Science.gov

Sample records for pretreatment protects myocardium

  1. Protective effect of pretreatment with the calcium antagonist anipamil on the ischemic-reperfused rat myocardium: a phosphorus-31 nuclear magnetic resonance study

    SciTech Connect

    Kirkels, J.H.; Ruigrok, T.J.; Van Echteld, C.J.; Meijler, F.L.

    1988-05-01

    To assess whether the prophylactic administration of anipamil, a new calcium antagonist, protects the heart against the effects of ischemia and reperfusion, rats were injected intraperitoneally twice daily for 5 days with 5 mg/kg body weight of this drug. The heart was then isolated and perfused by the Langendorff technique. Phosphorus-31 nuclear magnetic resonance spectroscopy was used to monitor myocardial energy metabolism and intracellular pH during control perfusion and 30 min of total ischemia (37/sup 0/C), followed by 30 min of reperfusion. Pretreatment with anipamil altered neither left ventricular developed pressure under normoxic conditions nor the rate and extent of depletion of adenosine triphosphate (ATP) and creatine phosphate during ischemia. Intracellular acidification, however, was attenuated. On reperfusion, hearts from anipamil-pretreated animals recovered significantly better than untreated hearts with respect to replenishment of ATP and creatine phosphate stores, restitution of low levels of intracellular inorganic phosphate and recovery of left ventricular function and coronary flow. Intracellular pH recovered rapidly to preischemic levels, whereas in untreated hearts a complex intracellular inorganic phosphate peak indicated the existence of areas of different pH within the myocardium. It is concluded that anipamil pretreatment protects the heart against some of the deleterious effects of ischemia and reperfusion. Because this protection occurred in the absence of a negative inotropic effect during normoxia, it cannot be attributed to an energy-sparing effect during ischemia. Therefore, alternative mechanisms of action are to be considered.

  2. Liver X receptor activation protects against inflammation and enhances autophagy in myocardium of neonatal mouse challenged by lipopolysaccharides.

    PubMed

    Liu, Peng; He, Siyi; Gao, Junwei; Li, Jingwei; Fan, Xiaotang; Xiao, Ying-Bin

    2014-01-01

    Liver X receptors (LXRs) has been emerged as negative regulators of cardiomyocytic inflammation. The cellular process of autophagy is believed to play a protective role in myocardium during the inflammatory status. In this study, we investigated the role of LXRs agonist TO901317 (TO) on lipopolysaccharides (LPS)-induced myocardial inflammation and autophagy. The results showed that TO pretreatment significantly reduced the LPS-induced infiltration of inflammatory cells, elevation of NF-κB protein, TNF-α, and IL-6 mRNA levels in the myocardium. Moreover, LPS stimulated autophagy in neonatal mice heart, and this effect was further enhanced by TO pretreatment as evidenced by increased LC3-II/GAPDH ratio increment. Furthermore, TUNEL assay revealed LPS stimulation also increased the number of apoptotic cells in the myocardium, and the increment was inhibited by TO pretreatment. Our findings suggested that attenuation of inflammation and apoptosis, and enhancement of autophagy by TO may contribute to the protection of myocardium under inflammatory condition.

  3. Protection of the myocardium with high-energy solutions.

    PubMed

    Levitsky, S; Feinberg, H

    1975-07-01

    An approach to intraoperative protection of the myocardium is described that attempts to increase glucose utilization by infusion of high-energy solutions during aortic cross-clamping. Infusion of hypertonic glucose or glucose plus insulin prior to aortic cross-clamping has enhanced contractility and increased high-energy phosphate moieties in animals with induced ischemia. Recent pilot experiments in our laboratory suggest that infusions of creatine may result in increased production of creatine phosphate, which in turn induces phosphorylation of adenosine diphosphate to adenosine triphosphate, possibly enhancing myocardial contractility. The intraoperative clinical benefits of these infusions remain to be proved, however.

  4. Protective effect of ischemic postconditioning against ischemia reperfusion-induced myocardium oxidative injury in IR rats.

    PubMed

    Zhang, Li; Ma, Jiangwei; Liu, Huajin

    2012-03-27

    Brief episodes of myocardial ischemia-reperfusion (IR) employed during reperfusion after a prolonged ischemic insult may attenuate the total ischemia-reperfusion injury. This phenomenon has been termed ischemic postconditioning. In the present study, we studied the possible effect of ischemic postconditioning on an ischemic reperfusion (IR)-induced myocardium oxidative injury in rat model. Results showed that ischemic postconditioning could improve arrhythmia cordis, reduce myocardium infarction and serum creatin kinase (CK), lactate dehydrogenase (LDH) and aspartate transaminase (AST) activities in IR rats. In addition, ischemic postconditioning could still decrease myocardium malondialdehyde (MDA) level, and increased myocardium Na+-K+-ATPase, Ca2+-Mg2+-ATPase, superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) and glutathione reductase (GR) activities. It can be concluded that ischemic postconditioning possesses strong protective effects against ischemia reperfusion-induced myocardium oxidative injury in IR rats.

  5. Ghrelin protects infarcted myocardium by induction of autophagy and AMP-activated protein kinase pathway.

    PubMed

    Yuan, Ming-Jie; Kong, Bin; Wang, Tao; Wang, Xin; Huang, He; Maghsoudi, Taneen

    2016-08-01

    The majority of studies have reported that enhancing autophagy in the myocardium is cardioprotective. Here, we tested the hypothesis that ghrelin, a growth hormone-releasing peptide, will protect infarcted myocardium by inducing of autophagy. Myocardial infarction was induced in mice by left coronary artery ligation the surviving mice 24 h after surgical were started on 2 week treatments with one of the following: vehicle, acylated ghrelin(50 mg/kg per day) or acylated ghrelin plus 3-MA(an autophagy inhibitor, 15 mg/kg, per day). We found that ghrelin significantly improved the cardiac function, and autophagy was enhanced by elevated LC3-II/LC-I ratio and mRNA expression of autophagy related protein. In vitro, cultured neonatal rat ventricular cardiomyocytes were subjected to simulate ischemia/reperfusion, 3-MA significantly attenuated ghrelin-induced autophagy, which was associated with activated AMP-activated protein kinase (AMPK) signal pathway. Moreover, ghrelin reduced cell death, and RNAi-mediated knockdown of autophagy protein 5 (Atg5) partly abolished ghrelin's cardioprotective effect. It is the first time to demonstrate that the cardioprotective effect of ghrelin on ischemia myocardium in part through regulating of autophagy signal pathway. PMID:27235554

  6. Cardiac progenitor-derived exosomes protect ischemic myocardium from acute ischemia/reperfusion injury

    SciTech Connect

    Chen, Lijuan; Wang, Yingjie; Pan, Yaohua; Zhang, Lan; Shen, Chengxing; Qin, Gangjian; Ashraf, Muhammad; Weintraub, Neal; Ma, Genshan; Tang, Yaoliang

    2013-02-15

    Highlights: ► Cardiac progenitor-derived (CPC) Exosomes protect H9C2 from apoptosis in vitro. ► CPC-exosomes protect cardiomyoyctes from MI/R induced apoptosis in vivo. ► CPC-exosomes were taken up by H9C2 with high efficiency using PKH26 labeling. ► miR-451, one of GATA4-responsive miRNA cluster, is enriched in CPC-exosomes. -- Abstract: Background: Cardiac progenitors (CPC) mediate cardioprotection via paracrine effects. To date, most of studies focused on secreted paracrine proteins. Here we investigated the CPC-derived-exosomes on protecting myocardium from acute ischemia/reperfusion (MI/R) injury. Methods and results: CPC were isolated from mouse heart using two-step protocol. Exosomes were purified from conditional medium, and confirmed by electron micrograph and Western blot using CD63 as a marker. qRT-PCR shows that CPC-exosomes have high level expression of GATA4-responsive-miR-451. Exosomes were ex vivo labeled with PKH26, We observed exosomes can be uptaken by H9C2 cardiomyoblasts with high efficiency after 12 h incubation. CPC-exosomes protect H9C2 from oxidative stress by inhibiting caspase 3/7 activation invitro. In vivo delivery of CPC-exosomes in an acute mouse myocardial ischemia/reperfusion model inhibited cardiomyocyte apoptosis by about 53% in comparison with PBS control (p < 0.05). Conclusion: Our results suggest, for the first time, the CPC-exosomes can be used as a therapeutic vehicle for cardioprotection, and highlights a new perspective for using non-cell exosomes for cardiac disease.

  7. Study of possible mechanism of protective effect of phosphocreatine on ischemic myocardium

    SciTech Connect

    Preobrazhenskii, A.N.; Dzhavadov, S.A.; Saks, V.A.

    1986-10-20

    The accumulation of (/sup 32/P)phosphocreatine by control and isolated perfused ischemic rat hearts was studied. It was found that at phosphocreatine concentrations of 0.5-10 mM in the perfusing solution the rate of phosphocreatine accumulation was twice as high in hearts subjected to ischemia for 35 min as in the control hearts and constituted 182 nmoles/min/g dry weight tissue at a phosphocreatine concentrations in the perfusate of 10 mM. 5'-Nucleotidase and phosphatase activities were found in the crude plasma membrane fraction from rat hearts. The pH-dependence of the activity of these enzymes was studied. The 5'-nucleotidase activity decreased 4- to 5-fold with a drop in the pH from 8.0 to 6.0. The phosphatase activity of the preparations increased 2-fold with a drop in the pH from 8.0 to 6.0. The 5'-nucleotidase activity was inhibited by 10 mM phosphocreatine in the presence of 5 mM Mg/sup 2 +/, and the degree of the inhibition depended on the pH. Maximum inhibition by phosphocreatine (58%) was observed at pH 6.0. The inhibition of phosphatase by phosphocreatine did not depend on the pH and reached 20% in the presence of 10 mM phosphocreatine. Some possible mechanisms of the protective effect of phosphocreatine on an ischemic myocardium are discussed.

  8. KATP channel blocker does not abolish the protective effect of NHE1 inhibition against ischaemia/reperfusion in aged myocardium

    PubMed Central

    Liu, Hong; Moore, Peter G

    2010-01-01

    Background and objective Aging is associated with an increase in myocardial susceptibility to ischaemia/reperfusion (I/R) injury. Na+/H+ exchange (NHE) inhibition and anaesthetic preconditioning (APC) are shown to protect myocardium from I/R injury. We set out to investigate if NHE inhibition can induce protection against I/R injury and whether KATP channel inhibition can enhance this effect in aged rat myocardium. Methods Hearts from 24-month old rats were assigned to 4 groups: (1) Control group; (2) APC group perfused with 2.5% sevoflurane before ischemia; (3) HOE group perfused with (3-methylsulfonyl-4-piperidinobenzoyl) guanidine methanesulfonate (HOE-694) prior to ischaemia; (4) HOE+5HD group perfused with both HOE and 5-hydroxydecanoic acid before ischaemia. We measured intracellular Na+ and Ca++ to quantitate the severity of myocardial injury. Results Both intracellular Na+ and Ca++ were significantly increased at the end of ischaemia and both were attenuated by NHE inhibition. Intracellular Na+ was 134±12 mEq/kg/dry weight in control group and 55±7 in HOE group (p<0.05). Intracellular Ca++ was 1764±142 nM in control group and 694±213 in HOE group (p<0.05). Infarct size was measured at 28±4% in control group vs. 17±2% in HOE group (p<0.05). High-energy phosphates and myocardial function were better preserved in HOE group compared to control (p<0.05). The beneficial effects of HOE on myocardial preservation was not blocked by 5HD nor were there any differences between APC and control groups. Conclusions NHE inhibition was effective in protecting myocardium from I/R injury in aged rats whereas APC was not. 5HD failed to block the protective effect of NHE inhibition. PMID:20216068

  9. Lipopolysaccharide Pretreatment Protects from Renal Ischemia/Reperfusion Injury

    PubMed Central

    Heemann, Uwe; Szabo, Attila; Hamar, Peter; Müller, Veronika; Witzke, Oliver; Lutz, Jens; Philipp, Thomas

    2000-01-01

    In vivo administration of low doses of lipopolysaccharide (LPS) to rodents can protect these animals from subsequently administrated, usually lethal doses of endotoxin or LPS. In this study we tested the effects of LPS pretreatment on ischemia/reperfusion injury in the kidney. Male C57/B1 mice were pretreated with different doses of LPS or phosphate-buffered saline on days −4 and −3. The right kidney was removed, and the vessels of the left kidney were clamped for 30 or 45 minutes on day 0. Creatinine levels and survival of animals were monitored. To test the involvement of cytokines, additional animals were harvested before (“time 0”) and 15 minutes, 1, 2, 8, and 16 hours after reperfusion for histology, immunohistochemistry, terminal deoxynucleotidyltransferase-mediated UTP end-labeling assay, and reverse transcriptase-polymerase chain reaction analysis (including tumor necrosis factor (TNF)-α, interleukin (IL)-1, IL-6, inducible nitric oxide synthase (iNOS), and interferon (IFN)-γ messenger RNA (mRNA)). In controls, renal ischemia of 30 minutes was nonlethal, whereas 73% of the animals died within 48 ± 18 hours, after 45 minutes of ischemia. All different doses of LPS protected the animals from lethal renal ischemia/reperfusion injury. Starting at similar levels, serum creatinine increased significantly in controls but not in LPS-pretreated animals over time. As early as 2 hours after reperfusion, tubular cell damage was significantly more pronounced in controls than in LPS-treated mice. In controls, tubules deteriorated progressively until 8 hours of reperfusion. At this time, more than 50% of tubular cells were destroyed. This destruction was accompanied by a pronounced leukocytic infiltration, predominantly by macrophages. In contrast, LPS pretreatment prevented the destruction of kidney tissue and infiltration by leukocytes. The terminal deoxynucleotidyltransferase-mediated UTP end-labeling assay revealed significantly more apoptotic cells in

  10. RhNRG-1β Protects the Myocardium against Irradiation-Induced Damage via the ErbB2-ERK-SIRT1 Signaling Pathway.

    PubMed

    Gu, Anxin; Jie, Yamin; Sun, Liang; Zhao, Shuping; E, Mingyan; You, Qingshan

    2015-01-01

    Radiation-induced heart disease (RIHD), which is a serious side effect of the radiotherapy applied for various tumors due to the inevitable irradiation of the heart, cannot be treated effectively using current clinical therapies. Here, we demonstrated that rhNRG-1β, an epidermal growth factor (EGF)-like protein, protects myocardium tissue against irradiation-induced damage and preserves cardiac function. rhNRG-1β effectively ameliorated irradiation-induced myocardial nuclear damage in both cultured adult rat-derived cardiomyocytes and rat myocardium tissue via NRG/ErbB2 signaling. By activating ErbB2, rhNRG-1β maintained mitochondrial integrity, ATP production, respiratory chain function and the Krebs cycle status in irradiated cardiomyocytes. Moreover, the protection of irradiated cardiomyocytes and myocardium tissue by rhNRG-1β was at least partly mediated by the activation of the ErbB2-ERK-SIRT1 signaling pathway. Long-term observations further showed that rhNRG-1β administered in the peri-irradiation period exerts continuous protective effects on cardiac pump function, the myocardial energy metabolism, cardiomyocyte volume and interstitial fibrosis in the rats receiving radiation via NRG/ErbB2 signaling. Our findings indicate that rhNRG-1β can protect the myocardium against irradiation-induced damage and preserve cardiac function via the ErbB2-ERK-SIRT1 signaling pathway. PMID:26332771

  11. RhNRG-1β Protects the Myocardium against Irradiation-Induced Damage via the ErbB2-ERK-SIRT1 Signaling Pathway.

    PubMed

    Gu, Anxin; Jie, Yamin; Sun, Liang; Zhao, Shuping; E, Mingyan; You, Qingshan

    2015-01-01

    Radiation-induced heart disease (RIHD), which is a serious side effect of the radiotherapy applied for various tumors due to the inevitable irradiation of the heart, cannot be treated effectively using current clinical therapies. Here, we demonstrated that rhNRG-1β, an epidermal growth factor (EGF)-like protein, protects myocardium tissue against irradiation-induced damage and preserves cardiac function. rhNRG-1β effectively ameliorated irradiation-induced myocardial nuclear damage in both cultured adult rat-derived cardiomyocytes and rat myocardium tissue via NRG/ErbB2 signaling. By activating ErbB2, rhNRG-1β maintained mitochondrial integrity, ATP production, respiratory chain function and the Krebs cycle status in irradiated cardiomyocytes. Moreover, the protection of irradiated cardiomyocytes and myocardium tissue by rhNRG-1β was at least partly mediated by the activation of the ErbB2-ERK-SIRT1 signaling pathway. Long-term observations further showed that rhNRG-1β administered in the peri-irradiation period exerts continuous protective effects on cardiac pump function, the myocardial energy metabolism, cardiomyocyte volume and interstitial fibrosis in the rats receiving radiation via NRG/ErbB2 signaling. Our findings indicate that rhNRG-1β can protect the myocardium against irradiation-induced damage and preserve cardiac function via the ErbB2-ERK-SIRT1 signaling pathway.

  12. RhNRG-1β Protects the Myocardium against Irradiation-Induced Damage via the ErbB2-ERK-SIRT1 Signaling Pathway

    PubMed Central

    Gu, Anxin; Jie, Yamin; Sun, Liang; Zhao, Shuping; E, Mingyan; You, Qingshan

    2015-01-01

    Radiation-induced heart disease (RIHD), which is a serious side effect of the radiotherapy applied for various tumors due to the inevitable irradiation of the heart, cannot be treated effectively using current clinical therapies. Here, we demonstrated that rhNRG-1β, an epidermal growth factor (EGF)-like protein, protects myocardium tissue against irradiation-induced damage and preserves cardiac function. rhNRG-1β effectively ameliorated irradiation-induced myocardial nuclear damage in both cultured adult rat-derived cardiomyocytes and rat myocardium tissue via NRG/ErbB2 signaling. By activating ErbB2, rhNRG-1β maintained mitochondrial integrity, ATP production, respiratory chain function and the Krebs cycle status in irradiated cardiomyocytes. Moreover, the protection of irradiated cardiomyocytes and myocardium tissue by rhNRG-1β was at least partly mediated by the activation of the ErbB2-ERK-SIRT1 signaling pathway. Long-term observations further showed that rhNRG-1β administered in the peri-irradiation period exerts continuous protective effects on cardiac pump function, the myocardial energy metabolism, cardiomyocyte volume and interstitial fibrosis in the rats receiving radiation via NRG/ErbB2 signaling. Our findings indicate that rhNRG-1β can protect the myocardium against irradiation-induced damage and preserve cardiac function via the ErbB2-ERK-SIRT1 signaling pathway. PMID:26332771

  13. Sildenafil Augments Early Protective Transcriptional Changes After Ischemia In Mouse Myocardium

    PubMed Central

    Vidavalur, Ramesh; Penumathsa, Suresh Varma; Thirunavukkarasu, Mahesh; Zhan, Lijun; Krueger, Winfried; Maulik, Nilanjana

    2009-01-01

    Recently, targeting cyclic-GMP specific phosphodiesterase-5 (PDE5) has attracted much interest in several cardiopulmonary diseases, in particular myocardial ischemia (MI). Although multiple mechanisms were postulated for these beneficial effects at cellular level, early transcriptional changes were unknown. The aim of present study was to examine gene expression profiles in response to MI after 24h of ischemia in murine model and compare transcriptional modulation by sildenafil, a popular phosphodiesterase 5 (PDE5) inhibitor. Mice were divided into four groups: Control sham (C), Sildenafil sham (S), Control MI (CMI) and Sildenafil MI (SMI). Sildenafil was given at a dose of 0.7 mg/kg intraperitoneally 30 minutes before LAD occlusion. cDNA microarray analysis of peri-infarct tissue was done using a custom cloneset and employing a looped dye swap design. Replicate signals were median averaged and normalized using LOWESS algorithm. R/MAANOVA analysis was used and false discovery rate corrected permutation p-values < 0.005 were employed as significance thresholds. 156 genes were identified as significantly regulated demonstrating fold difference >1.5 in atleast one of the four groups. 52 genes were significantly upregulated in SMI compared to CMI. For a randomly chosen subset of genes (9), microarray data were confirmed through real time RT-PCR. The differentially expressed genes could be classified into following groups based on their function: Phosphorylation/dephosphorylation, Apoptosis, differentiation, ATP binding. Our results suggest that sildenafil treatment might regulate early genetic reprogramming strategy for preservation of the ischemic myocardium. PMID:19013509

  14. Antiarrhythmic action and protection of ischaemia myocardium after beta-blockade with bevantolol.

    PubMed

    Verdouw, P D; Van Bremen, R H; Verkeste, C M; Van der Giessen, W J

    1985-05-20

    In the present study 12 of 13 untreated pigs died of ventricular fibrillation during three 10 min episodes of left anterior descending coronary artery occlusion interrupted by 20 min of reperfusion. The selective beta-adrenoceptor antagonist bevantolol in a dose of 1.5 mg X kg-1, but not 0.5 mg X kg-1, offered nearly complete protection against this fatal arrhythmia. Evidence is also presented that bevantolol enhanced the recovery of regional myocardial function after these ischaemic events.

  15. Improved myocardium transducer

    NASA Technical Reports Server (NTRS)

    Culler, V. H.; Feldstein, C.; Lewis, G. W.

    1979-01-01

    Method of implanting myocardium transducer uses special indented pins that are caught and securely held by epicardial fibers. Pins are small enough to cause minimum of trauma to myocardium during implantation or removal.

  16. Growth differentiation factor 15 may protect the myocardium from no-reflow by inhibiting the inflammatory-like response that predominantly involves neutrophil infiltration

    PubMed Central

    ZHANG, MEI; PAN, KUNYING; LIU, QIANPING; ZHOU, XIN; JIANG, TIEMIN; LI, YUMING

    2016-01-01

    significant no-reflow in ischemic myocardium. GDF-15 may protect the I/R myocardium from no-reflow by inhibiting the inflammatory-like response, which involves neutrophil infiltration and transendothelial migration. PMID:26647773

  17. Growth differentiation factor 15 may protect the myocardium from no‑reflow by inhibiting the inflammatory‑like response that predominantly involves neutrophil infiltration.

    PubMed

    Zhang, Mei; Pan, Kunying; Liu, Qianping; Zhou, Xin; Jiang, Tiemin; Li, Yuming

    2016-01-01

    times (6 h) resulting in significant no‑reflow in ischemic myocardium. GDF‑15 may protect the I/R myocardium from no‑reflow by inhibiting the inflammatory‑like response, which involves neutrophil infiltration and transendothelial migration.

  18. Docosahexaenoic Acid Pretreatment Confers Protection and Functional Improvements after Acute Spinal Cord Injury in Adult Rats

    PubMed Central

    Figueroa, Johnny D.; Cordero, Kathia; Baldeosingh, Keisha; Torrado, Aranza I.; Walker, Robert L.; Miranda, Jorge D.

