breeding for durable anthracnose resistance requires a good understanding of the resistance mechanisms to different pathotypes and inoculation methods. This study aimed to investigate the inheritances of differential resistances as responding to two different Colletotrichum pathotypes, PCa2 and PCa3 and as by two different inoculation methods, microinjection (MI) and high pressure spray (HP). Detached ripe fruit of Capsicum baccatum ‘PBC80’ derived F2 and BC1s populations was assessed for anthracnose resistance. Two dominant genes were identified responsible for the differential resistance to anthracnose. One was responsible for the resistance to PCa2 and PCa3 by MI and the other was responsible for the resistance to PCa3 by HP. The two genes were linked with 16.7 cM distance. PMID:24273429

  19. Differential resistances to anthracnose in Capsicum baccatum as responding to two Colletotrichum pathotypes and inoculation methods.

    PubMed

    Mahasuk, Pitchayapa; Chinthaisong, Jittima; Mongkolporn, Orarat

    2013-09-01

    Chili anthracnose, caused by Colletotrichum spp., is one of the major diseases to chili production in the tropics and subtropics worldwide. Breeding for durable anthracnose resistance requires a good understanding of the resistance mechanisms to different pathotypes and inoculation methods. This study aimed to investigate the inheritances of differential resistances as responding to two different Colletotrichum pathotypes, PCa2 and PCa3 and as by two different inoculation methods, microinjection (MI) and high pressure spray (HP). Detached ripe fruit of Capsicum baccatum 'PBC80' derived F2 and BC1s populations was assessed for anthracnose resistance. Two dominant genes were identified responsible for the differential resistance to anthracnose. One was responsible for the resistance to PCa2 and PCa3 by MI and the other was responsible for the resistance to PCa3 by HP. The two genes were linked with 16.7 cM distance. PMID:24273429

  20. Co-segregation analysis and mapping of the anthracnose Co-10 and angular leaf spot Phg-ON disease resistance genes in common bean cultivar Ouro Negro

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Anthracnose (ANT) and angular leaf spot (ALS) are devastating diseases of common bean. Ouro Negro is a highly productive Mesoamerican black-seeded common bean cultivar possessing the dominant Co-10 and Phg-ON genes that confer resistance to ANT and ALS, respectively. In this study we elucidate the ...

  1. Sorghum germplasm resistance to anthracnose

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Anthracnose is one of the most damaging diseases for sorghum production. The disease can be successfully managed through the use of resistant cultivars, but the development of resistant cultivars is hindered by extensive variation in virulence within the pathogen population. Additional sources of ...

  2. Strawberry Anthracnose: Cultural Control Options

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Colletotrichum species incite serious diseases of many fruit and vegetable crops worldwide, and three species, C. acutatum, C. fragariae, and C. gloeosporioides, are major pathogens of strawberry. Strawberry anthracnose crown rot has been a destructive disease in strawberry nurseries and fruit prod...

  3. First report of leaf anthracnose caused by Phomopsis convolvuli on field bindweed in turkey

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Field bindweed (Convolvulus arvensis L., Convolvulaceae) is a troublesome perennial weed in many important crops in the world. In May of 2007, dying field bindweed plants were found along the edge of a wheat field between Bafra and Taflan, Turkey. Disease lesions on leaves were irregular and varia...

  4. Molecular mapping of Cg1, a gene for resistance to anthracnose (Colletotrichum sublineolum) in sorghum

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Anthracnose, caused by the fungus Colletotrichum sublineolum is one of the most destructive diseases of sorghum and has been reported in most areas where the crop is grown. Several control strategies have been developed but host plant resistance has been regarded as the most effective strategy for ...

  5. Phenotypic and molecular characterization of Colletotrichum species associated with anthracnose of banana (Musa spp) in Malaysia.

    PubMed

    Intan Sakinah, M A; Suzianti, I V; Latiffah, Z

    2014-01-01

    Anthracnose caused by Colletotrichum species is a common postharvest disease of banana fruit. We investigated and identified Colletotrichum species associated with anthracnose in several local banana cultivars based on morphological characteristics and sequencing of ITS regions and of the β-tubulin gene. Thirty-eight Colletotrichum isolates were encountered in anthracnose lesions of five local banana cultivars, 'berangan', 'mas', 'awak', 'rastali', and 'nangka'. Based on morphological characteristics, 32 isolates were identified as Colletotrichum gloeosporioides and 6 isolates as C. musae. C. gloeosporioides isolates were divided into two morphotypes, with differences in colony color, shape of the conidia and growth rate. Based on ITS regions and β-tubulin sequences, 35 of the isolates were identified as C. gloeosporioides and only 3 isolates as C. musae; the percentage of similarity from BLAST ranged from 95-100% for ITS regions and 97-100% for β-tubulin. C. gloeosporioides isolates were more prevalent compared to C. musae. This is the first record of C. gloeosporioides associated with banana anthracnose in Malaysia. In a phylogenetic analysis of the combined dataset of ITS regions and β-tubulin using a maximum likelihood method, C. gloeosporioides and C. musae isolates were clearly separated into two groups. We concluded that C. gloeosporioides and C. musae isolates are associated with anthracnose in the local banana cultivars and that C. gloeosporioides is more prevalent than C. musae. PMID:24854442

  6. Development and optimization of sequence-tagged microsatellite site markers to detect genetic diversity within Colletotrichum capsici, a causal agent of chilli pepper anthracnose disease.

    PubMed

    Ranathunge, N P; Ford, R; Taylor, P W J

    2009-07-01

    Genomic libraries enriched for microsatellites from Colletotrichum capsici, one of the major causal agents of anthracnose disease in chilli pepper (Capsicum spp.), were developed using a modified hybridization procedure. Twenty-seven robust primer pairs were designed from microsatellite flanking sequences and were characterized using 52 isolates from three countries India, Sri Lanka and Thailand. Highest gene diversity of 0.857 was observed at the CCSSR1 with up to 18 alleles among all the isolates whereas the differentiation ranged from 0.05 to 0.45. The sequence-tagged microsatellite site markers developed in this study will be useful for genetic analyses of C. capsici populations. PMID:21564867

  7. Characterization of Glomerella strains recovered from anthracnose lesions on common bean plants in Brazil.

    PubMed

    Barcelos, Quélen L; Pinto, Joyce M A; Vaillancourt, Lisa J; Souza, Elaine A

    2014-01-01

    Anthracnose caused by Colletotrichum lindemuthianum is an important disease of common bean, resulting in major economic losses worldwide. Genetic diversity of the C. lindemuthianum population contributes to its ability to adapt rapidly to new sources of host resistance. The origin of this diversity is unknown, but sexual recombination, via the Glomerella teleomorph, is one possibility. This study tested the hypothesis that Glomerella strains that are frequently recovered from bean anthracnose lesions represent the teleomorph of C. lindemuthianum. A large collection of Glomerella isolates could be separated into two groups based on phylogenetic analysis, morphology, and pathogenicity to beans. Both groups were unrelated to C. lindemuthianum. One group clustered with the C. gloeosporioides species complex and produced mild symptoms on bean tissues. The other group, which belonged to a clade that included the cucurbit anthracnose pathogen C. magna, caused no symptoms. Individual ascospores recovered from Glomerella perithecia gave rise to either fertile (perithecial) or infertile (conidial) colonies. Some pairings of perithecial and conidial strains resulted in induced homothallism in the conidial partner, while others led to apparent heterothallic matings. Pairings involving two perithecial, or two conidial, colonies produced neither outcome. Conidia efficiently formed conidial anastomosis tubes (CATs), but ascospores never formed CATs. The Glomerella strains formed appressoria and hyphae on the plant surface, but did not penetrate or form infection structures within the tissues. Their behavior was similar whether the beans were susceptible or resistant to anthracnose. These same Glomerella strains produced thick intracellular hyphae, and eventually acervuli, if host cell death was induced. When Glomerella was co-inoculated with C. lindemuthianum, it readily invaded anthracnose lesions. Thus, the hypothesis was not supported: Glomerella strains from anthracnose

  8. Characterization of Glomerella Strains Recovered from Anthracnose Lesions on Common Bean Plants in Brazil

    PubMed Central

    Barcelos, Quélen L.; Pinto, Joyce M. A.; Vaillancourt, Lisa J.; Souza, Elaine A.

    2014-01-01

    Anthracnose caused by Colletotrichum lindemuthianum is an important disease of common bean, resulting in major economic losses worldwide. Genetic diversity of the C. lindemuthianum population contributes to its ability to adapt rapidly to new sources of host resistance. The origin of this diversity is unknown, but sexual recombination, via the Glomerella teleomorph, is one possibility. This study tested the hypothesis that Glomerella strains that are frequently recovered from bean anthracnose lesions represent the teleomorph of C. lindemuthianum. A large collection of Glomerella isolates could be separated into two groups based on phylogenetic analysis, morphology, and pathogenicity to beans. Both groups were unrelated to C. lindemuthianum. One group clustered with the C. gloeosporioides species complex and produced mild symptoms on bean tissues. The other group, which belonged to a clade that included the cucurbit anthracnose pathogen C. magna, caused no symptoms. Individual ascospores recovered from Glomerella perithecia gave rise to either fertile (perithecial) or infertile (conidial) colonies. Some pairings of perithecial and conidial strains resulted in induced homothallism in the conidial partner, while others led to apparent heterothallic matings. Pairings involving two perithecial, or two conidial, colonies produced neither outcome. Conidia efficiently formed conidial anastomosis tubes (CATs), but ascospores never formed CATs. The Glomerella strains formed appressoria and hyphae on the plant surface, but did not penetrate or form infection structures within the tissues. Their behavior was similar whether the beans were susceptible or resistant to anthracnose. These same Glomerella strains produced thick intracellular hyphae, and eventually acervuli, if host cell death was induced. When Glomerella was co-inoculated with C. lindemuthianum, it readily invaded anthracnose lesions. Thus, the hypothesis was not supported: Glomerella strains from anthracnose

  9. Biological Control of Apple Anthracnose by Paenibacillus polymyxa APEC128, an Antagonistic Rhizobacterium

    PubMed Central

    Kim, Young Soo; Balaraju, Kotnala; Jeon, Yongho

    2016-01-01

    The present study investigated the suppression of the disease development of anthracnose caused by Colletotrichum gloeosporioides and C. acutatum in harvested apples using an antagonistic rhizobacterium Paenibacillus polymyxa APEC128 (APEC128). Out of 30 bacterial isolates from apple rhizosphere screened for antagonistic activity, the most effective strain was APEC128 as inferred from the size of the inhibition zone. This strain showed a greater growth in brain-heart infusion (BHI) broth compared to other growth media. There was a reduction in anthracnose symptoms caused by the two fungal pathogens in harvested apples after their treatment with APEC128 in comparison with non-treated control. This effect is explained by the increased production of protease and amylase by APEC128, which might have inhibited mycelial growth. In apples treated with different APEC128 suspensions, the disease caused by C. gloeosporioides and C. acutatum was greatly suppressed (by 83.6% and 79%, respectively) in treatments with the concentration of 1 × 108 colony forming units (cfu)/ml compared to other lower dosages, suggesting that the suppression of anthracnose development on harvested apples is dose-dependent. These results indicated that APEC128 is one of the promising agents in the biocontrol of apple anthracnose, which might help to increase the shelf-life of apple fruit during the post-harvest period. PMID:27298600

  10. Biological Control of Apple Anthracnose by Paenibacillus polymyxa APEC128, an Antagonistic Rhizobacterium.

    PubMed

    Kim, Young Soo; Balaraju, Kotnala; Jeon, Yongho

    2016-06-01

    The present study investigated the suppression of the disease development of anthracnose caused by Colletotrichum gloeosporioides and C. acutatum in harvested apples using an antagonistic rhizobacterium Paenibacillus polymyxa APEC128 (APEC128). Out of 30 bacterial isolates from apple rhizosphere screened for antagonistic activity, the most effective strain was APEC128 as inferred from the size of the inhibition zone. This strain showed a greater growth in brain-heart infusion (BHI) broth compared to other growth media. There was a reduction in anthracnose symptoms caused by the two fungal pathogens in harvested apples after their treatment with APEC128 in comparison with non-treated control. This effect is explained by the increased production of protease and amylase by APEC128, which might have inhibited mycelial growth. In apples treated with different APEC128 suspensions, the disease caused by C. gloeosporioides and C. acutatum was greatly suppressed (by 83.6% and 79%, respectively) in treatments with the concentration of 1 × 10(8) colony forming units (cfu)/ml compared to other lower dosages, suggesting that the suppression of anthracnose development on harvested apples is dose-dependent. These results indicated that APEC128 is one of the promising agents in the biocontrol of apple anthracnose, which might help to increase the shelf-life of apple fruit during the post-harvest period. PMID:27298600

  11. Field assessment of anthracnose disease response for the sorghum germplasm collection from the Mopti region of Mali

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Sorghum anthracnose (Colletotrichum sublineolum) is a highly variable pathogen and new sources of host plant resistance are required for the development of resistant sorghum varieties. Germplasm collections are an important source of host plant resistance and screening germplasm will be essential t...

  12. Field evaluation of foliar anthracnose disease response for sorghum germplasm from the Matabeleland North Province of Zimbabwe

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Anthracnose occurs in most sorghum producing regions worldwide and the pathogen is highly variable; thus, additional sources of resistance are needed for sorghum improvement. To identify resistant sources, 41 sorghum accessions from the Matabeleland North Province of Zimbabwe were evaluated for fol...

  13. Field evaluation of anthracnose disease response for the sorghum germplasm collection from the Kayes region of Mali

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Sorghum germplasm from the Kayes region of Mali maintained in the USDA, ARS National Plant Germplasm System was inoculated with Colletotrichum sublineolum and evaluated for foliar anthracnose resistance in 2003 and 2004 at the USDA, ARS Tropical Agriculture Research Station in Isabela, Puerto Rico. ...

  14. [Does vaccination cause disease?].

    PubMed

    Zingg, W

    2005-10-01

    Not many inventions in medical history have influenced our society as much as vaccination. The concept is old and simple. When Edward Jenner published his work on cowpox, "variolation" was quite common. In this procedure, pus of patients with mild smallpox was transferred to healthy individuals. Meanwhile smallpox has been eradicated worldwide. Diseases such as poliomyelitis, diphtheria or tetanus almost disappeared in industrialized countries. The same happened with epiglottitis and meningitis due to Haemophilus influenzae type b (Hib) after vaccination against Hib was introduced in Switzerland in 1990. This success was possible because of routine vaccination. Immunization is a save procedure and adverse events are much lower than complications in the natural course of the prevented diseases. However vaccinations were accused to cause diseases themselves such as asthma, multiple sclerosis, diabetes mellitus, chronic arthritis or autism. Hitherto no large cohort study or case-control-study was able to proof responsibility of vaccines in any of these diseases. Public media are eager to publish early data from surveillance reports or case reports which are descriptive and never a principle of cause and effect. In large controlled trials there was no proof that vaccination causes asthma, hepatitis-B-vaccination causes multiple sclerosis or macrophagic myofasciitis, Hib-vaccination causes diabetes mellitus, rubella-vaccination causes chronic arthritis, measles-mumps-rubella-vaccination causes gait disturbance or thiomersal causes autism. These results are rarely published in newspapers or television. Thus, many caring parents are left with negative ideas about immunization. Looking for the best for their children they withhold vaccination and give way to resurgence of preventable diseases in our communities. This must be prevented. There is more evidence than expected that vaccination is safe and this can and must be told to parents. PMID:16277033

  15. AnthracnoseTracer: A Spatiotemporal Model for Simulating the Spread of Anthracnose in a Lupin Field.

    PubMed

    Diggle, A J; Salam, M U; Thomas, G J; Yang, H A; O'Connell, M; Sweetingham, M W

    2002-10-01

    ABSTRACT A spatiotemporal model has been developed to simulate the spread of anthracnose, initiated by infected seed, in a lupin field. The model quantifies the loss of healthy growing points of lupin in all 1-m(2) subunits of a field throughout a growing season. The development of growing points is modeled as a function of temperature using a 1-day time step, and disease-induced compensatory growth is accounted for. Dispersal of spores is simulated explicitly using Monte Carlo techniques. Spread of spores occurs during rainfall events on a 1-h time step. The distance traveled by spores is partially dependent on wind speed and is generated by adding the values selected from half-Cauchy distributions. The direction of travel of the spores is influenced by wind direction. The model has been employed to produce a theoretical assessment of damage from disease in two environments at five levels of seed infection. It was calculated that in a susceptible lupin cultivar with a 0.01% initial seed infection, anthracnose would cause approximately 15% loss of healthy growing points in a high rainfall environment in Western Australia. In a low rainfall environment, similar damage would be unlikely even with a much higher (1%) level of seed infection. PMID:18944222

  16. What Causes Coronary Microvascular Disease?

    MedlinePlus

    ... Living With Clinical Trials Links Related Topics Angina Atherosclerosis Coronary Heart Disease Coronary Heart Disease Risk Factors ... Microvascular Disease? The same risk factors that cause atherosclerosis may cause coronary microvascular disease. Atherosclerosis is a ...

  17. Particles causing lung disease.

    PubMed Central

    Kilburn, K H

    1984-01-01

    The lung has a limited number of patterns of reaction to inhaled particles. The disease observed depends upon the location: conducting airways, terminal bronchioles and alveoli, and upon the nature of inflammation induced: acute, subacute or chronic. Many different agents cause narrowing of conducting airways (asthma) and some of these cause permanent distortion or obliteration of airways as well. Terminal bronchioles appear to be particularly susceptible to particles which cause goblet cell metaplasia, mucous plugging and ultimately peribronchiolar fibrosis. Cancer is the last outcome at the bronchial level and appears to depend upon continuous exposure to or retention of an agent in the airway and failure of the affected cells to be exfoliated which may be due to squamous metaplasia. Alveoli are populated by endothelial cells, Type I or pavement epithelial cells and metabolically active cuboidal Type II cells that produce the lungs specific surfactant, dipalmytol lecithin. Disturbances of surfactant lead to edema in distal lung while laryngeal edema due to anaphylaxis or fumes may produce asphyxia. Physical retention of indigestible particles or retention by immune memory responses may provoke hyaline membranes, stimulate alveolar lipoproteinosis and finally fibrosis. This later exuberant deposition of connective tissue has been best studied in the occupational pneumoconioses especially silicosis and asbestosis. In contrast emphysema a catabolic response, appears frequently to result from leakage or release of lysosomal proteases into the lung during processing of cigarette smoke particles. The insidious and probably most important human lung disease due to particles is bronchiolar obstruction and obliteration, producing progressive impairment of air flow. The responsible particle is the complex combination of poorly digestive lipids and complex carbohydrates with active chemicals which we call cigarette smoke. More research is needed to perfect, correct and

  18. Biology and pathology of turfgrass anthracnose

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Anthracnose is a destructive fungal disease of weakened turf that occurs throughout the United States, Canada, and Western Europe and is particularly severe on annual bluegrass (Poa annua). In this article, we provide an overview of the biology, host range and epidemiology of the fungus responsible...

  19. Biology and pathology of turfgrass anthracnose

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Anthracnose is a destructive fungal disease of weakened turf that occurs throughout the United States, Canada, and Western Europe and is particularly severe on annual bluegrass (Poa annua). In this article, we provide an overview of the biology, host range and epidemiology of the fungus responsible ...

  20. Linkage mapping of the Phg-1 and Co-14 genes for resistance to angular leaf spot and anthracnose in the common bean cultivar AND 277

    Technology Transfer Automated Retrieval System (TEKTRAN)

    The Andean common bean (Phaseolus vulgaris L.) cultivar AND 277 is an important source of disease resistance to angular leaf spot (ALS, caused by Pseudocercospora griseola) and anthracnose (caused by Colletotrichum lindemuthianum). AND 277 has the Phg-1 gene that confers resistance to eight races of...

  1. Particles causing lung disease

    SciTech Connect

    Kilburn, K.H.

    1984-04-01

    The lung has a limited number of patterns of reaction to inhaled particles. The disease observed depends upon the location: conducting airways, terminal bronchioles and alveoli, and upon the nature of inflammation induced: acute, subacute or chronic. Many different agents cause narrowing of conducting airways (asthma) and some of these cause permanent distortion or obliteration of airways as well. Terminal bronchioles appear to be particularly susceptible to particles which cause goblet cell metaplasia, mucous plugging and ultimately peribronchiolar fibrosis. Cancer is the last outcome at the bronchial level and appears to depend upon continuous exposure to or retention of an agent in the airway and failure of the affected cells to be exfoliated which may be due to squamous metaplasia. Alveoli are populated by endothelial cells, Type I or pavement epithelial cells and metabolically active cuboidal Type II cells that produce the lungs specific surfactant, dipalmytol lecithin. Disturbances of surfactant lead to edema in distal lung while laryngeal edema due to anaphylaxis or fumes may produce asphyxia. Physical retention of indigestible particles or retention by immune memory responses may provoke hyaline membranes, stimulate alveolar lipoproteinosis and finally fibrosis. This later exuberant deposition of connective tissue has been best studied in the occupational pneumoconioses especially silicosis and asbestosis. In contrast emphysema a catabolic response appears frequently to result from leakage or release of lysosomal proteases into the lung during processing of cigarette smoke particles. 164 references, 1 figure, 2 tables.

  2. Using genotyping by sequencing to map two novel anthracnose resistance loci in Sorghum bicolor

    DOE PAGESBeta

    Felderhoff, Tery J.; McIntyre, Lauren M.; Saballos, Ana; Vermerris, Wilfred

    2016-05-18

    Colletotrichum sublineola is an aggressive fungal pathogen that causes anthracnose in sorghum [Sorghum bicolor (L.) Moench]. The obvious symptoms of anthracnose are leaf blight and stem rot. Sorghum, the fifth most widely grown cereal crop in the world, can be highly susceptible to the disease, most notably in hot and humid environments. In the southeastern United States the acreage of sorghum has been increasing steadily in recent years, spurred by growing interest in producing biofuels, bio-based products, and animal feed. Resistance to anthracnose is, therefore, of paramount importance for successful sorghum production in this region. To identify anthracnose resistance locimore » present in the highly resistant cultivar ‘Bk7’, a biparental mapping population of F3:4 and F4:5 sorghum lines was generated by crossing ‘Bk7’ with the susceptible inbred ‘Early Hegari-Sart’. Lines were phenotyped in three environments and in two different years following natural infection. The population was genotyped by sequencing. Following a stringent custom filtering protocol, totals of 5186 and 2759 informative SNP markers were identified in the two populations. Segregation data and association analysis identified resistance loci on chromosomes 7 and 9, with the resistance alleles derived from ‘Bk7’. Both loci contain multiple classes of defense-related genes based on sequence similarity and gene ontologies. Genetic analysis following an independent selection experiment of lines derived from a cross between ‘Bk7’ and sweet sorghum ‘Mer81-4’ narrowed the resistance locus on chromosome 9 substantially, validating this QTL. As observed in other species, sorghum appears to have regions of clustered resistance genes. Lastly, further characterization of these regions will facilitate the development of novel germplasm with resistance to anthracnose and other diseases.« less

  3. Using genotyping by sequencing to map two novel anthracnose resistance Loci in Sorghum bicolor

    DOE PAGESBeta

    Felderhoff, Terry J.; McIntyre, Lauren M.; Saballos, Ana; Vermerris, Wilfred

    2016-05-18

    Colletotrichum sublineola is an aggressive fungal pathogen that causes anthracnose in sorghum [Sorghum bicolor (L.) Moench]. The obvious symptoms of anthracnose are leaf blight and stem rot. Sorghum, the fifth most widely grown cereal crop in the world, can be highly susceptible to the disease, most notably in hot and humid environments. In the southeastern United States the acreage of sorghum has been increasing steadily in recent years, spurred by growing interest in producing biofuels, bio-based products, and animal feed. Resistance to anthracnose is, therefore, of paramount importance for successful sorghum production in this region. To identify anthracnose resistance locimore » present in the highly resistant cultivar ‘Bk7’, a biparental mapping population of F3:4 and F4:5 sorghum lines was generated by crossing ‘Bk7’ with the susceptible inbred ‘Early Hegari-Sart’. Lines were phenotyped in three environments and in two different years following natural infection. The population was genotyped by sequencing. Following a stringent custom filtering protocol, totals of 5186 and 2759 informative SNP markers were identified in the two populations. Segregation data and association analysis identified resistance loci on chromosomes 7 and 9, with the resistance alleles derived from ‘Bk7’. Both loci contain multiple classes of defense-related genes based on sequence similarity and gene ontologies. In addition, genetic analysis following an independent selection experiment of lines derived from a cross between ‘Bk7’ and sweet sorghum ‘Mer81-4’ narrowed the resistance locus on chromosome 9 substantially, validating this QTL. As observed in other species, sorghum appears to have regions of clustered resistance genes. Further characterization of these regions will facilitate the development of novel germplasm with resistance to anthracnose and other diseases.« less

  4. Endophytic bacterial diversity in the phyllosphere of Amazon Paullinia cupana associated with asymptomatic and symptomatic anthracnose.

    PubMed

    Bogas, Andréa Cristina; Ferreira, Almir José; Araújo, Welington Luiz; Astolfi-Filho, Spartaco; Kitajima, Elliot Watanabe; Lacava, Paulo Teixeira; Azevedo, João Lúcio

    2015-01-01

    Endophytes colonize an ecological niche similar to that of phytopathogens, which make them candidate for disease suppression. Anthracnose is a disease caused by Colletotrichum spp., a phytopathogen that can infect guarana (Paullinia cupana), an important commercial crop in the Brazilian Amazon. We investigated the diversity of endophytic bacteria inhabiting the phyllosphere of asymptomatic and symptomatic anthracnose guarana plants. The PCR-denaturation gradient gel electrophoresis (PCR-DGGE) fingerprints revealed differences in the structure of the evaluated communities. Detailed analysis of endophytic bacteria composition using culture-dependent and 16S rRNA clone libraries revealed the presence of Firmicutes, Proteobacteria, Actinobacteria, Bacteroidetes, and Acidobacteria phyla. Firmicutes comprised the majority of isolates in asymptomatic plants (2.40E(-4)). However, cloning and sequencing of 16S rRNA revealed differences at the genus level for Neisseria (1.4E(-4)), Haemophilus (2.1E(-3)) and Arsenophonus (3.6E(-5)) in asymptomatic plants, Aquicella (3.5E(-3)) in symptomatic anthracnose plants, and Pseudomonas (1.1E(-3)), which was mainly identified in asymptomatic plants. In cross-comparisons of the endophytic bacterial communities as a whole, symptomatic anthracnose plants contained higher diversity, as reflected in the Shannon-Weaver and Simpson indices estimation (P < 0.05). Similarly, comparisons using LIBSHUFF and heatmap analysis for the relative abundance of operational taxonomic units (OTUs) showed differences between endophytic bacterial communities. These data are in agreement with the NMSD and ANOSIM analysis of DGGE profiles. Our results suggest that anthracnose can restructure endophytic bacterial communities by selecting certain strains in the phyllosphere of P. cupana. The understanding of these interactions is important for the development of strategies of biocontrol for Colletotrichum. PMID:26090305

  5. Using Genotyping by Sequencing to Map Two Novel Anthracnose Resistance Loci in Sorghum bicolor

    PubMed Central

    J. Felderhoff, Terry; M. McIntyre, Lauren; Saballos, Ana; Vermerris, Wilfred

    2016-01-01

    Colletotrichum sublineola is an aggressive fungal pathogen that causes anthracnose in sorghum [Sorghum bicolor (L.) Moench]. The obvious symptoms of anthracnose are leaf blight and stem rot. Sorghum, the fifth most widely grown cereal crop in the world, can be highly susceptible to the disease, most notably in hot and humid environments. In the southeastern United States the acreage of sorghum has been increasing steadily in recent years, spurred by growing interest in producing biofuels, bio-based products, and animal feed. Resistance to anthracnose is, therefore, of paramount importance for successful sorghum production in this region. To identify anthracnose resistance loci present in the highly resistant cultivar ‘Bk7’, a biparental mapping population of F3:4 and F4:5 sorghum lines was generated by crossing ‘Bk7’ with the susceptible inbred ‘Early Hegari-Sart’. Lines were phenotyped in three environments and in two different years following natural infection. The population was genotyped by sequencing. Following a stringent custom filtering protocol, totals of 5186 and 2759 informative SNP markers were identified in the two populations. Segregation data and association analysis identified resistance loci on chromosomes 7 and 9, with the resistance alleles derived from ‘Bk7’. Both loci contain multiple classes of defense-related genes based on sequence similarity and gene ontologies. Genetic analysis following an independent selection experiment of lines derived from a cross between ‘Bk7’ and sweet sorghum ‘Mer81-4’ narrowed the resistance locus on chromosome 9 substantially, validating this QTL. As observed in other species, sorghum appears to have regions of clustered resistance genes. Further characterization of these regions will facilitate the development of novel germplasm with resistance to anthracnose and other diseases. PMID:27194807

  6. Using Genotyping by Sequencing to Map Two Novel Anthracnose Resistance Loci in Sorghum bicolor.

    PubMed

    J Felderhoff, Terry; M McIntyre, Lauren; Saballos, Ana; Vermerris, Wilfred

    2016-01-01

    Colletotrichum sublineola is an aggressive fungal pathogen that causes anthracnose in sorghum [Sorghum bicolor (L.) Moench]. The obvious symptoms of anthracnose are leaf blight and stem rot. Sorghum, the fifth most widely grown cereal crop in the world, can be highly susceptible to the disease, most notably in hot and humid environments. In the southeastern United States the acreage of sorghum has been increasing steadily in recent years, spurred by growing interest in producing biofuels, bio-based products, and animal feed. Resistance to anthracnose is, therefore, of paramount importance for successful sorghum production in this region. To identify anthracnose resistance loci present in the highly resistant cultivar 'Bk7', a biparental mapping population of F3:4 and F4:5 sorghum lines was generated by crossing 'Bk7' with the susceptible inbred 'Early Hegari-Sart'. Lines were phenotyped in three environments and in two different years following natural infection. The population was genotyped by sequencing. Following a stringent custom filtering protocol, totals of 5186 and 2759 informative SNP markers were identified in the two populations. Segregation data and association analysis identified resistance loci on chromosomes 7 and 9, with the resistance alleles derived from 'Bk7'. Both loci contain multiple classes of defense-related genes based on sequence similarity and gene ontologies. Genetic analysis following an independent selection experiment of lines derived from a cross between 'Bk7' and sweet sorghum 'Mer81-4' narrowed the resistance locus on chromosome 9 substantially, validating this QTL. As observed in other species, sorghum appears to have regions of clustered resistance genes. Further characterization of these regions will facilitate the development of novel germplasm with resistance to anthracnose and other diseases. PMID:27194807

  7. Real-Time PCR Detection of Dogwood Anthracnose Fungus in Historical Herbarium Specimens from Asia

    PubMed Central

    Miller, Stephen; Masuya, Hayato; Zhang, Jian; Walsh, Emily; Zhang, Ning

    2016-01-01

    Cornus species (dogwoods) are popular ornamental trees and important understory plants in natural forests of northern hemisphere. Dogwood anthracnose, one of the major diseases affecting the native North American Cornus species, such as C. florida, is caused by the fungal pathogen Discula destructiva. The origin of this fungus is not known, but it is hypothesized that it was imported to North America with its host plants from Asia. In this study, a TaqMan real-time PCR assay was used to detect D. destructiva in dried herbarium and fresh Cornus samples. Several herbarium specimens from Japan and China were detected positive for D. destructiva, some of which were collected before the first report of the dogwood anthracnose in North America. Our findings further support that D. destructiva was introduced to North America from Asia where the fungus likely does not cause severe disease. PMID:27096929

  8. Real-Time PCR Detection of Dogwood Anthracnose Fungus in Historical Herbarium Specimens from Asia.

    PubMed

    Miller, Stephen; Masuya, Hayato; Zhang, Jian; Walsh, Emily; Zhang, Ning

    2016-01-01

    Cornus species (dogwoods) are popular ornamental trees and important understory plants in natural forests of northern hemisphere. Dogwood anthracnose, one of the major diseases affecting the native North American Cornus species, such as C. florida, is caused by the fungal pathogen Discula destructiva. The origin of this fungus is not known, but it is hypothesized that it was imported to North America with its host plants from Asia. In this study, a TaqMan real-time PCR assay was used to detect D. destructiva in dried herbarium and fresh Cornus samples. Several herbarium specimens from Japan and China were detected positive for D. destructiva, some of which were collected before the first report of the dogwood anthracnose in North America. Our findings further support that D. destructiva was introduced to North America from Asia where the fungus likely does not cause severe disease. PMID:27096929

  9. What Causes Sickle Cell Disease?

    MedlinePlus

    ... from the NHLBI on Twitter. What Causes Sickle Cell Disease? Abnormal hemoglobin, called hemoglobin S , causes sickle cell ... that hemoglobin works. ( See Overview. ) How Is Sickle Cell Disease Inherited? When the hemoglobin S gene is inherited ...

  10. First report of anthracnose of mile-a-minute (Persicaria perfoliata) caused by Colletotrichum gloeosporioides in Turkey

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Mile-a-minute (Persicaria perfoliata (L.) H. Gross; family Polygonaceae) is an exotic annual barbed vine that is now invasive in the northeastern USA, Mississippi, and Oregon and is a target of biological control efforts. In July, 2010, diseased P. perfoliata plants were found along the Firtina Rive...

  11. Diseases Caused by Viruses

    Technology Transfer Automated Retrieval System (TEKTRAN)

    The symptoms, causal agents, epidemiology and management of important virus diseases in chickpea and lentil crops were reviewed in depth. The virus diseases include.Alflafa mosaic virus, Cucumber mosaiv virus, Faba bean necrotic yellows virus, Pea enation mosaic virus, Pea seed-borne mosaci virus,...

  12. Chitosan controls postharvest anthracnose in bell pepper by activating defense-related enzymes.

    PubMed

    Edirisinghe, Madushani; Ali, Asgar; Maqbool, Mehdi; Alderson, Peter G

    2014-12-01

    Anthracnose, a postharvest disease caused by the fungus Colletotrichum capsici is the most devastating disease of bell pepper that causes great economic losses especially in tropical climates. Therefore, the objective of this study was to evaluate the antifungal properties of chitosan (low molecular weight from crab shell, Mw: 50 kDa and 75-85 % deacetylated) against anthracnose by inducing defense-related enzymes. The concentrations of 0, 0.5, 1.0, 1.5 and 2.0 % chitosan were used to control the fungus in vitro and postharvest. There was a reduction in C. capsici mycelial growth and the highest chitosan concentration (2.0 %) reduced the growth by 70 % after 7 days incubation. In germination test, the concentration of 1.5 and 2.0 % chitosan reduced spore germination in C. capsici between 80 % and 84 %, respectively. In postharvest trial the concentration of 1.5 % decreased the anthracnose severity in pepper fruit by approximately 76 % after 28 days of storage (10 ± 1 °C; 80 % RH). For enzymatic activities, the concentration of 1.5 and 2.0 % chitosan increased the polyphenol oxidase (PPO), peroxidase (POD) and total phenolics in inoculated bell pepper during storage. Based on these results, the chitosan presents antifungal properties against C. capsici, as well as potential to induce resistance on bell pepper. PMID:25477684

  13. Causes of Alzheimer's disease

    PubMed Central

    Munoz, D G; Feldman, H

    2000-01-01

    It is now understood that genetic factors play a crucial role in the risk of developing Alzheimer's disease (AD). Rare mutations in at least 3 genes are responsible for early-onset familial AD. A common polymorphism in the apolipoprotein E gene is the major determinant of risk in families with late-onset AD, as well as in the general population. Advanced age, however, remains the major established risk factor for AD, although environmental variables may also have some role in disease expression. Some pathogenic factors directly associated with aging include oxidative damage and mutations in messenger RNA. Other factors unrelated to the aging process may, in the future, be amenable to therapeutic intervention by way of estrogen replacement therapy for postmenopausal women, anti-inflammatory drug therapy and reducing vascular risk factors. Older theories, such as aluminum playing a role in the pathogenesis of AD, have been mostly discarded as our understanding of pathogenic mechanisms of AD has advanced. PMID:11216203

  14. Inheritance and molecular mapping of anthracnose resistance genes present in sorghum line SC112-14

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Anthracnose (Colletotrichum sublineolum) is one of the most destructive diseases of sorghum (Sorghum bicolor L. Moench) affecting all aerial tissues of the plant. The most effective strategy for its control is the incorporation of resistance genes. Therefore, the anthracnose resistance response pr...

  15. A New Anthracnose Resistance Gene in Andean Common Bean Cultivar Jalo Listras Pretas

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Anthracnose is one of the most widespread and economically important diseases of common bean worldwide. Most anthracnose resistance genes in common bean are from beans of the Mesoamerican gene pool. The resistant reaction of the Andean common bean cultivar Jalo Listras Pretas to races 9, 64, 65 and ...

  16. Developmental Stage and Temperature Affect Strawberry Flower and Fruit Susceptibility to Anthracnose

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Colletotrichum acutatum and C. fragariae both cause anthracnose flower blight and fruit rot of strawberry. Anthracnose lesions on ripe fruit are circular and tan to light brown initially, later becoming dark brown and sunken with pink masses of conidia. Lesions on green fruit often originate on in...

  17. Application of Volatile Antifungal Plant Essential Oils for Controlling Pepper Fruit Anthracnose by Colletotrichum gloeosporioides.

    PubMed

    Hong, Jeum Kyu; Yang, Hye Ji; Jung, Heesoo; Yoon, Dong June; Sang, Mee Kyung; Jeun, Yong-Chull

    2015-09-01

    Anthracnose caused by Colletotrichum gloeosporioides has been destructive during pepper fruit production in outdoor fields in Korea. In vitro antifungal activities of 15 different plant essential oils or its components were evaluated during conidial germination and mycelial growth of C. gloeosporioides. In vitro conidial germination was most drastically inhibited by vapour treatments with carvacrol, cinnamon oil, trans-cinnamaldehyde, citral, p-cymene and linalool. Inhibition of the mycelial growth by indirect vapour treatment with essential oils was also demonstrated compared with untreated control. Carvacrol, cinnamon oil, trans-cinnamaldehyde, citral and eugenol were among the most inhibitory plant essential oils by the indirect antifungal efficacies. Plant protection efficacies of the plant essential oils were demonstrated by reduced lesion diameter on the C. gloeosporioides-inoculated immature green pepper fruits compared to the inoculated control fruits without any plant essential oil treatment. In planta test showed that all plant essential oils tested in this study demonstrated plant protection efficacies against pepper fruit anthracnose with similar levels. Thus, application of different plant essential oils can be used for eco-friendly disease management of anthracnose during pepper fruit production. PMID:26361475

  18. Application of Volatile Antifungal Plant Essential Oils for Controlling Pepper Fruit Anthracnose by Colletotrichum gloeosporioides

    PubMed Central

    Hong, Jeum Kyu; Yang, Hye Ji; Jung, Heesoo; Yoon, Dong June; Sang, Mee Kyung; Jeun, Yong-Chull

    2015-01-01

    Anthracnose caused by Colletotrichum gloeosporioides has been destructive during pepper fruit production in outdoor fields in Korea. In vitro antifungal activities of 15 different plant essential oils or its components were evaluated during conidial germination and mycelial growth of C. gloeosporioides. In vitro conidial germination was most drastically inhibited by vapour treatments with carvacrol, cinnamon oil, trans-cinnamaldehyde, citral, p-cymene and linalool. Inhibition of the mycelial growth by indirect vapour treatment with essential oils was also demonstrated compared with untreated control. Carvacrol, cinnamon oil, trans-cinnamaldehyde, citral and eugenol were among the most inhibitory plant essential oils by the indirect antifungal efficacies. Plant protection efficacies of the plant essential oils were demonstrated by reduced lesion diameter on the C. gloeosporioides-inoculated immature green pepper fruits compared to the inoculated control fruits without any plant essential oil treatment. In planta test showed that all plant essential oils tested in this study demonstrated plant protection efficacies against pepper fruit anthracnose with similar levels. Thus, application of different plant essential oils can be used for eco-friendly disease management of anthracnose during pepper fruit production. PMID:26361475

  19. Anthracnose field evaluation of sorghum germplasm from Botswana

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Sorghum anthracnose is a disease of worldwide importance and host-plant resistance is the most practical method of disease management. In this study, 154 sorghum accessions from the Botswana collection maintained by the United States National Plant Germplasm System were inoculated with Colletotrich...

  20. Inheritance of anthracnose resistance for the sorghum cultivar 'Redlan'

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Anthracnose occurs worldwide and is one of the most important diseases limiting sorghum production. The development of resistant varieties to control the disease is hindered by extensive variation in virulence for the pathogen. The sorghum cultivar, ‘Redlan’, has been used to evaluate virulence wi...

  1. Antagonistic Activities of Bacillus spp. Strains Isolated from Tidal Flat Sediment Towards Anthracnose Pathogens Colletotrichum acutatum and C. gloeosporioides in South Korea.

    PubMed

    Han, Joon-Hee; Shim, Hongsik; Shin, Jong-Hwan; Kim, Kyoung Su

    2015-06-01

    Anthracnose is a fungal disease caused by Colletotrichum species that is detrimental to numerous plant species. Anthracnose control with fungicides has both human health and environmental safety implications. Despite increasing public concerns, fungicide use will continue in the absence of viable alternatives. There have been relatively less efforts to search antagonistic bacteria from mudflats harboring microbial diversity. A total of 420 bacterial strains were isolated from mudflats near the western sea of South Korea. Five bacterial strains, LB01, LB14, HM03, HM17, and LB15, were characterized as having antifungal properties in the presence of C. acutatum and C. gloeosporioides. The three Bacillus atrophaeus strains, LB14, HM03, and HM17, produced large quantities of chitinase and protease enzymes, whereas the B. amyloliquefaciens strain LB01 produced protease and cellulase enzymes. Two important antagonistic traits, siderophore production and solubilization of insoluble phosphate, were observed in the three B. atrophaeus strains. Analyses of disease suppression revealed that LB14 was most effective for suppressing the incidence of anthracnose symptoms on pepper fruits. LB14 produced antagonistic compounds and suppressed conidial germination of C. acutatum and C. gloeosporioides. The results from the present study will provide a basis for developing a reliable alternative to fungicides for anthracnose control. PMID:26060435

  2. Antagonistic Activities of Bacillus spp. Strains Isolated from Tidal Flat Sediment Towards Anthracnose Pathogens Colletotrichum acutatum and C. gloeosporioides in South Korea

    PubMed Central

    Han, Joon-Hee; Shim, Hongsik; Shin, Jong-Hwan; Kim, Kyoung Su

    2015-01-01

    Anthracnose is a fungal disease caused by Colletotrichum species that is detrimental to numerous plant species. Anthracnose control with fungicides has both human health and environmental safety implications. Despite increasing public concerns, fungicide use will continue in the absence of viable alternatives. There have been relatively less efforts to search antagonistic bacteria from mudflats harboring microbial diversity. A total of 420 bacterial strains were isolated from mudflats near the western sea of South Korea. Five bacterial strains, LB01, LB14, HM03, HM17, and LB15, were characterized as having antifungal properties in the presence of C. acutatum and C. gloeosporioides. The three Bacillus atrophaeus strains, LB14, HM03, and HM17, produced large quantities of chitinase and protease enzymes, whereas the B. amyloliquefaciens strain LB01 produced protease and cellulase enzymes. Two important antagonistic traits, siderophore production and solubilization of insoluble phosphate, were observed in the three B. atrophaeus strains. Analyses of disease suppression revealed that LB14 was most effective for suppressing the incidence of anthracnose symptoms on pepper fruits. LB14 produced antagonistic compounds and suppressed conidial germination of C. acutatum and C. gloeosporioides. The results from the present study will provide a basis for developing a reliable alternative to fungicides for anthracnose control. PMID:26060435

  3. Disease Outbreaks Caused by Water.

    ERIC Educational Resources Information Center

    Craun, Gunther F.

    1978-01-01

    Presents a literature review of the disease outbreaks caused by drinking polluted water, covering publications of 1976-77. Some of the waterborn outbreaks included are: (1) cholera; (2) gastroenteritis; (3) giardiasis; and (4) typhoid fever and salmonellosis. A list of 66 references is also presented. (HM)

  4. Can Infections Cause Alzheimer's Disease?

    PubMed Central

    Mawanda, Francis; Wallace, Robert

    2013-01-01

    Late-onset Alzheimer's disease (AD) is the most prevalent cause of dementia among older adults, yet more than a century of research has not determined why this disease develops. One prevailing hypothesis is that late-onset AD is caused by infectious pathogens, an idea widely studied in both humans and experimental animal models. This review examines the infectious AD etiology hypothesis and summarizes existing evidence associating infectious agents with AD in humans. The various mechanisms through which different clinical and subclinical infections could cause or promote the progression of AD are considered, as is the concordance between putative infectious agents and the epidemiology of AD. We searched the PubMed, Web of Science, and EBSCO databases for research articles pertaining to infections and AD and systematically reviewed the evidence linking specific infectious pathogens to AD. The evidence compiled from the literature linking AD to an infectious cause is inconclusive, but the amount of evidence suggestive of an association is too substantial to ignore. Epidemiologic, clinical, and basic science studies that could improve on current understanding of the associations between AD and infections and possibly uncover ways to control this highly prevalent and debilitating disease are suggested. PMID:23349428

  5. Pediatric genetic diseases causing glaucoma

    PubMed Central

    Ichhpujani, Parul; Singh, Rohan B.

    2014-01-01

    Glaucomatous optic neuropathy may be considered as an endpoint of multiple systemic factors. Genetic conditions commonly causing glaucoma in children and adolescents include Axenfeld-Reiger syndrome, aniridia, Marfan syndrome, Weill-Marchessani syndrome, Sturge-Weber syndrome, Rubinstein-Taybi syndrome, nevus of Ota, congenital rubella and neurofibromatosis type 1. In the recent years, with the advancements in genetic research our understanding of the fundamental causes of glaucoma associated with inherited disorders has improved. In addition to intraocular pressure reduction, it is important for the clinician to be familiar with the multiple systemic associations with glaucoma, to re-evaluate treatment frequently, and to target the underlying disease process, if present.

  6. Biocontrol activity and primed systemic resistance by compost water extracts against anthracnoses of pepper and cucumber.

    PubMed

    Sang, Mee Kyung; Kim, Ki Deok

    2011-06-01

    We investigated direct and indirect effects of compost water extracts (CWEs) from Iljuk-3, Iljuk-7, Shinong-8, and Shinong-9 for the control of anthracnoses caused by Colletotrichum coccodes on pepper and C. orbiculare on cucumber. All tested CWEs significantly (P < 0.05) inhibited in vitro conidial germination and appressorium formation of the fungal pathogens; however, DL-β-amino-n-butyric acid (BABA) failed to inhibit the conidial development of the pathogens. Direct treatments of the CWEs and BABA on pepper and cucumber leaves at 1 and 3 days before or after inoculation significantly (P < 0.05) reduced anthracnose severities; Iljuk-3, Shinong-9, and BABA for pepper and Iljuk-7 for cucumber had more protective activities than curative activities. In addition, root treatment of CWEs suppressed anthracnoses on the plants by the pathogens; however, CWE treatment on lower leaves failed to reduce the diseases on the upper leaves of the plants. The CWE root treatments enhanced not only the expression of the pathogenesis-related (PR) genes CABPR1, CABGLU, CAChi2, CaPR-4, CAPO1, and CaPR-10 in pepper and PR1-1a, PR-2, PR-3, and APOX in cucumber but also the activity of β-1,3-glucanase, chitinase, and peroxidase and the generation of hydrogen peroxide in pepper and cucumber under pathogen-inoculated conditions. However, the CWE treatments failed to induce the plant responses under pathogen-free conditions. These results indicated that the CWEs had direct effects, reducing anthracnoses by C. coccodes on pepper leaves and C. orbiculare on cucumber leaves through protective and curative effects. In addition, CWE root treatments could induce systemic resistance in the primed state against pathogens on plant leaves that enhanced PR gene expression, defense-related enzyme production, and hydrogen peroxide generation rapidly and effectively immediately after pathogen infection. Thus, the CWEs might suppress anthracnoses on leaves of both pepper and cucumber through primed

  7. Disease Caused by Rotavirus Infection

    PubMed Central

    Lin, Che-Liang; Chen, Shou-Chien; Liu, Shyun-Yeu; Chen, Kow-Tong

    2014-01-01

    Although rotavirus vaccines are available, rotaviruses remain the major cause of childhood diarrheal disease worldwide. The Rotarix (GlaxoSmithKline Biologicals Rixensart, Belgium) and RotaTeq (Merck and Co., Inc. Whitehouse Station, New Jersey, USA) vaccines are effective for reducing the morbidity and mortality of rotavirus infection. This article aims to assess the epidemiology of rotaviral gastroenteritis and the efficacy and effectiveness of licensed rotavirus vaccines. This review concludes by presenting challenges in the field that require further exploration by and perspectives from basic and translational research in the future. PMID:25553142

  8. Optimal control of anthracnose using mixed strategies.

    PubMed

    Fotsa Mbogne, David Jaures; Thron, Christopher

    2015-11-01

    In this paper we propose and study a spatial diffusion model for the control of anthracnose disease in a bounded domain. The model is a generalization of the one previously developed in [15]. We use the model to simulate two different types of control strategies against anthracnose disease. Strategies that employ chemical fungicides are modeled using a continuous control function; while strategies that rely on cultivational practices (such as pruning and removal of mummified fruits) are modeled with a control function which is discrete in time (though not in space). For comparative purposes, we perform our analyses for a spatially-averaged model as well as the space-dependent diffusion model. Under weak smoothness conditions on parameters we demonstrate the well-posedness of both models by verifying existence and uniqueness of the solution for the growth inhibition rate for given initial conditions. We also show that the set [0, 1] is positively invariant. We first study control by impulsive strategies, then analyze the simultaneous use of mixed continuous and pulse strategies. In each case we specify a cost functional to be minimized, and we demonstrate the existence of optimal control strategies. In the case of pulse-only strategies, we provide explicit algorithms for finding the optimal control strategies for both the spatially-averaged model and the space-dependent model. We verify the algorithms for both models via simulation, and discuss properties of the optimal solutions. PMID:26407644

  9. Classical endocrine diseases causing obesity.

    PubMed

    Weaver, Jolanta U

    2008-01-01

    Obesity is associated with several endocrine diseases, including common ones such as hypothyroidism and polycystic ovarian syndrome to rare ones such as Cushing's syndrome, central hypothyroidism and hypothalamic disorders. The mechanisms for the development of obesity vary in according to the endocrine condition. Hypothyroidism is associated with accumulation of hyaluronic acid within various tissues, additional fluid retention due to reduced cardiac output and reduced thermogenesis. The pathophysiology of obesity associated with polycystic ovarian syndrome remains complex as obesity itself may simultaneously be the cause and the effect of the syndrome. Net excess of androgen appears to be pivotal in the development of central obesity. In Cushing's syndrome, an interaction with thyroid and growth hormones plays an important role in addition to an increased adipocyte differentiation and adipogenesis. This review also describes remaining rare cases: hypothalamic obesity due to central hypothyroidism and combined hormone deficiencies. PMID:18230905

  10. Microsatellite isolation and characterization for Colletotrichum spp, causal agent of anthracnose in Andean blackberry.

    PubMed

    Marulanda, M L; López, A M; Isaza, L; López, P

    2014-01-01

    The genus Colletotrichum, comprised of pathogenic fungi that affect plants grown worldwide, causes the disease known as anthracnose in several fruit and vegetable species. Several studies conducted on plants have shown that the disease is characterized by the presence of one or several species of the fungus attacking the fruit or other organs of the same host. To develop and implement effective control strategies, it is vital to understand the genetic structure of the fungus in agricultural systems, identify associated Colletotrichum species, and define the subpopulations responsible for the disease. Molecular tools were accordingly developed to characterize genotypic populations of Colletotrichum spp, causal agent of anthracnose in commercial crops of Andean blackberry (Rubus glaucus Benth.). A microsatellite-enriched library for Colletotrichum gloeosporioides was developed to identify and characterize microsatellite loci among isolates collected in R. glaucus plantations. Thirty microsatellites were developed and tested in 36 isolates gathered from eight different blackberry-production areas of Colombia. Ten pairs of microsatellites were polymorphic. PMID:25299081

  11. Inheritance of downy mildew (Plasmopara viticola) and anthracnose (Sphaceloma ampelinum) resistance in grapevines.

    PubMed

    Poolsawat, O; Mahanil, S; Laosuwan, P; Wongkaew, S; Tharapreuksapong, A; Reisch, B I; Tantasawat, P A

    2013-01-01

    Downy mildew (Plasmopara viticola) and anthracnose (Sphaceloma ampelinum) are two of the major diseases of most grapevine (Vitis vinifera L.) cultivars grown in Thailand. Therefore, breeding grapevines for improved downy mildew and anthracnose resistance is crucial. Factorial crosses were made between three downy mildew and/or anthracnose resistant lines ('NY88.0517.01', 'NY65.0550.04', and 'NY65.0551.05'; male parents) and two or three susceptible cultivars of V. vinifera ('Black Queen', 'Carolina Black Rose', and/or 'Italia'; female parents). F1 hybrid seedlings were evaluated for downy mildew and anthracnose resistance using a detached/excised leaf assay. For both diseases, the general combining ability (GCA) variance among male parents was significant, while the variance of GCA among females and the specific combining ability (SCA) variance were not significant, indicating the prevalence of additive over non-additive gene actions. The estimated narrow sense heritabilities of downy mildew and anthracnose resistance were 55.6 and 79.2%, respectively, suggesting that downy mildew/anthracnose resistance gene(s) were highly heritable. The 'Carolina Black Rose x NY65.0550.04' cross combination is recommended for future use. PMID:24391016

  12. Genome-Wide Association Study of Anthracnose Resistance in Andean Beans (Phaseolus vulgaris)

    PubMed Central

    Zuiderveen, Grady H.; Padder, Bilal A.; Kamfwa, Kelvin; Song, Qijian; Kelly, James D.

    2016-01-01

    Anthracnose is a seed-borne disease of common bean (Phaseolus vulgaris L.) caused by the fungus Colletotrichum lindemuthianum, and the pathogen is cosmopolitan in distribution. The objectives of this study were to identify new sources of anthracnose resistance in a diverse panel of 230 Andean beans comprised of multiple seed types and market classes from the Americas, Africa, and Europe, and explore the genetic basis of this resistance using genome-wide association mapping analysis (GWAS). Twenty-eight of the 230 lines tested were resistant to six out of the eight races screened, but only one cultivar Uyole98 was resistant to all eight races (7, 39, 55, 65, 73, 109, 2047, and 3481) included in the study. Outputs from the GWAS indicated major quantitative trait loci (QTL) for resistance on chromosomes, Pv01, Pv02, and Pv04 and two minor QTL on Pv10 and Pv11. Candidate genes associated with the significant SNPs were detected on all five chromosomes. An independent QTL study was conducted to confirm the physical location of the Co-1 locus identified on Pv01 in an F4:6 recombinant inbred line (RIL) population. Resistance was determined to be conditioned by the single dominant gene Co-1 that mapped between 50.16 and 50.30 Mb on Pv01, and an InDel marker (NDSU_IND_1_50.2219) tightly linked to the gene was developed. The information reported will provide breeders with new and diverse sources of resistance and genomic regions to target in the development of anthracnose resistance in Andean beans. PMID:27270627

  13. Genome-Wide Association Study of Anthracnose Resistance in Andean Beans (Phaseolus vulgaris).

    PubMed

    Zuiderveen, Grady H; Padder, Bilal A; Kamfwa, Kelvin; Song, Qijian; Kelly, James D

    2016-01-01

    Anthracnose is a seed-borne disease of common bean (Phaseolus vulgaris L.) caused by the fungus Colletotrichum lindemuthianum, and the pathogen is cosmopolitan in distribution. The objectives of this study were to identify new sources of anthracnose resistance in a diverse panel of 230 Andean beans comprised of multiple seed types and market classes from the Americas, Africa, and Europe, and explore the genetic basis of this resistance using genome-wide association mapping analysis (GWAS). Twenty-eight of the 230 lines tested were resistant to six out of the eight races screened, but only one cultivar Uyole98 was resistant to all eight races (7, 39, 55, 65, 73, 109, 2047, and 3481) included in the study. Outputs from the GWAS indicated major quantitative trait loci (QTL) for resistance on chromosomes, Pv01, Pv02, and Pv04 and two minor QTL on Pv10 and Pv11. Candidate genes associated with the significant SNPs were detected on all five chromosomes. An independent QTL study was conducted to confirm the physical location of the Co-1 locus identified on Pv01 in an F4:6 recombinant inbred line (RIL) population. Resistance was determined to be conditioned by the single dominant gene Co-1 that mapped between 50.16 and 50.30 Mb on Pv01, and an InDel marker (NDSU_IND_1_50.2219) tightly linked to the gene was developed. The information reported will provide breeders with new and diverse sources of resistance and genomic regions to target in the development of anthracnose resistance in Andean beans. PMID:27270627

  14. DISEASES CAUSED BY WATER CONTACT

    EPA Science Inventory

    Diseases associated with water contact are reviewed with respect to the sources of etiological agents, the types of diseases and the conditions under which they occur. The sources of disease agents fall into three general groups; point sources such as sewage treatment plants; dis...

  15. Thailandins A and B, New Polyene Macrolactone Compounds Isolated from Actinokineospora bangkokensis Strain 44EHW(T), Possessing Antifungal Activity against Anthracnose Fungi and Pathogenic Yeasts.

    PubMed

    Intra, Bungonsiri; Greule, Anja; Bechthold, Andreas; Euanorasetr, Jirayut; Paululat, Thomas; Panbangred, Watanalai

    2016-06-29

    Two new polyene macrolactone antibiotics, thailandins A, 1, and B, 2, were isolated from the fermentation broth of rhizosphere soil-associated Actinokineospora bangkokensis strain 44EHW(T). The new compounds from this strain were purified using semipreparative HPLC and Sephadex LH-20 gel filtration while following an antifungal activity guided fractionation. Their structures were elucidated through spectroscopic techniques including UV, HR-ESI-MS, and NMR. These compounds demonstrated broad spectrum antifungal activity against fungi causing anthracnose disease (Colletotrichum gloeosporioides DoA d0762, Colletotrichum gloeosporiodes DoA c1060, and Colletotrichum capsici DoA c1511) as well as pathogenic yeasts (Candida albicans MT 2013/1, Candida parasilopsis DKMU 434, and Cryptococcus neoformans MT 2013/2) with minimum inhibitory concentrations ranging between 16 and 32 μg/mL. This is the first report of polyene antibiotics produced by Actinokineospora species as bioactive compounds against anthracnose fungi and pathogenic yeast strains. PMID:27267862

  16. Improved control of anthracnose rot in loquat fruit by a combination treatment of Pichia membranifaciens with CaCl(2).

    PubMed

    Cao, Shifeng; Zheng, Yonghua; Tang, Shuangshuang; Wang, Kaituo

    2008-08-15

    The beneficial effect of 2% CaCl(2) (w/v) on the antagonistic yeast Pichia membranifaciens for control of anthracnose rot caused by Colletotrichum acutatum in postharvest loquat fruit (Eriobotrya japonica L.) and the possible mechanisms involved were investigated. The results showed that treatment with P. membranifaciens at 1x10(8) CFU ml(-1) or 2% CaCl(2) alone both resulted in significantly smaller lesion diameter and lower disease incidence of anthracnose rot on loquat fruit wounds compared with the controls. The biocontrol activity of P. membranifaciens on the disease was enhanced by the addition of 2% CaCl(2), the combined treatment of P. membranifaciens with CaCl(2) resulted in a remarkably improved control of the disease in comparison with the treatment of P. membranifaciens or CaCl(2) alone. P. membranifaciens in combination with CaCl(2) induced higher activities of two defense-related enzymes chitinase and beta-1,3-glucanase in loquat fruit than applying the yeast or CaCl(2) alone. The in vitro experiment showed that the addition of 2% CaCl(2) in the suspensions of P. membranifaciens significantly inhibited spore germination and germ tube elongation of C. acutatum than the yeast or CaCl(2) alone. However, adding CaCl(2) did not significantly influence the population of P. membranifaciens in NYDB medium or fruit wounds. These results suggest that CaCl(2) could improve the biocontrol activity of P. membranifaciens on anthracnose rot in loquat fruit. It is postulated that the improved control of the disease is directly because of the higher inhibitory effect on pathogen growth and indirectly because of the enhanced disease resistance in loquat fruit by the combination treatment. PMID:18590937

  17. Meningococcal Disease: Causes and Transmission

    MedlinePlus

    ... Vaccine Campaign Podcast: Meningitis Immunization for Adolescents Meningitis Sepsis Causes & Transmission Recommend on Facebook Tweet Share Compartir ... Vaccine Campaign Podcast: Meningitis Immunization for Adolescents Meningitis Sepsis File Formats Help: How do I view different ...

  18. Treatments for Diseases That Cause Infertility

    MedlinePlus

    ... for Males Fertility Treatments for Females Assisted Reproductive Technology ... for Diseases That Cause Infertility Skip sharing on social media links Share this: Page Content Specific treatments for ...

  19. Response to anthracnose infection for a random selection of sorghum germplasm

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Anthracnose is one of the most important diseases of sorghum and substantial grain yield losses can occur during disease epidemics. The disease can be successfully managed through the use of resistant cultivars. Germplasm collections provide important sources of genetic diversity for the identific...

  20. Waterfowl diseases: causes, prevention, and control

    USGS Publications Warehouse

    Friend, M.; Cross, D.H.

    1995-01-01

    Preventing and controlling disease in waterfowl is a difficult job. Few tools are available to deal with disease in highly mobile, unconfined animal populations, and few managers are trained and experienced in the prevention and control of avian diseases. Furthermore, the geographic distribution, frequency of occurrence, magnitude of losses, and causes of diseases in waterfowl, as in other life forms, change over time. Waterfowl mortality from infectious diseases, for example, has increased in the past 20 years (Friend 1992).

  1. Colletotrichum gloeosporioides, causing anthracnose of mile-a-minute (Persicaria perfoliata) in Turkey, is a potential biological control agent of this weed in the U.S.

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Mile-a-minute (Persicaria perfoliata (L.) H. Gross; family Polygonaceae) is an exotic annual barbed vine that has invaded the northeastern USA, Mississippi, and Oregon. In July of 2010, in a search for potential biological control pathogens, diseased P. perfoliata plants were found along the Firtina...

  2. Inheritance and molecular mapping of anthracnose resistance gene present in the differential line PI533918

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Anthracnose (Collectrotichum sublineolum) is considered one of the most destructive diseases of sorghum (Sorghum bicolor L. Moench) because it infects all aerial tissues of the plant. The best strategy to control the disease is the incorporation of resistance genes. At present, eighteen sorghum line...

  3. Reaction of sorghum hybrids to anthracnose, grain mold and grain weathering in Burleson County, Texas, 2007

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Thirty commercial hybrids were evaluated for resistance against anthracnose, caused by Colletotrichum sublineolum and grain mold or grain weathering caused by a number of fungal species at the Texas A&M University Agricultural Experiment Station in College Station (Burleson County). Six hybrids wer...

  4. Respiratory Diseases Caused by Coal Mine Dust

    PubMed Central

    Laney, A. Scott; Weissman, David N.

    2015-01-01

    Objective To provide an update on respiratory diseases caused by coal mine dust. Methods This article presents the results of a literature review initially performed for an International Conference on Occupational and Environmental Lung Disease held in summer 2013. Results Coal mine dust causes a spectrum of lung diseases collectively termed coal mine dust lung disease (CMDLD). These include Coal Workers’ Pneumoconiosis, silicosis, mixed dust pneumoconiosis, dust-related diffuse fibrosis (which can be mistaken for idiopathic pulmonary fibrosis), and chronic obstructive pulmonary disease. CMDLD continues to be a problem in the United States, particularly in the central Appalachian region. Treatment of CMDLD is symptomatic. Those with end-stage disease are candidates for lung transplantation. Because CMDLD cannot be cured, prevention is critical. Conclusions Coal mine dust remains a relevant occupational hazard and miners remain at risk for CMDLD. PMID:25285970

  5. [Adrenomyeloneuropathy as the cause of Addison's disease].

    PubMed

    Benová, L; Ochodnický, M; Misovicová, N; Mokán, M

    2000-12-01

    The authors describe adrenoleukodystrophy and adrenomyeloneuropathy found in one family. This disease is a less frequent cause of Addison's disease, but it is very serious from the prognostic aspect. The authors recommend therefore to examine very long chain fatty acid plasma levels in patients with adrenal insufficiency. PMID:11214371

  6. An unusual cause of pancytopenia: Whipple's disease

    PubMed Central

    Tun, Nay T.; Shukla, Shwetanshu; Krishnakurup, Jaykrishnan; Pappachen, Binu; Krishnamurthy, Mahesh; Salib, Hayman

    2014-01-01

    Whipple's disease is a systemic infectious disease caused by the bacteria Tropheryma whipplei. The most common clinical manifestations of Whipple's disease are weight loss (92%), hypoalbuminemia and steatorrhea (91%, respectively), diarrhea (72%), arthralgia (67%), and abdominal pain (55%). Neurological signs and symptoms from dementia to oculomasticatory myorhythmia or oculofacioskeletal myorhythmia (pathognomonic of Whipple's disease), lymphadenopathy, and fatigue can also be present. Pancytopenia is a rare and less recognized clinical feature in Whipple's disease patients. We are describing a case where a middle-aged Caucasian male diagnosed with Whipple's disease was found to have pancytopenia. Etiology of pancytopenia is postulated to be due to the invasion of bone marrow by T. whipplei. It is important to recognize that bone marrow involvement by the Whipple bacillus is not uncommon. In the presence of lymphadenopathy and pancytopenia, clinicians should think of Whipple's disease as a differential diagnosis apart from lymphoma or other non-specific granulomatous reticuloendothelial disorders. PMID:24765256

  7. Genetic differentiation of Colletotrichum gloeosporioides and C. truncatum associated with Anthracnose disease of papaya (Carica papaya L.) and bell pepper (Capsium annuum L.) based on ITS PCR-RFLP fingerprinting.

    PubMed

    Maharaj, Ariana; Rampersad, Sephra N

    2012-03-01

    Members of the genus Colletotrichum include some of the most economically important fungal pathogens in the world. Accurate diagnosis is critical to devising disease management strategies. Two species, Colletotrichum gloeosporioides and C. truncatum, are responsible for anthracnose disease in papaya (Carica papaya L.) and bell pepper (Capsicum annuum L.) in Trinidad. The ITS1-5.8S-ITS2 region of 48 Colletotrichum isolates was sequenced, and the ITS PCR products were analyzed by PCR-RFLP analysis. Restriction site polymorphisms generated from 11 restriction enzymes enabled the identification of specific enzymes that were successful in distinguishing between C. gloeosporioides and C. truncatum isolates. Species-specific restriction fragment length polymorphisms generated by the enzymes AluI, HaeIII, PvuII, RsaI, and Sau3A were used to consistently resolve C. gloeosporioides and C. truncatum isolates from papaya. AluI, ApaI, PvuII, RsaI, and SmaI reliably separated isolates of C. gloeosporioides and C. truncatum from bell pepper. PvuII, RsaI, and Sau3A were also capable of distinguishing among the C. gloeosporioides isolates from papaya based on the different restriction patterns that were obtained as a result of intra-specific variation in restriction enzyme recognition sites in the ITS1-5.8S-ITS2 rDNA region. Of all the isolates tested, C. gloeosporioides from papaya also had the highest number of PCR-RFLP haplotypes. Cluster analysis of sequence and PCR-RFLP data demonstrated that all C. gloeosporioides and C. truncatum isolates clustered separately into species-specific clades regardless of host species. Phylograms also revealed consistent topologies which suggested that the genetic distances for PCR-RFLP-generated data were comparable to that of ITS sequence data. ITS PCR-RFLP fingerprinting is a rapid and reliable method to identify and differentiate between Colletotrichum species. PMID:21720933

  8. Pulmonary disease caused by Mycobacterium malmoense.

    PubMed

    Alberts, W M; Chandler, K W; Solomon, D A; Goldman, A L

    1987-06-01

    Mycobacterium malmoense was isolated from pulmonary material from 4 patients. Two patients had repeatedly positive smears and cultures along with roentgenographic progression of pulmonary disease in the absence of another pathogen. These 2 patients therefore meet the criteria for diagnosis of pulmonary mycobacteriosis. Isolation of the organism may represent colonization in a third patient, and M. malmoense has been isolated from a fourth patient on 2 occasions. It is not yet definite, however, that the pulmonary process is due to mycobacterial disease. Although uncommon, pulmonary disease caused by this organism has been reported from Europe. Only 1 prior case of pulmonary disease caused by M. malmoense, however, has been reported in the United States. PMID:3592410

  9. Introgression and pyramiding into common bean market class fabada of genes conferring resistance to anthracnose and potyvirus.