    2012-01-01

    Abstract Currently, few interventions have been shown to successfully limit the progression of secondary damage events associated with the acute phase of spinal cord injury (SCI). Docosahexaenoic acid (DHA, C22:6 n-3) is neuroprotective when administered following SCI, but its potential as a pretreatment modality has not been addressed. This study used a novel DHA pretreatment experimental paradigm that targets acute cellular and molecular events during the first week after SCI in rats. We found that DHA pretreatment reduced functional deficits during the acute phase of injury, as shown by significant improvements in Basso-Beattie-Bresnahan (BBB) locomotor scores, and the detection of transcranial magnetic motor evoked potentials (tcMMEPs) compared to vehicle-pretreated animals. We demonstrated that, at 7 days post-injury, DHA pretreatment significantly increased the percentage of white matter sparing, and resulted in axonal preservation, compared to the vehicle injections. We found a significant increase in the survival of NG2+, APC+, and NeuN+ cells in the ventrolateral funiculus (VLF), dorsal corticospinal tract (dCST), and ventral horns, respectively. Interestingly, these DHA protective effects were observed despite the lack of inhibition of inflammatory markers for monocytes/macrophages and astrocytes, ED1/OX42 and GFAP, respectively. DHA pretreatment induced levels of Akt and cyclic AMP responsive element binding protein (CREB) mRNA and protein. This study shows for the first time that DHA pretreatment ameliorates functional deficits, and increases tissue sparing and precursor cell survival. Further, our data suggest that DHA-mediated activation of pro-survival/anti-apoptotic pathways may be independent of its anti-inflammatory effects. PMID:21970623

  19. The effect of various cosmetic pretreatments on protecting hair from thermal damage by hot flat ironing.

    PubMed

    Zhou, Y; Rigoletto, R; Koelmel, D; Zhang, G; Gillece, T W; Foltis, L; Moore, D J; Qu, X; Sun, C

    2011-01-01

    Hot flat irons are used to create straight hair styles. As these devices operate at temperatures over 200 °C they can cause significant damage to hair keratin. In this study, hair thermal damage and the effect of various polymeric pretreatments were investigated using FTIR imaging spectroscopy, DSC, dynamic vapor sorption (DVS), AFM, SEM, and thermal image analysis. FTIR imaging spectroscopy of hair cross sections provides spatially resolved molecular information such as protein distribution and structure. This approach was used to monitor thermally induced modification of hair protein, including the conversion of α-helix to β-sheet and protein degradation. DSC measurements of thermally treated hair also demonstrated degradation of hair keratin. DVS of thermally treated hair shows the reduced water regain and lower water retention, compared to the non-thermally treated hair, which might be attributed to the protein conformation changes due to heat damage. The protection of native protein structure associated with selected polymer pretreatments leads to improved moisture restoration and water retention of hair. This contributes to heat control on repeated hot flat ironing. Thermally stressing hair led to significantly increased hair breakage when subjected to combing. These studies indicate that hair breakage can be reduced significantly when hair is pretreated with selected polymers such as VP/acrylates/lauryl methacrylate copolymer, polyquaternium-55, and a polyelectrolyte complex of PVM/MA copolymer and polyquaternium-28. In addition, polymeric pretreatments provide thermal protection against thermal degradation of keratin in the cortex as well as hair surface damage. The morphological improvement in cuticle integrity and smoothness with the polymer pretreatment plays an important role in their anti-breakage effect. Insights into structure-property relationships necessary to provide thermal protection to hair are presented.

  20. The effect of various cosmetic pretreatments on protecting hair from thermal damage by hot flat ironing.

    PubMed

    Zhou, Y; Rigoletto, R; Koelmel, D; Zhang, G; Gillece, T W; Foltis, L; Moore, D J; Qu, X; Sun, C

    2011-01-01

    Hot flat irons are used to create straight hair styles. As these devices operate at temperatures over 200 °C they can cause significant damage to hair keratin. In this study, hair thermal damage and the effect of various polymeric pretreatments were investigated using FTIR imaging spectroscopy, DSC, dynamic vapor sorption (DVS), AFM, SEM, and thermal image analysis. FTIR imaging spectroscopy of hair cross sections provides spatially resolved molecular information such as protein distribution and structure. This approach was used to monitor thermally induced modification of hair protein, including the conversion of α-helix to β-sheet and protein degradation. DSC measurements of thermally treated hair also demonstrated degradation of hair keratin. DVS of thermally treated hair shows the reduced water regain and lower water retention, compared to the non-thermally treated hair, which might be attributed to the protein conformation changes due to heat damage. The protection of native protein structure associated with selected polymer pretreatments leads to improved moisture restoration and water retention of hair. This contributes to heat control on repeated hot flat ironing. Thermally stressing hair led to significantly increased hair breakage when subjected to combing. These studies indicate that hair breakage can be reduced significantly when hair is pretreated with selected polymers such as VP/acrylates/lauryl methacrylate copolymer, polyquaternium-55, and a polyelectrolyte complex of PVM/MA copolymer and polyquaternium-28. In addition, polymeric pretreatments provide thermal protection against thermal degradation of keratin in the cortex as well as hair surface damage. The morphological improvement in cuticle integrity and smoothness with the polymer pretreatment plays an important role in their anti-breakage effect. Insights into structure-property relationships necessary to provide thermal protection to hair are presented. PMID:21635854

  1. Protection of ischemic myocardium: comparison of effects of propranolol, bevantolol and N-dimethyl propranolol on infarct size following coronary artery occlusion in anesthetized dogs.

    PubMed

    Warltier, D C; Gross, G J; Jesmok, G J; Brooks, H L; Hardman, H F

    1980-01-01

    The relative extent of myocardial infarction produced by occlusion of the left anterior descendens coronary artery in anesthetized dogs was determined under control conditions or following treatment (4 h after ligation) with propranolol (1 mg/kg), bevantolol (3 mg/kg) or N-dimethyl propranolol (10 mg/kg). Doses of drugs were selected to provide similar reductions in heart rate, aortic blood pressure and contractility. Infarct size was estimated indirectly from levels of plasma creatine phosphokinase and measured histochemically by nitroblue tetrazolium stain. A significant ( p < 0.001) correlation between methods was found. Propranolol and bevantolol (beta adrenergic antagonists) produced a significant (p < 0.05) reduction (approximately 50% decrease) in infarct size, measured at 8 h following induction of ischemia, while N-dimemthyl propranolol (no beta antagonist activity) produced no effect. While all three agents produced similar hemodynamic actions and thereby reduced primary determinants of myocardial oxygen demand, only the beta blockers were able to afford protection of ischemic myocardium.

  2. Emodin-mediated protection from acute myocardial infarction via inhibition of inflammation and apoptosis in local ischemic myocardium.

    PubMed

    Wu, Yanxia; Tu, Xin; Lin, Guosheng; Xia, Hao; Huang, Hao; Wan, Jing; Cheng, Zhide; Liu, Mengyuan; Chen, Gao; Zhang, Haimou; Fu, Jinrong; Liu, Qian; Liu, Dong-Xu

    2007-10-13

    Acute myocardial infarction (AMI) is associated with inflammation and apoptosis. Emodin plays an anti-inflammatory role in several inflammatory diseases. Recent studies have demonstrated that emodin protects against myocardial ischemia/reperfusion injury. However, its mechanism underlying its effects remains unknown. In a murine model of AMI, based on ligation of the left coronary artery, administration of emodin reduced myocardial infarct size (MIS) in a dose-dependent manner. Emodin significantly suppressed TNF-alpha expression and NF-kappaB activation in the local myocardial infarction area. Treatment with emodin inhibited myocardial cell apoptosis by inhibiting caspase-3 activation. Therefore, these studies demonstrate that emodin protects against myocardial cell injury via suppression of local inflammation and apoptosis.

  3. Over-expression of HSPA12B protects mice against myocardium ischemic/reperfusion injury through a PPARγ-dependent PI3K/Akt/eNOS pathway

    PubMed Central

    Sun, Yanjun; Ye, Lincai; Jiang, Chuan; Jiang, Jun; Hong, Haifa; Qiu, Lisheng

    2015-01-01

    Acute myocardial ischemia/reperfusion (MIR) injury leads to severe arrhythmias and a high lethality. We aim to determine the effect of heat shock protein A12B (HSPA12B), a newly discovered member of the Hsp70 family, on heart injury parameters following MIR surgery. We used HSPA12B transgenic mice to determine its effects on heart function parameters, infarct size and cellular apoptosis following MIR surgery. Proinflammatory cytokines, oxidative products and anti-oxidative enzymes in the myocardium were measured to evaluate the anti-inflammatory and anti-oxidative effects of HSPA12B over-expression. The role of PPARs/eNOS/PI3k/Akt pathway was investigated using their inhibitors. The alteration of hemodynamic parameters, histopathological, apoptotic and infarct size caused by MIR was greatly attenuated in HSPA12B over-expressed mice. HSPA12B also greatly mitigated the inflammatory response, demonstrated by the decrease in the levels of IL-1β, IL-6, TNF-a and MPO. Anti-oxidative enzymes (SOD, Catalase and GPx) were restored by HSPA12B; oxidative products (8-OHdG, MDA and protein carbonyl) were decreased. HSPA12B activated the PPARγ-dependent eNOS/PI3k/Akt pathway, and the influence of HSPA12B on cardiac function was reversed by the inhibitors of eNOS, PPARγ, Akt and PI3K. Our results present a novel signaling mechanism that HSPA12B protects MIR injury through a PPARγ-dependent PI3K/Akt/eNOS pathway. PMID:26885270

  4. Salicylic acid and heat acclimation pretreatment protects Laminaria japonica sporophyte (Phaeophyceae) from heat stress

    NASA Astrophysics Data System (ADS)

    Zhou, Bin; Tang, Xuexi; Wang, You

    2010-07-01

    Possible mediatory roles of heat acclimation and salicylic acid in protecting the sporophyte of marine macroalga Laminaria japonica (Phaeophyceae) from heat stress were studied. Heat stress resulted in oxidative injury in the kelp blades. Under heat stress significant accumulation of hydrogen peroxide (H2O2) and malonaldehyde (MDA), a membrane lipid peroxidation product, and a drastic decrease in chlorophyll a content were recorded. Activity of the enzymatic antioxidant system was drastically affected by heat stress. The activity of superoxide dismutase (SOD) was significantly increased while peroxidase (POD), catalase (CAT) and glutathione peroxidase (GPX) were greatly inhibited and, simultaneously, phenylalanine ammonia-lyase was activated while polyphenol oxidase (PPO) was inhibited. Both heat acclimation pretreatment and exogenous application of salicylic acid alleviated oxidative damage in kelp blades. Blades receiving heat acclimation pretreatment and exogenous salicylic acid prior to heat stress exhibited a reduced increase in H2O2 and MDA content, and a lower reduction in chlorophyll a content. Pretreatment with heat acclimation and salicylic acid elevated activities of SOD, POD, CAT, GPX and PPO. Considering these results collectively, we speculate that the inhibition of antioxidant enzymes is a possible cause of the heat-stress-induced oxidative stress in L. japonica, and enhanced thermotolerance may be associated, at least in part, with the elevated activity of the enzymatic antioxidant system.

  5. Protective Effect of Pretreatment with Acenocoumarol in Cerulein-Induced Acute Pancreatitis

    PubMed Central

    Warzecha, Zygmunt; Sendur, Paweł; Ceranowicz, Piotr; Dembiński, Marcin; Cieszkowski, Jakub; Kuśnierz-Cabala, Beata; Olszanecki, Rafał; Tomaszewska, Romana; Ambroży, Tadeusz; Dembiński, Artur

    2016-01-01

    Coagulation is recognized as a key player in inflammatory and autoimmune diseases. The aim of the current research was to examine the effect of pretreatment with acenocoumarol on the development of acute pancreatitis (AP) evoked by cerulein. Methods: AP was induced in rats by cerulein administered intraperitoneally. Acenocoumarol (50, 100 or 150 µg/kg/dose/day) or saline were given once daily for seven days before AP induction. Results: In rats with AP, pretreatment with acenocoumarol administered at the dose of 50 or 100 µg/kg/dose/day improved pancreatic histology, reducing the degree of edema and inflammatory infiltration, and vacuolization of acinar cells. Moreover, pretreatment with acenocoumarol given at the dose of 50 or 100 µg/kg/dose/day reduced the AP-evoked increase in pancreatic weight, serum activity of amylase and lipase, and serum concentration of pro-inflammatory interleukin-1β, as well as ameliorated pancreatic DNA synthesis and pancreatic blood flow. In contrast, acenocoumarol given at the dose of 150 μg/kg/dose did not exhibit any protective effect against cerulein-induced pancreatitis. Conclusion: Low doses of acenocoumarol, given before induction of AP by cerulein, inhibit the development of that inflammation. PMID:27754317

  6. Waterborne chitosan-epoxysilane hybrid pretreatments for corrosion protection of zinc.

    PubMed

    Fernández-Solis, Christian; Erbe, Andreas

    2016-06-23

    Biopolymer-based systems are extensively studied as green alternatives for traditional polymer coatings, e.g., in corrosion protection. Chitosan-epoxysilane hybrid films are presented in this work as a chitosan-based protective system, which could, e.g., be applied in a pretreatment step. For the preparation of the chitosan-epoxysilane hybrid systems, a sol-gel procedure was applied. The function of the silane is to ensure adhesion to the substrate. On zinc substrates, homogeneous thin films with thickness of 50-70 nm were obtained after thermal curing. The hybrid-coated zinc substrates were characterized by infrared spectroscopy, ellipsometry, and x-ray photoelectron spectroscopy. As model corrosion experiments, linear polarization resistance was measured, and cathodic delamination of the weak polymer coating poly(vinylbutyral) (PVB) was studied using scanning Kelvin probe. Overall, chitosan-epoxysilane hybrid pretreated samples showed lower delamination rates than unmodified chitosan coatings and pure PVB. Electrochemical impedance spectroscopy confirmed a reduced ion permeability and water uptake by chitosan-epoxysilane films compared to that of a nonmodified chitosan coating. Even though the coatings are hydrophobic and contain water, they slow down cathodic delamination by limiting ion transport.

  7. Pretreatment with Apoaequorin Protects Hippocampal CA1 Neurons from Oxygen-Glucose Deprivation

    PubMed Central

    Detert, Julia A.; Adams, Erin L.; Lescher, Jacob D.; Lyons, Jeri-Anne; Moyer, James R.

    2013-01-01

    Ischemic stroke affects ∼795,000 people each year in the U.S., which results in an estimated annual cost of $73.7 billion. Calcium is pivotal in a variety of neuronal signaling cascades, however, during ischemia, excess calcium influx can trigger excitotoxic cell death. Calcium binding proteins help neurons regulate/buffer intracellular calcium levels during ischemia. Aequorin is a calcium binding protein isolated from the jellyfish Aequorea victoria, and has been used for years as a calcium indicator, but little is known about its neuroprotective properties. The present study used an in vitro rat brain slice preparation to test the hypothesis that an intra-hippocampal infusion of apoaequorin (the calcium binding component of aequorin) protects neurons from ischemic cell death. Bilaterally cannulated rats received an apoaequorin infusion in one hemisphere and vehicle control in the other. Hippocampal slices were then prepared and subjected to 5 minutes of oxygen-glucose deprivation (OGD), and cell death was assayed by trypan blue exclusion. Apoaequorin dose-dependently protected neurons from OGD – doses of 1% and 4% (but not 0.4%) significantly decreased the number of trypan blue-labeled neurons. This effect was also time dependent, lasting up to 48 hours. This time dependent effect was paralleled by changes in cytokine and chemokine expression, indicating that apoaequorin may protect neurons via a neuroimmunomodulatory mechanism. These data support the hypothesis that pretreatment with apoaequorin protects neurons against ischemic cell death, and may be an effective neurotherapeutic. PMID:24244400

  8. Pretreatment with Danhong injection protects the brain against ischemia-reperfusion injury.

    PubMed

    Wang, Shaoxia; Guo, Hong; Wang, Xumei; Chai, Lijuan; Hu, Limin; Zhao, Tao; Zhao, Buchang; Tan, Xiaoxu; Jia, Feifei

    2014-08-01

    Danhong injection (DHI), a Chinese Materia Medica standardized product extracted from Radix Salviae miltiorrhizae and Flos Carthami tinctorii, is widely used in China for treating acute ischemic stroke. In the present study, we explored the neuroprotective efficacy of DHI in a rat model of temporary middle cerebral artery occlusion, and evaluated the potential mechanisms underlying its effects. Pretreatment with DHI (0.9 and 1.8 mL/kg) resulted in a significantly smaller infarct volume and better neurological scores than pretreatment with saline. Furthermore, DHI significantly reduced the permeability of the blood-brain barrier, increased occludin protein expression and decreased neutrophil infiltration, as well as profoundly suppressing the upregulation of matrix metallopeptidase-9 expression seen in rats that had received vehicle. Matrix metallopeptidase-2 expression was not affected by ischemia or DHI. Moreover, DHI (1.8 mL/kg) administered 3 hours after the onset of ischemia also improved neurological scores and reduced infarct size. Our results indicate that the neuroprotective efficacy of DHI in a rat model of cerebral ischemia-reperfusion injury is mediated by a protective effect on the blood-brain barrier and the reversal of neutrophil infiltration.

  9. Pulmonary delivery of an aerosolized recombinant human butyrylcholinesterase pretreatment protects against aerosolized paraoxon in macaques.

    PubMed

    Rosenberg, Yvonne J; Laube, Beth; Mao, Lingjun; Jiang, Xiaoming; Hernandez-Abanto, Segundo; Lee, Keunmyoung D; Adams, Robert

    2013-03-25

    Butyrylcholinesterase (BChE) is the leading pretreatment candidate against exposure to organophosphates (OPs), which pose an ever increasing public and military health. Since respiratory failure is the primary cause of death following acute OP poisoning, an inhaled BChE therapeutic could prove highly efficacious in preventing acute toxicity as well as the associated delayed neuropathy. To address this, studies have been performed in mice and macaques using Chinese Hamster Ovary cells (CHO)-derived recombinant (r) BChE delivered by the pulmonary route, to examine whether the deposition of both macaque (Ma) and human (Hu) rBChE administered as aerosols (aer) favored the creation and retention of an efficient protective "pulmonary bioshield" that could scavenge incoming (inhaled) OPs in situ thereby preventing entry into the circulation and inhibition of plasma BChE and AChE on red blood cells (RBC-AChE) and in cholinergic synapses. In contrast to parenteral delivery of rBChE, which currently requires posttranslational modification for good plasma stability, an unmodified aer-rBChE pretreatment given 1-40 h prior to >1 LD50 of aer-paraoxon (Px) was able to prevent inhibition of circulating cholinesterase in a dose-dependent manner. These studies are the first to show protection by rBChE against a pesticide such as paraoxon when delivered directly into the lung and bode well for the use of a non-invasive and consumer friendly method of rHuBChE delivery as a human treatment to counteract OP toxicity. PMID:23178380

  10. Amelioration of Isoproterenol-Induced Oxidative Damage in Rat Myocardium by Withania somnifera Leaf Extract

    PubMed Central

    Khalil, Md. Ibrahim; Ahmmed, Istiyak; Ahmed, Romana; Tanvir, E. M.; Afroz, Rizwana; Paul, Sudip; Gan, Siew Hua; Alam, Nadia

    2015-01-01

    We investigated the protective role of Withania somnifera leaf extract (WSLEt) on isoproterenol- (ISO-) induced myocardial infarction (MI) in rats. Subcutaneous injection of ISO (85 mg/kg body weight (b.w.)) administered to rats for two consecutive days caused a significant increase in cardiac troponin I (cTnI) levels and serum lipid profiles, as well as the activities of some marker enzymes. In addition to these diagnostic markers, there were increased levels of lipid peroxidation (LPO) and decreased activities of enzymatic antioxidants (superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GRx), and glutathione-S-transferase (GST)) in the myocardium. However, oral pretreatment (100 mg/kg b.w.) with WSLEt for 4 weeks elicited a significant cardioprotective activity by lowering the levels of cTnI, lipid profiles, and marker enzymes. The levels of LPO products were also significantly decreased. Elevated activities of antioxidant enzymes were also observed in rats pretreated with WSLEt. As further confirmed histopathologically, our findings strongly suggest that the cardioprotective effect of WSLEt on myocardium experiencing ISO-induced oxidative damage may be due to an augmentation of the endogenous antioxidant system and an inhibition of LPO in the myocardial membrane. We conclude that WSLEt confers some protection against oxidative damage in ISO-induced MI in rats. PMID:26539517

  11. Amelioration of Isoproterenol-Induced Oxidative Damage in Rat Myocardium by Withania somnifera Leaf Extract.

    PubMed

    Khalil, Md Ibrahim; Ahmmed, Istiyak; Ahmed, Romana; Tanvir, E M; Afroz, Rizwana; Paul, Sudip; Gan, Siew Hua; Alam, Nadia

    2015-01-01

    We investigated the protective role of Withania somnifera leaf extract (WSLEt) on isoproterenol- (ISO-) induced myocardial infarction (MI) in rats. Subcutaneous injection of ISO (85 mg/kg body weight (b.w.)) administered to rats for two consecutive days caused a significant increase in cardiac troponin I (cTnI) levels and serum lipid profiles, as well as the activities of some marker enzymes. In addition to these diagnostic markers, there were increased levels of lipid peroxidation (LPO) and decreased activities of enzymatic antioxidants (superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GRx), and glutathione-S-transferase (GST)) in the myocardium. However, oral pretreatment (100 mg/kg b.w.) with WSLEt for 4 weeks elicited a significant cardioprotective activity by lowering the levels of cTnI, lipid profiles, and marker enzymes. The levels of LPO products were also significantly decreased. Elevated activities of antioxidant enzymes were also observed in rats pretreated with WSLEt. As further confirmed histopathologically, our findings strongly suggest that the cardioprotective effect of WSLEt on myocardium experiencing ISO-induced oxidative damage may be due to an augmentation of the endogenous antioxidant system and an inhibition of LPO in the myocardial membrane. We conclude that WSLEt confers some protection against oxidative damage in ISO-induced MI in rats.