    PubMed

    Ferreira, Juan José; Campa, Ana; Pérez-Vega, Elena; Rodríguez-Suárez, Cristina; Giraldez, Ramón

    2012-03-01

    Anthracnose and bean common mosaic (BCM) are considered major diseases in common bean crop causing severe yield losses worldwide. This work describes the introgression and pyramiding of genes conferring genetic resistance to BCM and anthracnose local races into line A25, a bean genotype classified as market class fabada. Resistant plants were selected using resistance tests or combining resistance tests and marker-assisted selection. Lines A252, A321, A493, Sanilac BC6-Are, and BRB130 were used as resistance sources. Resistance genes to anthracnose (Co-2 ( C ), Co-2 ( A252 ) and Co-3/9) and/or BCM (I and bc-3) were introgressed in line A25 through six parallel backcrossing programs, and six breeding lines showing a fabada seed phenotype were obtained after six backcross generations: line A1258 from A252; A1231 from A321; A1220 from A493; A1183 and A1878 from Sanilac BC6-Are; and line A2418 from BRB130. Pyramiding of different genes were developed using the pedigree method from a single cross between lines obtained in the introgression step: line A1699 (derived from cross A1258 × A1220), A2438 (A1220 × A1183), A2806 (A1878 × A2418), and A3308 (A1699 × A2806). A characterization based on eight morpho-agronomic traits revealed a limited differentiation among the obtained breeding lines and the recurrent line A25. However, using a set of seven molecular markers linked to the loci used in the breeding programs it was possible to differentiate the 11 fabada lines. Considering the genetic control of the resistance in resistant donor lines, the observed segregations in the last backcrossing generation, the reaction against the pathogens, and the expression of the molecular markers it was also possible to infer the genotype conferring resistance in the ten fabada breeding lines obtained. As a result of these breeding programs, genetic resistance to three anthracnose races controlled by genes included in clusters Co-2 and Co-3/9, and genetic resistance to BCM controlled

  10. Evaluation of Pseudomonas syringae Strain ESC11 for Biocontrol of Crown Rot and Anthracnose of Banana

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Pseudomonas syringae strain ESC11, and 250 'g/ml each of thiabendazole (TBZ) and imazalil reduced crown rot of banana caused by a Fusarium sp. by 0-88% and 73-88%, respectively, in laboratory experiments. ESC11 alone did not significantly reduce rot, mold, or anthracnose in most field trials. TBZ an...

  11. Analysis of genetic diversity of flowering dogwood natural stands using microsatellites the effects of dogwood anthracnose

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Flowering dogwood (Cornus florida) populations recently have experienced severe declines caused by dogwood anthracnose. Mortality ranged from 48-98%, raising the concern that genetic diversity has been reduced significantly. Microsatellite data was used to evaluate the level and distribution of ge...

  12. Genetic dissection of resistance to anthracnose and powdery mildew in Medicago truncatula

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Medicago truncatula was used to characterize resistance to anthracnose and powdery mildew, respectively caused by Colletotrichum trifolii and Erysiphe pisi. Two isolates of E. pisi (Ep-p from pea and Ep-a from alfalfa) and two races of C. trifolii (races 1 and 2) were used in this study. The A17 gen...

  13. Occupational respiratory disease caused by acrylates.

    PubMed

    Savonius, B; Keskinen, H; Tuppurainen, M; Kanerva, L

    1993-05-01

    Acrylates are compounds used in a variety of industrial fields and their use is increasing. They have many features which make them superior to formerly used chemicals, regarding both their industrial use and their possible health effects. Contact sensitization is, however, one of their well known adverse health effects but they may also cause respiratory symptoms. We report on 18 cases of respiratory disease, mainly asthma, caused by different acrylates, 10 cases caused by cyanoacrylates, four by methacrylates and two cases by other acrylates. PMID:8334539

  14. Association of RGA-SSCP markers with resistance to downy mildew and anthracnose in grapevines.

    PubMed

    Tantasawat, P A; Poolsawat, O; Prajongjai, T; Chaowiset, W; Tharapreuksapong, A

    2012-01-01

    Downy mildew (Plasmopara viticola) and anthracnose (Sphaceloma ampelinum) are two major diseases that severely affect most grapevine (Vitis vinifera) cultivars grown commercially in Thailand. Progress of conventional breeding programs of grapevine for improved resistance to these diseases can be speeded up by selection of molecular markers associated with resistance traits. We evaluated the association between 13 resistance gene analog (RGA)-single-strand conformation polymorphism (SSCP) markers with resistance to downy mildew and anthracnose in 71 segregating progenies of seven cross combinations between susceptible cultivars and resistant lines. F(1) hybrids from each cross were assessed for resistance to downy mildew and anthracnose (isolates Nk4-1 and Rc2-1) under laboratory conditions. Association of resistance traits with RGA-SSCP markers was evaluated using simple linear regression analysis. Three RGA-SSCP markers were found to be significantly correlated with anthracnose resistance, whereas significant correlation with downy mildew resistance was observed for only one RGA-SSCP marker. These results demonstrate the usefulness of RGA-SSCP markers. Four candidate markers with significant associations to resistance to these two major diseases of grapevine were identified. However, these putative associations between markers and resistance need to be verified with larger segregating populations before they can be used for marker-assisted selection. PMID:22869536

  15. Endocrine causes of nonalcoholic fatty liver disease

    PubMed Central

    Marino, Laura; Jornayvaz, François R

    2015-01-01

    Nonalcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease in the industrialized world. The prevalence of NAFLD is increasing, becoming a substantial public health burden. NAFLD includes a broad spectrum of disorders, from simple conditions such as steatosis to severe manifestations such as fibrosis and cirrhosis. The relationship of NAFLD with metabolic alterations such as type 2 diabetes is well described and related to insulin resistance, with NAFLD being recognized as the hepatic manifestation of metabolic syndrome. However, NAFLD may also coincide with endocrine diseases such as polycystic ovary syndrome, hypothyroidism, growth hormone deficiency or hypercortisolism. It is therefore essential to remember, when discovering altered liver enzymes or hepatic steatosis on radiological exams, that endocrine diseases can cause NAFLD. Indeed, the overall prognosis of NAFLD may be modified by treatment of the underlying endocrine pathology. In this review, we will discuss endocrine diseases that can cause NALFD. Underlying pathophysiological mechanisms will be presented and specific treatments will be reviewed. PMID:26494962

  16. [Treatment of bone disease caused by gastrectomy].

    PubMed

    Iwamoto, Jun

    2015-11-01

    Gastrectomy is undergone mainly in patients with gastric cancer. Bone diseases(osteoporosis and osteomalacia)caused by gastractomy are associated with weight loss, calcium and vitamin D inadequancy, and malnutrition. Most patients after gastrectomy have multile risk factors of bone diseases and subsequently are at a higher risk for fractures. In particular, sex hormone deficiency and aging enhance the risk for fractures. The management of bone diseases caused by gastraectomy include adequet intake of calcium, vitamin D and protein, sunlight exposure, and regular weight-bearing exercise, as well as non-smoking and avoiding excess alcohol drinking. The patients at a high risk for fractures shoud be treated with bisphosphonates. PMID:26503874

  17. Co-segregation analysis and mapping of the anthracnose Co-10 and angular leaf spot Phg-ON disease-resistance genes in the common bean cultivar Ouro Negro.

    PubMed

    Gonçalves-Vidigal, M C; Cruz, A S; Lacanallo, G F; Vidigal Filho, P S; Sousa, L L; Pacheco, C M N A; McClean, P; Gepts, P; Pastor-Corrales, M A

    2013-09-01

    Anthracnose (ANT) and angular leaf spot (ALS) are devastating diseases of common bean (Phaseolus vulgaris L.). Ouro Negro is a highly productive common bean cultivar, which contains the Co-10 and Phg-ON genes for resistance to ANT and ALS, respectively. In this study, we performed a genetic co-segregation analysis of resistance to ANT and ALS using an F2 population from the Rudá × Ouro Negro cross and the F2:3 families from the AND 277 × Ouro Negro cross. Ouro Negro is resistant to races 7 and 73 of the ANT and race 63-39 of the ALS pathogens. Conversely, cultivars AND 277 and Rudá are susceptible to races 7 and 73 of ANT, respectively. Both cultivars are susceptible to race 63-39 of ALS. Co-segregation analysis revealed that Co-10 and Phg-ON were inherited together, conferring resistance to races 7 and 73 of ANT and race 63-39 of ALS. The Co-10 and Phg-ON genes were co-segregated and were tightly linked at a distance of 0.0 cM on chromosome Pv04. The molecular marker g2303 was linked to Co-10 and Phg-ON at a distance of 0.0 cM. Because of their physical linkage in a cis configuration, the Co-10 and Phg-ON resistance alleles are inherited together and can be monitored with great efficiency using g2303. The close linkage between the Co-10 and Phg-ON genes and prior evidence are consistent with the existence of a resistance gene cluster at one end of chromosome Pv04, which also contains the Co-3 locus and ANT resistance quantitative trait loci. These results will be very useful for breeding programs aimed at developing bean cultivars with ANT and ALS resistance using marker-assisted selection. PMID:23760652

  18. Invasive Disease Caused by Nontypeable Haemophilus influenzae

    PubMed Central

    de Jonge, Marien I.

    2015-01-01

    The incidence of severe Haemophilus influenza infections, such as sepsis and meningitis, has declined substantially since the introduction of the H. influenzae serotype b vaccine. However, the H. influenzae type b vaccine fails to protect against nontypeable H. influenzae strains, which have become increasingly frequent causes of invasive disease, especially among children and the elderly. We summarize recent literature supporting the emergence of invasive nontypeable H. influenzae and describe mechanisms that may explain its increasing prevalence over the past 2 decades. PMID:26407156

  19. Molecular and Phenotypic Analyses Reveal Association of Diverse Colletotrichum acutatum Groups and a Low Level of C. gloeosporioides with Olive Anthracnose

    PubMed Central

    Talhinhas, Pedro; Sreenivasaprasad, S.; Neves-Martins, João; Oliveira, Helena

    2005-01-01

    Anthracnose (Colletotrichum spp.) is an important disease causing major yield losses and poor oil quality in olives. The objectives were to determine the diversity and distribution pattern of Colletotrichum spp. populations prevalent in olives and their relatedness to anthracnose pathogens in other hosts, assess their pathogenic variability and host preference, and develop diagnostic tools. A total of 128 Colletotrichum spp. isolates representing all olive-growing areas in Portugal and a few isolates from other countries were characterized by molecular and phenotypic assays and compared with reference isolates. Arbitrarily primed PCR data, internal transcribed spacer of rRNA gene and β-tubulin 2 nucleotide sequences, colony characteristics, and benomyl sensitivity showed Colletotrichum acutatum to be dominant (>97%) with limited occurrence of Colletotrichum gloeosporioides (<3%). Among C. acutatum populations, five molecular groups, A2 to A6, were identified. A2 was widely prevalent (89%), coinciding with a high incidence of anthracnose and environmental conditions suitable to disease spread. A4 was dominant in a particular region, while other C. acutatum groups and C. gloeosporioides were sporadic in their occurrence, mostly related to marginal areas of olive cultivation. C. gloeosporioides, isolated from olive fruits with symptoms indistinguishable from those of C. acutatum, showed same virulence rating as the most virulent C. acutatum isolate from group A2. C. acutatum and C. gloeosporioides isolates tested in infected strawberry fruits and strawberry and lupin plants revealed their cross-infection potential. Diagnostic tools were developed from β-tubulin 2 sequences to enable rapid and reliable pathogen detection and differentiation of C. acutatum groups. PMID:15932994

  20. Pulmonary disease caused by nontuberculous mycobacteria.

    PubMed

    Weiss, Curtis H; Glassroth, Jeffrey

    2012-12-01

    The propensity of various nontuberculous mycobacteria to cause lung disease varies widely and is conditioned by host factors; infection is believed to occur from environmental sources. Nontuberculous mycobacteria pulmonary disease (PNTM) is increasing worldwide and Mycobacterium avium complex is the most common cause. PNTM usually occurs in one of three prototypical forms: hypersensitivity pneumonitis, cavitary tuberculosis-like disease or nodular bronchiectasis. PNTM has been linked in some patients to genetic variants of the cystic fibrosis transmembrane conductance regulator gene and a distinct patient phenotype. Interactions between PNTM and other comorbidities are also increasingly appreciated. Guidelines for diagnosis, emphasizing chest imaging and microbiology, have been published; speciation using molecular techniques is critical for accuracy and for treatment decisions. Clinical trials are lacking to inform treatment for many species and experience with M. avium complex and several others species serves as a guide instead. Use of multiple drugs for a period of at least 12 months following sputum conversion is the norm for most species. In vitro drug susceptibility results for many drugs may not correlate with clinical outcomes and such testing should be done on a selective basis. PMID:23234447

  1. Plant growth-promoting Pseudomonas sp. Strains reduce natural occurrence of anthracnose in soybean (Glycine max L.) in central Himalayan region.

    PubMed

    Tripathi, Manisha; Johri, Bhavdish N; Sharma, Alok

    2006-05-01

    Biological control is an accepted important component of current plant disease management strategies. Introduction of bacterized seeds carrying bacterial isolates with proven growth-promotion capabilities and antagonistic characteristics offer a valid alternative to chemical protectants. Root colonization of disease-susceptible (PS 1024) and moderately resistant (PS1042) varieties of soyabean (Glycine Max L) by fluorescent pseudomonad (FLPs) strains GRP3, PEn-4, PRS1, and WRS-24 was studied in relation to natural occurrence of anthracnose caused by Colletotrichum dematium (Pers Ex Fr.) Grove. Rhizoplane population of FLPs was maintained at a critical level (5.3 cfu) up to 30 days of plant growth, followed by a steep decline. Indigenous FLPs population, however, remained nearly unchanged (3.0 to 2.4 log g(-1) root) between 30 days and 75 days of plant growth. The relative FLPs population in rhizosphere was lower than that in rhizoplane. Although intervarietal difference was observed, the root/shoot length remained unaffected. Compared to nonbacterized control, dry root weight was improved by FLPs treatment. Severity of foliar anthracnose was reduced significantly after FLPs treatment in the variety PS 1042. Because the point of FLPs treatment (seed bacterization) was away from the site of disease appearance (leaf), operation of induced systemic resistance in strains PEn-4 and GRP3 appears imminent. PMID:16604418

  2. Genome-Wide Association Studies of Anthracnose and Angular Leaf Spot Resistance in Common Bean (Phaseolus vulgaris L.).

    PubMed

    Perseguini, Juliana Morini Küpper Cardoso; Oblessuc, Paula Rodrigues; Rosa, João Ricardo Bachega Feijó; Gomes, Kleber Alves; Chiorato, Alisson Fernando; Carbonell, Sérgio Augusto Morais; Garcia, Antonio Augusto Franco; Vianello, Rosana Pereira; Benchimol-Reis, Luciana Lasry

    2016-01-01

    The common bean (Phaseolus vulgaris L.) is the world's most important legume for human consumption. Anthracnose (ANT; Colletotrichum lindemuthianum) and angular leaf spot (ALS; Pseudocercospora griseola) are complex diseases that cause major yield losses in common bean. Depending on the cultivar and environmental conditions, anthracnose and angular leaf spot infections can reduce crop yield drastically. This study aimed to estimate linkage disequilibrium levels and identify quantitative resistance loci (QRL) controlling resistance to both ANT and ALS diseases of 180 accessions of common bean using genome-wide association analysis. A randomized complete block design with four replicates was performed for the ANT and ALS experiments, with four plants per genotype in each replicate. Association mapping analyses were performed for ANT and ALS using a mixed linear model approach implemented in TASSEL. A total of 17 and 11 significant statistically associations involving SSRs were detected for ANT and ALS resistance loci, respectively. Using SNPs, 21 and 17 significant statistically associations were obtained for ANT and angular ALS, respectively, providing more associations with this marker. The SSR-IAC167 and PvM95 markers, both located on chromosome Pv03, and the SNP scaffold00021_89379, were associated with both diseases. The other markers were distributed across the entire common bean genome, with chromosomes Pv03 and Pv08 showing the greatest number of loci associated with ANT resistance. The chromosome Pv04 was the most saturated one, with six markers associated with ALS resistance. The telomeric region of this chromosome showed four markers located between approximately 2.5 Mb and 4.4 Mb. Our results demonstrate the great potential of genome-wide association studies to identify QRLs related to ANT and ALS in common bean. The results indicate a quantitative and complex inheritance pattern for both diseases in common bean. Our findings will contribute to more

  3. Genome-Wide Association Studies of Anthracnose and Angular Leaf Spot Resistance in Common Bean (Phaseolus vulgaris L.)

    PubMed Central

    Perseguini, Juliana Morini Küpper Cardoso; Oblessuc, Paula Rodrigues; Rosa, João Ricardo Bachega Feijó; Gomes, Kleber Alves; Chiorato, Alisson Fernando; Carbonell, Sérgio Augusto Morais; Garcia, Antonio Augusto Franco; Vianello, Rosana Pereira; Benchimol-Reis, Luciana Lasry

    2016-01-01

    The common bean (Phaseolus vulgaris L.) is the world’s most important legume for human consumption. Anthracnose (ANT; Colletotrichum lindemuthianum) and angular leaf spot (ALS; Pseudocercospora griseola) are complex diseases that cause major yield losses in common bean. Depending on the cultivar and environmental conditions, anthracnose and angular leaf spot infections can reduce crop yield drastically. This study aimed to estimate linkage disequilibrium levels and identify quantitative resistance loci (QRL) controlling resistance to both ANT and ALS diseases of 180 accessions of common bean using genome-wide association analysis. A randomized complete block design with four replicates was performed for the ANT and ALS experiments, with four plants per genotype in each replicate. Association mapping analyses were performed for ANT and ALS using a mixed linear model approach implemented in TASSEL. A total of 17 and 11 significant statistically associations involving SSRs were detected for ANT and ALS resistance loci, respectively. Using SNPs, 21 and 17 significant statistically associations were obtained for ANT and angular ALS, respectively, providing more associations with this marker. The SSR-IAC167 and PvM95 markers, both located on chromosome Pv03, and the SNP scaffold00021_89379, were associated with both diseases. The other markers were distributed across the entire common bean genome, with chromosomes Pv03 and Pv08 showing the greatest number of loci associated with ANT resistance. The chromosome Pv04 was the most saturated one, with six markers associated with ALS resistance. The telomeric region of this chromosome showed four markers located between approximately 2.5 Mb and 4.4 Mb. Our results demonstrate the great potential of genome-wide association studies to identify QRLs related to ANT and ALS in common bean. The results indicate a quantitative and complex inheritance pattern for both diseases in common bean. Our findings will contribute to more

  4. Corals diseases are a major cause of coral death

    EPA Science Inventory

    Corals, like humans, are susceptible to diseases. Some coral diseases are associated with pathogenic bacteria; however, the causes of most remain unknown. Some diseases trigger rapid and extensive mortality, while others slowly cause localized color changes or injure coral tiss...

  5. Biocontrol of Postharvest Anthracnose of Mango Fruit with Debaryomyces Nepalensis and Effects on Storage Quality and Postharvest Physiology.

    PubMed

    Luo, Shanshan; Wan, Bin; Feng, Shuhan; Shao, Yuanzhi

    2015-11-01

    Anthracnose is presently recognized as one of the most important postharvest disease of mango worldwide. To control the disease, chemical fungicides for a long time was widely used among fruit farmers, but recently found that pathogen had developed increasingly resistance to it. With people's growing desire of healthy and green food, finding new and environmentally friendly biological control approach was very necessary. In this paper, we provided a kind of new antagonistic yeast which enriched the strain resources and the efficacy of Debaryomyces nepalensis against postharvest anthracnose of mango fruit and the influence on quality parameters were investigated. The results showed that the decay incidence and lesion diameter of postharvest anthracnose of mango treated by D. nepalensis were significantly reduced compared with the control fruit stored at 25 °C for 30 d or at 15 °C for 40 d, and the higher concentration of D. nepalensis was, the better the efficacy of the biocontrol was. Study also found that 1 h was the best treatment duration and antagonistic yeast inoculated earlier had good biocontrol effect on anthracnose. Meanwhile, treatment by D. nepalensis could significantly reduce postharvest anthracnose of mango, delay the decrease in firmness, TSS, TA, and ascorbic acid value, and do not impair surface color during postharvest storage. Moreover, the increase in MDA (malondialdehyde) content and increase in cell membrane permeability of fruit treated by D. nepalensis was highly inhibited. The results suggested D. nepalensis treatment could not only maintain storage quality of mango fruit, but also decrease the decay incidence to anthracnose disease. All these results indicated that D. nepalensis has great potential for development of commercial formulations to control postharvest pathogens of mango fruit. PMID:26445226

  6. Allergens causing atopic diseases in canine.

    PubMed

    Youn, Hwa-Young; Kang, Hyung-Seok; Bhang, Dong-Ha; Kim, Min-Kue; Hwang, Cheol-Yong; Han, Hong-Ryul

    2002-12-01

    Canine atopic skin disease is seasonal or sometimes non-seasonal immune-mediated skin disease which occurs commonly in Korea. The definite clinical sign is systemic pruritus, especially on periocular parts, external ear, interdigit spaces and lateral flank. For diagnosis of this dermatitis, complete history taking followed by intradermal skin test and serum in vitro IgE test needs to be performed. Allergen selection for the diagnosis and treatment of atopic dermatitis should be varied geographically. In this study, with intradermal skin test(IDST) the prevalence of atopic disease and what allergens are involved in are researched. Allergens used for IDST included 26 allergen extracts from six allergen groups: grasses, trees, weeds, molds, epidermal allergens and environmental allergens. The number of allergens was 42 in which the positive and negative controls are included. The most common positive allergen reaction was the house dust mites on IDST(22/35, 63%). The other positive allergen reactions were to flea(3/35, 9%), molds(1/35, 3%), house dusts(2/35, 6%), feathers (1/35, 3%), cedar/juniper(1/35, 3%), timothy grass(1/35, 3%) and dandelion(1/35, 3%). In this study, the most prevalent allergen causing atopic dermatitis in dogs in Korea was the house dust mites followed by the flea. PMID:12819384

  7. [Diseases caused by mutations in mitochondrial DNA].

    PubMed

    Wojewoda, Marta; Zabłocki, Krzysztof; Szczepanowska, Joanna

    2011-01-01

    Mitochondrial diseases associated with mutations within mitochondrial genome are a subgroup of metabolic disorders since their common consequence is reduced metabolic efficiency caused by impaired oxidative phophorylation and shortage of ATP. Although the vast majority of mitochondrial proteins (approximately 1500) is encoded by nuclear genome, mtDNA encodes 11 subunits of respiratory chain complexes, 2 subunits of ATP synthase, 22 tRNAs and 2 rRNAs. Up to now, more than 250 pathogenic mutations have been described within mtDNA. The most common are point mutations in genes encoding mitochondrial tRNAs such as 3243A-->G and 8344T-->G that cause, respectively, MELAS (mitochondrial encephalopathy, lactic acidosis and stroke-like episodes) or MIDD (maternally-inherited diabetes and deafness) and MERRF (myoclonic epilepsy with ragged red fibres) syndromes. There have been also found mutations in genes encoding subunits of ATP synthase such as 8993T-->G substitution associated with NARP (neuropathy, ataxia and retinitis pigmentosa) syndrome. It is worth to note that mitochondrial dysfunction can also be caused by mutations within nuclear genes coding for mitochondrial proteins. PMID:21913424

  8. Infection and disease: cause and cure.

    PubMed

    Herrington, C Simon; Douek, Daniel C

    2006-01-01

    Much can be learnt about the mechanisms by which micro-organisms cause disease from the ways that they interact with cells and tissues. This issue of The Journal of Pathology contains articles that address the roles that cell and tissue biology and pathology are playing in the elucidation of these mechanisms. A review of variant Creutzfeldt-Jakob disease is followed by a discussion of severe acute respiratory syndrome (SARS). Two articles on human papillomavirus (HPV) infection address the association between viral infection and neoplasia, as do reviews on viruses and lymphoma/leukaemia, and Kaposi's sarcoma-associated herpesvirus (human herpesvirus 8, HHV8). The section on viral disease concludes with an article on morbilliviruses. The intracellular effects of bacteria are addressed in a review of Listeria infection and a further review outlines recent advances in our knowledge of syphilis. Reviews on Helicobacter and gastric neoplasia, innate defences against methicillin-resistant Staphylococcus aureus (MRSA) infection, and the function of granulomas in tuberculosis also address aspects of tissue responses to bacterial infection. Following a review of the function of immunoglobulin A in defence against infection, a group of articles considers vaccination and gene therapy approaches, the latter involving consideration of both viral and bacterial strategies. The reviews assembled here bridge several gaps: between microbiology and cellular pathology; between host and infecting organism; and between disease and therapy. It is clear that cell and tissue pathology approaches are of value in all of these spheres, providing cell and tissue relevance to microbiological and immunological observations. PMID:16362991

  9. Genetic and physical localization of an anthracnose resistance gene in Medicago truncatula.

    PubMed

    Yang, Shengming; Gao, Muqiang; Deshpande, Shweta; Lin, Shaoping; Roe, Bruce A; Zhu, Hongyan

    2007-12-01

    Anthracnose of alfalfa, caused by the fungal pathogen Colletotrichum trifolii, is one of the most destructive diseases of alfalfa worldwide. An improved understanding of the genetic and molecular mechanisms underlying host resistance will facilitate the development of resistant alfalfa cultivars, thus providing the most efficient and environmentally sound strategy to control alfalfa diseases. Unfortunately, cultivated alfalfa has an intractable genetic system because of its tetrasomic inheritance and out-crossing nature. Nevertheless, the model legume Medicago truncatula, a close relative of alfalfa, has the potential to serve as a surrogate to map and clone the counterparts of agronomically important genes in alfalfa -- particularly, disease resistance genes against economically important pathogens. Here we describe the high-resolution genetic and physical mapping of RCT1, a host resistance gene against C. trifolii race 1 in M. truncatula. We have delimited the RCT1 locus within a physical interval spanning approximately 200 kb located on the top of M. truncatula linkage group 4. RCT1 is part of a complex locus containing numerous genes homologous to previously characterized TIR-NBS-LRR type resistance genes. The result presented in this paper will facilitate the positional cloning of RCT1 in Medicago. PMID:17891371

  10. Diseases caused by enterovirus 71 infection.

    PubMed

    Lee, Ta-Chung; Guo, How-Ran; Su, Huey-Jen Jenny; Yang, Yi-Ching; Chang, Hsiao-Ling; Chen, Kow-Tong

    2009-10-01

    The purpose of this review was to explore the epidemiology, pathogenesis, virology, and management of enterovirus 71 (EV71) infection. Published literature was surveyed by Medline using the keyword "EV71." The reported incidence of cases of hand-foot-mouth disease/herpangina varied from year to year; seasonal variations in incidence were observed, with a peak in incidence during the summer season. Most cases of hand-foot-mouth disease/herpangina hospitalized for complications occurred in children less than 5 years old. The brainstem was the most likely major target of EV71 infection. Different enteroviruses cocirculate in the community annually. The emergence of the EV71 epidemic in the Asia Pacific region has been associated with the circulation of 5 genetic lineages (genotypes B3, B4, C1, C2, C4) that appear to be undergoing rapid evolutionary changes. The relationship between the gene structure of the EV71 virus and the factors that ensure its survival, ease of transmission, and evasion of immunity is still unclear. EV71 central nervous system involvement causes serious clinical illness, death, and long-term neurologic and psychiatric disorders in young children. EV71 infection has emerged as an important public health problem. Vaccine development is recommended for the prevention of EV71 infection in the future. PMID:20118685

  11. Overexpression of a defensin enhances resistance to a fruit-specific anthracnose fungus in pepper.

    PubMed

    Seo, Hyo-Hyoun; Park, Sangkyu; Park, Soomin; Oh, Byung-Jun; Back, Kyoungwhan; Han, Oksoo; Kim, Jeong-Il; Kim, Young Soon

    2014-01-01

    Functional characterization of a defensin, J1-1, was conducted to evaluate its biotechnological potentiality in transgenic pepper plants against the causal agent of anthracnose disease, Colletotrichum gloeosporioides. To determine antifungal activity, J1-1 recombinant protein was generated and tested for the activity against C. gloeosporioides, resulting in 50% inhibition of fungal growth at a protein concentration of 0.1 mg·mL-1. To develop transgenic pepper plants resistant to anthracnose disease, J1-1 cDNA under the control of 35S promoter was introduced into pepper via Agrobacterium-mediated genetic transformation method. Southern and Northern blot analyses confirmed that a single copy of the transgene in selected transgenic plants was normally expressed and also stably transmitted to subsequent generations. The insertion of T-DNA was further analyzed in three independent homozygous lines using inverse PCR, and confirmed the integration of transgene in non-coding region of genomic DNA. Immunoblot results showed that the level of J1-1 proteins, which was not normally accumulated in unripe fruits, accumulated high in transgenic plants but appeared to differ among transgenic lines. Moreover, the expression of jasmonic acid-biosynthetic genes and pathogenesis-related genes were up-regulated in the transgenic lines, which is co-related with the resistance of J1-1 transgenic plants to anthracnose disease. Consequently, the constitutive expression of J1-1 in transgenic pepper plants provided strong resistance to the anthracnose fungus that was associated with highly reduced lesion formation and fungal colonization. These results implied the significance of the antifungal protein, J1-1, as a useful agronomic trait to control fungal disease. PMID:24848280

  12. Symptoms and Causes of Peptic Ulcer Disease

    MedlinePlus

    ... Ulcer Disease Next: Diagnosis of Peptic Ulcer Disease Digestive Disease Organizations Many organizations provide support to patients and medical professionals. View the full list of Digestive Disease Organizations​​ (PDF, 341 KB)​​​​​ NIH...Turning Discovery ...

  13. Candidate Gene Identification with SNP Marker-Based Fine Mapping of Anthracnose Resistance Gene Co-4 in Common Bean

    PubMed Central

    Burt, Andrew J.; William, H. Manilal; Perry, Gregory; Khanal, Raja; Pauls, K. Peter; Kelly, James D.; Navabi, Alireza

    2015-01-01

    Anthracnose, caused by Colletotrichum lindemuthianum, is an important fungal disease of common bean (Phaseolus vulgaris). Alleles at the Co–4 locus confer resistance to a number of races of C. lindemuthianum. A population of 94 F4:5 recombinant inbred lines of a cross between resistant black bean genotype B09197 and susceptible navy bean cultivar Nautica was used to identify markers associated with resistance in bean chromosome 8 (Pv08) where Co–4 is localized. Three SCAR markers with known linkage to Co–4 and a panel of single nucleotide markers were used for genotyping. A refined physical region on Pv08 with significant association with anthracnose resistance identified by markers was used in BLAST searches with the genomic sequence of common bean accession G19833. Thirty two unique annotated candidate genes were identified that spanned a physical region of 936.46 kb. A majority of the annotated genes identified had functional similarity to leucine rich repeats/receptor like kinase domains. Three annotated genes had similarity to 1, 3-β-glucanase domains. There were sequence similarities between some of the annotated genes found in the study and the genes associated with phosphoinositide-specific phosphilipases C associated with Co-x and the COK–4 loci found in previous studies. It is possible that the Co–4 locus is structured as a group of genes with functional domains dominated by protein tyrosine kinase along with leucine rich repeats/nucleotide binding site, phosphilipases C as well as β-glucanases. PMID:26431031

  14. Candidate Gene Identification with SNP Marker-Based Fine Mapping of Anthracnose Resistance Gene Co-4 in Common Bean.

    PubMed

    Burt, Andrew J; William, H Manilal; Perry, Gregory; Khanal, Raja; Pauls, K Peter; Kelly, James D; Navabi, Alireza

    2015-01-01

    Anthracnose, caused by Colletotrichum lindemuthianum, is an important fungal disease of common bean (Phaseolus vulgaris). Alleles at the Co-4 locus confer resistance to a number of races of C. lindemuthianum. A population of 94 F4:5 recombinant inbred lines of a cross between resistant black bean genotype B09197 and susceptible navy bean cultivar Nautica was used to identify markers associated with resistance in bean chromosome 8 (Pv08) where Co-4 is localized. Three SCAR markers with known linkage to Co-4 and a panel of single nucleotide markers were used for genotyping. A refined physical region on Pv08 with significant association with anthracnose resistance identified by markers was used in BLAST searches with the genomic sequence of common bean accession G19833. Thirty two unique annotated candidate genes were identified that spanned a physical region of 936.46 kb. A majority of the annotated genes identified had functional similarity to leucine rich repeats/receptor like kinase domains. Three annotated genes had similarity to 1, 3-β-glucanase domains. There were sequence similarities between some of the annotated genes found in the study and the genes associated with phosphoinositide-specific phosphilipases C associated with Co-x and the COK-4 loci found in previous studies. It is possible that the Co-4 locus is structured as a group of genes with functional domains dominated by protein tyrosine kinase along with leucine rich repeats/nucleotide binding site, phosphilipases C as well as β-glucanases. PMID:26431031

  15. DISEASE OUTBREAKS CAUSED BY DRINKING WATER

    EPA Science Inventory

    Thirty-two waterborne disease outbreaks were reported to the Centers for Disease Control (CDC) and the Environmental Protection Agency in 1981. The outbreaks occurred in 17 states and involved 4430 cases. This was only 64% of the number of outbreaks that were reported in 1980 and...

  16. Animal Diseases Caused by Orbiviruses, Algeria

    PubMed Central

    Madani, Hafsa; Casal, Jordi; Alba, Anna; Allepuz, Alberto; Cêtre-Sossah, Catherine; Hafsi, Leila; Kount-Chareb, Houria; Bouayed-Chaouach, Nadera; Saadaoui, Hassiba

    2011-01-01

    Antibodies against bluetongue virus were detected in cattle, sheep, goats, and camels in Algeria in 2008. Antibodies against epizootic hemorrhagic disease virus were detected in cattle, but antibodies against African horse sickness virus were not detected in horses and mules. Epizootic hemorrhagic disease in northern Africa poses a major risk for the European Union. PMID:22172371

  17. SUBCHRONIC ENDOTOXIN INHALATION CAUSES PERSISTENT AIRWAY DISEASE

    EPA Science Inventory

    ABSTRACT

    The endotoxin component of organic dusts causes acute reversible airflow obstruction and airway inflammation. To test the hypothesis that endotoxin alone causes airway remodeling, we have compared the response of two inbred mouse strains to subchronic endotoxin ...

  18. Detecting Rare Disease-Causing Glitches

    MedlinePlus

    ... to other members. Instead of sequencing the entire human genome , which has 3 billion DNA base pairs, whole- ... Arthritis and Musculoskeletal and Skin Diseases (NIAMS), National Human Genome Research Institute (NHGRI), National Institute of Neurological Disorders ...

  19. Biocontrol of Phytophthora Blight and Anthracnose in Pepper by Sequentially Selected Antagonistic Rhizobacteria against Phytophthora capsici

    PubMed Central

    Sang, Mee Kyung; Shrestha, Anupama; Kim, Du-Yeon; Park, Kyungseok; Pak, Chun Ho; Kim, Ki Deok

    2013-01-01

    We previously developed a sequential screening procedure to select antagonistic bacterial strains against Phytophthora capsici in pepper plants. In this study, we used a modified screening procedure to select effective biocontrol strains against P. capsici; we evaluated the effect of selected strains on Phytophthora blight and anthracnose occurrence and fruit yield in pepper plants under field and plastic house conditions from 2007 to 2009. We selected four potential biocontrol strains (Pseudomonas otitidis YJR27, P. putida YJR92, Tsukamurella tyrosinosolvens YJR102, and Novosphingobium capsulatum YJR107) among 239 bacterial strains. In the 3-year field tests, all the selected strains significantly (P < 0.05) reduced Phytophthora blight without influencing rhizosphere microbial populations; they showed similar or better levels of disease suppressions than in metalaxyl treatment in the 2007 and 2009 tests, but not in the 2008 test. In the 2-year plastic house tests, all the selected strains significantly (P < 0.05) reduced anthracnose incidence in at least one of the test years, but their biocontrol activities were variable. In addition, strains YJR27, YJR92, and YJR102, in certain harvests, increased pepper fruit numbers in field tests and red fruit weights in plastic house tests. Taken together, these results indicate that the screening procedure is rapid and reliable for the selection of potential biocontrol strains against P. capsici in pepper plants. In addition, these selected strains exhibited biocontrol activities against anthracnose, and some of the strains showed plant growth-promotion activities on pepper fruit. PMID:25288942

  20. Haemophilus haemolyticus Isolates Causing Clinical Disease

    PubMed Central

    Wang, Xin; Briere, Elizabeth C.; Katz, Lee S.; Cohn, Amanda C.; Clark, Thomas A.; Messonnier, Nancy E.; Mayer, Leonard W.

    2012-01-01

    We report seven cases of Haemophilus haemolyticus invasive disease detected in the United States, which were previously misidentified as nontypeable Haemophilus influenzae. All cases had different symptoms and presentations. Our study suggests that a testing scheme that includes reliable PCR assays and standard microbiological methods should be used in order to improve H. haemolyticus identification. PMID:22573587

  1. Genetic defect causing familial Alzheimer's disease maps on chromosome 21

    SciTech Connect

    St. George-Hyslop, P.H.; Tanzi, R.E.; Polinsky, R.J.; Haines, J.L.; Nee, L.; Watkins, P.C.; Myers, R.H.; Feldman, R.G.; Pollen, D.; Drachman, D.; Growdon, J.

    1987-02-20

    Alzheimer's disease is a leading cause of morbidity and mortality among the elderly. Several families have been described in which Alzheimer's disease is caused by an autosomal dominant gene defect. The chromosomal location of this defective gene has been discovered by using genetic linkage to DNA markers on chromosome 21. The localization on chromosome 21 provides an explanation for the occurrence of Alzheimer's disease-like pathology in Down syndrome. Isolation and characterization of the gene at this locus may yield new insights into the nature of the defect causing familial Alzheimer's disease and possibly, into the etiology of all forms of Alzheimer's disease.

  2. Assessment of sorghum germplasm from Burkina Faso and South Africa to identify new sources of resistance to grain mold and anthracnose

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Sorghum is an important worldwide crop whose yield can be significantly reduced by anthracnose (Colletotrichum sublineola) and grain mold diseases (multiple fungi). The identification of new genetic sources of resistance to both diseases is imperative for the development of new sorghum varieties. T...

  3. Lung Disease Caused by Mycobacterium malmoense in an Immunocompetent Patient

    PubMed Central

    Jeon, Min Kyung; Yoon, Jung A; Kim, Junhwan; Yi, Sangyoung; Sung, Heungsup; Shim, Tae Sun

    2015-01-01

    Mycobacterium malmoense is a very rare cause of lung disease in South Korea. We reported the first case of lung disease caused by M. malmoense in an immunocompetent patient. The patient was successfully treated with a 14-month course of antibiotics. PMID:26175789

  4. Does aluminum smelting cause lung disease?

    PubMed

    Abramson, M J; Wlodarczyk, J H; Saunders, N A; Hensley, M J

    1989-04-01

    The evidence concerning a relationship between work in the aluminum industry and lung disease has been reviewed using epidemiologic criteria. Adequate data on environmental exposure are rarely presented. Case series on aluminum potroom workers over the past 50 years have identified an asthmalike syndrome that appears to be due to an irritant rather than an allergic mechanism. These studies have been supported by evidence of within shift variability of measures of lung function. However, to date, there is inadequate evidence to resolve the question of whether potroom exposure initiates asthma or merely precipitates asthmalike symptoms in a predisposed individual. Cross-sectional studies have demonstrated evidence of reduced lung function, consistent with chronic airflow limitation. In exposed aluminum smelter workers compared to unexposed control subjects. Cigarette smoking, the major potential confounding variable, has been measured and accounted for in multivariate analyses. To date, evidence is lacking from longitudinal studies about the development of disabling chronic obstructive lung disease. Exposure to coal tar pitch volatiles in the production and consumption of anodes has biologic plausibility for an association of lung cancer with work in an aluminum smelter. Although retrospective mortality studies have failed to account for the probable high prevalence of smoking in blue collar workers, the relative risk of lung cancer is very low if present at all. Pulmonary fibrosis has not been shown to be a significant problem in aluminum smelter workers. Future research in the aluminum industry needs to concentrate on longitudinal studies, preferably with an inception cohort for the investigation of potroom asthma. PMID:2648910

  5. Does aluminum smelting cause lung disease

    SciTech Connect

    Abramson, M.J.; Wlodarczyk, J.H.; Saunders, N.A.; Hensley, M.J.

    1989-04-01

    The evidence concerning a relationship between work in the aluminum industry and lung disease has been reviewed using epidemiologic criteria. Adequate data on environmental exposure are rarely presented. Case series on aluminum potroom workers over the past 50 years have identified an asthmalike syndrome that appears to be due to an irritant rather than an allergic mechanism. These studies have been supported by evidence of within shift variability of measures of lung function. However, to date, there is inadequate evidence to resolve the question of whether potroom exposure initiates asthma or merely precipitates asthmalike symptoms in a predisposed individual. Cross-sectional studies have demonstrated evidence of reduced lung function, consistent with chronic airflow limitation. In exposed aluminum smelter workers compared to unexposed control subjects. Cigarette smoking, the major potential confounding variable, has been measured and accounted for in multivariate analyses. To date, evidence is lacking from longitudinal studies about the development of disabling chronic obstructive lung disease. Exposure to coal tar pitch volatiles in the production and consumption of anodes has biologic plausibility for an association of lung cancer with work in an aluminum smelter. Although retrospective mortality studies have failed to account for the probable high prevalence of smoking in blue collar workers, the relative risk of lung cancer is very low if present at all. Pulmonary fibrosis has not been shown to be a significant problem in aluminum smelter workers. Future research in the aluminum industry needs to concentrate on longitudinal studies, preferably with an inception cohort for the investigation of potroom asthma. 92 references.

  6. Diseases and Their Management

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Important diseases and their management practices of lentil were reviewed. The diseases reveiwed include Ascochyta blight (Ascochyta lentis), Anthracnose (Colletotrichum truncatum), White mold (Sclerotinia sclerotiorum), rust (Uromyces viciae-fabae), Botrytis gray mold (Botrytis cinerea and B. faba...

  7. Reversible renal impairment caused by thyroid disease.

    PubMed

    Chakera, Aron; Paul, Hans-Joerg; O'Callaghan, Chris A

    2010-04-01

    Renal impairment is a common finding in clinical practice and is increasingly recognized with the routine reporting of estimated glomerular filtration rates. Clinical assessment is essential to determine which of the many possible investigations are appropriate. Thyroid hormones regulate many cellular functions, and abnormalities of the active thyroid hormones, thyroxine (T(4)) and tri-iodothyronine (T(3)), can influence serum creatinine levels. Evaluation of thyroid function is easily overlooked, but important in this context, as hypothyroidism is common and can cause renal impairment, which is typically reversible. Renal dysfunction may also be more frequent in hyperthyroidism than is recognized. This report describe how a dramatic elevation in serum creatinine paralleled the development of hyperthyroidism, with a return of the creatinine to normal following treatment of the hyperthyroid state. PMID:20199343

  8. Respiratory disease caused by synthetic fibres: a new occupational disease.

    PubMed Central

    Pimentel, J C; Avila, R; Lourenço, A G

    1975-01-01

    Seven patients exposed to the inhalation of synthetic fibres presented with various bronchopulmonary diseases, such as asthma, extrinsic allergic alveolitis, chronic bronchitis with bronchiectasis, spontaneous pneumothorax, and chronic pneumonia. The histological features are described and an attempt has been made to set up immunological techniques for the diagnosis. A series of histochemical techniques, based on textile chemistry, are proposed for the identification of the inclusions found in bronchopulmonary lesions. The results of the experimental production of the disease in guinea-pigs by the inhalation of synthetic fibre dusts are presented. The prognosis of these cases is good in the acute or recently established cases but is poor when widespread and irreversible fibrosis has set in. The authors consider that pulmonary disease due to inhaled particles is probably set off by an individual factor, possibly immunological. Images PMID:1179318

  9. Celiac disease: A missed cause of metabolic bone disease

    PubMed Central

    Rastogi, Ashu; Bhadada, Sanjay K.; Bhansali, Anil; Kochhar, Rakesh; Santosh, Ramakrishnan

    2012-01-01

    Introduction: Celiac disease (CD) is a highly prevalent autoimmune disease. The symptoms of CD are varied and atypical, with many patients having no gastrointestinal symptoms. Metabolic bone disease (MBD) is a less recognized manifestation of CD associated with spectrum of musculoskeletal signs and symptoms, viz. bone pains, proximal muscle weakness, osteopenia, osteoporosis, and fracture. We here report five patients who presented with severe MBD as the only manifestation of CD. Materials and Methods: Records of 825 patients of CD diagnosed during 2002–2010 were retrospectively analyzed for clinical features, risk factors, signs, biochemical, and radiological parameters. Results: We were able to identify five patients (0.6%) of CD who had monosymptomatic presentation with musculoskeletal symptoms and signs in the form of bone pains, proximal myopathy, and fragility fractures without any gastrointestinal manifestation. All the five patients had severe MBD in the form of osteopenia, osteoporosis, and fragility fractures. Four of the five patients had additional risk factors such as antiepileptic drugs, chronic alcohol consumption, malnutrition, and associated vitamin D deficiency which might have contributed to the severity of MBD. Conclusion: Severe metabolic disease as the only presentation of CD is rare. Patients show significant improvement in clinical, biochemical, and radiological parameters with gluten-free diet, calcium, and vitamin D supplementation. CD should be looked for routinely in patients presenting with unexplained MBD. PMID:23087864

  10. SEPARATING THE CAUSES AND CONSEQUENCES IN DISEASE TRANSCRIPTOME

    PubMed Central

    Li, Yong Fuga; Xin, Fuxiao; Altman, Russ B.

    2015-01-01

    The causes of complex diseases are multifactorial and the phenotypes of complex diseases are typically heterogeneous, posting significant challenges for both the experiment design and statistical inference in the study of such diseases. Transcriptome profiling can potentially provide key insights on the pathogenesis of diseases, but the signals from the disease causes and consequences are intertwined, leaving it to speculations what are likely causal. Genome-wide association study on the other hand provides direct evidences on the potential genetic causes of diseases, but it does not provide a comprehensive view of disease pathogenesis, and it has difficulties in detecting the weak signals from individual genes. Here we propose an approach diseaseExPatho that combines transcriptome data, regulome knowledge, and GWAS results if available, for separating the causes and consequences in the disease transcriptome. DiseaseExPatho computationally de-convolutes the expression data into gene expression modules, hierarchically ranks the modules based on regulome using a novel algorithm, and given GWAS data, it directly labels the potential causal gene modules based on their correlations with genome-wide gene-disease associations. Strikingly, we observed that the putative causal modules are not necessarily differentially expressed in disease, while the other modules can show strong differential expression without enrichment of top GWAS variations. On the other hand, we showed that the regulatory network based module ranking prioritized the putative causal modules consistently in 6 diseases, We suggest that the approach is applicable to other common and rare complex diseases to prioritize causal pathways with or without genome-wide association studies. PMID:26776202

  11. Do We Know What Causes Gestational Trophoblastic Disease?

    MedlinePlus

    ... know what causes gestational trophoblastic disease? Normally, the sperm and egg cells each provide a set of ... hydatidiform (HY-duh-TIH-dih-form) moles , a sperm cell fertilizes an abnormal egg cell that has ...

  12. Transcriptome Analysis of an Anthracnose-Resistant Tea Plant Cultivar Reveals Genes Associated with Resistance to Colletotrichum camelliae

    PubMed Central

    Wang, Lu; Wang, Yuchun; Cao, Hongli; Hao, Xinyuan; Zeng, Jianming; Yang, Yajun; Wang, Xinchao

    2016-01-01

    Tea plant breeding is a topic of great economic importance. However, disease remains a major cause of yield and quality losses. In this study, an anthracnose-resistant cultivar, ZC108, was developed. An infection assay revealed different responses to Colletotrichum sp. infection between ZC108 and its parent cultivar LJ43. ZC108 had greater resistance than LJ43 to Colletotrichum camelliae. Additionally, ZC108 exhibited earlier sprouting in the spring, as well as different leaf shape and plant architecture. Microarray data revealed that the genes that are differentially expressed between LJ43 and ZC108 mapped to secondary metabolism-related pathways, including phenylpropanoid biosynthesis, phenylalanine metabolism, and flavonoid biosynthesis pathways. In addition, genes involved in plant hormone biosynthesis and signaling as well as plant-pathogen interaction pathways were also changed. Quantitative real-time PCR was used to examine the expression of 27 selected genes in infected and uninfected tea plant leaves. Genes encoding a MADS-box transcription factor, NBS-LRR disease-resistance protein, and phenylpropanoid metabolism pathway components (CAD, CCR, POD, beta-glucosidase, ALDH and PAL) were among those differentially expressed in ZC108. PMID:26849553

  13. Hereditary Causes of Kidney Stones and Chronic Kidney Disease

    PubMed Central

    Edvardsson, Vidar O.; Goldfarb, David S.; Lieske, John C.; Beara-Lasic, Lada; Anglani, Franca; Milliner, Dawn S.; Palsson, Runolfur

    2013-01-01

    Adenine phosphoribosyltransferase (APRT) deficiency, cystinuria, Dent disease, familial hypomagnesemia with hypercalciuria and nephrocalcinosis (FHHNC) and primary hyperoxaluria (PH) are rare but important causes of severe kidney stone disease and/or chronic kidney disease in children. Recurrent kidney stone disease and nephrocalcinosis, particularly in pre-pubertal children, should alert the physician to the possibility of an inborn error of metabolism as the underlying cause. Unfortunately, the lack of recognition and knowledge of the five disorders has frequently resulted in an unacceptable delay in diagnosis and treatment, sometimes with grave consequences. A high index of suspicion coupled with early diagnosis may reduce or even prevent the serious long-term complications of these diseases. In this paper, we review the epidemiology, clinical features, diagnosis, treatment and outcome of patients with APRT deficiency, cystinuria, Dent disease, FHHNC and PH with emphasis on childhood manifestations. PMID:23334384

  14. [Professional diseases caused by the action of antibiotics].

    PubMed

    Gerasimova, M M; Bogoslovskaia, I A; Karcharova, S V; Litovskaia, A V

    1989-05-01

    A follow-up study is presented of the clinical aspects and pathogenesis of professional diseases due to the effect of antibiotics. A progressing, stable and regressing course of the disease was singled out. It is shown that in the long-term period the main pathogenetic mechanism was allergic vasculitis caused by penicillin, streptomycin and Candida fungi. PMID:2773415

  15. [A brief history of the natural causes of human disease].

    PubMed

    Lips-Castro, Walter

    2015-01-01

    In the study of the causes of disease that have arisen during the development of humankind, one can distinguish three major perspectives: the natural, the supernatural, and the artificial. In this paper we distinguish the rational natural causes of disease from the irrational natural causes. Within the natural and rational causal approaches of disease, we can highlight the Egyptian theory of putrid intestinal materials called "wechdu", the humoral theory, the atomistic theory, the contagious theory, the cellular theory, the molecular (genetic) theory, and the ecogenetic theory. Regarding the irrational, esoteric, and mystic causal approaches to disease, we highlight the astrological, the alchemical, the iatrochemical, the iatromechanical, and others (irritability, solidism, brownism, and mesmerism). PMID:26581540

  16. Molecular Diversity of Anthracnose Pathogen Populations Associated with UK Strawberry Production Suggests Multiple Introductions of Three Different Colletotrichum Species

    PubMed Central

    Baroncelli, Riccardo; Zapparata, Antonio; Sarrocco, Sabrina; Sukno, Serenella A.; Lane, Charles R.; Thon, Michael R.; Vannacci, Giovanni; Holub, Eric; Sreenivasaprasad, Surapareddy

    2015-01-01

    Fragaria × ananassa (common name: strawberry) is a globally cultivated hybrid species belonging to Rosaceae family. Colletotrichum acutatum sensu lato (s.l.) is considered to be the second most economically important pathogen worldwide affecting strawberries. A collection of 148 Colletotrichum spp. isolates including 67 C. acutatum s.l. isolates associated with the phytosanitary history of UK strawberry production were used to characterize multi-locus genetic variation of this pathogen in the UK, relative to additional reference isolates that represent a worldwide sampling of the diversity of the fungus. The evidence indicates that three different species C. nymphaeae, C. godetiae and C. fioriniae are associated with strawberry production in the UK, which correspond to previously designated genetic groups A2, A4 and A3, respectively. Among these species, 12 distinct haplotypes were identified suggesting multiple introductions into the country. A subset of isolates was also used to compare aggressiveness in causing disease on strawberry plants and fruits. Isolates belonging to C. nymphaeae, C. godetiae and C. fioriniae representative of the UK anthracnose pathogen populations showed variation in their aggressiveness. Among the three species, C. nymphaeae and C. fioriniae appeared to be more aggressive compared to C. godetiae. This study highlights the genetic and pathogenic heterogeneity of the C. acutatum s.l. populations introduced into the UK linked to strawberry production. PMID:26086351

  17. Novel clones of Streptococcus pneumoniae causing invasive disease in Malaysia.

    PubMed

    Jefferies, Johanna M; Mohd Yusof, Mohd Yasim; Devi Sekaran, Shamala; Clarke, Stuart C

    2014-01-01

    Although Streptococcus pneumoniae is a leading cause of childhood disease in South East Asia, little has previously been reported regarding the epidemiology of invasive pneumococcal disease in Malaysia and very few studies have explored pneumococcal epidemiology using multilocus sequence typing (MLST). Here we describe serotype, multilocus sequence type (ST), and penicillin susceptibility of thirty pneumococcal invasive disease isolates received by the University of Malaya Medical Centre between February 2000 and January 2007 and relate this to the serotypes included in current pneumococcal conjugate vaccines. A high level of diversity was observed; fourteen serotypes and 26 sequence types (ST), (11 of which were not previously described) were detected from 30 isolates. Penicillin non-susceptible pneumococci accounted for 33% of isolates. The extent of molecular heterogeneity within carried and disease-causing Malaysian pneumococci remains unknown. Larger surveillance and epidemiological studies are now required in this region to provide robust evidence on which to base future vaccine policy. PMID:24941079

  18. Causes of Mortality and Diseases in Farmed Deer in Switzerland

    PubMed Central

    Sieber, Veronika; Robert, Nadia; Schybli, Martina; Sager, Heinz; Miserez, Raymond; Engels, Monika; Ryser-Degiorgis, Marie-Pierre

    2010-01-01

    To investigate diseases and causes of mortality in Swiss farmed deer, deer found dead or shot due to diseased condition between March 2003 and December 2004 were requested for a complete postmortem examination. One hundred and sixty-two animals were submitted. Perinatal mortality, necrobacillosis in 3 week to 6 month old deer, and endoparasitosis in 6 month to 2 year old deer were identified as the most important causes of loss, followed by ruminal acidosis, which was diagnosed in 22% of deer older than 1 year. Congenital malformations were observed in 15% of deer less than 6 months old. Reportable infectious diseases known as major problems in deer farming in other countries were rare (yersiniosis, malignant catarrhal fever) or not observed (tuberculosis, chronic wasting disease). Overall, the results indicate that the Swiss deer population does not present major health problems of concern for domestic animals. PMID:20706668

  19. Effects of pretreatment with simulated acid rain on the severity of dogwood anthracnose

    SciTech Connect

    Britton, K.O.; Berrang, P.; Mavity, E.

    1996-06-01

    The effects of simulated acid rain on dogwood anthracnose severity were evaluated in a series of greenhouse and field experiments over a 4-year period. In 1990 and 1991, Cornus florida seedlings received 10 weekly foliar applications of simulated rain adjusted to pH 2.5, 3.5, 4.5, and 5.5. They were then placed under mature dogwoods naturally infected with Discula destructive. In both years, the percent leaf area infected increased significantly as the pH of the simulated rain solution decreased. In 1992 and 1993, seedlings were wrapped in plastic bags below the root collar to permit separate application of simulated acid rain (pH 2.5) or normal rain (pH 5.5) to the foliage or the growing medium or both. Application of pH 2.5 rain to the growing medium increased disease severity. Foliar applications alone did not increase disease. These results suggest that changes in nutrient availability, rather than foliar damage, are responsible for the increase in anthracnose severity in dogwoods pretreated with simulated acid rain. 41 refs., 1 fig., 1 tab.

  20. Lack of exercise is a major cause of chronic diseases

    PubMed Central

    Booth, Frank W.; Roberts, Christian K.; Laye, Matthew J.

    2014-01-01

    Chronic diseases are major killers in the modern era. Physical inactivity is a primary cause of most chronic diseases. The initial third of the article considers: activity and prevention definitions; historical evidence showing physical inactivity is detrimental to health and normal organ functional capacities; cause vs. treatment; physical activity and inactivity mechanisms differ; gene-environment interaction [including aerobic training adaptations, personalized medicine, and co-twin physical activity]; and specificity of adaptations to type of training. Next, physical activity/exercise is examined as primary prevention against 35 chronic conditions [Accelerated biological aging/premature death, low cardiorespiratory fitness (VO2max), sarcopenia, metabolic syndrome, obesity, insulin resistance, prediabetes, type 2 diabetes, non-alcoholic fatty liver disease, coronary heart disease, peripheral artery disease, hypertension, stroke, congestive heart failure, endothelial dysfunction, arterial dyslipidemia, hemostasis, deep vein thrombosis, cognitive dysfunction, depression and anxiety, osteoporosis, osteoarthritis, balance, bone fracture/falls, rheumatoid arthritis, colon cancer, breast cancer, endometrial cancer, gestational diabetes, preeclampsia, polycystic ovary syndrome, erectile dysfunction, pain, diverticulitis, constipation, and gallbladder diseases]. The article ends with consideration of deterioration of risk factors in longer-term sedentary groups; clinical consequences of inactive childhood/adolescence; and public policy. In summary, the body rapidly maladapts to insufficient physical activity, and if continued, results in substantial decreases in both total and quality years of life. Taken together, conclusive evidence exists that physical inactivity is one important cause of most chronic diseases. In addition, physical activity primarily prevents, or delays, chronic diseases, implying that chronic disease need not be an inevitable outcome during life

  1. Lack of exercise is a major cause of chronic diseases.

    PubMed

    Booth, Frank W; Roberts, Christian K; Laye, Matthew J

    2012-04-01

    Chronic diseases are major killers in the modern era. Physical inactivity is a primary cause of most chronic diseases. The initial third of the article considers: activity and prevention definitions; historical evidence showing physical inactivity is detrimental to health and normal organ functional capacities; cause versus treatment; physical activity and inactivity mechanisms differ; gene-environment interaction (including aerobic training adaptations, personalized medicine, and co-twin physical activity); and specificity of adaptations to type of training. Next, physical activity/exercise is examined as primary prevention against 35 chronic conditions [accelerated biological aging/premature death, low cardiorespiratory fitness (VO2max), sarcopenia, metabolic syndrome, obesity, insulin resistance, prediabetes, type 2 diabetes, nonalcoholic fatty liver disease, coronary heart disease, peripheral artery disease, hypertension, stroke, congestive heart failure, endothelial dysfunction, arterial dyslipidemia, hemostasis, deep vein thrombosis, cognitive dysfunction, depression and anxiety, osteoporosis, osteoarthritis, balance, bone fracture/falls, rheumatoid arthritis, colon cancer, breast cancer, endometrial cancer, gestational diabetes, pre-eclampsia, polycystic ovary syndrome, erectile dysfunction, pain, diverticulitis, constipation, and gallbladder diseases]. The article ends with consideration of deterioration of risk factors in longer-term sedentary groups; clinical consequences of inactive childhood/adolescence; and public policy. In summary, the body rapidly maladapts to insufficient physical activity, and if continued, results in substantial decreases in both total and quality years of life. Taken together, conclusive evidence exists that physical inactivity is one important cause of most chronic diseases. In addition, physical activity primarily prevents, or delays, chronic diseases, implying that chronic disease need not be an inevitable outcome during life

  2. Neuromuscular Electrical Stimulation Therapy for Dysphagia Caused by Wilson's Disease

    PubMed Central

    Lee, Seon Yeong; Yang, Hee Seung; Lee, Seung Hwa; Jeung, Hae Won; Park, Young Ok

    2012-01-01

    Wilson's disease is an autosomal recessive disorder of abnormal copper metabolism. Although dysphagia is a common complaint of patients with Wilson's disease and pneumonia is an important cause of death in these patients, management of swallowing function has rarely been reported in the context of Wilson's disease. Hence, we report a case of Wilson's disease presenting with dysphagia. A 33-year-old man visited our hospital with a complaint of difficulty in swallowing, since about last 7 years and which had worsened since the last 2-3 months. He was diagnosed with Wilson's disease about 13 years ago. On the initial VFSS, reduced hyoid bone movement, impaired epiglottic movement and moderate amount of residue in the valleculae during the pharyngeal phase were noted. After 10 sessions of neuromuscular electrical stimulation for 1 hour per day, decreased amount of residue was observed in the valleculae during the pharyngeal phase on the follow-up VFSS. PMID:22837979

  3. Expression of pathogenesis-related (PR) genes in avocados fumigated with thyme oil vapours and control of anthracnose.

    PubMed

    Bill, Malick; Sivakumar, Dharini; Beukes, Mervyn; Korsten, Lise

    2016-03-01

    Thyme oil (TO) fumigation (96μll(-1)) to cv. Hass and Ryan avocados significantly reduced anthracnose incidence compared to prochloraz and the untreated control. Also, enhanced activities of β-1,3-glucanase, chitinase were noted in both cultivars. TO fumigation induced the expression of both β-1,3-glucanase and chitinase genes in naturally infected fruit of both cultivars, during storage at 7 or 7.5°C for up to 21d and during subsequent simulated market shelf conditions at 20°C for 5d. However, the impact of TO fumigation on the β-1,3-glucanase gene expression was higher in both cultivars. Higher gene regulation and β-1,3-glucanase, chitinase activities were observed in cv. Ryan compared to Hass. Although TO fumigation significantly reduced anthracnose incidence in both naturally infected cultivars, the inhibitory effect was slightly higher in cv. Ryan than Hass. Thus, postharvest TO fumigation had positive effects on enhancing anthracnose disease resistance during storage and also gave a residual effect during the simulated shelf life. PMID:26471637

  4. Genetic Factors Are Not the Major Causes of Chronic Diseases.

    PubMed

    Rappaport, Stephen M

    2016-01-01

    The risk of acquiring a chronic disease is influenced by a person's genetics (G) and exposures received during life (the 'exposome', E) plus their interactions (G×E). Yet, investigators use genome-wide association studies (GWAS) to characterize G while relying on self-reported information to classify E. If E and G×E dominate disease risks, this imbalance obscures important causal factors. To estimate proportions of disease risk attributable to G (plus shared exposures), published data from Western European monozygotic (MZ) twins were used to estimate population attributable fractions (PAFs) for 28 chronic diseases. Genetic PAFs ranged from 3.4% for leukemia to 48.6% for asthma with a median value of 18.5%. Cancers had the lowest PAFs (median = 8.26%) while neurological (median = 26.1%) and lung (median = 33.6%) diseases had the highest PAFs. These PAFs were then linked with Western European mortality statistics to estimate deaths attributable to G for heart disease and nine cancer types. Of 1.53 million Western European deaths in 2000, 0.25 million (16.4%) could be attributed to genetics plus shared exposures. Given the modest influences of G-related factors on the risks of chronic diseases in MZ twins, the disparity in coverage of G and E in etiological research is problematic. To discover causes of disease, GWAS should be complemented with exposome-wide association studies (EWAS) that profile chemicals in biospecimens from incident disease cases and matched controls. PMID:27105432

  5. Credibility Analysis of Putative Disease-Causing Genes Using Bioinformatics

    PubMed Central

    Abel, Olubunmi; Powell, John F.; Andersen, Peter M.; Al-Chalabi, Ammar

    2013-01-01

    Background Genetic studies are challenging in many complex diseases, particularly those with limited diagnostic certainty, low prevalence or of old age. The result is that genes may be reported as disease-causing with varying levels of evidence, and in some cases, the data may be so limited as to be indistinguishable from chance findings. When there are large numbers of such genes, an objective method for ranking the evidence is useful. Using the neurodegenerative and complex disease amyotrophic lateral sclerosis (ALS) as a model, and the disease-specific database ALSoD, the objective is to develop a method using publicly available data to generate a credibility score for putative disease-causing genes. Methods Genes with at least one publication suggesting involvement in adult onset familial ALS were collated following an exhaustive literature search. SQL was used to generate a score by extracting information from the publications and combined with a pathogenicity analysis using bioinformatics tools. The resulting score allowed us to rank genes in order of credibility. To validate the method, we compared the objective ranking with a rank generated by ALS genetics experts. Spearman's Rho was used to compare rankings generated by the different methods. Results The automated method ranked ALS genes in the following order: SOD1, TARDBP, FUS, ANG, SPG11, NEFH, OPTN, ALS2, SETX, FIG4, VAPB, DCTN1, TAF15, VCP, DAO. This compared very well to the ranking of ALS genetics experts, with Spearman's Rho of 0.69 (P = 0.009). Conclusion We have presented an automated method for scoring the level of evidence for a gene being disease-causing. In developing the method we have used the model disease ALS, but it could equally be applied to any disease in which there is genotypic uncertainty. PMID:23755159

  6. Anthracnose resistance in sorghum breeding lines developed from Ethiopian germplasm

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Ninety-nine dwarf and photoperiod-insensitive breeding lines developed from Ethiopian sorghum germplasm were inoculated with Colletotrichum sublineolum and evaluated for anthracnose resistance at the Tropical Agriculture Research Station in Isabela, Puerto Rico during the 2008 and 2009 growing seaso...

  7. Noroviruses: The Principal Cause of Foodborne Disease Worldwide

    PubMed Central

    Koo, Hoonmo L.; Ajami, Nadim; Atmar, Robert L.; DuPont, Herbert L.

    2011-01-01

    Noroviruses are the leading cause of foodborne disease outbreaks worldwide, and may soon eclipse rotaviruses as the most common cause of severe pediatric gastroenteritis, as the use of rotavirus vaccines becomes more widespread. Genetic mutations and recombinations contribute to the broad heterogeneity of noroviruses and the emergence of new epidemic strains. Although typically a self-limited disease, norovirus gastroenteritis can cause significant morbidity and mortality among children, the elderly, and the immunocompromised. The lack of a cell culture or small animal model has hindered norovirus research and the development of novel therapeutic and preventative interventions. However, vaccines based on norovirus capsid protein virus-like particles are promising and may one day become widely available through transgenic expression in plants. PMID:20670600

  8. Congenital Heart Disease: Causes, Diagnosis, Symptoms, and Treatments.

    PubMed

    Sun, RongRong; Liu, Min; Lu, Lei; Zheng, Yi; Zhang, Peiying

    2015-07-01

    The congenital heart disease includes abnormalities in heart structure that occur before birth. Such defects occur in the fetus while it is developing in the uterus during pregnancy. About 500,000 adults have congenital heart disease in USA (WebMD, Congenital heart defects medications, www.WebMD.com/heart-disease/tc/congenital-heart-defects-medications , 2014). 1 in every 100 children has defects in their heart due to genetic or chromosomal abnormalities, such as Down syndrome. The excessive alcohol consumption during pregnancy and use of medications, maternal viral infection, such as Rubella virus, measles (German), in the first trimester of pregnancy, all these are risk factors for congenital heart disease in children, and the risk increases if parent or sibling has a congenital heart defect. These are heart valves defects, atrial and ventricular septa defects, stenosis, the heart muscle abnormalities, and a hole inside wall of the heart which causes defect in blood circulation, heart failure, and eventual death. There are no particular symptoms of congenital heart disease, but shortness of breath and limited ability to do exercise, fatigue, abnormal sound of heart as heart murmur, which is diagnosed by a physician while listening to the heart beats. The echocardiogram or transesophageal echocardiogram, electrocardiogram, chest X-ray, cardiac catheterization, and MRI methods are used to detect congenital heart disease. Several medications are given depending on the severity of this disease, and catheter method and surgery are required for serious cases to repair heart valves or heart transplantation as in endocarditis. For genetic study, first DNA is extracted from blood followed by DNA sequence analysis and any defect in nucleotide sequence of DNA is determined. For congenital heart disease, genes in chromosome 1 show some defects in nucleotide sequence. In this review the causes, diagnosis, symptoms, and treatments of congenital heart disease are described

  9. Chemicals and environmentally caused diseases in developing countries

    SciTech Connect

    Jamall, I.S.; Davis, B. )

    1991-06-01

    This chapter discusses international aspects of diseases resulting from exposure to chemical pollutants in the environment, with an emphasis on developing countries. These countries share many of the same problems of air, water, and pesticide pollution that face the more industrialized countries. In developing countries, however, the problems are compounded by a number of unique situations, viz., economic priorities, high burden of infectious diseases, impoverishment, and absence of a regulatory framework for the disposal of toxic chemicals. This discussion emphasizes the importance of interactions among toxicants, malnutrition, and infectious diseases for both urban and rural populations insofar as these interactions contribute to disease. Toxicants not only produce disease directly but also exacerbate diseases with other causes. Specific examples from developing countries demonstrate how human health effects from exposures to environmental chemicals can be assessed. While they do not strictly fall under the rubric of developing countries, the public health consequences of inadequate control of environmental pollution in the East European countries should demonstrate the magnitude of the problem, except that in developing countries the public health consequence of environmental chemicals will be aggravated by the widespread malnutrition and high prevalence of infectious diseases. Much needs to be done before we can adequately quantify the contribution of environmental chemicals to morbidity and mortality in developing countries with the level of sophistication now evident in the charting of infectious diseases in these countries. 52 references.

  10. Helicobacter pylori and autoimmune disease: Cause or bystander

    PubMed Central

    Smyk, Daniel S; Koutsoumpas, Andreas L; Mytilinaiou, Maria G; Rigopoulou, Eirini I; Sakkas, Lazaros I; Bogdanos, Dimitrios P

    2014-01-01

    Helicobacter pylori (H. pylori) is the main cause of chronic gastritis and a major risk factor for gastric cancer. This pathogen has also been considered a potential trigger of gastric autoimmunity, and in particular of autoimmune gastritis. However, a considerable number of reports have attempted to link H. pylori infection with the development of extra-gastrointestinal autoimmune disorders, affecting organs not immediately relevant to the stomach. This review discusses the current evidence in support or against the role of H. pylori as a potential trigger of autoimmune rheumatic and skin diseases, as well as organ specific autoimmune diseases. We discuss epidemiological, serological, immunological and experimental evidence associating this pathogen with autoimmune diseases. Although over one hundred autoimmune diseases have been investigated in relation to H. pylori, we discuss a select number of papers with a larger literature base, and include Sjögrens syndrome, rheumatoid arthritis, systemic lupus erythematosus, vasculitides, autoimmune skin conditions, idiopathic thrombocytopenic purpura, autoimmune thyroid disease, multiple sclerosis, neuromyelitis optica and autoimmune liver diseases. Specific mention is given to those studies reporting an association of anti-H. pylori antibodies with the presence of autoimmune disease-specific clinical parameters, as well as those failing to find such associations. We also provide helpful hints for future research. PMID:24574735

  11. Genetic Factors Are Not the Major Causes of Chronic Diseases

    PubMed Central

    Rappaport, Stephen M.

    2016-01-01

    The risk of acquiring a chronic disease is influenced by a person’s genetics (G) and exposures received during life (the ‘exposome’, E) plus their interactions (G×E). Yet, investigators use genome-wide association studies (GWAS) to characterize G while relying on self-reported information to classify E. If E and G×E dominate disease risks, this imbalance obscures important causal factors. To estimate proportions of disease risk attributable to G (plus shared exposures), published data from Western European monozygotic (MZ) twins were used to estimate population attributable fractions (PAFs) for 28 chronic diseases. Genetic PAFs ranged from 3.4% for leukemia to 48.6% for asthma with a median value of 18.5%. Cancers had the lowest PAFs (median = 8.26%) while neurological (median = 26.1%) and lung (median = 33.6%) diseases had the highest PAFs. These PAFs were then linked with Western European mortality statistics to estimate deaths attributable to G for heart disease and nine cancer types. Of 1.53 million Western European deaths in 2000, 0.25 million (16.4%) could be attributed to genetics plus shared exposures. Given the modest influences of G-related factors on the risks of chronic diseases in MZ twins, the disparity in coverage of G and E in etiological research is problematic. To discover causes of disease, GWAS should be complemented with exposome-wide association studies (EWAS) that profile chemicals in biospecimens from incident disease cases and matched controls. PMID:27105432

  12. Chronic mild cerebrovascular dysfunction as a cause for Alzheimer's disease?

    PubMed Central

    Humpel, Christian

    2011-01-01

    Alzheimer's disease (AD) is a progressive chronic disorder and is characterized by β-amyloid plaques and angiopathy, tau pathology, neuronal cell death, and inflammatory responses. The reasons for this disease are not known. This review proposes the hypothesis that a chronic mild longlasting cerebrovascular dysfunction could initiate a cascade of events leading to AD. It is suggested that (vascular) risk factors (e.g. hypercholesterolemia, type 2 diabetes, hyperhomocysteinemia) causes either damage of the cerebrovascular system including silent strokes or causes dysregulation of beta-amyloid clearance at the blood-brain barrier resulting in increased brain beta-amyloid. A cascade of subsequent downstream events may lead to disturbed metabolic changes, and neuroinflammation and tau pathology. The role of NGF on the cell death of cholinergic neurons is discussed. Additional risk factors (e.g. acidosis, metals) contribute to plaque development. PMID:21112383

  13. Legionnaires' disease caused by Legionella dumoffii in distilled water.

    PubMed Central

    Joly, J R; Déry, P; Gauvreau, L; Coté, L; Trépanier, C

    1986-01-01

    Five cases of Legionnaires' disease caused by Legionella dumoffii were identified within an 11-month period in a hospital in the Quebec City area. In four cases bacterial isolates were obtained from clinical specimens, and in one case seroconversion was demonstrated. All the patients had been admitted to hospital within 10 days before diagnosis. Two of the patients were immunosuppressed children. Only 1 of the 40 hot water samples from the hospital yielded L. dumoffii; however, 6 of 11 distilled water samples contained the bacterium. All the patients had been exposed to distilled water, four through respiratory therapy equipment and one through a room humidifier. Following the use of sterile distilled water in the apparatus, no further cases were identified. This is the first reported outbreak of Legionnaires' disease caused by L. dumoffii, and it is the first time that nosocomial legionellosis has been linked to contaminated distilled water in Canada. PMID:3536052

  14. Viral Agents Causing Brown Cap Mushroom Disease of Agaricus bisporus.

    PubMed

    Eastwood, Daniel; Green, Julian; Grogan, Helen; Burton, Kerry

    2015-10-01

    The symptoms of viral infections of fungi range from cryptic to severe, but there is little knowledge of the factors involved in this transition of fungal/viral interactions. Brown cap mushroom disease of the cultivated Agaricus bisporus is economically important and represents a model system to describe this transition. Differentially expressed transcript fragments between mushrooms showing the symptoms of brown cap mushroom disease and control white noninfected mushrooms have been identified and sequenced. Ten of these RNA fragments have been found to be upregulated over 1,000-fold between diseased and nondiseased tissue but are absent from the Agaricus bisporus genome sequence and hybridize to double-stranded RNAs extracted from diseased tissue. We hypothesize that these transcript fragments are viral and represent components of the disease-causing agent, a bipartite virus with similarities to the family Partitiviridae. The virus fragments were found at two distinct levels within infected mushrooms, at raised levels in infected, nonsymptomatic, white mushrooms and at much greater levels (3,500 to 87,000 times greater) in infected mushrooms exhibiting brown coloration. In addition, differential screening revealed 9 upregulated and 32 downregulated host Agaricus bisporus transcripts. Chromametric analysis was able to distinguish color differences between noninfected white mushrooms and white infected mushrooms at an early stage of mushroom growth. This method may be the basis for an "on-farm" disease detection assay. PMID:26253676

  15. Viral Agents Causing Brown Cap Mushroom Disease of Agaricus bisporus

    PubMed Central

    Eastwood, Daniel; Green, Julian; Grogan, Helen

    2015-01-01

    The symptoms of viral infections of fungi range from cryptic to severe, but there is little knowledge of the factors involved in this transition of fungal/viral interactions. Brown cap mushroom disease of the cultivated Agaricus bisporus is economically important and represents a model system to describe this transition. Differentially expressed transcript fragments between mushrooms showing the symptoms of brown cap mushroom disease and control white noninfected mushrooms have been identified and sequenced. Ten of these RNA fragments have been found to be upregulated over 1,000-fold between diseased and nondiseased tissue but are absent from the Agaricus bisporus genome sequence and hybridize to double-stranded RNAs extracted from diseased tissue. We hypothesize that these transcript fragments are viral and represent components of the disease-causing agent, a bipartite virus with similarities to the family Partitiviridae. The virus fragments were found at two distinct levels within infected mushrooms, at raised levels in infected, nonsymptomatic, white mushrooms and at much greater levels (3,500 to 87,000 times greater) in infected mushrooms exhibiting brown coloration. In addition, differential screening revealed 9 upregulated and 32 downregulated host Agaricus bisporus transcripts. Chromametric analysis was able to distinguish color differences between noninfected white mushrooms and white infected mushrooms at an early stage of mushroom growth. This method may be the basis for an “on-farm” disease detection assay. PMID:26253676

  16. The unresolved puzzle why alanine extensions cause disease.

    PubMed

    Winter, Reno; Liebold, Jens; Schwarz, Elisabeth

    2013-08-01

    The prospective increase in life expectancy will be accompanied by a rise in the number of elderly people who suffer from ill health caused by old age. Many diseases caused by aging are protein misfolding diseases. The molecular mechanisms underlying these disorders receive constant scientific interest. In addition to old age, mutations also cause congenital protein misfolding disorders. Chorea Huntington, one of the most well-known examples, is caused by triplet extensions that can lead to more than 100 glutamines in the N-terminal region of huntingtin, accompanied by huntingtin aggregation. So far, nine disease-associated triplet extensions have also been described for alanine codons. The extensions lead primarily to skeletal malformations. Eight of these proteins represent transcription factors, while the nuclear poly-adenylate binding protein 1, PABPN1, is an RNA binding protein. Additional alanines in PABPN1 lead to the disease oculopharyngeal muscular dystrophy (OPMD). The alanine extension affects the N-terminal domain of the protein, which has been shown to lack tertiary contacts. Biochemical analyses of the N-terminal domain revealed an alanine-dependent fibril formation. However, fibril formation of full-length protein did not recapitulate the findings of the N-terminal domain. Fibril formation of intact PABPN1 was independent of the alanine segment, and the fibrils displayed biochemical properties that were completely different from those of the N-terminal domain. Although intranuclear inclusions have been shown to represent the histochemical hallmark of OPMD, their role in pathogenesis is currently unclear. Several cell culture and animal models have been generated to study the molecular processes involved in OPMD. These studies revealed a number of promising future therapeutic strategies that could one day improve the quality of life for the patients. PMID:23612654

  17. A rare cause of secondary amyloidosis: common variable immunodeficiency disease.

    PubMed

    Kadiroğlu, Ali Kemal; Yıldırım, Yaşar; Yılmaz, Zülfükar; Kayabaşı, Hasan; Avcı, Yahya; Yıldırım, M Serdar; Yılmaz, M Emin

    2012-01-01

    The common variable immunodeficiency disease (CVID) is the most common symptomatic primary antibody deficiency. It is the most frequently observed cause of panhypogammaglobulinemia in adults. Here, we present a case of systemic amyloidosis that developed secondary to the common variable immunodeficiency disease causing recurrent infections in a young female patient. A 24-year-old female patient, who was under treatment at the gynecology and obstetrics clinic for pelvic inflammatory disease, was referred to our clinic when she was observed to have swellings in her legs, hands, and face. She had proteinuria at a rate of 3.5 gr/day, and her serum albumin was 1.5 gr/dl. The levels of immunoglobulins are IgG: 138 mg/dl, IgA: 22,6 mg/dl, and IgM: 16,8 mg/dl. The renal USG revealed that the kidneys were observed to be enlarged. Since the patient had recurrent infections, hypogammaglobulinemia, nephrotic range proteinuria, and enlarged kidneys in the renal USG, she was thought to have type AA amyloidosis and therefore underwent a renal biopsy. The kidney biopsy revealed amyloid (+). So the patient was diagnosed with AA type of amyloidosis secondary to common variable immunodeficiency disease. A treatment regimen (an ACE inhibitor and a statin) with monthly administration of intravenous immunoglobulin was started. PMID:24558615

  18. Is mad cow disease caused by a bacteria?

    PubMed

    Broxmeyer, L

    2004-01-01

    Transmissible spongioform enchephalopathies (TSE's), include bovine spongiform encephalopathy (also called BSE or "mad cow disease"), Creutzfeldt-Jakob disease (CJD) in humans, and scrapie in sheep. They remain a mystery, their cause hotly debated. But between 1994 and 1996, 12 people in England came down with CJD, the human form of mad cow, and all had eaten beef from suspect cows. Current mad cow diagnosis lies solely in the detection of late appearing "prions", an acronym for hypothesized, gene-less, misfolded proteins, somehow claimed to cause the disease. Yet laboratory preparations of prions contain other things, which could include unidentified bacteria or viruses. Furthermore, the rigors of prion purification alone, might, in and of themselves, have killed the causative virus or bacteria. Therefore, even if samples appear to infect animals, it is impossible to prove that prions are causative. Manuelidis found viral-like particles, which even when separated from prions, were responsible for spongiform STE's. Subsequently, Lasmezas's study showed that 55% of mice injected with cattle BSE, and who came down with disease, had no detectable prions. Still, incredibly, prions, are held as existing TSE dogma and Heino Dringer, who did pioneer work on their nature, candidly predicts "it will turn out that the prion concept is wrong." Many animals that die of spongiform TSE's never show evidence of misfolded proteins, and Dr. Frank Bastian, of Tulane, an authority, thinks the disorder is caused by the bacterial DNA he found in this group of diseases. Recently, Roels and Walravens isolated Mycobacterium bovis it from the brain of a cow with the clinical and histopathological signs of mad cow. Moreover, epidemiologic maps of the origins and peak incidence of BSE in the UK, suggestively match those of England's areas of highest bovine tuberculosis, the Southwest, where Britain's mad cow epidemic began. The neurotoxic potential for cow tuberculosis was shown in pre-1960

  19. Plant growth-promoting fungus Penicillium spp. GP15-1 enhances growth and confers protection against damping-off and anthracnose in the cucumber.

    PubMed

    Hossain, Md Motaher; Sultana, Farjana; Miyazawa, Mitsuo; Hyakumachi, Mitsuro

    2014-01-01

    Plant growth-promoting fungi (PGPF) have the potential to confer several benefits to plants in terms of growth and protection against pests and pathogens. In the present study, we tested whether a PGPF isolate, Penicillium spp. GP15-1 (derived from zoysiagrass rhizospheres), stimulates growth and disease resistance in the cucumber plant. The use of the barley grain inoculum GP15-1 significantly enhanced root and shoot growth and biomass of cucumber plants. A root colonization study revealed that GP15-1 was a very rapid and efficient root colonizer and was isolated in significantly higher frequencies from the upper root parts than from the middle and lower root parts during the first 14 d of seedling growth. Inoculating the cucumber seedlings with GP15-1 significantly reduced the damping-off disease caused by Rhizoctonia solani, and the disease suppression effects of GP15-1 were considerably influenced by the inoculum potential of both GP15-1 and the pathogen. Treatment with the barley grain inoculum or a cell-free filtrate of GP15-1 increased systemic resistance against leaf infection by the anthracnose pathogen Colletotrichum orbiculare, resulting in a significant decrease in lesion number and size. Molecular and phylogenetic analyses of internal transcribed spacer sequences of the genomic DNA of GP15-1 revealed that the fungal isolate is a strain of either Penicillium neoechinulatum or Penicillium viridicatum. PMID:24671024

  20. Compensation for occupational disease with multiple causes: the case of coal miners respiratory diseases

    SciTech Connect

    Weeks, J.L.; Wagner, G.R.

    1986-01-01

    Many diseases associated with occupational exposures are clinically indistinguishable from diseases with non-occupational causes. Given this, how are fair decisions made about eligibility for compensation. This problem is discussed in relation to the federal black lung program. Conflicting definitions of terms--coal workers pneumoconiosis as defined by the medical profession, pneumoconiosis as defined by the United States Congress, and the popular term, black lung--are important considerations in this discussion. Each is embedded in different logical interpretations of the causes of occupational disease and of disability. Alternative views are presented and critically discussed.

  1. A Novel Virus Causes Scale Drop Disease in Lates calcarifer.

    PubMed

    de Groof, Ad; Guelen, Lars; Deijs, Martin; van der Wal, Yorick; Miyata, Masato; Ng, Kah Sing; van Grinsven, Lotte; Simmelink, Bartjan; Biermann, Yvonne; Grisez, Luc; van Lent, Jan; de Ronde, Anthony; Chang, Siow Foong; Schrier, Carla; van der Hoek, Lia

    2015-08-01

    From 1992 onwards, outbreaks of a previously unknown illness have been reported in Asian seabass (Lates calcarifer) kept in maricultures in Southeast Asia. The most striking symptom of this emerging disease is the loss of scales. It was referred to as scale drop syndrome, but the etiology remained enigmatic. By using a next-generation virus discovery technique, VIDISCA-454, sequences of an unknown virus were detected in serum of diseased fish. The near complete genome sequence of the virus was determined, which shows a unique genome organization, and low levels of identity to known members of the Iridoviridae. Based on homology of a series of putatively encoded proteins, the virus is a novel member of the Megalocytivirus genus of the Iridoviridae family. The virus was isolated and propagated in cell culture, where it caused a cytopathogenic effect in infected Asian seabass kidney and brain cells. Electron microscopy revealed icosahedral virions of about 140 nm, characteristic for the Iridoviridae. In vitro cultured virus induced scale drop syndrome in Asian seabass in vivo and the virus could be reisolated from these infected fish. These findings show that the virus is the causative agent for the scale drop syndrome, as each of Koch's postulates is fulfilled. We have named the virus Scale Drop Disease Virus. Vaccines prepared from BEI- and formalin inactivated virus, as well as from E. coli produced major capsid protein provide efficacious protection against scale drop disease. PMID:26252390

  2. A Novel Virus Causes Scale Drop Disease in Lates calcarifer

    PubMed Central

    de Groof, Ad; Guelen, Lars; Deijs, Martin; van der Wal, Yorick; Miyata, Masato; Ng, Kah Sing; van Grinsven, Lotte; Simmelink, Bartjan; Biermann, Yvonne; Grisez, Luc; van Lent, Jan; de Ronde, Anthony; Chang, Siow Foong; Schrier, Carla; van der Hoek, Lia

    2015-01-01

    From 1992 onwards, outbreaks of a previously unknown illness have been reported in Asian seabass (Lates calcarifer) kept in maricultures in Southeast Asia. The most striking symptom of this emerging disease is the loss of scales. It was referred to as scale drop syndrome, but the etiology remained enigmatic. By using a next-generation virus discovery technique, VIDISCA-454, sequences of an unknown virus were detected in serum of diseased fish. The near complete genome sequence of the virus was determined, which shows a unique genome organization, and low levels of identity to known members of the Iridoviridae. Based on homology of a series of putatively encoded proteins, the virus is a novel member of the Megalocytivirus genus of the Iridoviridae family. The virus was isolated and propagated in cell culture, where it caused a cytopathogenic effect in infected Asian seabass kidney and brain cells. Electron microscopy revealed icosahedral virions of about 140 nm, characteristic for the Iridoviridae. In vitro cultured virus induced scale drop syndrome in Asian seabass in vivo and the virus could be reisolated from these infected fish. These findings show that the virus is the causative agent for the scale drop syndrome, as each of Koch’s postulates is fulfilled. We have named the virus Scale Drop Disease Virus. Vaccines prepared from BEI- and formalin inactivated virus, as well as from E. coli produced major capsid protein provide efficacious protection against scale drop disease. PMID:26252390

  3. Chronic exposure to ozone causes restrictive lung disease

    SciTech Connect

    Grose, E.C.; Costa, D.L.; Hatch, G.E.; Miller, F.J.; Graham, J.A.

    1989-01-01

    A chronic study to determine the progression and/or reversibility of ozone-induced lung disease was conducted. Male rats were exposed to a diurnal pattern of ozone (O{sub 3}) for 1 week, 3 weeks, 3 months, 12 months, or 18 months. The occurrence of chronic lung disease was determined by structural and functional endpoints. Structurally, a biphasic response was observed with an initial acute inflammatory response after 1 week of exposure, a reduced acute response after 3 weeks of exposure, and an epithelial and interstitial response observed after 3 months which persisted or increased in intensity up to 18 months of exposure. Functional studies showed a persistence of decreased total lung capacity and residual volumes at 3, 12, and 18 months of exposure, a response indicative of restrictive lung disease. Biochemical changes in antioxidant metabolism were also observed after 12 and 18 months of exposure. Most significant changes were resolved after the clean-air recovery period. The study has shown that chronic exposure to O{sub 3} causes restrictive lung disease as characterized by the development of focal interstitial fibrosis.

  4. New insights into the cause of Parkinson's disease

    SciTech Connect

    Jenner, P.; Schapira, A.H.; Marsden, C.D. )

    1992-12-01

    Current concepts as to the cause of Parkinson's disease (PD) suggest an inherited predisposition to environmental or endogenous toxic agents. Study of the substantia nigra after death in PD has highlighted three major changes: (1) evidence of oxidative stress and depletion of reduced glutathione; (2) high levels of total iron, with reduced ferritin buffering; and (3) mitochondrial complex I deficiency. Which of these is the primary event, generating a secondary cascade of changes culminating in nigral cell death, is unknown. In presymptomatic Lewy body-positive control brains, the nigra shows depletion of reduced glutathione content and, possibly, a reduction of complex I activity. Whatever the significance of these various abnormalities, be they causal or secondary, they provide novel targets for the development of new strategies to treat the cause of PD.104 references.

  5. Burden of disease caused by local transport in Warsaw, Poland

    PubMed Central

    Tainio, Marko

    2015-01-01

    Transport is a major source of air pollution, noise, injuries and physical activity in the urban environment. The quantification of the health risks and benefits arising from these factors would provide useful information for the planning of cost-effective mitigation actions. In this study we quantified the burden of disease caused by local transport in the city of Warsaw, Poland. The disability-adjusted life-years (DALYs) were estimated for transport related air pollution (particulate matter (PM), nitrogen oxides (NOx), sulfur dioxide (SO2), benzo[a]pyrene (BaP), cadmium, lead and nickel), noise, injuries and physical activity. Exposure to these factors was based on local and international data, and the exposure-response functions (ERFs) were based on published reviews and recommendations. The uncertainties were quantified and propagated with the Monte Carlo method. Local transport generated air pollution, noise and injuries were estimated to cause approximately 58,000 DALYs in the study area. From this burden 44% was due to air pollution and 46% due to noise. Transport related physical activity was estimated to cause a health benefit of 17,000 DALYs. Main quantified uncertainties were related to disability weight for the annoyance (due to noise) and to the ERFs for fine particulate matter (PM2.5) air pollution and walking. The results indicate that the health burden of transport could be mitigated by reducing motorized transport, which causes air pollution and noise, and by encouraging walking and cycling in the study area. PMID:26516622

  6. Multifactorial pathogenesis: ought we to classify disease or treat the individual's causes of disease?

    PubMed

    Ahlqvist, J

    1985-03-01

    Added to the uniqueness of most of us imparted by HLA, our individual differences in the expression of other genetic traits, foetal period steroid imprints on brain and other functions, and regulators shared by body and mind indicate that each one of us (except most monozygotic twins) is born as a unique individual whole (I). Mechanisms suspected to be contributing ones in classified synovitides appear to correspond to individually exaggerated or depressed modes of response by physiological mechanisms linked to our unique individual wholes (II). If we upgrade the importance of influences of combinations of 'contributing' mechanisms, the importance of the alleged unknown fundamental causes of these diseases diminishes (III). This broad interpretation of 'multifactorial pathogenesis' can probably be applied to many common types of disease (IV), implying that disease classifications may poorly reflect the individual's causes of disease (V). There is reason to challenge modern concepts about disease (VI). PMID:3889563

  7. EST mining identifies proteins putatively secreted by the anthracnose pathogen Colletotrichum truncatum

    PubMed Central

    2011-01-01

    Background Colletotrichum truncatum is a haploid, hemibiotrophic, ascomycete fungal pathogen that causes anthracnose disease on many economically important leguminous crops. This pathogen exploits sequential biotrophic- and necrotrophic- infection strategies to colonize the host. Transition from biotrophy to a destructive necrotrophic phase called the biotrophy-necrotrophy switch is critical in symptom development. C. truncatum likely secretes an arsenal of proteins that are implicated in maintaining a compatible interaction with its host. Some of them might be transition specific. Results A directional cDNA library was constructed from mRNA isolated from infected Lens culinaris leaflet tissues displaying the biotrophy-necrotrophy switch of C. truncatum and 5000 expressed sequence tags (ESTs) with an average read of > 600 bp from the 5-prime end were generated. Nearly 39% of the ESTs were predicted to encode proteins of fungal origin and among these, 162 ESTs were predicted to contain N-terminal signal peptides (SPs) in their deduced open reading frames (ORFs). The 162 sequences could be assembled into 122 tentative unigenes comprising 32 contigs and 90 singletons. Sequence analyses of unigenes revealed four potential groups: hydrolases, cell envelope associated proteins (CEAPs), candidate effectors and other proteins. Eleven candidate effector genes were identified based on features common to characterized fungal effectors, i.e. they encode small, soluble (lack of transmembrane domain), cysteine-rich proteins with a putative SP. For a selected subset of CEAPs and candidate effectors, semiquantitative RT-PCR showed that these transcripts were either expressed constitutively in both in vitro and in planta or induced during plant infection. Using potato virus X (PVX) based transient expression assays, we showed that one of the candidate effectors, i. e. contig 8 that encodes a cerato-platanin (CP) domain containing protein, unlike CP proteins from other fungal

  8. Effect of MeJA treatment on polyamine, energy status and anthracnose rot of loquat fruit.

    PubMed

    Cao, Shifeng; Cai, Yuting; Yang, Zhenfeng; Joyce, Daryl C; Zheng, Yonghua

    2014-02-15

    The effect of methyl jasmonate (MeJA) on changes in polyamines content and energy status and their relation to disease resistance was investigated. Freshly harvested loquat fruit were treated with 10 μmol l(-1) MeJA and wound inoculated with Colletotrichum acutatum spore suspension (1.0 × 10(5) spores ml(-1)) after 24h, and then stored at 20 °C for 6 days. MeJA treatment significantly reduced decay incidence. MeJA treated fruit manifested higher contents of polyamines (putrescine, spermidine and spermine) compared with the control fruit, during storage. MeJA treatment also maintained higher levels of adenosine triphosphate, and suppressed an increase in adenosine monophosphate content in loquat fruit. These results suggest that MeJA treatment may inhibit anthracnose rot by increasing polyamine content and maintaining the energy status. PMID:24128452

  9. Streptococcus acidominimus causing invasive disease in humans: a case series

    PubMed Central

    2014-01-01

    Introduction Streptococcus acidominimus is a member of the viridans group streptococci and is rarely pathogenic in humans, making it difficult to assess its epidemiologic and clinical significance. Case presentation We report the cases of five Han Chinese patients with invasive diseases caused by S. acidominimus over a one-year time frame. Three of the patients developed continuous fever after surgery, consisting of a successful elective laparoscopic cholecystectomy (case 1), a laparoscopic esophageal resection and gastroesophageal anastomosis (case 2), and a liver transplant in a patient with liver cancer (case 3). For these three patients, cultures of the purulent drainage material grew S. acidominimus. Case 4 concerns a 52-year-old man who developed sepsis 48 hours after hospitalization for hepatitis, liver cirrhosis and hepatitis-related glomerulonephritis. Case 5 concerns a 55-year-old woman receiving regular hemodialysis who had low-grade fever for one month. For these two patients, blood cultures grew S. acidominimus. An antimicrobial susceptibility test revealed that S. acidominimus was resistant to clindamycin and, to some degree, beta-lactam or macrolides. The S. acidominimus from the patient on hemodialysis was resistant to multiple antibiotics. Conclusion S. acidominimus is an ever-increasing cause of disease, especially in patients who are critically ill. It is showing increased resistance to antimicrobial agents, so in patients with viridans group streptococci infections, it is necessary to identify the species to improve the clinical management of S. acidominimus. PMID:24529345

  10. [Occupational diseases caused by exposure to sensitizing metals].

    PubMed

    Kusaka, Y

    1993-03-01

    Diseases caused by occupational exposure to sensitizing metals including platinum (Pt), rhodium (Rh), nickel (Ni), chromium (Cr), cobalt (Co), gold (Au), mercury (Hg), zirconium (Zr) and beryllium (Be) are reviewed. Allergic reactions induced by the metals are described according to the classification by Coombs and Gell. Metals with unproven sensitizing potential are not discussed if reports on these are either very rare or devoid of convincing evidence for allergic involvement. The sensitizing metals are haptens which are not themselves able to act as antigens. There is evidence that combination of the metals with circulating or tissue protein gives rise to new antigens. An alternative hypothesis is that these metals interfere with the antigen recognition step of the immune response. Immunomodulatory effects or immunotoxicity of the metals may be also involved in metal-induced hypersensitivity. Occupational exposure to Pt, Rh, Ni, Cr, and Co causes allergic asthma via type I allergic reaction in which serum from affected individuals shows specific IgE antibodies against mental-human serum albumin conjugates. Some rheumatoid arthritis patients treated with gold salt therapy develop glomerulonephritis, thrombocytopenia, or agranulocytosis, which arise from type II and/or type III allergic reactions. Occupational exposure to mercury causes glomerulonephritis in which involvement of type III reaction is suggested. Type IV hypersensitivity reaction of the skin also takes place following exposure to the metals: allergic contact dermatitis is evoked by exposure to Ni, Cr, Co, Rh, and Hg; cutaneous granuloma is formed by contact with Zr and Be. Be is also a sensitizer of the lungs, resulting in granulomatous disease. Diagnosis of metal-induced allergic diseases is made on the basis of allergological tests with metal antigens including skin tests, radioallergosorbent test for specific antibody, lymphocyte transformation test, macrophage migration inhibition test, and

  11. The impact of weather conditions on response of sorghum genotypes to anthracnose (Colletotrichum sublineola) infection

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Rainfall is a major climatic factor influencing anthracnose development and in this study, 68 sorghum accessions were evaluated for anthracnose resistance under dry and wet growing conditions at the Texas A&M Agricultural Experiment Station, near College Station, Texas. Accessions, planted in a ran...

  12. [Environmental causes of the distal airways disease. Hypersensitivity pneumonitis and rare causes].

    PubMed

    Dalphin, J-C; Didier, A

    2013-10-01

    Hypersensitivity pneumonitis is one of the most frequent causes of distal airways disease. It is associated with inflammation of the bronchioles, predominantly by lymphocytic infiltrates, and with granuloma formation causing bronchial obstruction. This inflammation explains the clinical manifestations and the airways obstruction seen on pulmonary function tests, most often in the distal airways but proximal in almost 20%. CT scan abnormalities reflect the lymphocytic infiltrates and air trapping and, in some cases, the presence of emphysema. Bronchiolitis induced by chronic inhalation of mineral particles or acute inhalation of toxic gases (such as NO2) are other examples of small airways damage due to environmental exposure. The pathophysiological mechanisms are different and bronchiolar damage is either exclusive or predominant. Bronchiolitis induced by tobacco smoke exposure, usually classified as interstitial pneumonitis, is easily diagnosed thanks to broncho-alveolar lavage. Its prognosis is linked to the other consequences of tobacco smoke exposure including respiratory insufficiency. Finally, the complex lung exposure observed in some rare cases (such as the World Trade Center fire or during wars) may lead to a less characteristic pattern of small airways disease. PMID:24182653

  13. Baastrup's Disease: a poorly recognised cause of back pain.

    PubMed

    Farinha, F; Raínho, C; Cunha, I; Barcelos, A

    2015-01-01

    A 56-year-old male complained about progressive mechanical back pain for more than 10 years, which worsened with prolonged orthostatism and spine extension and improved in fetal position. His lumbar spine radiography revealed enlargement and sclerosis of the spinous processes which was confirmed by computed tomography, suggesting Baastrup's disease. This condition is characterized by enlargement, close approximation and impingement of one spinous process on another ("kissing spines"). There are few studies on Baastrup´s disease epidemiology and their results are inconsistent. Patients often complain of back pain, typically increased with extension and relieved by flexion. Radiographically, spinous process impingement leads to reactive sclerosis, enlargement, flattening, and remodeling of the involved vertebral spines. Physicians frequently miss it on radiographs due to lack of knowledge and overexposure of spinous processes in most X rays. Both conservative and surgical options are available for treatment. Baastrup's disease should be considered in differential diagnosis of back pain, although one must be aware the typical radiographic changes appear to be common with aging and may not be the cause of patient's symptoms. PMID:25782695

  14. Mutations that Cause Human Disease: A Computational/Experimental Approach

    SciTech Connect

    Beernink, P; Barsky, D; Pesavento, B

    2006-01-11

    International genome sequencing projects have produced billions of nucleotides (letters) of DNA sequence data, including the complete genome sequences of 74 organisms. These genome sequences have created many new scientific opportunities, including the ability to identify sequence variations among individuals within a species. These genetic differences, which are known as single nucleotide polymorphisms (SNPs), are particularly important in understanding the genetic basis for disease susceptibility. Since the report of the complete human genome sequence, over two million human SNPs have been identified, including a large-scale comparison of an entire chromosome from twenty individuals. Of the protein coding SNPs (cSNPs), approximately half leads to a single amino acid change in the encoded protein (non-synonymous coding SNPs). Most of these changes are functionally silent, while the remainder negatively impact the protein and sometimes cause human disease. To date, over 550 SNPs have been found to cause single locus (monogenic) diseases and many others have been associated with polygenic diseases. SNPs have been linked to specific human diseases, including late-onset Parkinson disease, autism, rheumatoid arthritis and cancer. The ability to predict accurately the effects of these SNPs on protein function would represent a major advance toward understanding these diseases. To date several attempts have been made toward predicting the effects of such mutations. The most successful of these is a computational approach called ''Sorting Intolerant From Tolerant'' (SIFT). This method uses sequence conservation among many similar proteins to predict which residues in a protein are functionally important. However, this method suffers from several limitations. First, a query sequence must have a sufficient number of relatives to infer sequence conservation. Second, this method does not make use of or provide any information on protein structure, which can be used to

  15. Deletions of recessive disease genes: CNV contribution to carrier states and disease-causing alleles

    PubMed Central

    Boone, Philip M.; Campbell, Ian M.; Baggett, Brett C.; Soens, Zachry T.; Rao, Mitchell M.; Hixson, Patricia M.; Patel, Ankita; Bi, Weimin; Cheung, Sau Wai; Lalani, Seema R.; Beaudet, Arthur L.; Stankiewicz, Pawel; Shaw, Chad A.; Lupski, James R.

    2013-01-01

    Over 1200 recessive disease genes have been described in humans. The prevalence, allelic architecture, and per-genome load of pathogenic alleles in these genes remain to be fully elucidated, as does the contribution of DNA copy-number variants (CNVs) to carrier status and recessive disease. We mined CNV data from 21,470 individuals obtained by array-comparative genomic hybridization in a clinical diagnostic setting to identify deletions encompassing or disrupting recessive disease genes. We identified 3212 heterozygous potential carrier deletions affecting 419 unique recessive disease genes. Deletion frequency of these genes ranged from one occurrence to 1.5%. When compared with recessive disease genes never deleted in our cohort, the 419 recessive disease genes affected by at least one carrier deletion were longer and located farther from known dominant disease genes, suggesting that the formation and/or prevalence of carrier CNVs may be affected by both local and adjacent genomic features and by selection. Some subjects had multiple carrier CNVs (307 subjects) and/or carrier deletions encompassing more than one recessive disease gene (206 deletions). Heterozygous deletions spanning multiple recessive disease genes may confer carrier status for multiple single-gene disorders, for complex syndromes resulting from the combination of two or more recessive conditions, or may potentially cause clinical phenotypes due to a multiply heterozygous state. In addition to carrier mutations, we identified homozygous and hemizygous deletions potentially causative for recessive disease. We provide further evidence that CNVs contribute to the allelic architecture of both carrier and recessive disease-causing mutations. Thus, a complete recessive carrier screening method or diagnostic test should detect CNV alleles. PMID:23685542

  16. Splicing in action: assessing disease causing sequence changes

    PubMed Central

    Baralle, D; Baralle, M

    2005-01-01

    Variations in new splicing regulatory elements are difficult to identify exclusively by sequence inspection and may result in deleterious effects on precursor (pre) mRNA splicing. These mutations can result in either complete skipping of the exon, retention of the intron, or the introduction of a new splice site within an exon or intron. Sometimes mutations that do not disrupt or create a splice site activate pre-existing pseudo splice sites, consistent with the proposal that introns contain splicing inhibitory sequences. These variants can also affect the fine balance of isoforms produced by alternatively spliced exons and in consequence cause disease. Available genomic pathology data reveal that we are still partly ignorant of the basic mechanisms that underlie the pre-mRNA splicing process. The fact that human pathology can provide pointers to new modulatory elements of splicing should be exploited. PMID:16199547

  17. SURF1 deficiency causes demyelinating Charcot-Marie-Tooth disease

    PubMed Central

    Ghezzi, Daniele; Chassagne, Maïté; Mayençon, Martine; Padet, Sylvie; Melchionda, Laura; Rouvet, Isabelle; Lannes, Béatrice; Bozon, Dominique; Latour, Philippe; Zeviani, Massimo; Mousson de Camaret, Bénédicte

    2013-01-01

    Objective: To investigate whether mutations in the SURF1 gene are a cause of Charcot-Marie-Tooth (CMT) disease. Methods: We describe 2 patients from a consanguineous family with demyelinating autosomal recessive CMT disease (CMT4) associated with the homozygous splice site mutation c.107-2A>G in the SURF1 gene, encoding an assembly factor of the mitochondrial respiratory chain complex IV. This observation led us to hypothesize that mutations in SURF1 might be an unrecognized cause of CMT4, and we investigated SURF1 in a total of 40 unrelated patients with CMT4 after exclusion of mutations in known CMT4 genes. The functional impact of c.107-2A>G on splicing, amount of SURF1 protein, and on complex IV activity and assembly was analyzed. Results: Another patient with CMT4 was found to harbor 2 additional SURF1 mutations. All 3 patients with SURF1-associated CMT4 presented with severe childhood-onset neuropathy, motor nerve conduction velocities <25 m/s, and lactic acidosis. Two patients had brain MRI abnormalities, including putaminal and periaqueductal lesions, and developed cerebellar ataxia years after polyneuropathy. The c.107-2A>G mutation produced no normally spliced transcript, leading to SURF1 absence. However, complex IV remained partially functional in muscle and fibroblasts. Conclusions: We found SURF1 mutations in 5% of families (2/41) presenting with CMT4. SURF1 should be systematically screened in patients with childhood-onset severe demyelinating neuropathy and additional features such as lactic acidosis, brain MRI abnormalities, and cerebellar ataxia developing years after polyneuropathy. PMID:24027061

  18. [Neurologic characteristics of diseases caused by Inkoo and Tahyna viruses].

    PubMed

    Demikhov, V G; Chaĭtsev, V G

    1995-01-01

    Two principal forms of diseases caused by Inkoo and Tahyna viruses were observed, fever (25 pts, 61%) and neuroinfection (13 pts, 31.7%). In 3 (7.3%) subjects the infection was inapparent. Ten patients presented with mixed forms of infection (virus-virus or virus-bacterial). Clinical manifestations were characterized by marked polymorphism and low specificity. The onset was acute with expressed symptoms of infection and weak catarrhal manifestations. Of the patients with the neuroinfectious form of the disease 3 presented with aseptic meningitis, 2 with meningoencephalitis, and 5 with encephalitis. Aseptic meningitis was characterized by a combination of general infectious and moderately expressed meningeal syndromes with weak inflammatory changes in the spinal fluid. Encephalitides were associated with numerous neurological symptoms which manifested on days 3-7 of the illness. These symptoms were asymmetry of nasolabial folds, hemiparesis, dysarthria, dysphagia, generalized tremor, tongue deviation. No significant differences in the clinical manifestations of Inkoo and Tahyna infections were observed. PMID:7740783

  19. Detection and Heterogeneity of Herpesviruses Causing Pacheco's Disease in Parrots

    PubMed Central

    Tomaszewski, Elizabeth; Wilson, Van G.; Wigle, William L.; Phalen, David N.

    2001-01-01

    Pacheco's disease (PD) is a common, often fatal, disease of parrots. We cloned a virus isolate from a parrot that had characteristic lesions of PD. Three viral clones were partially sequenced, demonstrating that this virus was an alphaherpesvirus most closely related to the gallid herpesvirus 1. Five primer sets were developed from these sequences. The primer sets were used with PCR to screen tissues or tissue culture media suspected to contain viruses from 54 outbreaks of PD. The primer sets amplified DNA from all but one sample. Ten amplification patterns were detected, indicating that PD is caused by a genetically heterogeneous population of viruses. A single genetic variant (psittacid herpesvirus variant 1) amplified with all primer sets and was the most common virus variant (62.7%). A single primer set (23F) amplified DNA from all of the positive samples, suggesting that PCR could be used as a rapid postmortem assay for these viruses. PCR was found to be significantly more sensitive than tissue culture for the detection of psittacid herpesviruses. PMID:11158102

  20. [DIABETIC NEPHROPATHY AS A CAUSE OF CHRONIC KIDNEY DISEASE].

    PubMed

    Kos, Ivan; Prkačin, Ingrid

    2014-12-01

    Diabetic nephropathy is the leading cause of end-stage chronic kidney disease in most developed countries. Hyperglycemia, hypertension and genetic predisposition are the main risk factors for the development of diabetic nephropathy. Elevated serum lipids, smoking habits, and the amount and origin of dietary protein also seem to play a role as risk factors. Clinical picture includes a progressive increase in albuminuria, decline in glomerular filtration, hypertension, and a high risk of cardiovascular morbidity and mortality. Screening for albuminuria should be performed yearly, starting 5 years after diagnosis in type 1 diabetes or earlier in the presence of adolescence or poor metabolic control. In patients with type 2 diabetes, screening should be performed at diagnosis and yearly thereafter. Patients with albuminuria should undergo evaluation regarding the presence of associated comorbidities, especially retinopathy and macrovascular disease. Achieving the best metabolic control (HbA1c < 7%), treating hypertension (target blood pressure < 140/85 mm Hg), using drugs with blockade effect on the renin-angiotensin-aldosterone system, treating dyslipidemia and anemia are effective strategies for preventing the development of albuminuria, delaying the progression to more advanced stages of nephropathy and reducing cardiovascular mortality in patients with type 1 and type 2 diabetes. PMID:26285470

  1. Hypoxemia in patients with COPD: cause, effects, and disease progression

    PubMed Central

    Kent, Brian D; Mitchell, Patrick D; McNicholas, Walter T

    2011-01-01

    Chronic obstructive pulmonary disease (COPD) is a leading cause of death and disability internationally. Alveolar hypoxia and consequent hypoxemia increase in prevalence as disease severity increases. Ventilation/perfusion mismatch resulting from progressive airflow limitation and emphysema is the key driver of this hypoxia, which may be exacerbated by sleep and exercise. Uncorrected chronic hypoxemia is associated with the development of adverse sequelae of COPD, including pulmonary hypertension, secondary polycythemia, systemic inflammation, and skeletal muscle dysfunction. A combination of these factors leads to diminished quality of life, reduced exercise tolerance, increased risk of cardiovascular morbidity, and greater risk of death. Concomitant sleep-disordered breathing may place a small but significant subset of COPD patients at increased risk of these complications. Long-term oxygen therapy has been shown to improve pulmonary hemodynamics, reduce erythrocytosis, and improve survival in selected patients with severe hypoxemic respiratory failure. However, the optimal treatment for patients with exertional oxyhemoglobin desaturation, isolated nocturnal hypoxemia, or mild-to-moderate resting daytime hypoxemia remains uncertain. PMID:21660297

  2. [Research Progress in Black Queen Cell Virus Causing Disease].

    PubMed

    Yang, Qian; Zhang, Jian; Song, Zhanyun; Zheng, Yan; Wang, Xianghui; Sui, Jiachen; Wang, Zhenguo; Mou, Jun

    2015-05-01

    In nature, honeybees are the most important pollinators. They play a vital role in both protecting the diversity of natural ecosystems, and maintaining the yield-improving effects of agroecosystems. But in recent years, epidemic disease in bees has caused huge losses. Black Queen Cell Virus (BQCV) is a bee pathogen that was first reported in 1955. It mainly infects bee larvae and pupae, making their bodies turn dark and black, and causing a massive decrease in the bee population. More specifically, the virus makes the exterior of the cell walls in the larvae and pupae turn black. BQCV is a seasonal epidemic, spread by means horizontal and vertical transmission, and is often unapparent. BQCV not only infects a variety of bee species, but also spiders, centipedes and other arthropods. It can also be coinfected with other honeybee viruses. In recent years, research has shown that the Nosema intestinal parasite plays an important role in BQCV transmission and bees carrying Nosema that become infected with BQCV have increased mortality. Here we summarize current research on the incidence, prevalence, geographical distribution and transmission of BQCV. PMID:26470541

  3. [Effects of silicon on flowering Chinese cabbage's anthracnose occurence, flower stalk formation, and silicon uptake and accumulation].

    PubMed

    Yang, Xian; Feng, Hong-Xian; Yang, Yue-Sheng

    2008-05-01

    Different concentrations of silicon (Si) were applied to flowering Chinese cabbbage (Brassica campestris L. ssp. chinensis var. utilis Tsen et Lee) to study their effects on the flowering Chinese cabbage's anthracnose occurrence, flower stalk formation, and Si uptake and accumulation. The results indicated that Si could obviously control the occurrence of anthracnose, and the effect was genotype-dependant. The plants of susceptible cultivar applied with 2.5 mmol L(-1) Si and those of resistant cultivar applied with 0.5 mmol L(-1) Si exhibited the highest resistance to Colletotrichum higginsianum, with the lowest disease index and the higheist flower stalk yield. Si application also obviously affected the quality of flower stalk. For susceptible cultivar, Si application promoted the synthesis of chlorophyll, crude fiber and vitamin C, and induced the formation of soluble sugars. The contents of chlorophyll and crude fiber increased with increasing Si level. For resistant cultivar, the chlorophyll content increased while vitamin C content decreased with increasing Si level, but Si application had less effect on the contents of crude fiber and soluble sugars. For both cultivars, Si application did not have significant effect on the contents of crude protein and soluble protein but remarkably increased the Si accumulation in plant leaves, and the leaf Si content was significantly increased with increasing Si level. The Si granules deposited in leaf tissues were not equal in size, and distributed unevenly in epidermis tissues. It was concluded that the accumulation of Si in leaves could increase the resistance of plant to anthracnose, but there was no linear correlation between the accumulated amount of Si and the resistance. PMID:18655585

  4. Mortality from Alzheimer's disease in Canada: A multiple-cause-of-death analysis, 2004 to 2011.

    PubMed

    Park, Jungwee

    2016-05-18

    Using multiple-cause-of-death data, this study investigates mortality from Alzheimer's disease. From 2004 through 2011, Alzheimer's disease was coded as a cause of 80,868 deaths-more often the underlying than a contributing cause. The rate of Alzheimer's disease deaths was higher for women and older individuals than for men and younger people, and varied considerably by province/territory. Regardless of whether Alzheimer's disease was coded as the underlying or a contributing cause, on average, two other causes were also listed on the death certificate. When Alzheimer's disease was the underlying cause, cardiovascular diseases were most often listed as a contributing cause; when Alzheimer's disease was a contributing cause, cardiovascular diseases were most often listed as the underlying cause. PMID:27192207

  5. Astrocyte pathology in Alexander disease causes a marked inflammatory environment.

    PubMed

    Olabarria, Markel; Putilina, Maria; Riemer, Ellen C; Goldman, James E

    2015-10-01

    Astrocytes and microglia are commonly involved in a wide variety of CNS pathologies. However, they are typically involved in a secondary response in which many cell types are affected simultaneously and therefore it is difficult to know their contributions to the pathology. Here, we show that pathological astrocytes in a mouse model of Alexander disease (AxD; GFAP (Tg);Gfap (+/R236H)) cause a pronounced immune response. We have studied the inflammatory response in the hippocampus and spinal cord of these mice and have found marked microglial activation, which follows that of astrocytes in a spatial pathological progression, as shown by increased levels of Iba1 and microglial cell (Iba1+) density. RNA sequencing and subsequent gene ontology (GO) analysis revealed that a majority of the most upregulated genes in GFAP (Tg);Gfap (+/R236H) mice are directly associated with immune function and that cytokine and chemokine GO attributes represent nearly a third of the total immune attributes. Cytokine and chemokine analysis showed CXCL10 and CCL2 to be the most and earliest increased molecules, showing concentrations as high as EAE or stroke models. CXCL10 was localized exclusively to astrocytes while CCL2 was also present in microglia. Despite the high levels of CXCL10 and CCL2, T cell infiltration was mild and no B cells were found. Thus, mutations in GFAP are sufficient to trigger a profound inflammatory response. The cellular stress caused by the accumulation of GFAP likely leads to the production of inflammatory molecules and microglial activation. Examination of human AxD CNS tissues also revealed microglial activation and T cell infiltrates. Therefore, the inflammatory environment may play an important role in producing the neuronal dysfunction and seizures of AxD. PMID:26296699

  6. Attention! Cardiac tamponade may be caused by underlying Castleman's disease.

    PubMed

    Atay, Hilmi; Kelkitli, Engin; Okuyucu, Muhammed; Yildiz, Levent; Turgut, Mehmet

    2015-05-01

    Castleman's disease is a rarely observed lymphoproliferative disease. In the literature, various signs and symptoms of the disease have been reported; one of these is secondary cardiac tamponade. We describe the case of a 41-year-old man who developed cardiac tamponade during examination, and who was later diagnosed with Castleman's disease, based on his lymph node biopsies. PMID:24887912

  7. Comparative Pathogenomics of Bacteria Causing Infectious Diseases in Fish

    PubMed Central

    Sudheesh, Ponnerassery S.; Al-Ghabshi, Aliya; Al-Mazrooei, Nashwa; Al-Habsi, Saoud

    2012-01-01

    Fish living in the wild as well as reared in the aquaculture facilities are susceptible to infectious diseases caused by a phylogenetically diverse collection of bacterial pathogens. Control and treatment options using vaccines and drugs are either inadequate, inefficient, or impracticable. The classical approach in studying fish bacterial pathogens has been looking at individual or few virulence factors. Recently, genome sequencing of a number of bacterial fish pathogens has tremendously increased our understanding of the biology, host adaptation, and virulence factors of these important pathogens. This paper attempts to compile the scattered literature on genome sequence information of fish pathogenic bacteria published and available to date. The genome sequencing has uncovered several complex adaptive evolutionary strategies mediated by horizontal gene transfer, insertion sequence elements, mutations and prophage sequences operating in fish pathogens, and how their genomes evolved from generalist environmental strains to highly virulent obligatory pathogens. In addition, the comparative genomics has allowed the identification of unique pathogen-specific gene clusters. The paper focuses on the comparative analysis of the virulogenomes of important fish bacterial pathogens, and the genes involved in their evolutionary adaptation to different ecological niches. The paper also proposes some new directions on finding novel vaccine and chemotherapeutic targets in the genomes of bacterial pathogens of fish. PMID:22675651

  8. Autosomal dominant Parkinson's disease caused by SNCA duplications.

    PubMed

    Konno, Takuya; Ross, Owen A; Puschmann, Andreas; Dickson, Dennis W; Wszolek, Zbigniew K

    2016-01-01

    The discovery in 1997 that mutations in the SNCA gene cause Parkinson's disease (PD) greatly advanced our understanding of this illness. There are pathogenic missense mutations and multiplication mutations in SNCA. Thus, not only a mutant protein, but also an increased dose of wild-type protein can produce autosomal dominant parkinsonism. We review the literature on SNCA duplications and focus on pathologically-confirmed cases. We also report a newly-identified American family with SNCA duplication whose proband was autopsied. We found that over half of the reported cases with SNCA duplication had early-onset parkinsonism and non-motor features, such as dysautonomia, rapid eye movement sleep behavior disorder (RBD), hallucinations (usually visual) and cognitive deficits leading to dementia. Only a few cases have presented with typical features of PD. Our case presented with depression and RBD that preceded parkinsonism, and dysautonomia that led to an initial diagnosis of multiple system atrophy. Dementia and visual hallucinations followed. Our patient and the other reported cases with SNCA duplications had widespread cortical Lewy pathology. Neuronal loss in the hippocampal cornu ammonis 2/3 regions were seen in about half of the autopsied SNCA duplication cases. Similar pathology was also observed in SNCA missense mutation and triplication carriers. PMID:26350119

  9. Upper extremity ischemia caused by small artery disease.

    PubMed Central

    Mills, J L; Friedman, E I; Taylor, L M; Porter, J M

    1987-01-01

    One hundred patients with ischemic finger ulceration had detailed prospective evaluation to determine the incidence of associated diseases, response to treatment, and natural history of the condition. A potentially serious associated disease was detected in each patient including autoimmune disease in 54%, Buerger's disease in 9%, arteriosclerosis obliterans in 9%, hypersensitivity angiitis in 22%, and miscellaneous diseases in 6%. Conservative treatment with soap and water scrubs, antibiotics, and local resection/debridement resulted in long-term healing without recurrence in 88% of patients. Most recurrences occurred in patients with autoimmune disease, usually scleroderma or CRST. Images Fig. 2. Figs. 3A and B. PMID:3662661

  10. Mycobacterium avium subspecies paratuberculosis causes Crohn's disease in some inflammatory bowel disease patients.

    PubMed

    Naser, Saleh A; Sagramsingh, Sudesh R; Naser, Abed S; Thanigachalam, Saisathya

    2014-06-21

    Crohn's disease (CD) is a chronic inflammatory condition that plagues millions all over the world. This debilitating bowel disease can start in early childhood and continue into late adulthood. Signs and symptoms are usually many and multiple tests are often required for the diagnosis and confirmation of this disease. However, little is still understood about the cause(s) of CD. As a result, several theories have been proposed over the years. One theory in particular is that Mycobacterium avium subspecies paratuberculosis (MAP) is intimately linked to the etiology of CD. This fastidious bacterium also known to cause Johne's disease in cattle has infected the intestines of animals for years. It is believed that due to the thick, waxy cell wall of MAP it is able to survive the process of pasteurization as well as chemical processes seen in irrigation purification systems. Subsequently meat, dairy products and water serve as key vehicles in the transmission of MAP infection to humans (from farm to fork) who have a genetic predisposition, thus leading to the development of CD. The challenges faced in culturing this bacterium from CD are many. Examples include its extreme slow growth, lack of cell wall, low abundance, and its mycobactin dependency. In this review article, data from 60 studies showing the detection and isolation of MAP by PCR and culture techniques have been reviewed. Although this review may not be 100% comprehensive of all studies, clearly the majority of the studies overwhelmingly and definitively support the role of MAP in at least 30%-50% of CD patients. It is very possible that lack of detection of MAP from some CD patients may be due to the absence of MAP role in these patients. The latter statement is conditional on utilization of methodology appropriate for detection of human MAP strains. Ultimately, stratification of CD and inflammatory bowel disease patients for the presence or absence of MAP is necessary for appropriate and effective

  11. Identification of SCAR markers linked to Rca 2 anthracnose resistance gene and their assessment in strawberry germ plasm.

    PubMed

    Lerceteau-Köhler, E; Guérin, G; Denoyes-Rothan, B

    2005-09-01

    Bulked segregant analysis combined with AFLPs was used to identify molecular markers linked to the Rca 2 gene conferring resistance to Colletotrichum acutatum pathogenicity group 2 which causes anthracnose in the octoploid strawberry Fragaria x ananassa. DNA bulks originating from a cross between the resistant cultivar 'Capitola' and the susceptible cultivar 'Pajaro' were screened with 110 EcoRI/M se IAFLP combinations. Four AFLP markers were found linked in coupling phase to Rca 2 with recombination percentages between 0% and 17.7%. Among the four markers linked to the resistance gene, two were converted into SCAR markers (STS-Rca 2417 and STS-Rca 2240) and screened in a large segregating population including 179 genotypes. The Rca 2 resistance gene was estimated to be 0.6 cM from STS-Rca 2417 and 2.8 cM from STS-Rca 2240. The presence/absence of the two SCAR markers was further studied in 43 cultivars of F. x ananassa, including 14 susceptible, 28 resistant, and one intermediate genotype. Results showed that 81.4% and 62.8% of the resistant/susceptible genotypes were correctly predicted by using STS-Rca 2417 and STS-Rca 2240, respectively. The 14 susceptible genotypes showed no amplification for either SCARs. These developed SCARs constitute new tools for indirect selection criteria of anthracnose resistance genotypes in strawberry breeding programs. PMID:16003555

  12. Diseases and Causes of Death in European Bats: Dynamics in Disease Susceptibility and Infection Rates

    PubMed Central

    Mühldorfer, Kristin; Speck, Stephanie; Kurth, Andreas; Lesnik, René; Freuling, Conrad; Müller, Thomas; Kramer-Schadt, Stephanie; Wibbelt, Gudrun

    2011-01-01

    Background Bats receive increasing attention in infectious disease studies, because of their well recognized status as reservoir species for various infectious agents. This is even more important, as bats with their capability of long distance dispersal and complex social structures are unique in the way microbes could be spread by these mammalian species. Nevertheless, infection studies in bats are predominantly limited to the identification of specific pathogens presenting a potential health threat to humans. But the impact of infectious agents on the individual host and their importance on bat mortality is largely unknown and has been neglected in most studies published to date. Methodology/Principal Findings Between 2002 and 2009, 486 deceased bats of 19 European species (family Vespertilionidae) were collected in different geographic regions in Germany. Most animals represented individual cases that have been incidentally found close to roosting sites or near human habitation in urban and urban-like environments. The bat carcasses were subjected to a post-mortem examination and investigated histo-pathologically, bacteriologically and virologically. Trauma and disease represented the most important causes of death in these bats. Comparative analysis of pathological findings and microbiological results show that microbial agents indeed have an impact on bats succumbing to infectious diseases, with fatal bacterial, viral and parasitic infections found in at least 12% of the bats investigated. Conclusions/Significance Our data demonstrate the importance of diseases and infectious agents as cause of death in European bat species. The clear seasonal and individual variations in disease prevalence and infection rates indicate that maternity colonies are more susceptible to infectious agents, underlining the possible important role of host physiology, immunity and roosting behavior as risk factors for infection of bats. PMID:22216354

  13. Historical perspectives on music as a cause of disease.

    PubMed

    Kennaway, James

    2015-01-01

    The relationship between music and medicine is generally understood in the benign context of music therapy, but, as this chapter shows, there is a long parallel history of medical theories that suggest that music can cause real physical and mental illness. During the seventeenth and eighteenth centuries, the idea of music as an expression of universal harmony was challenged by a more mechanistic model of nervous stimulation. By the 1790s, there was a substantial discourse on the dangers of musical overstimulation to health in medicine, literature, and etiquette books. During the nineteenth century, the sense of music as a pathogenic stimulant gained in influence. It was often linked to fears about sexuality, female gynecological health, and theories of hypnosis and degeneration. In the twentieth century, the debate on the medical perils of the wrong kinds of music became overtly politicized in Germany and the Soviet Union. Likewise, the opponents of jazz, particularly in the United States, often turned to medicine to fend off its supposed social, moral, and physical consequences. The Cold War saw an extensive discourse on the idea of musical "brainwashing," that rumbled on into the 1990s. Today, regular media panics about pathological music are mirrored by alarming evidence of the deliberate use of music to harm listeners in the context of the so-called War on Terror. Can music make you ill? Music therapy is a common if perhaps rather neglected part of medicine, but its diametric opposite, the notion that music might lead to real mental and physical illness, may seem improbable. In fact, over the last two hundred years, there have been many times when as much was written about the medical dangers of music as about its potential benefits. Since the eighteenth century, fears about music's effects on the nerves and the mind have created a remarkably extensive discourse on pathological music based on a view of both music and the causation of disease as matters of

  14. Blackberry Yellow Vein Disease is Caused by Multiple Virus Complexes

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Blackberry yellow vein disease, with symptoms of vein clearing, yellow mottling, ringspots and plant decline has been observed in blackberry in the southeastern United States since about 2000. At least six viruses have been identified by cloning and sequencing of double-stranded RNA from diseased p...

  15. Can Epiphytes reduce disease symptoms caused by Phytophthora ramorum

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Leaf infection of ornamental species by Phytophthora ramorum has a significant impact on the spread of this disease. Fungicides have had limited effects on controlling this disease. With increasing concerns that repeated fungicide applications will exasperate the potential for fungicide resistance...

  16. CHRONIC EXPOSURE TO OZONE CAUSES RESTRICTIVE LUNG DISEASE

    EPA Science Inventory

    A chronic study to determine the progression and or/reversibility of ozone-induced lung disease was conducted. ale rats were exposed to a diurnal pattern of ozone (O3) for 1 wk, 3 wk, 3 mo, 12 mo, or 18 mo. he occurrence of chronic lung disease was determined by structural and fu...

  17. Anthracnose disease response in the Burundi sorghum germplasm collection

    Technology Transfer Automated Retrieval System (TEKTRAN)

    The United States National Plant Germplasm System maintains 151 sorghum accessions from Burundi of which 148 accessions were evaluated for resistance to Colletotrichum sublineolum at the Tropical Agriculture Research Station in Isabela, Puerto Rico in replicated evaluations during the 2007 and 2008 ...

  18. Anthracnose disease evaluation of sorghum germplasm from Honduras

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Germplasm collections are important resources for sorghum improvement and 17 accessions from Honduras were inoculated with Colletotrichum sublineolum and evaluated at the Tropical Agriculture Research Station in Isabela, Puerto Rico during the 2005 and 2006 growing seasons to identify sources of ant...

  19. Causes and histopathology of ascending aortic disease in children and young adults

    PubMed Central

    Jain, Deepali; Dietz, Harry C.; Oswald, Gretchen L.; Maleszewski, Joseph J.; Halushka, Marc K.

    2011-01-01

    Background Ascending aortic diseases (aneurysms, dissections, and stenosis) and associated aortic valve disease are rare but important causes of morbidity and mortality in children and young adults. Certain genetic causes, such as Marfan syndrome and congenital bicuspid aortic valve disease, are well known. However, other rarer genetic and nongenetic causes of aortic disease exist. Methods We performed an extensive literature search to identify known causes of ascending aortic pathology in children and young adults. We catalogued both aortic pathologies and other defining systemic features of these diseases. Results We describe 17 predominantly genetic entities that have been associated with thoracic aortic disease in this age group. Conclusions While extensive literature on the common causes of ascending aortic disease exists, there is a need for better histologic documentation of aortic pathology in rarer diseases. PMID:19926309

  20. Chylomicron retention disease: A rare cause of chronic diarrhea.

    PubMed

    Ben Ameur, S; Aloulou, H; Jlidi, N; Kamoun, F; Chabchoub, I; Di Filippo, M; Sfaihi, L; Hachicha, M

    2016-07-01

    Chylomicron retention disease (CRD) is a rare autosomal recessive hereditary hypocholesterolemic disorder. The disease most frequently presents in infants and is characterized by a lipid malabsorption syndrome with steatorrhea, chronic diarrhea, and growth retardation. The disease is characterized by normal fasting serum triglyceride levels combined with the absence of apolipoprotein (apo) B48 and chylomicrons after a fat load. In this report, we describe the clinical, laboratory, and histological data as well as the molecular DNA analysis of a 12-month-old girl from Tunisia with CRD. The patient was treated with a low-fat diet and fat-soluble vitamin supplementation resulting in significant improvement. PMID:27266643

  1. Mycobacterium avium subspecies paratuberculosis causes Crohn's disease in some inflammatory bowel disease patients

    PubMed Central

    Naser, Saleh A; Sagramsingh, Sudesh R; Naser, Abed S; Thanigachalam, Saisathya

    2014-01-01

    Crohn’s disease (CD) is a chronic inflammatory condition that plagues millions all over the world. This debilitating bowel disease can start in early childhood and continue into late adulthood. Signs and symptoms are usually many and multiple tests are often required for the diagnosis and confirmation of this disease. However, little is still understood about the cause(s) of CD. As a result, several theories have been proposed over the years. One theory in particular is that Mycobacterium avium subspecies paratuberculosis (MAP) is intimately linked to the etiology of CD. This fastidious bacterium also known to cause Johne’s disease in cattle has infected the intestines of animals for years. It is believed that due to the thick, waxy cell wall of MAP it is able to survive the process of pasteurization as well as chemical processes seen in irrigation purification systems. Subsequently meat, dairy products and water serve as key vehicles in the transmission of MAP infection to humans (from farm to fork) who have a genetic predisposition, thus leading to the development of CD. The challenges faced in culturing this bacterium from CD are many. Examples include its extreme slow growth, lack of cell wall, low abundance, and its mycobactin dependency. In this review article, data from 60 studies showing the detection and isolation of MAP by PCR and culture techniques have been reviewed. Although this review may not be 100% comprehensive of all studies, clearly the majority of the studies overwhelmingly and definitively support the role of MAP in at least 30%-50% of CD patients. It is very possible that lack of detection of MAP from some CD patients may be due to the absence of MAP role in these patients. The latter statement is conditional on utilization of methodology appropriate for detection of human MAP strains. Ultimately, stratification of CD and inflammatory bowel disease patients for the presence or absence of MAP is necessary for appropriate and effective

  2. Lipophilic chemical exposure as a cause of cardiovascular disease

    PubMed Central

    2013-01-01

    Environmental chemical exposure has been linked to numerous diseases in humans. These diseases include cancers; neurological and neurodegenerative diseases; metabolic disorders including type 2 diabetes, metabolic syndrome and obesity; reproductive and developmental disorders; and endocrine disorders. Many studies have associated the link between exposures to environmental chemicals and cardiovascular disease (CVD). These chemicals include persistent organic pollutants (POPs); the plastic exudates bisphenol A and phthalates; low molecular weight hydrocarbons (LMWHCs); and poly nuclear aromatic hydrocarbons (PAHs). Here it is reported that though the chemicals reported on differ widely in chemical properties and known points of attack in humans, a common link exists between them. All are lipophilic species that are found in serum. Environmentally induced CVD is related to total lipophilic chemical load in the blood. Lipophiles serve to promote the absorption of otherwise not absorbed toxic hydrophilic species that promote CVD. PMID:24179429

  3. Could inhibition of the proteasome cause mad cow disease?

    PubMed

    Hooper, Nigel M

    2003-04-01

    The proteasome is the cellular machinery responsible for the degradation of normal and misfolded proteins. Inhibitors of the proteasome are being evaluated as therapeutic agents and recent work suggests that such inhibition might promote the neurotoxic properties of the prion protein (the causative agent of mad cow disease) and its conformational conversion to the infectious form, thus raising the question as to whether proteasome inhibitors might facilitate the development of prion diseases. PMID:12679058

  4. Causes of Charcot-Marie-Tooth Disease (CMT)

    MedlinePlus

    ... The peripheral nerve fibers, called axons , extend from sensory nerve cells in the body's periphery back toward ... which explains why CMT mostly causes motor and sensory problems in the body’s extremities. Inheritance patterns in ...

  5. Occult moyamoya disease causing fulminant infarction after septorhinoplasty

    PubMed Central

    Djedovic, Gabriel; Verstappen, Ralph; Matiasek, Johannes; Engelhardt, Timm O.; Pierer, Gerhard; Rieger, Ulrich M.

    2014-01-01

    Abstract Moyamoya disease is an extremely rare cerebrovascular condition that predisposes affected patients to stroke in association with progressive stenosis of the intracranial internal carotid arteries and their proximal branches. To our knowledge, this is the first report of a lethal complication due to moyamoya disease after septorhinoplasty. A 25-year-old female Caucasian patient presented to our outpatient clinic with impaired nasal breathing for septorhinoplasty. Regrettably the patient died 6 days postoperatively due to progressive infarct series affecting all major cerebral vessels. Despite a thorough knowledge of possible local complications after septorhinoplasty, it is of utmost importance to consider rare general complications like moyamoya disease. Although cerebral infarctions are very rare in young people, it is crucial to identify and correctly interpret underlying typical symptoms.