  12. Pyruvate-dependent preconditioning and cardioprotection in murine myocardium.

    PubMed

    Flood, Amanda; Hack, Benjamin D; Headrick, John P

    2003-03-01

    1. Whether pyruvate inhibits or can actually initiate myocardial preconditioning is unclear and whether pyruvate provides protection via its action as a 'cosubstrate' with glucose or via alternative mechanisms also remains controversial. We examined effects of a high concentration of pyruvate (10 mmol/L) alone or with 15 mmol/L glucose in mouse hearts subjected to 20 min ischaemia and 30 min reperfusion. 2. Provision of 10 mmol/L pyruvate alone or as a cosubstrate markedly reduced ischaemic contracture and enhanced postischaemic recovery. Time to contracture was increased from approximately 3 min to over 8 min, peak contracture was reduced from 90 mmHg to less than 60 mmHg and postischaemic pressure development was also improved. Effects on contracture were independent of the presence of pyruvate during ischaemia and improved postischaemic recovery was evident with pre-ischaemic pyruvate perfusion. 3. Cardioprotection did not require the presence of pyruvate during ischaemia or reperfusion and effects of pyruvate pretreatment could be mimicked by pretreatment with 1 mmol/L dichloroacetate (DCA), an activator of pyruvate dehydrogenase. 4. Myocardial adenosine efflux and Ca2+ content were elevated (by 215 and 65%, respectively) following pretreatment with pyruvate, potentially triggering a preconditioned state. A role for adenosine A1 receptors is supported by lack of added protection with pyruvate in hearts transgenically overexpressing adenosine A1 receptors. 5. Collectively, these observations demonstrate that pre-ischaemic treatment with pyruvate or DCA provides a beneficial preconditioning-like effect in ischaemic and postischaemic myocardium. The response appears unrelated to glycolytic inhibition, but may be mediated via transient changes in adenosine levels and/or cellular Ca2+.

  13. Comparative study of pre-treatment procedures for (3)H monitoring in water samples from environmental protection programs.

    PubMed

    Tarancón, A; Bagán, H; Rauret, G; García, J F

    2010-04-15

    The determination of tritium activity in water samples is included in most environmental protection programs, and the recommended procedure consists of sample distillation and further measurement by liquid scintillation. Distillation is a simple but time consuming pre-treatment, especially in routine analysis. Here we evaluate alternative pre-treatments for tritium activity determination, such as filtration or the use of multiple selective ion exchange columns. 52 samples from different water sources (rain, surface, underground, sea and drinking water) in Spanish environmental protection programs, together with an IAEA reference material were analyzed. Results show that both pre-treatments can be applied as a preliminary tool to discriminate between tritium active and non active waters in environmental monitoring programs. In addition, filtration and multiple selective ion exchange column pre-treatments can be used as alternative procedures for tritium activity determination in the routine analyses of water samples with known and reproducible chemical and isotopic composition. Both methods are less time consuming than distillation and, in the case of filtration, extremely cheap. For waters with complex matrices, especially sea water, distillation is the recommended procedure due to the interference from salts contained in the sample. PMID:20167352

  14. Comparative study of pre-treatment procedures for (3)H monitoring in water samples from environmental protection programs.

    PubMed

    Tarancón, A; Bagán, H; Rauret, G; García, J F

    2010-04-15

    The determination of tritium activity in water samples is included in most environmental protection programs, and the recommended procedure consists of sample distillation and further measurement by liquid scintillation. Distillation is a simple but time consuming pre-treatment, especially in routine analysis. Here we evaluate alternative pre-treatments for tritium activity determination, such as filtration or the use of multiple selective ion exchange columns. 52 samples from different water sources (rain, surface, underground, sea and drinking water) in Spanish environmental protection programs, together with an IAEA reference material were analyzed. Results show that both pre-treatments can be applied as a preliminary tool to discriminate between tritium active and non active waters in environmental monitoring programs. In addition, filtration and multiple selective ion exchange column pre-treatments can be used as alternative procedures for tritium activity determination in the routine analyses of water samples with known and reproducible chemical and isotopic composition. Both methods are less time consuming than distillation and, in the case of filtration, extremely cheap. For waters with complex matrices, especially sea water, distillation is the recommended procedure due to the interference from salts contained in the sample.

  15. Hyperthermic pre-treatment protects rat IPC-81 leukaemia cells against heat- and hydrogen peroxide-induced apoptosis.

    PubMed

    Zeise, E; Rensing, L

    2002-01-01

    It is well known that hyperthermia causes a transient tolerance of cells to a second heat challenge (acquired thermotolerance). The present study addresses the question of whether hyperthermic pre-treatment also increases the tolerance against heat- and hydrogen peroxide-induced apoptosis in rat IPC-81 leukaemia cells. This cell line exhibits an aberrant heat shock response which is characterized by a lack of the inducible Hsp70 isoform, even under conditions of heat or hydrogen peroxide stress, while the constitutively expressed Hsc70 and the inducible isoform of hemoxygenase (HO-1) are strongly enhanced by heat stress (43.5 degrees C; 30 min). In spite of this Hsp70 deficiency, hyperthermic pre-treatment protects IPC-81 leukaemia cells against apoptotic cell death induced by heat or hydrogen peroxide, but is less effective against necrosis induced by higher doses of the applied stressors. Addition of hydrogen peroxide (25 microM) enhances the amount of bax mRNA, while the level of bcl-2 mRNA remains unchanged. No increase of bax mRNA, in contrast, could be detected in heat shock-primed IPC-81 cells when treated with hydrogen peroxide after a 12h recovery. These results indicate that hyperthermic pre-treatment may exert its anti-apoptotic function not only by enhanced expression of constitutive as well as inducible HSPs but also by lowering the level of bax transcripts and thereby increasing the Bcl-2/Bax ratio.

  16. Exogenous selenium pretreatment protects rapeseed seedlings from cadmium-induced oxidative stress by upregulating antioxidant defense and methylglyoxal detoxification systems.

    PubMed

    Hasanuzzaman, Mirza; Hossain, Mohammad Anwar; Fujita, Masayuki

    2012-11-01

    The protective effect of selenium (Se) on antioxidant defense and methylglyoxal (MG) detoxification systems was investigated in leaves of rapeseed (Brassica napus cv. BINA sharisha 3) seedlings under cadmium (Cd)-induced oxidative stress. Two sets of 11-day-old seedlings were pretreated with both 50 and 100 μM Se (Na(2)SeO(4), sodium selenate) for 24 h. Two concentrations of CdCl(2) (0.5 and 1.0 mM) were imposed separately or on the Se-pretreated seedlings, which were grown for another 48 h. Cadmium stress at any levels resulted in the substantial increase in malondialdehyde and H(2)O(2) levels. The ascorbate (AsA) content of the seedlings decreased significantly upon exposure to Cd stress. The amount of reduced glutathione (GSH) increased only at 0.5 mM CdCl(2), while glutathione disulfide (GSSG) increased at any level of Cd, with concomitant decrease in GSH/GSSG ratio. The activities of ascorbate peroxidase (APX) and glutathione S-transferase (GST) increased significantly with increased concentration of Cd (both at 0.5 and 1.0 mM CdCl(2)), while the activities of glutathione reductase (GR) and glutathione peroxidase (GPX) increased only at moderate stress (0.5 mM CdCl(2)) and then decreased at 1.0 mM severe stress (1.0 mM CdCl(2)). Monodehydroascorbate reductase (MDHAR), dehydroascorbate reductase (DHAR), catalase (CAT), glyoxalase I (Gly I), and glyoxalase II (Gly II) activities decreased upon exposure to any levels of Cd. Selenium pretreatment had little effect on the nonenzymatic and enzymatic components of seedlings grown under normal conditions; i.e., they slightly increased the GSH content and the activities of APX, GR, GST, and GPX. On the other hand, Se pretreatment of seedlings under Cd-induced stress showed a synergistic effect; it increased the AsA and GSH contents, the GSH/GSSG ratio, and the activities of APX, MDHAR, DHAR, GR, GPX, CAT, Gly I, and Gly II which ultimately reduced the MDA and H(2)O(2) levels. However, in most cases, pretreatment with

  17. Exogenous selenium pretreatment protects rapeseed seedlings from cadmium-induced oxidative stress by upregulating antioxidant defense and methylglyoxal detoxification systems.

    PubMed

    Hasanuzzaman, Mirza; Hossain, Mohammad Anwar; Fujita, Masayuki

    2012-11-01

    The protective effect of selenium (Se) on antioxidant defense and methylglyoxal (MG) detoxification systems was investigated in leaves of rapeseed (Brassica napus cv. BINA sharisha 3) seedlings under cadmium (Cd)-induced oxidative stress. Two sets of 11-day-old seedlings were pretreated with both 50 and 100 μM Se (Na(2)SeO(4), sodium selenate) for 24 h. Two concentrations of CdCl(2) (0.5 and 1.0 mM) were imposed separately or on the Se-pretreated seedlings, which were grown for another 48 h. Cadmium stress at any levels resulted in the substantial increase in malondialdehyde and H(2)O(2) levels. The ascorbate (AsA) content of the seedlings decreased significantly upon exposure to Cd stress. The amount of reduced glutathione (GSH) increased only at 0.5 mM CdCl(2), while glutathione disulfide (GSSG) increased at any level of Cd, with concomitant decrease in GSH/GSSG ratio. The activities of ascorbate peroxidase (APX) and glutathione S-transferase (GST) increased significantly with increased concentration of Cd (both at 0.5 and 1.0 mM CdCl(2)), while the activities of glutathione reductase (GR) and glutathione peroxidase (GPX) increased only at moderate stress (0.5 mM CdCl(2)) and then decreased at 1.0 mM severe stress (1.0 mM CdCl(2)). Monodehydroascorbate reductase (MDHAR), dehydroascorbate reductase (DHAR), catalase (CAT), glyoxalase I (Gly I), and glyoxalase II (Gly II) activities decreased upon exposure to any levels of Cd. Selenium pretreatment had little effect on the nonenzymatic and enzymatic components of seedlings grown under normal conditions; i.e., they slightly increased the GSH content and the activities of APX, GR, GST, and GPX. On the other hand, Se pretreatment of seedlings under Cd-induced stress showed a synergistic effect; it increased the AsA and GSH contents, the GSH/GSSG ratio, and the activities of APX, MDHAR, DHAR, GR, GPX, CAT, Gly I, and Gly II which ultimately reduced the MDA and H(2)O(2) levels. However, in most cases, pretreatment with

  18. Partial Protection of PC12 Cells from Cellular Stress by Low-Dose Sodium Nitroprusside Pre-treatment.

    PubMed

    Varga, Judit; Bátor, Judit; Nádasdi, Gergő; Árvai, Zita; Schipp, Renáta; Szeberényi, József

    2016-10-01

    The PC12 rat pheochromocytoma cell line is an in vitro model system widely used for the investigation of intracellular signaling events contributing to neuronal differentiation and cell death. We found earlier that the nitric oxide donor compound sodium nitroprusside (SNP) induced apoptosis of PC12 cells if it was applied in high concentration (400 µM). Yoshioka et al. (J Pharmacol Sci 101:126-134, 2006) reported that cell death evoked by cytotoxic concentrations of SNP could be prevented by a 100 µM SNP pre-treatment in a murine macrophage cell line. The apoptosis caused by toxic-dose SNP treatment (400 µM) could be partially overcome in PC12 cells as well by the low-dose SNP pre-treatment. The partial inhibition of apoptosis was accompanied by reduced phosphorylation of certain proteins (such as stress-activated protein kinases, the p53, and the eIF2α proteins), decreased caspase activation, and less intense internucleosomal DNA fragmentation. The 100 µM SNP pre-treatment reduced the pro-apoptotic potential of certain other stress stimuli (serum withdrawal, cisplatin and tunicamycin treatments) as well, although the underlying biochemical changes were not entirely uniform. On the contrary, the 100 µM SNP pre-treatment was unable to prevent cell death caused by the protein synthesis inhibitor anisomycin. Further clarification of the above-mentioned processes may be important in understanding the mechanisms by which mild nitrosative stress protects cells against certain forms of cellular stress conditions.

  19. Adolescent pre-treatment with oxytocin protects against adult methamphetamine-seeking behavior in female rats.

    PubMed

    Hicks, Callum; Cornish, Jennifer L; Baracz, Sarah J; Suraev, Anastasia; McGregor, Iain S

    2016-03-01

    The neuropeptide oxytocin (OT), given acutely, reduces self-administration of the psychostimulant drug methamphetamine (METH). Additionally, chronic OT administration to adolescent rats reduces levels of alcohol consumption in adulthood, suggesting developmental neuroplasticity in the OT system relevant to addiction-related behaviors. Here, we examined whether OT exposure during adolescence might subsequently inhibit METH self-administration in adulthood. Female Sprague-Dawley rats were administered vehicle or OT (1 mg/kg, i.p.) once daily from postnatal days (PND) 28 to 37 (adolescence). At PND 62 (adulthood), rats were trained to self-administer METH (intravenous, i.v.) in daily 2-hour sessions for 10 days under a fixed ratio 1 (FR1) reinforcement schedule, followed by determination of dose-response functions (0.01-0.3 mg/kg/infusion, i.v.) under both FR1 and progressive ratio (PR) schedules of reinforcement. Responding was then extinguished, and relapse to METH-seeking behavior assessed following priming doses of non-contingent METH (0.1-1 mg/kg, i.p.). Finally, plasma was collected to determine pre-treatment effects on OT and corticosterone levels. Results showed that OT pre-treatment did not significantly inhibit the acquisition of METH self-administration or FR1 responding. However, rats pre-treated with OT responded significantly less for METH under a PR reinforcement schedule, and showed reduced METH-primed reinstatement with the 1 mg/kg prime. Plasma OT levels were also significantly higher in OT pre-treated rats. These results confirm earlier observations that adolescent OT exposure can subtly, yet significantly, inhibit addiction-relevant behaviors in adulthood.

  20. p27 kip1 haplo-insufficiency improves cardiac function in early-stages of myocardial infarction by protecting myocardium and increasing angiogenesis by promoting IKK activation.

    PubMed

    Zhou, Ningtian; Fu, Yuxuan; Wang, Yunle; Chen, Pengsheng; Meng, Haoyu; Guo, Shouyu; Zhang, Min; Yang, Zhijian; Ge, Yingbin

    2014-08-07

    p27(kip1) (p27) is widely known as a potent cell cycle inhibitor in several organs, especially in the heart. However, its role has not been fully defined during the early phase of myocardial infarction (MI). In this study, we investigated the relationships between p27, vascular endothelial growth factor/hepatocyte growth factor (VEGF/HGF) and NF-κB in post-MI cardiac function repair both in vivo and in the hypoxia/ischemia-induced rat myocardiocyte model. In vivo, haplo-insufficiency of p27 improved cardiac function, diminished the infarct zone, protected myocardiocytes and increased angiogenesis by enhancing the production of VEGF/HGF. In vitro, the presence of conditioned medium from hypoxia/ischemia-induced p27 knockdown myocardiocytes reduced the injury caused by hypoxia/ischemia in myocardiocytes, and this effect was reversed by VEGF/HGF neutralizing antibodies, consistent with the cardioprotection being due to VEGF/HGF secretion. We also observed that p27 bound to IKK and that p27 haplo-insufficiency promoted IKK/p65 activation both in vivo and in vitro, thereby inducing the NF-κB downstream regulator, VEGF/HGF. Furthermore, IKKi and IKK inhibitor negated the effect of VEGF/HGF. Therefore, we conclude that p27 haplo-insufficiency protects against heart injury by VEGF/HGF mediated cardioprotection and increased angiogenesis through promoting IKK activation.

  1. Impact of Sn/F Pre-Treatments on the Durability of Protective Coatings against Dentine Erosion/Abrasion

    PubMed Central

    Ganss, Carolina; Lussi, Adrian; Peutzfeldt, Anne; Naguib Attia, Nader; Schlueter, Nadine

    2015-01-01

    For preventing erosive wear in dentine, coating with adhesives has been suggested as an alternative to fluoridation. However, clinical studies have revealed limited efficacy. As there is first evidence that Sn2+ increases bond strength of the adhesive Clearfil SE (Kuraray), the aim of the present study was to investigate whether pre-treatment with different Sn2+/F− solutions improves the durability of Clearfil SE coatings. Dentine samples (eight groups, n=16/group) were freed of smear layer (0.5% citric acid, 10 s), treated (15 s) either with no solution (control), aminefluoride (AmF, 500 ppm F−, pH 4.5), SnCl2 (800/1600 ppm Sn2+; pH 1.5), SnCl2/AmF (500 ppm F−, 800 ppm Sn2+, pH 1.5/3.0/4.5), or Elmex Erosion Protection Rinse (EP, 500 ppm F−, 800 ppm Sn2+, pH 4.5; GABA International), then rinsed with water (15 s) and individually covered with Clearfil SE. Subsequently the specimens were subjected to an erosion/abrasion protocol consisting of 1320 cycles of immersion in 0.5% citric acid (5°C/55°C; 2 min) and automated brushing (15 s, 200 g, NaF-toothpaste, RDA 80). As the coatings proved stable up to 1320 cycles, 60 modified cycles (brushing time 30 min/cycle) were added. Wear was measured profilometrically. After SnCl2/AmF, pH 4.5 or EP pre-treatment all except one coating survived. In the other groups, almost all coatings were lost and there was no significant difference to the control group. Pre-treatment with a Sn2+/F− solution at pH 4.5 seems able to improve the durability of adhesive coatings, rendering these an attractive option in preventing erosive wear in dentine. PMID:26075906

  2. Impact of Sn/F Pre-Treatments on the Durability of Protective Coatings against Dentine Erosion/Abrasion.

    PubMed

    Ganss, Carolina; Lussi, Adrian; Peutzfeldt, Anne; Naguib Attia, Nader; Schlueter, Nadine

    2015-01-01

    For preventing erosive wear in dentine, coating with adhesives has been suggested as an alternative to fluoridation. However, clinical studies have revealed limited efficacy. As there is first evidence that Sn(2+) increases bond strength of the adhesive Clearfil SE (Kuraray), the aim of the present study was to investigate whether pre-treatment with different Sn(2+)/F(-) solutions improves the durability of Clearfil SE coatings. Dentine samples (eight groups, n=16/group) were freed of smear layer (0.5% citric acid, 10 s), treated (15 s) either with no solution (control), aminefluoride (AmF, 500 ppm F(-), pH 4.5), SnCl2 (800/1600 ppm Sn(2+); pH 1.5), SnCl2/AmF (500 ppm F(-), 800 ppm Sn(2+), pH 1.5/3.0/4.5), or Elmex Erosion Protection Rinse (EP, 500 ppm F-, 800 ppm Sn(2+), pH 4.5; GABA International), then rinsed with water (15 s) and individually covered with Clearfil SE. Subsequently the specimens were subjected to an erosion/abrasion protocol consisting of 1320 cycles of immersion in 0.5% citric acid (5 °C/55 °C; 2 min) and automated brushing (15 s, 200 g, NaF-toothpaste, RDA 80). As the coatings proved stable up to 1320 cycles, 60 modified cycles (brushing time 30 min/cycle) were added. Wear was measured profilometrically. After SnCl2/AmF, pH 4.5 or EP pre-treatment all except one coating survived. In the other groups, almost all coatings were lost and there was no significant difference to the control group. Pre-treatment with a Sn(2+)/F(-) solution at pH 4.5 seems able to improve the durability of adhesive coatings, rendering these an attractive option in preventing erosive wear in dentine. PMID:26075906

  3. Exercise preconditioning of the myocardium.

    PubMed

    Kavazis, Andreas N

    2009-01-01

    Diseases of the heart (e.g. myocardial ischaemia reperfusion injury) remain the major cause of death in the industrialized world. Therefore, developing a pragmatic countermeasure to reduce myocardial ischaemia reperfusion injury is vital. In this regard, a plethora of evidence indicates that regular exercise can protect the heart during an ischaemia reperfusion insult (i.e. cardioprotection). This review summarizes studies indicating that both short-term (i.e. 1-5 days) and long-term (i.e. weeks to months) endurance exercise provides cardioprotection. Data are presented showing that exercise duration and exercise intensity are both important factors in achieving a cardioprotective phenotype. Importantly, it appears that the exercise duration of a single exercise session should last for 60 minutes and should be performed at about 75% maximum oxygen consumption in order to achieve exercise-induced cardioprotection. Furthermore, data are presented showing that exercise-induced cardioprotection against myocardial stunning can persist for at least 9 days after the cessation of exercise training, but is lost 18 days after exercise. This review also summarizes the exercise-induced adaptations that occur to the myocardium. In particular, extrinsic changes observed in human and animal models include neural, hormonal, humoral, vascular and reduced body fat. Other anatomical and biochemical/molecular changes that have been studied as putative mechanisms in exercise-induced cardioprotection include alterations in anatomic coronary arteries, induction of myocardial heat shock proteins, increased myocardial cyclooxygenase-2 activity, elevated endoplasmic reticulum stress proteins, nitric oxide production, improved function of sarcolemmal and/or mitochondrial adenosine triphosphate (ATP)-sensitive potassium channels and increased myocardial antioxidant capacity. However, the most compelling evidence for exercise-induced cardioprotection is the fact that exercise training

  4. Mucuna pruriens Linn. seed extract pretreatment protects against cardiorespiratory and neuromuscular depressant effects of Naja sputatrix (Javan spitting cobra) venom in rats.

    PubMed

    Fung, Shin Yee; Tan, Nget Hong; Sim, Si Mui; Marinello, Enrico; Guerranti, Roberto; Aguiyi, John Chinyere

    2011-04-01

    Mucuna pruriens has been used by native Nigerians as a prophylactic for snakebite. The protective effects of M. pruriens seed extract (MPE) were investigated against the pharmacological actions of N. sputatrix (Javan spitting cobra) venom in rats. The results showed that MPE-pretreatment protected against cardiorespiratory and, to a lesser extent, neuromuscular depressant effects of N. sputatrix venom. These may be explained at least in part by the neutralisation of the cobra venom toxins by anti-MPE antibodies elicited by the MPE pretreatment. PMID:21614888

  5. Protective Effect of Low-dose Sevoflurane Inhalation and Propofol Anesthesia on the Myocardium after Carotid Endarterectomy: A Randomized Controlled Trial

    PubMed Central

    Wang, Qian; Li, Yan-Hong; Wang, Tian-Long; Feng, Hua; Cai, Bing

    2015-01-01

    Background: Myocardial infarction is an important cause of mortality after carotid endarterectomy (CEA). Sevoflurane provides myocardial protection to patients undergoing coronary surgery, but whether it also reduces the incidence of myocardial injury in CEA patients is unclear. In this study, we evaluated the cardioprotective effect of low-dose sevoflurane with propofol in patients undergoing CEA. Methods: This was a single-center, prospective, randomized study conducted between November 2011 and December 2013. The study population of 122 patients who underwent CEA were randomly assigned to two groups. Group A (n = 62) received propofol for anesthetic maintenance, and Group B (n = 60) additionally received 0.8% end-tidal sevoflurane. The bispectral index was kept at 40–60. Myocardial injury, defined as cardiac troponin I (cTnI) levels >0.04 ng/ml, was the primary end-point. Levels of cTnI were measured before anesthesia, and at 4, 24, and 72 h after surgery. Perioperative hemodynamic parameters and adverse cardiovascular events after surgery were also recorded. Results: Myocardial injury was detected in 18 patients in Group A and 7 in Group B. The difference was statistically significant (29.0% vs. 11.7%, P = 0.018). The hemodynamic parameters were comparable between the groups, as were adverse cardiovascular events (P = 0.619). Conclusions: Low-dose sevoflurane inhalation along with propofol reduces the incidence of myocardial injury in symptomatic patients after CEA. PMID:26168823

  6. The protective effect of zinc sulphate pretreatment against duodenal ulcers in the rat.

    PubMed

    Troskot, B; Simicevic, V N; Dodig, M; Rotkvic, I; Ivankovic, D; Duvnjak, M

    1997-10-01

    Exogenously administered zinc compounds have been shown to possess antiulcer activity in the development of gastric lesions. The aim of this study was to investigate the effects of zinc sulphate pretreatment of rats on cysteamine-induced duodenal ulcers and to correlate them with changes in zinc serum and tissue levels. Atomic absorption spectrophotometry was used to determine zinc serum and tissue concentrations in all animal groups. Cysteamine produced marked duodenal ulceration in control animals 24 h after application, with an increase in endogenous zinc tissue concentrations and a marked decrease in serum concentrations. Zinc sulphate (20, 40 or 80 mg kg-1) applied per os one hour prior to cysteamine application inhibited the development of duodenal lesions in a dose-related manner. The application of zinc sulphate in a single intraperitoneal (i.p.) application (80 mg kg-1) did not, however, prevent the formation of duodenal lesions. In order to assess zinc absorption from the gastrointestinal tract, one group of rats received a single oral dose of zinc sulphate (80 mg kg-1) without cysteamine application. The observations of this study seem to indicate that zinc plays an important cytoprotective role in duodenal ulcer disease.