  6. Molecular mechanisms of disease-causing missense mutations

    PubMed Central

    Stefl, Shannon; Nishi, Hafumi; Petukh, Marharyta; Panchenko, Anna R.; Alexov, Emil

    2013-01-01

    Genetic variations resulting in a change of amino acid sequence can have a dramatic effect on stability, hydrogen bond network, conformational dynamics, activity and many other physiologically important properties of proteins. The substitutions of only one residue in a protein sequence, so-called missense mutations, can be related to many pathological conditions, and may influence susceptibility to disease and drug treatment. The plausible effects of missense mutations range from affecting the macromolecular stability to perturbing macromolecular interactions and cellular localization. Here we review the individual cases and genome-wide studies which illustrate the association between missense mutations and diseases. In addition we emphasize that the molecular mechanisms of effects of mutations should be revealed in order to understand the disease origin. Finally we report the current state-of-the-art methodologies which predict the effects of mutations on protein stability, the hydrogen bond network, pH-dependence, conformational dynamics and protein function. PMID:23871686

  7. Node of Ranvier disruption as a cause of neurological diseases

    PubMed Central

    Susuki, Keiichiro

    2013-01-01

    Dysfunction and/or disruption of nodes of Ranvier are now recognized as key contributors to the pathophysiology of various neurological diseases. One reason is that the excitable nodal axolemma contains a high density of Nav (voltage-gated Na+ channels) that are required for the rapid and efficient saltatory conduction of action potentials. Nodal physiology is disturbed by altered function, localization, and expression of voltage-gated ion channels clustered at nodes and juxtaparanodes, and by disrupted axon–glial interactions at paranodes. This paper reviews recent discoveries in molecular/cellular neuroscience, genetics, immunology, and neurology that highlight the critical roles of nodes of Ranvier in health and disease. PMID:23834220

  8. Node of Ranvier disruption as a cause of neurological diseases.

    PubMed

    Susuki, Keiichiro

    2013-01-01

    Dysfunction and/or disruption of nodes of Ranvier are now recognized as key contributors to the pathophysiology of various neurological diseases. One reason is that the excitable nodal axolemma contains a high density of Nav (voltage-gated Na+ channels) that are required for the rapid and efficient saltatory conduction of action potentials. Nodal physiology is disturbed by altered function, localization, and expression of voltage-gated ion channels clustered at nodes and juxtaparanodes, and by disrupted axon-glial interactions at paranodes. This paper reviews recent discoveries in molecular/cellular neuroscience, genetics, immunology, and neurology that highlight the critical roles of nodes of Ranvier in health and disease. PMID:23834220

  9. Strategic Approaches to Unraveling Genetic Causes of Cardiovascular Diseases

    PubMed Central

    Marian, A.J.; Belmont, John

    2011-01-01

    DNA sequence variants (DSVs) are major components of the “causal field” for virtually all-medical phenotypes, whether single-gene familial disorders or complex traits without a clear familial aggregation. The causal variants in single gene disorders are necessary and sufficient to impart large effects. In contrast, complex traits are due to a much more complicated network of contributory components that in aggregate increase the probability of disease. The conventional approach to identification of the causal variants for single gene disorders is genetic linkage. However, it does not offer sufficient resolution to map the causal genes in small size families or sporadic cases. The approach to genetic studies of complex traits entails candidate gene or Genome Wide Association Studies (GWAS). GWAS provides an unbiased survey of the effects of common genetic variants (common disease - common variant hypothesis). GWAS have led to identification of a large number of alleles for various cardiovascular diseases. However, common alleles account for a relatively small fraction of the total heritability of the traits. Accordingly, the focus has shifted toward identification of rare variants that might impart larger effect sizes (rare variant-common disease hypothesis). This shift is made feasible by recent advances in massively parallel DNA sequencing platforms, which afford the opportunity to identify virtually all common as well as rare alleles in individuals. In this review, we discuss various strategies that are used to delineate the genetic contribution to medically important cardiovascular phenotypes, emphasizing the utility of the new deep sequencing approaches. PMID:21566222

  10. Immunogenetics of Disease-Causing Inflammation in Sarcoidosis.

    PubMed

    Grunewald, Johan; Spagnolo, Paolo; Wahlström, Jan; Eklund, Anders

    2015-08-01

    Sarcoidosis is a systemic inflammatory disorder characterised by tissue infiltration by mononuclear phagocytes and lymphocytes with associated non-caseating granuloma formation. Originally described as a disorder of the skin, sarcoidosis can involve any organ with wide-ranging clinical manifestations and disease course. Recent studies have provided new insights into the mechanisms involved in disease pathobiology, and we now know that sarcoidosis has a clear genetic basis largely involving human leukocyte antigen (HLA) genes. In contrast to Mendelian-monogenic disorders--which are generally due to specific and relatively rare mutations often leading to a single amino acid change in an encoded protein--sarcoidosis results from genetic variations relatively common in the general population and involving multiple genes, each contributing an effect of varying magnitude. However, an individual may have the necessary genetic profile and yet the disease will not develop unless an environmental or infectious factor is encountered. Genetics appears also to contribute to the huge variability in clinical phenotype and disease behaviour. Moreover, it has been established that sarcoidosis granulomatous inflammation is a highly polarized T helper 1 immune response that starts with an antigenic stimulus followed by T cell activation via a classic HLA class II-mediated pathway. A complex network of lymphocytes, macrophages, and cytokines is pivotal in the orchestration and evolution of the granulomatous process. Despite these advances, the aetiology of sarcoidosis remains elusive and its pathogenesis incompletely understood. As such, there is an urgent need for a better understanding of disease pathogenesis, which hopefully will translate into the development of truly effective therapies. PMID:25791751

  11. Sooty Mould Disease Caused by Leptoxyphium kurandae on Kenaf.

    PubMed

    Choi, In-Young; Kang, Chan-Ho; Lee, Geon-Hwi; Park, Ji-Hyun; Shin, Hyeon-Dong

    2015-09-01

    In September 2013, we discovered sooty mould growing on kenaf with the extrafloral nectaries in Iksan, Korea and identified the causative fungus as Leptoxyphium kurandae based on morphological characteristics and phylogenetic analyses. This is the first report of sooty mould caused by L. kurandae on kenaf in Korea and globally. PMID:26539054

  12. Sooty Mould Disease Caused by Leptoxyphium kurandae on Kenaf

    PubMed Central

    Choi, In-Young; Kang, Chan-Ho; Lee, Geon-Hwi; Park, Ji-Hyun

    2015-01-01

    In September 2013, we discovered sooty mould growing on kenaf with the extrafloral nectaries in Iksan, Korea and identified the causative fungus as Leptoxyphium kurandae based on morphological characteristics and phylogenetic analyses. This is the first report of sooty mould caused by L. kurandae on kenaf in Korea and globally. PMID:26539054

  13. Genotype-based databases for variants causing rare diseases.

    PubMed

    Lanthaler, Barbara; Wieser, Stefanie; Deutschmann, Andrea; Schossig, Anna; Fauth, Christine; Zschocke, Johannes; Witsch-Baumgartner, Martina

    2014-10-15

    Inherited diseases are the result of DNA sequence changes. In recessive diseases, the clinical phenotype results from the combined functional effects of variants in both copies of the gene. In some diseases there is often considerable variability of clinical presentation or disease severity, which may be predicted by the genotype. Additional effects may be triggered by environmental factors, as well as genetic modifiers which could be nucleotide polymorphisms in related genes, e.g. maternal ApoE or ABCA1 genotypes which may have an influence on the phenotype of SLOS individuals. Here we report the establishment of genotype variation databases for various rare diseases which provide individual clinical phenotypes associated with genotypes and include data about possible genetic modifiers. These databases aim to be an easy public access to information on rare and private variants with clinical data, which will facilitate the interpretation of genetic variants. The created databases include ACAD8 (isobutyryl-CoA dehydrogenase deficiency (IBD)), ACADSB (short-chain acyl-CoA dehydrogenase (SCAD) deficiency), AUH (3-methylglutaconic aciduria (3-MGCA)), DHCR7 (Smith-Lemli-Opitz syndrome), HMGCS2 (3-hydroxy-3-methylglutaryl-CoA synthase 2 deficiency), HSD17B10 (17-beta-hydroxysteroid dehydrogenase X deficiency), FKBP14 (Ehlers-Danlos syndrome with progressive kyphoscoliosis, myopathy, and hearing loss; EDSKMH) and ROGDI (Kohlschütter-Tönz syndrome). These genes have been selected because of our specific research interests in these rare and metabolic diseases. The aim of the database was to include all identified individuals with variants in these specific genes. Identical genotypes are listed multiple times if they were found in several patients, phenotypic descriptions and biochemical data are included as detailed as possible in view also of validating the proposed pathogenicity of these genotypes. For DHCR7 genetic modifier data (maternal APOE and ABCA1 genotypes) is

  14. [RENDU-OSLER DISEASE: A RARE CAUSE OF AMMONIA ENCEPHALOPATHY].

    PubMed

    Dumont, R; Loly, J-P; Delwaide, J; Louis, E

    2016-02-01

    Hereditary Hemorrhagic Telangiectasia (HHT) also known as Rendu-Osler disease is a group of related disorders inherited in an autosomal dominant fashion and characterized by the development of arteriovenous malformations (AVM) in the skin, mucous membranes, and/or internal organs such as the brain, lungs, and liver. The prevalence of liver involvement is clinically estimated between 8 and 31 percent. It can be revealed by the following clinical signs : ascites, edema of the lower extremities, abdominal pain, dyspnea, and, rarely, hepatic encephalopathy and gastrointestinal bleeding associated with portal hypertension. This case illustrates the highlight of liver damage revealed by an ammonia encephalopathy associated with iconographic anomalies on ultrasonography and magnetic resonance liver as part of Rendu-Osler disease. PMID:27141651

  15. Genetic causes of Parkinson's disease: extending the pathway.

    PubMed

    Riess, O; Krüger, R; Hochstrasser, H; Soehn, A S; Nuber, S; Franck, T; Berg, D

    2006-01-01

    The functional characterization of identified disease genes in monogenic forms of Parkinson's disease (PD) allows first insights into molecular pathways leading to neurodegeneration and dysfunction of the nigrostriatal system. There is increasing evidence that disturbance of the ubiquitin proteasome pathway is one important feature of this process underscoring the relevance of protein misfolding and accumulation in the neurodegenerative process of PD. Other genes are involved in mitochondrial homeostasis and still others link newly identified signalling pathways to the established paradigm of oxidative stress in PD. Additional factors are posttranslational modifications of key proteins such as phosphorylation. Also, molecular data support the role of altered iron metabolism in PD. Here we describe known genes and novel genetic susceptibility factors and define their role in neurodegeneration. PMID:17017528

  16. Corpora Amylacea in Neurodegenerative Diseases: Cause or Effect?

    PubMed Central

    Rohn, Troy T.

    2015-01-01

    The presence of corpora amylacea (CA) in the CNS is associated with both normal aging and neurodegenerative conditions including Alzheimer’s disease (AD) and vascular dementia (VaD). CA are spherical bodies ranging in diameter (10–50 μm) and whose origin has been documented to be derived from both neural and glial sources. CA are reported to be primarily composed of glucose polymers, but approximately 4% of the total weight of CA is consistently composed of protein. CA are typically localized in the subpial, periventricular and perivascular regions within the CNS. The presence of CA in VaD has recently been documented and of interest was the localization of CA within the hippocampus proper. Despite numerous efforts, the precise role of CA in normal aging or disease is not known. The purpose of this mini review is to highlight the potential function of CA in various neurodegenerative disorders with an emphasis on the potential role if any these structures may play in the etiology of these diseases. PMID:26550607

  17. Lipoprotein X Causes Renal Disease in LCAT Deficiency

    PubMed Central

    Thacker, Seth G.; Vaisman, Boris; Pryor, Milton; Freeman, Lita A.; Brantner, Christine A.; Baranova, Irina; Francone, Nicolás O.; Demosky, Stephen J.; Vitali, Cecilia; Locatelli, Monica; Abbate, Mauro; Zoja, Carlamaria; Franceschini, Guido; Calabresi, Laura; Remaley, Alan T.

    2016-01-01

    Human familial lecithin:cholesterol acyltransferase (LCAT) deficiency (FLD) is characterized by low HDL, accumulation of an abnormal cholesterol-rich multilamellar particle called lipoprotein-X (LpX) in plasma, and renal disease. The aim of our study was to determine if LpX is nephrotoxic and to gain insight into the pathogenesis of FLD renal disease. We administered a synthetic LpX, nearly identical to endogenous LpX in its physical, chemical and biologic characteristics, to wild-type and Lcat-/- mice. Our in vitro and in vivo studies demonstrated an apoA-I and LCAT-dependent pathway for LpX conversion to HDL-like particles, which likely mediates normal plasma clearance of LpX. Plasma clearance of exogenous LpX was markedly delayed in Lcat-/- mice, which have low HDL, but only minimal amounts of endogenous LpX and do not spontaneously develop renal disease. Chronically administered exogenous LpX deposited in all renal glomerular cellular and matrical compartments of Lcat-/- mice, and induced proteinuria and nephrotoxic gene changes, as well as all of the hallmarks of FLD renal disease as assessed by histological, TEM, and SEM analyses. Extensive in vivo EM studies revealed LpX uptake by macropinocytosis into mouse glomerular endothelial cells, podocytes, and mesangial cells and delivery to lysosomes where it was degraded. Endocytosed LpX appeared to be degraded by both human podocyte and mesangial cell lysosomal PLA2 and induced podocyte secretion of pro-inflammatory IL-6 in vitro and renal Cxl10 expression in Lcat-/- mice. In conclusion, LpX is a nephrotoxic particle that in the absence of Lcat induces all of the histological and functional hallmarks of FLD and hence may serve as a biomarker for monitoring recombinant LCAT therapy. In addition, our studies suggest that LpX-induced loss of endothelial barrier function and release of cytokines by renal glomerular cells likely plays a role in the initiation and progression of FLD nephrosis. PMID:26919698

  18. Lipoprotein X Causes Renal Disease in LCAT Deficiency.

    PubMed

    Ossoli, Alice; Neufeld, Edward B; Thacker, Seth G; Vaisman, Boris; Pryor, Milton; Freeman, Lita A; Brantner, Christine A; Baranova, Irina; Francone, Nicolás O; Demosky, Stephen J; Vitali, Cecilia; Locatelli, Monica; Abbate, Mauro; Zoja, Carlamaria; Franceschini, Guido; Calabresi, Laura; Remaley, Alan T

    2016-01-01

    Human familial lecithin:cholesterol acyltransferase (LCAT) deficiency (FLD) is characterized by low HDL, accumulation of an abnormal cholesterol-rich multilamellar particle called lipoprotein-X (LpX) in plasma, and renal disease. The aim of our study was to determine if LpX is nephrotoxic and to gain insight into the pathogenesis of FLD renal disease. We administered a synthetic LpX, nearly identical to endogenous LpX in its physical, chemical and biologic characteristics, to wild-type and Lcat-/- mice. Our in vitro and in vivo studies demonstrated an apoA-I and LCAT-dependent pathway for LpX conversion to HDL-like particles, which likely mediates normal plasma clearance of LpX. Plasma clearance of exogenous LpX was markedly delayed in Lcat-/- mice, which have low HDL, but only minimal amounts of endogenous LpX and do not spontaneously develop renal disease. Chronically administered exogenous LpX deposited in all renal glomerular cellular and matrical compartments of Lcat-/- mice, and induced proteinuria and nephrotoxic gene changes, as well as all of the hallmarks of FLD renal disease as assessed by histological, TEM, and SEM analyses. Extensive in vivo EM studies revealed LpX uptake by macropinocytosis into mouse glomerular endothelial cells, podocytes, and mesangial cells and delivery to lysosomes where it was degraded. Endocytosed LpX appeared to be degraded by both human podocyte and mesangial cell lysosomal PLA2 and induced podocyte secretion of pro-inflammatory IL-6 in vitro and renal Cxl10 expression in Lcat-/- mice. In conclusion, LpX is a nephrotoxic particle that in the absence of Lcat induces all of the histological and functional hallmarks of FLD and hence may serve as a biomarker for monitoring recombinant LCAT therapy. In addition, our studies suggest that LpX-induced loss of endothelial barrier function and release of cytokines by renal glomerular cells likely plays a role in the initiation and progression of FLD nephrosis. PMID:26919698

  19. [Respiratory disease caused by MMVF fibers and yarn].

    PubMed

    Riboldi, L; Rivolta, G; Barducci, M; Errigo, G; Picchi, O

    1999-01-01

    The non-carcinogenic effects of vitreous fibres on the human respiratory apparatus have been the subjects of numerous studies on large exposed populations. No evidence seems to have been produced of the existence of a fibrogenic effect. However, no definite and agreed opinion has yet been expressed by the main Agencies and Institutions working in the field of prevention. As a contribution to the discussion, the paper presents the experience of the Clinica del Lavoro of Milano involving 1000 subjects who underwent broncho-alveolar lavage during assessment and checking for suspected occupational respiratory disease. A group of 23 cases was selected who were exposed to vitreous fibres without other significant exposures to factors considered hazardous for the respiratory apparatus, especially asbestos. We observed 7 cases of alveolitis; 6 cases with pleural thickening; 2 cases of interstitial disease. On the basis of the nature of exposure (duration, latency from beginning and from the end of hazardous occupation), of the data obtained from the examination of the bronchial lavage liquid (presence of vitreous fibres, siderocytes, cellularity), and of the clinical and laboratory data (X-ray, PFR), the view expressed is tendentially reassuring concerning the possible effects of vitreous fibres on the respiratory apparatus. Although the existence of an irritative type of lesion that manifests in the form of alveolitis and localised pleural thickening seems possible, albeit in a limited number of cases, it does however appear much more difficult to admit the existence of a fibrogenic effect. PMID:10339954

  20. Deregulation of TNF expression can also cause heart valve disease.

    PubMed

    Lacey, Derek; Bouillet, Philippe

    2016-01-01

    High levels of the pro-inflammatory cytokine tumour necrosis factor (TNF) have been associated with many diseases including rheumatoid arthritis (RA), ankylosing spondylitis (AS), inflammatory bowel disease (IBD) and psoriasis. Although it has been clear for twenty-five years that TNF plays a major role in RA and AS, two major questions remain unanswered: (1) What mechanism underlies the loss of control of TNF levels in patients? (2) How does TNF exert its detrimental effects? Nonetheless, biological anti-TNF drugs have become the most successful treatment of these conditions with a third of patients entering remission, and the global market for biological TNF inhibitors is now estimated at around US$35 billions. However, their use is limited by their cost, the fact that they need to be injected, non-negligible side effects and the development of resistance due to the protein (thus antigenic) nature of these TNF inhibitors. It looks inevitable that new approaches to lower the amount of TNF should be considered. To do this, a better understanding of the regulation of TNF expression is necessary. PMID:26321488

  1. Mapping global potential risk of mango sudden decline disease caused by fungus Ceratocystis fimbriata

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Mango Sudden Decline (MSD), sometimes referred to as mango wilt, is an important disease of mango caused by one of the most significant fungal species causing disease in woody plants, Ceratocystis fimbriata. This species is mainly disseminated by the mango bark beetle, Hypocryphalus mangiferae (Steb...

  2. Infectious Diseases as Causes of Mental Retardation and Other Concomitant Neurological Sequelae.

    ERIC Educational Resources Information Center

    Iivanainen, Matti; Lahdevirta, Juhani

    1988-01-01

    Examination of 1,000 Finnish patients with mental retardation indicated that infectious diseases were the only cause of mental retardation in 11.1 percent and a contributory cause in a further 1.5 percent. Among the former group of 111 patients, the causative infectious disease operated prenatally in 18 percent and perinatally/postnatally in 82…

  3. Effect of host genotypes and weather variables on the severity and temporal dynamics of sorghum anthracnose in Ethiopia

    Technology Transfer Automated Retrieval System (TEKTRAN)

    The severity and temporal dynamics of anthracnose on susceptible (BTx623 and AL70) and resistant lines (2001PWColl#022 and 2001HararghieColl#12) were studied in field plots during the 2007 and 2008 growing seasons in southern Ethiopia. The initial, final, and mean anthracnose severities and area un...

  4. Whole genome sequence and genome annotation of Colletotrichum acutatum, causal agent of anthracnose in pepper plants in South Korea

    PubMed Central

    Han, Joon-Hee; Chon, Jae-Kyung; Ahn, Jong-Hwa; Choi, Ik-Young; Lee, Yong-Hwan; Kim, Kyoung Su

    2016-01-01

    Colletotrichum acutatum is a destructive fungal pathogen which causes anthracnose in a wide range of crops. Here we report the whole genome sequence and annotation of C. acutatum strain KC05, isolated from an infected pepper in Kangwon, South Korea. Genomic DNA from the KC05 strain was used for the whole genome sequencing using a PacBio sequencer and the MiSeq system. The KC05 genome was determined to be 52,190,760 bp in size with a G + C content of 51.73% in 27 scaffolds and to contain 13,559 genes with an average length of 1516 bp. Gene prediction and annotation were performed by incorporating RNA-Seq data. The genome sequence of the KC05 was deposited at DDBJ/ENA/GenBank under the accession number LUXP00000000. PMID:27114908

  5. Whole genome sequence and genome annotation of Colletotrichum acutatum, causal agent of anthracnose in pepper plants in South Korea.

    PubMed

    Han, Joon-Hee; Chon, Jae-Kyung; Ahn, Jong-Hwa; Choi, Ik-Young; Lee, Yong-Hwan; Kim, Kyoung Su

    2016-06-01

    Colletotrichum acutatum is a destructive fungal pathogen which causes anthracnose in a wide range of crops. Here we report the whole genome sequence and annotation of C. acutatum strain KC05, isolated from an infected pepper in Kangwon, South Korea. Genomic DNA from the KC05 strain was used for the whole genome sequencing using a PacBio sequencer and the MiSeq system. The KC05 genome was determined to be 52,190,760 bp in size with a G + C content of 51.73% in 27 scaffolds and to contain 13,559 genes with an average length of 1516 bp. Gene prediction and annotation were performed by incorporating RNA-Seq data. The genome sequence of the KC05 was deposited at DDBJ/ENA/GenBank under the accession number LUXP00000000. PMID:27114908

  6. Tight Bra in a 34-Year-Old Woman: An Unusual Cause of Mondor's Disease.

    PubMed

    Vincenza Polito, Maria; De Cicco, Pierluigi; Apicella, Rosa

    2014-01-01

    Mondor's disease is characterized by thrombophlebitis of the superficial veins of the breast and the chest wall. The list of causes is long. Various types of clothing, mainly tight bras and girdles, have been postulated as causes. We report a case of a 34-year-old woman who referred typical symptoms and signs of Mondor's disease, without other possible risk factors, and showed the cutaneous findings of the tight bra. Therefore, after distinguishing benign causes of Mondor's disease from hidden malignant causes, the clinicians should consider this clinical entity. PMID:24995060

  7. Just a sore throat? Uncommon causes of significant respiratory disease

    PubMed Central

    Wahab, Dalia; Bichard, Julia; Shah, Anand; Mann, Bhupinder

    2013-01-01

    We present two uncommon underlying causes of a sore throat which, if missed or delayed in diagnosis, can lead to disastrous consequences. Our first case is of Lemierre's syndrome diagnosed in a 21-year-old man presenting with a 5-day history of sore throat, fever, right-sided pleuritic chest pain and bilateral pulmonary nodules on CT imaging. Fusobacterium necrophorum cultured from peripheral blood and an occluded left internal jugular vein on ultrasound lead to an eventual diagnosis. Our second case presents a 29-year-old woman with a 5-day history of sore throat, fever and right-sided pleuritic chest pain. A left-sided quinsy was diagnosed and aspirated and the patient was discharged home. She represented shortly with worsening pleuritic pain and was found to have a right-sided pleural effusion with descending mediastinitis originating from the tonsillar abscess. Delayed diagnosis resulted in open thoracotomy, decortication and prolonged intravenous antibiotics. PMID:23632177

  8. The global tobacco disease pandemic: nature, causes, and cures.

    PubMed

    Warner, K E; Mackay, J

    2006-01-01

    Tobacco use kills 5 million citizens globally every year. The World Health Organization (WHO) projects that the number of deaths will double just 15 years from now. Tobacco will then constitute the leading cause of death in the developing world, as it already is in developed countries today. This paper describes the nature and extent of the tobacco pandemic, characteristics of the global tobacco industry, and national and international efforts to diminish the toll of tobacco. The review includes examination of the economic and political strategies employed by the multinational tobacco industry to increase cigarette consumption, as well as the policies that governments have adopted to combat smoking. The most promising development is the new Framework Convention on Tobacco Control, WHO's first-ever international health treaty. While aggressive tobacco control policies can and will diminish the toll of tobacco, the prospects for the foreseeable future appear grim. PMID:19153895

  9. Just a sore throat? Uncommon causes of significant respiratory disease.

    PubMed

    Wahab, Dalia; Bichard, Julia; Shah, Anand; Mann, Bhupinder

    2013-01-01

    We present two uncommon underlying causes of a sore throat which, if missed or delayed in diagnosis, can lead to disastrous consequences. Our first case is of Lemierre's syndrome diagnosed in a 21-year-old man presenting with a 5-day history of sore throat, fever, right-sided pleuritic chest pain and bilateral pulmonary nodules on CT imaging. Fusobacterium necrophorum cultured from peripheral blood and an occluded left internal jugular vein on ultrasound lead to an eventual diagnosis. Our second case presents a 29-year-old woman with a 5-day history of sore throat, fever and right-sided pleuritic chest pain. A left-sided quinsy was diagnosed and aspirated and the patient was discharged home. She represented shortly with worsening pleuritic pain and was found to have a right-sided pleural effusion with descending mediastinitis originating from the tonsillar abscess. Delayed diagnosis resulted in open thoracotomy, decortication and prolonged intravenous antibiotics. PMID:23632177

  10. EDEMA DISEASE CAUSED BY A CLONE OF ESCHERICHIA COLI O147

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Edema disease is a systemic disease of weaned pigs caused by host adapted strains of E. coli most commonly belonging to serogroups O138, O139 or O141. Recently, E. coli O147 strains containing the virulence genes f18, sta, stb and stx2e have been recovered from outbreaks of edema disease across the...

  11. The relationship between fire history and an exotic fungal disease in a deciduous forest.

    PubMed

    Holzmueller, Eric J; Jose, Shibu; Jenkins, Michael A

    2008-03-01

    Exotic diseases have fundamentally altered the structure and function of forest ecosystems. Controlling exotic diseases across large expanses of forest has proven difficult, but fire may reduce the levels of diseases that are sensitive to environmental conditions. We examined Cornus florida populations in burned and unburned Quercus-Carya stands to determine if burning prior to anthracnose infection has reduced the impacts of an exotic fungal disease, dogwood anthracnose, caused by Discula destructiva. We hypothesized that fire has altered stand structure and created open conditions less conducive to dogwood anthracnose. We compared C. florida density, C. florida health, and species composition and density among four sampling categories: unburned stands, and stands that had burned once, twice, and 3 times over a 20-year period (late 1960s to late 1980s). Double burn stands contained the greatest density of C. florida stems (770 stems ha(-1)) followed by triple burn stands (233 stems ha(-1)), single burn stands (225 stems ha(-1)) and unburned stands (70 stems ha(-1); P < 0.01). We observed less crown dieback in small C. florida trees (<5 cm diameter at breast height) in burned stands than in unburned stands (P < 0.05). Indicator species analysis showed that burning favored species historically associated with Quercus-Carya forests and excluded species associated with secondary succession following nearly a century of fire suppression. Our results suggest that fire may mitigate the decline of C. florida populations under attack by an exotic pathogen by altering forest structure and composition. Further, our results suggest that the burns we sampled have had an overall restorative effect on forest communities and were within the fire return interval of the historic fire regime. Consequently, prescribed fire may offer a management tool to reduce the impacts of fungal disease in forest ecosystems that developed under historic burning regimes. PMID:18026756

  12. Indoxyl sulphate and kidney disease: Causes, consequences and interventions.

    PubMed

    Ellis, Robert J; Small, David M; Vesey, David A; Johnson, David W; Francis, Ross; Vitetta, Luis; Gobe, Glenda C; Morais, Christudas

    2016-03-01

    In the last decade, chronic kidney disease (CKD), defined as reduced renal function (glomerular filtration rate (GFR) < 60 mL/min per 1.73 m(2) ) and/or evidence of kidney damage (typically manifested as albuminuria) for at least 3 months, has become one of the fastest-growing public health concerns worldwide. CKD is characterized by reduced clearance and increased serum accumulation of metabolic waste products (uremic retention solutes). At least 152 uremic retention solutes have been reported. This review focuses on indoxyl sulphate (IS), a protein-bound, tryptophan-derived metabolite that is generated by intestinal micro-organisms (microbiota). Animal studies have demonstrated an association between IS accumulation and increased fibrosis, and oxidative stress. This has been mirrored by in vitro studies, many of which report cytotoxic effects in kidney proximal tubular cells following IS exposure. Clinical studies have associated IS accumulation with deleterious effects, such as kidney functional decline and adverse cardiovascular events, although causality has not been conclusively established. The aims of this review are to: (i) establish factors associated with increased serum accumulation of IS; (ii) report effects of IS accumulation in clinical studies; (iii) critique the reported effects of IS in the kidney, when administered both in vivo and in vitro; and (iv) summarize both established and hypothetical therapeutic options for reducing serum IS or antagonizing its reported downstream effects in the kidney. PMID:26239363

  13. Waterborne Exophiala species causing disease in cold-blooded animals.

    PubMed

    de Hoog, G S; Vicente, V A; Najafzadeh, M J; Harrak, M J; Badali, H; Seyedmousavi, S

    2011-12-01

    The majority of mesophilic waterborne species of the black yeast genus Exophiala (Chaetothyriales) belong to a single clade judging from SSU rDNA data. Most taxa are also found to cause cutaneous or disseminated infections in cold-blooded, water animals, occasionally reaching epidemic proportions. Hosts are mainly fish, frogs, toads, turtles or crabs, all sharing smooth, moist or mucous skins and waterborne or amphibian lifestyles; occasionally superficial infections in humans are noted. Cold-blooded animals with strictly terrestrial life styles, such as reptiles and birds are missing. It is concluded that animals with moist skins, i.e. those being waterborne and those possessing sweat glands, are more susceptible to black yeast infection. Melanin and the ability to assimilate alkylbenzenes are purported general virulence factors. Thermotolerance influences the choice of host. Exophiala species in ocean water mostly have maximum growth temperatures below 30 °C, whereas those able to grow until 33(-36) °C are found in shallow waters and occasionally on humans. Tissue responses vary with the phylogenetic position of the host, the lower animals showing poor granulome formation. Species circumscriptions have been determined by multilocus analyses involving partial ITS, TEF1, BT2 and ACT1. PMID:22403476

  14. Hand, foot, and mouth disease caused by coxsackievirus A6, Thailand, 2012.

    PubMed

    Puenpa, Jiratchaya; Chieochansin, Thaweesak; Linsuwanon, Piyada; Korkong, Sumeth; Thongkomplew, Siwanat; Vichaiwattana, Preyaporn; Theamboonlers, Apiradee; Poovorawan, Yong

    2013-04-01

    In Thailand, hand, foot, and mouth disease (HFMD) is usually caused by enterovirus 71 or coxsackievirus A16. To determine the cause of a large outbreak of HFMD in Thailand during June-August 2012, we examined patient specimens. Coxsackievirus A6 was the causative agent. To improve prevention and control, causes of HFMD should be monitored. PMID:23631943

  15. Acute myeloid leukaemia as a cause of acute ischaemic heart disease

    PubMed Central

    van Haelst, P.L.; Schot, B.; Hoendermis, E.S.; van den Berg, M.P.

    2006-01-01

    Ischaemic heart disease is almost invariably the result of atherosclerotic degeneration of the coronary arteries. However, other causes of ischaemic heart disease should always be considered. Here we describe two patients with a classic presentation of ischaemic heart disease resulting from acute leukaemia. The pathophysiological mechanisms of acute leukaemia leading to ischaemic heart disease are discussed. ImagesFigure 1AFigure 1BFigure 2 PMID:25696595

  16. Acquired mitochondrial impairment as a cause of optic nerve disease.

    PubMed Central

    Sadun, A

    1998-01-01

    BACKGROUND: Blindness from an optic neuropathy recently occurred as an epidemic affecting 50,000 patients in Cuba (CEON) and had clinical features reminiscent of both tobacco-alcohol amblyopia (TAA) and Leber's hereditary optic neuropathy (Leber's; LHON). Selective damage to the papillomacular bundle was characteristic, and many patients also developed a peripheral neuropathy. Identified risk factors included vitamin deficiencies as well as exposure to methanol and cyanide. In all 3 syndromes, there is evidence that singular or combined insults to mitochondrial oxidative phosphorylation are associated with a clinically characteristic optic neuropathy. PURPOSE: First, to test the hypothesis that a common pathophysiologic mechanism involving impairment of mitochondria function and, consequently, axonal transport underlies both genetic optic nerve diseases such as Leber's and acquired toxic and nutritional deficiency optic neuropathies. According to this hypothesis, ATP depletion below a certain threshold leads to a blockage of orthograde axonal transport of mitochondria, which, in turn, leads to total ATP depletion and subsequent cell death. Second, to address several related questions, including (1) How does impaired energy production lead to optic neuropathy, particularly since it seems to relatively spare other metabolically active tissues, such as liver and heart? (2) Within the nervous system, why is the optic nerve, and most particularly the papillomacular bundle, so highly sensitive? Although there have been previous publications on the clinical features of the Cuban epidemic of blindness, the present hypothesis and the subsequent questions have not been previously addressed. METHODS: Patients in Cuba with epidemic optic neuropathy were personally evaluated through a comprehensive neuro-ophthalmologic examination. In addition, serum, lymphocytes for DNA analysis, cerebrospinal fluid (CSF), sural nerves, and eyes with attached optic nerves were obtained from

  17. An example of anti-s causing mild haemolytic disease of the newborn

    PubMed Central

    Davie, M. J.; Smith, D. S.; White, Ursula M.; Dyball, D.

    1972-01-01

    An example of anti-s found during routine antenatal tests and causing mild haemolytic disease of the newborn is described. The serological and immunological properties of the antibody are described. PMID:5086219

  18. NEW EYE DISEASE IN PEN-REARED CHINOOK SALMON CAUSED BY METACESTODES OF GILQUINIA SQUALI (TRYPANORHYNCHA)

    EPA Science Inventory

    Eye infections by metacestodes of Gilcruinia squali (Cestoda: Trypanorhyncha) caused mortality in seawater netpen reared chinook salmon, ncorhynchus tshawytscha, at two locations in British Columbia, Canada. ortality associated with the disease was approximately 105 at one site a...

  19. Osler-Weber-Rendu disease: A rare cause of recurrent hemoptysis.

    PubMed

    Khoja, Amir M; Jalan, Rahul K; Jain, Dheeraj L; Kajale, Omkar V

    2016-01-01

    Osler-Weber-Rendu disease, also known as hereditary hemorrhagic telangiectasia, is a rare autosomal dominant condition causing systemic fibrovascular dysplasia. It has an incidence of 1-2/100,000. Phenotypic variation is extreme ranging from asymptomatic to severely symptomatic, from cases with no or few mucocutaneous lesions to those with diffuse cutaneous telangiectasia. We discuss a case of Osler-Weber-Rendu disease causing diffuse cutaneous telangiectasia and hemoptysis. The patient presented with complaints of hemoptysis and was extensively examined and investigated before being diagnosed with Osler-Weber-Rendu disease. We successfully managed the patient's hemoptysis by bronchial artery embolization. This case emphasizes the need for careful examination and investigation and to consider such rare diseases when all the common causes of hemoptysis are ruled out. An early and proper diagnosis will lead to more effective management of such a rare disease with few treatment options available. PMID:27185997

  20. Osler-Weber-Rendu disease: A rare cause of recurrent hemoptysis

    PubMed Central

    Khoja, Amir M; Jalan, Rahul K; Jain, Dheeraj L; Kajale, Omkar V

    2016-01-01

    Osler-Weber-Rendu disease, also known as hereditary hemorrhagic telangiectasia, is a rare autosomal dominant condition causing systemic fibrovascular dysplasia. It has an incidence of 1-2/100,000. Phenotypic variation is extreme ranging from asymptomatic to severely symptomatic, from cases with no or few mucocutaneous lesions to those with diffuse cutaneous telangiectasia. We discuss a case of Osler-Weber-Rendu disease causing diffuse cutaneous telangiectasia and hemoptysis. The patient presented with complaints of hemoptysis and was extensively examined and investigated before being diagnosed with Osler-Weber-Rendu disease. We successfully managed the patient's hemoptysis by bronchial artery embolization. This case emphasizes the need for careful examination and investigation and to consider such rare diseases when all the common causes of hemoptysis are ruled out. An early and proper diagnosis will lead to more effective management of such a rare disease with few treatment options available. PMID:27185997

  1. On human disease-causing amino acid variants: statistical study of sequence and structural patterns

    PubMed Central

    Alexov, Emil

    2015-01-01

    Statistical analysis was carried out on large set of naturally occurring human amino acid variations and it was demonstrated that there is a preference for some amino acid substitutions to be associated with diseases. At an amino acid sequence level, it was shown that the disease-causing variants frequently involve drastic changes of amino acid physico-chemical properties of proteins such as charge, hydrophobicity and geometry. Structural analysis of variants involved in diseases and being frequently observed in human population showed similar trends: disease-causing variants tend to cause more changes of hydrogen bond network and salt bridges as compared with harmless amino acid mutations. Analysis of thermodynamics data reported in literature, both experimental and computational, indicated that disease-causing variants tend to destabilize proteins and their interactions, which prompted us to investigate the effects of amino acid mutations on large databases of experimentally measured energy changes in unrelated proteins. Although the experimental datasets were linked neither to diseases nor exclusory to human proteins, the observed trends were the same: amino acid mutations tend to destabilize proteins and their interactions. Having in mind that structural and thermodynamics properties are interrelated, it is pointed out that any large change of any of them is anticipated to cause a disease. PMID:25689729

  2. First report of mango malformation disease caused by Fusarium pseudocircinatum in Mexico

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Mango (Mangifera indica L.) malformation disease (MMD) is one of the most important diseases affecting this crop worldwide, causing severe economic loss due to reduction of yield. Subsequent to the first report in India in 1891 (3), MMD has spread worldwide to most mango-growing regions. Several spe...

  3. Rapid detection of Flavobacterium columnare, the bacterium causing Columnaris Disease in fish

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Flavobacterium columnare is a ubiquitous bacterium that causes columnaris disease in a wide variety of fish resulting in devastating losses particularly in the commercial aquaculture industry worldwide. Timely diagnosis of disease is imperative for prevention of spread and to reduce the economic los...

  4. The Importance of Esophageal and Gastric Diseases as Causes of Chest Pain

    PubMed Central

    Shin, Eun Jung; Kim, Nam Su; Lee, Young Ho; Nam, Eun Woo

    2015-01-01

    Purpose Pediatric chest pain is considered to be idiopathic or caused by benign diseases. This study was to find out how much upper gastrointestinal (UGI) diseases are major causes of chest pain in pediatric patients. Methods The records of 75 children (42 boys and 33 girls, aged 3-17 years old) who have presented with mainly chest pain from January 1995 to March 2015 were retrospectively reviewed. Chest X-ray and electrocardiography (ECG) were performed in all aptients. Further cardiologic and gastrointestinal (GI) evaluations were performed in indicated patients. Results Chest pain was most common in the children of 6 and 9 to 14 years old. Esopha-gogastric diseases were unexpectedly the most common direct causes of the chest pain, the next are idiopathic, cardiac diseases, chest trauma, respiratory disease, and psychosomatic disease. Even though 21 showed abnormal ECG findings and 7 showed abnormalities on echocardiography, cardiac diseases were determined to be the direct causes only in 9. UGI endoscopy was performed in 57 cases, and esophago-gastric diseases which thereafter were thought to be causative diseases were 48 cases. The mean age of the children with esophago-gastric diseases were different with marginal significance from that of the other children with chest pain not related with esophago-gastric diseases. All the 48 children diagnosed with treated with GI medicines based on the diagnosis, and 37 cases (77.1%) subsequently showed clinical improvement. Conclusion Diagnostic approaches to find out esophageal and gastric diseases in children with chest pain are important as well as cardiac and respiratory investigations. PMID:26770901

  5. Phoma species on beet: more cause disease than just Phoma betae

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Phoma can cause damage to sugar beet (Beta vulgaris) at multiple growth stages. It has historically been an important seedling disease, but this is largely managed by ensuring clean seed for planting. The pathogen also can cause a root rot, a leaf spot, and rotting of beets during storage. In the Un...

  6. Evaluation of virus resistant rootstocks to manage watermelon vine decline and diseases caused by other potyviruses

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Watermelon vine decline caused by Squash vein yellowing virus (SqVYV) is an emerging disease that has caused severe losses to Florida watermelon growers in recent years. Papaya ringspot virus type W (PRSV-W) is one of several watermelon-infecting potyviruses long present in the southeastern U.S. L...

  7. Occupational lung disease. Part 2. Discovering the cause of diffuse parenchymal lung disease.

    PubMed

    Kuschner, Ware G; Stark, Paul

    2003-04-01

    Diffuse parenchymal lung disease (also known as interstitial lung disease) and acute irritant reactions are much less commonly managed by primary care physicians than asthma. Acute irritant reactions are typically readily recognized because of the immediate exposure-response relationship. As with asthma, a diagnosis of diffuse parenchymal lung disease should prompt a careful review of the patient's work history. Findings from history taking and radiography provide most of the data needed to establish a diagnosis of asbestosis or silicosis. A pulmonologist should be consulted about lung disease that eludes diagnosis. In cases in which a link between work and illness is strongly suspected, an occupational medicine specialist may be consulted for assistance with preparing reports for a workers' compensation claim as well as characterizing and quantifying impairment. Various government agencies provide extensive information about specific toxic exposures and occupational lung diseases by telephone and on the World Wide Web. PMID:12718237

  8. Hemolytic disease of the newborn caused by maternal anti-Dib: a case report in Taiwan.

    PubMed

    Chen, C C; Broadberry, R E; Chang, F C; Ding, F; Lin, M

    1993-10-01

    Possibly the first case of hemolytic disease caused by anti-Dib in a Chinese infant is reported. The infant developed jaundice soon after birth; based on study, the jaundice has been diagnosed as a result of maternal anti-Dib which was most likely induced by previous pregnancies. The phenotype of the mother's red cells was Di (a+b-). The frequency of the Dia antigen among Chinese in Taiwan is 3.2%. In Orientals, hemolytic disease of the newborn caused by maternal anti-Dib is likely to be more severe than that caused by anti-Dia. PMID:8258120

  9. Is Mycobacterium avium subsp. paratuberculosis, the cause of Johne's disease in animals, a good candidate for Crohn's disease in man?

    PubMed

    Singh, A V; Singh, S V; Singh, P K; Sohal, J S

    2010-03-01

    Mycobacterium avium subspecies paratuberculosis (MAP) causes Johne's disease or paratuberculosis, a gastro intestinal inflammatory condition in ruminants and other animals, which is similar to Crohn's disease (CD) that occurs in man. The role of MAP in the causation of CD has been under intense investigation in the last few decades. This review summarizes the status of MAP in animals and the food chain and its association with CD in man. PMID:20443099

  10. Influence of Nitrogen, Phosphorus, and Potassium on the Severity of Strawberry Anthracnose Crown Rot

    Technology Transfer Automated Retrieval System (TEKTRAN)

    The influence of nitrogen, phosphorus, and potassium on the severity of anthracnose crown rot (causal fungus, Colletotrichum fragariae) was evaluated in three greenhouse studies. Strawberry plants were maintained under standard greenhouse conditions with one plant per 10 cm pot fertilized three tim...

  11. Effect of Fungicides on the Reaction of Sorghum Hybrids to Anthracnose in Burleson County, Texas, 2012

    Technology Transfer Automated Retrieval System (TEKTRAN)

    The use of three fungicides to control grain mold/weathering and anthracnose on two sorghum hybrids NC+7R34 and Warner W851-DR was conducted during the 2012 growing season. Three fungicides Headline, Quilt Xcel, and Topguard were used. On May 26, plots were inoculated by putting 10 Colletotrichum ...

  12. Evaluation of the Ugandan sorghum accessions for grain mold and anthracnose resistance

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Sorghum accessions from Uganda were evaluated for grain mold and anthracnose resistance during the 2005 and 2006 growing seasons at the Texas A&M University Research Farm, near College Station, TX. Accession PI534117 and SC719-11E exhibited the lowest grain mold severities of 2.4, whereas, accessio...

  13. Response of sorghum accessions from four African countries against Colletotrichum sublineolum, causal agent of sorghum anthracnose

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Seventy-two sorghum accessions were randomly selected from the Ethiopia, Mali, Sudan, and Uganda germplasm collections maintained by the US National Plant Germplasm System to evaluate variation in anthracnose resistance. The accessions were planted in a randomized complete block design in College S...

  14. Field evaluation of anthracnose resistance for sorghum germplasm from the Sikasso region in Mali

    Technology Transfer Automated Retrieval System (TEKTRAN)

    The USDA, ARS National Plant Germplasm System maintains 132 sorghum landraces from the Sikasso region of Mali. This germplasm was inoculated with Colletotrichum sublineolum and evaluated for foliar anthracnose resistance at the USDA, ARS Tropical Agriculture Research Station in Isabela, Puerto Rico...

  15. Inflammatory Bowel Disease Cause-specific Mortality: A Primer for Clinicians

    PubMed Central

    Kassam, Zain; Belga, Sara; Roifman, Idan; Hirota, Simon; Jijon, Humberto; Kaplan, Gilaad G.; Ghosh, Subrata

    2014-01-01

    Background: Inflammatory bowel disease (IBD), including Crohn's disease (CD) and ulcerative colitis (UC) is perceived to harbor significant morbidity but limited excess mortality, thought to be driven by colon cancer, compared with the general population. Recent studies suggest mortality rates seem higher than previously understood, and there are emerging threats to mortality. Clinicians must be up to date and able to clearly convey the causes of mortality to arm individual patients with information to meaningfully participate in decisions regarding IBD treatment and maintenance of health. Methods: A MEDLINE search was conducted to capture all relevant articles. Keyword search included: “inflammatory bowel disease,” “Crohn's disease,” “ulcerative colitis,” and “mortality.” Results: CD and UC have slightly different causes of mortality; however, malignancy and colorectal cancer–associated mortality remains controversial in IBD. CD mortality seems to be driven by gastrointestinal disease, infection, and respiratory diseases. UC mortality was primarily attributable to gastrointestinal disease and infection. Clostridium difficile infection is an emerging cause of mortality in IBD. UC and CD patients have a marked increase in risk of thromboembolic disease. With advances in medical and surgical interventions, the exploration of treatment-associated mortality must continue to be evaluated. Conclusions: Clinicians should be aware that conventional causes of death such as malignancy do not seem to be as significant a burden as originally perceived. However, emerging threats such as infection including C. difficile are noteworthy. Although CD and UC share similar causes of death, there seems to be some differences in cause-specific mortality. PMID:25185685

  16. Exonic rearrangements in the known Parkinson's disease-causing genes are a rare cause of the disease in South African patients.

    PubMed

    van der Merwe, Celia; Carr, Jonathan; Glanzmann, Brigitte; Bardien, Soraya

    2016-04-21

    Parkinson's disease (PD) is a neurodegenerative movement disorder characterized by the loss of dopaminergic neurons in the substantia nigra of the midbrain. To date, a number of PD-causing genes have been found, including SNCA, LRRK2, VPS35, PARK2, PINK1, DJ-1, ATP13A2, and most recently CHCHD2. Mutations in these genes range from point mutations to larger exonic rearrangements including deletions and duplications. This study aimed to detect possible copy number variation (CNV) in the known PD-causing genes in a cohort of South African patients with PD. Multiplex Ligation-dependent Probe Amplification (MLPA) analysis was performed on a total of 210 South African PD patients, and possible CNVs were verified using quantitative real time PCR. No homozygous or compound heterozygous exon rearrangements in the genes analysed were found in the patient group. A heterozygous PARK2 exon 4 deletion was found in a sporadic patient with an age at onset of 51 years. Sanger sequencing did not reveal any additional mutations in PARK2 in this patient. Combining our results with that of previous studies in a South African cohort, the frequency of exonic rearrangements in the known PD-causing genes is only 1.8% (8/439 patients). In conclusion, CNV in the known PD-causing genes are a rare cause of PD in a South African cohort, and there may be as yet unknown genetic causes of PD that are specific to patients of African ethnicity. PMID:27001088

  17. The spectrum of oculocutaneous disease: Part I. Infectious, inflammatory, and genetic causes of oculocutaneous disease.

    PubMed

    Horner, Mary E; Abramson, Amanda K; Warren, Richard B; Swanson, Susan; Menter, M Alan

    2014-05-01

    Many skin diseases are associated with ocular findings, emphasizing the need for dermatologists to be fully aware of their presence, and as a result, avoid overlooking conditions with potentially major ocular complications, including blindness. We review important oculocutaneous disease associations with recommendations for the management of the ocular complications and appropriate referral to our ophthalmology colleagues. Part I of this 2-part review focuses on the infectious, inflammatory, and genetic relationships. PMID:24742848

  18. Establishing Precise Evolutionary History of a Gene Improves Predicting Disease Causing Missense Mutations

    PubMed Central

    Adebali, Ogun; Reznik, Alexander O.; Ory, Daniel S.; Zhulin, Igor B.

    2015-01-01

    Purpose Predicting the phenotypic effects of mutations has become an important application in clinical genetic diagnostics. Computational tools evaluate the behavior of the variant over evolutionary time and assume that variations seen during the course of evolution are likely benign in humans. However, current tools do not take into account orthologous/paralogous relationships. Paralogs have dramatically different roles in Mendelian diseases. For example, while inactivating mutations in the NPC1 gene cause the neurodegenerative disorder Niemann-Pick C, inactivating mutations in its paralog NPC1L1 are not disease-causing and moreover are implicated in protection from coronary heart disease. Methods We identified major events in NPC1 evolution and revealed and compared orthologs and paralogs of the human NPC1 gene through phylogenetic and protein sequence analyses. We predicted whether an amino acid substitution affects protein function by reducing the organism’s fitness. Results Removing the paralogs and distant homologs improved the overall performance of categorizing disease-causing and benign amino acid substitutions. Conclusion The results show that a thorough evolutionary analysis followed by identification of orthologs improves the accuracy in predicting disease-causing missense mutations. We anticipate that this approach will be used as a reference in the interpretation of variants in other genetic diseases as well. PMID:26890452

  19. Coprinellus curtus (Hitoyo-take) prevents diseases of vegetables caused by pathogenic fungi.

    PubMed

    Nakasaki, Kiyohiko; Saito, Miyuki; Suzuki, Nobuaki

    2007-10-01

    A strain of Coprinellus curtus (designated GM-21), a basidiomycete that suppressed bottom-rot disease of Chinese cabbage, 'pak-choi' (Brassica campestris), caused by the pathogen Rhizoctonia solani Pak-choi 2 was isolated. The mechanism of plant disease suppression was discovered to be hyphal interference, a combative fungal interaction between strain GM-21 and the pathogen. The antifungal spectrum of strain GM-21 was shown to include R. solani and Fusarium sp., i.e. strain GM-21 showed disease-suppressive ability against bottom-rot disease of lettuce and Rhizoctonia-patch disease of mascarene grass caused by strains of R. solani. In addition, clear evidence of hyphal interference between strain GM-21 and Fusarium pathogens that cause crown (foot) and root-rot disease of tomato and Fusarium wilt of melon, respectively, was demonstrated. It was thus considered that GM-21 is effective for suppressing soil-borne pathogens, and that GM-21 presents new possibilities for biological control of vegetable diseases. PMID:17850327

  20. Human mitochondrial diseases caused by lack of taurine modification in mitochondrial tRNAs.

    PubMed

    Suzuki, Tsutomu; Nagao, Asuteka; Suzuki, Takeo

    2011-01-01

    Mitochondrial DNA mutations that cause mitochondrial dysfunction are responsible for a wide spectrum of human diseases, referred to as mitochondrial diseases. Pathogenic point mutations are found frequently in genes encoding mitochondrial (mt) tRNAs, indicating that impaired functioning of mutant mt tRNAs is the primary cause of mitochondrial dysfunction. Our previous studies revealed the absence of posttranscriptional taurine modification at the anticodon wobble uridine in mutant mt tRNAs isolated from cells derived from patients with two major classes of mitochondrial diseases, MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes) and MERRF (myoclonus epilepsy associated with ragged red fibers). Defective taurine modification of the mutant mt tRNAs results in a deficiency in protein synthesis as the cognate codons of the mutant mt tRNA cannot be decoded. These findings represent the first evidence of a molecular pathogenesis caused by an RNA modification disorder. PMID:21957023

  1. Nonhuman primate models used to study pelvic inflammatory disease caused by Chlamydia trachomatis.

    PubMed

    Bell, Jason D; Bergin, Ingrid L; Schmidt, Kelsey; Zochowski, Melissa K; Aronoff, David M; Patton, Dorothy L

    2011-01-01

    Pelvic inflammatory disease (PID) is a global health concern that is associated with significant morbidity and is a major cause of infertility. Throughout history animals have been used for anatomical studies and later as models of human disease. In particular, nonhuman primates (NHPs) have permitted investigations of human disease in a biologically, physiologically, and anatomically similar system. The use of NHPs as human PID models has led to a greater understanding of the primary microorganisms that cause disease (e.g., Chlamydia trachomatis and Neisseria gonorroheae), the pathogenesis of infection and its complications, and the treatment of people with PID. This paper explores historical and contemporary aspects of NHP modeling of chlamydial PID, with an emphasis on advantages and limitations of this approach and future directions for this research. PMID:21869858

  2. Taxonomy of fungi causing mucormycosis and entomophthoramycosis (zygomycosis) and nomenclature of the disease: molecular mycologic perspectives.

    PubMed

    Kwon-Chung, Kyung J

    2012-02-01

    Molecular phylogenetic analysis confirmed the phylum Zygomycota to be polyphyletic, and the taxa conventionally classified in Zygomycota are now distributed among the new phylum Glomeromycota and 4 subphyla incertae sedis (uncertain placement). Because the nomenclature of the disease zygomycosis was based on the phylum Zygomycota (Zygomycetes) in which the etiologic agents had been classified, the new classification profoundly affects the name of the disease. Zygomycosis was originally described as a convenient and inclusive name for 2 clinicopathologically different diseases, mucormycosis caused by members of Mucorales and entomophthoramycosis caused by species in the order Entomophthorales of Zygomycota. Without revision of original definition, the name "zygomycosis," however, has more often been used as a synonym only for mucormycosis. This article reviews the progress and changes in taxonomy and nomenclature of Zygomycota and the disease zygomycosis. The article also reiterates the reasons why the classic names "mucormycosis" and "entomophthoramycosis" are more appropriate than "zygomycosis." PMID:22247451

  3. Alternative projections of mortality and disability by cause 1990-2020: Global Burden of Disease Study.

    PubMed

    Murray, C J; Lopez, A D

    1997-05-24

    As part of the Global Burden of Disease Study, three scenarios of future mortality and disability were identified. The scenarios were based on future health status as a function of projected changes in key socioeconomic variables that influence health status. Regression equations for mortality rates for nine cause-of-death clusters were developed by region based on gross domestic product per person, average number of years of education, time (as a proxy for technological change), and smoking intensity. Life expectancy at birth was projected, in all three scenarios, to increase for women (to about 90 years in established market economies by 2020), with far smaller gains in male life expectancy. Worldwide, annual mortality from communicable maternal, perinatal, and nutritional disorders (group 1 causes) is expected to decline from 17.2 million to 10.3 million in 2020 in the baseline model. Also expected is a very large increase in deaths from non-communicable diseases (group 2 causes) from 28.1 million in 1990 to 49.7 million in 2020. Deaths from injuries (group 3) are projected to increase from 5.1 million to 8.4 million. Diarrheal diseases, perinatal disorders, measles, and malaria are expected to decline dramatically as causes of death in the 1990-2020 period, while lung cancer, stomach cancer, war injuries, liver cancer, and HIV are expected to move up five or more places in the ranking. In 2020, the 10 leading causes of disability-adjusted life-years (in descending order) are projected to be ischemic heart disease, unipolar major depression, road traffic accidents, cerebrovascular disease, chronic obstructive pulmonary disease, lower respiratory infections, tuberculosis, war injuries, diarrheal diseases, and HIV. Tobacco-attributable mortality is projected to increase from 3.0 million in 1990 to 8.4 million in 2020 (9% of the worldwide mortality burden). PMID:9167458

  4. Change in alcohol consumption and risk of death from all causes and from ischaemic heart disease.

    PubMed Central

    Lazarus, N B; Kaplan, G A; Cohen, R D; Leu, D J

    1991-01-01

    OBJECTIVE--To examine the association between alcohol consumption and mortality from all causes and from ischaemic heart disease with a focus on differentiating between long term abstainers and more recent non-drinkers. DESIGN--Cohort study of changes in alcohol consumption from 1965 to 1974 and mortality from all causes and ischaemic heart disease during 1974-84. SETTING--Population based study of adult residents of Alameda County, California. SUBJECTS--2225 women and 1845 men aged 35 and over in 1965. MAIN OUTCOME MEASURES--Alcohol consumption in 1964 and 1974 and mortality from all causes and from ischaemic heart disease during 1974-84. RESULTS--There was a significantly higher risk of death from all causes and from ischaemic heart disease in women who gave up drinking between 1965 and 1974 than in women who continued to drink (relative risk 1.72, 95% confidence interval 1.11 to 2.66, and 2.75, 1.44 to 5.23, for all causes and ischaemic heart disease respectively). A significant increase in risk was not seen in men who gave up drinking (1.32, 0.87 to 2.01, and 0.95, 0.41 to 2.20, respectively). Among men, long term abstainers compared with drinkers were at increased risk of death from all causes and from ischaemic heart disease, though the associations were not significant (1.40, 0.98 to 2.00, and 1.40, 0.76 to 2.58, for all causes and ischaemic heart disease respectively). CONCLUSION--Some of the increased risk of death from all causes and from ischaemic heart disease associated with not drinking in women seems to be accounted for by higher risks among those who gave up drinking. Men who are long term abstainers may also be at an increased risk of death. The heterogeneity of the non-drinking group should be considered when comparisons are made with drinkers. PMID:1912885

  5. Whole exome sequencing unravels disease-causing genes in consanguineous families in Qatar.

    PubMed

    Fahiminiya, S; Almuriekhi, M; Nawaz, Z; Staffa, A; Lepage, P; Ali, R; Hashim, L; Schwartzentruber, J; Abu Khadija, K; Zaineddin, S; Gamal, H; Majewski, J; Ben-Omran, T

    2014-08-01

    Whole exome sequencing (WES) has greatly facilitated the identification of causal mutations for diverse human genetic disorders. We applied WES as a molecular diagnostic tool to identify disease-causing genes in consanguineous families in Qatar. Seventeen consanguineous families with diverse disorders were recruited. Initial mutation screening of known genes related to the clinical diagnoses did not reveal the causative mutations. Using WES approach, we identified the definitive disease-causing mutations in four families: (i) a novel nonsense homozygous (c.1034C>G) in PHKG2 causing glycogen storage disease type 9C (GSD9C) in a male with initial diagnosis of GSD3; (ii) a novel homozygous 1-bp deletion (c.915del) in NSUN2 in a male proband with Noonan-like syndrome; (iii) a homozygous SNV (c.1598C>G) in exon 11 of IDUA causing Hurler syndrome in a female proband with unknown clinical diagnosis; (iv) a de novo known splicing mutation (c.1645+1G>A) in PHEX in a female proband with initial diagnosis of autosomal recessive hypophosphatemic rickets. Applying WES as a diagnostic tool led to the unambiguous identification of disease-causing mutations in phenotypically complex disorders or correction of the initial clinical diagnosis in ˜25% of our cases. PMID:24102521

  6. Infantile onset spinocerebellar ataxia caused by compound heterozygosity for Twinkle mutations and modeling of Twinkle mutations causing recessive disease.

    PubMed

    Pierce, Sarah B; Gulsuner, Suleyman; Stapleton, Gail A; Walsh, Tom; Lee, Ming K; Mandell, Jessica B; Morales, Augusto; Klevit, Rachel E; King, Mary-Claire; Rogers, R Curtis

    2016-07-01

    Mutations in nuclear genes required for the replication and maintenance of mitochondrial DNA cause progressive multisystemic neuromuscular disorders with overlapping phenotypes. Biallelic mutations in C10orf2, encoding the Twinkle mitochondrial DNA helicase, lead to infantile-onset cerebellar ataxia (IOSCA), as well as milder and more severe phenotypes. We present a 13-year-old girl with ataxia, severe hearing loss, optic atrophy, peripheral neuropathy, and hypergonadotropic hypogonadism. Whole-exome sequencing revealed that the patient is compound heterozygous for previously unreported variants in the C10orf2 gene: a paternally inherited frameshift variant (c.333delT; p.L112Sfs*3) and a maternally inherited missense variant (c.904C>T; p.R302W). The identification of novel C10orf2 mutations extends the spectrum of mutations in the Twinkle helicase causing recessive disease, in particular the intermediate IOSCA phenotype. Structural modeling suggests that the p.R302W mutation and many other recessively inherited Twinkle mutations impact the position or interactions of the linker region, which is critical for the oligomeric ring structure and activity of the helicase. This study emphasizes the utility of whole-exome sequencing for the genetic diagnosis of a complex multisystemic disorder. PMID:27551684

  7. Infantile onset spinocerebellar ataxia caused by compound heterozygosity for Twinkle mutations and modeling of Twinkle mutations causing recessive disease

    PubMed Central

    Gulsuner, Suleyman; Stapleton, Gail A.; Walsh, Tom; Lee, Ming K.; Mandell, Jessica B.; Morales, Augusto; Klevit, Rachel E.; King, Mary-Claire; Rogers, R. Curtis

    2016-01-01

    Mutations in nuclear genes required for the replication and maintenance of mitochondrial DNA cause progressive multisystemic neuromuscular disorders with overlapping phenotypes. Biallelic mutations in C10orf2, encoding the Twinkle mitochondrial DNA helicase, lead to infantile-onset cerebellar ataxia (IOSCA), as well as milder and more severe phenotypes. We present a 13-year-old girl with ataxia, severe hearing loss, optic atrophy, peripheral neuropathy, and hypergonadotropic hypogonadism. Whole-exome sequencing revealed that the patient is compound heterozygous for previously unreported variants in the C10orf2 gene: a paternally inherited frameshift variant (c.333delT; p.L112Sfs*3) and a maternally inherited missense variant (c.904C>T; p.R302W). The identification of novel C10orf2 mutations extends the spectrum of mutations in the Twinkle helicase causing recessive disease, in particular the intermediate IOSCA phenotype. Structural modeling suggests that the p.R302W mutation and many other recessively inherited Twinkle mutations impact the position or interactions of the linker region, which is critical for the oligomeric ring structure and activity of the helicase. This study emphasizes the utility of whole-exome sequencing for the genetic diagnosis of a complex multisystemic disorder. PMID:27551684

  8. Myocardial performance and perfusion during exercise in patients with coronary artery disease caused by Kawasaki disease

    SciTech Connect

    Paridon, S.M.; Ross, R.D.; Kuhns, L.R.; Pinsky, W.W. )

    1990-01-01

    For a study of the natural history of coronary artery lesions after Kawasaki disease and their effect on myocardial blood flow reserve with exercise, five such patients underwent exercise testing on a bicycle. Oxygen consumption, carbon dioxide production, minute ventilation, and electrocardiograms were monitored continuously. Thallium-201 scintigraphy was performed for all patients. One patient stopped exercise before exhaustion of cardiovascular reserve but had no evidence of myocardial perfusion abnormalities. Four patients terminated exercise because of exhaustion of cardiovascular reserve; one had normal cardiovascular reserve and thallium scintiscans, but the remaining patients had diminished cardiovascular reserve. Thallium scintigrams showed myocardial ischemia in two and infarction in one. No patient had exercise-induced electrocardiographic changes. These results indicate that patients with residual coronary artery lesions after Kawasaki disease frequently have reduced cardiovascular reserve during exercise. The addition of thallium scintigraphy and metabolic measurements to exercise testing improved the detection of exercise-induced abnormalities of myocardial perfusion.

  9. The spectrum of nephrocutaneous diseases and associations: Genetic causes of nephrocutaneous disease.

    PubMed

    Wofford, Jay; Fenves, Andrew Z; Jackson, J Mark; Kimball, Alexa B; Menter, Alan

    2016-02-01

    There are a significant number of diseases and treatment considerations of considerable importance relating to the skin and renal systems. This emphasizes the need for dermatologists in practice or in clinical training to be aware of these associations. Part I of this 2-part continuing medical education article reviews the genetic syndromes with both renal and cutaneous involvement that are most important for the dermatologist to be able to identify, manage, and appropriately refer to nephrology colleagues. Part II reviews the inflammatory syndromes with relevant renal manifestations and therapeutic agents commonly used by dermatologists that have drug-induced effects on or require close consideration of renal function. In addition, we will likewise review therapeutic agents commonly used by nephrologists that have drug-induced effects on the skin that dermatologists are likely to encounter in clinical practice. In both parts of this continuing medical education article, we discuss diagnosis, management, and appropriate referral to our nephrology colleagues in the context of each nephrocutaneous association. There are a significant number of dermatoses associated with renal abnormalities and disease, emphasizing the need for dermatologists to be keenly aware of their presence in order to avoid overlooking important skin conditions with potentially devastating renal complications. This review discusses important nephrocutaneous disease associations with recommendations for the appropriate urgency of referral to nephrology colleagues for diagnosis, surveillance, and early management of potential renal sequelae. PMID:26775773

  10. A genetic cause of Alzheimer disease: mechanistic insights from Down syndrome

    PubMed Central

    Wiseman, Frances K.; Al-Janabi, Tamara; Hardy, John; Karmiloff-Smith, Annette; Nizetic, Dean; Tybulewicz, Victor L. J.; Fisher, Elizabeth M. C.; Strydom, André

    2015-01-01

    Down syndrome, which arises in individuals carrying an extra copy of chromosome 21, is associated with a greatly increased risk of early-onset Alzheimer disease. It is thought that this risk is conferred by the presence of three copies of the gene encoding amyloid precursor protein (APP) — an Alzheimer disease risk factor — although the possession of extra copies of other chromosome 21 genes may also play a part. Further study of the mechanisms underlying the development of Alzheimer disease in people with Down syndrome could provide insights into the mechanisms that cause dementia in the general population. PMID:26243569

  11. Debating Diseases in Nineteenth-Century Colombia: Causes, Interests, and the Pasteurian Therapeutics.

    PubMed

    García, Mónica

    2015-01-01

    This article explores the medical conceptualization of the causes of diseases in nineteenth-century Colombia. It traces the history of some of the pathologies that were of major concern among nineteenth-century doctors: periodic fevers (yellow fever and malaria), continuous fevers (typhoid fever), and leprosy (Greek elephantiasis). By comparing the transforming conceptualizations of these diseases, this article shows that their changing pattern, the idea of climatic determinism of diseases (neo-Hippocratism and medical geography), the weak standing of the medical community in Colombian society, as well as Pasteurian germ practices were all crucial in the uneven and varied reshaping of their understanding. PMID:26095967

  12. Spontaneous retrotransposon insertion into TNF 3'UTR causes heart valve disease and chronic polyarthritis.

    PubMed

    Lacey, Derek; Hickey, Peter; Arhatari, Benedicta D; O'Reilly, Lorraine A; Rohrbeck, Leona; Kiriazis, Helen; Du, Xiao-Jun; Bouillet, Philippe

    2015-08-01

    Rheumatoid arthritis (RA) and ankylosing spondylitis (AS) are chronic inflammatory diseases that together affect 2-3% of the population. RA and AS predominantly involve joints, but heart disease is also a common feature in RA and AS patients. Here we have studied a new spontaneous mutation that causes severe polyarthritis in bone phenotype spontaneous mutation 1 (BPSM1) mice. In addition to joint destruction, mutant mice also develop aortic root aneurism and aorto-mitral valve disease that can be fatal depending on the genetic background. The cause of the disease is the spontaneous insertion of a retrotransposon into the 3' untranslated region (3'UTR) of the tumor necrosis factor (TNF), which triggers its strong overexpression in myeloid cells. We found that several members of a family of RNA-binding, CCCH-containing zinc-finger proteins control TNF expression through its 3'UTR, and we identified a previously unidentified regulatory element in the UTR. The disease in BPSM1 mice is independent of the adaptive immune system and does not appear to involve inflammatory cytokines other than TNF. To our knowledge, this is the first animal model showing both polyarthritis and heart disease as a direct result of TNF deregulation. These results emphasize the therapeutic potential of anti-TNF drugs for the treatment of heart valve disease and identify potential therapeutic targets to control TNF expression and inflammation. PMID:26195802

  13. Spontaneous retrotransposon insertion into TNF 3′UTR causes heart valve disease and chronic polyarthritis

    PubMed Central

    Lacey, Derek; Hickey, Peter; Arhatari, Benedicta D.; O’Reilly, Lorraine A.; Rohrbeck, Leona; Kiriazis, Helen; Du, Xiao-Jun; Bouillet, Philippe

    2015-01-01

    Rheumatoid arthritis (RA) and ankylosing spondylitis (AS) are chronic inflammatory diseases that together affect 2–3% of the population. RA and AS predominantly involve joints, but heart disease is also a common feature in RA and AS patients. Here we have studied a new spontaneous mutation that causes severe polyarthritis in bone phenotype spontaneous mutation 1 (BPSM1) mice. In addition to joint destruction, mutant mice also develop aortic root aneurism and aorto-mitral valve disease that can be fatal depending on the genetic background. The cause of the disease is the spontaneous insertion of a retrotransposon into the 3′ untranslated region (3′UTR) of the tumor necrosis factor (TNF), which triggers its strong overexpression in myeloid cells. We found that several members of a family of RNA-binding, CCCH-containing zinc-finger proteins control TNF expression through its 3′UTR, and we identified a previously unidentified regulatory element in the UTR. The disease in BPSM1 mice is independent of the adaptive immune system and does not appear to involve inflammatory cytokines other than TNF. To our knowledge, this is the first animal model showing both polyarthritis and heart disease as a direct result of TNF deregulation. These results emphasize the therapeutic potential of anti-TNF drugs for the treatment of heart valve disease and identify potential therapeutic targets to control TNF expression and inflammation. PMID:26195802

  14. Complete staghorn calculus in polycystic kidney disease: infection is still the cause

    PubMed Central

    2013-01-01

    Background Kidney stones in patients with autosomal dominant polycystic kidney disease are common, regarded as the consequence of the combination of anatomic abnormality and metabolic risk factors. However, complete staghorn calculus is rare in polycystic kidney disease and predicts a gloomy prognosis of kidney. For general population, recent data showed metabolic factors were the dominant causes for staghorn calculus, but for polycystic kidney disease patients, the cause for staghorn calculus remained elusive. Case presentation We report a case of complete staghorm calculus in a polycystic kidney disease patient induced by repeatedly urinary tract infections. This 37-year-old autosomal dominant polycystic kidney disease female with positive family history was admitted in this hospital for repeatedly upper urinary tract infection for 3 years. CT scan revealed the existence of a complete staghorn calculus in her right kidney, while there was no kidney stone 3 years before, and the urinary stone component analysis showed the composition of calculus was magnesium ammonium phosphate. Conclusion UTI is an important complication for polycystic kidney disease and will facilitate the formation of staghorn calculi. As staghorn calculi are associated with kidney fibrosis and high long-term renal deterioration rate, prompt control of urinary tract infection in polycystic kidney disease patient will be beneficial in preventing staghorn calculus formation. PMID:24070202

  15. A novel sponge disease caused by a consortium of micro-organisms

    NASA Astrophysics Data System (ADS)

    Sweet, Michael; Bulling, Mark; Cerrano, Carlo

    2015-09-01

    In healthy sponges, microbes have been shown to account for up to 40 % of tissues. The majority of these are thought to originate from survivors evading digestion and immune responses of the sponge and growing and residing in the microenvironments of the mesophyll. Although a large percentage of these microbes are likely commensals, they may also include potentially pathogenic agents, which under specific conditions, such as temperature stress, may cause disease. Here we report a novel disease (sponge necrosis syndrome) that is severely affecting populations of the sponge Callyspongia ( Euplacella) aff biru. Both ITS fungal and 16S rDNA bacterial diversities were assessed in healthy and diseased individuals, highlighting six potential primary causal agents for this new disease: two bacteria, a Rhodobacteraceae sp. and a cyanobacterium, Hormoscilla spongeliae (formally identified as Oscillatoria spongeliae), and four fungi, a Ascomycota sp., a Pleosporales sp., a Rhabdocline sp., and a Clasosporium sp. Furthermore, histological analysis showed the dominance of fungal hyphae rather than bacteria throughout the disease lesion, which was absent or rare in healthy tissues. Inoculation trails showed that only a combination of one bacterium and one fungus could replicate the disease, fulfilling Henle-Koch's postulates and showing that this sponge disease is caused by a poly-microbial consortium.

  16. Medical disease as a cause of maternal mortality: the pre-imminence of cardiovascular pathology.

    PubMed

    Mocumbi, A O; Sliwa, K; Soma-Pillay, P

    2016-01-01

    Maternal mortality ratio in low- to middle-income countries (LMIC) is 14 times higher than in high-income countries. This is partially due to lack of antenatal care, unmet needs for family planning and education, as well as low rates of birth managed by skilled attendants. While direct causes of maternal death such as complications of hypertension, obstetric haemorrhage and sepsis remain the largest cause of maternal death in LMICs, cardiovascular disease emerges as an important contributor to maternal mortality in both developing countries and the developed world, hampering the achievement of the millennium development goal 5, which aimed at reducing by three-quarters the maternal mortality ratio until the end of 2015. Systematic search for cardiac disease is usually not performed during pregnancy in LMICs despite hypertensive disease, rheumatic heart disease and cardiomyopathies being recognised as major health problems in these settings. New concern has been rising due to both the HIV/AIDS epidemic and the introduction of highly active antiretroviral therapy. Undetected or untreated congenital heart defects, undiagnosed pulmonary hypertension, uncontrolled heart failure and complications of sickle cell disease may also be important challenges. This article discusses issues related to the role of cardiovascular disease in determining a substantial portion of maternal morbidity and mortality. It also presents an algorhitm to be used for suspected and previously known cardiac disease in pregnancy in the context of LIMCs. PMID:27213855

  17. Compounds of Natural Origin and Acupuncture for the Treatment of Diseases Caused by Estrogen Deficiency.

    PubMed

    Thakur, Abhishek; Mandal, Subhash C; Banerjee, Sugato

    2016-06-01

    A predominant number of diseases affecting women are related to female hormones. In most of the cases, these diseases are reported to be associated with menstrual problems. These diseases affect female reproductive organs such as the breast, uterus, and ovaries. Estrogen is the main hormone responsible for the menstrual cycle, so irregular menstruation is primarily due to a disturbance in estrogen levels. Estrogen imbalance leads to various pathological conditions in premenopausal women, such as endometriosis, breast cancer, colorectal cancer, prostate cancer, poly cysts, intrahepatic cholestasis of pregnancy, osteoporosis, cardiovascular diseases, obesity, etc. In this review, we discuss common drug targets and therapeutic strategies, including acupuncture and compounds of natural origin, for the treatment of diseases caused by estrogen deficiency. PMID:27342884

  18. Celiac disease causing severe osteomalacia: an association still present in Morocco!

    PubMed

    Tahiri, Latifa; Azzouzi, Hamida; Squalli, Ghita; Abourazzak, Fatimazahra; Harzy, Taoufik

    2014-01-01

    Celiac disease (CD), a malabsorption syndrome caused by hypersensitivity to gliadin fraction of gluten. CD can manifest with classic symptoms; however, significant myopathy and multiple fractures are rarely the predominant presentation of untreated celiac disease. Osteomalacia complicating celiac disease had become more and more rare. We describe here a case of osteomalacia secondary to a longstanding untreated celiac disease. This patient complained about progressive bone and muscular pain, weakness, fractures and skeletal deformities. Radiological and laboratory findings were all in favor of severe osteomalacia. Improvement of patient's weakness and laboratory abnormalities was obvious after treatment with gluten free diet, vitamin D, calcium and iron. This case affirms that chronic untreated celiac disease, can lead to an important bone loss and irreversible complications like skeletal deformities. PMID:25667705

  19. Does Dent disease remain an underrecognized cause for young boys with focal glomerulosclerosis?

    PubMed

    Kubo, Kaori; Aizawa, Tomomi; Watanabe, Shojiro; Tsugawa, Koji; Tsuruga, Kazushi; Ito, Etsuro; Joh, Kensuke; Tanaka, Hiroshi

    2016-08-01

    Focal glomerulosclerosis (FGS) is a histologic entity that causes significant proteinuria in children. Although its etiology varies, recent reports indicated that some young male patients with FGS had underlying Dent disease. We describe the case of a 14-year-old Japanese boy who presented with persistent non-nephrotic range proteinuria, hematuria, and renal insufficiency. The patient was initially diagnosed as having FGS associated with scattered tubulointerstitial fibrosis. Although he had neither nephrocalcinosis nor family history of renal disease including urolithiasis, increased excretion of urinary β2 microglobulin was noted. Genetic analysis for Dent disease indicated a mutation (c.726 + 1G > A) in Chloride Channel, Voltage-Sensitive 5 (CLCN5). Given a recent hypothesis that Dent disease may be underrecognized in children with FGS, a careful diagnostic evaluation for possible underlying Dent disease should be considered in young boys who present with persistent albuminuria associated with high-grade low-molecular-weight proteinuria. PMID:27324082

  20. Diseases of Landscape Ornamentals. Slide Script.

    ERIC Educational Resources Information Center

    Powell, Charles C.; Sydnor, T. Davis

    This slide script, part of a series of slide scripts designed for use in vocational agriculture classes, deals with recognizing and controlling diseases found on ornamental landscape plants. Included in the script are narrations for use with a total of 80 slides illustrating various foliar diseases (anthracnose, black spot, hawthorn leaf blight,…

  1. The Blood Exposome and Its Role in Discovering Causes of Disease

    PubMed Central

    Barupal, Dinesh K.; Wishart, David; Vineis, Paolo; Scalbert, Augustin

    2014-01-01

    Background: Since 2001, researchers have examined the human genome (G) mainly to discover causes of disease, despite evidence that G explains relatively little risk. We posit that unexplained disease risks are caused by the exposome (E; representing all exposures) and G × E interactions. Thus, etiologic research has been hampered by scientists’ continuing reliance on low-tech methods to characterize E compared with high-tech omics for characterizing G. Objectives: Because exposures are inherently chemical in nature and arise from both endogenous and exogenous sources, blood specimens can be used to characterize exposomes. To explore the “blood exposome” and its connection to disease, we sought human blood concentrations of many chemicals, along with their sources, evidence of chronic-disease risks, and numbers of metabolic pathways. Methods: From the literature we obtained human blood concentrations of 1,561 small molecules and metals derived from foods, drugs, pollutants, and endogenous processes. We mapped chemical similarities after weighting by blood concentrations, disease-risk citations, and numbers of human metabolic pathways. Results: Blood concentrations spanned 11 orders of magnitude and were indistinguishable for endogenous and food chemicals and drugs, whereas those of pollutants were 1,000 times lower. Chemical similarities mapped by disease risks were equally distributed by source categories, but those mapped by metabolic pathways were dominated by endogenous molecules and essential nutrients. Conclusions: For studies of disease etiology, the complexity of human exposures motivates characterization of the blood exposome, which includes all biologically active chemicals. Because most small molecules in blood are not human metabolites, investigations of causal pathways should expand beyond the endogenous metabolome. Citation: Rappaport SM, Barupal DK, Wishart D, Vineis P, Scalbert A. 2014. The blood exposome and its role in discovering causes of

  2. Mutations Causing Complex Disease May under Certain Circumstances Be Protective in an Epidemiological Sense.

    PubMed

    Siegert, Sabine; Wolf, Andreas; Cooper, David N; Krawczak, Michael; Nothnagel, Michael

    2015-01-01

    Guided by the practice of classical epidemiology, research into the genetic basis of complex disease has usually taken for granted the dictum that causative mutations are invariably over-represented among clinically affected as compared to unaffected individuals. However, we show that this supposition is not true and that a mutation contributing to the etiology of a complex disease can, under certain circumstances, be depleted among patients. Populations with defined disease prevalence were repeatedly simulated under a Wright-Fisher model, assuming various types of population history and genotype-phenotype relationship. For each simulation, the resulting mutation-specific population frequencies and odds ratios (ORs) were evaluated. In addition, the relationship between mutation frequency and OR was studied using real data from the NIH GWAS catalogue of reported phenotype associations of single-nucleotide polymorphisms (SNPs). While rare diseases (prevalence <1%) were found to be consistently caused by rare mutations with ORs>1, up to 20% of mutations causing a pandemic disease (prevalence 10-20%) had ORs<1, and their population frequency ranged from 0% to 100%. Moreover, simulation-based ORs exhibited a wide distribution, irrespective of mutation frequency. In conclusion, a substantial proportion of mutations causing common complex diseases may appear 'protective' in genetic epidemiological studies and hence would normally tend to be excluded, albeit erroneously, from further study. This apparently paradoxical result is explicable in terms of mutual confounding of the respective genotype-phenotype relationships due to a negative correlation between causal mutations induced by their common gene genealogy. As would be predicted by our findings, a significant negative correlation became apparent in published genome-wide association studies between the OR of genetic variants associated with a particular disease and the prevalence of that disease. PMID:26161957

  3. Epididymitis Caused by Coxsackievirus A6 in Association with Hand, Foot, and Mouth Disease

    PubMed Central

    Österback, Riikka; Kuisma, Jani; Ylipalosaari, Pekka

    2014-01-01

    Coxsackievirus A6 (CV-A6) caused hand, foot, and mouth disease (HFMD) with a unique manifestation of epididymitis. The patient underwent operation due to suspicion of testicular torsion. Epididymitis was diagnosed by ultrasound examination. Enterovirus was detected from epididymal fluid by PCR and typed by partial sequencing of viral protein 1 as CV-A6. PMID:25232161

  4. [Acute respiratory distress syndrome caused by tropical eosinophilic lung disease: a case in Gabon].

    PubMed

    Chani, M; Iken, M; Eljahiri, Y; Nzenze, J R; Mion, G

    2011-04-01

    The purpose of this report is to describe the case of a 28-year-old woman in whom acute respiratory distress syndrome (ARDS) following cholecystectomy led to the discovery of eosinophilic lung disease. Outcome was favorable after oxygenotherapy and medical treatment using ivermectin and corticosteroids. The case shows that hypereosinophilic syndrome can be the underlying cause of ARDS. PMID:21695880

  5. Genome Sequence of Fusarium oxysporum f. sp. melonis, a fungus causing wilt disease on melon

    Technology Transfer Automated Retrieval System (TEKTRAN)

    This manuscript reports the genome sequence of F. oxysporum f. sp. melonis, a fungal pathogen that causes Fusarium wilt disease on melon (Cucumis melo). The project is part of a large comparative study designed to explore the genetic composition and evolutionary origin of this group of horizontally ...

  6. Genome sequence of Fusarium oxysporum f. sp. melonis, a fungus causing wilt disease on melon

    Technology Transfer Automated Retrieval System (TEKTRAN)

    This manuscript reports the genome sequence of F. oxysporum f. sp. melonis, a fungal pathogen that causes Fusarium wilt disease on melon (Cucumis melo). The project is part of a large comparative study designed to explore the genetic composition and evolutionary origin of this group of horizontally ...

  7. ANIMAL PATHOGENS THAT MAY CAUSE HUMAN DISEASE THAT ORIGINATE FROM FARM OPERATIONS

    EPA Science Inventory

    The recent increase in concentrated animal feeding operations in the United States has caused renewed concern regarding the infectious diseases that may be passed from farm animals to humans via the environment. It is also known that more than 20 recent epidemics among humans cou...

  8. A strain of Clover yellow vein virus that causes severe pod necrosis disease in snap bean

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Since 2000, the soybean aphid (Aphis glycines) has been associated with severe virus epidemics in snap bean (Phaseolus vulgaris) in the upper Midwestern states, New York, and Ontario, Canada. The causal agent of a disease causing severe mosaic, apical necrosis stunting and extensive pod necrosis wa...

  9. Infection and disease progress of motile Aeromonas septicemia caused by virulent Aeromonas hydrophila in channel catfish

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Motile Aeromonas septicemia (MAS), caused by virulent clonal isolates of Aeromonas hydrophila (vAh), is emerging as a major disease in channel catfish (Ictalurus punctatus) aquaculture in the Southeastern United States. Predisposing conditions leading to vAh infection in catfish were however largely...

  10. Heart disease is common in humans and chimpanzees, but is caused by different pathological processes.

    PubMed

    Varki, Nissi; Anderson, Dan; Herndon, James G; Pham, Tho; Gregg, Christopher J; Cheriyan, Monica; Murphy, James; Strobert, Elizabeth; Fritz, Jo; Else, James G; Varki, Ajit

    2009-02-01

    Heart disease is common in both humans and chimpanzees, manifesting typically as sudden cardiac arrest or progressive heart failure. Surprisingly, although chimpanzees are our closest evolutionary relatives, the major cause of heart disease is different in the two species. Histopathology data of affected chimpanzee hearts from two primate centers, and analysis of literature indicate that sudden death in chimpanzees (and in gorillas and orangutans) is commonly associated with diffuse interstitial myocardial fibrosis of unknown cause. In contrast, most human heart disease results from coronary artery atherosclerosis, which occludes myocardial blood supply, causing ischemic damage. The typical myocardial infarction of humans due to coronary artery thrombosis is rare in these apes, despite their human-like coronary-risk-prone blood lipid profiles. Instead, chimpanzee 'heart attacks' are likely due to arrythmias triggered by myocardial fibrosis. Why do humans not often suffer from the fibrotic heart disease so common in our closest evolutionary cousins? Conversely, why do chimpanzees not have the kind of heart disease so common in humans? The answers could be of value to medical care, as well as to understanding human evolution. A preliminary attempt is made to explore possibilities at the histological level, with a focus on glycosylation changes. PMID:25567850

  11. Molecular Phylogeny of the Psittacid Herpesviruses Causing Pacheco's Disease: Correlation of Genotype with Phenotypic Expression

    PubMed Central

    Tomaszewski, Elizabeth K.; Kaleta, Erhard F.; Phalen, David N.

    2003-01-01

    Fragments of 419 bp of the UL16 open reading frame from 73 psittacid herpesviruses (PsHVs) from the United States and Europe were sequenced. All viruses caused Pacheco's disease, and serotypes of the European isolates were known. A phylogenetic tree derived from these sequences demonstrated that the PsHVs that cause Pacheco's disease comprised four major genotypes, with each genotype including between two and four variants. With the exception of two viruses, the serotypes of the virus isolates could be predicted by the genotypes. Genotypes 1 and 4 corresponded to serotype 1 isolates, genotype 2 corresponded to serotype 2 isolates, and genotype 3 corresponded to serotype 3 isolates. The single serotype 4 virus mapped to genotype 4. DNA from a virus with a unique serotype could not be amplified with primers that amplified DNA from all other PsHVs, and its classification remains unknown. Viruses representing all four genotypes were found in both the United States and Europe, and it was therefore predicted that serotypes 1, 2, and 3 were present in the United States. Serotype 4 was represented by a single European isolate that could not be genetically distinguished from serotype 1 viruses; therefore, the presence of serotype 4 in the United States could not be predicted. Viruses of genotype 4 were found to be the most commonly associated with Pacheco's disease in macaws and conures and were least likely to be isolated in chicken embryo fibroblasts in the United States. All four genotypes caused deaths in Amazon parrots, but genotype 4 was associated with Pacheco's disease only in Amazons in Europe. Genotypes 2, 3, and 4, but not 1, were found in African grey parrots. Although parrots from the Pacific distribution represent a relatively small percentage of the total number of birds with Pacheco's disease, all four genotypes were found to cause disease in these species. PMID:14512573

  12. Molecular phylogeny of the psittacid herpesviruses causing Pacheco's disease: correlation of genotype with phenotypic expression.

    PubMed

    Tomaszewski, Elizabeth K; Kaleta, Erhard F; Phalen, David N

    2003-10-01

    Fragments of 419 bp of the UL16 open reading frame from 73 psittacid herpesviruses (PsHVs) from the United States and Europe were sequenced. All viruses caused Pacheco's disease, and serotypes of the European isolates were known. A phylogenetic tree derived from these sequences demonstrated that the PsHVs that cause Pacheco's disease comprised four major genotypes, with each genotype including between two and four variants. With the exception of two viruses, the serotypes of the virus isolates could be predicted by the genotypes. Genotypes 1 and 4 corresponded to serotype 1 isolates, genotype 2 corresponded to serotype 2 isolates, and genotype 3 corresponded to serotype 3 isolates. The single serotype 4 virus mapped to genotype 4. DNA from a virus with a unique serotype could not be amplified with primers that amplified DNA from all other PsHVs, and its classification remains unknown. Viruses representing all four genotypes were found in both the United States and Europe, and it was therefore predicted that serotypes 1, 2, and 3 were present in the United States. Serotype 4 was represented by a single European isolate that could not be genetically distinguished from serotype 1 viruses; therefore, the presence of serotype 4 in the United States could not be predicted. Viruses of genotype 4 were found to be the most commonly associated with Pacheco's disease in macaws and conures and were least likely to be isolated in chicken embryo fibroblasts in the United States. All four genotypes caused deaths in Amazon parrots, but genotype 4 was associated with Pacheco's disease only in Amazons in Europe. Genotypes 2, 3, and 4, but not 1, were found in African grey parrots. Although parrots from the Pacific distribution represent a relatively small percentage of the total number of birds with Pacheco's disease, all four genotypes were found to cause disease in these species. PMID:14512573

  13. Endophytic Fusarium verticillioides reduces disease severity caused by Ustilago maydis on maize.

    PubMed

    Lee, Keunsub; Pan, Jean J; May, Georgiana

    2009-10-01

    Endophytic fungi represent diverse taxa that inhabit plant hosts without causing disease symptoms. We used endophytic isolates of Fusarium verticillioides (Sacc.) Nirenberg to understand how endophytic fungi interact with pathogens, in this case, the corn smut pathogen, Ustilago maydis DC (Corda). Endophytic F. verticillioides strains were inoculated onto maize seedlings before, simultaneously, or after inoculation with U. maydis, and the effects on smut disease severity and on plant growth were assessed. When F. verticillioides is simultaneously coinoculated with U. maydis, smut disease severity is significantly decreased and plant growth is increased, compared with other treatments. Controls show that F. verticillioides by itself does not have measurable effects on plant growth. Together, our results suggest that a commonly occurring fungal endophyte on maize, F. verticillioides, ameliorates the effects of a host-specific pathogen, U. maydis, by interfering with the early infection process and limiting disease development, resulting in increased plant growth. PMID:19694816

  14. Tangier's disease: An uncommon cause of facial weakness and non-length dependent demyelinating neuropathy

    PubMed Central

    Nagappa, Madhu; Taly, Arun B.; Mahadevan, Anita; Pooja, M.; Bindu, P. S.; Chickabasaviah, Y. T.; Gayathri, N.; Sinha, Sanjib

    2016-01-01

    Tangier disease is an autosomal recessive disorder characterized by an abnormal accumulation of cholesterol esters in various organs secondary to adenotriphosphate binding cassette transporter A-1 (ABCA-1) transporter deficiency and disrupted reverse cholesterol transport. It causes neuropathy in half of the affected individuals. We present the clinical, electrophysiological, and histopathological findings in a middle aged gentleman of Tangier disease who was initially misdiagnosed leprosy and treated with antileprosy drugs. The presence of a demyelinating neuropathy on electrophysiology in a patient with predominant upper limb involvement and facial diplegia should raise the suspicion of Tangier disease. The characteristic lipid profile of Tangier disease was noted in this patient viz. extremely low high density lipoprotein (HDL), elevated triglyceride (TG), and reduced apolipoprotein A1. Estimation of serum lipids should form a part of routine evaluation in order to avoid misdiagnosis. PMID:27011649

  15. The role of disease resistance in alfalfa persistence

    Technology Transfer Automated Retrieval System (TEKTRAN)

    To evaluate the effect of disease resistance on alfalfa persistence, a five-year field study was conducted using sixteen cultivars with release dates from 1940 to 1996. Fusarium wilt and anthracnose were the prevalent lethal diseases observed. Disease was present in all cultivars, with higher incide...

  16. Reasoning over genetic variance information in cause-and-effect models of neurodegenerative diseases

    PubMed Central

    Naz, Mufassra; Kodamullil, Alpha Tom

    2016-01-01

    The work we present here is based on the recent extension of the syntax of the Biological Expression Language (BEL), which now allows for the representation of genetic variation information in cause-and-effect models. In our article, we describe, how genetic variation information can be used to identify candidate disease mechanisms in diseases with complex aetiology such as Alzheimer’s disease and Parkinson’s disease. In those diseases, we have to assume that many genetic variants contribute moderately to the overall dysregulation that in the case of neurodegenerative diseases has such a long incubation time until the first clinical symptoms are detectable. Owing to the multilevel nature of dysregulation events, systems biomedicine modelling approaches need to combine mechanistic information from various levels, including gene expression, microRNA (miRNA) expression, protein–protein interaction, genetic variation and pathway. OpenBEL, the open source version of BEL, has recently been extended to match this requirement, and we demonstrate in our article, how candidate mechanisms for early dysregulation events in Alzheimer’s disease can be identified based on an integrative mining approach that identifies ‘chains of causation’ that include single nucleotide polymorphism information in BEL models. PMID:26249223

  17. Causes of liver disease and its outcome in HIV-infected individuals.

    PubMed

    Shamanna, Suryanarayana Bettadpura; Naik, Ramavath Raghu Ramulu; Hamide, Abdoul

    2016-07-01

    Liver disease in HIV-infected patients has remained unaddressed in India. This study describes the causes of liver disease in HIV-infected patients and short-term outcome in them. Designed as a prospective observational study, it was conducted at Jawaharlal Institute of Postgraduate Medical Education and Research between September 2011 and March 2013. All consecutive HIV patients (>13 years) attending the antiretroviral therapy clinic or admitted in the Medicine Department were screened, and patients with liver disease or with either HBsAg or anti-HCV antibody positivity were included in the study. Of the 198 patients screened, 51 (26 %) had either abnormal liver function test or had HBsAg or anti-HCV positivity. The median age of the patients was 40 years and 82 % were males. The median CD4 count was 123 cells/mm(3). Eighteen (35 %) of them had alcoholic liver disease. Six patients had probable hepatic involvement due to tuberculosis. Ten patients had antituberculosis drug-induced hepatotoxicity. One patient had acute hepatitis B and seven patients had chronic hepatitis B. The cause could not be established in 10 patients (20 %). After a median period of 8 months of follow up, 23 patients had improved, 19 patients (37 %) had died, and six patients had been lost to follow up. Of the patients who had died, 11 patients (58 %) had tuberculosis, and 6 patients (30 %) had decompensated alcoholic liver disease. In conclusion, liver disease in HIV-infected patients was associated with high mortality. Alcohol abuse, tuberculosis, and antituberculosis drugs were the major causes. PMID:27435618

  18. Human ITCH E3 ubiquitin ligase deficiency causes syndromic multisystem autoimmune disease.

    PubMed

    Lohr, Naomi J; Molleston, Jean P; Strauss, Kevin A; Torres-Martinez, Wilfredo; Sherman, Eric A; Squires, Robert H; Rider, Nicholas L; Chikwava, Kudakwashe R; Cummings, Oscar W; Morton, D Holmes; Puffenberger, Erik G

    2010-03-12

    Ubiquitin ligases play an important role in the regulation of the immune system. Absence of Itch E3 ubiquitin ligase in mice has been shown to cause severe autoimmune disease. Using autozygosity mapping in a large Amish kindred, we identified a linkage region on chromosome 20 and selected candidate genes for screening. We describe, in ten patients, identification of a mutation resulting in truncation of ITCH. These patients represent the first reported human phenotype associated with ITCH deficiency. These patients not only have multisystem autoimmune disease but also display morphologic and developmental abnormalities. This disorder underscores the importance of ITCH ubiquitin ligase in many cellular processes. PMID:20170897

  19. Human ITCH E3 Ubiquitin Ligase Deficiency Causes Syndromic Multisystem Autoimmune Disease

    PubMed Central

    Lohr, Naomi J.; Molleston, Jean P.; Strauss, Kevin A.; Torres-Martinez, Wilfredo; Sherman, Eric A.; Squires, Robert H.; Rider, Nicholas L.; Chikwava, Kudakwashe R.; Cummings, Oscar W.; Morton, D. Holmes; Puffenberger, Erik G.

    2010-01-01

    Ubiquitin ligases play an important role in the regulation of the immune system. Absence of Itch E3 ubiquitin ligase in mice has been shown to cause severe autoimmune disease. Using autozygosity mapping in a large Amish kindred, we identified a linkage region on chromosome 20 and selected candidate genes for screening. We describe, in ten patients, identification of a mutation resulting in truncation of ITCH. These patients represent the first reported human phenotype associated with ITCH deficiency. These patients not only have multisystem autoimmune disease but also display morphologic and developmental abnormalities. This disorder underscores the importance of ITCH ubiquitin ligase in many cellular processes. PMID:20170897

  20. Candidate gene associated with a mutation causing recessive polycystic kidney disease in mice

    SciTech Connect

    Moyer, J.H.; Lee-Tischler, M.J.; Kwon, H.Y.; Schrick, J.J. ); Avner, E.D.; Sweeney, W.E. ); Godfrey, V.L.; Cacheiro, N.L.A.; Woychik, R.P. ); Wilkinson, J.E. )

    1994-05-27

    A line of transgenic mice was generated that contains an insertional mutation causing a phenotype similar to human autosomal recessive polycystic kidney disease. Homozygotes displayed a complex phenotype that included bilateral polycystic kidneys and an unusual liver lesion. The mutant locus was cloned and characterized through use of the transgene as a molecular marker. Additionally, a candidate polycystic kidney disease (PKD) gene was identified whose structure and expression are directly associated with the mutant locus. A complementary DNA derived from this gene predicted a peptide containing a motif that was originally identified in several genes involved in cell cycle control.

  1. The pathogen causing Dutch elm disease makes host trees attract insect vectors

    PubMed Central

    McLeod, Geoff; Gries, Regine; von Reuß, Stephan H; Rahe, James E; McIntosh, Rory; König, Wilfried A; Gries, Gerhard

    2005-01-01

    Dutch elm disease is caused by the fungal pathogen Ophiostoma novo-ulmi which is transmitted by the native elm bark beetle, Hylurgopinus rufipes. We have found that four semiochemicals (the monoterpene (−)-β-pinene and the sesquiterpenes (−)-α-cubebene, (+)-spiroaxa-5,7-diene and (+)-δ-cadinene) from diseased American elms, Ulmus americana, synergistically attract H. rufipes, and that sesquiterpene emission is upregulated in elm trees inoculated with O. novo-ulmi. The fungus thus manipulates host trees to enhance their apparency to foraging beetles, a strategy that increases the probability of transportation of the pathogen to new hosts. PMID:16271975

  2. First Report of Black Spot Disease Caused by Alternaria alternata on Sweet Persimmon Fruits

    PubMed Central

    Lee, Jung Han; Kim, Jinwoo

    2013-01-01

    Black spot of sweet persimmon, caused by Alternaria alternata, occurred in an orchard in Gyeongnam province, Korea in 2012. The symptom was appearance of 0.5 to 4 cm black spots on the surface of fruit. The pathogen was isolated from flesh of disease lesions. The causal agent was identified as A. alternata by morphological characteristics and sequencers of the internal transcribed spacer (ITS) 1 and ITS4 regions of rRNA. Artificial inoculation of the pathogen resulted in development of disease symptoms and the re-isolated pathogen showed characteristics of A. alternata. PMID:24198674

  3. Mortality Due to Chagas Disease in Brazil According to a Specific Cause

    PubMed Central

    da Nóbrega, Aglaêr Alves; de Araújo, Wildo Navegantes; Vasconcelos, Ana Maria Nogales

    2014-01-01

    A century after its discovery, Chagas disease (CD) is still considered a public health problem. Mortality caused by CD between 2000 and 2010 was described according to the specific underlying cause, year of occurrence, gender, age range, and region of Brazil. The standardized mortality rate decreased 32.4%, from 3.4% in 2000 to 2.3% in 2010. Most of the deaths (85.9%) occurred in male patients who were > 60 years of age caused by cardiac involvement. The mortality rate caused by cardiac involvement decreased in all regions of Brazil, except in the North region, where it increased by 1.6%. The Northeast had the smallest and the Central-West had the largest decrease. The mortality rate caused by a compromised digestive tract increased in all regions. Despite the control of transmission by vector and blood transfusions, CD should remain on the list of priority diseases for the public health service in Brazil, and surveillance actions cannot be interrupted. PMID:25002301

  4. A rare cause of acute abdominal disease: two reports of caecal diverticulum perforation.

    PubMed

    Çiftci, Fatih; Abdurrahman, İbrahim; Eren, Abdülkadir

    2016-05-01

    Diverticulum of the caecum is a rare lesion. From a clinical point of view, the inflammation it causes can mimic symptoms of acute appendicitis, causing difficulties in diagnosis and thus prescription of appropriate treatment. It is almost impossible to differentiate this disease from acute appendicitis through physical examination alone, and radiological imaging may also prove insufficient. For this reason, it is common to perioperatively diagnose diverticula of the caecum. Two cases of patients who underwent surgery for perforated caecal diverticula are presently described. PMID:27598596

  5. Association of Kidney Disease Measures with Cause-Specific Mortality: The Korean Heart Study

    PubMed Central

    Mok, Yejin; Matsushita, Kunihiro; Sang, Yingying; Ballew, Shoshana H.; Grams, Morgan; Shin, Sang Yop; Jee, Sun Ha; Coresh, Josef

    2016-01-01

    Background The link of low estimated glomerular filtration rate (eGFR) and high proteinuria to cardiovascular disease (CVD) mortality is well known. However, its link to mortality due to other causes is less clear. Methods We studied 367,932 adults (20–93 years old) in the Korean Heart Study (baseline between 1996–2004 and follow-up until 2011) and assessed the associations of creatinine-based eGFR and dipstick proteinuria with mortality due to CVD (1,608 cases), cancer (4,035 cases), and other (non-CVD/non-cancer) causes (3,152 cases) after adjusting for potential confounders. Results Although cancer was overall the most common cause of mortality, in participants with chronic kidney disease (CKD), non-CVD/non-cancer mortality accounted for approximately half of cause of death (47.0%for eGFR <60 ml/min/1.73m2 and 54.3% for proteinuria ≥1+). Lower eGFR (<60 vs. ≥60 ml/min/1.73m2) was significantly associated with mortality due to CVD (adjusted hazard ratio 1.49 [95% CI, 1.24–1.78]) and non-CVD/non-cancer causes (1.78 [1.54–2.05]). The risk of cancer mortality only reached significance at eGFR <45 ml/min/1.73m2 when eGFR 45–59 ml/min/1.73m2 was set as a reference (1.62 [1.10–2.39]). High proteinuria (dipstick ≥1+ vs. negative/trace) was consistently associated with mortality due to CVD (1.93 [1.66–2.25]), cancer (1.49 [1.32–1.68]), and other causes (2.19 [1.96–2.45]). Examining finer mortality causes, low eGFR and high proteinuria were commonly associated with mortality due to coronary heart disease, any infectious disease, diabetes, and renal failure. In addition, proteinuria was also related to death from stroke, cancers of stomach, liver, pancreas, and lung, myeloma, pneumonia, and viral hepatitis. Conclusion Low eGFR was associated with CVD and non-CVD/non-cancer mortality, whereas higher proteinuria was consistently related to mortality due to CVD, cancer, and other causes. These findings suggest the need for multidisciplinary prevention

  6. DIFFERENTIALLY EXPRESSED GENES IN RESPONSES TO LATE LEAF SPOT DISEASE CAUSED BY CERCOSPORIDIUM PERSONATUM IN PEANUT USING MICROARRAY ANALYSIS

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Late leaf spot disease caused by Cercosporidium personatum is one of the most destructive foliar diseases of peanut worldwide. This research was to identify resistance genes in response to leaf spot disease using miccroarray and real-time PCR. To identify transcripts involved in disease resistance, ...

  7. A small molecule, odanacatib, inhibits inflammation and bone loss caused by endodontic disease.

    PubMed

    Hao, Liang; Chen, Wei; McConnell, Matthew; Zhu, Zheng; Li, Sheng; Reddy, Michael; Eleazer, Paul D; Wang, Min; Li, Yi-Ping

    2015-04-01

    Periapical disease, an inflammatory disease mainly caused by dental caries, is one of the most prevalent infectious diseases of humans, affecting both children and adults. The infection travels through the root, leading to inflammation, bone destruction, and severe pain for the patient. Therefore, the development of a new class of anti-periapical disease therapies is necessary and critical for treatment and prevention. A small molecule, odanacatib (ODN), which is a cathepsin K (Ctsk) inhibitor, was investigated to determine its ability to treat this disease in a mouse model of periapical disease. While Ctsk was originally found in osteoclasts as an osteoclast-specific lysosomal protease, we were surprised to find that ODN can suppress the bacterium-induced immune response as well as bone destruction in the lesion area. X rays and microcomputed tomography (micro-CT) showed that ODN treatment had significant bone protection effects at different time points. Immunohistochemical and immunofluorescent staining show that ODN treatment dramatically decreased F4/80+ macrophages and CD3+ T cells in the lesion areas 42 days after infection. Consistent with these findings, quantitative real-time PCR (qRT-PCR) and enzyme-linked immunosorbent assay (ELISA) analysis showed low levels of proinflammatory mRNAs (for tumor necrosis factor alpha, interleukin 6, and interleukin 23α) and corresponding cytokine expression in the ODN-treated disease group. The levels of mRNA for Toll-like receptors 4, 5, and 9 also largely decreased in the ODN-treated disease group. Our results demonstrated that ODN can inhibit endodontic disease development, bone erosion, and immune response. These results indicate that application of this small molecule offers a new opportunity to design effective therapies that could prevent periapical inflammation and revolutionize current treatment options. PMID:25583522

  8. A Small Molecule, Odanacatib, Inhibits Inflammation and Bone Loss Caused by Endodontic Disease

    PubMed Central

    Hao, Liang; McConnell, Matthew; Zhu, Zheng; Li, Sheng; Reddy, Michael; Eleazer, Paul D.; Li, Yi-Ping

    2015-01-01

    Periapical disease, an inflammatory disease mainly caused by dental caries, is one of the most prevalent infectious diseases of humans, affecting both children and adults. The infection travels through the root, leading to inflammation, bone destruction, and severe pain for the patient. Therefore, the development of a new class of anti-periapical disease therapies is necessary and critical for treatment and prevention. A small molecule, odanacatib (ODN), which is a cathepsin K (Ctsk) inhibitor, was investigated to determine its ability to treat this disease in a mouse model of periapical disease. While Ctsk was originally found in osteoclasts as an osteoclast-specific lysosomal protease, we were surprised to find that ODN can suppress the bacterium-induced immune response as well as bone destruction in the lesion area. X rays and microcomputed tomography (micro-CT) showed that ODN treatment had significant bone protection effects at different time points. Immunohistochemical and immunofluorescent staining show that ODN treatment dramatically decreased F4/80+ macrophages and CD3+ T cells in the lesion areas 42 days after infection. Consistent with these findings, quantitative real-time PCR (qRT-PCR) and enzyme-linked immunosorbent assay (ELISA) analysis showed low levels of proinflammatory mRNAs (for tumor necrosis factor alpha, interleukin 6, and interleukin 23α) and corresponding cytokine expression in the ODN-treated disease group. The levels of mRNA for Toll-like receptors 4, 5, and 9 also largely decreased in the ODN-treated disease group. Our results demonstrated that ODN can inhibit endodontic disease development, bone erosion, and immune response. These results indicate that application of this small molecule offers a new opportunity to design effective therapies that could prevent periapical inflammation and revolutionize current treatment options. PMID:25583522

  9. Occupational obstructive airway diseases in Germany: Frequency and causes in an international comparison

    SciTech Connect

    Latza, U.; Baur, X.

    2005-08-01

    Occupational inhalative exposures contribute to a significant proportion of obstructive airway diseases (OAD), namely chronic obstructive pulmonary disease (COPD) and asthma. The number of occupational OAD in the German industrial sector for the year 2003 are presented. Other analyses of surveillance data were retrieved from Medline. Most confirmed reports of OAD are cases of sensitizer induced occupational asthma (625 confirmed cases) followed by COPD in coal miners (414 cases), irritant induced occupational asthma (156 cases), and isocyanate asthma (54 cases). Main causes of occupational asthma in Germany comprise flour/flour constituents (35.9%), food/feed dust (9.0%), and isocyanates (6.5%). Flour and grain dust is a frequent cause of occupational asthma in most European countries and South Africa. Isocyanates are still a problem worldwide. Although wide differences in the estimated incidences between countries exist due to deficits in the coverage of occupational OAD, the high numbers necessitate improvement of preventive measures.

  10. Nontuberculous Mycobacterial Lung Disease Caused by Mycobacterium simiae: The First Reported Case in South Korea

    PubMed Central

    Jeong, Suk Hyeon; Kim, Su-Young; Lee, Hyun; Ham, Jun Soo; Hwang, Keum Bit; Hwang, Subin; Shin, Sun Hye; Chung, Myung Jin; Lee, Seung Heon; Shin, Sung Jae

    2015-01-01

    This is a report of the first South Korean case of a lung disease caused by Mycobacterium simiae. The patient was a previously healthy 52-year-old female. All serial isolates were identified as M. simiae by multi-locus sequencing analysis, based on hsp65, rpoB, 16S-23S rRNA internal transcribed spacer, and 16S rRNA fragments. A chest radiography revealed deterioration, and the follow-up sputum cultures were persistently positive, despite combination antibiotic treatment, including azithromycin, ethambutol, and rifampin. To the best of our knowledge, this is the first confirmed case of a lung disease caused by M. simiae in South Korea. PMID:26508940

  11. Drug Resistance Mechanisms in Bacteria Causing Sexually Transmitted Diseases and Associated with Vaginosis

    PubMed Central

    Shaskolskiy, Boris; Dementieva, Ekaterina; Leinsoo, Arvo; Runina, Anastassia; Vorobyev, Denis; Plakhova, Xenia; Kubanov, Alexey; Deryabin, Dmitrii; Gryadunov, Dmitry

    2016-01-01

    Here, we review sexually transmitted diseases (STDs) caused by pathogenic bacteria and vaginal infections which result from an overgrowth of opportunistic bacterial microflora. First, we describe the STDs, the corresponding pathogens and the antimicrobials used for their treatment. In addition to the well-known diseases caused by single pathogens (i.e., syphilis, gonococcal infections, and chlamydiosis), we consider polymicrobial reproductive tract infections (especially those that are difficult to effectively clinically manage). Then, we summarize the biochemical mechanisms that lead to antimicrobial resistance and the most recent data on the emergence of drug resistance in STD pathogens and bacteria associated with vaginosis. A large amount of research performed in the last 10–15 years has shed light on the enormous diversity of mechanisms of resistance developed by bacteria. A detailed understanding of the mechanisms of antimicrobials action and the emergence of resistance is necessary to modify existing drugs and to develop new ones directed against new targets. PMID:27242760

  12. Drug Resistance Mechanisms in Bacteria Causing Sexually Transmitted Diseases and Associated with Vaginosis.

    PubMed

    Shaskolskiy, Boris; Dementieva, Ekaterina; Leinsoo, Arvo; Runina, Anastassia; Vorobyev, Denis; Plakhova, Xenia; Kubanov, Alexey; Deryabin, Dmitrii; Gryadunov, Dmitry

    2016-01-01

    Here, we review sexually transmitted diseases (STDs) caused by pathogenic bacteria and vaginal infections which result from an overgrowth of opportunistic bacterial microflora. First, we describe the STDs, the corresponding pathogens and the antimicrobials used for their treatment. In addition to the well-known diseases caused by single pathogens (i.e., syphilis, gonococcal infections, and chlamydiosis), we consider polymicrobial reproductive tract infections (especially those that are difficult to effectively clinically manage). Then, we summarize the biochemical mechanisms that lead to antimicrobial resistance and the most recent data on the emergence of drug resistance in STD pathogens and bacteria associated with vaginosis. A large amount of research performed in the last 10-15 years has shed light on the enormous diversity of mechanisms of resistance developed by bacteria. A detailed understanding of the mechanisms of antimicrobials action and the emergence of resistance is necessary to modify existing drugs and to develop new ones directed against new targets. PMID:27242760

  13. Evidence for Autoinduction and Quorum Sensing in White Band Disease-Causing Microbes on Acropora cervicornis

    NASA Astrophysics Data System (ADS)

    Certner, Rebecca H.; Vollmer, Steven V.

    2015-06-01

    Coral reefs have entered a state of global decline party due to an increasing incidence of coral disease. However, the diversity and complexity of coral-associated bacterial communities has made identifying the mechanisms underlying disease transmission and progression extremely difficult. This study explores the effects of coral cell-free culture fluid (CFCF) and autoinducer (a quorum sensing signaling molecule) on coral-associated bacterial growth and on coral tissue loss respectively. All experiments were conducted using the endangered Caribbean coral Acropora cervicornis. Coral-associated microbes were grown on selective media infused with CFCF derived from healthy and white band disease-infected A. cervicornis. Exposure to diseased CFCF increased proliferation of Cytophaga-Flavobacterium spp. while exposure to healthy CFCF inhibited growth of this group. Exposure to either CFCF did not significantly affect Vibrio spp. growth. In order to test whether disease symptoms can be induced in healthy corals, A. cervicornis was exposed to bacterial assemblages supplemented with exogenous, purified autoinducer. Incubation with autoinducer resulted in complete tissue loss in all corals tested in less than one week. These findings indicate that white band disease in A. cervicornis may be caused by opportunistic pathogenesis of resident microbes.

  14. Evidence for Autoinduction and Quorum Sensing in White Band Disease-Causing Microbes on Acropora cervicornis

    PubMed Central

    Certner, Rebecca H.; Vollmer, Steven V.

    2015-01-01

    Coral reefs have entered a state of global decline party due to an increasing incidence of coral disease. However, the diversity and complexity of coral-associated bacterial communities has made identifying the mechanisms underlying disease transmission and progression extremely difficult. This study explores the effects of coral cell-free culture fluid (CFCF) and autoinducer (a quorum sensing signaling molecule) on coral-associated bacterial growth and on coral tissue loss respectively. All experiments were conducted using the endangered Caribbean coral Acropora cervicornis. Coral-associated microbes were grown on selective media infused with CFCF derived from healthy and white band disease-infected A. cervicornis. Exposure to diseased CFCF increased proliferation of Cytophaga-Flavobacterium spp. while exposure to healthy CFCF inhibited growth of this group. Exposure to either CFCF did not significantly affect Vibrio spp. growth. In order to test whether disease symptoms can be induced in healthy corals, A. cervicornis was exposed to bacterial assemblages supplemented with exogenous, purified autoinducer. Incubation with autoinducer resulted in complete tissue loss in all corals tested in less than one week. These findings indicate that white band disease in A. cervicornis may be caused by opportunistic pathogenesis of resident microbes. PMID:26047488

  15. Does infectious disease cause global variation in the frequency of intrastate armed conflict and civil war?

    PubMed

    Letendre, Kenneth; Fincher, Corey L; Thornhill, Randy

    2010-08-01

    Geographic and cross-national variation in the frequency of intrastate armed conflict and civil war is a subject of great interest. Previous theory on this variation has focused on the influence on human behaviour of climate, resource competition, national wealth, and cultural characteristics. We present the parasite-stress model of intrastate conflict, which unites previous work on the correlates of intrastate conflict by linking frequency of the outbreak of such conflict, including civil war, to the intensity of infectious disease across countries of the world. High intensity of infectious disease leads to the emergence of xenophobic and ethnocentric cultural norms. These cultures suffer greater poverty and deprivation due to the morbidity and mortality caused by disease, and as a result of decreased investment in public health and welfare. Resource competition among xenophobic and ethnocentric groups within a nation leads to increased frequency of civil war. We present support for the parasite-stress model with regression analyses. We find support for a direct effect of infectious disease on intrastate armed conflict, and support for an indirect effect of infectious disease on the incidence of civil war via its negative effect on national wealth. We consider the entanglements of feedback of conflict into further reduced wealth and increased incidence of disease, and discuss implications for international warfare and global patterns of wealth and imperialism. PMID:20377573

  16. A Giant Intrathoracic Malignant Schwannoma Causing Respiratory Failure in a Patient without von Recklinghausen's Disease

    PubMed Central

    Angelopoulos, Epameinondas; Eleftheriou, Konstantinos; Kyriakopoulos, Georgios; Athanassiadi, Kalliopi; Rontogianni, Dimitra; Routsi, Christina

    2016-01-01

    We report an unusual case of a thoracic opacity due to a huge mediastinal malignant schwannoma which compressed the whole left lung and the mediastinum causing respiratory failure in a 73-year-old woman without von Recklinghausen's disease. Although the tumor was resected, the patient failed to wean from mechanical ventilation and died one month later because of multiple organ dysfunction syndrome. PMID:27118974

  17. Fatty liver disease: Disparate predictive ability for cardiometabolic risk and all-cause mortality

    PubMed Central

    Onat, Altan; Can, Günay; Kaya, Ayşem; Akbaş, Tuğba; Özpamuk-Karadeniz, Fatma; Şimşek, Barış; Çakır, Hakan; Yüksel, Hüsniye

    2015-01-01

    AIM: To assess the association of a surrogate of fatty liver disease (FLD) with incident type-2 diabetes, coronary heart disease, and all-cause mortality. METHODS: In a prospective population-based study on 1822 middle-aged adults, stratified to gender, we used an algorithm of fatty liver index (FLI) to identify associations with outcomes. An index ≥ 60 indicated the presence of FLD. In Cox regression models, adjusted for age, smoking status, high-density lipoprotein cholesterol, and systolic blood pressure, we assessed the predictive value of FLI for incident diabetes, coronary heart disease (CHD), and all-cause mortality. RESULTS: At a mean 8 year follow-up, 218 and 285 incident cases of diabetes and CHD, respectively, and 193 deaths were recorded. FLD was significantly associated in each gender with blood pressure, total cholesterol, apolipoprotein B, uric acid, and C-reactive protein; weakly with fasting glucose; and inversely with high-density lipoprotein-cholesterol and sex hormone-binding globulin. In adjusted Cox models, FLD was (with a 5-fold HR) the major determinant of diabetes development. Analyses further disclosed significant independent prediction of CHD by FLD in combined gender [hazard ratio (HR) = 1.72, 95% confidence interval (CI): 1.17-2.53] and men (HR = 2.35, 95%CI: 1.25-4.43). Similarly-adjusted models for all-cause mortality proved, however, not to confer risk, except for a tendency in prediabetics and diabetic women. CONCLUSION: A surrogate of FLD conferred significant high risk of diabetes and coronary heart disease, independent of some metabolic syndrome traits. All-cause mortality was not associated with FLD, except likely in the prediabetic state. Such a FLI may reliably be used in epidemiologic studies. PMID:26730168

  18. Mycetoma Caused by Acremonium Species in a Patient with Chronic Granulomatous Disease

    PubMed Central

    Wong, Gabriel; Jones, Julie; Huissoon, Aarnoud

    2016-01-01

    Patients with chronic granulomatous disease are predisposed to fungal infections and are therefore routinely prescribed antifungal prophylaxis. We report a case where acremonium was responsible for causing a cutaneous infection (mycetoma) despite antifungal prophylaxis. Treatment with voriconazole was initiated and the infection gradually resolved. This case highlights the need for careful clinical follow-up and thorough investigation of patients who have a neutrophil immunodeficiency. PMID:27022493

  19. Cluster of Legionnaires disease cases caused by Legionella longbeachae serogroup 1, Scotland, August to September 2013.

    PubMed

    Potts, A; Donaghy, M; Marley, M; Othieno, R; Stevenson, J; Hyland, J; Pollock, K G; Lindsay, D; Edwards, G; Hanson, M F; Helgason, K O

    2013-01-01

    We report six confirmed cases of Legionnaires' disease in Scotland caused by Legionella longbeachae serogroup 1, identified over a four-week period in August–September 2013. All cases required admission to hospital intensive care facilities. All cases were amateur gardeners with frequent exposure to horticultural growing media throughout their incubation period. L. longbeachae was identified in five samples of growing media linked to five cases. Product tracing did not identify a common product or manufacturer. PMID:24342515

  20. A systematic screening to identify de novo mutations causing sporadic early-onset Parkinson's disease

    PubMed Central

    Kun-Rodrigues, Celia; Ganos, Christos; Guerreiro, Rita; Schneider, Susanne A.; Schulte, Claudia; Lesage, Suzanne; Darwent, Lee; Holmans, Peter; Singleton, Andrew; Bhatia, Kailash; Bras, Jose

    2015-01-01

    Despite the many advances in our understanding of the genetic basis of Mendelian forms of Parkinson's disease (PD), a large number of early-onset cases still remain to be explained. Many of these cases, present with a form of disease that is identical to that underlined by genetic causes, but do not have mutations in any of the currently known disease-causing genes. Here, we hypothesized that de novo mutations may account for a proportion of these early-onset, sporadic cases. We performed exome sequencing in full parent–child trios where the proband presents with typical PD to unequivocally identify de novo mutations. This approach allows us to test all genes in the genome in an unbiased manner. We have identified and confirmed 20 coding de novo mutations in 21 trios. We have used publicly available population genetic data to compare variant frequencies and our independent in-house dataset of exome sequencing in PD (with over 1200 cases) to identify additional variants in the same genes. Of the genes identified to carry de novo mutations, PTEN, VAPB and ASNA1 are supported by various sources of data to be involved in PD. We show that these genes are reported to be within a protein–protein interaction network with PD genes and that they contain additional rare, case-specific, mutations in our independent cohort of PD cases. Our results support the involvement of these three genes in PD and suggest that testing for de novo mutations in sporadic disease may aid in the identification of novel disease-causing genes. PMID:26362251

  1. A systematic screening to identify de novo mutations causing sporadic early-onset Parkinson's disease.

    PubMed

    Kun-Rodrigues, Celia; Ganos, Christos; Guerreiro, Rita; Schneider, Susanne A; Schulte, Claudia; Lesage, Suzanne; Darwent, Lee; Holmans, Peter; Singleton, Andrew; Bhatia, Kailash; Bras, Jose

    2015-12-01

    Despite the many advances in our understanding of the genetic basis of Mendelian forms of Parkinson's disease (PD), a large number of early-onset cases still remain to be explained. Many of these cases, present with a form of disease that is identical to that underlined by genetic causes, but do not have mutations in any of the currently known disease-causing genes. Here, we hypothesized that de novo mutations may account for a proportion of these early-onset, sporadic cases. We performed exome sequencing in full parent-child trios where the proband presents with typical PD to unequivocally identify de novo mutations. This approach allows us to test all genes in the genome in an unbiased manner. We have identified and confirmed 20 coding de novo mutations in 21 trios. We have used publicly available population genetic data to compare variant frequencies and our independent in-house dataset of exome sequencing in PD (with over 1200 cases) to identify additional variants in the same genes. Of the genes identified to carry de novo mutations, PTEN, VAPB and ASNA1 are supported by various sources of data to be involved in PD. We show that these genes are reported to be within a protein-protein interaction network with PD genes and that they contain additional rare, case-specific, mutations in our independent cohort of PD cases. Our results support the involvement of these three genes in PD and suggest that testing for de novo mutations in sporadic disease may aid in the identification of novel disease-causing genes. PMID:26362251

  2. Successful therapy for protein-losing enteropathy caused by chronic neuronopathic Gaucher disease

    PubMed Central

    Mhanni, A.A.; Kozenko, M.; Hartley, J.N.; Deneau, M.; El-Matary, W.; Rockman-Greenberg, C.

    2015-01-01

    Gaucher disease (OMIM #230800) is caused by β-glucosidase deficiency and primarily involves the mononuclear phagocyte system (also called Reticuloendothelial System or Macrophage System). The disease is classified into three main phenotypes based on the presence or absence of neurological manifestations: non-neuronopathic (type 1), acute neuronopathic (type 2) and chronic neuronopathic (type 3). Typical manifestations include hepatosplenomegaly, skeletal deformities, hematological abnormalities, interstitial lung fibrosis and neurodegeneration in neuronopathic cases. Mesenteric lymphadenopathy with resultant protein losing enteropathy (PLE) has only been rarely described. Mesenteric lymphadenopathy may lead to intestinal lymphatic obstruction and secondary lymphangiectasia resulting in chronic diarrhea, abdominal pain and weight loss. Fecal protein loss with secondary hypoalbuminemia can be significant. We report a male with Chronic Neuronopathic Gaucher disease (GD) (homozygous for c.1448T > C (NM_000157.3) GBA mutation) who at 16 years of age developed intractable abdominal pain, diarrhea and weight loss. This was caused by PLE secondary to intestinal lymphangiectasia caused by calcified mesenteric lymphadenopathy despite prior long term enzyme replacement therapy (ERT) and/or substrate reduction therapy (SRT). His older similarly affected sister who had been receiving treatment with ERT and/or SRT remains stable on these treatments with no evidence of mesenteric lymphadenopathy. Medical management with total parenteral nutrition, daily medium chain triglyceride-oil (MCT) supplementation, low dose oral budesonide, continued oral SRT and an increased dose of parenteral ERT has stabilized his condition with resolution of the gastrointestinal symptoms and appropriate weight gain. PMID:27014572

  3. Cap disease caused by heterozygous deletion of the beta-tropomyosin gene TPM2.

    PubMed

    Lehtokari, Vilma-Lotta; Ceuterick-de Groote, Chantal; de Jonghe, Peter; Marttila, Minttu; Laing, Nigel G; Pelin, Katarina; Wallgren-Pettersson, Carina

    2007-06-01

    "Cap myopathy" or "cap disease" is a congenital myopathy characterised by cap-like structures at the periphery of muscle fibres, consisting of disarranged thin filaments with enlarged Z discs. Here we report a deletion in the beta-tropomyosin (TPM2) gene causing cap disease in a 36-year-old male patient with congenital muscle weakness, myopathic facies and respiratory insufficiency. The mutation identified in this patient is an in-frame deletion (c.415_417delGAG) of one codon in exon 4 of TPM2 removing a single glutamate residue (p.Glu139del) from the beta-tropomyosin protein. This is expected to disrupt the seven-amino acid repeat essential for making a coiled coil, and thus to impair tropomyosin-actin interaction. Missense mutations in TPM2 have previously been found to cause rare cases of nemaline myopathy and distal arthrogryposis. This mutation is one not previously described and the first genetic cause identified for cap disease. PMID:17434307

  4. Successful therapy for protein-losing enteropathy caused by chronic neuronopathic Gaucher disease.

    PubMed

    Mhanni, A A; Kozenko, M; Hartley, J N; Deneau, M; El-Matary, W; Rockman-Greenberg, C

    2016-03-01

    Gaucher disease (OMIM #230800) is caused by β-glucosidase deficiency and primarily involves the mononuclear phagocyte system (also called Reticuloendothelial System or Macrophage System). The disease is classified into three main phenotypes based on the presence or absence of neurological manifestations: non-neuronopathic (type 1), acute neuronopathic (type 2) and chronic neuronopathic (type 3). Typical manifestations include hepatosplenomegaly, skeletal deformities, hematological abnormalities, interstitial lung fibrosis and neurodegeneration in neuronopathic cases. Mesenteric lymphadenopathy with resultant protein losing enteropathy (PLE) has only been rarely described. Mesenteric lymphadenopathy may lead to intestinal lymphatic obstruction and secondary lymphangiectasia resulting in chronic diarrhea, abdominal pain and weight loss. Fecal protein loss with secondary hypoalbuminemia can be significant. We report a male with Chronic Neuronopathic Gaucher disease (GD) (homozygous for c.1448T > C (NM_000157.3) GBA mutation) who at 16 years of age developed intractable abdominal pain, diarrhea and weight loss. This was caused by PLE secondary to intestinal lymphangiectasia caused by calcified mesenteric lymphadenopathy despite prior long term enzyme replacement therapy (ERT) and/or substrate reduction therapy (SRT). His older similarly affected sister who had been receiving treatment with ERT and/or SRT remains stable on these treatments with no evidence of mesenteric lymphadenopathy. Medical management with total parenteral nutrition, daily medium chain triglyceride-oil (MCT) supplementation, low dose oral budesonide, continued oral SRT and an increased dose of parenteral ERT has stabilized his condition with resolution of the gastrointestinal symptoms and appropriate weight gain. PMID:27014572

  5. Biology, Systematics, Life Cycle, and Distribution of Angiostrongylus cantonensis, the Cause of Rat Lungworm Disease

    PubMed Central

    2013-01-01

    Angiostrongylus cantonensis is a metastrongyloid nematode in the family Angiostrongylidae. It is the cause of angiostrongyliasis (rat lungworm disease), which manifests as eosinophilic meningitis. First described in 1935 from rats in China, A. cantonensis was placed in the genus Parastrongylus in 1986, but most workers have not adopted this treatment. The taxonomy of A. cantonensis and related worms is largely based on adult morphology, notably of the male bursa. However, identification of infective third stage larvae is more difficult. The natural life cycle involves rats as the definitive host and snails or slugs as the intermediate host. Human infection, as accidental hosts, results in worms maturing in the brain, but dying there instead of moving back into the bloodstream, as in rats, thereby leading to eosinophilic meningitis. The disease is an emerging infectious disease; Angiostrongylus cantonensis continues to be reported in new regions beyond its native range. PMID:23901372

  6. First report of Oryctes rhinoceros nudivirus (Coleoptera: Scarabaeidae) causing severe disease in Allomyrina dichotoma in Korea.

    PubMed

    Lee, Seokhyun; Park, Kwan-Ho; Nam, Sung-Hee; Kwak, Kyu-Won; Choi, Ji-Young

    2015-01-01

    Oryctes rhinoceros nudivirus (OrNV) has been known to cause severe disease in coconut palm rhinoceros beetle, Oryctes rhinoceros, in Southeastern Asia and is used as a biological control to reduce the pest population. Here, we report for the first time that the OrNV may have landed on Korea and may be the major pathogen for diseased larvae of Korean horn beetle, Allomyrina dichotoma. After peroral inoculation, over 60% of infected larvae perished in 6 wk. This viral disease spreads very fast in several locations throughout Korea. This threat not only makes economic loss of local farms rearing A. dichotoma larvae but also may disturb the ecosystem by transmitting to wild A. dichotoma. PMID:25765317

  7. Crystal structure of glycogen debranching enzyme and insights into its catalysis and disease-causing mutations

    PubMed Central

    Zhai, Liting; Feng, Lingling; Xia, Lin; Yin, Huiyong; Xiang, Song

    2016-01-01

    Glycogen is a branched glucose polymer and serves as an important energy store. Its debranching is a critical step in its mobilization. In animals and fungi, the 170 kDa glycogen debranching enzyme (GDE) catalyses this reaction. GDE deficiencies in humans are associated with severe diseases collectively termed glycogen storage disease type III (GSDIII). We report crystal structures of GDE and its complex with oligosaccharides, and structure-guided mutagenesis and biochemical studies to assess the structural observations. These studies reveal that distinct domains in GDE catalyse sequential reactions in glycogen debranching, the mechanism of their catalysis and highly specific substrate recognition. The unique tertiary structure of GDE provides additional contacts to glycogen besides its active sites, and our biochemical experiments indicate that they mediate its recruitment to glycogen and regulate its activity. Combining the understanding of the GDE catalysis and functional characterizations of its disease-causing mutations provides molecular insights into GSDIII. PMID:27088557

  8. A derangement of the brain wound healing process may cause some cases of Alzheimer's disease.

    PubMed

    Lehrer, Steven; Rheinstein, Peter H

    2016-08-01

    A derangement of brain wound healing may cause some cases of Alzheimer's disease. Wound healing, a highly complex process, has four stages: hemostasis, inflammation, repair, and remodeling. Hemostasis and the initial phases of inflammation in brain tissue are typical of all vascularized tissue, such as skin. However, distinct differences arise in brain tissue during the later stages of inflammation, repair, and remodeling, and closely parallel the changes of Alzheimer's disease. Our hypothesis -- Alzheimer's disease is brain wound healing gone awry at least in some cases -- could be tested by measuring progression with biomarkers for the four stages of wound healing in humans or appropriate animal models. Autopsy studies might be done. Chronic traumatic encephalopathy might also result from the brain wound healing process. PMID:27585229

  9. First Report of Oryctes rhinoceros nudivirus (Coleoptera: Scarabaeidae) Causing Severe Disease in Allomyrina dichotoma in Korea

    PubMed Central

    Lee, Seokhyun; Park, Kwan-Ho; Nam, Sung-Hee; Kwak, Kyu-Won; Choi, Ji-Young

    2015-01-01

    Oryctes rhinoceros nudivirus (OrNV) has been known to cause severe disease in coconut palm rhinoceros beetle, Oryctes rhinoceros, in Southeastern Asia and is used as a biological control to reduce the pest population. Here, we report for the first time that the OrNV may have landed on Korea and may be the major pathogen for diseased larvae of Korean horn beetle, Allomyrina dichotoma. After peroral inoculation, over 60% of infected larvae perished in 6 wk. This viral disease spreads very fast in several locations throughout Korea. This threat not only makes economic loss of local farms rearing A. dichotoma larvae but also may disturb the ecosystem by transmitting to wild A. dichotoma. PMID:25765317

  10. Crystal structure of glycogen debranching enzyme and insights into its catalysis and disease-causing mutations.

    PubMed

    Zhai, Liting; Feng, Lingling; Xia, Lin; Yin, Huiyong; Xiang, Song

    2016-01-01

    Glycogen is a branched glucose polymer and serves as an important energy store. Its debranching is a critical step in its mobilization. In animals and fungi, the 170 kDa glycogen debranching enzyme (GDE) catalyses this reaction. GDE deficiencies in humans are associated with severe diseases collectively termed glycogen storage disease type III (GSDIII). We report crystal structures of GDE and its complex with oligosaccharides, and structure-guided mutagenesis and biochemical studies to assess the structural observations. These studies reveal that distinct domains in GDE catalyse sequential reactions in glycogen debranching, the mechanism of their catalysis and highly specific substrate recognition. The unique tertiary structure of GDE provides additional contacts to glycogen besides its active sites, and our biochemical experiments indicate that they mediate its recruitment to glycogen and regulate its activity. Combining the understanding of the GDE catalysis and functional characterizations of its disease-causing mutations provides molecular insights into GSDIII. PMID:27088557

  11. How do Lyme Borrelia Organisms Cause Disease? The Quest for Virulence Determinants#

    PubMed Central

    Norris, Steven J

    2012-01-01

    Lyme disease Borrelia are invasive, nontoxigenic, persistent pathogens, and little is known about their mechanisms of pathogenesis. In our laboratory, a signature-tagged mutagenesis (STM) library of over 4,000 Borrelia burgdorferi transposon mutants has been constructed and is being screened for infectivity in mice. In this manner, a global view of the virulence determinants (factors required for full infectivity) is being developed. Additionally, the mechanisms of immune evasion involving the VMP-like system (vls) are under analysis, and cryo-electron microscopy is providing a detailed view of the three-dimensional structure of B. burgdorferi. These approaches will contribute to the improved understanding of how Lyme disease Borrelia cause disease. PMID:23091573

  12. [EPIDEMIOLOGIC ANALYSIS OF OUTBREAKS OF DISEASES CAUSED BY AMERICAN EQUINE ENCEPHALITIS CAUSATIVE AGENTS IN ENDEMIC REGIONS].

    PubMed

    Petrov, A A; Lebedev, V N; Kulish, V S; Pyshnaya, N S; Stovba, L F; Borisevich, S V

    2015-01-01

    Epidemiologic analysis of epidemic outbreaks caused by American equine encephalitis causative agents is carried out in the review. Eastern equine encephalomyelitis (EEE), Western equine encephalomyelitis (WEE) and Venezuela equine encephalomyelitis (VEE) viruses are etiologic agents of dangerous transmissive diseases that are usually accompanied by fever and neurologic symptoms. Among the New World alphaviruses, VEE virus has the most potential danger for humans and domestic animals. Currently, enzootic strains of VEE play an increasing role as etiologic agents of human diseases. Most of the VEE cases in humans in endemic regions during inter-epidemic period are caused by infection with VEE subtype ID virus. A possibility of emergence of novel epidemic outbreaks of VEE is determined by mutations of ID subtype strains into IC subtype, and those currently pose a potential threat as an etiologic agent of the disease. Despite low morbidity, EEE and WEE are a problem for healthcare due to a relatively high frequency of lethal outcomes of the disease. PMID:26829861

  13. The dynamics of spreading bacterial diseases and ilnesses caused by helminthosis in Adjara Autonomous Republic 2011.

    PubMed

    Lomtatidze, N; Chachnelidze, R; Chkaidze, M

    2013-01-01

    According to the data of past few years it has been determined that the general incidence and the prevalence of the bacterial and helminthosis diseases have increased. Epidemic Supervision has registered a slight increase of such diseases in data of 2011. Taking into consideration this fact, this research is quite important for the region of Adjara. The aim of our research is to study the dynamics of spreading some bacterial and helminthosis diseases in Adjara Autonomous Republic. In particular, the diseases caused by different bacterias of leptospira family - leptospirosis and illnesses caused by helminthosis - ascariasis, enterobiasis and trichocephalosis. according to the reseaches held it has been determined that there have been several cases of leptospirosis registered in Adjara. Specifically, 10 cases in 2008, 6 in 2009, 30 in 2010 and 31 cases in 2011 out of which 10 of the cases where laboratorily claimed. There were cases of ascariasis, enterobiasis and trichocephalosis. According to data, there are 5 times less cases of trichocephalosis than of ascariasis. As for enterobiasis, it's less than ascariasis (the difference is 205 cases). In therms of the aging, all the cases occur more frequently in the group of children below the age of 14. PMID:23388532

  14. Diseases of comfort: primary cause of death in the 22nd century

    PubMed Central

    Choi, B.; Hunter, D.; Tsou, W.; Sainsbury, P.

    2005-01-01

    Objective: To describe the concept, causes, and prevention and control strategies of diseases of comfort. Methods: Brokered by a senior research scientist specialised in knowledge translation, a chair, a president, and a past president of national public health associations contributed their views on the subject. Results: Diseases of comfort have emerged as a price of living in a modern society. It is inevitable that these diseases will become more common and more disabling if human "progress" and civilisation continue toward better (more comfortable) living, without necessarily considering their effects on health. Modern technology must be combined with education, legislation, intersectoral action, and community involvement to create built and social environments that encourage, and make easy, walking, physical activity, and nutritious food choices, to reduce the health damaging effects of modern society for all citizens and not only the few. Conclusions: Public health needs to be more passionate about the health issues caused by human progress and adopt a health promotion stance, challenging the assumptions behind the notion of social "progress" that is giving rise to the burden of chronic disease and developing the skills to create more health promoting societies in which individual health thrives. PMID:16286489

  15. Epidemiology and Control of Strawberry Bacterial Angular Leaf Spot Disease Caused by Xanthomonas fragariae.

    PubMed

    Kim, Da-Ran; Gang, Gun-Hye; Jeon, Chang-Wook; Kang, Nam Jun; Lee, Sang-Woo; Kwak, Youn-Sig

    2016-08-01

    Strawberry bacterial angular leaf spot (ALS) disease, caused by Xanthomonas fragariae has become increasingly problematic in the strawberry agro-industry. ALS causes small angular water-soaked lesions to develop on the abaxial leaf surface. Studies reported optimum temperature conditions for X. fragariae are 20°C and the pathogen suffers mortality above 32°C. However, at the nursery stage, disease symptoms have been observed under high temperature conditions. In the present study, results showed X. fragariae transmission was via infected maternal plants, precipitation, and sprinkler irrigation systems. Systemic infections were detected using X. fragariae specific primers 245A/B and 295A/B, where 300-bp and 615-bp were respectively amplified. During the nursery stage (from May to August), the pathogen was PCR detected only in maternal plants, but not in soil or irrigation water through the nursery stage. During the cultivation period, from September to March, the pathogen was detected in maternal plants, progeny, and soil, but not in water. Additionally, un-infected plants, when planted with infected plants were positive for X. fragariae via PCR at the late cultivation stage. Chemical control for X. fragariae with oxolinic acid showed 87% control effects against the disease during the nursery period, in contrast to validamycin-A, which exhibited increased efficacy against the disease during the cultivation stage (control effect 95%). To our knowledge, this is the first epidemiological study of X. fragariae in Korean strawberry fields. PMID:27493604

  16. Epidemiology and Control of Strawberry Bacterial Angular Leaf Spot Disease Caused by Xanthomonas fragariae

    PubMed Central

    Kim, Da-Ran; Gang, Gun-hye; Jeon, Chang-Wook; Kang, Nam Jun; Lee, Sang-woo; Kwak, Youn-Sig

    2016-01-01

    Strawberry bacterial angular leaf spot (ALS) disease, caused by Xanthomonas fragariae has become increasingly problematic in the strawberry agro-industry. ALS causes small angular water-soaked lesions to develop on the abaxial leaf surface. Studies reported optimum temperature conditions for X. fragariae are 20°C and the pathogen suffers mortality above 32°C. However, at the nursery stage, disease symptoms have been observed under high temperature conditions. In the present study, results showed X. fragariae transmission was via infected maternal plants, precipitation, and sprinkler irrigation systems. Systemic infections were detected using X. fragariae specific primers 245A/B and 295A/B, where 300-bp and 615-bp were respectively amplified. During the nursery stage (from May to August), the pathogen was PCR detected only in maternal plants, but not in soil or irrigation water through the nursery stage. During the cultivation period, from September to March, the pathogen was detected in maternal plants, progeny, and soil, but not in water. Additionally, un-infected plants, when planted with infected plants were positive for X. fragariae via PCR at the late cultivation stage. Chemical control for X. fragariae with oxolinic acid showed 87% control effects against the disease during the nursery period, in contrast to validamycin-A, which exhibited increased efficacy against the disease during the cultivation stage (control effect 95%). To our knowledge, this is the first epidemiological study of X. fragariae in Korean strawberry fields. PMID:27493604

  17. An evaluation of weather and disease as causes of decline in two populations of boreal toads

    USGS Publications Warehouse

    Scherer, R. D.; Muths, E.; Noon, B.R.; Corn, P.S.

    2005-01-01

    Two populations of boreal toads (Bufo boreas) experienced drastic declines in abundance in the late 1990s. Evidence supported the hypothesis of disease (the chytrid fungus, Batrachochytrium dendrobatidis) as the cause of these declines, but other hypotheses had not been evaluated. We used an 11-year capture-recapture data set to evaluate weather and disease as causes of these declines. We developed sets of mathematical models that reflected hypothesized relationships between several weather variables and annual survival rates of adult males in these populations. In addition, models that reflected the possibility that the declines were caused by an introduced fungus were developed. All models were fit to the data and were evaluated using a model selection criterion (QAICc). Our analysis provided strong support for the hypothesis of an introduced fungus and little support for the hypothesis that weather conditions caused the declines. Our results also suggest a strong, negative 'marking effect' on survival rates of boreal toads. Model-averaged estimates of survival rate are presented.