  7. [Protective effects of d-chlorpheniramine maleate pre-treatment against acute side effects of Irinotecan(CPT- 11)].

    PubMed

    Misumi, Nobuhiro; Hiraike, Mikako; Nawata, Fusako; Hashimoto, Mirai; Tanigawa, Kayoko; Takase, Izumi; Nabeshima, Aya; Honda, Shinobu

    2011-07-01

    It is wellknown that cholinomimetic side effects, such as sedation, abdominal pain, nasal flow and watery eyes, may develop in patients in the early stage of Irinotecan (CPT-11) administration; however, there have been no investigations concerning methods for preventing the development of these side effects. To assess the protective effects of pre-treatment with d-CM on cholinomimetic side effects in the early stage after Irinotecan (CPT-11) administration, we prescribed d- Chlorpheniramine maleate (d-CM) to a group of patients prior to Irinotecan (CPT-11) administration. Twenty members from the group of non-d-CM-treated patients (n=39) and 4 members from the group of treated patients (n=20) complained of side effects. The pre-administration of d-CM significantly reduced the number of patients with side effects (p<0.05). The relative risk (RR) for the frequency of side effects was 0.39 (95% CI; 0.15-0.98), demonstrating that the frequency of side effects was significantly reduced. Based on theses findings, we concluded that the pre-administration of d-CM had protective effects against side effects that might develop in the early stage after Irinotecan (CPT-11) administration.

  8. Resveratrol pretreatment protects rat hearts from ischemia/reperfusion injury partly via a NALP3 inflammasome pathway

    PubMed Central

    Dong, Wusong; Yang, Rui; Yang, Jian; Yang, Jun; Ding, Jiawang; Wu, Hui; Zhang, Jing

    2015-01-01

    Caspase1 expression and IL-1β and IL-18 activation. These results suggest that the NALP3 inflammasome is activated during the myocardial I/R injury process and that the secretion of the inflammatory cytokines IL-1β and IL-18 mediates the cascade inflammatory response. Resveratrol may play an important role in protecting the myocardium against I/R injury in rats by inhibiting the expression and activation of the NALP3 inflammatory body. Therefore, the attenuation of the inflammatory response may be involved in the cardioprotective mechanisms of resveratrol in response to myocardial I/R injury. PMID:26464617

  9. Protective effect of pretreatment with thymoquinone against Aflatoxin B1 induced liver toxicity in mice

    PubMed Central

    Nili-Ahmadabadi, A.; Tavakoli, F.; Hasanzadeh, GR.; Rahimi, HR.; Sabzevari, O.

    2011-01-01

    Background and the purpose of the study Thymoquinone (TQ) is one of the active components of Nigella sativa. The plant has been used in herbal medicine for treatment of many diseases including liver complications. The present study aimed to investigate protective effects of TQ on Aflatoxin B1 (AFB1) induced liver toxicity in mice. Methods Animals were divided into six groups and treated intraperitoneally. Group 1 (blank) served as vehicle, group 2 (positive control) received AFB1, Group 3 was treated with 9 mg/kg of TQ, Groups 4, 5 and 6 were treated with 4.5, 9 and 18 mg/kg of TQ, respectively. After three consecutive days, except for groups 1 and 3, animals were administered with a single dose of AFB1 (2 mg/kg). All the animals were killed 24 hrs following the AFB1 administration under ether anesthesia. Biochemical parameters including AST, ALT and ALP in serum samples and glutathione (GSH) and malondialdehyde (MDA) contents in liver homogenates were determined. Liver sections were collected for histopathological examination. Results Findings of this study showed that AST, ALT, ALP and MDA levels were significantly lower in the TQ treated animals as compared to AFB1 group (group 2). Furthermore, TQ was able to recover glutathione content (GSH) of liver tissue. The best response, however, was observed with the dose of 9 mg/kg. Liver sections of AFB1 intoxicated mice showed inflammation, necrosis, hyperplasia of kupffer and infiltration of mononuclear cells, dilation of sinusoids and disruption of hepatocytes, while treatment with TQ helped to normalize liver architecture in accordance to biochemical findings. Conclusion Taken collectively, TQ has a protective role with optimum dose of 9 mg/kg in AFB1 hepatotoxicity. PMID:22615670

  10. Heat shock pretreatment may protect against heatstroke-induced circulatory shock and cerebral ischemia by reducing oxidative stress and energy depletion.

    PubMed

    Wang, Jui-Ling; Ke, Der-Shin; Lin, Mao-Tsun

    2005-02-01

    The mechanisms underlying the protective effects of heat shock pretreatment on heatstroke remain unclear. Here we attempted to ascertain whether the possible occurrence of oxidative stress and energy depletion exhibited during heatstroke can be reduced by heat shock preconditioning. In the present study, colonic temperature, mean arterial pressure, heart rate, striatal levels of heat shock protein 72 (HSP72), local Po2, brain temperature, cerebral blood flow, cellular ischemia and damage markers, dihydroxybenzoic acid (DHBA), lipid peroxidation, glutathione, glutathione peroxidase and reductase activities, and ATP were assayed in normothermic control rats and in heatstroke rats with or without preconditioning 16 or 96 h before initiation of heatstroke. Heatstroke was induced by exposing the anesthetized rats to a high ambient temperature (Ta = 43 degrees C) until the moment at which MAP decreased from its peak level. Sublethal heat shock pretreatment 16 h before initiation of heatstroke, in addition to increasing striatal HSP72 levels, conferred significant protection against heatstroke-induced arterial hypotension, striatal ischemia and damage, increment of hydroxyl radical formation, lipid peroxidation, glutathione oxidation, and decrement of glutathione peroxidase activity and ATP. However, at 96 h after heat shock, when striatal HSP72 expression returned to basal levels, the above responses that occurred during onset of heatstroke were indistinguishable between the two groups. These results suggest that heat shock pretreatment induces HSP72 overexpression in striatum and confers protection against heatstroke-induced striatal ischemia and damage by reducing oxidative stress and energy depletion.

  11. Protection of dichlorvos induced oxidative stress and nigrostriatal neuronal death by chronic Coenzyme Q{sub 10} pretreatment

    SciTech Connect

    Binukumar, BK; Gupta, Nidhi; Bal, Amanjit; Gill, Kiran Dip

    2011-10-01

    Numerous epidemiological studies have shown an association between pesticide exposure and increased risk of developing Parkinson's diseases. Oxidative stress generated as a result of mitochondrial dysfunction has been implicated as an important factor in the etiology of Parkinson's disease. Previously, we reported that chronic dichlorvos exposure causes mitochondrial impairments and nigrostriatal neuronal death in rats. The present study was designed to test whether Coenzyme Q{sub 10} (CoQ{sub 10}) administration has any neuroprotective effect against dichlorvos mediated nigrostriatal neuronal death, {alpha}-synuclein aggregation, and motor dysfunction. Male albino rats were administered dichlorvos by subcutaneous injection at a dose of 2.5 mg/kg body weight over a period of 12 weeks. Results obtained there after showed that dichlorvos exposure leads to enhanced mitochondrial ROS production, {alpha}-synuclein aggregation, decreased dopamine and its metabolite levels resulting in nigrostriatal neurodegeneration. Pretreatment by Coenzyme Q{sub 10} (4.5 mg/kg ip for 12 weeks) to dichlorvos treated animals significantly attenuated the extent of nigrostriatal neuronal damage, in terms of decreased ROS production, increased dopamine and its metabolite levels, and restoration of motor dysfunction when compared to dichlorvos treated animals. Thus, the present study shows that Coenzyme Q{sub 10} administration may attenuate dichlorvos induced nigrostriatal neurodegeneration, {alpha}-synuclein aggregation and motor dysfunction by virtue of its antioxidant action. - Highlights: > CoQ{sub 10} administration attenuates dichlorvos induced nigrostriatal neurodegenaration. > CoQ{sub 10} pre treatment leads to preservation of TH-IR neurons. > CoQ{sub 10} may decrease oxidative damage and {alpha}-synuclin aggregation. > CoQ{sub 10} treatment enhances motor function and protects rats from catalepsy.

  12. Pretreatment by low-dose fibrates protects against acute free fatty acid-induced renal tubule toxicity by counteracting PPAR{alpha} deterioration

    SciTech Connect

    Takahashi, Kyoko; Kamijo, Yuji; Hora, Kazuhiko; Hashimoto, Koji; Higuchi, Makoto; Nakajima, Takero; Ehara, Takashi; Shigematsu, Hidekazu; Gonzalez, Frank J.; Aoyama, Toshifumi

    2011-05-01

    Development of a preventive strategy against tubular damage associated with proteinuria is of great importance. Recently, free fatty acid (FFA) toxicities accompanying proteinuria were found to be a main cause of tubular damage, which was aggravated by insufficiency of peroxisome proliferator-activated receptor alpha (PPAR{alpha}), suggesting the benefit of PPAR{alpha} activation. However, an earlier study using a murine acute tubular injury model, FFA-overload nephropathy, demonstrated that high-dose treatment of PPAR{alpha} agonist (0.5% clofibrate diet) aggravated the tubular damage as a consequence of excess serum accumulation of clofibrate metabolites due to decreased kidney elimination. To induce the renoprotective effects of PPAR{alpha} agonists without drug accumulation, we tried a pretreatment study using low-dose clofibrate (0.1% clofibrate diet) using the same murine model. Low-dose clofibrate pretreatment prevented acute tubular injuries without accumulation of its metabolites. The tubular protective effects appeared to be associated with the counteraction of PPAR{alpha} deterioration, resulting in the decrease of FFAs influx to the kidney, maintenance of fatty acid oxidation, diminution of intracellular accumulation of undigested FFAs, and attenuation of disease developmental factors including oxidative stress, apoptosis, and NF{kappa}B activation. These effects are common to other fibrates and dependent on PPAR{alpha} function. Interestingly, however, clofibrate pretreatment also exerted PPAR{alpha}-independent tubular toxicities in PPAR{alpha}-null mice with FFA-overload nephropathy. The favorable properties of fibrates are evident when PPAR{alpha}-dependent tubular protective effects outweigh their PPAR{alpha}-independent tubular toxicities. This delicate balance seems to be easily affected by the drug dose. It will be important to establish the appropriate dosage of fibrates for treatment against kidney disease and to develop a novel PPAR

  13. [Stunned myocardium after acute ischemic stroke].

    PubMed

    Varela, Daniel; Díaz, Fernanda; Hlavnicka, Alejandro; Wainsztein, Néstor; Leiguarda, Ramón

    2006-01-01

    The so-called stunned myocardium, defined as transitory myocardial contractile dysfunction, has been clearly demonstrated in diverse clinical situations. However, stunned myocardium related to ischemic stroke has been poorly identified. We describe two patients with diagnosis of acute ischemic stroke who developed eletrocardiographic changes, cardiac enzyme increasing levels and myocardial dysfunction secondary to abnormal cardiac wall motion. At the same time the patients developed acute lung injury with rapid resolution, perhaps as a consequence of neurocardiogenic components.

  14. Protective role of hydrogen peroxide pretreatment on defense systems and BnMP1 gene expression in Cr(VI)-stressed canola seedlings.

    PubMed

    Yıldız, Mustafa; Terzi, Hakan; Bingül, Nagihan

    2013-10-01

    To evaluate the ameliorating effects of hydrogen peroxide (H2O2, 200 μM) on hexavalent chromium [Cr(VI)] toxicity in canola (Brassica napus L.), we focused on the plant growth, chlorophyll content, thiol contents, lipid peroxidation, antioxidant enzymes, and the expression of metallothionein protein (BnMP1) mRNA. Cr(VI) at 50 μM significantly decreased the plant growth (fresh and dry weights). The decrease in growth was accompanied by increased lipid peroxidation and decreased chlorophyll content in leaves. Hydrogen peroxide pretreatment, however, enhanced plant growth parameters and led to the reduced levels of lipid peroxidation and higher levels of pigment. In addition, H2O2 pretreatment increased Cr accumulation in aerial parts of seedlings. The tendency of increase in thiol content under Cr(VI) stress was further increased with H2O2 pretreatment. The activities of antioxidant enzymes such as superoxide dismutase (SOD), ascorbate peroxidase (APX), guaiacol peroxidase (POD) and catalase (CAT) were differentially altered. SOD and POD activities increased under Cr(VI) stress, whereas APX and CAT activities decreased. The SOD and CAT activities remained unaffected in both durations due to H2O2 pretreatment, but activities of APX and POD were promoted in the Cr(VI)-stressed seedlings. Metallothioneins are a family of low-molecular-weight Cys-rich proteins and are thought to play a possible role in metal metabolism or detoxification. In real-time quantitative PCR analysis, the expression level of BnMP1 mRNA was increased at 1 day after treatment (DAT), whereas it was decreased at 7 DAT in Cr(VI)-stressed seedlings. At 1 DAT, pretreatment of H2O2 before Cr(VI) stress reduced the expression of BnMP1 mRNA as compared to Cr(VI) stress alone, but this effect was not significant. At 7 DAT, H2O2 pretreatment alleviated the Cr(VI) stress-mediated decrease in the expression of BnMP1 mRNA. These results suggest that H2O2 may act as a signal that triggers defense mechanisms

  15. Protective role of hydrogen peroxide pretreatment on defense systems and BnMP1 gene expression in Cr(VI)-stressed canola seedlings.

    PubMed

    Yıldız, Mustafa; Terzi, Hakan; Bingül, Nagihan

    2013-10-01

    To evaluate the ameliorating effects of hydrogen peroxide (H2O2, 200 μM) on hexavalent chromium [Cr(VI)] toxicity in canola (Brassica napus L.), we focused on the plant growth, chlorophyll content, thiol contents, lipid peroxidation, antioxidant enzymes, and the expression of metallothionein protein (BnMP1) mRNA. Cr(VI) at 50 μM significantly decreased the plant growth (fresh and dry weights). The decrease in growth was accompanied by increased lipid peroxidation and decreased chlorophyll content in leaves. Hydrogen peroxide pretreatment, however, enhanced plant growth parameters and led to the reduced levels of lipid peroxidation and higher levels of pigment. In addition, H2O2 pretreatment increased Cr accumulation in aerial parts of seedlings. The tendency of increase in thiol content under Cr(VI) stress was further increased with H2O2 pretreatment. The activities of antioxidant enzymes such as superoxide dismutase (SOD), ascorbate peroxidase (APX), guaiacol peroxidase (POD) and catalase (CAT) were differentially altered. SOD and POD activities increased under Cr(VI) stress, whereas APX and CAT activities decreased. The SOD and CAT activities remained unaffected in both durations due to H2O2 pretreatment, but activities of APX and POD were promoted in the Cr(VI)-stressed seedlings. Metallothioneins are a family of low-molecular-weight Cys-rich proteins and are thought to play a possible role in metal metabolism or detoxification. In real-time quantitative PCR analysis, the expression level of BnMP1 mRNA was increased at 1 day after treatment (DAT), whereas it was decreased at 7 DAT in Cr(VI)-stressed seedlings. At 1 DAT, pretreatment of H2O2 before Cr(VI) stress reduced the expression of BnMP1 mRNA as compared to Cr(VI) stress alone, but this effect was not significant. At 7 DAT, H2O2 pretreatment alleviated the Cr(VI) stress-mediated decrease in the expression of BnMP1 mRNA. These results suggest that H2O2 may act as a signal that triggers defense mechanisms

  16. Experimental Calcification of the Myocardium

    PubMed Central

    Bonucci, Ermanno; Sadun, Raffaele

    1973-01-01

    Focal areas of calcification are frequent in rat myocardium 30 and 60 days after administration of dihydrotachysterol. These areas are PAS-positive, stain deeply with alcian blue and show high affinity for colloidal iron. Calcification is almost completely confined to intracellular structures. Small clusters of needle-shaped crystals are first found in apparently undamaged mitochondria in undamaged myocardial cells. When all the mitochondria are calcified, the cell degenerates, and inorganic crystals are laid down in relationship with its myofilaments. In other myocardial cells, clusters of amorphous or finely granular inorganic substance are found in both mitochondria and myofibrils. Both structures show signs of advanced degeneration. Inorganic substance has only occasionally been found within the structures of the sarcoplasmic reticulum. These structures do not seem to be involved in myocardial calcification under the present experimental conditions. Calcification of myocardial cells gives rise to a cellular reaction. Many macrophagic cells surround the calcified areas, which are rapidly reabsorbed. The present results show that myocardial mitochondria are actively engaged in controlling the intracellular concentration and movement of calcium ions. Their role in the myocardial contraction-relaxation cycle and the possible mechanism of myocardial calcification are discussed. ImagesFig 14Fig 1Fig 2Fig 3Fig 4Fig 5Fig 6Fig 7Fig 8Fig 9Fig 10Fig 11Fig 12Fig 13 PMID:4197422

  17. Modeling the dispersion in electromechanically coupled myocardium

    PubMed Central

    Eriksson, Thomas S. E.; Prassl, Anton J.; Plank, Gernot; Holzapfel, Gerhard A.

    2014-01-01

    SUMMARY We present an approach to model the dispersion of fiber and sheet orientations in the myocardium. By utilizing structure parameters, an existing orthotropic and invariant-based constitutive model developed to describe the passive behavior of the myocardium is augmented. Two dispersion parameters are fitted to experimentally observed angular dispersion data of the myocardial tissue. Computations are performed on a unit myocardium tissue cube and on a slice of the left ventricle indicating that the dispersion parameter has an effect on the myocardial deformation and stress development. The use of fiber dispersions relating to a pathological myocardium had a rather big effect. The final example represents an ellipsoidal model of the left ventricle indicating the influence of fiber and sheet dispersions upon contraction over a cardiac cycle. Although only a minor shift in the pressure–volume (PV) loops between the cases with no dispersions and with fiber and sheet dispersions for a healthy myocardium was observed, a remarkably different behavior is obtained with a fiber dispersion relating to a diseased myocardium. In future simulations, this dispersion model for myocardial tissue may advantageously be used together with models of, for example, growth and remodeling of various cardiac diseases. PMID:23868817

  18. Comparative transcriptome analyses indicate enhanced cellular protection against FMDV in PK15 cells pretreated with IFN-γ.

    PubMed

    Fu, Yin; Zhu, Zesen; Chang, Huiyun; Liu, Zaixin; Liu, Jing; Chen, Huiyong

    2016-07-25

    Interferon gamma (IFN-γ) can induce a host antiviral response to foot and mouth disease virus (FMDV) in vivo and in vitro. To elucidate the mechanism of IFN-γ anti FMDV infection in host cells, high-throughput RNA sequencing was analyzed for systemic changes in gene expression profiles in PK15 cells infected by FMDV with or without IFN-γ pretreatment. More than 25 million reads, covering 1.2-1.5 Gb, were analyzed from each experiment panel. FMDV challenge altered the transcription of genes involved in positively and negatively regulating cell death or apoptosis; however, the expected immune suppression response was not obvious. IFN-γ pretreatment combined with FMDV infection normalized the increase in apoptosis. Furthermore, the transcription factors required for IFN-γ functioning, STAT1 and IRF1 were up-regulated by IFN-γ pretreatment and stimulated downstream IFN-stimulated genes (ISGs). These induced ISGs are mainly responsible for antigen processing, antigen presentation or antiviral defense. Interestingly, a synergistic effect on some ISGs, including OAS1, OAS2, MX1, MX2, RIG-I and IFIT1, was observed in the combined treatment compared to the IFN-γ treatment alone. The suggested effects identified by RNA sequencing were consistent with cellular morphology changes and confirmed by related protein markers. This is the first report exploring transcriptome alterations introduced by FMDV infection with or without IFN-γ pretreatment. The identified key host genes that control cell survival in vitro broaden our comprehensive understanding of how IFN-γ inhibits FMDV infection and may shed light on developing improved FMD control approaches. PMID:27018244

  19. Captopril pretreatment protects the lung against severe acute pancreatitis induced injury via inhibiting angiotensin II production and suppressing Rho/ROCK pathway.

    PubMed

    Yu, Qi-Hong; Guo, Jie-Fang; Chen, Yan; Guo, Xiao-Rong; Du, Yi-Qi; Li, Zhao-Shen

    2016-09-01

    Acute pancreatitis (AP) usually causes acute lung injury, which is also known as acute pancreatitis associated lung injury (APALI). This study aimed to investigate whether captopril pretreatment was able to protect lung against APALI via inhibiting angiotensin II (Ang II) production and suppressing Rho/ROCK (Rho kinase) pathway in rats. Severe AP (SAP) was introduced to rats by bile-pancreatic duct retrograde injection of 5% sodium taurocholate. Rats were randomly divided into three groups. In the sham group, sham operation was performed; in the SAP group, SAP was introduced; in the pre-cpl + SAP group, rats were intragastrically injected with 5 mg/kg captopril 1 hour prior to SAP induction. Pathological examination of the lung and pancreas, evaluation of pulmonary vascular permeability by wet/dry ratio and Evans Blue staining, detection of serum amylase, Western blot assay for Ang II receptor type 1 (AT1), RhoA, ROCK (Rho kinase), and MLCK (myosin light chain kinase) were performed after the animals were sacrificed at 24 hours. After the surgery, characteristic findings of pancreatitis were observed, accompanied by lung injury. The serum amylase, Ang II, and lung expression of AT1, RhoA, ROCK, and MLCK increased dramatically in SAP rats. However, captopril pretreatment improved the histological changes, reduced the pathological score of the pancreas and lung, inhibited serum amylase and Ang II production, and decreased expression of AT1, RhoA, ROCK, and MLCK in the lung. These findings suggest that captopril pretreatment is able to protect the lung against APALI, which is, at least partially, related to the inhibition of Ang II production and the suppression of the Rho/ROCK pathway.