  18. Coxsackievirus A6: a new emerging pathogen causing hand, foot and mouth disease outbreaks worldwide.

    PubMed

    Bian, Lianlian; Wang, Yiping; Yao, Xin; Mao, Qunying; Xu, Miao; Liang, Zhenglun

    2015-01-01

    Enterovirus 71 (EV71) and coxsackievirus A16 (CA16) are the predominant pathogens causing outbreaks of hand, foot and mouth disease (HFMD) worldwide. Other human enterovirus A (HEV-A) serotypes tend to cause only sporadic HFMD cases. However, since a HFMD caused by coxsackievirus A6 broke out in Finland in 2008, CA6 has been identified as the responsible pathogen for a series of HFMD outbreaks in Europe, North America and Asia. Because of the severity of the clinical manifestations and the underestimated public health burden, the epidemic of CA6-associated HFMD presents a new challenge to the control of HFMD. This article reviewed the epidemic characteristics, molecular epidemiology, clinical features and laboratory diagnosis of CA6 infection. The genetic evolution of CA6 strains associated with HFMD was also analyzed. It indicated that the development of a multivalent vaccine combining EV71, CA16 and CA6 is an urgent necessity to control HFMD. PMID:26112307

  19. Effects of Running on Chronic Diseases and Cardiovascular and All-Cause Mortality.

    PubMed

    Lavie, Carl J; Lee, Duck-chul; Sui, Xuemei; Arena, Ross; O'Keefe, James H; Church, Timothy S; Milani, Richard V; Blair, Steven N

    2015-11-01

    Considerable evidence has established the link between high levels of physical activity (PA) and all-cause and cardiovascular disease (CVD)-specific mortality. Running is a popular form of vigorous PA that has been associated with better overall survival, but there is debate about the dose-response relationship between running and CVD and all-cause survival. In this review, we specifically reviewed studies published in PubMed since 2000 that included at least 500 runners and 5-year follow-up so as to analyze the relationship between vigorous aerobic PA, specifically running, and major health consequences, especially CVD and all-cause mortality. We also made recommendations on the optimal dose of running associated with protection against CVD and premature mortality, as well as briefly discuss the potential cardiotoxicity of a high dose of aerobic exercise, including running (eg, marathons). PMID:26362561

  20. Pancreatitis in hand-foot-and-mouth disease caused by enterovirus 71.

    PubMed

    Zhang, Yu-Feng; Deng, Hui-Ling; Fu, Jia; Zhang, Yu; Wei, Jian-Qiang

    2016-02-14

    Some viruses, including certain members of the enterovirus genus, have been reported to cause pancreatitis, especially Coxsackie virus. However, no case of human enterovirus 71 (EV71) associated with pancreatitis has been reported so far. We here report a case of EV71-induced hand-foot-and-mouth disease (HFMD) presenting with pancreatitis in a 2-year-old girl. This is the first report of a patient with acute pancreatitis in HFMD caused by EV71. We treated the patient conservatively with nasogastric suction, intravenous fluid and antivirals. The patient's symptoms improved after 8 d, and recovered without complications. We conclude that EV71 can cause acute pancreatitis in HFMD, which should be considered in differential diagnosis, especially in cases of idiopathic pancreatitis. PMID:26877620

  1. Pancreatitis in hand-foot-and-mouth disease caused by enterovirus 71

    PubMed Central

    Zhang, Yu-Feng; Deng, Hui-Ling; Fu, Jia; Zhang, Yu; Wei, Jian-Qiang

    2016-01-01

    Some viruses, including certain members of the enterovirus genus, have been reported to cause pancreatitis, especially Coxsackie virus. However, no case of human enterovirus 71 (EV71) associated with pancreatitis has been reported so far. We here report a case of EV71-induced hand-foot-and-mouth disease (HFMD) presenting with pancreatitis in a 2-year-old girl. This is the first report of a patient with acute pancreatitis in HFMD caused by EV71. We treated the patient conservatively with nasogastric suction, intravenous fluid and antivirals. The patient’s symptoms improved after 8 d, and recovered without complications. We conclude that EV71 can cause acute pancreatitis in HFMD, which should be considered in differential diagnosis, especially in cases of idiopathic pancreatitis. PMID:26877620

  2. A Mouse Model for Studying Viscerotropic Disease Caused by Yellow Fever Virus Infection

    PubMed Central

    Meier, Kathryn C.; Gardner, Christina L.; Khoretonenko, Mikhail V.; Klimstra, William B.; Ryman, Kate D.

    2009-01-01

    Mosquito-borne yellow fever virus (YFV) causes highly lethal, viscerotropic disease in humans and non-human primates. Despite the availability of efficacious live-attenuated vaccine strains, 17D-204 and 17DD, derived by serial passage of pathogenic YFV strain Asibi, YFV continues to pose a significant threat to human health. Neither the disease caused by wild-type YFV, nor the molecular determinants of vaccine attenuation and immunogenicity, have been well characterized, in large part due to the lack of a small animal model for viscerotropic YFV infection. Here, we describe a small animal model for wild-type YFV that manifests clinical disease representative of that seen in primates without adaptation of the virus to the host, which was required for the current hamster YF model. Investigation of the role of type I interferon (IFN-α/β) in protection of mice from viscerotropic YFV infection revealed that mice deficient in the IFN-α/β receptor (A129) or the STAT1 signaling molecule (STAT129) were highly susceptible to infection and disease, succumbing within 6–7 days. Importantly, these animals developed viscerotropic disease reminiscent of human YF, instead of the encephalitic signs typically observed in mice. Rapid viremic dissemination and extensive replication in visceral organs, spleen and liver, was associated with severe pathologies in these tissues and dramatically elevated MCP-1 and IL-6 levels, suggestive of a cytokine storm. In striking contrast, infection of A129 and STAT129 mice with the 17D-204 vaccine virus was subclinical, similar to immunization in humans. Although, like wild-type YFV, 17D-204 virus amplified within regional lymph nodes and seeded a serum viremia in A129 mice, infection of visceral organs was rarely established and rapidly cleared, possibly by type II IFN-dependent mechanisms. The ability to establish systemic infection and cause viscerotropic disease in A129 mice correlated with infectivity for A129-derived, but not WT129

  3. An unusual case caused by a common reason: Mondor's disease by oral contraceptives☆☆☆

    PubMed Central

    Kadioglu, Huseyin; Yildiz, Şeyma; Ersoy, Yeliz Emine; Yücel, Serap; Müslümanoğlu, Mahmut

    2013-01-01

    INTRODUCTION Mondor's disease (MD) of the breast is a rare condition at breast clinics. We do not have enough data to establish its real prevalence. As a known data, most of the patients that were admitted to breast clinics are not breast cancer. Also MD is a rare entity and diagnosing this entity and informing the patient about it is very important. We present here this case to remind breast clinic practitioners that MD can be seen without trauma (neither surgical nor physical). Also clinical and radiological findings and the treatmentof the MD were discussed. PRESENTATION OF CASE A 35 year old woman was admitted our clinic with cutaneous breast retraction. She had no risk for thrombosis else using oral contraceptives. Mondor's Disease was diagnosed and supported by radiological findings. Rheumatologic and hematologic causes were also explored. Patient healed in four weeks only with non-steroidal anti-inflammatory drug. DISCUSSION Mondor's Disease is rarely related with breast cancer. This rare entity can be diagnosed with doubt and patient should be informed about it. Anti-coagulant treatment does not required if disease is idiopathic. CONCLUSION Mondor's Disease should be reminded at a patient with retracted breast skin. PMID:23959419

  4. Staphylococcal superantigens interact with multiple host receptors to cause serious diseases.

    PubMed

    Stach, Christopher S; Herrera, Alfa; Schlievert, Patrick M

    2014-08-01

    Staphylococcus aureus strains that cause human diseases produce a large family of pyrogenic toxin superantigens (SAgs). These include toxic shock syndrome toxin-1 (TSST-1), the staphylococcal enterotoxins (SEs), and the SE-like proteins; to date, 23 staphylococcal SAgs have been described. Among the SAgs, three have been highly associated with human diseases (TSST-1, SEB, and SEC), likely because they are produced in high concentrations compared to other SAgs. Another major family of exotoxins produced by S. aureus is the cytolysins, particularly α-, β-, γ-, and δ-toxins, phenol soluble modulins, and leukocidins. This review discusses the association of SAgs with human diseases and particularly the "outside-in" signaling mechanism that leads to SAg-associated diseases. We discuss SAg interactions with three host immune cell receptors, including variable regions of the β-chain of the T cell receptor, MHC II α- and/or β-chains, and an epithelial/endothelial cell receptor that may include CD40. To a lesser extent, we discuss the role of cytolysins in facilitating disease production by SAgs. PMID:24838262

  5. Possibility of biological control of primocane fruiting raspberry disease caused by Fusarium sambucinum.

    PubMed

    Shternshis, Margarita V; Belyaev, Anatoly A; Matchenko, Nina S; Shpatova, Tatyana V; Lelyak, Anastasya A

    2015-10-01

    Biological control agents are a promising alternative to chemical pesticides for plant disease suppression. The main advantage of the natural biocontrol agents, such as antagonistic bacteria compared with chemicals, includes environmental pollution prevention and a decrease of chemical residues in fruits. This study is aimed to evaluate the impact of three Bacillus strains on disease of primocane fruiting raspberry canes caused by Fusarium sambucinum under controlled infection load and uncontrolled environmental factors. Bacillus subtilis, Bacillus licheniformis, and Bacillus amyloliquefaciens were used for biocontrol of plant disease in 2013 and 2014 which differed by environmental conditions. The test suspensions were 10(5) CFU/ml for each bacterial strain. To estimate the effect of biological agents on Fusarium disease, canes were cut at the end of vegetation, and the area of outer and internal lesions was measured. In addition to antagonistic effect, the strains revealed the ability to induce plant resistance comparable with chitosan-based formulation. Under variable ways of cane treatment by bacterial strains, the more effective were B. subtilis and B. licheniformis demonstrating dual biocontrol effect. However, environmental factors were shown to impact the strain biocontrol ability; changes in air temperature and humidity led to the enhanced activity of B. amyloliquefaciens. For the first time, the possibility of replacing chemicals with environmentally benign biological agents for ecologically safe control of the raspberry primocane fruiting disease was shown. PMID:26018288

  6. Revealing the causes of chronic disease epidemics: from research to prevention.

    PubMed

    Wynder, E L

    1994-02-01

    Descriptive epidemiology, with support from metabolic epidemiology and other laboratory studies, has demonstrated a causative relationship between lifestyles--what we smoke, drink and eat, use of illicit drugs, and unsafe sexual practices--and the morbidity and mortality from chronic diseases. What immunization, sanitation and hygiene have done to reduce the scourges of infectious diseases must also be done to reduce the incidence of chronic diseases that have man-made causes. The challenge of applied epidemiology and preventive medicine is to improve health-related behaviours beginning with children's health education, extending to economic incentives for adult populations for good health behaviour, and engaging responsible industry, media and governmental influences to manufacture and promote safer products, and to provide a social and economic environment that is conductive to greater self-esteem and enables people to make the right health decisions. There is ample research to prove that our lifestyles are responsible for much of our health care costs. The challenge of improving the health of all people and of reducing health care cost can be most effectively met by practising disease prevention. After all, the history of medicine shows that the elimination of disease has rarely been the result of therapy, but rather, a consequence of prevention. PMID:8166989

  7. Viral competition and maternal immunity influence the clinical disease caused by very virulent infectious bursal disease virus.

    PubMed

    Jackwood, Daral J

    2011-09-01

    The very virulent form of infectious bursal disease virus (vvIBDV) causes an immunosuppressive disease that is further characterized by the rapid onset of morbidity and high mortality in susceptible chickens. In 2009, vvIBDV was first reported in California, U. S. A., and since that time only a few cases of acute infectious bursal disease attributed to vvIBDV have been recognized in California. In other countries where vvIBDV has become established, it rapidly spreads to most poultry-producing regions. Two factors that may be involved in limiting the spread or reducing the severity of the clinical disease caused by vvIBDV in the U. S. A. are maternal immunity and competition with endemic variant strains of the virus. In this study, the ability of vvIBDV to infect and cause disease in maternally immune layer chickens was examined at weekly intervals over a 5-wk period during which their neutralizing maternal antibodies waned. Birds inoculated with vvIBDV at 2, 3, and 4 wk of age seemed healthy throughout the duration of the experiment, but macroscopic and microscopic lesions were observed in their bursa tissues. A real-time reverse transcriptase-polymerase chain reaction (RT-PCR) assay also confirmed the presence of vvIBDV RNA in their bursa tissues, indicating this virus was infecting the birds even at 2 wk of age when neutralizing maternal antibodies to infectious bursal disease virus were still relatively high (> 2000 geometric mean antibody titer). No mortality was observed in any birds when inoculated at 2, 3, or 4 wk of age; however, inoculation at 5 and 6 wk of age resulted in 10% and 20% mortality, respectively. Three experiments on the competition between vvIBDV and the two variant viruses T1 and FF6 were conducted. In all three experiments, specific-pathogen-free (SPF) birds that were inoculated with only the vvIBDV became acutely moribund, and except for Experiment 1 (62% mortality) all succumbed to the infection within 4 days of being exposed. When the

  8. Traffic air pollution and mortality from cardiovascular disease and all causes: a Danish cohort study

    PubMed Central

    2012-01-01

    Background Traffic air pollution has been linked to cardiovascular mortality, which might be due to co-exposure to road traffic noise. Further, personal and lifestyle characteristics might modify any association. Methods We followed up 52 061 participants in a Danish cohort for mortality in the nationwide Register of Causes of Death, from enrollment in 1993–1997 through 2009, and traced their residential addresses from 1971 onwards in the Central Population Registry. We used dispersion-modelled concentration of nitrogen dioxide (NO2) since 1971 as indicator of traffic air pollution and used Cox regression models to estimate mortality rate ratios (MRRs) with adjustment for potential confounders. Results Mean levels of NO2 at the residence since 1971 were significantly associated with mortality from cardiovascular disease (MRR, 1.26; 95% confidence interval [CI], 1.06–1.51, per doubling of NO2 concentration) and all causes (MRR, 1.13; 95% CI, 1.04–1.23, per doubling of NO2 concentration) after adjustment for potential confounders. For participants who ate < 200 g of fruit and vegetables per day, the MRR was 1.45 (95% CI, 1.13–1.87) for mortality from cardiovascular disease and 1.25 (95% CI, 1.11–1.42) for mortality from all causes. Conclusions Traffic air pollution is associated with mortality from cardiovascular diseases and all causes, after adjustment for traffic noise. The association was strongest for people with a low fruit and vegetable intake. PMID:22950554

  9. Chronic kidney disease of uncertain etiology in Sri Lanka: Are leptospirosis and Hantaviral infection likely causes?

    PubMed

    Gamage, Chandika Damesh; Sarathkumara, Yomani Dilukshi

    2016-06-01

    Chronic kidney disease of uncertain etiology (CKDu) has been a severe burden and a public health crisis in Sri Lanka over the past two decades. Many studies have established hypotheses to identify potential risk factors although causative agents, risk factors and etiology of this disease are still uncertain. Several studies have postulated that fungal and bacterial nephrotoxins are a possible etiological factor; however, the precise link between hypothesized risk factors and the pathogenesis of chronic kidney disease has yet to be proven in prior studies. Leptospirosis and Hantavirus infections are important zoonotic diseases that are naturally maintained and transmitted via infected rodent populations and which present similar clinical and epidemiological features. Both infections are known to be a cause of acute kidney damage that can proceed into chronic renal failure. Several studies have reported presence of both infections in Sri Lanka. Therefore, we hypothesized that pathogenic Leptospira or Hantavirus are possible causative agents of acute kidney damage which eventually progresses to chronic kidney disease in Sri Lanka. The proposed hypothesis will be evaluated by means of an observational study design. Past infection will be assessed by a cross-sectional study to detect the presence of IgG antibodies with further confirmatory testing among chronic kidney disease patients and individuals from the community in selected endemic areas compared to low prevalence areas. Identification of possible risk factors for these infections will be followed by a case-control study and causality will be further determined with a cohort study. If the current hypothesis is true, affected communities will be subjected for medical interventions related to the disease for patient management while considering supportive therapies. Furthermore and possibly enhance their preventive and control measures to improve vector control to decrease the risk of infection. PMID:27142134

  10. Acylated Cholesteryl Galactosides Are Specific Antigens of Borrelia Causing Lyme Disease and Frequently Induce Antibodies in Late Stages of Disease

    PubMed Central

    Stübs, Gunthard; Fingerle, Volker; Wilske, Bettina; Göbel, Ulf B.; Zähringer, Ulrich; Schumann, Ralf R.; Schröder, Nicolas W. J.

    2009-01-01

    Borrelia burgdorferi sensu lato is the causative agent of Lyme disease (LD), an infectious disease occurring in North America, Europe, and Asia in different clinical stages. B. burgdorferi sensu lato encompasses at least 12 species, with B. burgdorferi sensu stricto, B. garinii, and B. afzelii being of highest clinical importance. Immunologic testing for LD as well as recent vaccination strategies exclusively refer to proteinaceous antigens. However, B. burgdorferi sensu stricto exhibits glycolipid antigens, including 6-O-acylated cholesteryl β-d-galactopyranoside (ACGal), and first the data indicated that this compound may act as an immunogen. Here we investigated whether B. garinii and B. afzelii also possess this antigen, and whether antibodies directed against these compounds are abundant among patients suffering from different stages of LD. Gas-liquid chromatography/mass spectroscopy and NMR spectroscopy showed that both B. garinii and B. afzelii exhibit ACGal in high quantities. In contrast, B. hermsii causing relapsing fever features 6-O-acylated cholesteryl β-d-glucopyranoside (ACGlc). Sera derived from patients diagnosed for LD contained antibodies against ACGal, with 80% of patients suffering from late stage disease exhibiting this feature. Antibodies reacted with ACGal from all three B. burgdorferi species tested, but not with ACGlc from B. hermsii. These data show that ACGal is present in all clinically important B. burgdorferi species, and that specific antibodies against this compound are frequently found during LD. ACGal may thus be an interesting tool for improving diagnostics as well as for novel vaccination strategies. PMID:19307181

  11. WDR73 mutations cause infantile neurodegeneration and variable glomerular kidney disease

    PubMed Central

    Vodopiutz, Julia; Seidl, Rainer; Prayer, Daniela; Khan, M. Imran; Mayr, Johannes A.; Streubel, Berthold; Steiß, Jens-Oliver; Hahn, Andreas; Csaicsich, Dagmar; Castro, Christel; Assoum, Mirna; Müller, Thomas; Wieczorek, Dagmar; Mancini, Grazia M. S.; Sadowski, Carolin E.; Levy, Nicolas; Mégarbané, André; Godbole, Koumudi; Schanze, Denny; Hildebrandt, Friedhelm; Delague, Valérie; Janecke, Andreas R.; Zenker, Martin

    2015-01-01

    Infantile-onset cerebellar atrophy (CA) is a clinically and genetically heterogeneous trait. Galloway-Mowat syndrome (GMS) is a rare autosomal recessive disease, characterized by microcephaly with brain anomalies including CA in some cases, intellectual disability, and early-infantile-onset nephrotic syndrome. Very recently, WDR73 deficiency was identified as the cause of GMS in five individuals. To evaluate the role of WDR73 mutations as a cause of GMS and other forms of syndromic CA, we performed Sanger or exome sequencing in 51 unrelated patients with CA and variable brain anomalies and in 40 unrelated patients with a diagnosis of GMS. We identified 10 patients from three CA and from two GMS families with WDR73 mutations including the original family described with CA, mental retardation, optic atrophy and skin abnormalities (CAMOS). There were five novel mutations, of which two were truncating and three were missense mutations affecting highly conserved residues. Individuals carrying homozygous WDR73 mutations mainly presented with a pattern of neurological and neuroimaging findings as well as intellectual disability, while kidney involvement was variable. We document postnatal onset of CA, a retinopathy, basal ganglia degeneration, and short stature as novel features of WDR73-related disease, and define WDR73-related disease as a new entity of infantile neurodegeneration. PMID:26123727

  12. Two Novel De Novo GARS Mutations Cause Early-Onset Axonal Charcot-Marie-Tooth Disease

    PubMed Central

    Liao, Yi-Chu; Liu, Yo-Tsen; Tsai, Pei-Chien; Chang, Chia-Ching; Huang, Yen-Hua; Soong, Bing-Wen; Lee, Yi-Chung

    2015-01-01

    Background Mutations in the GARS gene have been identified in a small number of patients with Charcot-Marie-Tooth disease (CMT) type 2D or distal spinal muscular atrophy type V, for whom disease onset typically occurs during adolescence or young adulthood, initially manifesting as weakness and atrophy of the hand muscles. The role of GARS mutations in patients with inherited neuropathies in Taiwan remains elusive. Methodology and Principal Findings Mutational analyses of the coding regions of GARS were performed using targeted sequencing of 54 patients with molecularly unassigned axonal CMT, who were selected from 340 unrelated CMT patients. Two heterozygous mutations in GARS, p.Asp146Tyr and p.Met238Arg, were identified; one in each patient. Both are novel de novo mutations. The p.Asp146Tyr mutation is associated with a severe infantile-onset neuropathy and the p.Met238Arg mutation results in childhood-onset disability. Conclusion GARS mutations are an uncommon cause of CMT in Taiwan. The p.Asp146Tyr and p.Met238Arg mutations are associated with early-onset axonal CMT. These findings broaden the mutational spectrum of GARS and also highlight the importance of considering GARS mutations as a disease cause in patients with early-onset neuropathies. PMID:26244500

  13. Structural consequences of amino acid substitutions causing Tay-Sachs disease.

    PubMed

    Ohno, Kazuki; Saito, Seiji; Sugawara, Kanako; Sakuraba, Hitoshi

    2008-08-01

    To determine the structural changes in the alpha-subunit of beta-hexosaminidase due to amino acid substitutions causing Tay-Sachs disease, we built structural models of mutant alpha-subunits resulting from 33 missense mutations (24 infantile and 9 late-onset), and analyzed the influence of each amino acid replacement on the structure by calculating the number of atoms affected and determining the solvent-accessible surface area of the corresponding amino acid residue in the wild-type alpha-subunit. In the infantile Tay-Sachs group, the number of atoms influenced by a mutation was generally larger than that in the late-onset Tay-Sachs group in both the main chain and the side chain, and residues associated with the mutations found in the infantile Tay-Sachs group tended to be less solvent-accessible than those in the late-onset Tay-Sachs group. Furthermore, color imaging determined the distribution and degree of the structural changes caused by representative amino acid substitutions, and that there were also differences between the infantile and late-onset Tay-Sachs disease groups. Structural study is useful for elucidating the basis of Tay-Sachs disease. PMID:18490185

  14. Tight Bra in a 34-Year-Old Woman: An Unusual Cause of Mondor’s Disease

    PubMed Central

    2014-01-01

    Mondor’s disease is characterized by thrombophlebitis of the superficial veins of the breast and the chest wall. The list of causes is long. Various types of clothing, mainly tight bras and girdles, have been postulated as causes. We report a case of a 34-year-old woman who referred typical symptoms and signs of Mondor’s disease, without other possible risk factors, and showed the cutaneous findings of the tight bra. Therefore, after distinguishing benign causes of Mondor’s disease from hidden malignant causes, the clinicians should consider this clinical entity. PMID:24995060

  15. First report of anthracnose of Salsola tragus caused by Colletotrichum gloeosporioides in Russia

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Salsola tragus L. (Russian thistle, tumbleweed), family Chenopodiaceae, is a problematic invasive weed in the western United States and a target of biological control efforts. In October of 2006, dying Salsola tragus L. plants were found along the Azov Sea at Chushka, Russia. About 40 plants in th...

  16. Agrarian diet and diseases of affluence – Do evolutionary novel dietary lectins cause leptin resistance?

    PubMed Central

    Jönsson, Tommy; Olsson, Stefan; Ahrén, Bo; Bøg-Hansen, Thorkild C; Dole, Anita; Lindeberg, Staffan

    2005-01-01

    Background The global pattern of varying prevalence of diseases of affluence, such as obesity, cardiovascular disease and diabetes, suggests that some environmental factor specific to agrarian societies could initiate these diseases. Presentation of the hypothesis We propose that a cereal-based diet could be such an environmental factor. Through previous studies in archaeology and molecular evolution we conclude that humans and the human leptin system are not specifically adapted to a cereal-based diet, and that leptin resistance associated with diseases of affluence could be a sign of insufficient adaptation to such a diet. We further propose lectins as a cereal constituent with sufficient properties to cause leptin resistance, either through effects on metabolism central to the proper functions of the leptin system, and/or directly through binding to human leptin or human leptin receptor, thereby affecting the function. Testing the hypothesis Dietary interventions should compare effects of agrarian and non-agrarian diets on incidence of diseases of affluence, related risk factors and leptin resistance. A non-significant (p = 0.10) increase of cardiovascular mortality was noted in patients advised to eat more whole-grain cereals. Our lab conducted a study on 24 domestic pigs in which a cereal-free hunter-gatherer diet promoted significantly higher insulin sensitivity, lower diastolic blood pressure and lower C-reactive protein as compared to a cereal-based swine feed. Testing should also evaluate the effects of grass lectins on the leptin system in vivo by diet interventions, and in vitro in various leptin and leptin receptor models. Our group currently conducts such studies. Implications of the hypothesis If an agrarian diet initiates diseases of affluence it should be possible to identify the responsible constituents and modify or remove them so as to make an agrarian diet healthier. PMID:16336696

  17. Identification and Chacterization of new strains of Enterobacter spp. causing Mulberry (Morus alba) wilt disease in China

    Technology Transfer Automated Retrieval System (TEKTRAN)

    A new mulberry wilt disease (MWD) was recently identified in Hangzhou, Zhejiang province, China. Typical symptoms of the disease are dark brown discolorations in vascular tissues, leaf wilt, defoliation, and tree decline. Unlike the bacterial wilt disease caused by Ralstonia solanacearum, the leaf w...

  18. Managing scab diseases of potato and radish caused by Streptomyces spp. using Bacillus amyloliquefaciens BAC03 and other biomaterials

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Streptomyces spp. cause scab disease in plants like potato and radish. To seek effective control methods of this disease, biologically based materials were examined on their efficacies for disease control. In greenhouse or growth chamber tests, potting soil was infested with Streptomyces scabies (10...

  19. Newcastle disease viruses causing recent outbreaks worldwide show unexpectedly high genetic similarity with historical virulent isolates from the 1940s

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Virulent strains of Newcastle disease virus (NDV) cause Newcastle disease (ND), a devastating disease of poultry and wild birds. Phylogenetic analyses clearly distinguish historical isolates (obtained prior to 1960) from currently circulating viruses of class II genotypes V, VI, VII, and XII throug...

  20. Epidemiology of Diseases Caused by Xylella fastidiosa in California: Evaluation of Alfalfa As A Source of Vectors and Inocula

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Pierce’s disease of grape and almond leaf scorch disease have been chronic problems in California. Both diseases are caused by the xylem-limited, bacterial pathogen, Xylella fastidiosa. The pathogen is vectored by xylem feeding insects and within California key vectors vary by region. The potenti...

  1. Two whole genome sequences of Xylella fastidiosa (strains M12 and M23) causing almond leaf scorch disease in California

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Xylella fastidiosa is a Gram negative, nutritionally fastidious plant pathogenic bacterium that causes many economically important diseases including almond leaf scorch disease (ALSD) and Pierce’s disease of grape in California, as well as citrus variegated chlorosis in South America. Genome inform...

  2. Guanidino compounds as cause of cardiovascular damage in chronic kidney disease: an in vitro evaluation.

    PubMed

    Schepers, Eva; Glorieux, Griet; Dou, Laetitia; Cerini, Claire; Gayrard, Nathalie; Louvet, Loïc; Maugard, Charlotte; Preus, Pierre; Rodriguez-Ortiz, Maria; Argiles, Angel; Brunet, Philippe; Cohen, Gerald; Jankowski, Joachim; Jankowski, Vera; Massy, Ziad; Rodriguez, Mariano; Vanholder, Raymond

    2010-01-01

    Chronic kidney disease is considered a major cause of cardiovascular risk and non-traditional risk factors remain largely unknown. The in vitro toxicity of 10 guanidino compounds (GCs) was evaluated via a standardized approach on different cell systems of relevance in cardiovascular disease. The parameters evaluated were production of reactive oxygen species, expression of surface molecules, cell proliferation, cytotoxicity and calcification. Several GCs had a stimulatory effect on monocytes and granulocytes (SDMA, creatine and guanidinobutyric acid (GBA)). Some GCs (guandine (G), guanidinosuccinic acid (GSA) and SDMA) inhibited endothelial cell proliferation or reduced calcification in osteoblast-like human VSMC (ADMA, GSA and SDMA). Stimulation of osteoclastogenesis could be demonstrated for ADMA, G, guanidinoacetic acid and GBA in a RAW264.7 cell line. No compounds were cytotoxic to AoSMC or endothelial cells, nor influenced their viability. GCs, especially SDMA, likely contribute to cardiovascular complications in uremia, mainly those related to microinflammation and leukocyte activation. PMID:21079396

  3. Expert-novice differences in mental models of viruses, vaccines, and the causes of infectious disease.

    PubMed

    Jee, Benjamin D; Uttal, David H; Spiegel, Amy; Diamond, Judy

    2015-02-01

    Humans are exposed to viruses everywhere they live, play, and work. Yet people's beliefs about viruses may be confused or inaccurate, potentially impairing their understanding of scientific information. This study used semi-structured interviews to examine people's beliefs about viruses, vaccines, and the causes of infectious disease. We compared people at different levels of science expertise: middle school students, teachers, and professional virologists. The virologists described more entities involved in microbiological processes, how these entities behaved, and why. Quantitative and qualitative analyses revealed distinctions in the cognitive organization of several concepts, including infection and vaccination. For example, some students and teachers described viral replication in terms of cell division, independent of a host. Interestingly, most students held a mental model for vaccination in which the vaccine directly attacks a virus that is present in the body. Our findings have immediate implications for how to communicate about infectious disease to young people. PMID:23959975

  4. The causes of lower-extremity deep venous thrombosis in the children with cranial diseases

    PubMed Central

    Wang, Yan; Liu, Wei; Jia, Ge; Li, Na; Jia, Yulong

    2015-01-01

    In order to investigate the prevalence of lower-extremity deep venous thrombosis (DVT) and to explore its possible reasons in children patients who received neurosurgery operation. Clinical data of 4958 cases children patients with lower-extremity DVT and without the thrombosis after the neurosurgery operation from 2010 January to 2014 December in department of neurosurgery of Tian Tan hospital were collected and analyzed. 18 cases children were diagnosed with lower-extremity DVT. All of them had invasive operation of lower-extremity deep venous catheterization. The mainly primary diseases of thrombosis children were craniopharyngioma. They have longer operation time compared with those without thrombosis (P<0.05). Therefore, the causes of DVT in neurosurgical children involve not only deep venous catheter-related but also neurological primary disease and operation time. PMID:26885175

  5. Recent Trends in Control Methods for Bacterial Wilt Diseases Caused by Ralstonia solanacearum

    PubMed Central

    Yuliar; Nion, Yanetri Asi; Toyota, Koki

    2015-01-01

    Previous studies have described the development of control methods against bacterial wilt diseases caused by Ralstonia solanacearum. This review focused on recent advances in control measures, such as biological, physical, chemical, cultural, and integral measures, as well as biocontrol efficacy and suppression mechanisms. Biological control agents (BCAs) have been dominated by bacteria (90%) and fungi (10%). Avirulent strains of R. solanacearum, Pseudomonas spp., Bacillus spp., and Streptomyces spp. are well-known BCAs. New or uncommon BCAs have also been identified such as Acinetobacter sp., Burkholderia sp., and Paenibacillus sp. Inoculation methods for BCAs affect biocontrol efficacy, such as pouring or drenching soil, dipping of roots, and seed coatings. The amendment of different organic matter, such as plant residue, animal waste, and simple organic compounds, have frequently been reported to suppress bacterial wilt diseases. The combined application of BCAs and their substrates was shown to more effectively suppress bacterial wilt in the tomato. Suppression mechanisms are typically attributed to the antibacterial metabolites produced by BCAs or those present in natural products; however, the number of studies related to host resistance to the pathogen is increasing. Enhanced/modified soil microbial communities are also indirectly involved in disease suppression. New promising types of control measures include biological soil disinfection using substrates that release volatile compounds. This review described recent advances in different control measures. We focused on the importance of integrated pest management (IPM) for bacterial wilt diseases. PMID:25762345

  6. A long-lasting pandemic: diseases caused by dust containing silica: Italy within the international context.

    PubMed

    Carnevale, F; Baldasseroni, A

    2005-01-01

    Diseases caused by dust containing silica represent an exemplary case study in the field of work-related diseases and in the history of the discovery of chronic industrial disease and its relationship to industrial society. Both dust and steam are indissolubly linked to the Industrial Revolution which everywhere was expected to replace slaves with masses of proletarians alike lesser gods. The identification of different nosological entities of dust-related diseases, the discovery that the most harmful dust particles in gold mines were invisible, insurance compensation and the development of the silicosis threshold limit value were all subjects of intense political negotiation that accompanied, with the connivance of doctors and scientists, a compromise between the health of workers and the economic health of industry. The preference for damage compensation (insurance system) over risk prevention (industrial hygienic measures) was also asserted and maintained in post-war Italy. Decline and modification of silicosis in Italy proceeded at the same rate as the introduction and subsequent application of more effective preventative legislation, especially with the protest movements of the working class at the end of the 1960s, together with the elimination of entire sectors of industrial activities, first those specialising in extraction and then the metallurgy. PMID:16001517

  7. Primary osteoarthritis of the hip: a genetic disease caused by European genetic variants.

    PubMed

    Hoaglund, Franklin T

    2013-03-01

    Primary osteoarthritis of the hip is a separate phenotype that occurs at a rate of 3% to 6% in the populations of the world with European ancestry. In all non-European populations, there is a consistent rarity of primary osteoarthritis that suggests a different etiology for these few patients. Family, sibling, and twin studies prove primary osteoarthritis to be a genetic disease with a 50% heritability caused by European genetic variants. The genetic basis is reinforced by the lower rate of primary osteoarthritis in American minorities consistent with their degree of European gene admixture. Whether the mechanism of degeneration of primary osteoarthritis may be secondary through a morphologic deformity, such as femoroacetabular impingement, remains unknown. The virtual absence of the disease in non-Europeans indicates that the European gene component is necessary for the expression of this separate phenotype of osteoarthritis. PMID:23467870

  8. Mycobacterium avium subspecies paratuberculosis in the etiology of Crohn’s disease, cause or epiphenomenon?

    PubMed Central

    Liverani, Elisa; Scaioli, Eleonora; Cardamone, Carla; Dal Monte, Paola; Belluzzi, Andrea

    2014-01-01

    The origin of inflammatory bowel disease is unknown. Attempts have been made to isolate a microorganism that could explain the onset of inflammation, but no pathological agent has ever been identified. Johne’s disease is a granulomatous chronic enteritis of cattle and sheep caused by Mycobacterium avium subspecies paratuberculosis (MAP) and shows some analogies with Crohn’s disease (CD). Several studies have tried to clarify if MAP has a role in the etiology of CD. The present article provides an overview of the evidence in favor and against the “MAP-hypothesis”, analyzing the methods commonly adopted to detect MAP and the role of antimycobacterial therapy in patients with inflammatory bowel disease. Studies were identified through the electronic database, MEDLINE, and were selected based on their relevance to the objective of the review. The presence of MAP was investigated using multiple diagnostic methods for MAP detection and in different tissue samples from patients affected by CD or ulcerative colitis and in healthy controls. On the basis of their studies, several authors support a close relationship between MAP and CD. Although increasing evidence of MAP detection in CD patients is unquestionable, a clear etiological link still needs to be proven. PMID:25278700

  9. Mycobacterium avium subspecies paratuberculosis in the etiology of Crohn's disease, cause or epiphenomenon?

    PubMed

    Liverani, Elisa; Scaioli, Eleonora; Cardamone, Carla; Dal Monte, Paola; Belluzzi, Andrea

    2014-09-28

    The origin of inflammatory bowel disease is unknown. Attempts have been made to isolate a microorganism that could explain the onset of inflammation, but no pathological agent has ever been identified. Johne's disease is a granulomatous chronic enteritis of cattle and sheep caused by Mycobacterium avium subspecies paratuberculosis (MAP) and shows some analogies with Crohn's disease (CD). Several studies have tried to clarify if MAP has a role in the etiology of CD. The present article provides an overview of the evidence in favor and against the "MAP-hypothesis", analyzing the methods commonly adopted to detect MAP and the role of antimycobacterial therapy in patients with inflammatory bowel disease. Studies were identified through the electronic database, MEDLINE, and were selected based on their relevance to the objective of the review. The presence of MAP was investigated using multiple diagnostic methods for MAP detection and in different tissue samples from patients affected by CD or ulcerative colitis and in healthy controls. On the basis of their studies, several authors support a close relationship between MAP and CD. Although increasing evidence of MAP detection in CD patients is unquestionable, a clear etiological link still needs to be proven. PMID:25278700

  10. The probable cause of civilization diseases and the structural limits of pleasure.

    PubMed

    Gracia, M C

    2009-11-01

    This article provides a theoretical basis and experimental evidence for the following rules: (1) All mental activities involving some level of intelligence ultimately follow the laws of operant conditioning and can exert a long-term control of behaviour only if they regularly provide the midbrain centres with the minimal set of neural rewards that these centres expect (2) Mental activity is always accompanied by a proportional amount of efferent-controlled physiological activity, which may be, for example, voluntary muscular work, but also internal, possibly surreptitious phenomena like inflammation, immune reactions, blood pressure increase, etc. These rules provide an explanation for most 'civilization' diseases whose ultimate causes are currently unknown or uncontrollable, e.g. cardiovascular troubles, cancer, allergies, auto-immune disorders, non-congenital degenerative diseases, neural dysfunctions including Alzheimer and Parkinson diseases, ALS or multiple sclerosis, emotional troubles including depression, cyclothymic/bipolar disorders, uncontrollable compulsions, etc. Potentially, this explanation also provides a cure for all these diseases as long as there is no accumulation of many of them because, for example, of very advanced age, and only if we are ready to adopt a philosophy of happiness based on moderation and appreciation of the value of life, dignity and empathy, instead of attempting an unlimited accumulation of pleasure, which does not seem neurologically viable. PMID:19527923

  11. Chimpanzee deaths at Mahale caused by a flu-like disease.

    PubMed

    Hanamura, Shunkichi; Kiyono, Mieko; Lukasik-Braum, Magdalena; Mlengeya, Titus; Fujimoto, Mariko; Nakamura, Michio; Nishida, Toshisada

    2008-01-01

    A flu-like disease spread among chimpanzees (Pan troglodytes schweinfurthii) of the M group at Mahale Mountains National Park, Tanzania, from June to July 2006. This epizootic or epidemic killed up to 12 chimpanzees. The obvious evidence of their deaths came from finding the bodies of three infants who had previously shown some symptoms of the disease. At least one of these infants died of pneumonia. In addition, nine chimpanzees were missing after the outbreak. These individuals were assumed to have been killed by this epizootic because most of them had contact with the infected individuals on the last days they were observed. We also found two dead bodies during this period, which were thought to be those of two missing individuals. We confirmed 23 (35.4%) of 65 individuals of the M group showed some symptoms of the disease, although most of them (20/23) did not die. More than half of them (14/23) had kin showing symptoms. Since this epizootic may have been caused by contact with humans, it will be necessary to establish and follow appropriate protocols for researchers, tourists, and park staff to observe chimpanzees, and to explore the mechanism of disease transmission from humans to chimpanzees and among chimpanzees. PMID:17721678

  12. Shining Light on the Cause of Alzheimer's Disease (411th Brookhaven Lecture)

    SciTech Connect

    Miller, Lisa

    2006-01-18

    Alzheimer’s disease is a progressive brain disorder that gradually destroys a person’s memory and ability to learn, reason, communicate and carry out daily activities. An estimated 4.5 million Americans have it, a number that is expected to triple over the next 50 years. Today, one in ten people aged 65 and half of people over 85 are affected. The cause of Alzheimer’s disease is thought to involve the formation of “plaques” — tiny aggregates of a naturally occurring, but misfolded or misshapen protein — in the brain. Recently, the formation of these plaques has been associated with the binding of metal ions such as iron, copper, and zinc. Yet the function of these metal ions and the misfolded proteins in the disease process is not well understood. Now, synchrotron infrared and x-ray microscopes are used to image the protein structure and metal content in the Alzheimer’s-affected brain tissue, providing a better understanding of how the disease occurs and potential ways of preventing it in the future.

  13. Expert-Novice Differences in Mental Models of Viruses, Vaccines, and the Causes of Infectious Disease

    PubMed Central

    Jee, Benjamin D.; Uttal, David H.; Spiegel, Amy; Diamond, Judy

    2014-01-01

    Humans are exposed to viruses everywhere they live, play, and work. Yet people’s beliefs about viruses may be confused or inaccurate, potentially impairing their understanding of scientific information. This study used semi-structured interviews to examine people’s beliefs about viruses, vaccines, and the causes of infectious disease. We compared people at different levels of science expertise: middle school students, teachers, and professional virologists. The virologists described more entities involved in microbiological processes, how these entities behaved, and why. Quantitative and qualitative analyses revealed distinctions in the cognitive organization of several concepts, including infection and vaccination. For example, some students and teachers described viral replication in terms of cell division, independent of a host. Interestingly, most students held a mental model for vaccination in which the vaccine directly attacks a virus that is present in the body. Our findings have immediate implications for how to communicate about infectious disease to young people. PMID:23959975

  14. Eosinophilic meningitis caused by Angiostrongylus cantonensis: an emergent disease in Brazil

    PubMed Central

    Morassutti, Alessandra Loureiro; Thiengo, Silvana Carvalho; Fernandez, Monica; Sawanyawisuth, Kittisak; Graeff-Teixeira, Carlos

    2014-01-01

    Eosinophilic meningitis (EoM) is an acute disease that affects the central nervous system. It is primarily caused by infection with the nematode Angiostrongylus cantonensis. This infection was previously restricted to certain Asian countries and the Pacific Islands, but it was first reported in Brazil in 2007. Since then, intermediate and definitive hosts infected with A. cantonensis have been identified within the urban areas of many states in Brazil, including those in the northern, northeastern, southeastern and southern regions. The goals of this review are to draw the attention of the medical community and health centres to the emergence of EoM in Brazil, to compile information about several aspects of the human infection and mode of transmission and to provide a short protocol of procedures for the diagnosis of this disease. PMID:25075779

  15. Exome sequencing reveals riboflavin transporter mutations as a cause of motor neuron disease.

    PubMed

    Johnson, Janel O; Gibbs, J Raphael; Megarbane, Andre; Urtizberea, J Andoni; Hernandez, Dena G; Foley, A Reghan; Arepalli, Sampath; Pandraud, Amelie; Simón-Sánchez, Javier; Clayton, Peter; Reilly, Mary M; Muntoni, Francesco; Abramzon, Yevgeniya; Houlden, Henry; Singleton, Andrew B

    2012-09-01

    Brown-Vialetto-Van Laere syndrome was first described in 1894 as a rare neurodegenerative disorder characterized by progressive sensorineural deafness in combination with childhood amyotrophic lateral sclerosis. Mutations in the gene, SLC52A3 (formerly C20orf54), one of three known riboflavin transporter genes, have recently been shown to underlie a number of severe cases of Brown-Vialetto-Van Laere syndrome; however, cases and families with this disease exist that do not appear to be caused by SLC52A3 mutations. We used a combination of linkage and exome sequencing to identify the disease causing mutation in an extended Lebanese Brown-Vialetto-Van Laere kindred, whose affected members were negative for SLC52A3 mutations. We identified a novel mutation in a second member of the riboflavin transporter gene family (gene symbol: SLC52A2) as the cause of disease in this family. The same mutation was identified in one additional subject, from 44 screened. Within this group of 44 patients, we also identified two additional cases with SLC52A3 mutations, but none with mutations in the remaining member of this gene family, SLC52A1. We believe this strongly supports the notion that defective riboflavin transport plays an important role in Brown-Vialetto-Van Laere syndrome. Initial work has indicated that patients with SLC52A3 defects respond to riboflavin treatment clinically and biochemically. Clearly, this makes an excellent candidate therapy for the SLC52A2 mutation-positive patients identified here. Initial riboflavin treatment of one of these patients shows promising results. PMID:22740598

  16. Exome sequencing reveals riboflavin transporter mutations as a cause of motor neuron disease

    PubMed Central

    Johnson, Janel O.; Gibbs, J. Raphael; Megarbane, Andre; Urtizberea, J. Andoni; Hernandez, Dena G.; Foley, A. Reghan; Arepalli, Sampath; Pandraud, Amelie; Simón-Sánchez, Javier; Clayton, Peter; Reilly, Mary M.; Muntoni, Francesco; Abramzon, Yevgeniya; Houlden, Henry

    2012-01-01

    Brown–Vialetto–Van Laere syndrome was first described in 1894 as a rare neurodegenerative disorder characterized by progressive sensorineural deafness in combination with childhood amyotrophic lateral sclerosis. Mutations in the gene, SLC52A3 (formerly C20orf54), one of three known riboflavin transporter genes, have recently been shown to underlie a number of severe cases of Brown–Vialetto–Van Laere syndrome; however, cases and families with this disease exist that do not appear to be caused by SLC52A3 mutations. We used a combination of linkage and exome sequencing to identify the disease causing mutation in an extended Lebanese Brown–Vialetto–Van Laere kindred, whose affected members were negative for SLC52A3 mutations. We identified a novel mutation in a second member of the riboflavin transporter gene family (gene symbol: SLC52A2) as the cause of disease in this family. The same mutation was identified in one additional subject, from 44 screened. Within this group of 44 patients, we also identified two additional cases with SLC52A3 mutations, but none with mutations in the remaining member of this gene family, SLC52A1. We believe this strongly supports the notion that defective riboflavin transport plays an important role in Brown–Vialetto–Van Laere syndrome. Initial work has indicated that patients with SLC52A3 defects respond to riboflavin treatment clinically and biochemically. Clearly, this makes an excellent candidate therapy for the SLC52A2 mutation-positive patients identified here. Initial riboflavin treatment of one of these patients shows promising results. PMID:22740598

  17. Deletion of the meq gene significantly decreases immunosuppression in chickens caused by pathogenic marek's disease virus

    PubMed Central

    2011-01-01

    Background Marek's disease virus (MDV) causes an acute lymphoproliferative disease in chickens, resulting in immunosuppression, which is considered to be an integral aspect of the pathogenesis of Marek's disease (MD). A recent study showed that deletion of the Meq gene resulted in loss of transformation of T-cells in chickens and a Meq-null virus, rMd5ΔMeq, could provide protection superior to CVI988/Rispens. Results In the present study, to investigate whether the Meq-null virus could be a safe vaccine candidate, we constructed a Meq deletion strain, GX0101ΔMeq, by deleting both copies of the Meq gene from a pathogenic MDV, GX0101 strain, which was isolated in China. Pathogenesis experiments showed that the GX0101ΔMeq virus was fully attenuated in specific pathogen-free chickens because none of the infected chickens developed Marek's disease-associated lymphomas. The study also evaluated the effects of GX0101ΔMeq on the immune system in chickens after infection with GX0101ΔMeq virus. Immune system variables, including relative lymphoid organ weight, blood lymphocytes and antibody production following vaccination against AIV and NDV were used to assess the immune status of chickens. Experimental infection with GX0101ΔMeq showed that deletion of the Meq gene significantly decreased immunosuppression in chickens caused by pathogenic MDV. Conclusion These findings suggested that the Meq gene played an important role not only in tumor formation but also in inducing immunosuppressive effects in MDV-infected chickens. PMID:21205328

  18. Development of low-density oligonucleotide microarrays for detecting mutations causing Wilson's disease

    PubMed Central

    Mathur, Manjula; Singh, Ekta; Poduval, T.B.; Rao, Akkipeddi V.S.S.N.

    2015-01-01

    Background & objectives: Wilson's disease (WD) is an autosomal recessive disorder caused by mutations in ATP7B, a copper transporter gene, leading to hepatic and neuropsychiatric manifestations due to copper accumulation. If diagnosed early, WD patients can be managed by medicines reducing morbidity and mortality. Diagnosis of this disease requires a combination of tests and at times is inconclusive due to overlap of the symptoms with other disorders. Genetic testing is the preferred alternative in such cases particularly for individuals with a family history. Use of DNA microarray for detecting mutations in ATP7B gene is gaining popularity because of the advantages it offers in terms of throughput and sensitivity. This study attempts to establish the quality analysis procedures for microarray based diagnosis of Wilson's disease. Methods: A home-made microarrayer was used to print oligonucleotide based low-density microarrays for addressing 62 mutations causing Wilson's disease reported from Indian population. Inter- and intra- array comparisons were used to study quality of the arrays. The arrays were validated by using mutant samples generated by site directed mutagenesis. Results: The hybridization reaction were found to be consistent across the surface of a given microarray. Our results have shown that 52 °C post-hybridization wash yields better reproducibility across experiments compared to 42 °C. Our arrays have shown > 80 per cent sensitivity in detecting these 62 mutations. Interpretation & conclusions: The present results demonstrate the design and evaluation of a low-density microarray for the detection of 62 mutations in ATP7B gene, and show that a microarray based approach can be cost-effective for detecting a large number of mutations simultaneously. This study also provides information on some of the important parameters required for microarray based diagnosis of genetic disorders. PMID:25900953

  19. Changes in insulin and insulin signaling in Alzheimer's disease: cause or consequence?

    PubMed

    Stanley, Molly; Macauley, Shannon L; Holtzman, David M

    2016-07-25

    Individuals with type 2 diabetes have an increased risk for developing Alzheimer's disease (AD), although the causal relationship remains poorly understood. Alterations in insulin signaling (IS) are reported in the AD brain. Moreover, oligomers/fibrils of amyloid-β (Aβ) can lead to neuronal insulin resistance and intranasal insulin is being explored as a potential therapy for AD. Conversely, elevated insulin levels (ins) are found in AD patients and high insulin has been reported to increase Aβ levels and tau phosphorylation, which could exacerbate AD pathology. Herein, we explore whether changes in ins and IS are a cause or consequence of AD. PMID:27432942

  20. Is Chronic Obstructive Pulmonary Disease Caused by Wood Smoke a Different Phenotype or a Different Entity?

    PubMed

    Torres-Duque, Carlos A; García-Rodriguez, María Carmen; González-García, Mauricio

    2016-08-01

    Around 40% of the world's population continue using solid fuel, including wood, for cooking or heating their homes. Chronic exposure to wood smoke is a risk factor for developing chronic obstructive pulmonary disease (COPD). In some regions of the world, this can be a more important cause of COPD than exposure to tobacco smoke from cigarettes. Significant differences between COPD associated with wood smoke (W-COPD) and that caused by smoking (S-COPD) have led some authors to suggest that W-COPD should be considered a new COPD phenotype. We present a review of the differences between W-COPD and S-COPD. On the premise that wood smoke and tobacco smoke are not the same and the physiopathological mechanisms they induce may differ, we have analyzed whether W-COPD can be considered as another COPD phenotype or a distinct nosological entity. PMID:27207325

  1. Epidemiology of Foodborne Disease Outbreaks Caused by Clostridium perfringens, United States, 1998–2010

    PubMed Central

    Grass, Julian E.; Gould, L. Hannah; Mahon, Barbara E.

    2015-01-01

    Clostridium perfringens is estimated to be the second most common bacterial cause of foodborne illness in the United States, causing one million illnesses each year. Local, state, and territorial health departments voluntarily report C. perfringens outbreaks to the U.S. Centers for Disease Control and Prevention through the Foodborne Disease Outbreak Surveillance System. Our analysis included outbreaks confirmed by laboratory evidence during 1998–2010. A food item was implicated if C. perfringens was isolated from food or based on epidemiologic evidence. Implicated foods were classified into one of 17 standard food commodities when possible. From 1998 to 2010, 289 confirmed outbreaks of C. perfringens illness were reported with 15,208 illnesses, 83 hospitalizations, and eight deaths. The number of outbreaks reported each year ranged from 16 to 31 with no apparent trend over time. The annual number of outbreak-associated illnesses ranged from 359 to 2,173, and the median outbreak size was 24 illnesses. Outbreaks occurred year round, with the largest number in November and December. Restaurants (43%) were the most common setting of food preparation. Other settings included catering facility (19%), private home (16%), prison or jail (11%), and other (10%). Among the 144 (50%) outbreaks attributed to a single food commodity, beef was the most common commodity (66 outbreaks, 46%), followed by poultry (43 outbreaks, 30%), and pork (23 outbreaks, 16%). Meat and poultry outbreaks accounted for 92% of outbreaks with an identified single food commodity. Outbreaks caused by C. perfringens occur regularly, are often large, and can cause substantial morbidity yet are preventable if contamination of raw meat and poultry products is prevented at the farm or slaughterhouse or, after contamination, if these products are properly handled and prepared, particularly in restaurants and catering facilities. PMID:23379281

  2. Whole grain consumption and risk of cardiovascular disease, cancer, and all cause and cause specific mortality: systematic review and dose-response meta-analysis of prospective studies

    PubMed Central

    Keum, NaNa; Giovannucci, Edward; Fadnes, Lars T; Boffetta, Paolo; Greenwood, Darren C; Tonstad, Serena; Vatten, Lars J; Riboli, Elio; Norat, Teresa

    2016-01-01

    Objective To quantify the dose-response relation between consumption of whole grain and specific types of grains and the risk of cardiovascular disease, total cancer, and all cause and cause specific mortality. Data sources PubMed and Embase searched up to 3 April 2016. Study selection Prospective studies reporting adjusted relative risk estimates for the association between intake of whole grains or specific types of grains and cardiovascular disease, total cancer, all cause or cause specific mortality. Data synthesis Summary relative risks and 95% confidence intervals calculated with a random effects model. Results 45 studies (64 publications) were included. The summary relative risks per 90 g/day increase in whole grain intake (90 g is equivalent to three servings—for example, two slices of bread and one bowl of cereal or one and a half pieces of pita bread made from whole grains) was 0.81 (95% confidence interval 0.75 to 0.87; I2=9%, n=7 studies) for coronary heart disease, 0.88 (0.75 to 1.03; I2=56%, n=6) for stroke, and 0.78 (0.73 to 0.85; I2=40%, n=10) for cardiovascular disease, with similar results when studies were stratified by whether the outcome was incidence or mortality. The relative risks for morality were 0.85 (0.80 to 0.91; I2=37%, n=6) for total cancer, 0.83 (0.77 to 0.90; I2=83%, n=11) for all causes, 0.78 (0.70 to 0.87; I2=0%, n=4) for respiratory disease, 0.49 (0.23 to 1.05; I2=85%, n=4) for diabetes, 0.74 (0.56 to 0.96; I2=0%, n=3) for infectious diseases, 1.15 (0.66 to 2.02; I2=79%, n=2) for diseases of the nervous system disease, and 0.78 (0.75 to 0.82; I2=0%, n=5) for all non-cardiovascular, non-cancer causes. Reductions in risk were observed up to an intake of 210-225 g/day (seven to seven and a half servings per day) for most of the outcomes. Intakes of specific types of whole grains including whole grain bread, whole grain breakfast cereals, and added bran, as well as total bread and total breakfast cereals were also associated

  3. Mortality from Parkinson's disease and other causes among a workforce manufacturing paraquat: a retrospective cohort study

    PubMed Central

    Campbell, Clive

    2011-01-01

    Objective To assess the risk of Parkinson's disease (PD) and update information on mortality from major causes of death among a UK workforce who manufactured paraquat (PQ) between 1961 and 1995. There have been no previous studies of the incidence of PD among PQ production workers, although much epidemiological literature exists concerning the relationship between pesticides and PD, and interest has focused on PQ and its users. Methods The cohort included all employees who had ever worked on any of the four plants at Widnes where PQ was manufactured between 1961 and 1995, and 926 male and 42 female workers were followed through 30 June 2009. Mortalities for males were compared with national and local rates, including rates for PD as a mentioned cause of death. Results Overall, 307 workers had died by 30 June 2009. One male death was due to PD, and no other death certificate mentioned PD. At least 3.3 death certificates of male employees would have been expected to have mentioned PD (standardised mortality ratio=31; 95% CI 1 to 171). Personal monitoring results were indicative that the exposure of a PQ production worker on a daily basis was at least comparable with that of a PQ sprayer or mixer/loader. Reduced mortalities compared with local rates were found for major causes of death. Conclusions The study provided no evidence of an increased risk of PD, or increased mortalities from other causes. PMID:22080539

  4. Difficulties experienced in defining the microbial cause of pelvic inflammatory disease.

    PubMed

    Taylor-Robinson, D; Jensen, J S; Svenstrup, H; Stacey, C M

    2012-01-01

    Clinical assessment of women with pelvic pain was a poor indicator of disease seen at laparoscopy. Thus, of 109 women, 22 at laparoscopy had salpingitis, 19 had adhesions without salpingitis, 20 had endometriosis or ovarian pathology and 48 no observable abnormality. In all laparoscopic categories, Ureaplasma spp. and Mycoplasma hominis, but not Mycoplasma genitalium, were at least as common in the cervix/vagina as Chlamydia trachomatis and equally frequent in the endometrium. However, C. trachomatis had the greatest propensity for spread to the Fallopian tubes. Thus, of 28 women who had C. trachomatis organisms in the vagina/cervix, 13 had them in a Fallopian tube (ratio 2.2:1); the ratio was 6:1 for Neisseria gonorrhoeae, 8:1 for M. genitalium, 21:1 for M. hominis and 31:1 for Ureaplasma spp. M. hominis organisms in a large number were detected most often in women with salpingitis. The likelihood of spread of Ureaplasma urealyticum and U. parvum from the lower to the upper genital tract was about the same and they were detected only once each in a tube, which was not inflamed in either case. Multiple bacteria were often detected at a single site, making it difficult to establish the exact cause of disease. However N. gonorrhoeae was considered to be the sole cause of salpingitis in one woman and the primary or equal primary contributor in four others; C. trachomatis was involved in at least 11 women, mostly as the sole cause or as the primary contributor; M. genitalium was considered the cause in one woman and had possible involvement in three others; and M. hominis was a questionable sole cause in one woman and the primary or equal primary contributor in three. Serologically, C. trachomatis was related to adhesions, without salpingitis, more often (63%) than any other micro-organism. M. genitalium may have been implicated in one case. Serologically, a previous C. trachomatis infection was indicated in 40% of women without an observable laparoscopic abnormality

  5. Escalating chronic kidney diseases of multi-factorial origin in Sri Lanka: causes, solutions, and recommendations.

    PubMed

    Wimalawansa, Sunil J

    2014-11-01

    During the last two decades, Sri Lanka, located close to the equator, has experienced an escalating incidence of chronic kidney disease (CKD) of unknown aetiology (CKDue) in dry zonal areas. Similar incidences of unusual CKDs have been reported in the dry zonal, agricultural areas of several other equatorial countries. In Sri Lanka, the incidence of CKDue is highest in the North Central Province (NCP), where approximately 45 % of the country's paddy fields are located. However, in recent years, the disease has spread into areas adjacent to as well as distant from the NCP. The cause of CKD in Sri Lanka is unknown, and may likely due to interactions of different potential agents; thus, CKD is of multi-factorial origin (CKD-mfo). These factors include, the negative effects from overuse of agrochemicals. Nevertheless, the potential interactions and synergism between probable agents have not been studied. This systematic review discusses the proposed hypotheses and causes of CKD-mfo in Sri Lanka, and ways to decrease the incidence of this disease and to eradicate it, and provide some recommendations. During the past decade, a number of groups have investigated this disorder using different methodologies and reported various correlations, but failed to find a cause. Research has focussed on the contamination of water with heavy metals, agrochemicals, hard water, algae, ionicity, climate change, and so forth. Nevertheless, the levels of any of the pollutants or conditions reported in water in NPC are inconsistent not correlated with the prevalence of the disease, and are too low to be the sole cause of CKD-mfo. Meanwhile, several nephrotoxins prevalent in the region, including medications, leptospirosis, toxic herbs, illicit alcohol, locally grown tobacco, and petrochemicals, as well as the effects of changed habits occured over the past four decades have not been studied to date. Taken together, the geographical distribution and overall findings indicate that

  6. Identification of virulence genes in the crucifer anthracnose fungus Colletotrichum higginsianum by insertional mutagenesis.

    PubMed

    Liu, Liping; Zhao, Dian; Zheng, Lu; Hsiang, Tom; Wei, Yangdou; Fu, Yanping; Huang, Junbin

    2013-11-01

    To investigate the molecular and genetic mechanisms underlying virulence of Colletotrichum higginsianum on Arabidopsis thaliana, a T-DNA insertion mutant library of C. higginsianum, the causal agent of crucifer anthracnose, was established using Agrobacterium tumefaciens-mediated transformation. Among 875 transformants tested for virulence on Arabidopsis, six mutants with altered virulence, including an appressorial melanin-deficient mutant T734, two mutants defective in penetration, T45 and B30, and three mutants, T679, T732 and T801, that cause hypersensitive reactions on host Arabidopsis, were obtained. Southern blot analysis indicated that the mutants T732 and T734 harbored single-site T-DNA integrations, while B30 harbored two T-DNA insertions. Border flanking sequences of T-DNAs from these mutants were recovered by inverse polymerase chain reaction (PCR) and thermal asymmetric interlaced PCR. Sequence analyses revealed that single T-DNA insertions in mutant T734 targeted the coding region of a gene with unknown function, and in mutant T732 targeted a gene encoding a copper amine oxidase. The two T-DNA insertion sites in mutant B30 were found in the coding region of a gene encoding an exosome component and in the upstream region of a DUF221-domain gene. None of these genes have previously been implicated in virulence of the phytopathogenic fungi. Among these avirulent mutants, T734 showed altered color in colony growth and produced melanin-deficient, albino appressoria. The T-DNA insert in T734 was detected in the coding region of a gene named C. higginsianum melanin-deficiency gene (Ch-MEL1), which is highly similar to a gene encoding a hypothetical protein in Colletotrichum gloeosporioides (GenBank ELA33048). To validate whether the Ch-MEL1 gene was associated with virulence of the mutant T734, a targeted gene disruption and complementation approach was used. The appressoria of ▵Ch-mel1 null mutants were defective in melanization and failed to penetrate

  7. Human pathogen shown to cause disease in the threatened eklhorn coral Acropora palmata.

    PubMed

    Sutherland, Kathryn Patterson; Shaban, Sameera; Joyner, Jessica L; Porter, James W; Lipp, Erin K

    2011-01-01

    Coral reefs are in severe decline. Infections by the human pathogen Serratia marcescens have contributed to precipitous losses in the common Caribbean elkhorn coral, Acropora palmata, culminating in its listing under the United States Endangered Species Act. During a 2003 outbreak of this coral disease, called acroporid serratiosis (APS), a unique strain of the pathogen, Serratia marcescens strain PDR60, was identified from diseased A. palmata, human wastewater, the non-host coral Siderastrea siderea and the corallivorous snail Coralliophila abbreviata. In order to examine humans as a source and other marine invertebrates as vectors and/or reservoirs of the APS pathogen, challenge experiments were conducted with A. palmata maintained in closed aquaria to determine infectivity of strain PDR60 from reef and wastewater sources. Strain PDR60 from wastewater and diseased A. palmata caused disease signs in elkhorn coral in as little as four and five days, respectively, demonstrating that wastewater is a definitive source of APS and identifying human strain PDR60 as a coral pathogen through fulfillment of Koch's postulates. A. palmata inoculated with strain PDR60 from C. abbreviata showed limited virulence, with one of three inoculated fragments developing APS signs within 13 days. Strain PDR60 from non-host coral S. siderea showed a delayed pathogenic effect, with disease signs developing within an average of 20 days. These results suggest that C. abbreviata and non-host corals may function as reservoirs or vectors of the APS pathogen. Our results provide the first example of a marine "reverse zoonosis" involving the transmission of a human pathogen (S. marcescens) to a marine invertebrate (A. palmata). These findings underscore the interaction between public health practices and environmental health indices such as coral reef survival. PMID:21858132

  8. Atherosclerosis and Alzheimer - diseases with a common cause? Inflammation, oxysterols, vasculature

    PubMed Central

    2014-01-01

    Background Aging is accompanied by increasing vulnerability to pathologies such as atherosclerosis (ATH) and Alzheimer disease (AD). Are these different pathologies, or different presentations with a similar underlying pathoetiology? Discussion Both ATH and AD involve inflammation, macrophage infiltration, and occlusion of the vasculature. Allelic variants in common genes including APOE predispose to both diseases. In both there is strong evidence of disease association with viral and bacterial pathogens including herpes simplex and Chlamydophila. Furthermore, ablation of components of the immune system (or of bone marrow-derived macrophages alone) in animal models restricts disease development in both cases, arguing that both are accentuated by inflammatory/immune pathways. We discuss that amyloid β, a distinguishing feature of AD, also plays a key role in ATH. Several drugs, at least in mouse models, are effective in preventing the development of both ATH and AD. Given similar age-dependence, genetic underpinnings, involvement of the vasculature, association with infection, Aβ involvement, the central role of macrophages, and drug overlap, we conclude that the two conditions reflect different manifestations of a common pathoetiology. Mechanism Infection and inflammation selectively induce the expression of cholesterol 25-hydroxylase (CH25H). Acutely, the production of ‘immunosterol’ 25-hydroxycholesterol (25OHC) defends against enveloped viruses. We present evidence that chronic macrophage CH25H upregulation leads to catalyzed esterification of sterols via 25OHC-driven allosteric activation of ACAT (acyl-CoA cholesterol acyltransferase/SOAT), intracellular accumulation of cholesteryl esters and lipid droplets, vascular occlusion, and overt disease. Summary We postulate that AD and ATH are both caused by chronic immunologic challenge that induces CH25H expression and protection against particular infectious agents, but at the expense of longer-term pathology

  9. ALS5/SPG11/KIAA1840 mutations cause autosomal recessive axonal Charcot-Marie-Tooth disease.

    PubMed

    Montecchiani, Celeste; Pedace, Lucia; Lo Giudice, Temistocle; Casella, Antonella; Mearini, Marzia; Gaudiello, Fabrizio; Pedroso, José L; Terracciano, Chiara; Caltagirone, Carlo; Massa, Roberto; St George-Hyslop, Peter H; Barsottini, Orlando G P; Kawarai, Toshitaka; Orlacchio, Antonio

    2016-01-01

    Charcot-Marie-Tooth disease is a group of hereditary peripheral neuropathies that share clinical characteristics of progressive distal muscle weakness and atrophy, foot deformities, distal sensory loss, as well as diminished tendon reflexes. Hundreds of causative DNA changes have been found, but much of the genetic basis of the disease is still unexplained. Mutations in the ALS5/SPG11/KIAA1840 gene are a frequent cause of autosomal recessive hereditary spastic paraplegia with thin corpus callosum and peripheral axonal neuropathy, and account for ∼ 40% of autosomal recessive juvenile amyotrophic lateral sclerosis. The overlap of axonal Charcot-Marie-Tooth disease with both diseases, as well as the common autosomal recessive inheritance pattern of thin corpus callosum and axonal Charcot-Marie-Tooth disease in three related patients, prompted us to analyse the ALS5/SPG11/KIAA1840 gene in affected individuals with autosomal recessive axonal Charcot-Marie-Tooth disease. We investigated 28 unrelated families with autosomal recessive axonal Charcot-Marie-Tooth disease defined by clinical, electrophysiological, as well as pathological evaluation. Besides, we screened for all the known genes related to axonal autosomal recessive Charcot-Marie-Tooth disease (CMT2A2/HMSN2A2/MFN2, CMT2B1/LMNA, CMT2B2/MED25, CMT2B5/NEFL, ARCMT2F/dHMN2B/HSPB1, CMT2K/GDAP1, CMT2P/LRSAM1, CMT2R/TRIM2, CMT2S/IGHMBP2, CMT2T/HSJ1, CMTRID/COX6A1, ARAN-NM/HINT and GAN/GAN), for the genes related to autosomal recessive hereditary spastic paraplegia with thin corpus callosum and axonal peripheral neuropathy (SPG7/PGN, SPG15/ZFYVE26, SPG21/ACP33, SPG35/FA2H, SPG46/GBA2, SPG55/C12orf65 and SPG56/CYP2U1), as well as for the causative gene of peripheral neuropathy with or without agenesis of the corpus callosum (SLC12A6). Mitochondrial disorders related to Charcot-Marie-Tooth disease type 2 were also excluded by sequencing POLG and TYMP genes. An additional locus for autosomal recessive Charcot

  10. Animal models of Parkinson's disease: a source of novel treatments and clues to the cause of the disease

    PubMed Central

    Duty, Susan; Jenner, Peter

    2011-01-01

    Animal models of Parkinson's disease (PD) have proved highly effective in the discovery of novel treatments for motor symptoms of PD and in the search for clues to the underlying cause of the illness. Models based on specific pathogenic mechanisms may subsequently lead to the development of neuroprotective agents for PD that stop or slow disease progression. The array of available rodent models is large and ranges from acute pharmacological models, such as the reserpine- or haloperidol-treated rats that display one or more parkinsonian signs, to models exhibiting destruction of the dopaminergic nigro-striatal pathway, such as the classical 6-hydroxydopamine (6-OHDA) rat and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse models. All of these have provided test beds in which new molecules for treating the motor symptoms of PD can be assessed. In addition, the emergence of abnormal involuntary movements (AIMs) with repeated treatment of 6-OHDA-lesioned rats with L-DOPA has allowed for examination of the mechanisms responsible for treatment-related dyskinesia in PD, and the detection of molecules able to prevent or reverse their appearance. Other toxin-based models of nigro-striatal tract degeneration include the systemic administration of the pesticides rotenone and paraquat, but whilst providing clues to disease pathogenesis, these are not so commonly used for drug development. The MPTP-treated primate model of PD, which closely mimics the clinical features of PD and in which all currently used anti-parkinsonian medications have been shown to be effective, is undoubtedly the most clinically-relevant of all available models. The MPTP-treated primate develops clear dyskinesia when repeatedly exposed to L-DOPA, and these parkinsonian animals have shown responses to novel dopaminergic agents that are highly predictive of their effect in man. Whether non-dopaminergic drugs show the same degree of predictability of response is a matter of debate. As our

  11. Mitochondrial diseases caused by toxic compound accumulation: from etiopathology to therapeutic approaches.

    PubMed

    Di Meo, Ivano; Lamperti, Costanza; Tiranti, Valeria

    2015-10-01

    Mitochondrial disorders are a group of highly invalidating human conditions for which effective treatment is currently unavailable and characterized by faulty energy supply due to defective oxidative phosphorylation (OXPHOS). Given the complexity of mitochondrial genetics and biochemistry, mitochondrial inherited diseases may present with a vast range of symptoms, organ involvement, severity, age of onset, and outcome. Despite the wide spectrum of clinical signs and biochemical underpinnings of this group of dis-orders, some common traits can be identified, based on both pathogenic mechanisms and potential therapeutic approaches. Here, we will review two peculiar mitochondrial disorders, ethylmalonic encephalopathy (EE) and mitochondrial neurogastrointestinal encephalomyopathy (MNGIE), caused by mutations in the ETHE1 and TYMP nuclear genes, respectively. ETHE1 encodes for a mitochondrial enzyme involved in sulfide detoxification and TYMP for a cytosolic enzyme involved in the thymidine/deoxyuridine catabolic pathway. We will discuss these two clinical entities as a paradigm of mitochondrial diseases caused by the accumulation of compounds normally present in traces, which exerts a toxic and inhibitory effect on the OXPHOS system. PMID:26194912

  12. Mitochondrial diseases caused by toxic compound accumulation: from etiopathology to therapeutic approaches

    PubMed Central

    Di Meo, Ivano; Lamperti, Costanza; Tiranti, Valeria

    2015-01-01

    Mitochondrial disorders are a group of highly invalidating human conditions for which effective treatment is currently unavailable and characterized by faulty energy supply due to defective oxidative phosphorylation (OXPHOS). Given the complexity of mitochondrial genetics and biochemistry, mitochondrial inherited diseases may present with a vast range of symptoms, organ involvement, severity, age of onset, and outcome. Despite the wide spectrum of clinical signs and biochemical underpinnings of this group of dis-orders, some common traits can be identified, based on both pathogenic mechanisms and potential therapeutic approaches. Here, we will review two peculiar mitochondrial disorders, ethylmalonic encephalopathy (EE) and mitochondrial neurogastrointestinal encephalomyopathy (MNGIE), caused by mutations in the ETHE1 and TYMP nuclear genes, respectively. ETHE1 encodes for a mitochondrial enzyme involved in sulfide detoxification and TYMP for a cytosolic enzyme involved in the thymidine/deoxyuridine catabolic pathway. We will discuss these two clinical entities as a paradigm of mitochondrial diseases caused by the accumulation of compounds normally present in traces, which exerts a toxic and inhibitory effect on the OXPHOS system. PMID:26194912

  13. Bacteria causing important diseases of citrus utilise distinct modes of pathogenesis to attack a common host.

    PubMed

    Vojnov, Adrián Alberto; do Amaral, Alexandre Morais; Dow, John Maxwell; Castagnaro, Atilio Pedro; Marano, Marìa Rosa

    2010-06-01

    In this review, we summarise the current knowledge on three pathogens that exhibit distinct tissue specificity and modes of pathogenesis in citrus plants. Xanthomonas axonopodis pv. citri causes canker disease and invades the host leaf mesophyll tissue through natural openings and can also survive as an epiphyte. Xylella fastidiosa and Candidatus Liberibacter are vectored by insects and proliferate in the vascular system of the host, either in the phloem (Candidatus Liberibacter) or xylem (X. fastidiosa) causing variegated chlorosis and huanglongbing diseases, respectively. Candidatus Liberibacter can be found within host cells and is thus unique as an intracellular phytopathogenic bacterium. Genome sequence comparisons have identified groups of species-specific genes that may be associated with the particular lifestyle, mode of transmission or symptoms produced by each phytopathogen. In addition, components that are conserved amongst bacteria may have diverse regulatory actions underpinning the different bacterial lifestyles; one example is the divergent role of the Rpf/DSF cell-cell signalling system in X. citri and X. fastidiosa. Biofilm plays a key role in epiphytic fitness and canker development in X. citri and in the symptoms produced by X. fastidiosa. Bacterial aggregation may be associated with vascular occlusion of the xylem vessels and symptomatology of variegated chlorosis. PMID:20449739

  14. Alcohol binging causes peliosis hepatis during azathioprine therapy in Crohn's disease.

    PubMed

    Elsing, Christoph; Placke, Joerg; Herrmann, Thomas

    2007-09-14

    Patients with inflammatory bowel disease have normal life expectancy and, due to modern immunosuppressive therapies, also a normal quality of life. Since mostly young people are affected, their social behaviour suits this environment. Alcohol binging is an increasingly disturbing factor among young people. We describe a patient with Crohn's disease, treated with azathioprine, who developed peliosis hepatis after three epsiodes of alcohol binging. Liver toxicity was not observed previously during the course of the treatment. Azathioprine-induced peliosis hepatis is thought to be idiosyncratic in humans. From animal studies, however, it is clear that hepatic depletion of glutathione leads to azathioprine toxicity to the sinusoidal endothelial cells. Damage of these cells causes peliosis hepatis. Since alcohol binging leads to hepatic glutathione depletion, we conclude that in our patient the episodes of binging have reduced liver gluathione content and therefore this has increased azathioprine toxicity causing peliosis hepatis. The problem of alcohol binging has not yet been addressed in IBD patients undertaking immunosuppressive therapy. This should be reviewed in future considerations regarding patients advice. PMID:17729423

  15. Bud Rot Caused by Phytophthora palmivora: A Destructive Emerging Disease of Oil Palm.

    PubMed

    Torres, G A; Sarria, G A; Martinez, G; Varon, F; Drenth, A; Guest, D I

    2016-04-01

    Oomycetes from the genus Phytophthora are among the most important plant pathogens in agriculture. Epidemics caused by P. infestans precipitated the great Irish famine and had a major impact on society and human history. In the tropics, P. palmivora is a pathogen of many plant species including cacao (Theobroma cacao), citrus (Citrus sp.), durian (Durio zibethines), jackfruit (Artrocarpus heterophyllus), rubber (Hevea brasiliensis), and several palm species including coconut (Cocos nucifera), and the African oil palm (Elaeis guineensis) as determined recently. The first localized epidemics of bud rot in oil palm in Colombia were reported in 1964. However, recent epidemics of bud rot have destroyed more than 70,000 ha of oil palm in the Western and Central oil palm growing regions of Colombia. The agricultural, social, and economic implications of these outbreaks have been significant in Colombia. Identification of the pathogen after 100 years of investigating the disease in the world enabled further understanding of infection, expression of a range of symptoms, and epidemiology of the disease. This review examines the identification of P. palmivora as the cause of bud rot in Colombia, its epidemiology, and discusses the importance of P. palmivora as a major threat to oil palm plantings globally. PMID:26714102

  16. Human Hemorrhagic Fever Causing Arenaviruses: Molecular Mechanisms Contributing to Virus Virulence and Disease Pathogenesis

    PubMed Central

    Shao, Junjie; Liang, Yuying; Ly, Hinh

    2015-01-01

    Arenaviruses include multiple human pathogens ranging from the low-risk lymphocytic choriomeningitis virus (LCMV) to highly virulent hemorrhagic fever (HF) causing viruses such as Lassa (LASV), Junin (JUNV), Machupo (MACV), Lujo (LUJV), Sabia (SABV), Guanarito (GTOV), and Chapare (CHPV), for which there are limited preventative and therapeutic measures. Why some arenaviruses can cause virulent human infections while others cannot, even though they are isolated from the same rodent hosts, is an enigma. Recent studies have revealed several potential pathogenic mechanisms of arenaviruses, including factors that increase viral replication capacity and suppress host innate immunity, which leads to high viremia and generalized immune suppression as the hallmarks of severe and lethal arenaviral HF diseases. This review summarizes current knowledge of the roles of each of the four viral proteins and some known cellular factors in the pathogenesis of arenaviral HF as well as of some human primary cell-culture and animal models that lend themselves to studying arenavirus-induced HF disease pathogenesis. Knowledge gained from these studies can be applied towards the development of novel therapeutics and vaccines against these deadly human pathogens. PMID:26011826

  17. The nature and causes of chronic obstructive pulmonary disease: A historical perspective

    PubMed Central

    Warren, C Peter W

    2009-01-01

    Chronic obstructive pulmonary disease (COPD) is the currently favoured name for the diseases formerly known as emphysema and bronchitis. COPD has been recognized for more than 200 years. Its cardinal symptoms are cough, phlegm and dyspnea, and its pathology is characterized by enlarged airspaces and obstructed airways. In the 19th century, the diagnosis of COPD depended on its symptoms and signs of a hyperinflated chest, and reduced expiratory breath sounds. The airflow obstruction evident on spirometry was identified in that century, but did not enter into clinical practice. Bronchitis, and the mechanical forces required to overcome its obstruction, was believed to be responsible for emphysema, although the inflammation present was recognized. The causes of bronchitis, and hence emphysema, included atmospheric and domestic air pollution, as well as dusty occupations. Cigarette smoking only became recognized as the dominant cause in the 20th century. The lessons learned of the risks for COPD in 19th-century Britain are very pertinent to the world today. PMID:19262908

  18. Life-threatening hemorrhagic pneumonia caused by Stenotrophomonas maltophilia in the treatment of hematologic diseases.

    PubMed

    Mori, Minako; Tsunemine, Hiroko; Imada, Kazunori; Ito, Kiminari; Kodaka, Taiichi; Takahashi, Takayuki

    2014-06-01

    Since the late 1990s, Stenotrophomonas maltophilia (S. maltophilia) has become one of the most common nonfermenting Gram-negative bacilli that cause opportunistic infection. Patients with hematologic diseases are the most risky candidate for S. maltophilia pneumonia or sepsis because of chemotherapy-induced neutropenia or immunodeficiency. Frequent exposure to broad-spectrum antibiotics and prolonged insertion of central venous catheter further enhance the risk of S. maltophilia infection. One of the most severe S. maltophilia infections is hemorrhagic pneumonia. This type of infection is mostly fatal because of pulmonary alveolar hemorrhage that leads to acute respiratory failure. Furthermore, S. maltophilia exhibits a high-level intrinsic resistance to conventional antibiotics such as β-lactams and aminoglycosides and, more recently, the increasing acquired resistance to co-trimoxazole and quinolones. According to our experienced and previously reported cases, all of the patients with hemorrhagic pneumonia caused by S. maltophilia had a fatal course within a few days after the onset of the pneumonia. In this article, we perform a systematic review on a total 30 cases of hemorrhagic pneumonia induced by S. maltophilia from our institutions and the literature, and we describe its early diagnosis, prophylaxis, and recommended therapeutic strategy for the infection in the treatment of hematologic disease. PMID:24535696

  19. Deregulation of Fas ligand expression as a novel cause of autoimmune lymphoproliferative syndrome-like disease

    PubMed Central

    Nabhani, Schafiq; Ginzel, Sebastian; Miskin, Hagit; Revel-Vilk, Shoshana; Harlev, Dan; Fleckenstein, Bernhard; Hönscheid, Andrea; Oommen, Prasad T.; Kuhlen, Michaela; Thiele, Ralf; Laws, Hans-Jürgen; Borkhardt, Arndt; Stepensky, Polina; Fischer, Ute

    2015-01-01

    Autoimmune lymphoproliferative syndrome is frequently caused by mutations in genes involved in the Fas death receptor pathway, but for 20–30% of patients the genetic defect is unknown. We observed that treatment of healthy T cells with interleukin-12 induces upregulation of Fas ligand and Fas ligand-dependent apoptosis. Consistently, interleukin-12 could not induce apoptosis in Fas ligand-deficient T cells from patients with autoimmune lymphoproliferative syndrome. We hypothesized that defects in the interleukin-12 signaling pathway may cause a similar phenotype as that caused by mutations of the Fas ligand gene. To test this, we analyzed 20 patients with autoimmune lymphoproliferative syndrome of unknown cause by whole-exome sequencing. We identified a homozygous nonsense mutation (c.698G>A, p.R212*) in the interleukin-12/interleukin-23 receptor-component IL12RB1 in one of these patients. The mutation led to IL12RB1 protein truncation and loss of cell surface expression. Interleukin-12 and -23 signaling was completely abrogated as demonstrated by deficient STAT4 phosphorylation and interferon γ production. Interleukin-12-mediated expression of membrane-bound and soluble Fas ligand was lacking and basal expression was much lower than in healthy controls. The patient presented with the classical symptoms of autoimmune lymphoproliferative syndrome: chronic non-malignant, non-infectious lymphadenopathy, splenomegaly, hepatomegaly, elevated numbers of double-negative T cells, autoimmune cytopenias, and increased levels of vitamin B12 and interleukin-10. Sanger sequencing and whole-exome sequencing excluded the presence of germline or somatic mutations in genes known to be associated with the autoimmune lymphoproliferative syndrome. Our data suggest that deficient regulation of Fas ligand expression by regulators such as the interleukin-12 signaling pathway may be an alternative cause of autoimmune lymphoproliferative syndrome-like disease. PMID:26113417

  20. Phenotypic and Genotypic Characteristics of Neisseria meningitidis Disease-Causing Strains in Argentina, 2010

    PubMed Central

    Sorhouet-Pereira, Cecilia; Efron, Adriana; Gagetti, Paula; Faccone, Diego; Regueira, Mabel; Corso, Alejandra; Gabastou, Jean-Marc; Ibarz-Pavón, Ana Belén

    2013-01-01

    Phenotypic and genotypic characterization of 133 isolates of Neisseria meningitidis obtained from meningococcal disease cases in Argentina during 2010 were performed by the National Reference Laboratory as part of a project coordinated by the PAHO within the SIREVA II network. Serogroup, serotype, serosubtype and MLST characterization were performed. Minimum Inhibitory Concentration to penicillin, ampicillin, ceftriaxone, rifampin, chloramphenicol, tetracycline and ciprofloxacin were determined and interpreted according to CLSI guidelines. Almost 49% of isolates were W135, and two serotype:serosubtype combinations, W135∶2a:P1.5,2:ST-11 and W135∶2a:P1.2:ST-11 accounted for 78% of all W135 isolates. Serogroup B accounted for 42.1% of isolates, and was both phenotypically and genotypically diverse. Serogroup C isolates represented 5.3% of the dataset, and one isolate belonging to the ST-198 complex was non-groupable. Isolates belonged mainly to the ST-11 complex (48%) and to a lesser extent to the ST-865 (18%), ST-32 (9,8%) and the ST-35 complexes (9%). Intermediate resistance to penicillin and ampicillin was detected in 35.4% and 33.1% of isolates respectively. Two W135∶2a:P1.5,2:ST-11:ST-11 isolates presented resistance to ciprofloxacin associated with a mutation in the QRDR of gyrA gene Thr91-Ile. These data show serogroup W135 was the first cause of disease in Argentina in 2010, and was strongly associated with the W135∶2a:P1.5,2:ST-11 epidemic clone. Serogroup B was the second cause of disease and isolates belonging to this serogroup were phenotypically and genotypically diverse. The presence of isolates with intermediate resistance to penicillin and the presence of fluorquinolone-resistant isolates highlight the necessity and importance of maintaining and strengthening National Surveillance Programs. PMID:23483970

  1. Malnutrition as an underlying cause of childhood deaths associated with infectious diseases in developing countries.

    PubMed Central

    Rice, A. L.; Sacco, L.; Hyder, A.; Black, R. E.

    2000-01-01

    INTRODUCTION: Recent estimates suggest that malnutrition (measured as poor anthropometric status) is associated with about 50% of all deaths among children. Although the association between malnutrition and all-cause mortality is well documented, the malnutrition-related risk of death associated with specific diseases is less well described. We reviewed published literature to examine the evidence for a relation between malnutrition and child mortality from diarrhoea, acute respiratory illness, malaria and measles, conditions that account for over 50% of deaths in children worldwide. METHODS: MEDLINE was searched for suitable review articles and original reports of community-based and hospital-based studies. Findings from cohort studies and case-control studies were reviewed and summarized. RESULTS: The strongest and most consistent relation between malnutrition and an increased risk of death was observed for diarrhoea and acute respiratory infection. The evidence, although limited, also suggests a potentially increased risk for death from malaria. A less consistent association was observed between nutritional status and death from measles. Although some hospital-based studies and case-control studies reported an increased risk of mortality from measles, few community-based studies reported any association. DISCUSSION: The risk of malnutrition-related mortality seems to vary for different diseases. These findings have important implications for the evaluation of nutritional intervention programmes and child survival programmes being implemented in settings with different disease profiles. PMID:11100616

  2. Notification of Huntington's disease as primary cause of death in Brazil from 1984 to 2008.

    PubMed

    Vaz, I P; Paiva, C L A

    2016-01-01

    The aim of this article was to conduct a retrospective observational study on reported deaths due to Huntington's disease (HD) in Brazil in the past 25 years (from 1984 to 2008). Data were obtained from the Brazilian Mortality Information System (SIM/DATASUS), the official system of Brazilian Mortality Database. The data obtained included information regarding the gender of the deceased and the number of death notifications, which we stratified by demographic regions and states. HD mortality per 100,000 was calculated and plotted in a graph. Linear regression was calculated using ordinary least square technique. We observed that the mortality due to HD recorded by SIM/DATASUS from 1984 to 2008 had increased at much higher rates than the population in the same period. Also, some Brazilian regions still show very low rates of HD mortality compared to the national average of deaths due to HD. These findings suggest that HD mortality has been underestimated. Ignorance about the disease as well as the fact that death from HD can occur as a consequence of heart disease, pneumonia, or suicide can strongly contribute to the misguided notification of HD as the cause of death in the official reports. PMID:27421006

  3. Isolation and Characterization of Bacteriophages Against Pseudomonas syringae pv. actinidiae Causing Bacterial Canker Disease in Kiwifruit.

    PubMed

    Yu, Ji-Gang; Lim, Jeong-A; Song, Yu-Rim; Heu, Sunggi; Kim, Gyoung Hee; Koh, Young Jin; Oh, Chang-Sik

    2016-02-01

    Pseudomonas syringae pv. actinidiae causes bacterial canker disease in kiwifruit. Owing to the prohibition of agricultural antibiotic use in major kiwifruit-cultivating countries, alternative methods need to be developed to manage this disease. Bacteriophages are viruses that specifically infect target bacteria and have recently been reconsidered as potential biological control agents for bacterial pathogens owing to their specificity in terms of host range. In this study, we isolated bacteriophages against P. syringae pv. actinidiae from soils collected from kiwifruit orchards in Korea and selected seven bacteriophages for further characterization based on restriction enzyme digestion patterns of genomic DNA. Among the studied bacteriophages, two belong to the Myoviridae family and three belong to the Podoviridae family, based on morphology observed by transmission electron microscopy. The host range of the selected bacteriophages was confirmed using 18 strains of P. syringae pv. actinidiae, including the Psa2 and Psa3 groups, and some were also effective against other P. syringae pathovars. Lytic activity of the selected bacteriophages was sustained in vitro until 80 h, and their activity remained stable up to 50°C, at pH 11, and under UV-B light. These results indicate that the isolated bacteriophages are specific to P. syringae species and are resistant to various environmental factors, implying their potential use in control of bacterial canker disease in kiwifruits. PMID:26628254

  4. Predicting Mendelian Disease-Causing Non-Synonymous Single Nucleotide Variants in Exome Sequencing Studies

    PubMed Central

    Bao, Su-Ying; Yang, Wanling; Ho, Shu-Leong; Song, Yong-Qiang; Sham, Pak C.

    2013-01-01

    Exome sequencing is becoming a standard tool for mapping Mendelian disease-causing (or pathogenic) non-synonymous single nucleotide variants (nsSNVs). Minor allele frequency (MAF) filtering approach and functional prediction methods are commonly used to identify candidate pathogenic mutations in these studies. Combining multiple functional prediction methods may increase accuracy in prediction. Here, we propose to use a logit model to combine multiple prediction methods and compute an unbiased probability of a rare variant being pathogenic. Also, for the first time we assess the predictive power of seven prediction methods (including SIFT, PolyPhen2, CONDEL, and logit) in predicting pathogenic nsSNVs from other rare variants, which reflects the situation after MAF filtering is done in exome-sequencing studies. We found that a logit model combining all or some original prediction methods outperforms other methods examined, but is unable to discriminate between autosomal dominant and autosomal recessive disease mutations. Finally, based on the predictions of the logit model, we estimate that an individual has around 5% of rare nsSNVs that are pathogenic and carries ∼22 pathogenic derived alleles at least, which if made homozygous by consanguineous marriages may lead to recessive diseases. PMID:23341771

  5. Predicting mendelian disease-causing non-synonymous single nucleotide variants in exome sequencing studies.

    PubMed

    Li, Miao-Xin; Kwan, Johnny S H; Bao, Su-Ying; Yang, Wanling; Ho, Shu-Leong; Song, Yong-Qiang; Sham, Pak C

    2013-01-01

    Exome sequencing is becoming a standard tool for mapping Mendelian disease-causing (or pathogenic) non-synonymous single nucleotide variants (nsSNVs). Minor allele frequency (MAF) filtering approach and functional prediction methods are commonly used to identify candidate pathogenic mutations in these studies. Combining multiple functional prediction methods may increase accuracy in prediction. Here, we propose to use a logit model to combine multiple prediction methods and compute an unbiased probability of a rare variant being pathogenic. Also, for the first time we assess the predictive power of seven prediction methods (including SIFT, PolyPhen2, CONDEL, and logit) in predicting pathogenic nsSNVs from other rare variants, which reflects the situation after MAF filtering is done in exome-sequencing studies. We found that a logit model combining all or some original prediction methods outperforms other methods examined, but is unable to discriminate between autosomal dominant and autosomal recessive disease mutations. Finally, based on the predictions of the logit model, we estimate that an individual has around 5% of rare nsSNVs that are pathogenic and carries ~22 pathogenic derived alleles at least, which if made homozygous by consanguineous marriages may lead to recessive diseases. PMID:23341771

  6. Low disease-causing threshold in a frog species susceptible to chytridiomycosis.

    PubMed

    Stockwell, Michelle P; Garnham, James I; Bower, Deborah S; Clulow, John; Mahony, Michael J

    2016-06-01

    A simple diagnosis of the presence or absence of an infection is an uninformative metric when individuals differ considerably in their tolerance to different infection loads or resistance to rates of disease progression. Models that incorporate the relationship between the progression of the infection with the potential alternate outcomes provide a far more powerful predictive tool than diagnosis alone. The global decline of amphibians has been amplified by Batrachochytrium dendrobatidis, a pathogen that can cause the fatal disease chytridiomycosis. We measured the infection load and observed signs of disease in Litoria aurea Receiver operating characteristic curves were used to quantify the dissimilarity between the infection loads of L. aurea that showed signs associated with chytridiomycosis and those that did not. Litoria aurea had a 78% probability of developing chytridiomycosis past a threshold of 68 zoospore equivalents (ZE) per swab and chytridiomycosis occurred within a variable range of 0.5-490 ZE. Studies should incorporate a species-specific threshold as a predictor of chytridiomycosis, rather than a binary diagnosis. Measures of susceptibility to chytridiomycosis must account not only for the ability of B. dendrobatidis to increase its abundance on the skin of amphibians but also to determine how each species tolerates these infection loads. PMID:27190153

  7. Aspartoacylase catalytic deficiency as the cause of Canavan disease: a structural perspective.

    PubMed

    Wijayasinghe, Yasanandana S; Pavlovsky, Alexander G; Viola, Ronald E

    2014-08-01

    Canavan disease (CD) is a fatal, childhood neurological disorder caused by mutations in the ASPA gene, leading to catalytic deficiencies in the aspartoacylase (ASPA) enzyme and impaired N-acetyl-l-aspartic acid metabolism in the brain. To study the possible structural defects triggered by these mutations, four ASPA missense mutations associated with different disease severities have been structurally characterized. These mutant enzymes each have overall structures similar to that of the native ASPA enzyme, but with varying degrees of alterations that offer explanations for the respective loss of catalytic activity. The K213E mutant, a nonconservative mutant associated with a mild disease phenotype, has minimal structural differences compared to the native enzyme. In contrast, the loss of van der Waals contacts in the F295S mutant and the loss of hydrophobic and hydrogen bonding interactions in the Y231C mutant lead to a local collapse of the hydrophobic core structure in the carboxyl-terminal domain, contributing to a decrease in protein stability. The structure of the E285A mutant, the most common clinical mutant, reveals that the loss of hydrogen bonding interactions with the carboxylate side chain of Glu285 disturbs the active site architecture, leading to altered substrate binding and lower catalytic activity. Our improved understanding of the nature of these structural defects provides a basis for the development of treatment therapies for CD. PMID:25003821

  8. Clinical and Molecular Epidemiology of Haemophilus influenzae Causing Invasive Disease in Adult Patients

    PubMed Central

    Puig, Carmen; Grau, Imma; Tubau, Fe; Calatayud, Laura; Pallares, Roman; Liñares, Josefina

    2014-01-01

    Objectives The epidemiology of invasive Haemophilus influenzae (Hi) has changed since the introduction of the Hi type b (Hib) vaccine. The aim of this study was to analyze the clinical and molecular epidemiology of Hi invasive disease in adults. Methods Clinical data of the 82 patients with Hi invasive infections were analyzed. Antimicrobial susceptibility, serotyping, and genotyping were studied (2008–2013). Results Men accounted for 63.4% of patients (whose mean age was 64.3 years). The most frequent comorbidities were immunosuppressive therapy (34.1%), malignancy (31.7%), diabetes, and COPD (both 22%). The 30-day mortality rate was 20.7%. The majority of the strains (84.3%) were nontypeable (NTHi) and serotype f was the most prevalent serotype in the capsulated strains. The highest antimicrobial resistance was for cotrimoxazole (27.1%) and ampicillin (14.3%). Twenty-three isolates (32.9%) had amino acid changes in the PBP3 involved in resistance. Capsulated strains were clonal and belonged to clonal complexes 6 (serotype b), 124 (serotype f), and 18 (serotype e), whereas NTHi were genetically diverse. Conclusions Invasive Hi disease occurred mainly in elderly and those with underlying conditions, and it was associated with a high mortality rate. NTHi were the most common cause of invasive disease and showed high genetic diversity. PMID:25379704

  9. Atypical hand, foot, and mouth disease: a vesiculobullous eruption caused by Coxsackie virus A6.

    PubMed

    Feder, Henry M; Bennett, Nicholas; Modlin, John F

    2014-01-01

    A previously well infant aged 9 months presented with an acute, self-limiting illness characterised by high fever and a papular eruption that started on the face. Although fever subsided within 3 days, the rash worsened and extended over the whole body, with some papules evolving into vesiculobullous lesions. The infant had been exposed to children with a similar illness 1 week before onset. PCR of vesicular swabs and stool samples taken on day 6 of illness showed Coxsackie virus A6. The illness resolved within 10 days of onset, although onychomadesis was seen on both big toes at follow-up 5 weeks later. Our case exemplifies the severe, atypical cases of hand, foot, and mouth disease that have been reported worldwide since 2008, and in the USA since the 2011. Atypical hand, foot, and mouth disease is caused by a new lineage of Coxsackie virus A6 and is characterised by high fever and vesiculobullous eruptions on the calves and backs of the hands. Infants with eczema might be predisposed to severe disease. PMID:24287184

  10. Genetic variants of Kudoa septempunctata (Myxozoa: Multivalvulida), a flounder parasite causing foodborne disease.

    PubMed

    Takeuchi, F; Ogasawara, Y; Kato, K; Sekizuka, T; Nozaki, T; Sugita-Konishi, Y; Ohnishi, T; Kuroda, M

    2016-06-01

    Foodborne disease outbreaks caused by raw olive flounders (Paralichthys olivaceus) parasitized with Kudoa septempunctata have been reported in Japan. Origins of olive flounders consumed in Japan vary, being either domestic or imported, and aquaculture-raised or natural. Although it is unknown whether different sources are associated with different outcomes, it is desirable to identify whether this is the case by determining whether unique K. septempunctata strains occur and if so, whether some are associated with foodborne illness. We here developed an intraspecific genotyping method, using the sequence variation of mitochondrial genes. We collected olive flounder samples from foodborne disease outbreaks, domestic fish farms or quarantine offices and investigated whether K. septempunctata genotype is associated with pathogenicity or geographic origin. The 104 samples were classified into three genotypes, ST1, ST2 and ST3. Frequency of symptomatic cases differed by genotypes, but the association was not statistically significant. Whereas K. septempunctata detected from aquaculture-raised and natural fish from Japan were either ST1 or ST2, those from fish inspected at quarantine from Korea to Japan were ST3. Our method can be applied to phylogeographic analysis of K. septempunctata and contribute to containing the foodborne disease. The genotype database is hosted in the PubMLST website (http://pubmlst.org/kseptempunctata/). PMID:26096292

  11. Molecular analysis of Streptococcus pneumoniae clones causing invasive disease in children in Singapore.

    PubMed

    Jefferies, J M C; Tee, W S N; Clarke, S C

    2011-06-01

    Streptococcus pneumoniae remains a leading cause of serious paediatric disease. However, there are few published epidemiological data regarding invasive pneumococcal disease (IPD) in many countries in South East Asia, including Singapore. Baseline data for IPD are essential to inform policy regarding pneumococcal conjugate vaccine (PCV) use in Singapore. To our knowledge, this is the first study to use multilocus sequence typing (MLST) to investigate clonal relationships among Singaporean IPD isolates. We characterized 86 invasive pneumococci isolated from Singaporean children between 2001 and 2006 using serotyping and MLST. The objectives were to compare Singaporean MLST data to worldwide data and to assess serotype distribution in relation to current PCV formulations. We observed 50 sequence types (STs), a high proportion of which (n = 16) were novel STs. Despite the presence of these novel STs, serotype distribution was similar to that observed elsewhere. Serotypes 14, 6B, 19A and 19F accounted for 85 % of IPD cases. PCV7, PCV10 and PCV13 covered 85 %, 86 % and 97 % of IPD isolates, respectively. We have demonstrated a pressing need for larger studies to determine the molecular epidemiology and antibiotic susceptibility of circulating pneumococcal clones from both carriage and disease in Singapore. PMID:21330410

  12. HAX1 Mutations causing SCN and Neurological Disease Lead to Microstructural Abnormalities Revealed by Quantitative MRI

    PubMed Central

    Boztug, Kaan; Ding, Xiao-Qi; Hartmann, Hans; Ziesenitz, Lena; Schäffer, Alejandro A.; Diestelhorst, Jana; Pfeifer, Dietmar; Appaswamy, Giridharan; Kehbel, Sonja; Simon, Thorsten; Jefri, Abdullah Al; Lanfermann, Heinrich; Klein, Christoph

    2011-01-01

    Biallelic mutations in the gene encoding HCLS-associated protein X-1 (HAX1) cause autosomal recessive severe congenital neutropenia. Some of these patients display neurological abnormalities including developmental delay, cognitive impairment and/or epilepsy. Recent genotype-phenotype studies have shown that mutations in HAX1 affecting transcripts A (NM_006118.3) and B (NM_001018837.1) cause the phenotype of SCN with neurological impairment, while mutations affecting isoform A but not B lead to SCN without neurological aberrations. In this study, we identified a consanguineous family with two patients suffering from SCN and neurological disease caused by a novel, homozygous genomic deletion including exons 4–7 of the HAX1 gene. Quantitative MRI analyses revealed general alterations in cerebral proton density in both of the patients, as well as in an additional unrelated patient with another HAX1 mutation (Arg86X) known to be associated with neurological manifestations. This study provides first in vivo evidence of general neurodegeneration associated with HAX1 deficiency in SCN patients. PMID:21108402

  13. Computed tomography findings of hepatic veno-occlusive disease caused by Sedum aizoon with histopathological correlation

    PubMed Central

    Shao, H.; Chen, H. Z.; Zhu, J. S.; Ruan, B.; Zhang, Z. Q.; Lin, X.; Gan, M. F.

    2015-01-01

    This study investigated the value of computed tomography (CT) in the diagnosis and treatment of hepatic veno-occlusive disease (HVOD) caused by Sedum aizoon (SA). The clinical manifestations, treatment results, imaging findings, and histological findings of the liver were analyzed in 39 patients with HVOD caused by SA. Hepatomegaly, liver dysfunction, abdominal effusion, and geographic density changes on liver CT scans were found in all 39 patients. The pathological findings of histological liver examination included swelling and point-like necrosis of liver cells, significant expansion and congestion of the sinuses, endothelial swelling, and wall thickening with incomplete lumen occlusion of small liver vessels. CT geographic density changes were confirmed by histological examination of the liver in 18 patients. Sixteen patients with small amounts of ascites that started within 4 weeks of treatment recovered completely or significantly improved after symptomatic and supportive treatment. However, only 43.75% of the patients with larger amounts of ascites improved following symptomatic and supportive treatment. In conclusion, liver CT examination is a valuable, safe, and noninvasive tool for the diagnosis of HVOD caused by SA. In selected cases, liver CT examination may replace liver biopsy and histological analysis. PMID:26517336

  14. An infectious disease of ducks caused by a newly emerged Tembusu virus strain in mainland China.

    PubMed

    Yan, Pixi; Zhao, Youshu; Zhang, Xu; Xu, Dawei; Dai, Xiaoguang; Teng, Qiaoyang; Yan, Liping; Zhou, Jiewen; Ji, Xiwen; Zhang, Shumei; Liu, Guangqing; Zhou, Yanjun; Kawaoka, Yoshihiro; Tong, Guangzhi; Li, Zejun

    2011-08-15

    During investigations into an outbreak of egg production decline, retarded growth, and even death among ducks in Southeast China, a novel Tembusu virus strain named Tembusu virus Fengxian 2010 (FX2010) was isolated. This virus replicated in embryonated chicken eggs and caused embryo death. In cross-neutralization tests, antiserum to the partial E protein of Tembusu virus Mm1775 strain neutralized FX2010, whereas antiserum to Japanese encephalitis virus did not. FX2010 is an enveloped RNA virus of approximately 45-50 nm in diameter. Sequence analysis of its E and NS5 genes showed that both genes share up to 99.6% nucleotide sequence identity with Baiyangdian virus, and up to 88% nucleotide sequence identity with their counterparts in Tembusu virus. FX2010 was transmitted without mosquito, and caused systemic infection and lesions in experimentally infected ducks. These results indicate that FX2010 and BYD virus are newly emerged Tembusu virus strains that cause an infectious disease in ducks. PMID:21722935

  15. Intestinal Microbiota and Celiac Disease: Cause, Consequence or Co-Evolution?

    PubMed

    Cenit, María Carmen; Olivares, Marta; Codoñer-Franch, Pilar; Sanz, Yolanda

    2015-08-01

    It is widely recognized that the intestinal microbiota plays a role in the initiation and perpetuation of intestinal inflammation in numerous chronic conditions. Most studies report intestinal dysbiosis in celiac disease (CD) patients, untreated and treated with a gluten-free diet (GFD), compared to healthy controls. CD patients with gastrointestinal symptoms are also known to have a different microbiota compared to patients with dermatitis herpetiformis and controls, suggesting that the microbiota is involved in disease manifestation. Furthermore, a dysbiotic microbiota seems to be associated with persistent gastrointestinal symptoms in treated CD patients, suggesting its pathogenic implication in these particular cases. GFD per se influences gut microbiota composition, and thus constitutes an inevitable confounding factor in studies conducted in CD patients. To improve our understanding of whether intestinal dysbiosis is the cause or consequence of disease, prospective studies in healthy infants at family risk of CD are underway. These studies have revealed that the CD host genotype selects for the early colonizers of the infant's gut, which together with environmental factors (e.g., breast-feeding, antibiotics, etc.) could influence the development of oral tolerance to gluten. Indeed, some CD genes and/or their altered expression play a role in bacterial colonization and sensing. In turn, intestinal dysbiosis could promote an abnormal response to gluten or other environmental CD-promoting factors (e.g., infections) in predisposed individuals. Here, we review the current knowledge of host-microbe interactions and how host genetics/epigenetics and environmental factors shape gut microbiota and may influence disease risk. We also summarize the current knowledge about the potential mechanisms of action of the intestinal microbiota and specific components that affect CD pathogenesis. PMID:26287240

  16. Intestinal Microbiota and Celiac Disease: Cause, Consequence or Co-Evolution?

    PubMed Central

    Cenit, María Carmen; Olivares, Marta; Codoñer-Franch, Pilar; Sanz, Yolanda

    2015-01-01

    It is widely recognized that the intestinal microbiota plays a role in the initiation and perpetuation of intestinal inflammation in numerous chronic conditions. Most studies report intestinal dysbiosis in celiac disease (CD) patients, untreated and treated with a gluten-free diet (GFD), compared to healthy controls. CD patients with gastrointestinal symptoms are also known to have a different microbiota compared to patients with dermatitis herpetiformis and controls, suggesting that the microbiota is involved in disease manifestation. Furthermore, a dysbiotic microbiota seems to be associated with persistent gastrointestinal symptoms in treated CD patients, suggesting its pathogenic implication in these particular cases. GFD per se influences gut microbiota composition, and thus constitutes an inevitable confounding factor in studies conducted in CD patients. To improve our understanding of whether intestinal dysbiosis is the cause or consequence of disease, prospective studies in healthy infants at family risk of CD are underway. These studies have revealed that the CD host genotype selects for the early colonizers of the infant’s gut, which together with environmental factors (e.g., breast-feeding, antibiotics, etc.) could influence the development of oral tolerance to gluten. Indeed, some CD genes and/or their altered expression play a role in bacterial colonization and sensing. In turn, intestinal dysbiosis could promote an abnormal response to gluten or other environmental CD-promoting factors (e.g., infections) in predisposed individuals. Here, we review the current knowledge of host-microbe interactions and how host genetics/epigenetics and environmental factors shape gut microbiota and may influence disease risk. We also summarize the current knowledge about the potential mechanisms of action of the intestinal microbiota and specific components that affect CD pathogenesis. PMID:26287240

  17. Variable Clinical Presentation of an MUC1 Mutation Causing Medullary Cystic Kidney Disease Type 1

    PubMed Central

    Kmoch, Stanislav; Antignac, Corinne; Robins, Vicki; Kidd, Kendrah; Kelsoe, John R.; Hladik, Gerald; Klemmer, Philip; Knohl, Stephen J.; Scheinman, Steven J.; Vo, Nam; Santi, Ann; Harris, Alese; Canaday, Omar; Weller, Nelson; Hulick, Peter J.; Vogel, Kristen; Rahbari-Oskoui, Frederick F.; Tuazon, Jennifer; Deltas, Constantinos; Somers, Douglas; Megarbane, Andre; Kimmel, Paul L.; Sperati, C. John; Orr-Urtreger, Avi; Ben-Shachar, Shay; Waugh, David A.; McGinn, Stella; Hodaňová, Kateřina; Vylet'al, Petr; Živná, Martina; Hart, Thomas C.; Hart, P. Suzanne

    2014-01-01

    Background and objectives The genetic cause of medullary cystic kidney disease type 1 was recently identified as a cytosine insertion in the variable number of tandem repeat region of MUC1 encoding mucoprotein-1 (MUC1), a protein that is present in skin, breast, and lung tissue, the gastrointestinal tract, and the distal tubules of the kidney. The purpose of this investigation was to analyze the clinical characteristics of families and individuals with this mutation. Design, setting, participants, & measurements Families with autosomal dominant interstitial kidney disease were referred for genetic analysis over a 14-year period. Families without UMOD or REN mutations prospectively underwent genotyping for the presence of the MUC1 mutation. Clinical characteristics were retrospectively evaluated in individuals with the MUC1 mutation and historically affected individuals (persons who were both related to genetically affected individuals in such a way that ensured that they could be genetically affected and had a history of CKD stage IV or kidney failure resulting in death, dialysis, or transplantation). Results Twenty-four families were identified with the MUC1 mutation. Of 186 family members undergoing MUC1 mutational analysis, the mutation was identified in 95 individuals, 91 individuals did not have the mutation, and111 individuals were identified as historically affected. Individuals with the MUC1 mutation suffered from chronic kidney failure with a widely variable age of onset of end stage kidney disease ranging from 16 to >80 years. Urinalyses revealed minimal protein and no blood. Ultrasounds of 35 individuals showed no medullary cysts. There were no clinical manifestations of the MUC1 mutation detected in the breasts, skin, respiratory system, or gastrointestinal tract. Conclusion MUC1 mutation results in progressive chronic kidney failure with a bland urinary sediment. The age of onset of end stage kidney disease is highly variable, suggesting that gene

  18. Mutations in the MORC2 gene cause axonal Charcot-Marie-Tooth disease.

    PubMed

    Sevilla, Teresa; Lupo, Vincenzo; Martínez-Rubio, Dolores; Sancho, Paula; Sivera, Rafael; Chumillas, María J; García-Romero, Mar; Pascual-Pascual, Samuel I; Muelas, Nuria; Dopazo, Joaquín; Vílchez, Juan J; Palau, Francesc; Espinós, Carmen

    2016-01-01

    new pathogenic mechanism to the long list of causes of Charcot-Marie-Tooth disease. PMID:26497905

  19. LRPPRC mutations cause early-onset multisystem mitochondrial disease outside of the French-Canadian population.

    PubMed

    Oláhová, Monika; Hardy, Steven A; Hall, Julie; Yarham, John W; Haack, Tobias B; Wilson, William C; Alston, Charlotte L; He, Langping; Aznauryan, Erik; Brown, Ruth M; Brown, Garry K; Morris, Andrew A M; Mundy, Helen; Broomfield, Alex; Barbosa, Ines A; Simpson, Michael A; Deshpande, Charu; Moeslinger, Dorothea; Koch, Johannes; Stettner, Georg M; Bonnen, Penelope E; Prokisch, Holger; Lightowlers, Robert N; McFarland, Robert; Chrzanowska-Lightowlers, Zofia M A; Taylor, Robert W

    2015-12-01

    Mitochondrial Complex IV [cytochrome c oxidase (COX)] deficiency is one of the most common respiratory chain defects in humans. The clinical phenotypes associated with COX deficiency include liver disease, cardiomyopathy and Leigh syndrome, a neurodegenerative disorder characterized by bilateral high signal lesions in the brainstem and basal ganglia. COX deficiency can result from mutations affecting many different mitochondrial proteins. The French-Canadian variant of COX-deficient Leigh syndrome is unique to the Saguenay-Lac-Saint-Jean region of Québec and is caused by a founder mutation in the LRPPRC gene. This encodes the leucine-rich pentatricopeptide repeat domain protein (LRPPRC), which is involved in post-transcriptional regulation of mitochondrial gene expression. Here, we present the clinical and molecular characterization of novel, recessive LRPPRC gene mutations, identified using whole exome and candidate gene sequencing. The 10 patients come from seven unrelated families of UK-Caucasian, UK-Pakistani, UK-Indian, Turkish and Iraqi origin. They resemble the French-Canadian Leigh syndrome patients in having intermittent severe lactic acidosis and early-onset neurodevelopmental problems with episodes of deterioration. In addition, many of our patients have had neonatal cardiomyopathy or congenital malformations, most commonly affecting the heart and the brain. All patients who were tested had isolated COX deficiency in skeletal muscle. Functional characterization of patients' fibroblasts and skeletal muscle homogenates showed decreased levels of mutant LRPPRC protein and impaired Complex IV enzyme activity, associated with abnormal COX assembly and reduced steady-state levels of numerous oxidative phosphorylation subunits. We also identified a Complex I assembly defect in skeletal muscle, indicating different roles for LRPPRC in post-transcriptional regulation of mitochondrial mRNAs between tissues. Patient fibroblasts showed decreased steady-state levels

  20. LRPPRC mutations cause early-onset multisystem mitochondrial disease outside of the French-Canadian population

    PubMed Central

    Oláhová, Monika; Hardy, Steven A.; Hall, Julie; Yarham, John W.; Haack, Tobias B.; Wilson, William C.; Alston, Charlotte L.; He, Langping; Aznauryan, Erik; Brown, Ruth M.; Brown, Garry K.; Morris, Andrew A. M.; Mundy, Helen; Broomfield, Alex; Barbosa, Ines A.; Simpson, Michael A.; Deshpande, Charu; Moeslinger, Dorothea; Koch, Johannes; Stettner, Georg M.; Bonnen, Penelope E.; Prokisch, Holger; Lightowlers, Robert N.; McFarland, Robert; Chrzanowska-Lightowlers, Zofia M. A.

    2015-01-01

    Mitochondrial Complex IV [cytochrome c oxidase (COX)] deficiency is one of the most common respiratory chain defects in humans. The clinical phenotypes associated with COX deficiency include liver disease, cardiomyopathy and Leigh syndrome, a neurodegenerative disorder characterized by bilateral high signal lesions in the brainstem and basal ganglia. COX deficiency can result from mutations affecting many different mitochondrial proteins. The French-Canadian variant of COX-deficient Leigh syndrome is unique to the Saguenay-Lac-Saint-Jean region of Québec and is caused by a founder mutation in the LRPPRC gene. This encodes the leucine-rich pentatricopeptide repeat domain protein (LRPPRC), which is involved in post-transcriptional regulation of mitochondrial gene expression. Here, we present the clinical and molecular characterization of novel, recessive LRPPRC gene mutations, identified using whole exome and candidate gene sequencing. The 10 patients come from seven unrelated families of UK-Caucasian, UK-Pakistani, UK-Indian, Turkish and Iraqi origin. They resemble the French-Canadian Leigh syndrome patients in having intermittent severe lactic acidosis and early-onset neurodevelopmental problems with episodes of deterioration. In addition, many of our patients have had neonatal cardiomyopathy or congenital malformations, most commonly affecting the heart and the brain. All patients who were tested had isolated COX deficiency in skeletal muscle. Functional characterization of patients’ fibroblasts and skeletal muscle homogenates showed decreased levels of mutant LRPPRC protein and impaired Complex IV enzyme activity, associated with abnormal COX assembly and reduced steady-state levels of numerous oxidative phosphorylation subunits. We also identified a Complex I assembly defect in skeletal muscle, indicating different roles for LRPPRC in post-transcriptional regulation of mitochondrial mRNAs between tissues. Patient fibroblasts showed decreased steady

  1. Influenza A (H10N7) Virus Causes Respiratory Tract Disease in Harbor Seals and Ferrets

    PubMed Central

    Herfst, Sander; Bodewes, Rogier; Pfankuche, Vanessa M.; van de Bildt, Marco W. G.; Seehusen, Frauke; Puff, Christina; Richard, Mathilde; Siebert, Ursula; Lehnert, Kristina; Bestebroer, Theo; Lexmond, Pascal; Fouchier, Ron A. M.; Prenger-Berninghoff, Ellen; Herbst, Werner; Koopmans, Marion; Osterhaus, Albert D. M. E.

    2016-01-01

    Avian influenza viruses sporadically cross the species barrier to mammals, including humans, in which they may cause epidemic disease. Recently such an epidemic occurred due to the emergence of avian influenza virus of the subtype H10N7 (Seal/H10N7) in harbor seals (Phoca vitulina). This epidemic caused high mortality in seals along the north-west coast of Europe and represented a potential risk for human health. To characterize the spectrum of lesions and to identify the target cells and viral distribution, findings in 16 harbor seals spontaneously infected with Seal/H10N7 are described. The seals had respiratory tract inflammation extending from the nasal cavity to bronchi associated with intralesional virus antigen in respiratory epithelial cells. Virus infection was restricted to the respiratory tract. The fatal outcome of the viral infection in seals was most likely caused by secondary bacterial infections. To investigate the pathogenic potential of H10N7 infection for humans, we inoculated the seal virus intratracheally into six ferrets and performed pathological and virological analyses at 3 and 7 days post inoculation. These experimentally inoculated ferrets displayed mild clinical signs, virus excretion from the pharynx and respiratory tract inflammation extending from bronchi to alveoli that was associated with virus antigen expression exclusively in the respiratory epithelium. Virus was isolated only from the respiratory tract. In conclusion, Seal/H10N7 infection in naturally infected harbor seals and experimentally infected ferrets shows that respiratory epithelial cells are the permissive cells for viral replication. Fatal outcome in seals was caused by secondary bacterial pneumonia similar to that in fatal human cases during influenza pandemics. Productive infection of ferrets indicates that seal/H10N7 may possess a zoonotic potential. This outbreak of LPAI from wild birds to seals demonstrates the risk of such occasions for mammals and thus humans

  2. Influenza A (H10N7) Virus Causes Respiratory Tract Disease in Harbor Seals and Ferrets.

    PubMed

    van den Brand, Judith M A; Wohlsein, Peter; Herfst, Sander; Bodewes, Rogier; Pfankuche, Vanessa M; van de Bildt, Marco W G; Seehusen, Frauke; Puff, Christina; Richard, Mathilde; Siebert, Ursula; Lehnert, Kristina; Bestebroer, Theo; Lexmond, Pascal; Fouchier, Ron A M; Prenger-Berninghoff, Ellen; Herbst, Werner; Koopmans, Marion; Osterhaus, Albert D M E; Kuiken, Thijs; Baumgärtner, Wolfgang

    2016-01-01

    Avian influenza viruses sporadically cross the species barrier to mammals, including humans, in which they may cause epidemic disease. Recently such an epidemic occurred due to the emergence of avian influenza virus of the subtype H10N7 (Seal/H10N7) in harbor seals (Phoca vitulina). This epidemic caused high mortality in seals along the north-west coast of Europe and represented a potential risk for human health. To characterize the spectrum of lesions and to identify the target cells and viral distribution, findings in 16 harbor seals spontaneously infected with Seal/H10N7 are described. The seals had respiratory tract inflammation extending from the nasal cavity to bronchi associated with intralesional virus antigen in respiratory epithelial cells. Virus infection was restricted to the respiratory tract. The fatal outcome of the viral infection in seals was most likely caused by secondary bacterial infections. To investigate the pathogenic potential of H10N7 infection for humans, we inoculated the seal virus intratracheally into six ferrets and performed pathological and virological analyses at 3 and 7 days post inoculation. These experimentally inoculated ferrets displayed mild clinical signs, virus excretion from the pharynx and respiratory tract inflammation extending from bronchi to alveoli that was associated with virus antigen expression exclusively in the respiratory epithelium. Virus was isolated only from the respiratory tract. In conclusion, Seal/H10N7 infection in naturally infected harbor seals and experimentally infected ferrets shows that respiratory epithelial cells are the permissive cells for viral replication. Fatal outcome in seals was caused by secondary bacterial pneumonia similar to that in fatal human cases during influenza pandemics. Productive infection of ferrets indicates that seal/H10N7 may possess a zoonotic potential. This outbreak of LPAI from wild birds to seals demonstrates the risk of such occasions for mammals and thus humans

  3. Mapping QTL conferring resistance in maize to gray leaf spot disease caused by Cercospora zeina

    PubMed Central

    2014-01-01

    Background Gray leaf spot (GLS) is a globally important foliar disease of maize. Cercospora zeina, one of the two fungal species that cause the disease, is prevalent in southern Africa, China, Brazil and the eastern corn belt of the USA. Identification of QTL for GLS resistance in subtropical germplasm is important to support breeding programmes in developing countries where C. zeina limits production of this staple food crop. Results A maize RIL population (F7:S6) from a cross between CML444 and SC Malawi was field-tested under GLS disease pressure at five field sites over three seasons in KwaZulu-Natal, South Africa. Thirty QTL identified from eleven field trials (environments) were consolidated to seven QTL for GLS resistance based on their expression in at least two environments and location in the same core maize bins. Four GLS resistance alleles were derived from the more resistant parent CML444 (bin 1.10, 4.08, 9.04/9.05, 10.06/10.07), whereas the remainder were from SC Malawi (bin 6.06/6.07, 7.02/7.03, 9.06). QTLs in bin 4.08 and bin 6.06/6.07 were also detected as joint QTLs, each explained more than 11% of the phenotypic variation, and were identified in four and seven environments, respectively. Common markers were used to allocate GLS QTL from eleven previous studies to bins on the IBM2005 map, and GLS QTL “hotspots” were noted. Bin 4.08 and 7.02/7.03 GLS QTL from this study overlapped with hotspots, whereas the bin 6.06/6.07 and bin 9.06 QTLs appeared to be unique. QTL for flowering time (bin 1.07, 4.09) in this population did not correspond to QTL for GLS resistance. Conclusions QTL mapping of a RIL population from the subtropical maize parents CML444 and SC Malawi identified seven QTL for resistance to gray leaf spot disease caused by C. zeina. These QTL together with QTL from eleven studies were allocated to bins on the IBM2005 map to provide a basis for comparison. Hotspots of GLS QTL were identified on chromosomes one, two, four, five and

  4. PROGRESSION OF DISEASES CAUSED BY THE OYSTER PARASITES, PERKINSUS MARINUS AND HAPLOSPORIDIUM NELSONI IN CRASSOSTREA VIRGINICA ON CONSTRUCTED INTERTIDAL REEFS

    EPA Science Inventory

    The progression of diseases caused by the oyster parasites, Perkinsus marinus and Haplosporidium nelsoni, were evaluated by periodic sampling (May 1994 - December 1995) of oysters, Crassostrea virginica, on an artificial reef located in the Piankatank River, Virginia. The infecti...

  5. Kcne2 deletion causes early-onset nonalcoholic fatty liver disease via iron deficiency anemia

    PubMed Central

    Lee, Soo Min; Nguyen, Dara; Anand, Marie; Kant, Ritu; Köhncke, Clemens; Lisewski, Ulrike; Roepke, Torsten K.; Hu, Zhaoyang; Abbott, Geoffrey W.

    2016-01-01

    Nonalcoholic fatty liver disease (NAFLD) is an increasing health problem worldwide, with genetic, epigenetic, and environmental components. Here, we describe the first example of NAFLD caused by genetic disruption of a mammalian potassium channel subunit. Mice with germline deletion of the KCNE2 potassium channel β subunit exhibited NAFLD as early as postnatal day 7. Using mouse genetics, histology, liver damage assays and transcriptomics we discovered that iron deficiency arising from KCNE2-dependent achlorhydria is a major factor in early-onset NAFLD in Kcne2─/─ mice, while two other KCNE2-dependent defects did not initiate NAFLD. The findings uncover a novel genetic basis for NAFLD and an unexpected potential factor in human KCNE2-associated cardiovascular pathologies, including atherosclerosis. PMID:26984260

  6. Kcne2 deletion causes early-onset nonalcoholic fatty liver disease via iron deficiency anemia.

    PubMed

    Lee, Soo Min; Nguyen, Dara; Anand, Marie; Kant, Ritu; Köhncke, Clemens; Lisewski, Ulrike; Roepke, Torsten K; Hu, Zhaoyang; Abbott, Geoffrey W

    2016-01-01

    Nonalcoholic fatty liver disease (NAFLD) is an increasing health problem worldwide, with genetic, epigenetic, and environmental components. Here, we describe the first example of NAFLD caused by genetic disruption of a mammalian potassium channel subunit. Mice with germline deletion of the KCNE2 potassium channel β subunit exhibited NAFLD as early as postnatal day 7. Using mouse genetics, histology, liver damage assays and transcriptomics we discovered that iron deficiency arising from KCNE2-dependent achlorhydria is a major factor in early-onset NAFLD in Kcne2(─/─) mice, while two other KCNE2-dependent defects did not initiate NAFLD. The findings uncover a novel genetic basis for NAFLD and an unexpected potential factor in human KCNE2-associated cardiovascular pathologies, including atherosclerosis. PMID:26984260

  7. Sepsis Caused by Achromobacter Xylosoxidans in a Child with Cystic Fibrosis and Severe Lung Disease.

    PubMed

    Stobbelaar, Kim; Van Hoorenbeeck, Kim; Lequesne, Monique; De Dooy, Jozef; Ho, Erwin; Vlieghe, Erika; Ieven, Margaretha; Verhulst, Stijn

    2016-01-01

    BACKGROUND Achromobacter xylosoxidans is an aerobic, motile, Gram-negative, opportunistic pathogen that can be responsible for various severe nosocomial and community-acquired infections. It has been found in immunocompromised patients and patients with several other underlying conditions, but the clinical role of this microorganism in cystic fibrosis is unclear. CASE REPORT We describe a case of septic shock caused by A. xylosoxidans in a 10-year-old child with cystic fibrosis and severe lung disease. CONCLUSIONS As the prevalence of A. xylosoxidans in cystic fibrosis patients is rising and patient-to-patient transmission is highly probable, further studies are warranted to determine its role and to document the appropriate treatment strategy for eradication and long-term treatment of this organism. PMID:27498677

  8. Legionnaires' disease caused by Legionella longbeachae in Taiwan, 2006-2010.

    PubMed

    Wei, Sung-Hsi; Tseng, Lei-Ron; Tan, Jei-Kai; Cheng, Chin-Yu; Hsu, Yen-Tao; Cheng, En-Tsung; Lu, Chia-Sheng; Hsiao, Yao-Chuan; Wu, Tsai-Hung; Hsu, Jui-Feng; Liu, Ming-Tsan; Mu, Jung-Jung; Chen, Wan-Chin; Tsou, Tsung-Pei; Hung, Min-Nan; Chiang, Chuen-Sheue

    2014-02-01

    The aim of the present study was to investigate the epidemiology of Legionnaires' disease (LD) caused by Legionella longbeachae in Taiwan during 2006-2010. A total of six cases were identified prospectively, accounting for 1.6% of all laboratory-confirmed LD cases and 4.4% of culture-positive LD cases. All six cases occurred between April and August. The male to female ratio was 0.5. These six LD patients had a higher median age than those with LD due to Legionella pneumophila. Four of the six patients presented with pleural effusion and five survived the infection episode. Only two patients had a potential soil contact history prior to LD onset. The patients resided in divergent geographical areas without a common exposure history. The individual genomic DNA banding patterns of the six L. longbeachae isolates analyzed by pulsed-field gel electrophoresis (PFGE) were unique, supporting the hypothesis that the L. longbeachae infections occurred sporadically. PMID:24269651

  9. McKeown and the idea that social conditions are fundamental causes of disease.

    PubMed

    Link, Bruce G; Phelan, Jo C

    2002-05-01

    In an accompanying commentary, Colgrove indicates that McKeown's thesis-that dramatic reductions in mortality over the past 2 centuries were due to improved socioeconomic conditions rather than to medical or public health interventions-has been "overturned" and his theory "discredited." McKeown sought to explain a very prominent trend in population health and did so with a strong emphasis on the importance of basic social and economic conditions. If Colgrove is right about the McKeown thesis, social epidemiology is left with a gaping hole in its explanatory repertoire and a challenge to a cherished principle about the importance of social factors in health. We return to the trend McKeown focused upon-post-McKeown and post-Colgrove-to indicate how and why social conditions must continue to be seen as fundamental causes of disease. PMID:11988436

  10. Sepsis Caused by Achromobacter Xylosoxidans in a Child with Cystic Fibrosis and Severe Lung Disease

    PubMed Central

    Stobbelaar, Kim; Van Hoorenbeeck, Kim; Lequesne, Monique; De Dooy, Jozef; Ho, Erwin; Vlieghe, Erika; Ieven, Margaretha; Verhulst, Stijn

    2016-01-01

    Patient: Female, 10 Final Diagnosis: Sepsis Symptoms: Fever • hypotension • not tollerating enteral feeds • respiratory deterioration Medication: — Clinical Procedure: IV antibiotics • lungtransplantion Specialty: Pediatrics and Neonatology Objective: Unusual clinical course Background: Achromobacter xylosoxidans is an aerobic, motile, Gram-negative, opportunistic pathogen that can be responsible for various severe nosocomial and community-acquired infections. It has been found in immunocompromised patients and patients with several other underlying conditions, but the clinical role of this microorganism in cystic fibrosis is unclear. Case Report: We describe a case of septic shock caused by A. xylosoxidans in a 10-year-old child with cystic fibrosis and severe lung disease. Conclusions: As the prevalence of A. xylosoxidans in cystic fibrosis patients is rising and patient-to-patient transmission is highly probable, further studies are warranted to determine its role and to document the appropriate treatment strategy for eradication and long-term treatment of this organism. PMID:27498677

  11. Herpes Simplex Virus 1 Reactivates from Autonomic Ciliary Ganglia Independently from Sensory Trigeminal Ganglia To Cause Recurrent Ocular Disease

    PubMed Central

    Lee, Sungseok; Ives, Angela M.

    2015-01-01

    ABSTRACT Herpes simplex virus 1 (HSV-1) and HSV-2 establish latency in sensory and autonomic neurons after ocular or genital infection, but their recurrence patterns differ. HSV-1 reactivates from latency to cause recurrent orofacial disease, and while HSV-1 also causes genital lesions, HSV-2 recurs more efficiently in the genital region and rarely causes ocular disease. The mechanisms regulating these anatomical preferences are unclear. To determine whether differences in latent infection and reactivation in autonomic ganglia contribute to differences in HSV-1 and HSV-2 anatomical preferences for recurrent disease, we compared HSV-1 and HSV-2 clinical disease, acute and latent viral loads, and viral gene expression in sensory trigeminal and autonomic superior cervical and ciliary ganglia in a guinea pig ocular infection model. HSV-2 produced more severe acute disease, correlating with higher viral DNA loads in sensory and autonomic ganglia, as well as higher levels of thymidine kinase expression, a marker of productive infection, in autonomic ganglia. HSV-1 reactivated in ciliary ganglia, independently from trigeminal ganglia, to cause more frequent recurrent symptoms, while HSV-2 replicated simultaneously in autonomic and sensory ganglia to cause more persistent disease. While both HSV-1 and HSV-2 expressed the latency-associated transcript (LAT) in the trigeminal and superior cervical ganglia, only HSV-1 expressed LAT in ciliary ganglia, suggesting that HSV-2 is not reactivation competent or does not fully establish latency in ciliary ganglia. Thus, differences in replication and viral gene expression in autonomic ganglia may contribute to differences in HSV-1 and HSV-2 acute and recurrent clinical disease. IMPORTANCE Herpes simplex virus 1 (HSV-1) and HSV-2 establish latent infections, from which the viruses reactivate to cause recurrent disease throughout the life of the host. However, the viruses exhibit different manifestations and frequencies of recurrent

  12. Infection dynamics in frog populations with different histories of decline caused by a deadly disease.

    PubMed

    Sapsford, Sarah J; Voordouw, Maarten J; Alford, Ross A; Schwarzkopf, Lin

    2015-12-01

    Pathogens can drive host population dynamics. Chytridiomycosis is a fungal disease of amphibians that is caused by the fungus Batrachochytrium dendrobatidis (Bd). This pathogen has caused declines and extinctions in some host species whereas other host species coexist with Bd without suffering declines. In the early 1990s, Bd extirpated populations of the endangered common mistfrog, Litoria rheocola, at high-elevation sites, while populations of the species persisted at low-elevation sites. Today, populations have reappeared at many high-elevation sites where they presently co-exist with the fungus. We conducted a capture-mark-recapture (CMR) study of six populations of L. rheocola over 1 year, at high and low elevations. We used multistate CMR models to determine which factors (Bd infection status, site type, and season) influenced rates of frog survival, recapture, infection, and recovery from infection. We observed Bd-induced mortality of individual frogs, but did not find any significant effect of Bd infection on the survival rate of L. rheocola at the population level. Survival and recapture rates depended on site type and season. Infection rate was highest in winter when temperatures were favourable for pathogen growth, and differed among site types. The recovery rate was high (75.7-85.8%) across seasons, and did not differ among site types. The coexistence of L. rheocola with Bd suggests that (1) frog populations are becoming resistant to the fungus, (2) Bd may have evolved lower virulence, or (3) current environmental conditions may be inhibiting outbreaks of the fatal disease. PMID:26293680

  13. Evidence that climate change has caused 'emergence' of tick-borne diseases in Europe?

    PubMed

    Randolph, Sarah E

    2004-04-01

    Even though tick-borne disease systems are highly susceptible to climatic influences, climate change to date is not necessarily the cause of the marked increased incidence of a variety of tick-borne diseases in many parts of Europe over the past two decades. To test for causality, rather than coincidence, we need to examine whether the right sorts of climate change have occurred at the right time and in the right places to account for the observed heterogeneous temporal and spatial patterns of tick-borne disease 'emergence'. Tick-borne encephalitis (TBE) incidence, for example, showed a 3-fold step increase from 1983 to 1986 in Sweden, doubled in 1993 in the Czech Republic, increased even more dramatically in the same year in Lithuania and Poland, but declined markedly in 1997 in Hungary, Croatia and Slovenia. Within each country, TBE incidence has changed to different degrees in different regions. Because other tick-borne diseases, notably Lyme borreliosis, has commonly 'emerged' in parallel with TBE, we should first examine climate variables predicted to have a general effect on tick abundance, which has indeed increased in the past decade. These include temperature and moisture stress, which have seasonally differential impacts. Monthly mean records for 1960-2000 from the UK Climate Research Unit's interpolated global climate surface reveal that mean spring, spring-autumn and winter temperatures have all increased gradually over the past 40 years, but apparently most sharply in the late 1980s, when moisture stress also increased. These climate data do not reveal any obvious differences between sites where TBE did or did not 'emerge', and in Sweden increases in TBE pre-dated the onset of warmer springs and winters. If recorded climate changes cannot yet satisfactorily explain the temporal and spatial patterns of tick-borne disease change in Europe, the impact of biotic factors, such as increases in deer abundance and changing habitat structure, and of socio

  14. Risk factors and ultrasound can predict chronic hepatitis caused by nonalcoholic fatty liver disease.

    PubMed

    Riley, Thomas R; Kahn, Amin

    2006-01-01

    The diagnosis of nonalcoholic fatty liver disease (NAFLD) is under-recognized. The aim of this study was to develop a scoring system that separates NAFLD diagnosis as a cause of chronic hepatitis from controls by using clinical features and liver ultrasound. A retrospective review of consecutive NAFLD cases and other liver disease controls was undertaken selecting patients from an abnormal liver function test code. To qualify for analysis all patients had to have elevated liver injury tests for more then 6 months, a biopsy-confirmed diagnosis, and an ultrasound as part of the evaluation. There were 84 cases of NAFLD and 75 liver disease controls. The NAFLD group had a larger body mass index (BMI) (34.9 versus 26.1; P < or = 0.0001), a larger liver span (9.8 versus 8.1 cm; P < or = 0.0001), and higher triglycerides (252 versus 142.6; P < or = 0.0001). The ultrasound reports recorded features consistent with fatty infiltration in 65.5% of NAFLD cases, compared to 5.3% of other liver diseases (P < or = 0.0001). Diabetes mellitus was found in 35% of NAFLD and 6.7% of other cases (P < or = 0.0001). The BMI was >30 in 79.8% of NAFLD cases and 22.7% of other liver disease cases (P < or = 0.0001). The liver span was >8 cm in 78.6% of NAFLD cases and in only 16% of controls (P = 0.0001). On multivariate analysis using logistic regression, the odds ratio of having ultrasound report findings suggestive of fatty infiltration was 15.9 (CI, 4.1-60). The odds ratio was 9.4 (CI, 2.3-37.9) for diabetes, 5.0 (CI, 1.7-14.6) for BMI >30, and 2.3 for liver span >8 cm (CI, 1.36-3.90). A scoring system using clinical features and ultrasound was shown to reliably separate NAFLD from other cases of chronic hepatitis. PMID:16416209

  15. Muscle dysfunction in chronic obstructive pulmonary disease: update on causes and biological findings

    PubMed Central

    Pascual, Sergi; Casadevall, Carme; Orozco-Levi, Mauricio; Barreiro, Esther

    2015-01-01

    Respiratory and/or limb muscle dysfunction, which are frequently observed in chronic obstructive pulmonary disease (COPD) patients, contribute to their disease prognosis irrespective of the lung function. Muscle dysfunction is caused by the interaction of local and systemic factors. The key deleterious etiologic factors are pulmonary hyperinflation for the respiratory muscles and deconditioning secondary to reduced physical activity for limb muscles. Nonetheless, cigarette smoke, systemic inflammation, nutritional abnormalities, exercise, exacerbations, anabolic insufficiency, drugs and comorbidities also seem to play a relevant role. All these factors modify the phenotype of the muscles, through the induction of several biological phenomena in patients with COPD. While respiratory muscles improve their aerobic phenotype (percentage of oxidative fibers, capillarization, mitochondrial density, enzyme activity in the aerobic pathways, etc.), limb muscles exhibit the opposite phenotype. In addition, both muscle groups show oxidative stress, signs of damage and epigenetic changes. However, fiber atrophy, increased number of inflammatory cells, altered regenerative capacity; signs of apoptosis and autophagy, and an imbalance between protein synthesis and breakdown are rather characteristic features of the limb muscles, mostly in patients with reduced body weight. Despite that significant progress has been achieved in the last decades, full elucidation of the specific roles of the target biological mechanisms involved in COPD muscle dysfunction is still required. Such an achievement will be crucial to adequately tackle with this relevant clinical problem of COPD patients in the near-future. PMID:26623119

  16. A nairovirus isolated from African bats causes haemorrhagic gastroenteritis and severe hepatic disease in mice.

    PubMed

    Ishii, Akihiro; Ueno, Keisuke; Orba, Yasuko; Sasaki, Michihito; Moonga, Ladslav; Hang'ombe, Bernard M; Mweene, Aaron S; Umemura, Takashi; Ito, Kimihito; Hall, William W; Sawa, Hirofumi

    2014-01-01

    Bats can carry important zoonotic pathogens. Here we use a combination of next-generation sequencing and classical virus isolation methods to identify novel nairoviruses from bats captured from a cave in Zambia. This nairovirus infection is highly prevalent among giant leaf-nosed bats, Hipposideros gigas (detected in samples from 16 individuals out of 38). Whole-genome analysis of three viral isolates (11SB17, 11SB19 and 11SB23) reveals a typical bunyavirus tri-segmented genome. The strains form a single phylogenetic clade that is divergent from other known nairoviruses, and are hereafter designated as Leopards Hill virus (LPHV). When i.p. injected into mice, the 11SB17 strain causes only slight body weight loss, whereas 11SB23 produces acute and lethal disease closely resembling that observed with Crimean-Congo Haemorrhagic Fever virus in humans. We believe that our LPHV mouse model will be useful for research on the pathogenesis of nairoviral haemorrhagic disease. PMID:25451856

  17. A nairovirus isolated from African bats causes haemorrhagic gastroenteritis and severe hepatic disease in mice

    PubMed Central

    Ishii, Akihiro; Ueno, Keisuke; Orba, Yasuko; Sasaki, Michihito; Moonga, Ladslav; Hang’ombe, Bernard M.; Mweene, Aaron S.; Umemura, Takashi; Ito, Kimihito; Hall, William W.; Sawa, Hirofumi

    2014-01-01

    Bats can carry important zoonotic pathogens. Here we use a combination of next-generation sequencing and classical virus isolation methods to identify novel nairoviruses from bats captured from a cave in Zambia. This nairovirus infection is highly prevalent among giant leaf-nosed bats, Hipposideros gigas (detected in samples from 16 individuals out of 38). Whole-genome analysis of three viral isolates (11SB17, 11SB19 and 11SB23) reveals a typical bunyavirus tri-segmented genome. The strains form a single phylogenetic clade that is divergent from other known nairoviruses, and are hereafter designated as Leopards Hill virus (LPHV). When i.p. injected into mice, the 11SB17 strain causes only slight body weight loss, whereas 11SB23 produces acute and lethal disease closely resembling that observed with Crimean–Congo Haemorrhagic Fever virus in humans. We believe that our LPHV mouse model will be useful for research on the pathogenesis of nairoviral haemorrhagic disease. PMID:25451856

  18. Mutations in MYH7 cause Multi-minicore Disease (MmD) with variable cardiac involvement.

    PubMed

    Cullup, T; Lamont, P J; Cirak, S; Damian, M S; Wallefeld, W; Gooding, R; Tan, S V; Sheehan, J; Muntoni, F; Abbs, S; Sewry, C A; Dubowitz, V; Laing, N G; Jungbluth, H

    2012-12-01

    Central Core Disease (CCD) and Multi-minicore Disease (MmD) (the "core myopathies") have been mainly associated with mutations in the skeletal muscle ryanodine receptor (RYR1) and the selenoprotein N (SEPN1) gene. A proportion of cases remain unresolved. Mutations in MYH7 encoding the beta myosin heavy chain protein have been implicated in cardiac and, less frequently, skeletal muscle disorders. Here we report four patients from two families with a histopathological diagnosis of MmD, presenting in childhood with slowly progressive muscle weakness, more proximal in Family 1 and more distal in Family 2, and variable degrees of cardiorespiratory impairment evolving later in life. There was also a strong family history of sudden death in the first family. Muscle biopsies obtained in early childhood showed multiple minicores as the most prominent feature. Sequencing of the MYH7 gene revealed heterozygous missense mutations, c.4399C>G; p.Leu1467Val (exon 32) in Family 1 and c.4763G>C; p.Arg1588Pro (exon 34) in Family 2. These findings suggest MYH7 mutations as another cause of a myopathy with multiple cores, in particular if associated with dominant inheritance and cardiac involvement. However, clinical features previously associated with this genetic background, namely a more distal distribution of weakness and an associated cardiomyopathy, may only evolve over time. PMID:22784669

  19. Mutations in the cofilin partner Aip1/Wdr1 cause autoinflammatory disease and macrothrombocytopenia

    PubMed Central

    Panopoulos, Athanasia D.; Stirzaker, Roslynn A.; Hacking, Douglas F.; Tahtamouni, Lubna H.; Willson, Tracy A.; Mielke, Lisa A.; Henley, Katya J.; Zhang, Jian-Guo; Wicks, Ian P.; Stevenson, William S.; Nurden, Paquita; Watowich, Stephanie S.; Justice, Monica J.