  20. Captopril pretreatment protects the lung against severe acute pancreatitis induced injury via inhibiting angiotensin II production and suppressing Rho/ROCK pathway.

    PubMed

    Yu, Qi-Hong; Guo, Jie-Fang; Chen, Yan; Guo, Xiao-Rong; Du, Yi-Qi; Li, Zhao-Shen

    2016-09-01

    Acute pancreatitis (AP) usually causes acute lung injury, which is also known as acute pancreatitis associated lung injury (APALI). This study aimed to investigate whether captopril pretreatment was able to protect lung against APALI via inhibiting angiotensin II (Ang II) production and suppressing Rho/ROCK (Rho kinase) pathway in rats. Severe AP (SAP) was introduced to rats by bile-pancreatic duct retrograde injection of 5% sodium taurocholate. Rats were randomly divided into three groups. In the sham group, sham operation was performed; in the SAP group, SAP was introduced; in the pre-cpl + SAP group, rats were intragastrically injected with 5 mg/kg captopril 1 hour prior to SAP induction. Pathological examination of the lung and pancreas, evaluation of pulmonary vascular permeability by wet/dry ratio and Evans Blue staining, detection of serum amylase, Western blot assay for Ang II receptor type 1 (AT1), RhoA, ROCK (Rho kinase), and MLCK (myosin light chain kinase) were performed after the animals were sacrificed at 24 hours. After the surgery, characteristic findings of pancreatitis were observed, accompanied by lung injury. The serum amylase, Ang II, and lung expression of AT1, RhoA, ROCK, and MLCK increased dramatically in SAP rats. However, captopril pretreatment improved the histological changes, reduced the pathological score of the pancreas and lung, inhibited serum amylase and Ang II production, and decreased expression of AT1, RhoA, ROCK, and MLCK in the lung. These findings suggest that captopril pretreatment is able to protect the lung against APALI, which is, at least partially, related to the inhibition of Ang II production and the suppression of the Rho/ROCK pathway. PMID:27638402

  1. Biomass pretreatment

    DOEpatents

    Hennessey, Susan Marie; Friend, Julie; Elander, Richard T; Tucker, III, Melvin P

    2013-05-21

    A method is provided for producing an improved pretreated biomass product for use in saccharification followed by fermentation to produce a target chemical that includes removal of saccharification and or fermentation inhibitors from the pretreated biomass product. Specifically, the pretreated biomass product derived from using the present method has fewer inhibitors of saccharification and/or fermentation without a loss in sugar content.

  2. Pre-treatment with cardamonin protects against cisplatin-induced nephrotoxicity in rats: Impact on NOX-1, inflammation and apoptosis

    SciTech Connect

    El-Naga, Reem N.

    2014-01-01

    Cisplatin is an effective anti-cancer drug; however, its clinical use is usually associated with nephrotoxicity as a dose-limiting side effect. Several molecular mechanisms have been found to be involved in this nephrotoxicity such as oxidative stress, inflammation and apoptosis. The aim of this study was to explore the potential nephroprotective effect of cardamonin, a flavone found in Alpinia plant, in a rat model of cisplatin-induced nephrotoxicity. The possible mechanisms underlying this nephroprotective effect were investigated. Cardamonin was given at two different doses; 10 and 30 mg/kg orally for two weeks, starting one week before giving a single nephrotoxic dose of cisplatin (7 mg/kg). Acute nephrtoxicity was evident by significantly increased blood urea nitrogen and serum creatinine levels. Also, cisplatin increased lipid peroxidation and depleted reduced glutathione level and superoxide dismutase. Additionally, cisplatin showed a marked pro-inflammatory response as evidenced by significant increase in tissue levels of IL-1β, TNF-α, NF-kB, iNOS, ICAM-1 and MCP-1. Pre-treatment with cardamonin significantly attenuated the nephrotoxic effects, oxidative stress and inflammation induced by cisplatin, in a dose-dependent manner. Also, cardamonin decreased caspase-3 expression and Bax/Bcl-2 ratio as compared to cisplatin group. Besides, cradamonin reversed cisplatin-induced decrease in EGF. Furthermore, up-regulation of NOX-1 was found to be involved in cisplatin-induced nephrotoxicity and its expression was significantly reduced by cardamonin. Histopathological examination further confirmed the nephroprotective effect of cardamonin. Moreover, pre-treatment with subtoxic concentration of cardamonin has significantly enhanced cisplatin cytotoxic activity in four different human cancer cell lines; hela, hepG2, PC3 and HCT116 cancer cell lines. In conclusion, these findings suggest that cardamonin improves therapeutic index of cisplatin and that NOX-1 is

  3. Lime Pretreatment

    NASA Astrophysics Data System (ADS)

    Sierra, Rocio; Granda, Cesar Benigno; Holtzapple, Mark T.

    Lime pretreatment has proven to be a useful method for selectively reducing the lignin content of lignocellulosic biomass without significant loss in carbohydrates, thus realizing an important increase in biodigestibility. In lime pretreatment, the biomass is pretreated with calcium hydroxide and water under different conditions of temperature and pressure. It can be accomplished in one of three fashions: (1) short-term pretreatment that lasts up to 6 h, requires temperatures of 100-160°C, and can be applied with or without oxygen (pressure ~200 psig); (2) long-term pretreatment taking up to 8 weeks, requiring only 55-65°C, and capable of running with or without air (atmospheric pressure); and (3) simple pretreatment requiring 1 h in boiling water, without air or oxygen. Nonoxidative conditions are effective at low lignin contents (below ~18% lignin), whereas oxidative conditions are required for high lignin contents (above ~18% lignin).

  4. Bioreducible Polymer-Transfected Skeletal Myoblasts for VEGF Delivery to Acutely Ischemic Myocardium

    PubMed Central

    McGinn, Arlo N.; Nam, Hye Yeong; Ou, Mei; Straub, Catherine M.; Hu, Norman; Yockman, James W.; Bull, David A.; Kim, Sung Wan

    2010-01-01

    Implantation of skeletal myoblasts to the heart has been investigated as a means to regenerate and protect the myocardium from damage after myocardial infarction. While several animal studies utilizing skeletal myoblasts have reported positive findings, results from clinical studies have been mixed. In this study we utilize a newly developed bioreducible polymer system to transfect skeletal myoblasts with a plasmid encoding vascular endothelial growth factor (VEGF) prior to implantation into acutely ischemic myocardium. VEGF has been demonstrated to promote revascularization of the myocardium following myocardial infarction. We report that implanting VEGF expressing skeletal myoblasts into acutely ischemic myocardium produces superior results compared to implantation of untransfected skeletal myoblasts. Skeletal myoblasts expressing secreted VEGF were able to restore cardiac function to non-diseased levels as measured by ejection fraction, to limit remodeling of the heart chamber as measured by end systolic and diastolic volumes, and to prevent myocardial wall thinning. Additionally, arteriole and capillary formation, retention of viable cardiomyocytes, and prevention of apoptosis was significantly improved by VEGF expressing skeletal myoblasts compared to untransfected myoblasts. This work demonstrates the feasibility of using bioreducible cationic polymers to create engineered skeletal myoblasts to treat acutely ischemic myocardium. PMID:20970850

  5. Pretreatment with Fucoidan from Fucus vesiculosus Protected against ConA-Induced Acute Liver Injury by Inhibiting Both Intrinsic and Extrinsic Apoptosis.

    PubMed

    Li, Jingjing; Chen, Kan; Li, Sainan; Liu, Tong; Wang, Fan; Xia, Yujing; Lu, Jie; Zhou, Yingqun; Guo, Chuanyong

    2016-01-01

    This study aimed to explore the effects of fucoidan from Fucus vesiculosus on concanavalin A (ConA)-induced acute liver injury in mice. Pretreatment with fucoidan protected liver function indicated by ALT, AST and histopathological changes by suppressing inflammatory cytokines, such as tumor necrosis factor alpha (TNF-α) and interferon gamma (IFN-γ). In addition, intrinsic and extrinsic apoptosis mediated by Bax, Bid, Bcl-2, Bcl-xL and Caspase 3, 8, and 9 were inhibited by fucoidan and the action was associated with the TRADD/TRAF2 and JAK2/STAT1 signal pathways. Our results demonstrated that fucoidan from Fucus vesiculosus alleviated ConA-induced acute liver injury via the inhibition of intrinsic and extrinsic apoptosis mediated by the TRADD/TRAF2 and JAK2/STAT1 pathways which were activated by TNF-α and IFN-γ. These findings could provide a potential powerful therapy for T cell-related hepatitis.

  6. Prolonged Cardiac Dysfunction After Intraparenchymal Hemorrhage and Neurogenic Stunned Myocardium.

    PubMed

    Krishnamoorthy, Vijay; Wilson, Thomas; Sharma, Deepak; Vavilala, Monica S

    2016-01-01

    Cardiac dysfunction occurring secondary to neurologic disease, termed neurogenic stunned myocardium, is an incompletely understood phenomenon that has been described after several distinct neurologic processes. We present a case of neurogenic stunned myocardium, discovered intraoperatively after anesthetic induction, in a patient who presented to our operating room with a recent intraparenchymal hemorrhage. We discuss the longitudinal cardiac functional course after neurogenic stunned myocardium. Finally, we discuss the pathophysiology of neurogenic stunned myocardium, as well as its implications for anesthesiologists caring for neurosurgical patients.

  7. Association of high expression in rat gastric mucosal heat shock protein 70 induced by moxibustion pretreatment with protection against stress injury

    PubMed Central

    Chang, Xiao-Rong; Peng, La; Yi, Shou-Xiang; Peng, Yan; Yan, Jie

    2007-01-01

    AIM: To study the effect of moxibustion on Zusanli or Liangmeng point on gastric mucosa injury in stress-induced ulcer rats and its correlation with the expression of heat shock protein 70 (HSP70). METHODS: Sixty healthy SD rats (30 males, 30 females) were divided into control group, injury model group, Zushanli point group, Liangmeng point group. Stress gastric ulcer model was induced by binding cold stress method. Gastric mucosa ulcer injury (UI) index was calculated by Guth method. Gastric mucosa blood flow (GMBF) was recorded with a biological signal analyzer. Protein content and gene expression in gastric mucosal HSP70 were detected by immunohistochemistry (IHC) and reverse transcription polymerase chain reaction (RT-PCR). Thiobarbital method was used to determine malondialdehyde (MDA) content. Gastric mucosal endothelin (ET) and prostaglandin E2 (PGE2) were analyzed by radioimmunoassay. RESULTS: High gastric mucosal UI index, high HSP70 expression, low GMBF and PGF2, elevated MDA and ET were observed in gastric mucosa of rats subjected to cold stress. Moxibustion on Zusanli or Liangmeng point decreased rat gastric mucosal UI index, MDA and ET. Conversely, the expression of HSP70, GMBF, and PGE2 was elevated in gastric mucosa after pretreatment with moxibustion on Zusanli or Liangmeng point. The observed parameters were significantly different between Zusanli and Liangmeng points. CONCLUSION: Pretreatment with moxibustion on Zusanli or Liangmeng point protects gastric mucosa against stress injury. This protection is associated with the higher expression of HSP70 mRNA and protein, leading to release of PGE2 and inhibition of MDA and ET, impairment of gastric mucosal index. PMID:17708611

  8. Myocardium wall thickness transducer and measuring method

    NASA Technical Reports Server (NTRS)

    Feldstein, C.; Lewis, G. W.; Silver, R. H.; Culler, V. H. (Inventor)

    1976-01-01

    A miniature transducer for measuring changes of thickness of the myocardium is described. The device is easily implantable without traumatizing the subject, without affecting the normal muscle behavior, and is removable and implantable at a different muscle location. Operating features of the device are described.

  9. Influence of the surface pre-treatment of aluminum on the processes of formation of cerium oxides protective films

    NASA Astrophysics Data System (ADS)

    Andreeva, R.; Stoyanova, E.; Tsanev, A.; Stoychev, D.

    2016-03-01

    It is known that there is special interest in the contemporary investigations on conversion treatment of aluminum aimed at promoting its corrosion stability, which is focused on electrolytes on the basis of salts of metals belonging to the group of rare-earth elements. Their application is especially attractive, as it enables a successful substitution of the presently applied highly efficient, but at the same time toxic Cr6+-containing electrolytes. The present paper presents a study on the influence of the preliminary alkaline activation and acidic de-oxidation of the aluminum surface on the processes of immersion formation of protective cerium oxides films on Al 1050. The results obtained show that their deposition from simple electrolytes (containing only salts of Ce3+ ions) on the Al surface, treated only in alkaline solution, occurs at a higher rate, which leads to preparing thicker oxide films having a better protective ability. In the cases when the formation of oxide films is realized in a complex electrolyte (containing salts of Ce3+ and Cu2+ ions), better results are obtained with respect to the morphology and protective action of cerium oxides film on samples that have been consecutively activated in alkaline solution and deoxidized in acidic solution. Electrochemical investigations were carried out in a model corrosion medium (0.1 M NaCl); it was shown that the cerium protective films, deposited by immersion, have a cathodic character with regard to the aluminum support and inhibit the occurrence of the depolarizing corrosion process -- the reaction of oxygen reduction.

  10. Simvastatin pretreatment protects cerebrum from neuronal injury by decreasing the expressions of phosphor-CaMK II and AQP4 in ischemic stroke rats.

    PubMed

    Zhu, Min-xia; Lu, Chao; Xia, Chun-mei; Qiao, Zhong-wei; Zhu, Da-nian

    2014-12-01

    Excitotoxicity and cytotoxic edema are the two major factors resulting in neuronal injury during brain ischemia and reperfusion. Ca2+/calmodulin-dependent protein kinase II (CaMK II), the downstream signal molecular of N-methyl-D-aspartate receptors (NMDARs), is a mediator in the excitotoxicity. Aquaporin 4 (AQP4), expressed mainly in the brain, is an important aquaporin to control the flux of water. In a previous study, we had reported that pretreatment of simvastatin protected the cerebrum from ischemia and reperfusion injury by decreasing neurological deficit score and infarct area (Zhu et al. PLoS One 7:e51552, 2012). The present study used a middle cerebral artery occlusion (MCAO) model to further explore the pleiotropic effect of simvastatin via CaMK II and AQP4. The results showed that simvastatin reduced degenerated cells and brain edema while decreasing the protein expressions of phosphor-CaMK II and AQP4, and increasing the ratios of Bcl-2/Bax, which was independent of cholesterol-lowering effect. Immunocomplexes formed between the subunit of NMDARs-NR3A and AQP4 were detected for the first time. It was concluded that simvastatin could protect the cerebrum from neuronal excitotoxicity and cytotoxic edema by downregulating the expressions of phosphor-CaMK II and AQP4, and that the interaction between NR3A and AQP4 might provide the base for AQP4 involving in the signaling pathways mediated by NMDARs.

  11. U0126 attenuates ischemia/reperfusion-induced apoptosis and autophagy in myocardium through MEK/ERK/EGR-1 pathway.

    PubMed

    Wang, Anxing; Zhang, Huijun; Liang, Zeming; Xu, Kai; Qiu, Weifeng; Tian, Yongbo; Guo, Hong; Jia, Junzheng; Xing, Erke; Chen, Rufei; Xiang, Zongxing; Liu, Jia

    2016-10-01

    Myocardial ischemia is one of the main causes of sudden cardiac death worldwide. Depending on the cell type and stimulus, ERK activity mediates different anti-proliferative events, such as apoptosis, autophagy, and senescence. The aim of this study was to determine the protective effect of 1,4-diamino-2,3-dicyano-1,4-bis[2-aminophenylthio] butadiene (U0126), an ERK kinase inhibitor, on myocardial ischemia/reperfusion (I/R) injury and the mechanisms involved. An I/R model was established in vivo in C57BL/6 mice and in vitro using mouse cardiomyocytes, respectively. To evaluate the protective effects of U0126 on I/R injury, we measured the myocardial infarct area, apoptosis, and autophagy. Our data indicated that pretreatment with U0126 significantly reduced the infarct area caused by I/R. Moreover, U0126 reduced the caspase-3 activity and the number of TUNEL-positive cardiomyocytes, which together indicate decreased apoptosis. Additionally, U0126 remarkable reduced the level of Beclin-1 and LC3 and increased p62 expression, which indicates that U0126 suppressed H/R-induced autophagy. Furthermore, the relationship between U0126 and MEK/ERK pathway activation in H/R-induced cardiomyocytes was also investigated. U0126 ameliorated H/R injury through inhibition of the MEK/ERK pathway and by suppressing in the downstream EGR-1 expression. Together, our research suggests that U0126 may protect against H/R injury by preventing H/R-induced myocardium apoptosis and autophagy via the MEK/ERK/EGR-1 pathway, and may be a potential therapeutic approach for attenuating myocardial I/R injury. PMID:27343376

  12. Protective effect of cholesterol-loaded cyclodextrin pretreatment against hydrogen peroxide induced oxidative damage in ram sperm.

    PubMed

    Naseer, Zahid; Ahmad, Ejaz; Aksoy, Melih; Küçük, Niyazi; Serin, İlker; Ceylan, Ahmet; Boyacıoğlu, Murat; Kum, Cavit

    2015-08-01

    Three experiments were conducted to determine the protective effect of cholesterol-loaded cyclodextrin (CLC) against hydrogen peroxide (H2O2) or cryo-induced damage in ram sperm. In Experiment 1, the fresh ejaculates were either treated with CLC or remained untreated. Both CLC treated and untreated samples were then incubated with 0, 250 or 500 μM H2O2 at 35°C for 12 h. After incubation period of 12 h, the motility, viability and membrane integrity remained higher in CLC treated sperm even in the presence of 250 or 500 μM H2O2. The H2O2 treatment affected all the sperm parameters adversely (P<0.05). However, compared to CLC untreated counterpart, the motility, viability and membrane integrity remained higher (P<0.05) in treated sperm, even in the presence of 250 or 500 μM H2O2 during 12 h of incubation. In Experiment 2, semen was cryopreserved in the presence or absence of CLC. The post-thaw results revealed that CLC treated sperm has higher (P<0.05) motility, viability and membrane integrity compared to the control. In Experiment 3, lipid peroxidation levels were assessed by determining malondialdehyde (MDA) concentrations during the H2O2-induced oxidative stress in CLC treated and untreated sperm. However, no difference (P>0.05) in MDA level was observed among the groups at any stage of incubation. In conclusion, the CLC incorporation in ram sperm membrane may protects it against H2O2 or cryo-induced oxidative damage. The cryoprotective influence of CLC on ram sperm might be resulted from, at least partly, its antioxidative property.

  13. Backscatter and attenuation characterization of ventricular myocardium

    NASA Astrophysics Data System (ADS)

    Gibson, Allyson Ann

    2009-12-01

    This Dissertation presents quantitative ultrasonic measurements of the myocardium in fetal hearts and adult human hearts with the goal of studying the physics of sound waves incident upon anisotropic and inhomogeneous materials. Ultrasound has been used as a clinical tool to assess heart structure and function for several decades. The clinical usefulness of this noninvasive approach has grown with our understanding of the physical mechanisms underlying the interaction of ultrasonic waves with the myocardium. In this Dissertation, integrated backscatter and attenuation analyses were performed on midgestational fetal hearts to assess potential differences in the left and right ventricular myocardium. The hearts were interrogated using a 50 MHz transducer that enabled finer spatial resolution than could be achieved at more typical clinical frequencies. Ultrasonic data analyses demonstrated different patterns and relative levels of backscatter and attenuation from the myocardium of the left ventricle and the right ventricle. Ultrasonic data of adult human hearts were acquired with a clinical imaging system and quantified by their magnitude and time delay of cyclic variation of myocardial backscatter. The results were analyzing using Bayes Classification and ROC analysis to quantify potential advantages of using a combination of two features of cyclic variation of myocardial backscatter over using only one or the other feature to distinguish between groups of subjects. When the subjects were classified based on hemoglobin A1c, the homeostasis model assessment of insulin resistance, and the ratio of triglyceride to high-density lipoprotein-cholesterol, differences in the magnitude and normalized time delay of cyclic variation of myocardial backscatter were observed. The cyclic variation results also suggested a trend toward a larger area under the ROC curve when information from magnitude and time delay of cyclic variation is combined using Bayes classification than when

  14. Pretreatment with transforming growth factor beta-3 protects small intestinal stem cells against radiation damage in vivo.

    PubMed Central

    Potten, C. S.; Booth, D.; Haley, J. D.

    1997-01-01

    The gastrointestinal tract, with its rapid cell replacement, is sensitive to cytotoxic damage and can be a site of dose-limiting toxicity in cancer therapy. Here, we have investigated the use of one growth modulator to manipulate the cell cycle status of gastrointestinal stem cells before cytotoxic exposure to minimize damage to this normal tissue. Transforming growth factor beta-3 (TGF-beta3), a known inhibitor of cell cycle progression through G1, was used to alter intestinal crypt stem cell sensitivity before 12-16 Gy of gamma irradiation, which was used as a model cytotoxic agent. Using a crypt microcolony assay as a measure of functional competence of gastrointestinal stem cells, it was shown that the administration of TGF-beta3 over a 24-h period before irradiation increased the number of surviving crypts by four- to six-fold. To test whether changes in crypt survival are reflected in the well-being of the animal, survival time analyses were performed. After 14.5 Gy of radiation, only 35% of the animals survived within a period of about 12 days, while prior treatment with TGF-beta3 provided significant protection against this early gastrointestinal animal death, with 95% of the treated animals surviving for greater than 30 days. PMID:9166937

  15. Enhanced self-cleaning, antibacterial and UV protection properties of nano TiO2 treated textile through enzymatic pretreatment.

    PubMed

    Montazer, Majid; Seifollahzadeh, Samira

    2011-01-01

    Textile materials can be treated with some enzymes to improve their functionality. The usual enzymatic treatment hydrolyzes the textile surfaces that leads to increase the functional groups. Here, the polyester/wool fabric as a blend of fibers fabric was selected and treated with the two different types of enzymes to increase the surface activity with a propose of higher nano-TiO(2) adsorption. The fabric was first treated with proteases and lipases to hydrolyze the wool and the polyester surfaces, respectively. It has been then dipped into an ultrasound bath containing nano TiO(2) and cross-linking agent followed by curing. The cross-linking agent, butane tetracarboxylic acid (BTCA), also assisted to enhance the nano-particles adsorption and stabilization on the fabric surface. The self-cleaning properties of the fabrics were examined through evaluating the color removal from the stained fabric with Acid Blue 113. The antibacterial properties were determined by reduction growth of a Gram-negative bacteria E. coli. and the UV protection was assessed by UV-reflectance spectrum. The SEM pictures and EDX spectrums of some samples were also reported.

  16. Pretreatment with Fucoidan from Fucus vesiculosus Protected against ConA-Induced Acute Liver Injury by Inhibiting Both Intrinsic and Extrinsic Apoptosis

    PubMed Central

    Li, Jingjing; Chen, Kan; Li, Sainan; Liu, Tong; Wang, Fan; Xia, Yujing; Lu, Jie; Zhou, Yingqun; Guo, Chuanyong

    2016-01-01

    This study aimed to explore the effects of fucoidan from Fucus vesiculosus on concanavalin A (ConA)-induced acute liver injury in mice. Pretreatment with fucoidan protected liver function indicated by ALT, AST and histopathological changes by suppressing inflammatory cytokines, such as tumor necrosis factor alpha (TNF-α) and interferon gamma (IFN-γ). In addition, intrinsic and extrinsic apoptosis mediated by Bax, Bid, Bcl-2, Bcl-xL and Caspase 3, 8, and 9 were inhibited by fucoidan and the action was associated with the TRADD/TRAF2 and JAK2/STAT1 signal pathways. Our results demonstrated that fucoidan from Fucus vesiculosus alleviated ConA-induced acute liver injury via the inhibition of intrinsic and extrinsic apoptosis mediated by the TRADD/TRAF2 and JAK2/STAT1 pathways which were activated by TNF-α and IFN-γ. These findings could provide a potential powerful therapy for T cell-related hepatitis. PMID:27035150

  17. Pretreatment with antibody to eosinophil major basic protein prevents hyperresponsiveness by protecting neuronal M2 muscarinic receptors in antigen-challenged guinea pigs.

    PubMed Central

    Evans, C M; Fryer, A D; Jacoby, D B; Gleich, G J; Costello, R W

    1997-01-01

    In antigen-challenged guinea pigs there is recruitment of eosinophils into the lungs and to airway nerves, decreased function of inhibitory M2 muscarinic autoreceptors on parasympathetic nerves in the lungs, and airway hyperresponsiveness. A rabbit antibody to guinea pig eosinophil major basic protein was used to determine whether M2 muscarinic receptor dysfunction, and the subsequent hyperresponsiveness, are due to antagonism of the M2 receptor by eosinophil major basic protein. Guinea pigs were sensitized, challenged with ovalbumin and hyperresponsiveness, and M2 receptor function tested 24 h later with the muscarinic agonist pilocarpine. Antigen-challenged guinea pigs were hyperresponsive to electrical stimulation of the vagus nerves compared with controls. Likewise, loss of M2 receptor function was demonstrated since the agonist pilocarpine inhibited vagally-induced bronchoconstriction in control but not challenged animals. Pretreatment with rabbit antibody to guinea pig eosinophil major basic protein prevented hyperresponsiveness, and protected M2 receptor function in the antigen-challenged animals without inhibiting eosinophil accumulation in the lungs or around the nerves. Thus, hyperresponsiveness is a result of inhibition of neuronal M2 muscarinic receptor function by eosinophil major basic protein in antigen-challenged guinea pigs. PMID:9410903

  18. Lignocellulosic biomass pretreatment using AFEX.

    PubMed

    Balan, Venkatesh; Bals, Bryan; Chundawat, Shishir P S; Marshall, Derek; Dale, Bruce E

    2009-01-01

    Although cellulose is the most abundant organic molecule, its susceptibility to hydrolysis is restricted due to the rigid lignin and hemicellulose protection surrounding the cellulose micro fibrils. Therefore, an effective pretreatment is necessary to liberate the cellulose from the lignin-hemicellulose seal and also reduce cellulosic crystallinity. Some of the available pretreatment techniques include acid hydrolysis, steam explosion, ammonia fiber expansion (AFEX), alkaline wet oxidation, and hot water pretreatment. Besides reducing lignocellulosic recalcitrance, an ideal pretreatment must also minimize formation of degradation products that inhibit subsequent hydrolysis and fermentation. AFEX is an important pretreatment technology that utilizes both physical (high temperature and pressure) and chemical (ammonia) processes to achieve effective pretreatment. Besides increasing the surface accessibility for hydrolysis, AFEX promotes cellulose decrystallization and partial hemicellulose depolymerization and reduces the lignin recalcitrance in the treated biomass. Theoretical glucose yield upon optimal enzymatic hydrolysis on AFEX-treated corn stover is approximately 98%. Furthermore, AFEX offers several unique advantages over other pretreatments, which include near complete recovery of the pretreatment chemical (ammonia), nutrient addition for microbial growth through the remaining ammonia on pretreated biomass, and not requiring a washing step during the process which facilitates high solid loading hydrolysis. This chapter provides a detailed practical procedure to perform AFEX, design the reactor, determine the mass balances, and conduct the process safely.

  19. Thallium-201 kinetics in nonischemic canine myocardium

    SciTech Connect

    Okada, R.D.; Jacobs, M.L.; Daggett, W.M.

    1982-01-01

    Myocardial thallium-201 (/sup 201/Tl) kinetics have not been precisely defined because reliable techniques to determine continuous activity in vivo have not been available. In this study, an implantable miniature cadmium telluride radiation detection device was inserted through the left ventricular apex, positioned against the endocardium, and used for continuous on-line monitoring of myocardial /sup 201/Tl activity for 260-810 minutes in 18 dogs. Blood was serially sampled and counted. Microsphere-determined myocardial blood flow was measured before administration of /sup 201/Tl and was not significantly different from that measured at the end of the experiment in 11 of 18 dogs. Thallium was administered intravenously. Myocardial and blood activity curves were analyzed using a nonlinear least-squares estimation of the decay constant lambda (min/sup -1/). The mean final blood lambda/sub 3/ was almost identical to the mean myocardial lambda. The data suggest that /sup 201/Tl washout after peak activity is reached in nonischemic myocardium is mono-exponential. The rate of /sup 201/Tl clearance from the myocardium is related to the rate of /sup 201/Tl clearance from the blood after i.v. administration of the tracer.

  20. Substrate use in ischemic and reperfused canine myocardium: quantitative considerations

    SciTech Connect

    Myears, D.W.; Sobel, B.E.; Bergmann, S.R.

    1987-07-01

    The patterns of use of substrate in reperfused myocardium are not yet well elucidated, and their delineation is essential for adequate interpretation of results of analyses performed after positron emission tomography with labeled substrates to differentiate normal from abnormal heart muscle. Accordingly, in open-chest, anesthetized dogs the authors measured glucose and fatty acid utilization in normal, ischemic, and reperfused myocardium and assessed the contributions of metabolism of each substrate to overall oxidative metabolism. Intracoronary (/sup 3/H)glucose and (/sup 14/C)palmitate were administered in five control dogs, eight dogs subjected to 1 h of coronary occlusion, and nine dogs subjected to reperfusion after 1 h of ischemia. Regional coronary venous blood samples were assayed sequentially. In reperfused myocardium, utilization of glucose was 103% greater than that in ischemic and 273% greater than in normal myocardium. Utilization of fatty acid during reperfusion, although greater than that in ischemic myocardium, was significantly less than that in normal myocardium despite restoration of flow to 80% of control values. Despite diminished net uptake of fatty acid, oxidation of fatty acid accounted for 63% of total oxygen consumption in reperfused myocardium. These studies indicate that canine myocardium reperfused after 1 h of ischemia exhibits enhanced uptake of glucose and impaired utilization of palmitate. Nevertheless, palmitate continues to comprise the substrate primarily utilized for oxidative metabolism.

  1. Inhibition of anti-apoptotic signals by Wortmannin induces apoptosis in the remote myocardium after LAD ligation: evidence for a protein kinase C-δ-dependent pathway.

    PubMed

    Wiedemann, Stephan; Wessela, Teresa; Schwarz, Kerstin; Joachim, Dirk; Jercke, Marcel; Strasser, Ruth H; Ebner, Bernd; Simonis, Gregor

    2013-01-01

    It has been shown that, in the remote myocardium after infarction (MI), protein kinase C (PKC) inhibition reduces apoptosis both by blocking proapoptotic pathways and by activating antiapoptotic signals including the Akt pathway. However, it was open if vice versa, blockade of antiapoptotic pathways may influence proapoptotic signals. To clarify this, the present study tested the effects of the PI3-kinase blocker Wortmannin on proapoptotic signals and on apoptosis execution in the remote myocardium after infarction. Rats were subjected to MI by LAD ligation in situ. Some were pre-treated with Wortmannin alone or in combination with the PKC inhibitor Chelerythrine. After 24 h, pro- and anti-apoptotic signals (caspase-3, PKC isoforms, p38-MAPK, p42/44-MAPK, Akt, Bad), and marker of apoptosis execution (TUNEL) were quantified in the myocardium remote from the infarction. Wortmannin treatment increased apoptosis in the remote myocardium both at baseline and after MI, together with an activation of the PKC-δ/p38-MAPK-pathway. PKC-ε and p42/44-MAPK were unaffected. Combined treatment with Wortmannin and Chelerythrine fully reversed the pro-apoptotic effects of Wortmannin both at baseline and after MI. The PKC-δ-p38-MAPK-pathway as a strong signal for apoptosis in the non-infarcted myocardium can be influenced by targeting the anti-apoptotic PI3-kinase pathway. This gives evidence of a bi-directional crosstalk of pro- and anti-apoptotic signals after infarction.

  2. Metastatic Midgut Carcinoid in the Myocardium.

    PubMed

    Bukowczan, Jakub; Lois, Konstantinos B; Skinner, Jane; Petrides, George; James, Robert Andrew; Perros, Petros

    2015-09-01

    Metastasis of neuroendocrine tumor to the myocardium is rare. We present a case of 64-year-old woman, who presented initially with abdominal pain and large adnexal mass. The image-guided biopsy showed low-grade neuroendocrine tumor with Ki67 less than 2% within the ovarian tissue. CT staging revealed bilateral adnexal masses, liver metastases, and primary lesion in the terminal ileum. Octreoscan showed marked tracer uptake within the lower esophagus not related to obvious mass on CT scan; the echocardiography confirmed the presence of a 2.7 cm LV/LA mass. In this case, close correlation between ECHO and the octreoscan obviated need for myocardial biopsy. PMID:26164175

  3. Non-excitatory electrical stimulation attenuates myocardial infarction via homeostasis of calcitonin gene-related peptide in myocardium.

    PubMed

    Guo, Zhi-Jia; Guo, Zheng

    2015-03-01

    Electrical stimulation has been shown protection of brain, retina, optic nerves and pancreatic β-cells but the effect on cardio-protection is still unknown. Calcitonin gene-related peptide (CGRP) participates in the pathology of injury and protection of myocardium but whether or not electrical stimulation modulates endogenous CGRP is not clear. Male Sprague-Dawley rats were divided into 4 groups: (1) control group, without any treatment. (2) I/R group, animals were subjected to 30 min of myocardial ischemia followed by 60 min reperfusion. (3) NES+I/R group, non-excitatory electrical stimulation (NES) was commenced from 15 min before coronary artery occlusion till the end of reperfusion. (4) I/R+CGRP8-37 group, animals were given with CGRP8-37 (an antagonist of CGRP receptor, 10(-7) mol/L, 0.3 ml, i.v.) at 5 min before reperfusion without any electrical stimulation. The hemodynamics and electrocardiogram were monitored and recorded. Infarct size and troponin I were examined and CGRP expression in the myocardium and serum was analyzed. It was found that the infarct size and TnI were significantly reduced in NES+I/R group, by 45% and 58% respectively, accompanied by an obvious fall back of CGRP in myocardium, compared to I/R group (all p<0.05). Treatment with CGRP8-37 resulted in the same protection on myocardium as NES did. No significant difference in hemodynamics or ventricular tachycardia was detected among the groups (all p>0.05). It can be concluded that NES reduced the infarction size after acute myocardial ischemia and reperfusion, for which the underlying mechanism may be associated with modulation of endogenous CGRP in myocardium.

  4. OCT imaging of myocardium extending to pulmonary vein

    NASA Astrophysics Data System (ADS)

    Li, Zhifang; Dickfeld, Timm; Tang, Qinggong; Wang, Bohan; Chen, Yu

    2016-02-01

    In this study, we propose to use optical coherence tomography to enable a direct visualization of myocardium extending into the pulmonary vein (PV). The results showed that there are obvious differences in the morphology of myocardium and fibrous tissue in the transition region of myocardial sleeve, which is in agreement with the histological analysis. In addition, the myocardial area in transition point has three layers in the depth of 1 mm, and the depth-resolved myocardial fiber show different orientation in the different layers. This characteristic was applied for segmentation of the structures of myocardium extending into PV.

  5. Heat shock proteins, end effectors of myocardium ischemic preconditioning?

    PubMed Central

    Guisasola, María Concepcion; Desco, Maria del Mar; Gonzalez, Fernanda Silvana; Asensio, Fernando; Dulin, Elena; Suarez, Antonio; Garcia Barreno, Pedro

    2006-01-01

    The purpose of this study was to investigate (1) whether ischemia-reperfusion increased the content of heat shock protein 72 (Hsp72) transcripts and (2) whether myocardial content of Hsp72 is increased by ischemic preconditioning so that they can be considered as end effectors of preconditioning. Twelve male minipigs (8 protocol, 4 sham) were used, with the following ischemic preconditioning protocol: 3 ischemia and reperfusion 5-minute alternative cycles and last reperfusion cycle of 3 hours. Initial and final transmural biopsies (both in healthy and ischemic areas) were taken in all animals. Heat shock protein 72 messenger ribonucleic acid (mRNA) expression was measured by a semiquantitative reverse transcriptase-polymerase chain reaction (RT-PCR) method using complementary DNA normalized against the housekeeping gene cyclophilin. The identification of heat shock protein 72 was performed by immunoblot. In our “classic” preconditioning model, we found no changes in mRNA hsp72 levels or heat shock protein 72 content in the myocardium after 3 hours of reperfusion. Our experimental model is valid and the experimental techniques are appropriate, but the induction of heat shock proteins 72 as end effectors of cardioprotection in ischemic preconditioning does not occur in the first hours after ischemia, but probably at least 24 hours after it, in the so-called “second protection window.” PMID:17009598

  6. 40 CFR 405.76 - Pretreatment standards for new sources.

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... comply with 40 CFR part 403. ... 40 Protection of Environment 28 2010-07-01 2010-07-01 true Pretreatment standards for new sources. 405.76 Section 405.76 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED)...

  7. Spiral waves in a model of myocardium

    NASA Astrophysics Data System (ADS)

    Tyson, John J.; Keener, James P.

    1987-11-01

    Myocardial tissue is an excitable medium through which propagate waves of electrical stimulation and muscular contraction. In addition to radially expanding waves of neuromuscular activity characterizing the normal heartbeat, myocardial tissue may also support high frequency, rotating spiral waves of activity which are associated with cardiac pathologies (flutter and fibrillation). Recently Pertsov, Ermakova and Panfilov have presented a numerical study of rotating spiral waves in a two-dimensional excitable medium modeled on the FitzHugh-Nagumo equations, suitably modified to reflect the electrical properties of myocardium. We show that some of their principal numerical results can be reproduced in quantitative detail by a general theory of rotating spiral waves in excitable media. The critical ingredients of our theory are the dispersion of nonlinear plane waves and the effects of curvature on the propagation of wave fronts in two-dimensional media. The close comparison of our analytical results with numerical simulations of the full reaction-diffusion equations lends credence to our theoretical description of spiral waves in excitable media.

  8. Shock-induced arrhythmogenesis in the myocardium

    NASA Astrophysics Data System (ADS)

    Trayanova, Natalia; Eason, James

    2002-09-01

    The focus of this article is the investigation of the electrical behavior of the normal myocardium following the delivery of high-strength defibrillation shocks. To achieve its goal, the study employs a complex three-dimensional defibrillation model of a slice of the canine heart characterized with realistic geometry and fiber architecture. Defibrillation shocks of various strengths and electrode configurations are delivered to the model preparation in which a sustained ventricular tachycardia is induced. Instead of analyzing the post-shock electrical events as progressions of transmembrane potential maps, the study examines the evolution of the postshock phase singularities (PSs) which represent the organizing centers of reentry. The simulation results demonstrate that the shock induces numerous PSs the majority of which vanish before the reentrant wavefronts associated with them complete half of a single rotation. Failed shocks are characterized with one or more PSs that survive the initial period of PS annihilation to establish a new postshock arrhythmia. The increase in shock strength results in an overall decrease of the number of PSs that survive over 200 ms after the end of the shock; however, the exact behavior of the PSs is strongly dependent on the shock electrode configuration.

  9. Murine myocardium OCT imaging with a blood substitute

    NASA Astrophysics Data System (ADS)

    Kim, Jeehyun; Villard, Joseph W.; Lee, Ho; Feldman, Marc D.; Milner, Thomas E.

    2002-06-01

    Imaging of the in vivo murine myocardium using optical coherence tomography (OCT) is described. Application of conventional techniques (e.g. MRI, Ultrasound imaging) for imaging the murine myocardium is problematic because the wall thickness is less than 1.5mm (20g mouse), and the heart rate can be as high as six-hundred beats per minute. To acquire a real-time image of the murine myocardium, OCT can provide sufficient spatial resolution (10 micrometers ) and imaging speed (1000 A-Scans/s). Strong light scattering by blood in the heart causes significant light attenuation making delineation of the endocardium-chamber boundary problematic. By replacing whole blood in the mouse with an artificial blood substitute we demonstrate significant reduction of light scattering in the murine myocardium. The results indicate a significant reduction in light scattering as whole blood hematocrit is diminished below 5%. To measure thickness change of the myocardium during one cycle, a myocardium edge detection algorithm is developed and demonstrated.

  10. 40 CFR 403.2 - Objectives of general pretreatment regulations.

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... 40 Protection of Environment 28 2010-07-01 2010-07-01 true Objectives of general pretreatment regulations. 403.2 Section 403.2 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS GENERAL PRE-TREAT-MENT REGULATIONS FOR EXIST-ING AND NEW SOURCES...

  11. 40 CFR 403.2 - Objectives of general pretreatment regulations.

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... 40 Protection of Environment 29 2011-07-01 2009-07-01 true Objectives of general pretreatment regulations. 403.2 Section 403.2 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS GENERAL PRE-TREAT-MENT REGULATIONS FOR EXIST-ING AND NEW SOURCES...

  12. 40 CFR 405.64 - Pretreatment standards for existing sources.

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... comply with 40 CFR part 403. In addition, the following pretreatment standard establishes the quantity or... 40 Protection of Environment 29 2011-07-01 2009-07-01 true Pretreatment standards for existing sources. 405.64 Section 405.64 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY...

  13. Fatty acid uptake in normal human myocardium

    SciTech Connect

    Vyska, K.; Meyer, W.; Stremmel, W.; Notohamiprodjo, G.; Minami, K.; Machulla, H.J.; Gleichmann, U.; Meyer, H.; Koerfer, R. )

    1991-09-01

    Fatty acid binding protein has been found in rat aortic endothelial cell membrane. It has been identified to be a 40-kDa protein that corresponds to a 40-kDa fatty acid binding protein with high affinity for a variety of long chain fatty acids isolated from rat heart myocytes. It is proposed that this endothelial membrane fatty acid binding protein might mediate the myocardial uptake of fatty acids. For evaluation of this hypothesis in vivo, influx kinetics of tracer-labeled fatty acids was examined in 15 normal subjects by scintigraphic techniques. Variation of the plasma fatty acid concentration and plasma perfusion rate has been achieved by modulation of nutrition state and exercise conditions. The clinical results suggest that the myocardial fatty acid influx rate is saturable by increasing fatty acid plasma concentration as well as by increasing plasma flow. For analysis of these data, functional relations describing fatty acid transport from plasma into myocardial tissue in the presence and absence of an unstirred layer were developed. The fitting of these relations to experimental data indicate that the free fatty acid influx into myocardial tissue reveals the criteria of a reaction on a capillary surface in the vicinity of flowing plasma but not of a reaction in extravascular space or in an unstirred layer and that the fatty acid influx into normal myocardium is a saturable process that is characterized by the quantity corresponding to the Michaelis-Menten constant, Km, and the maximal velocity, Vmax, 0.24 {plus minus} 0.024 mumol/g and 0.37 {plus minus} 0.013 mumol/g(g.min), respectively. These data are compatible with a nondiffusional uptake process mediated by the initial interaction of fatty acids with the 40-kDa membrane fatty acid binding protein of cardiac endothelial cells.

  14. 40 CFR 421.65 - Pretreatment standards for existing sources.

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... Subcategory § 421.65 Pretreatment standards for existing sources. Except as provided in 40 CFR 403.7 and 403... treatment works must comply with 40 CFR part 403 and achieve the following pretreatment standards for... 40 Protection of Environment 28 2010-07-01 2010-07-01 true Pretreatment standards for...

  15. Hibernating myocardium results in partial sympathetic denervation and nerve sprouting.

    PubMed

    Fernandez, Stanley F; Ovchinnikov, Vladislav; Canty, John M; Fallavollita, James A

    2013-01-15

    Hibernating myocardium due to chronic repetitive ischemia is associated with regional sympathetic nerve dysfunction and spontaneous arrhythmic death in the absence of infarction. Although inhomogeneity in regional sympathetic innervation is an acknowledged substrate for sudden death, the mechanism(s) responsible for these abnormalities in viable, dysfunctional myocardium (i.e., neural stunning vs. sympathetic denervation) and their association with nerve sprouting are unknown. Accordingly, markers of sympathetic nerve function and nerve sprouting were assessed in subendocardial tissue collected from chronically instrumented pigs with hibernating myocardium (n = 18) as well as sham-instrumented controls (n = 7). Hibernating myocardium exhibited evidence of partial sympathetic denervation compared with the normally perfused region and sham controls, with corresponding regional reductions in tyrosine hydroxylase protein (-32%, P < 0.001), norepinephrine uptake transport protein (-25%, P = 0.01), and tissue norepinephrine content (-45%, P < 0.001). Partial denervation induced nerve sprouting with regional increases in nerve growth factor precursor protein (31%, P = 0.01) and growth associated protein-43 (38%, P < 0.05). All of the changes in sympathetic nerve markers were similar in animals that developed sudden death (n = 9) compared with electively terminated pigs with hibernating myocardium (n = 9). In conclusion, sympathetic nerve dysfunction in hibernating myocardium is most consistent with partial sympathetic denervation and is associated with regional nerve sprouting. The extent of sympathetic remodeling is similar in animals that develop sudden death compared with survivors; this suggests that sympathetic remodeling in hibernating myocardium is not an independent trigger for sudden death. Nevertheless, sympathetic remodeling likely contributes to electrical instability in combination with other factors.