    2007-01-01

    A pivotal mediator of actin dynamics is the protein cofilin, which promotes filament severing and depolymerization, facilitating the breakdown of existing filaments, and the enhancement of filament growth from newly created barbed ends. It does so in concert with actin interacting protein 1 (Aip1), which serves to accelerate cofilin's activity. While progress has been made in understanding its biochemical functions, the physiologic processes the cofilin/Aip1 complex regulates, particularly in higher organisms, are yet to be determined. We have generated an allelic series for WD40 repeat protein 1 (Wdr1), the mammalian homolog of Aip1, and report that reductions in Wdr1 function produce a dramatic phenotype gradient. While severe loss of function at the Wdr1 locus causes embryonic lethality, macrothrombocytopenia and autoinflammatory disease develop in mice carrying hypomorphic alleles. Macrothrombocytopenia is the result of megakaryocyte maturation defects, which lead to a failure of normal platelet shedding. Autoinflammatory disease, which is bone marrow–derived yet nonlymphoid in origin, is characterized by a massive infiltration of neutrophils into inflammatory lesions. Cytoskeletal responses are impaired in Wdr1 mutant neutrophils. These studies establish an essential requirement for Wdr1 in megakaryocytes and neutrophils, indicating that cofilin-mediated actin dynamics are critically important to the development and function of both cell types. PMID:17515402

  20. HGCS: an online tool for prioritizing disease-causing gene variants by biological distance

    PubMed Central

    2014-01-01

    Background Identifying the genotypes underlying human disease phenotypes is a fundamental step in human genetics and medicine. High-throughput genomic technologies provide thousands of genetic variants per individual. The causal genes of a specific phenotype are usually expected to be functionally close to each other. According to this hypothesis, candidate genes are picked from high-throughput data on the basis of their biological proximity to core genes — genes already known to be responsible for the phenotype. There is currently no effective gene-centric online interface for this purpose. Results We describe here the human gene connectome server (HGCS), a powerful, easy-to-use interactive online tool enabling researchers to prioritize any list of genes according to their biological proximity to core genes associated with the phenotype of interest. We also make available an updated and extended version for all human gene-specific connectomes. The HGCS is freely available to noncommercial users from: http://hgc.rockefeller.edu/. Conclusions The HGCS should help investigators from diverse fields to identify new disease-causing candidate genes more effectively, via a user-friendly online interface. PMID:24694260

  1. Muscle dysfunction in chronic obstructive pulmonary disease: update on causes and biological findings.

    PubMed

    Gea, Joaquim; Pascual, Sergi; Casadevall, Carme; Orozco-Levi, Mauricio; Barreiro, Esther

    2015-10-01

    Respiratory and/or limb muscle dysfunction, which are frequently observed in chronic obstructive pulmonary disease (COPD) patients, contribute to their disease prognosis irrespective of the lung function. Muscle dysfunction is caused by the interaction of local and systemic factors. The key deleterious etiologic factors are pulmonary hyperinflation for the respiratory muscles and deconditioning secondary to reduced physical activity for limb muscles. Nonetheless, cigarette smoke, systemic inflammation, nutritional abnormalities, exercise, exacerbations, anabolic insufficiency, drugs and comorbidities also seem to play a relevant role. All these factors modify the phenotype of the muscles, through the induction of several biological phenomena in patients with COPD. While respiratory muscles improve their aerobic phenotype (percentage of oxidative fibers, capillarization, mitochondrial density, enzyme activity in the aerobic pathways, etc.), limb muscles exhibit the opposite phenotype. In addition, both muscle groups show oxidative stress, signs of damage and epigenetic changes. However, fiber atrophy, increased number of inflammatory cells, altered regenerative capacity; signs of apoptosis and autophagy, and an imbalance between protein synthesis and breakdown are rather characteristic features of the limb muscles, mostly in patients with reduced body weight. Despite that significant progress has been achieved in the last decades, full elucidation of the specific roles of the target biological mechanisms involved in COPD muscle dysfunction is still required. Such an achievement will be crucial to adequately tackle with this relevant clinical problem of COPD patients in the near-future. PMID:26623119

  2. Characterization of a novel Canine distemper virus causing disease in wildlife.

    PubMed

    Pope, Jenny P; Miller, Debra L; Riley, Matthew C; Anis, Eman; Wilkes, Rebecca P

    2016-09-01

    Canine distemper virus (CDV) is a common cause of a multisystemic disease in both domestic dogs and wildlife species, including raccoons and foxes. Outbreaks of CDV in domestic dogs in eastern Tennessee have occurred since 2012, and it was determined that these outbreaks resulted from a novel genotype of CDV. We hypothesized that this virus is also infecting area wildlife and may be a source of the virus for these outbreaks in dogs. From 2013 to 2014, autopsies were performed and tissues collected from raccoons (Procyon lotor; n = 50) and gray foxes (Urocyon cinereoargenteus; n = 8) for CDV testing. A real-time reverse transcription PCR was used to document the presence of CDV in tissue samples, and a portion of the virus was subsequently sequenced for phylogenetic analysis. A high percentage of wildlife, both with (86%) and without (55%) clinical signs, tested positive for CDV, with the majority (77%) testing positive for the novel genotype. Microscopic findings, including syncytia in the lungs and viral inclusion bodies in urothelium, astrocytes, neurons, and bronchiolar epithelium, were also consistent with canine distemper. Minimal inflammation in the central nervous system of affected animals was indicative of the acute neurologic form of the disease. Pneumonia and parasitism were also commonly found in CDV-infected animals. Based on these results, CDV appears to be prevalent in eastern Tennessee wildlife. Subclinical or clinically recovered shedders are a potential source of this novel genotype for domestic dogs, and this genotype is genetically distinct from vaccine strains. PMID:27400957

  3. Schizophrenia: A Pathogenetic Autoimmune Disease Caused by Viruses and Pathogens and Dependent on Genes

    PubMed Central

    Carter, C. J.

    2011-01-01

    Many genes have been implicated in schizophrenia as have viral prenatal or adult infections and toxoplasmosis or Lyme disease. Several autoantigens also target key pathology-related proteins. These factors are interrelated. Susceptibility genes encode for proteins homologous to those of the pathogens while the autoantigens are homologous to pathogens' proteins, suggesting that the risk-promoting effects of genes and risk factors are conditional upon each other, and dependent upon protein matching between pathogen and susceptibility gene products. Pathogens' proteins may act as dummy ligands, decoy receptors, or via interactome interference. Many such proteins are immunogenic suggesting that antibody mediated knockdown of multiple schizophrenia gene products could contribute to the disease, explaining the immune activation in the brain and lymphocytes in schizophrenia, and the preponderance of immune-related gene variants in the schizophrenia genome. Schizophrenia may thus be a “pathogenetic” autoimmune disorder, caused by pathogens, genes, and the immune system acting together, and perhaps preventable by pathogen elimination, or curable by the removal of culpable antibodies and antigens. PMID:22567321

  4. NPMc+ cooperates with Flt3/ITD mutations to cause acute leukemia recapitulating human disease

    PubMed Central

    Rau, Rachel; Magoon, Daniel; Greenblatt, Sarah; Li, Li; Annesley, Colleen; Duffield, Amy S.; Huso, David; McIntyre, Emily; Clohessy, John G.; Reschke, Markus; Pandolfi, Pier Paolo; Small, Donald; Brown, Patrick

    2013-01-01

    Cytoplasmic nucleophosmin (NPMc+) mutations and FMS-like tyrosine kinase 3 (FLT3) internal tandem duplication (ITD) mutations are two of the most common known molecular alterations in acute myeloid leukemia (AML), and they frequently occur together suggesting cooperative leukemogenesis. To explore the specific relationship between NPMc+ and FLT3/ITD in vivo, we crossed Flt3/ITD knock-in mice with transgenic NPMc+ mice. Mice with both mutations develop a transplantable leukemia of either myeloid or lymphoid lineage, definitively demonstrating cooperation between Flt3/ITD and NPMc+. In mice with myeloid leukemia, functionally significant loss of heterozygosity of the wild-type Flt3 allele is common, similar to what is observed in human FLT3/ITD+ AML, providing further in vivo evidence of the importance of loss of wild-type FLT3 in leukemic initiation and progression. Additionally, in vitro clonogenic assays reveal that the combination of Flt3/ITD and NPMc+ mutations causes a profound monocytic expansion, in excess of that seen with either mutation alone consistent with the predominance of myelomonocytic phenotype in human FLT3/ITD+/NPMc+ AML. This in vivo model of Flt3/ITD+/NPMc+ leukemia closely recapitulates human disease and will therefore serve as a tool for the investigation of the biology of this common disease entity. PMID:24184354

  5. Pulmonary Veno-Occlusive Disease: A Newly Recognized Cause of Severe Pulmonary Hypertension in Dogs.

    PubMed

    Williams, K; Andrie, K; Cartoceti, A; French, S; Goldsmith, D; Jennings, S; Priestnall, S L; Wilson, D; Jutkowitz, A

    2016-07-01

    Pulmonary hypertension is a well-known though poorly characterized disease in veterinary medicine. In humans, pulmonary veno-occlusive disease (PVOD) is a rare cause of severe pulmonary hypertension with a mean survival time of 2 years without lung transplantation. Eleven adult dogs (5 males, 6 females; median age 10.5 years, representing various breeds) were examined following the development of severe respiratory signs. Lungs of affected animals were evaluated morphologically and with immunohistochemistry for alpha smooth muscle actin, desmin, CD31, CD3, CD20, and CD204. All dogs had pulmonary lesions consistent with PVOD, consisting of occlusive remodeling of small- to medium-sized pulmonary veins, foci of pulmonary capillary hemangiomatosis (PCH), and accumulation of hemosiderophages; 6 of 11 dogs had substantial pulmonary arterial medial and intimal thickening. Ultrastructural examination and immunohistochemistry showed that smooth muscle cells contributed to the venous occlusion. Increased expression of CD31 was evident in regions of PCH indicating increased numbers of endothelial cells in these foci. Spindle cells strongly expressing alpha smooth muscle actin and desmin co-localized with foci of PCH; similar cells were present but less intensely labeled elsewhere in non-PCH alveoli. B cells and macrophages, detected by immunohistochemistry, were not co-localized with the venous lesions of canine PVOD; small numbers of CD3-positive T cells were occasionally in and around the wall of remodeled veins. These findings indicate a condition in dogs with clinically severe respiratory disease and pathologic features resembling human PVOD, including foci of pulmonary venous remodeling and PCH. PMID:26926086

  6. Linking global climate and temperature variability to widespread amphibian declines putatively caused by disease.

    PubMed

    Rohr, Jason R; Raffel, Thomas R

    2010-05-01

    The role of global climate change in the decline of biodiversity and the emergence of infectious diseases remains controversial, and the effect of climatic variability, in particular, has largely been ignored. For instance, it was recently revealed that the proposed link between climate change and widespread amphibian declines, putatively caused by the chytrid fungus Batrachochytrium dendrobatidis (Bd), was tenuous because it was based on a temporally confounded correlation. Here we provide temporally unconfounded evidence that global El Niño climatic events drive widespread amphibian losses in genus Atelopus via increased regional temperature variability, which can reduce amphibian defenses against pathogens. Of 26 climate variables tested, only factors associated with temperature variability could account for the spatiotemporal patterns of declines thought to be associated with Bd. Climatic predictors of declines became significant only after controlling for a pattern consistent with epidemic spread (by temporally detrending the data). This presumed spread accounted for 59% of the temporal variation in amphibian losses, whereas El Niño accounted for 59% of the remaining variation. Hence, we could account for 83% of the variation in declines with these two variables alone. Given that global climate change seems to increase temperature variability, extreme climatic events, and the strength of Central Pacific El Niño episodes, climate change might exacerbate worldwide enigmatic declines of amphibians, presumably by increasing susceptibility to disease. These results suggest that changes to temperature variability associated with climate change might be as significant to biodiversity losses and disease emergence as changes to mean temperature. PMID:20404180

  7. Effects of habitual coffee consumption on cardiometabolic disease, cardiovascular health, and all-cause mortality.

    PubMed

    O'Keefe, James H; Bhatti, Salman K; Patil, Harshal R; DiNicolantonio, James J; Lucan, Sean C; Lavie, Carl J

    2013-09-17

    Coffee, after water, is the most widely consumed beverage in the United States, and is the principal source of caffeine intake among adults. The biological effects of coffee may be substantial and are not limited to the actions of caffeine. Coffee is a complex beverage containing hundreds of biologically active compounds, and the health effects of chronic coffee intake are wide ranging. From a cardiovascular (CV) standpoint, coffee consumption may reduce the risk of type 2 diabetes mellitus and hypertension, as well as other conditions associated with CV risk such as obesity and depression; but it may adversely affect lipid profiles depending on how the beverage is prepared. Regardless, a growing body of data suggests that habitual coffee consumption is neutral to beneficial regarding the risks of a variety of adverse CV outcomes including coronary heart disease, congestive heart failure, arrhythmias, and stroke. Moreover, large epidemiological studies suggest that regular coffee drinkers have reduced risks of mortality, both CV and all-cause. The potential benefits also include protection against neurodegenerative diseases, improved asthma control, and lower risk of select gastrointestinal diseases. A daily intake of ∼2 to 3 cups of coffee appears to be safe and is associated with neutral to beneficial effects for most of the studied health outcomes. However, most of the data on coffee's health effects are based on observational data, with very few randomized, controlled studies, and association does not prove causation. Additionally, the possible advantages of regular coffee consumption have to be weighed against potential risks (which are mostly related to its high caffeine content) including anxiety, insomnia, tremulousness, and palpitations, as well as bone loss and possibly increased risk of fractures. PMID:23871889

  8. Glycogen Storage Disease type 1a – a secondary cause for hyperlipidemia: report of five cases

    PubMed Central

    2013-01-01

    Background and aims Glycogen storage disease type Ia (GSD Ia) is a rare metabolic disorder, caused by deficient activity of glucose-6-phosphatase-α. It produces fasting induced hypoglycemia and hepatomegaly, usually manifested in the first semester of life. Besides, it is also associated with growth delay, anemia, platelet dysfunction, osteopenia and sometimes osteoporosis. Hyperlipidemia and hyperuricemia are almost always present and hepatocellular adenomas and renal dysfunction frequent late complications. Methods The authors present a report of five adult patients with GSD Ia followed in internal medicine appointments and subspecialties. Results Four out of five patients were diagnosed in the first 6 months of life, while the other one was diagnosed in adult life after the discovery of hepatocellular adenomas. In two cases genetic tests were performed, being identified the missense mutation R83C in one, and the mutation IVS4-3C > G in the intron 4 of glucose-6-phosphatase gene, not previously described, in the other. Growth retardation was present in 3 patients, and all of them had anemia, increased bleeding tendency and hepatocellular adenomas; osteopenia/osteoporosis was present in three cases. All but one patient had marked hyperlipidemia and hyperuricemia, with evidence of endothelial dysfunction in one case and of brain damage with refractory epilepsy in another case. Proteinuria was present in two cases and end-stage renal disease in another case. There was a great variability in the dietary measures; in one case, liver transplantation was performed, with correction of the metabolic derangements. Conclusions Hyperlipidemia is almost always present and only partially responds to dietary and drug therapy; liver transplantation is the only definitive solution. Although its association with premature atherosclerosis is rare, there have been reports of endothelial dysfunction, raising the possibility for increased cardiovascular risk in this group of

  9. Long-term disease dynamics in lakes: causes and consequences of chytrid infections in Daphnia populations.

    PubMed

    Johnson, Pieter T J; Ives, Anthony R; Lathrop, Richard C; Carpenter, Stephen R

    2009-01-01

    Understanding the drivers and consequences of disease epidemics is an important frontier in ecology. However, long-term data on hosts, their parasites, and the corresponding environmental conditions necessary to explore these interactions are often unavailable. We examined the dynamics of Daphnia pulicaria, a keystone zooplankter in lake ecosystems, to explore the long-term causes and consequences of infection by a chytridiomycete parasitoid (Polycaryum laeve). After quantifying host-pathogen dynamics from vouchered samples collected over 15 years, we used autoregressive models to evaluate (1) hypothesized drivers of infection, including host density, water temperature, dissolved oxygen, host-food availability, and lake mixing; and (2) the effects of epidemics on host populations. Infection was present in most years but varied widely in prevalence, from < 1% to 34%, with seasonal peaks in early spring and late fall. Within years, lake stratification strongly inhibited P. laeve transmission, such that epidemics occurred primarily during periods of water mixing. Development of the thermocline likely reduced transmission by spatially separating susceptible hosts from infectious zoospores. Among years, ice duration and cumulative snowfall correlated negatively with infection prevalence, likely because of reductions in spring phytoplankton and D. pulicaria density in years with extended winters. Epidemics also influenced dynamics of the host population. Infected D. pulicaria rarely (< 1%) contained eggs, and P. laeve prevalence was positively correlated with sexual reproduction in D. pulicaria. Analyses of D. pulicaria density-dependent population dynamics predicted that, in the absence of P. laeve infection, host abundance would be 11-50% higher than what was observed. By underscoring the importance of complex physical processes in controlling host-parasite interactions and of epidemic disease in influencing host populations, our results highlight the value of long

  10. Gastroesophageal Reflux Disease and overall and Cause-specific Mortality: A Prospective Study of 50000 Individuals

    PubMed Central

    Islami, Farhad; Pourshams, Akram; Nasseri-Moghaddam, Siavosh; Khademi, Hooman; Poutschi, Hossein; Khoshnia, Masoud; Norouzi, Alireza; Amiriani, Taghi; Sohrabpour, Amir Ali; Aliasgari, Ali; Jafari, Elham; Semnani, Shahryar; Abnet, Christian C.; Pharaoh, Paul D.; Brennan, Paul; Kamangar, Farin; Dawsey, Sanford M.; Boffetta, Paolo; Malekzadeh, Reza

    2014-01-01

    BACKGROUND Only a few studies in Western countries have investigated the association between gastroesophageal reflux disease (GERD) and mortality at the general population level and they have shown mixed results. This study investigated the association between GERD symptoms and overall and cause-specific mortality in a large prospective population-based study in Golestan Province, Iran. METHODS Baseline data on frequency, onset time, and patient-perceived severity of GERD symptoms were available for 50001 participants in the Golestan Cohort Study (GCS). We identified 3107 deaths (including 1146 circulatory and 470 cancer-related) with an average follow-up of 6.4 years and calculated hazard ratios (HR) and 95% confidence intervals (CI) adjusted for multiple potential confounders. RESULTS Severe daily symptoms (defined as symptoms interfering with daily work or causing nighttime awakenings on a daily bases, reported by 4.3% of participants) were associated with cancer mortality (HR 1.48, 95% CI: 1.04-2.05). This increase was too small to noticeably affect overall mortality. Mortality was not associated with onset time or frequency of GERD and was not increased with mild to moderate symptoms. CONCLUSION We have observed an association with GERD and increased cancer mortality in a small group of individuals that had severe symptoms. Most patients with mild to moderate GERD can be re-assured that their symptoms are not associated with increased mortality. PMID:24872865

  11. Gastroesophageal Reflux Disease and overall and Cause-specific Mortality: A Prospective Study of 50000 Individuals.

    PubMed

    Islami, Farhad; Pourshams, Akram; Nasseri-Moghaddam, Siavosh; Khademi, Hooman; Poutschi, Hossein; Khoshnia, Masoud; Norouzi, Alireza; Amiriani, Taghi; Sohrabpour, Amir Ali; Aliasgari, Ali; Jafari, Elham; Semnani, Shahryar; Abnet, Christian C; Pharaoh, Paul D; Brennan, Paul; Kamangar, Farin; Dawsey, Sanford M; Boffetta, Paolo; Malekzadeh, Reza

    2014-04-01

    BACKGROUND Only a few studies in Western countries have investigated the association between gastroesophageal reflux disease (GERD) and mortality at the general population level and they have shown mixed results. This study investigated the association between GERD symptoms and overall and cause-specific mortality in a large prospective population-based study in Golestan Province, Iran. METHODS Baseline data on frequency, onset time, and patient-perceived severity of GERD symptoms were available for 50001 participants in the Golestan Cohort Study (GCS). We identified 3107 deaths (including 1146 circulatory and 470 cancer-related) with an average follow-up of 6.4 years and calculated hazard ratios (HR) and 95% confidence intervals (CI) adjusted for multiple potential confounders. RESULTS Severe daily symptoms (defined as symptoms interfering with daily work or causing nighttime awakenings on a daily bases, reported by 4.3% of participants) were associated with cancer mortality (HR 1.48, 95% CI: 1.04-2.05). This increase was too small to noticeably affect overall mortality. Mortality was not associated with onset time or frequency of GERD and was not increased with mild to moderate symptoms. CONCLUSION We have observed an association with GERD and increased cancer mortality in a small group of individuals that had severe symptoms. Most patients with mild to moderate GERD can be re-assured that their symptoms are not associated with increased mortality. PMID:24872865

  12. VCP recruitment to mitochondria causes mitophagy impairment and neurodegeneration in models of Huntington's disease

    PubMed Central

    Guo, Xing; Sun, XiaoYan; Hu, Di; Wang, Ya-Juan; Fujioka, Hisashi; Vyas, Rajan; Chakrapani, Sudha; Joshi, Amit Umesh; Luo, Yu; Mochly-Rosen, Daria; Qi, Xin

    2016-01-01

    Mutant Huntingtin (mtHtt) causes neurodegeneration in Huntington's disease (HD) by evoking defects in the mitochondria, but the underlying mechanisms remains elusive. Our proteomic analysis identifies valosin-containing protein (VCP) as an mtHtt-binding protein on the mitochondria. Here we show that VCP is selectively translocated to the mitochondria, where it is bound to mtHtt in various HD models. Mitochondria-accumulated VCP elicits excessive mitophagy, causing neuronal cell death. Blocking mtHtt/VCP mitochondrial interaction with a peptide, HV-3, abolishes VCP translocation to the mitochondria, corrects excessive mitophagy and reduces cell death in HD mouse- and patient-derived cells and HD transgenic mouse brains. Treatment with HV-3 reduces behavioural and neuropathological phenotypes of HD in both fragment- and full-length mtHtt transgenic mice. Our findings demonstrate a causal role of mtHtt-induced VCP mitochondrial accumulation in HD pathogenesis and suggest that the peptide HV-3 might be a useful tool for developing new therapeutics to treat HD. PMID:27561680

  13. Transcriptome Remodeling Contributes to Epidemic Disease Caused by the Human Pathogen Streptococcus pyogenes

    PubMed Central

    Beres, Stephen B.; Kachroo, Priyanka; Nasser, Waleed; Olsen, Randall J.; Zhu, Luchang; Flores, Anthony R.; de la Riva, Ivan; Paez-Mayorga, Jesus; Jimenez, Francisco E.; Cantu, Concepcion; Vuopio, Jaana; Jalava, Jari; Kristinsson, Karl G.; Gottfredsson, Magnus; Corander, Jukka; Fittipaldi, Nahuel; Di Luca, Maria Chiara; Petrelli, Dezemona; Vitali, Luca A.; Raiford, Annessa; Jenkins, Leslie

    2016-01-01

    ABSTRACT For over a century, a fundamental objective in infection biology research has been to understand the molecular processes contributing to the origin and perpetuation of epidemics. Divergent hypotheses have emerged concerning the extent to which environmental events or pathogen evolution dominates in these processes. Remarkably few studies bear on this important issue. Based on population pathogenomic analysis of 1,200 Streptococcus pyogenes type emm89 infection isolates, we report that a series of horizontal gene transfer events produced a new pathogenic genotype with increased ability to cause infection, leading to an epidemic wave of disease on at least two continents. In the aggregate, these and other genetic changes substantially remodeled the transcriptomes of the evolved progeny, causing extensive differential expression of virulence genes and altered pathogen-host interaction, including enhanced immune evasion. Our findings delineate the precise molecular genetic changes that occurred and enhance our understanding of the evolutionary processes that contribute to the emergence and persistence of epidemically successful pathogen clones. The data have significant implications for understanding bacterial epidemics and for translational research efforts to blunt their detrimental effects. PMID:27247229

  14. Parkinson disease-associated mutant VPS35 causes mitochondrial dysfunction by recycling DLP1 complexes

    PubMed Central

    Fujioka, Hisashi; Hoppel, Charles; Whone, Alan L.; Caldwell, Maeve A.; Cullen, Peter J.; Liu, Jun; Zhu, Xiongwei

    2015-01-01

    Mitochondrial dysfunction represents a critical step during the pathogenesis of Parkinson disease (PD) and increasing evidence suggests abnormal mitochondrial dynamics and quality control as important underlying mechanisms. The VPS35 gene, encoding a key component of the retromer complex, is the third autosomal-dominant gene associated with PD. However, how VPS35 mutations may lead to neurodegeneration remains unclear. Here we demonstrate that PD-associated VPS35 mutations caused mitochondrial fragmentation and cell death in cultured neurons in vitro, in mouse substantia nigra neurons in vivo, and in human fibroblasts from PD patient bearing the D620N mutation. VPS35-induced mitochondrial deficits and neuronal dysfunction could be prevented by inhibition of mitochondrial fission. VPS35 mutation caused increased interactions with DLP1 which enhanced mitochondrial DLP1 complex turnover via mitochondria-derived vesicles-dependent trafficking to lysosomes for degradation. Importantly, oxidative stress increased the VPS35–DLP1 interaction which was also increased in the brains of sporadic PD cases. These results revealed a novel cellular mechanism for the involvement of VPS35 in mitochondrial fission, dysregulation of which is likely involved in the pathogenesis of familial, and possibly sporadic, PD. PMID:26618722

  15. [In vitro activity of doripenem against strains from pediatric diseases and strains causing purulent meningitis].

    PubMed

    Ohta, Merime; Toba, Shinsuke; Ito, Akinobu; Nakamura, Rio; Tsuji, Masakatsu

    2012-12-01

    This study evaluated the in vitro activity of doripenem (DRPM) against 200 Streptococcus pneumoniae and 197 Haemophilus influenzae from children and adults in 2007, 50 H. influenzae type b in 2006, 20 Listeria monocytogenes in 1990-2005, 23 Neisseria meningitidis in 2007-2009 and 83 Bordetella pertussis in 1989-2003. All strains were isolated from Japanese clinical facilities. We also investigated in vitro activity of other carbapenems (meropenem, imipenem, panipenem, biapenem), cephems (ceftriaxone, cefotaxime), ampicillin and clarithromycin. The all MICs were determined by a broth micro dilution method or an agar dilution method according to CLSI. The MIC90(s) of DRPM against S. pneumoniae and H. influenzae from children were 0.25 microg/mL, 1 microg/mL, respectively, which were similar to strains from adults. These results suggested that antibacterial activity of DRPM is not variable by patient's age. DRPM also showed excellent activities against H. influenzae type b, L. monocytogenes and N. meningitidis, which cause purulent meningitis, and B. pertussis causing whooping cough more than the other carbapenems. DRPM showed superior activities against serious strains of pediatric infection diseases. PMID:23593734

  16. How do Mutations in GJB1 Cause X-linked Charcot-Marie-Tooth Disease?

    PubMed Central

    Kleopa, Kleopas A.; Abrams, Charles K.; Scherer, Steven S.

    2012-01-01

    The X-linked form of Charcot-Marie-Tooth disease (CMT1X) is the second most common form of hereditary motor and sensory neuropathy. The clinical phenotype is characterized by progressive weakness, atrophy, and sensory abnormalities that are most pronounced in the distal extremities. Some patients have CNS manifestations. Affected males have moderate to severe symptoms, whereas heterozygous females are usually less affected. Neurophysiology shows intermediate slowing of conduction and length-dependent axonal loss. Nerve biopsies show more prominent axonal degeneration than de/remyelination. Mutations in GJB1, the gene that encodes the gap junction (GJ) protein connexin32 (Cx32) cause CMT1X; more than 400 different mutations have been described. Many Cx32 mutants fail to form functional GJs, or form GJs with abnormal biophysical properties. Schwann cells and oligodendrocytes express Cx32, and the GJs formed by Cx32 play an important role in the homeostasis of myelinated axons. Animal models of CMT1X demonstrate that loss of Cx32 in myelinating Schwann cells causes a demyelinating neuropathy. Effective therapies remain to be developed. PMID:22771394

  17. Gender differences and disparities in all-cause and coronary heart disease mortality: epidemiological aspects.

    PubMed

    Barrett-Connor, Elizabeth

    2013-08-01

    This overview is primarily concerned with large recent prospective cohort studies of adult populations, not patients, because the latter studies are confounded by differences in medical and surgical management for men vs. women. When early papers are uniquely informative they are also included. Because the focus is on epidemiology, details of age, sex, sample size, and source as well as study methods are provided. Usually the primary outcomes were all-cause or coronary heart disease (CHD) mortality using baseline data from midlife or older adults. Fifty years ago few prospective cohort studies of all-cause or CHD mortality included women. Most epidemiologic studies that included community-dwelling adults did not include both sexes and still do not report men and women separately. Few studies consider both sex (biology) and gender (behavior and environment) differences. Lifespan studies describing survival after live birth are not considered here. The important effects of prenatal and early childhood biologic and behavioral factors on adult mortality are beyond the scope of this review. Clinical trials are not discussed. Overall, presumptive evidence for causality was equivalent for psychosocial and biological exposures, and these attributes were often associated with each other. Inconsistencies or gaps were particularly obvious for studies of sex or gender differences in age and optimal measures of body size for CHD outcomes, and in the striking interface of diabetes and people with the metabolic syndrome, most of whom have unrecognized diabetes. PMID:24054926

  18. Geosmithia argillacea: An Emerging Cause of Invasive Mycosis in Human Chronic Granulomatous Disease

    PubMed Central

    Challipalli, Malliswari; Anderson, Victoria; Shea, Yvonne R.; Marciano, Beatriz; Hilligoss, Dianne; Marquesen, Martha; DeCastro, Rosamma; Liu, Yen-chun; Sutton, Deanna A.; Wickes, Brian L.; Kammeyer, Patricia L.; Sigler, Lynne; Sullivan, Kathleen; Kang, Elizabeth M.; Malech, Harry L.; Holland, Steven M.; Zelazny, Adrian M.

    2011-01-01

    Background. Chronic granulomatous disease (CGD) is an inherited disorder of the nicotinamide adenine dinucleotide phosphate oxidase that leads to defective production of microbicidal superoxide and other oxidative radicals, resulting in increased susceptibility to invasive infections, especially those due to fungi. Methods. Geosmithia argillacea was identified from cultured isolates by genomic sequencing of the internal transcribed spacer region. Isolates previously identified as Paecilomyces variotii, a filamentous fungus closely resembling G. argillacea, were also examined. Results. We identified G. argillacea as the cause of invasive mycosis in 7 CGD patients. In 5 cases, the fungus had been previously identified morphologically as P. variotii. All patients had pulmonary lesions; 1 had disseminated lesions following inhalational pneumonia. Infections involved the chest wall and contiguous ribs in 2 patients and disseminated to the brain in 1 patient. Four patients with pneumonia underwent surgical intervention. All patients responded poorly to medical treatment, and 3 died. Conclusions. We report the first cases of invasive mycosis caused by G. argillacea in CGD patients. G. argillacea infections in CGD are often refractory and severe with a high fatality rate. Surgical intervention has been effective in some cases. G. argillacea is a previously underappreciated and frequently misidentified pathogen in CGD that should be excluded when P. variotii is identified morphologically. PMID:21367720

  19. Characterization of Vibrio parahaemolyticus causing acute hepatopancreatic necrosis disease in southern Thailand.

    PubMed

    Kongrueng, J; Yingkajorn, M; Bunpa, S; Sermwittayawong, N; Singkhamanan, K; Vuddhakul, V

    2015-11-01

    Vibrio parahaemolyticus was isolated from shrimp of five farms located in the Pattani and Songkhla provinces of southern Thailand. Using a PCR method targeted to the unique DNA sequences derived from the plasmid (AP2 primers) and the toxin gene (AP3 primers) of V. parahaemolyticus that caused acute hepatopancreatic necrosis disease (AHPND), a total of 33 of 108 isolates were positive. In contrast, all 63 and 66 isolates of clinical and environmental V. parahaemolyticus, respectively, obtained previously from 2008 to 2014 from the same area were negative. This implied that these strains were likely to be the cause of the outbreak of AHPND in this area. Intestinal samples proved to be a better source for the isolation of V. parahaemolyticus AHPND than the hepatopancreas. All isolates were investigated for haemolytic activity, virulence genes, serotypes, genotypes and antibiotic susceptibility. All the AHPND isolates had a unique O antigen, but small variations of the K antigens were detected from different farms. In addition, the DNA profiles of V. parahaemolyticus AHPND isolates were similar, but distinct from those clinical and environmental isolates. It is postulated that the causative agent of AHPND might have originated from one clone and then slightly different serotypes subsequently developed. PMID:25287127

  20. VCP recruitment to mitochondria causes mitophagy impairment and neurodegeneration in models of Huntington's disease.

    PubMed

    Guo, Xing; Sun, XiaoYan; Hu, Di; Wang, Ya-Juan; Fujioka, Hisashi; Vyas, Rajan; Chakrapani, Sudha; Joshi, Amit Umesh; Luo, Yu; Mochly-Rosen, Daria; Qi, Xin

    2016-01-01

    Mutant Huntingtin (mtHtt) causes neurodegeneration in Huntington's disease (HD) by evoking defects in the mitochondria, but the underlying mechanisms remains elusive. Our proteomic analysis identifies valosin-containing protein (VCP) as an mtHtt-binding protein on the mitochondria. Here we show that VCP is selectively translocated to the mitochondria, where it is bound to mtHtt in various HD models. Mitochondria-accumulated VCP elicits excessive mitophagy, causing neuronal cell death. Blocking mtHtt/VCP mitochondrial interaction with a peptide, HV-3, abolishes VCP translocation to the mitochondria, corrects excessive mitophagy and reduces cell death in HD mouse- and patient-derived cells and HD transgenic mouse brains. Treatment with HV-3 reduces behavioural and neuropathological phenotypes of HD in both fragment- and full-length mtHtt transgenic mice. Our findings demonstrate a causal role of mtHtt-induced VCP mitochondrial accumulation in HD pathogenesis and suggest that the peptide HV-3 might be a useful tool for developing new therapeutics to treat HD. PMID:27561680

  1. Performance-based regulation: enterprise responsibility for reducing death, injury, and disease caused by consumer products.

    PubMed

    Sugarman, Stephen D

    2009-12-01

    This article offers a bold new idea for confronting the staggering level of death, injury, and disease caused by five consumer products: cigarettes, alcohol, guns, junk food, and motor vehicles. Business leaders try to frame these negative outcomes as "collateral damage" that is someone else's problem. That framing not only is morally objectionable but also overlooks the possibility that, with proper prodding, industry could substantially lessen these public health disasters. I seek to reframe the public perception of who is responsible and propose to deploy a promising approach called "performance-based regulation" to combat the problem. Performance-based regulation would impose on manufacturers a legal obligation to reduce the negative social costs of their products. Rather than involving them in litigation or forcing them to operate differently (as "command-and-control" regimes do), performance-based regulation allows the firms to determine how best to decrease bad public health consequences. Like other public health strategies, performance-based regulation focuses on those who are far more likely than individual consumers to achieve real gains. Analogous to a tax on causing harm that exceeds a threshold level, performance-based regulation seeks to harness private initiative in pursuit of the public good. PMID:20018990

  2. Genotypes of the Enterovirus Causing Hand Foot and Mouth Disease in Shanghai, China, 2012-2013

    PubMed Central

    Xu, Menghua; Su, Liyun; Cao, Lingfeng; Zhong, Huaqing; Dong, Niuniu; Dong, Zuoquan; Xu, Jin

    2015-01-01

    Sporadic HFMD (hand foot and mouth disease, HFMD) cases and outbreaks caused by etiologic agents other than EV71 and CA16 have increased globally. We conducted this study to investigate the prevalence and genetic characteristics of enteroviruses, especially the non-EV71 and non-CA16 enteroviruses, causing HFMD in Shanghai. Clinical specimens were collected from patients with a diagnosis of HFMD. A partial length of VP1 was amplified with RT-PCR and subjected to direct sequencing. Phylogenetic analyses were performed using MEGA 5.0. The ages of the HFMD cases ranged from 3 to 96 months, and the male/female ratio was 1.41. The median hospital stay was 2.96 days. Up to 18.0% of patients had neurologic system complications such as encephalitis, meningoencephalitis or meningitis. Of the 480 samples, 417 were positive for enterovirus (86.9%) with RT-PCR. A total of 13 enterovirus genotypes were identified. The most frequent genotypes were CA6 (31.9%), EV71 (30.6%), CA16 (8.8%) and CA10 (7.5%). Infections with CA6, EV71, CA16 and CA10 were prevalent throughout the years of study, while the proportion of CA6 notably increased from Sep. 2012 to Dec. 2013. Phylogenetic analyses showed that EV71 strains belonged to the C4a subgenogroup and CA16 was identified as B1b subgenogroup. The CA6 strains were assigned to genogroup F, whereas the CA10 strains were assigned to genogroup D. Patients infected with CA6 were typically younger, had a shorter hospital stay and had a lower incidence of neurologic system complications when compared to patients infected with EV71. Our study demonstrates that the enterovirus genotypes causing HFMD were diversified, and there was an increasing prevalence of the non-EV71 and non-CA16 enteroviruses from 2012 to 2013. CA6 was the most predominant pathogen causing HFMD from Sep. 2012 to Dec. 2013, and it often caused relatively mild HFMD symptoms. Most severe HFMD cases were associated with EV71 infection. PMID:26398767

  3. Mucor rot - An emerging postharvest disease of mandarin fruit caused by Mucor piriformis and other Mucor spp. in California

    Technology Transfer Automated Retrieval System (TEKTRAN)

    In recent years, an emerging, undescribed postharvest fruit rot disease was observed on mandarin fruit after extended storage in California. We collected decayed mandarin fruit from three citrus packinghouses in the Central Valley of California in 2015 and identified this disease as Mucor rot caused...

  4. Myelin-associated glycoprotein gene mutation causes Pelizaeus-Merzbacher disease-like disorder.

    PubMed

    Lossos, Alexander; Elazar, Nimrod; Lerer, Israela; Schueler-Furman, Ora; Fellig, Yakov; Glick, Benjamin; Zimmerman, Bat-El; Azulay, Haim; Dotan, Shlomo; Goldberg, Sharon; Gomori, John M; Ponger, Penina; Newman, J P; Marreed, Hodaifah; Steck, Andreas J; Schaeren-Wiemers, Nicole; Mor, Nofar; Harel, Michal; Geiger, Tamar; Eshed-Eisenbach, Yael; Meiner, Vardiella; Peles, Elior

    2015-09-01

    Pelizaeus-Merzbacher disease is an X-linked hypomyelinating leukodystrophy caused by mutations or rearrangements in PLP1. It presents in infancy with nystagmus, jerky head movements, hypotonia and developmental delay evolving into spastic tetraplegia with optic atrophy and variable movement disorders. A clinically similar phenotype caused by recessive mutations in GJC2 is known as Pelizaeus-Merzbacher-like disease. Both genes encode proteins associated with myelin. We describe three siblings of a consanguineous family manifesting the typical infantile-onset Pelizaeus-Merzbacher disease-like phenotype slowly evolving into a form of complicated hereditary spastic paraplegia with mental retardation, dysarthria, optic atrophy and peripheral neuropathy in adulthood. Magnetic resonance imaging and spectroscopy were consistent with a demyelinating leukodystrophy. Using genetic linkage and exome sequencing, we identified a homozygous missense c.399C>G; p.S133R mutation in MAG. This gene, previously associated with hereditary spastic paraplegia, encodes myelin-associated glycoprotein, which is involved in myelin maintenance and glia-axon interaction. This mutation is predicted to destabilize the protein and affect its tertiary structure. Examination of the sural nerve biopsy sample obtained in childhood in the oldest sibling revealed complete absence of myelin-associated glycoprotein accompanied by ill-formed onion-bulb structures and a relatively thin myelin sheath of the affected axons. Immunofluorescence, cell surface labelling, biochemical analysis and mass spectrometry-based proteomics studies in a variety of cell types demonstrated a devastating effect of the mutation on post-translational processing, steady state expression and subcellular localization of myelin-associated glycoprotein. In contrast to the wild-type protein, the p.S133R mutant was retained in the endoplasmic reticulum and was subjected to endoplasmic reticulum-associated protein degradation by the

  5. Proportion of Pelvic Inflammatory Disease Cases Caused by Chlamydia trachomatis: Consistent Picture From Different Methods

    PubMed Central

    Price, Malcolm J.; Ades, A. E.; Welton, Nicky J.; Simms, Ian; Macleod, John; Horner, Paddy J.

    2016-01-01

    Background. Pelvic inflammatory disease (PID) is a leading cause of both tubal factor infertility and ectopic pregnancy. Chlamydia trachomatis is an important risk factor for PID, but the proportion of PID cases caused by C. trachomatis is unclear. Estimates of this are required to evaluate control measures. Methods. We consider 5 separate methods of estimating age-group-specific population excess fractions (PEFs) of PID due to C. trachomatis, using routine data, surveys, case-control studies, and randomized controlled trials, and apply these to data from the United Kingdom before introduction of the National Chlamydia Screening Programme. Results. As they are informed by randomized comparisons and national exposure and outcome estimates, our preferred estimates of the proportion of PID cases caused by C. trachomatis are 35% (95% credible interval [CrI], 11%–69%) in women aged 16–24 years and 20% (95% CrI, 6%–38%) in women aged 16–44 years in the United Kingdom. There is a fair degree of consistency between adjusted estimates of PEF, but all have wide 95% CrIs. The PEF decreases from 53.5% (95% CrI, 15.6%–100%) in women aged 16–19 years to 11.5% (95% CrI, 3.0%–25.7%) in women aged 35–44 years. Conclusions. The PEFs of PID due to C. trachomatis decline steeply with age by a factor of around 5-fold between younger and older women. Further studies of the etiology of PID in different age groups are required. PMID:27260786

  6. Interleukin-6 Deficiency Does Not Affect Motor Neuron Disease Caused by Superoxide Dismutase 1 Mutation

    PubMed Central

    Han, Yongmei; Ripley, Barry; Serada, Satoshi; Naka, Tetsuji; Fujimoto, Minoru

    2016-01-01

    Background & Aim Amyotrophic Lateral Sclerosis (ALS) is an adult-onset, progressive, motor neuron degenerative disease. Recent evidence indicates that inflammation is associated with many neurodegenerative diseases including ALS. Previously, abnormal levels of inflammatory cytokines including IL-1β, IL-6 and TNF-α were described in ALS patients and/or in mouse ALS models. In addition, one study showed that blocking IL-1β could slow down progression of ALS-like symptoms in mice. In this study, we examined a role for IL-6 in ALS, using an animal model for familial ALS. Methods Mice with mutant SOD1 (G93A) transgene, a model for familial ALS, were used in this study. The expression of the major inflammatory cytokines, IL-6, IL-1β and TNF-α, in spinal cords of these SOD1 transgenic (TG) mice were assessed by real time PCR. Mice were then crossed with IL-6(-/-) mice to generate SOD1TG/IL-6(-/-) mice. SOD1 TG/IL-6(-/-) mice (n = 17) were compared with SOD1 TG/IL-6(+/-) mice (n = 18), SOD1 TG/IL-6(+/+) mice (n = 11), WT mice (n = 15), IL-6(+/-) mice (n = 5) and IL-6(-/-) mice (n = 8), with respect to neurological disease severity score, body weight and the survival. We also histologically compared the motor neuron loss in lumber spinal cords and the atrophy of hamstring muscles between these mouse groups. Results Levels of IL-6, IL-1β and TNF-α in spinal cords of SOD1 TG mice was increased compared to WT mice. However, SOD1 TG/IL-6(-/-) mice exhibited weight loss, deterioration in motor function and shortened lifespan (167.55 ± 11.52 days), similarly to SOD1 TG /IL-6(+/+) mice (164.31±12.16 days). Motor neuron numbers and IL-1β and TNF-α levels in spinal cords were not significantly different in SOD1 TG /IL-6(-/-) mice and SOD1 TG /IL-6 (+/+) mice. Conclusion These results provide compelling preclinical evidence indicating that IL-6 does not directly contribute to motor neuron disease caused by SOD1 mutations. PMID:27070121

  7. Disease and Predation: Sorting out Causes of a Bighorn Sheep (Ovis canadensis) Decline

    PubMed Central

    Smith, Joshua B.; Jenks, Jonathan A.; Grovenburg, Troy W.; Klaver, Robert W.

    2014-01-01

    Estimating survival and documenting causes and timing of mortality events in neonate bighorn sheep (Ovis canadensis) improves understanding of population ecology and factors influencing recruitment. During 2010–2012, we captured and radiocollared 74 neonates in the Black Hills, South Dakota, of which 95% (70) died before 52 weeks of age. Pneumonia (36%) was the leading cause of mortality followed by predation (30%). We used known fate analysis in Program MARK to estimate weekly survival rates and investigate the influence of intrinsic variables on 52-week survival. Model {S1 wk, 2–8 wks, >8 wks} had the lowest AICc (Akaike’s Information Criterion corrected for small sample size) value, indicating that age (3-stage age-interval: 1 week, 2–8 weeks, and >8 weeks) best explained survival. Weekly survival estimates for 1 week, 2–8 weeks, and >8 weeks were 0.81 (95% CI = 0.70–0.88), 0.86 (95% CI = 0.81–0.90), and 0.94 (95% CI = 0.91–0.96), respectively. Overall probability of surviving 52 weeks was 0.02 (95% CI = 0.01–0.07). Of 70 documented mortalities, 21% occurred during the first week, 55% during weeks 2–8, and 23% occurred >8 weeks of age. We found pneumonia and predation were temporally heterogeneous with lambs most susceptible to predation during the first 2–3 weeks of life, while the greatest risk from pneumonia occurred from weeks 4–8. Our results indicated pneumonia was the major factor limiting recruitment followed by predation. Mortality from predation may have been partly compensatory to pneumonia and its effects were less pronounced as alternative prey became available. Given the high rates of pneumonia-caused mortality we observed, and the apparent lack of pneumonia-causing pathogens in bighorn populations in the western Black Hills, management activities should be geared towards eliminating contact between diseased and healthy populations. PMID:24516623

  8. Moko Disease-Causing Strains of Ralstonia solanacearum from Brazil Extend Known Diversity in Paraphyletic Phylotype II.

    PubMed

    Albuquerque, Greecy M R; Santos, Liliana A; Felix, Kátia C S; Rollemberg, Christtianno L; Silva, Adriano M F; Souza, Elineide B; Cellier, Gilles; Prior, Philippe; Mariano, Rosa L R

    2014-11-01

    The epidemic situation of Moko disease-causing strains in Latin America and Brazil is unclear. Thirty-seven Ralstonia solanacearum strains from Brazil that cause the Moko disease on banana and heliconia plants were sampled and phylogenetically typed using the endoglucanase (egl) and DNA repair (mutS) genes according to the phylotype and sequevar classification. All of the strains belonged to phylotype II and a portion of the strains was typed as the Moko disease-related sequevars IIA-6 and IIA-24. Nevertheless, two unsuspected sequevars also harbored the Moko disease-causing strains IIA-41 and IIB-25, and a new sequevar was described and named IIA-53. All of the strains were pathogenic to banana and some of the strains of sequevars IIA-6, IIA-24, and IIA-41 were also pathogenic to tomato. The Moko disease-causing strains from sequevar IIB-25 were pathogenic to potato but not to tomato. These results highlight the high diversity of strains of Moko in Brazil, reinforce the efficiency of the egl gene to reveal relationships among these strains, and contribute to a better understanding of the diversity of paraphyletic Moko disease-causing strains of the R. solanacearum species complex, where the following seven distinct genetic clusters have been described: IIA-6, IIA-24, IIA-41, IIA-53, IIB-3, IIB-4, and IIB-25. PMID:24848276

  9. Unusual pecan diseases that might appear during a wet year

    Technology Transfer Automated Retrieval System (TEKTRAN)

    In most growing seasons the diseases of most concern to pecan growers in the southeastern United States are pecan scab (particularly in wet years) and anthracnose (most often a problem when trees are stressed in mid-late season). Pecan is known to also be affected by at least 17 other pathogens, onl...

  10. Is severe progressive liver disease caused by alpha-1-antitrypsin deficiency more common in children or adults?

    PubMed

    Chu, Andrew S; Chopra, Kapil B; Perlmutter, David H

    2016-07-01

    The classical form of alpha-1-antitrypsin deficiency (A1ATD) is known to cause liver disease in children and adults, but there is relatively little information about the risk of severe, progressive liver disease and the need for liver transplantation. To better understand how newly evolving pharmacological, genetic, and cellular therapies may be targeted according to risk for progressive liver disease, we sought to determine the age distribution of A1ATD as a cause of severe liver disease, as defined by the need for liver transplantation. Using 3 US liver transplantation databases for the period 1991-2012, we found 77.2% of 1677 liver transplants with a reported diagnosis of A1ATD were adults. The peak age range was 50-64 years. Using 2 of the databases which included specific A1AT phenotypes, we found that many of these adults who undergo liver transplantation with A1ATD as the diagnosis are heterozygotes and have other potential causes of liver disease, most notably obesity and ethanol abuse. However, even when these cases are excluded and only ZZ and SZ phenotypes are considered, severe liver disease requiring transplantation is more than 2.5 times as likely in adults. The analysis also showed a markedly increased risk for males. In the pediatric group, almost all of the transplants are done in children less than 5 years of age. In conclusion, A1ATD causes progressive liver disease most commonly in adults with males in the highest risk category. In the pediatric group, children less than 5 years of age are highest in risk. These results suggest that A1ATD most commonly causes liver disease by mechanisms similar to age-dependent degenerative diseases and more rarely in children by powerful modifiers. Liver Transplantation 22 886-894 2016 AASLD. PMID:26946192

  11. Amyloid Triggers Extensive Cerebral Angiogenesis Causing Blood Brain Barrier Permeability and Hypervascularity in Alzheimer's Disease

    PubMed Central

    Biron, Kaan E.; Dickstein, Dara L.; Gopaul, Rayshad; Jefferies, Wilfred A.

    2011-01-01

    Evidence of reduced blood-brain barrier (BBB) integrity preceding other Alzheimer's disease (AD) pathology provides a strong link between cerebrovascular angiopathy and AD. However, the “Vascular hypothesis”, holds that BBB leakiness in AD is likely due to hypoxia and neuroinflammation leading to vascular deterioration and apoptosis. We propose an alternative hypothesis: amyloidogenesis promotes extensive neoangiogenesis leading to increased vascular permeability and subsequent hypervascularization in AD. Cerebrovascular integrity was characterized in Tg2576 AD model mice that overexpress the human amyloid precursor protein (APP) containing the double missense mutations, APPsw, found in a Swedish family, that causes early-onset AD. The expression of tight junction (TJ) proteins, occludin and ZO-1, were examined in conjunction with markers of apoptosis and angiogenesis. In aged Tg2576 AD mice, a significant increase in the incidence of disrupted TJs, compared to age matched wild-type littermates and young mice of both genotypes, was directly linked to an increased microvascular density but not apoptosis, which strongly supports amyloidogenic triggered hypervascularity as the basis for BBB disruption. Hypervascularity in human patients was corroborated in a comparison of postmortem brain tissues from AD and controls. Our results demonstrate that amylodogenesis mediates BBB disruption and leakiness through promoting neoangiogenesis and hypervascularity, resulting in the redistribution of TJs that maintain the barrier and thus, provides a new paradigm for integrating vascular remodeling with the pathophysiology observed in AD. Thus the extensive angiogenesis identified in AD brain, exhibits parallels to the neovascularity evident in the pathophysiology of other diseases such as age-related macular degeneration. PMID:21909359

  12. Rising to the challenge of multiple Cryptococcus species and the diseases they cause

    PubMed Central

    Idnurm, Alexander; Lin, Xiaorong

    2015-01-01

    Cryptococcus neoformans and C. gattii are well-studied basidiomyceteous yeasts that are capable of causing disease in healthy and immunocompromised people. The Conference on Cryptococcus and Cryptococcosis (ICCC) is held every three years: the accompanying Special Issue stems from the 9th ICCC and covers a subset of the topics related to these fungi in detail. This conference started with a revised and reduced estimate of disease burden globally, in part due to improved treatment for HIV+ people. However, mortality from cryptococcosis remains consistently high for those unfortunate to have limited access to therapies or without underlying immunodefiencies. As such, there are yet still great distances to be covered to address antifungal drug availability, the need for new antifungal agents and the timing and doses of these agents in conjunction with antiviral therapy, underscoring the importance of continued research. A notable point from the 9th ICCC was the research addressing the variation in the pathogen and host populations. Analysis of cryptococcal strain variability, particularly at the molecular level, has resolved distinct lineages with the consequence of a taxonomic revision that divides C. neoformans and C. gattii into seven Cryptococcus species. Similarly, analysis of host factors in so called “immune-competent” individuals revealed previously unrecognized risk factors. Research on these species has established them as important model organisms to understand gene evolution and function in other fungi and eukaryotes. The stage is set for the refinement of research directions, leading ultimately to better treatment of this pathogenic monophyletic clade in the genus Cryptococcus.  PMID:25983191

  13. Antisynthetase syndrome: An under-recognized cause of interstitial lung disease

    PubMed Central

    Maturu, Venkata Nagarjuna; Lakshman, Arjun; Bal, Amanjit; Dhir, Varun; Sharma, Aman; Garg, Mandeep; Saikia, Biman; Agarwal, Ritesh

    2016-01-01

    Background: Antisynthetase syndrome (AS) is an uncommon and under-recognised connective tissue disease characterized by the presence of antibodies to anti-aminoacyl t-RNA synthetase along with features of interstitial lung disease (ILD), myositis and arthritis. The aim of the current study is to describe our experience with management of AS. Materials and Methods: This was a 2-year (2013-2014) retrospective analysis of patients diagnosed with anti-Jo-1-related AS. The presence of anti-Jo-1 antibody was tested by the immunoblot assay. All patients underwent high-resolution computed tomography of the chest, transthoracic echocardiography and evaluation for inflammatory myositis. Transbronchial lung biopsies and muscle biopsies were obtained when clinically indicated. Results: Nine patients (mean age: 43.8 years) were diagnosed with anti-Jo-1-related AS. The median duration of symptoms before diagnosis of AS was 6 months. All patients were negative for antinuclear antibodies by indirect immunofluorescence. The prevalence of ILD, myositis and arthritis at presentation was 100%, 77.8% and 55.6%, respectively. The most common ILD pattern was non-specific interstitial pneumonia (n = 6) followed by organizing pneumonia (n = 2) and usual interstitial pneumonia (n = 1). ILD was the sole manifestation in two patients and was subclinical in two patients. Six patients had pleuropericardial effusions, three patients had pulmonary artery hypertension and two patients had venous thromboembolism. Eight of the nine patients improved after treatment with steroids and other immunosuppressants. Conclusion: Antisynthetase syndrome is an important and a treatable cause of ILD. Strong clinical suspicion is needed to achieve an early diagnosis. PMID:26933302

  14. Paternal Age Effect Mutations and Selfish Spermatogonial Selection: Causes and Consequences for Human Disease

    PubMed Central

    Goriely, Anne; Wilkie, Andrew O.M.

    2012-01-01

    Advanced paternal age has been associated with an increased risk for spontaneous congenital disorders and common complex diseases (such as some cancers, schizophrenia, and autism), but the mechanisms that mediate this effect have been poorly understood. A small group of disorders, including Apert syndrome (caused by FGFR2 mutations), achondroplasia, and thanatophoric dysplasia (FGFR3), and Costello syndrome (HRAS), which we collectively term “paternal age effect” (PAE) disorders, provides a good model to study the biological and molecular basis of this phenomenon. Recent evidence from direct quantification of PAE mutations in sperm and testes suggests that the common factor in the paternal age effect lies in the dysregulation of spermatogonial cell behavior, an effect mediated molecularly through the growth factor receptor-RAS signal transduction pathway. The data show that PAE mutations, although arising rarely, are positively selected and expand clonally in normal testes through a process akin to oncogenesis. This clonal expansion, which is likely to take place in the testes of all men, leads to the relative enrichment of mutant sperm over time—explaining the observed paternal age effect associated with these disorders—and in rare cases to the formation of testicular tumors. As regulation of RAS and other mediators of cellular proliferation and survival is important in many different biological contexts, for example during tumorigenesis, organ homeostasis and neurogenesis, the consequences of selfish mutations that hijack this process within the testis are likely to extend far beyond congenital skeletal disorders to include complex diseases, such as neurocognitive disorders and cancer predisposition. PMID:22325359

  15. Complex Regional Pain Syndrome Caused by Lumbar Herniated Intervertebral Disc Disease.

    PubMed

    Kim, Se Hee; Choi, Sang Sik; Lee, Mi Kyung; Kin, Jung Eun

    2016-07-01

    Most cases of complex regional pain syndrome (CRPS) occur after some inciting injury. There are a few cases of CRPS after an operation for disc disease. CRPS from a mild herniated intervertebral disc (HIVD) without surgical intervention is even rarer than CRPS after an operation for disc disease.A 22-year-old man was transferred to a pain clinic. He had continuously complained about back and right leg pain. He presented with a skin color change in the right lower leg, intermittent resting tremor, stiffness, and swelling in the right leg. He complained of a pulling sensation and numbness in his right buttock, posterior thigh, lateral calf, and ankle. This symptom was in accordance with L4/5 radiculopathy. Magnetic resonance imaging (MRI) also showed L4/5 HIVD that was central to the bilateral subarticular protrusion.He was diagnosed as having CRPS, which fits the revised International Association for the Study of Pain (IASP) criteria. He fulfilled 4 symptom categories (allodynia, temperature asymmetry and skin color change, sweating changes, decreased range of motion and motor dysfunction) and 3 of 4 sign categories (allodynia, temperature asymmetry and skin color changes, decreased range of motion and motor dysfunction). The bone scan and thermography also revealed CRPS.For the past 2 months, we have performed intensive treatments. But, he never became pain-free and walking for 5 minutes led to persistent leg pain. We decided to perform percutaneous nucleoplasty, which can directly decompress a HIVD. On the next day, he achieved dramatic symptom relief. The visual analog scale (VAS) score improved to 3, compared to the VAS score of 9 at the first visit. The skin color change, allodynia, and tremor in the right leg disappeared, and the temperature asymmetry normalized. Motor weakness of the right leg also recovered.We report an unusual case of CRPS that was caused by L4/5 HIVD without a history of trauma or surgery. It has a clear causal relationship between HIVD

  16. Achievements and challenges in legume breeding for pest and disease resistance

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Yield stability of legume crops is constrained by a number of pest and diseases. Major diseases are rusts, powdery and downy mildews, ascochyta blight, botrytis gray molds, anthracnoses, damping-off, root rots, collar rot, vascular wilts and white mold. Parasitic weeds, viruses, bacteria, nematodes ...

  17. Mutations in the glucose-6-phosphatase gene that cause glycogen storage disease type 1a

    SciTech Connect

    Chou, J.Y.; Lei, K.J.; Shelly, L.L.

    1994-09-01

    Glycogen storage disease (GSD) type la (von Gierke disease) is caused by the deficiency of glucose-6-phosphatase (G6Pase), the key enzyme in glucose homeostasis. The disease presents with clinical manifestations of severe hypoglycemia, hepatomegaly, growth retardation, lactic acidemia, hyperlipidemia, and hyperuricemia. We have succeeded in isolating a murine G6Pase cDNA from a normal mouse liver cDNA library by differentially screening method. We then isolated the human G6Pase cDNA and gene. To date, we have characterized the G6Pase genes of twelve GSD type la patients and uncovered a total of six different mutations. The mutations are comprised of R83C (an Arg at codon 83 to a Cys), Q347X (a Gly at codon 347 to a stop codon), 459insTA (a two basepair insertion at nucleotide 459 yielding a truncated G6Pase of 129 residues), R295C (an Arg at codon 295 to a Cys), G222R (a Gly at codon 222 to an Arg) and {delta}F327 (a codon deletion for Phe-327 at nucleotides 1058 to 1060). The relative incidences of these mutations are 37.5% (R83C), 33.3% (Q347X), 16.6% (459insTA), 4.2% (G222R), 4.2% (R295C) and 4.2% ({delta}F327). Site-directed mutagenesis and transient expression assays demonstrated that the R83C, Q347X, R295C, and {delta}F327 mutations abolished whereas the G222R mutation greatly reduced G6Pase activity. We further characterized the structure-function requirements of amino acids 83, 222, and 295 in G6Pase catalysis. The identification of mutations in GSD type la patients has unequivocally established the molecular basis of the type la disorder. Knowledge of the mutations may be applied to prenatal diagnosis and opens the way for developing and evaluating new therapeutic approaches.

  18. Efficacy of a pyrimidine derivative to control spot disease on Solanum melongena caused by Alternaria alternata.

    PubMed

    Hassan, Nemat M; Abu-Doubara, Mohamed I; Waly, Mohamed A; Nemat Alla, Mamdouh M

    2013-07-01

    The pyrimidine derivative (4,6-dimethyl-N-phenyldiethyl pyrimidine, DPDP) was tested as a foliar spray fungicide at 50 mg l(-1) for protection of eggplant (Solanum melongena) from spot disease caused by Alternaria alternata. Varied concentrations of DPDP (10-50 mg l(-1)) differentially inhibited mycelial growth, conidial count and conidial germination of A. alternata growth in vitro; the magnitude of inhibition increased with increasing concentration. In vivo, an experiment was conducted in pots using a complete block randomized design and repeated twice with three replications and four treatments (control, A. alternata alone, DPDP alone and combination of DPDP and A. alternata) for 5 weeks (1 plant in pot × 3 pots per set (3 replications per treatment) × 4 sets (4 treatments) × 5 weeks × 2 experimental repetitions = 120 pots). In this experiment, 10-day-old eggplant seedlings were transplanted in pots and then inoculated with A. alternata, DPDP or their combination 1 week later. Leaves of the A. alternata-infected eggplant suffered from chlorosis, necrosis and brown spots during the subsequent 5 weeks. Disease intensity was obvious in infected leaves but withdrawn by DPDP. There were relationships between incidence and severity, greater in plant leaves infected A. alternata alone and diminished with the presence of DPDP. Moreover, the infection resulted in reductions in growth, decreases in contents of anthocyanins, chlorophylls, carotenoids and thiols as well as inhibitions in activities of superoxide dismutase (SOD), glutathione peroxidase (GPX) and glutathione-S-transferase (GST). Nonetheless, the application of DPDP at 50 mg led to a recovery of the infected eggplant; the infection-induced deleterious effects were mostly reversed by DPDP. However, treatment with DPDP alone seemed with no significant impacts. Due to its safe use to host and the inhibition for the pathogen, DPDP could be suggested as an efficient fungicide for protection

  19. Homozygous mutations in caveolin-3 cause a severe form of rippling muscle disease.

    PubMed

    Kubisch, Christian; Schoser, Benedikt G H; von Düring, Monika; Betz, Regina C; Goebel, Hans-Hilmar; Zahn, Susanne; Ehrbrecht, Antje; Aasly, Jan; Schroers, Anja; Popovic, Nikola; Lochmüller, Hanns; Schröder, J Michael; Brüning, Thomas; Malin, Jean-Pierre; Fricke, Britta; Meinck, Hans-Michael; Torbergsen, Torberg; Engels, Hartmut; Voss, Bruno; Vorgerd, Matthias

    2003-04-01

    Heterozygous missense mutations in the caveolin-3 gene (CAV3) cause different muscle disorders. Most patients with CAV3 alterations present with rippling muscle disease (RMD) characterized by signs of increased muscle irritability without muscle weakness. In some patients, CAV3 mutations underlie the progressive limb-girdle muscular dystrophy type 1C (LGMD1C). Here, we report two unrelated patients with novel homozygous mutations (L86P and A92T) in CAV3. Both presented with a more severe clinical phenotype than usually seen in RMD. Immunohistochemical and immunoblot analyses of muscle biopsies showed a strong reduction of caveolin-3 in both homozygous RMD patients similar to the findings in heterozygous RMD. Electron microscopy studies showed a nearly complete absence of caveolae in the sarcolemma in all RMD patients analyzed. Additional plasma membrane irregularities (small plasmalemmal discontinuities, subsarcolemmal vacuoles, abnormal papillary projections) were more pronounced in homozygous than in heterozygous RMD patients. A stronger activation of nitric oxide synthase was observed in both homozygous patients compared with heterozygous RMD. Like in LGMD1C, dysferlin immunoreactivity is reduced in RMD but more pronounced in homozygous as compared with heterozygous RMD. Thus, we further extend the phenotypic variability of muscle caveolinopathies by identification of a severe form of RMD associated with homozygous CAV3 mutations. PMID:12666119

  20. A Role for Non-B DNA Forming Sequences in Mediating Microlesions Causing Human Inherited Disease.

    PubMed

    Kamat, Mihir Anant; Bacolla, Albino; Cooper, David N; Chuzhanova, Nadia

    2016-01-01

    Missense/nonsense mutations and microdeletions/microinsertions (<21 bp) represent ∼ 76% of all mutations causing human inherited disease, and their occurrence has been associated with sequence motifs (direct, inverted, and mirror repeats; G-quartets) capable of adopting non-B DNA structures. We found that a significant proportion (∼ 21%) of both microdeletions and microinsertions occur within direct repeats, and are explicable by slipped misalignment. A novel mutational mechanism, DNA triplex formation followed by DNA repair, may explain ∼ 5% of microdeletions and microinsertions at mirror repeats. Further, G-quartets, direct, and inverted repeats also appear to play a prominent role in mediating missense mutations, whereas only direct and inverted repeats mediate nonsense mutations. We suggest a mutational mechanism involving slipped strand mispairing, slipped structure formation, and DNA repair, to explain ∼ 15% of missense and ∼ 12% of nonsense mutations yielding perfect direct repeats from imperfect repeats, or the extension of existing direct repeats. Similar proportions of missense and nonsense mutations were explicable by hairpin/loop formation and DNA repair, yielding perfect inverted repeats from imperfect repeats. We also propose a model for single base-pair substitution based on one-electron oxidation reactions at G-quadruplex DNA. Overall, the proposed mechanisms provide support for a role for non-B DNA structures in human gene mutagenesis. PMID:26466920