  16. Long-term preservation of ischemic myocardium in the dog by hyaluronidase.

    PubMed

    Kloner, R A; Braunwald, E; Maroko, P R

    1978-08-01

    The administration of hyaluronidase is a promising intervention to protect the ischemic myocardium in man, but evidence of the extent to which it may reduce the ultimate size of an infarct is not well-defined. Hence, open chest, anesthetized dogs were randomized into 10 control dogs which received saline and eight treated dogs which received three doses of hyaluronidase (500 NF units/kg I.V.) at 15 minutes, 2 hours and 24 hours after occlusion of the left anterior descending coronary artery (CAO). Regional myocardial blood flow (RMBF) assessed by the microsphere technique was measured 12 minutes after CAO. The chest was then closed and the dogs were allowed to recover. Twenty-one days after CAO, the hearts were excised, divided into 1 cm thick slices and incubated in triphenyl tetrazolium chloride. Infarct size was then determined by planimetry. The left ventricular myocardium was divided into multiple samples for RMBF analysis. In control dogs 23.2 +/- 2% of the left ventricle was infarcted, compared to only 9 +/- 2.8% (P less than 0.001) in hyaluronidase-treated dogs. RMBF in noninfarcted myocardium directly adjacent to the infarct was similar to that in the normal zone remote from the infarct in the control dogs; however, in the hyaluronidase-treated dogs, blood flow in the myocardium adjacent to the infarct was significantly reduced to 68% of normal (P less than 0.01) in the outer myocardial wall and to 86% of normal (P less than 0.02) in the inner myocardial wall, which indicates that this tissue, at least in some part, was in jeopardy, but was salvaged by hyaluronidase. Epicardial electrocardiographic data showed that three weeks after CAO, Q waves were less frequent and smaller in hyaluronidase compared to untreated dogs. Preservation of the frequency and magnitude of R waves was greater in the hyaluronidase-treated group at three weeks. We conclude that hyaluronidase resulted in long-term preservation of the ischemic myocardium.

  17. Long-term pretreatment with desethylamiodarone (DEA) or amiodarone (AMIO) protects against coronary artery occlusion induced ventricular arrhythmias in conscious rats.

    PubMed

    Morvay, Nikolett; Baczkó, István; Sztojkov-Ivanov, Anita; Falkay, György; Papp, Julius Gy; Varró, András; Leprán, István

    2015-09-01

    The aim of this investigation was to compare the effectiveness of long-term pretreatment with amiodarone (AMIO) and its active metabolite desethylamiodarone (DEA) on arrhythmias induced by acute myocardial infarction in rats. Acute myocardial infarction was induced in conscious, male, Sprague-Dawley rats by pulling a previously inserted loose silk loop around the left main coronary artery. Long-term oral pretreatment with AMIO (30 or 100 mg·(kg body mass)(-1)·day(-1), loading dose 100 or 300 mg·kg(-1) for 3 days) or DEA (15 or 50 mg·kg(-1)·day(-1), loading dose 100 or 300 mg·kg(-1) for 3 days), was applied for 1 month before the coronary artery occlusion. Chronic oral treatment with DEA (50 mg·kg(-1)·day(-1)) resulted in a similar myocardial DEA concentration as chronic AMIO treatment (100 mg·kg(-1)·day(-1)) in rats (7.4 ± 0.7 μg·g(-1) and 8.9 ± 2.2 μg·g(-1)). Both pretreatments in the larger doses significantly improved the survival rate during the acute phase of experimental myocardial infarction (82% and 64% by AMIO and DEA, respectively, vs. 31% in controls). Our results demonstrate that chronic oral treatment with DEA resulted in similar cardiac tissue levels to that of chronic AMIO treatment, and offered an equivalent degree of antiarrhythmic effect against acute coronary artery ligation induced ventricular arrhythmias in conscious rats.

  18. Pretreatment Technology Plan

    SciTech Connect

    Barker, S.A.; Thornhill, C.K.; Holton, L.K. Jr.

    1993-03-01

    This technology plan presents a strategy for the identification, evaluation, and development of technologies for the pretreatment of radioactive wastes stored in underground storage tanks at the Hanford Site. This strategy includes deployment of facilities and process development schedules to support the other program elements. This document also presents schedule information for alternative pretreatment systems: (1) the reference pretreatment technology development system, (2) an enhanced pretreatment technology development system, and (3) alternative pretreatment technology development systems.

  19. Protective effect of Guaraná (Paullinia cupana var. sorbilis) pre-treatment on cadmium-induced damages in adult Wistar testis.

    PubMed

    Leite, Rodrigo Paula; Wada, Ronaldo Seichi; Monteiro, Juliana Castro; Predes, Fabrícia Souza; Dolder, Heidi

    2011-06-01

    Guaraná (Paullinia cupana) is an Amazonian plant. Its antioxidant potential was demonstrated to be due to the high polyphenol concentration. On the other hand, one of the mechanisms underlying cadmium-induced cellular damage is free radical mediated, resulting in increased oxidative processes. This study investigated P. cupana's potential to attenuate cadmium-induced damages in Wistar rat testis. Adult male Wistar rats were either pre-treated with 2 mg/g body weight (BW) of powdered P. cupana seed during 56 days and/or injected with cadmium chloride at a dose of 1.15 mg/kg BW. After cadmium exposition (48 h), testes samples were evaluated by histological and stereological analyses. Both groups exposed to cadmium presented evident morphological alterations relative to control animals. A few rodents showed massive cell death in the seminiferous epithelium and intertubular space, indicating that some animals are more sensitive to cadmium. Despite the alterations observed in both groups, pre-treatment with P. cupana was effective in attenuating morphological changes in Leydig cells, as well as reducing inflammatory response, relative to animals exclusively exposed to the metal. Animals treated only with P. cupana presented a significant increase in plasma testosterone levels and a significant increase in volumetric proportions of seminiferous tubules, which are indicative of spermatogenic stimulation.

  20. Noncompaction myocardium in association with type Ib glycogen storage disease.

    PubMed

    Goeppert, Benjamin; Lindner, Martin; Vogel, Monika Nadja; Warth, Arne; Stenzinger, Albrecht; Renner, Marcus; Schnabel, Philipp; Schirmacher, Peter; Autschbach, Frank; Weichert, Wilko

    2012-10-15

    Noncompaction myocardium is a rare disorder assumed to occur as an arrest of the compaction process during the normal development of the heart. Left ventricular noncompaction has been reported to be associated with a variety of cardiac and extracardiac, especially neuromuscular abnormalities. Moreover, it has been suggested that metabolic alterations could be responsible for the noncompaction. However, no association of noncompaction myocardium with type Ib glycogen storage disease (GSD) has been reported so far. Type Ib GSD is due to a defect of a transmembrane protein which results, similar to type Ia GSD, in hypoglycemia, a markedly enlarged liver and, additionally, in neutropenia, recurrent infections, and inflammatory bowel disease. Until now, no muscular or cardiac involvement has been described in type Ib GSD patients. The present case represents the first report of a noncompaction myocardium in a child with type Ib GSD who died of sudden clinical deterioration at the age of four.

  1. System of scale-selective tomography of myocardium birefringence

    NASA Astrophysics Data System (ADS)

    Ushenko, O. G.; Boichuk, T. M.; Bachinskiy, V. T.; Vanchuliak, O. Ya.; Minzer, O. P.; Ushenko, Yu. O.; Dubolazov, O. V.; Savich, V. O.

    2015-09-01

    This research presents the results of investigation of laser polarization fluorescence of biological layers (histological sections of the myocardium). The polarized structure of autofluorescence imaging layers of biological tissues was detected and investigated. Proposed the model of describing the formation of polarization inhomogeneous of autofluorescence imaging biological optically anisotropic layers. On this basis, analytically and experimentally tested to justify the method of laser polarimetry autofluorescent. Analyzed the effectiveness of this method in the postmortem diagnosis of infarction. The objective criteria (statistical moments) of differentiation of autofluorescent images of histological sections myocardium were defined. The operational characteristics (sensitivity, specificity, accuracy) of these technique were determined.

  2. [Effect of biologically active food supplement coenzyme Q10 on metabolic processes in the myocardium of rats kept in different temperature conditions].

    PubMed

    Mikashinovich, Z I; Novoderzhkina, Iu G; Belousova, E S

    2007-01-01

    In present research the action of coenzyme Q10 on energetic metabolism and antioxidant system at different temperature conditions has been studied. It was established that the addition of coenzyme Q10 caused inadequate stimulation of main metabolic systems that could lead to running out of functional reserves of cardiomyocytes. The use of coenzyme Q10 helped to optimize intracellular compensating mechanisms supplying the defense of myocardium. Introduction in a diet coenzyme Q10 in conditions of a temperature's comfort threshold excess and development of a histic hypoxia can promote the decrease of gravity of hypoxic myocardium's lesions and to glycogenolysis' amplification that promotes maintenance of an energy homeostasis of a myocardium in posthypoxia term. It is possible to assume, that the augmentation of duration of reception coenzyme Q10 or its dosages can render more expressed protective effect.

  3. Early Recovery of Regional Performance in Salvaged Ischemic Myocardium following Coronary Artery Occlusion in the Dog

    PubMed Central

    Darsee, John R.; Kloner, Robert A.; Braunwald, Eugene

    1981-01-01

    Although numerous agents have been shown experimentally to protect ischemic myocardium, a critical unanswered question is whether function is preserved in the salvaged tissue. Accordingly, 38 openchest dogs had measurements of percent segment length shortening (%SS) and velocity of segment length shortening either in midmyocardial or subepicardial and subendocardial ischemic segments before and after 60 min of left anterior descending coronary artery occlusion during 5 h of reperfusion; 10 additional dogs were subjected to 3 h of coronary occlusion followed by 72 h of reperfusion. 15 min after coronary artery occlusion, radiolabeled microspheres were injected into the left atrium for measurement of regional myocardial blood flow, and dogs were treated with 1 mg/kg i.v. (n = 23) of an anti-inflammatory drug, flurbiprofen or an equal volume of saline (n = 25). The ischemic myocardium-at-risk for necrosis was determined by injecting methylene blue dye into the left atrium with the coronary artery reoccluded at the end of the reperfusion period, slicing the left ventricle into thin transverse sections, and measuring the areas of each slice that were not perfused (pink unstained tissue) by methylene blue. The quantity of necrotic tissue in each transverse section was measured by planimetry after incubation of the slices in triphenyltetrazolium chloride, and by direct histological examination in dogs with 72 h of reperfusion. Regional myocardial blood flow of the ischemic segments between the ultrasonic dimension crystals was similar in treated (0.34±0.03 ml/min per g) and control dogs (0.35±0.03 ml/min per g). In saline-treated control dogs subjected to a l-h coronary occlusion, 17.9±1.8% of the myocardium-at-risk became necrotic but in flurbiprofen-treated dogs none of the tissue became necrotic. In saline-treated dogs passive lengthening of the previously ischemic segments persisted through 5 h of reperfusion in all three regions of myocardium after a 1-h coronary

  4. 40 CFR 408.326 - Pretreatment standards for new sources.

    Code of Federal Regulations, 2014 CFR

    2014-07-01

    ... comply with 40 CFR part 403. In addition, the following pretreatment standard establishes the quantity or.... 408.326 Section 408.326 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT... Fillet Processing Subcategory § 408.326 Pretreatment standards for new sources. Any new source subject...

  5. 40 CFR 408.326 - Pretreatment standards for new sources.

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ... comply with 40 CFR part 403. In addition, the following pretreatment standard establishes the quantity or.... 408.326 Section 408.326 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT... Fillet Processing Subcategory § 408.326 Pretreatment standards for new sources. Any new source subject...

  6. 40 CFR 408.326 - Pretreatment standards for new sources.

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... comply with 40 CFR part 403. In addition, the following pretreatment standard establishes the quantity or.... 408.326 Section 408.326 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT... Fillet Processing Subcategory § 408.326 Pretreatment standards for new sources. Any new source subject...

  7. 40 CFR 408.326 - Pretreatment standards for new sources.

    Code of Federal Regulations, 2012 CFR

    2012-07-01

    ... comply with 40 CFR part 403. In addition, the following pretreatment standard establishes the quantity or.... 408.326 Section 408.326 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT... Fillet Processing Subcategory § 408.326 Pretreatment standards for new sources. Any new source subject...

  8. 40 CFR 408.326 - Pretreatment standards for new sources.

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... comply with 40 CFR part 403. In addition, the following pretreatment standard establishes the quantity or.... 408.326 Section 408.326 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT... Fillet Processing Subcategory § 408.326 Pretreatment standards for new sources. Any new source subject...

  9. 40 CFR 443.36 - Pretreatment standard for new sources.

    Code of Federal Regulations, 2014 CFR

    2014-07-01

    .... 443.36 Section 443.36 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT...) POINT SOURCE CATEGORY Asphalt Roofing Subcategory § 443.36 Pretreatment standard for new sources. Any... treatment works must comply with 40 CFR part 403. In addition, the following pretreatment...

  10. Recombinant Human Erythropoietin Protects Myocardial Cells from Apoptosis via the Janus-Activated Kinase 2/Signal Transducer and Activator of Transcription 5 Pathway in Rats with Epilepsy

    PubMed Central

    Ma, Bao-Xin; Li, Jie; Li, Hua; Wu, Sui-Sheng

    2015-01-01

    Objective To investigate the potential mechanisms underlying the protective effects of recombinant human erythropoietin (rhEPO) and carbamylated EPO (CEPO) against myocardial cell apoptosis in epilepsy. Methods Rats were given an intra-amygdala injection of kainic acid to induce epilepsy. Groups of rats were treated with rhEPO or CEPO before induction of epilepsy, whereas additional rats were given a caudal vein injection of AG490, a selective inhibitor of Janus kinase 2 (JAK2). At different time points after seizure onset, electroencephalogram changes were recorded, and myocardium samples were taken for the detection of myocardial cell apoptosis and expression of JAK2, signal transducer and activator of transcription 5 (STAT5), caspase-3, and bcl-xl mRNAs and proteins. Results Induction of epilepsy significantly enhanced myocardial cell apoptosis and upregulated the expression of caspase-3 and bcl-xl proteins and JAK2 and STAT5a at both the mRNA and protein levels. Pretreatment with either rhEPO or CEPO reduced the number of apoptotic cells, upregulated bcl-xl expression, and downregulated caspase-3 expression in the myocardium of epileptic rats. Both myocardial JAK2 and STAT5a mRNAs, as well as phosphorylated species of JAK2 and STAT5a, were upregulated in epileptic rats in response to rhEPO—but not to CEPO—pretreatment. AG490 treatment increased apoptosis, upregulated caspase-3 protein expression, and downregulated bcl-xl protein expression in the myocardium of epileptic rats. Conclusions These results indicate that myocardial cell apoptosis may contribute to myocardial injury in epilepsy. EPO protects myocardial cells from apoptosis via the JAK2/STAT5 pathway in rats with experimental epilepsy, whereas CEPO exerts antiapoptotic activity perhaps via a pathway independent of JAK2/STAT5 signaling. PMID:26649078

  11. Engineering and visualization of bacteria for targeting infarcted myocardium.

    PubMed

    Le, Uyenchi N; Kim, Hyung-Seok; Kwon, Jin-Sook; Kim, Mi Yeon; Nguyen, Vu H; Jiang, Sheng Nan; Lee, Byeong-Il; Hong, Yeongjin; Shin, Myung Geun; Rhee, Joon Haeng; Bom, Hee-Seung; Ahn, Youngkeun; Gambhir, Sanjiv S; Choy, Hyon E; Min, Jung-Joon

    2011-05-01

    Optimization of the specific affinity of cardiac delivery vector could significantly improve the efficiency of gene/protein delivery, yet no cardiac vectors to date have sufficient target specificity for myocardial infarction (MI). In this study, we explored bacterial tropism for infarcted myocardium based on our previous observations that certain bacteria are capable of targeting the hypoxic regions in solid tumors. Out of several Escherichia coli or Salmonella typhimurium strains, the S. typhimurium defective in the synthesis of ppGpp (ΔppGpp S. typhimurium) revealed accumulation and selective proliferation in the infarcted myocardium without spillover to noncardiac tissue. The Salmonellae that were engineered to express a variant of Renilla luciferase gene (RLuc8), under the control of the E. coli arabinose operon promoter (P(BAD)), selectively targeted and delivered RLuc8 in the infarcted myocardium only upon injection of L-arabinose. An examination of the infarct size before and after infection, and estimations of C-reactive protein (CRP) and procalcitonin indicated that intravenous injection of ΔppGpp S. typhimurium did not induce serious local or systemic immune reactions. This current proof-of-principle study demonstrates for the first time the capacity of Salmonellae to target infarcted myocardium and to serve as a vehicle for the selective delivery of therapeutic agents in MI.

  12. From Molecules to Myofibers: Multiscale Imaging of the Myocardium

    PubMed Central

    Goergen, Craig J.

    2012-01-01

    Pathology in the heart can be examined at several scales, ranging from the molecular to the macroscopic. Traditionally, fluorescence-based techniques such as flow cytometry have been used to study the myocardium at the molecular, cellular, and microscopic levels. Recent advances in magnetic resonance imaging (MRI), however, have made it possible to image certain cellular and molecular events in the myocardium noninvasively in vivo. In addition, diffusion MRI has been used to image myocardial fiber architecture and microstructure in the intact heart. Diffusion MRI tractography, in particular, is providing novel insights into myocardial microsctructure in both health and disease. Recent developments have also been made in fluorescence imaging, making it possible to image fluorescent probes in the heart of small animals non-invasively in vivo. Moreover, techniques have been developed to perform in vivo fluorescence tomography of the mouse heart. These advances in MRI and fluorescence imaging allow events in the myocardium to be imaged at several scales linking molecular changes to alterations in microstructure and microstructural changes to gross function. A complete and integrated picture of pathophysiology in the myocardium is thus obtained. This multiscale approach has the potential to be of significant value not only in preclinical research but, ultimately, in the clinical arena as well. PMID:21643889

  13. Arachidonic acid metabolism in fibroblasts derived from canine myocardium

    SciTech Connect

    Weber, D.R.; Prescott, S.M.

    1986-03-05

    Canine fibroblasts from normal or healing infarcted myocardium were grown in culture. The cells were morphologically indistinguishable, but the doubling time of cells from healing myocardium was 39.6 +/- 3.5 hr whereas that of normals was 24 +/- 3.7 (n=5, p < .025). Fibroblasts incorporated (/sup 3/H)arachidonate (AA) into phospholipids. Calcium ionophore A23187 (10 ..mu..M) caused release and metabolism of (/sup 3/H) AA. A23187 or AA (10..mu..M) induced production of 6-keto PGF1..cap alpha.., PGE2, and a hydroxy metabolite of AA. RIA of 6-keto PGF1..cap alpha.. showed that subconfluent cells from healing myocardium produced 1202 +/- 354 pg/mg protein whereas that of normals was 551 +/- 222 (n=7, p < .025). Histamine and bradykinin also induced AA metabolism but were less potent. They examined the effect of AA released from deteriorating myocytes on AA metabolism by cultured fibroblasts. They confirmed that isolated myocytes labelled with (/sup 3/H)AA released but did not metabolize (/sup 3/H)AA. In coincubations, fibroblasts incorporated myocyte-derived AA. Subsequent stimulation of the fibroblasts with A23187 induced the synthesis of 6-keto PGF1..cap alpha.., PGE2 and a hydroxy metabolite. The fibroblast content of healing myocardium was 35-1000 times that of normal tissue (n=7). Thus even a moderate change in AA metabolism, amplified by the AA released from deteriorating myocytes, may be a significant physiologic or pathologic event.

  14. Three-dimensional imaging of the myocardium with isotopes

    NASA Technical Reports Server (NTRS)

    Budinger, T. F.

    1975-01-01

    Three methods of imaging the three-dimensional distribution of isotopes in the myocardium are discussed. Three-dimensional imaging was examined using multiple Anger-camera views. Longitudinal tomographic images with compensation for blurring were studied. Transverse-section reconstruction using coincidence detection of annihilation gammas from positron emitting isotopes was investigated.

  15. Estrogen protects the heart from ischemia-reperfusion injury via COX-2-derived PGI2.

    PubMed

    Booth, Erin Anne; Flint, RaShonda Renee; Lucas, Kathryn Louise; Knittel, Andrea Kathleen; Lucchesi, Benedict R

    2008-09-01

    There is an accumulating body of data to suggest that estrogen mediates its cardioprotective effects via cyclooxygenase activation and synthesis of prostaglandins (PG), specifically PGI2. We hypothesized that inhibition of COX-2 would prevent estrogen's cardioprotective effects after myocardial ischemia-reperfusion. Acute treatment with 17beta-estradiol (E2; 20 microg/rabbit) increased COX-2 protein expression and activity in the myocardium. To determine the effects of COX-2 inhibition on infarct size after E2 treatment, New Zealand white rabbits were anesthetized and administered the COX-2 inhibitor nimesulide (5 mg/kg) or vehicle intravenously 30 minutes before an intravenous injection of E2. Thirty minutes after estrogen treatment, the coronary artery was occluded for 30 minutes followed by 4 hours of reperfusion. E2 significantly decreased infarct size as a percent of area at risk when compared to vehicle (18.9 +/- 3.1 versus 47.0 +/- 4.1; P < 0.001). Pretreatment with nimesulide nullified the infarct size sparing effect of E2 (55.8 +/- 5.6). Treatment with the PGI2 receptor antagonist RO3244794 also abolished the protective effects of E2 (45.3 +/- 4.5). The results indicate that estrogen protects the myocardium from ischemia-reperfusion injury through increased production of COX-2-derived PGI2. The data indicate that selective COX-2 inhibitors might counteract the potential cytoprotective effects of estrogen in premenopausal or postmenopausal women.

  16. N-acetyl-L-cysteine pre-treatment protects cryopreserved bovine spermatozoa from reactive oxygen species without compromising the in vitro developmental potential of intracytoplasmic sperm injection embryos.

    PubMed

    Pérez, L; Arias, M E; Sánchez, R; Felmer, R

    2015-12-01

    Excess of reactive oxygen species (ROS) on in vitro embryo production systems negatively affects the quality and developmental potential of embryos, as result of a decreased sperm quality and increased DNA fragmentation. This issue is of major importance in assisted fertilisation procedures such as intracytoplasmic sperm injection (ICSI), because this technique does not allow the natural selection of competent spermatozoa, and therefore, DNA-damaged spermatozoa might be used to fertilise an egg. The aim of this study was to investigate a new strategy to prevent the potential deleterious effect of ROS on cryopreserved bovine spermatozoa. We evaluated the effect of a sperm pre-treatment with different concentrations of N-acetyl-L-cysteine (NAC) on ROS production, viability and DNA fragmentation and assessed the effect of this treatment on the in vitro developmental potential and quality of embryos generated by ICSI. The results show a strong scavenging effect of 1 and 10 mm NAC after exposure of spermatozoa to a ROS inducer, without compromising the viability and DNA integrity. Importantly, in vitro developmental potential and quality of embryos generated by ICSI with spermatozoa treated with NAC were not affected, confirming the feasibility of using this treatment before an ICSI cycle.

  17. Melatonin-induced glycosaminoglycans augmentation in myocardium remote to infarction.

    PubMed

    Drobnik, J; Tosik, D; Piera, L; Szczepanowska, A; Olczak, S; Zielinska, A; Liberski, P P; Ciosek, J

    2013-12-01

    Elevated levels of collagen as well as transient increases of glycosaminoglycans (GAG) have been shown in the myocardium remote to the infarction. The aim of the study is to observe the effect of melatonin on the accumulation of collagen and GAG in the left ventricle wall, remote to the infarction. A second aim is to determine whether the effect of the pineal indole is mediated by the membrane melatonin receptors of heart fibroblasts. Rats with myocardial infarction induced by ligation of the left coronary artery were treated with melatonin at a dose of 60 μg/100 g b.w. or vehicle (2% ethanol in 0.9% NaCl). The results were compared with an untreated control. In the second part of the study, the fibroblasts from the non-infarcted part of myocardium were isolated and cultured. Melatonin at a range of concentrations from 10(-8) M to 10(-6) M was applied to the fibroblast cultures. In the final part of the study, the influence of luzindole (10(-6) M), the melatonin membrane receptor inhibitor, on melatonin-induced GAG augmentation was investigated. Both collagen and GAG content were measured in the experiment. Melatonin elevated GAG content in the myocardium remote to the infarcted heart. Collagen level was not changed by pineal indoleamine. Fibroblasts isolated from the myocardium varied in shape from fusiform to spindle-shaped. Moreover, the pineal hormone (10(-7)M and 10(-6)M) increased GAG accumulation in the fibroblast culture. Luzindole inhibited melatonin-induced elevation of GAG content at 10(-6)M. Melatonin increased GAG content in the myocardium remote to infarction. This effect was dependent on the direct influence of the pineal indole on the heart fibroblasts. The melatonin-induced GAG elevation is blocked by luzindole, the melatonin membrane receptors inhibitor, indicating a direct effect of this indole.

  18. Stromal derived factor 1α: a chemokine that delivers a two-pronged defence of the myocardium.

    PubMed

    Bromage, Daniel I; Davidson, Sean M; Yellon, Derek M

    2014-09-01

    Alleviating myocardial injury associated with ST elevation myocardial infarction is central to improving the global burden of coronary heart disease. The chemokine stromal cell-derived factor 1α (SDF-1α) has dual potential benefit in this regard. Firstly, SDF-1α is up-regulated in experimental and clinical studies of acute myocardial infarction (AMI) and regulates stem cell migration to sites of injury. SDF-1α delivery to the myocardium after AMI is associated with improved stem cell homing, angiogenesis, and left ventricular function in animal models, and improvements in heart failure and quality of life in humans. Secondly, SDF-1α may have a role in remote ischaemic conditioning (RIC), the phenomenon whereby non-lethal ischaemia-reperfusion applied to an organ or tissue remote from the heart protects the myocardium from lethal ischaemia-reperfusion injury (IRI). SDF-1α is increased in the serum of rats subjected to RIC and protects against myocardial IRI in ex vivo studies. Despite these potential pleiotropic effects, a limitation of SDF-1α is its short plasma half-life due to cleavage by dipeptidyl peptidase-4 (DPP-4). However, DPP-4 inhibitors increase the half-life of SDF-1α by preventing its degradation and are also protective against lethal IRI. In summary, SDF-1 potentially delivers a 'two-pronged' defence of the myocardium: acutely protecting it from IRI while simultaneously stimulating repair by recruiting stem cells to the site of injury. In this article we examine the evidence for acute and chronic cardioprotective roles of SDF-1α and discuss potential therapeutic manipulations of this mechanism with DPP-4 inhibitors to protect against lethal tissue injury in the clinical setting.

  19. Remote ischemic postconditioning enhances cell retention in the myocardium after intravenous administration of bone marrow mesenchymal stromal cells.

    PubMed

    Jiang, Qin; Song, Peng; Wang, Enshi; Li, Jun; Hu, Shengshou; Zhang, Hao

    2013-03-01

    Efficacy of intravenous administration of mesenchymal stromal cells (MSCs) for myocardial infarction (MI) is limited by low cell retention in the damaged myocardium. Previous studies indicated that remote ischemic conditioning could protect against ischemia-reperfusion-induced injury by release of various cytokines including stromal cell derived factor-1 alpha (SDF-1α). However, whether remote ischemic postconditioning (RIPostC) can also enhance the retention of infused cells in the myocardium by activating MSC homing is unclear. In this study, RIPostC was induced with 4cycles of 5min occlusion and reperfusion of the abdominal aorta in female Sprague-Dawley (SD) rats which underwent ligation of the coronary artery 1week previously. Cytokine levels in serum and myocardium were evaluated by enzyme-linked immunosorbent assay (ELISA) at 1, 6, 24 and 48h after RIPostC. Then, a total of 4×10(6) male MSCs were infused intravenously at 24h after RIPostC. The number of survived cells in the myocardium was evaluated by real-time polymerase chain reaction analysis for Y chromosome and the heart function was evaluated by echocardiography at 1month after cell infusion. Furthermore, 10μg/kg rabbit anti-rat CXCR4 polyclonal antibody was injected intraperitoneally to prove the role of SDF-1α for RIPostC. RIPostC induced an increase in SDF-1α in serum at 1h and enhanced SDF-1α transcription and protein synthesis in the myocardium at 24h after the procedure. 1month after cell transplantation, RIPostC significantly increased MSC myocardial retention by 79.1±12.3% and thereby contributed to enhanced cardiac function in comparison with cell transplantation without RIPostC. Furthermore, blockade with a CXCR4-specific antibody after RIPostC markedly attenuated the enhancement of therapeutic efficacy. We conclude that RIPostC activated SDF-1α expression and enhanced retention of the infused MSCs in the injured myocardium. Priming of the heart with RIPostC might be a novel

  20. MiR-22/Sp-1 Links Estrogens With the Up-Regulation of Cystathionine γ-Lyase in Myocardium, Which Contributes to Estrogenic Cardioprotection Against Oxidative Stress.

    PubMed

    Wang, Long; Tang, Zhi-Ping; Zhao, Wei; Cong, Bing-Hai; Lu, Jian-Qiang; Tang, Xiao-Lu; Li, Xiao-Han; Zhu, Xiao-Yan; Ni, Xin

    2015-06-01

    Hydrogen sulfide, generated in the myocardium predominantly via cystathionine-γ-lyase (CSE), is cardioprotective. Our previous study has shown that estrogens enhance CSE expression in myocardium of female rats. The present study aims to explore the mechanisms by which estrogens regulate CSE expression, in particular to clarify the role of estrogen receptor subtypes and the transcriptional factor responsible for the estrogenic effects. We found that either the CSE inhibitor or the CSE small interfering RNA attenuated the protective effect of 17β-estradiol (E2) against H2O2- and hypoxia/reoxygenation-induced injury in primary cultured neonatal cardiomyocytes. E2 stimulates CSE expression via estrogen receptor (ER)-α both in cultured cardiomyocytes in vitro and in the myocardium of female mice in vivo. A specificity protein-1 (Sp-1) consensus site was identified in the rat CSE promoter and was found to mediate the E2-induced CSE expression. E2 increases ERα and Sp-1 and inhibits microRNA (miR)-22 expression in myocardium of ovariectomized rats. In primary cardiomyocytes, E2 stimulates Sp-1 expression through the ERα-mediated down-regulation of miR-22. It was confirmed that both ERα and Sp-1 were targeted by miR-22. In the myocardium of ovariectomized rats, the level of miR-22 inversely correlated to CSE, ERα, Sp-1, and antioxidant biomarkers and positively correlated to oxidative biomarkers. In summary, this study demonstrates that estrogens stimulate Sp-1 through the ERα-mediated down-regulation of miR-22 in cardiomyocytes, leading to the up-regulation of CSE, which in turn results in an increase of antioxidative defense. Interaction of ERα, miR-22, and Sp-1 may play a critical role in the control of oxidative stress status in the myocardium of female rats.

  1. Genetic Modification of Mesenchymal Stem Cells Overexpressing CCR1 Increases Cell Viability, Migration, Engraftment and Capillary Density in the Injured Myocardium

    PubMed Central

    Huang, Jing; Zhang, Zhiping; Guo, Jian; Ni, Aiguo; Deb, Arjun; Zhang, Lunan; Mirotsou, Maria; Pratt, Richard E; Dzau, Victor J

    2010-01-01

    Rationale Although mesenchymal stem cell (MSC) transplantation has been shown to promote cardiac repair in acute myocardial injury in vivo, its overall restorative capacity appears to be restricted mainly due to poor cell viability and low engraftment in the ischemic myocardium. Specific chemokines are upregulated in the infarcted myocardium. However the expression levels of the corresponding chemokine receptors (e.g. CCR1, CXCR2) in MSCs are very low. We hypothesized that this discordance may account for the poor MSC engraftment and survival. Objective To determine whether overexpression of CCR1 or CXCR2 chemokine receptors in MSCs augments their cell survival, migration and engraftment after injection in the infarcted myocardium. Methods and Results Overexpression of CCR1, but not CXCR2, dramatically increased chemokine-induced murine MSC migration and protected MSC from apoptosis in vitro. Moreover, when MSCs were injected intramyocardially one hour after coronary artery ligation, CCR1-MSCs accumulated in the infarcted myocardium at significantly higher levels than control-MSCs or CXCR2-MSCs three days post-myocardial infarction (MI). CCR1-MSC injected hearts exhibited a significant reduction in infarct size, reduced cardiomyocytes apoptosis and increased capillary density in injured myocardium three days post-MI. Furthermore, intramyocardial injection of CCR1-MSCs prevented cardiac remodeling and restored cardiac function 4 weeks post-MI. Conclusions Our results demonstrate the in vitro and in vivo salutary effects of genetic modification of stem cells. Specifically, overexpression of chemokine receptor enhances the migration, survival and engraftment of MSCs, and may provide a new therapeutic strategy for the injured myocardium. PMID:20378860

  2. The iron-regulatory peptide hepcidin is upregulated in the ischemic and in the remote myocardium after myocardial infarction.

    PubMed

    Simonis, Gregor; Mueller, Katrin; Schwarz, Peggy; Wiedemann, Stephan; Adler, Guido; Strasser, Ruth H; Kulaksiz, Hasan

    2010-09-01

    Recent evidence suggests that iron metabolism contributes to the ischemic damage after myocardial infarction. Hepcidin, a recently discovered peptide hormone, regulates iron uptake and metabolism, protecting the body from iron overload. In this study we analyzed the regulation of hepcidin in the heart and blood of rats after myocardial infarction. To induce a myocardial infarction in the rats, left anterior descending coronary artery ligation was performed. After 1-24h, biopsies from the ischemic and the non-ischemic myocardium were taken. In these biopsies, the mRNA levels and the protein expression of hepcidin were analyzed by quantitative RT-PCR and immunoblot analysis, respectively. In parallel, the serum levels of prohepcidin were measured by ELISA. Six hours after myocardial infarction, the hepcidin mRNA expression was temporally upregulated in the ischemic and in the non-ischemic myocardium. The upregulation was specific for hepcidin, since other iron-related genes (hemojuvelin, IREG-1) remained unchanged. Furthermore, the alteration of the hepcidin protein expression in the ischemic area was connected to the level of hepcidin in the serum of the infarcted rats, where hepcidin also raised up. Angiotensin receptor blockade with candesartan did not influence the mRNA regulation of hepcidin. Together, these data show a particular upregulation of the iron-regulatory peptide hepcidin in the ischemic and the non-ischemic myocardium after myocardial infarction. It is speculated that upregulation of hepcidin may reduce iron toxicity and thus infarct size expansion in an infarcted heart.

  3. Licorice treatment prevents oxidative stress, restores cardiac function, and salvages myocardium in rat model of myocardial injury.

    PubMed

    Ojha, Shreesh Kumar; Sharma, Charu; Golechha, Mahaveer Jain; Bhatia, Jagriti; Kumari, Santosh; Arya, Dharamvir Singh

    2015-02-01

    The present study examined the effects of licorice on antioxidant defense, functional impairment, histopathology, and ultrastructural alterations in isoproterenol (ISP)-induced myocardial injury in rats. Myocardial necrosis was induced by two subcutaneous injection of ISP (85 mg/kg) at an interval of 24 h. Licorice was administered orally for 30 days in the doses of 100, 200, 400, or 800 mg/kg. ISP-treated rats showed impaired hemodynamics, left ventricular dysfunction, and caused depletion of antioxidants and marker enzymes along with lipid peroxidation from myocardium. ISP also induced histopathological and ultrastructural alterations in myocardium. Pretreatment with licorice prevented the depletion of endogenous antioxidants and myocyte injury marker enzymes, inhibited lipid peroxidation, and showed recovery of hemodynamic and ventricular functions. Licorice treatment also reduced myonecrosis, edema, and infiltration of inflammatory cells and showed preservation of subcellular and ultrastructural components. Our results demonstrate that licorice exerts cardioprotection by reducing oxidative stress, augmenting endogenous antioxidants, and restoring functional parameters as well as maintaining structural integrity.

  4. Protective action of taurine, given as a pretreatment or as a posttreatment, against endotoxin-induced acute lung inflammation in hamsters.

    PubMed

    Bhavsar, Tapan M; Patel, Sanket N; Lau-Cam, Cesar A

    2010-01-01

    To assess the effect of taurine on lipopolysaccharide (LPS)-induced lung inflammation, oxidative stress and apoptosis, female Golden Syrian hamsters were intratracheally instilled with bacterial LPS (0.02 mg in phosphate buffered saline (PBS) pH 7.4), before or after a 3-day intraperitoneal treatment with a single dose of taurine (50 mg/kg/day in PBS pH 7.4), and bronchoalveolar lavage fluid (BALF) and lung tissue samples were collected at 24 hr after the last treatment. In comparison to BALF samples from animals receiving only PBS pH 7.4, and serving as controls, those of LPS-stimulated animals exhibited a higher count of both total leukocytes and neutrophils and increased expression of tumor necrosis factor receptor 1. In comparison to lungs from control animals, those from LPS-treated animals showed increased cellular apoptosis, lipid peroxidation, decreased glutathione levels, altered activities of antioxidant enzymes (catalase, glutathione peroxidase, superoxide dismutase) and focal inflammation confined to the parenchyma. A treatment with taurine was found to significantly attenuate all these alterations, with the protection being, in all instances, greater when given before rather than after LPS. The present results suggest that taurine is endowed with antiinflammatory and antioxidant properties that are protective in the lung against the deleterious actions of Gram negative bacterial endotoxin.

  5. Effect of levosimendan injection on oxidative stress of rat myocardium.

    PubMed

    Basel, Halil; Kavak, Servet; Demir, Halit; Meral, Ismail; Ekim, Hasan; Bektas, Hava

    2013-06-01

    This experiment was designed to investigate the effect of levosimendan injection on lipid peroxidation product malondialdehyde (MDA) and antioxidant glutathione (GSH) levels, and activities of antioxidant enzymes in myocardium of rats. Twenty male Wistar-albino rats were divided randomly into 2 study groups, each consisting of 10 rats. The animals in the first group were not treated with drug and served as control. It was found that the MDA and GSH levels decreased in levosimendan injected group. Superoxide dismutase, glutathione peroxidase, catalase and carbonic anhydrase enzyme activities were lower in levosimendan injected group than controls. It was concluded that lower tissue free radical level caused by levosimendan injection led to a lower antioxidant enzymes synthesis in the body and a decrease in the antioxidant enzyme activity and free radical scavenger level in myocardium of rat.

  6. Myocardium and BMP signaling are required for endocardial differentiation.

    PubMed

    Palencia-Desai, Sharina; Rost, Megan S; Schumacher, Jennifer A; Ton, Quynh V; Craig, Michael P; Baltrunaite, Kristina; Koenig, Andrew L; Wang, Jinhu; Poss, Kenneth D; Chi, Neil C; Stainier, Didier Y R; Sumanas, Saulius

    2015-07-01

    Endocardial and myocardial progenitors originate in distinct regions of the anterior lateral plate mesoderm and migrate to the midline where they coalesce to form the cardiac tube. Endocardial progenitors acquire a molecular identity distinct from other vascular endothelial cells and initiate expression of specific genes such as nfatc1. Yet the molecular pathways and tissue interactions involved in establishing endocardial identity are poorly understood. The endocardium develops in tight association with cardiomyocytes. To test for a potential role of the myocardium in endocardial morphogenesis, we used two different zebrafish models deficient in cardiomyocytes: the hand2 mutant and a myocardial-specific genetic ablation method. We show that in hand2 mutants endocardial progenitors migrate to the midline but fail to assemble into a cardiac cone and do not express markers of differentiated endocardium. Endocardial differentiation defects were rescued by myocardial but not endocardial-specific expression of hand2. In metronidazole-treated myl7:nitroreductase embryos, myocardial cells were targeted for apoptosis, which resulted in the loss of endocardial nfatc1 expression. However, endocardial cells were present and retained expression of general vascular endothelial markers. We further identified bone morphogenetic protein (BMP) as a candidate myocardium-derived signal required for endocardial differentiation. Chemical and genetic inhibition of BMP signaling at the tailbud stage resulted in severe inhibition of endocardial differentiation while there was little effect on myocardial development. Heat-shock-induced bmp2b expression rescued endocardial nfatc1 expression in hand2 mutants and in myocardium-depleted embryos. Our results indicate that the myocardium is crucial for endocardial morphogenesis and differentiation, and identify BMP as a signal involved in endocardial differentiation.

  7. C-reactive protein activates complement in infarcted human myocardium.

    PubMed

    Nijmeijer, Remco; Lagrand, Wim K; Lubbers, Yvonne T P; Visser, Cees A; Meijer, Chris J L M; Niessen, Hans W M; Hack, C Erik

    2003-07-01

    Circulating levels of C-reactive protein (CRP) constitute a cardiovascular risk marker. Immunohistochemical studies have revealed co-localization of CRP and activated complement in human infarcted myocardium suggesting CRP to enhance inflammation in ischemic myocardium by inducing local complement activation. The aim was to establish whether CRP activates complement in infarcted human myocardium and to assess the relationship between this activation and the duration of infarction. Myocardial tissue samples from 56 patients that had died from acute myocardial infarction were evaluated. Specimens were taken from infarcted as well as noninfarcted sites of the heart. CRP-mediated complement activation was assessed by immunohistochemistry and by measuring levels of complement, CRP, and CRP-complement complexes, specific markers for CRP-mediated activation, in homogenates of the heart. Infarctions of 12 hours to 5 days had significantly more extensive depositions of complement and CRP and contained significantly more CRP, activated complement, and CRP-complement complexes than infarctions that were less than 12 hours old. Levels of CRP complexes correlated significantly with CRP and complement concentrations in the infarctions, as well as with the extent of complement and CRP depositions as measured via immunohistochemistry. Specific activation products of CRP-mediated activation of complement are increased in infarcts of more than 12 hours in duration and correlate with the extent of complement depositions. Hence, CRP seems to enhance local inflammatory reactions ensuing in human myocardial infarcts of more than 12 hours duration.

  8. Ultrastructural and functional effects of lead poisoning on adult canine myocardium: assessment of thiamin treatment

    SciTech Connect

    Kincaid, N.G.

    1985-01-01

    The effects of lead (Pb) poisoning on the adult canine myocardium were assessed quantitatively using stereological techniques, functional testing, and blood analyses as well as qualitatively by morphological investigation. Relative measurements using stereological techniques compared the volume fractions of cellular components of the three groups. Blood was analyzed for lead, hemoglobin, hematocrit, total erythrocytes, total leukocytes, thiamin pyrophosphate (TPP), delta-aminolevulinic acid dehydratase activity (ALAD), and zinc protoporphyrin (ZPP). The major finding of the stereological analysis was the statistically significant increase of 3.2% in myofilament volume in the Pb treated group and the significant decrease in mitochondrial volume in both the Pb treated and Pb + B/sub 1/ treated groups. A statistically significant decrease in the mitochondria/myofilament volume ratio was found in the Pb treated, but no Pb + B/sub 1/ treated group. This may indicate either a protective effect of thiamin on mitochondria or a reduced compensatory need of the myocyte to increase myofilament volume.

  9. Potent In Vitro Protection Against PM₂.₅-Caused ROS Generation and Vascular Permeability by Long-Term Pretreatment with Ganoderma tsugae.

    PubMed

    Tseng, Chia-Yi; Chung, Meng-Chi; Wang, Jhih-Syuan; Chang, Yu-Jung; Chang, Jing-Fen; Lin, Chin-Hung; Hseu, Ruey-Shyang; Chao, Ming-Wei

    2016-01-01

    Epidemiological studies show increased particulate matter (PM[Formula: see text]) particles in ambient air are correlated with increased myocardial infarctions. Given the close association of capillaries and alveoli, the dysfunction is caused when inhaled PM[Formula: see text] particles come in close proximity to capillary endothelial cells. We previously suggested that the inhalation of PM[Formula: see text] diesel exhaust particles (DEP) induces oxidative stress and upregulates the Nrf2/HO-1 pathway, inducing vascular permeability factor VEGFA secretion, which results in cell-cell adherens junction disruption and PM[Formula: see text] transmigratation into circulation. Here, we minimized the level that PM[Formula: see text] traveled in the bloodstream by pre-supplementing with a traditional Chinese medicine (TCM) Ganoderma tsugae DMSO extract (GTDE) prior to PM[Formula: see text] exposure. Our results show that PM[Formula: see text] caused alterations in enzyme activities and cellular anti-oxidant balance. We found decreased glutathione levels, a reduced cellular redox ratio, increased ROS generation and cytotoxicity in the cellular fractions. The oxidative stress caused DNA damage and apoptosis, likely causing downstream molecular events that trigger vasculature permeabilization and, eventually, cardiovascular disorders. Our results show long-term GTDE treatment increased endogenous glutathione level, while PM[Formula: see text]-reduced glutathione levels and the cellular redox ratio. GTDE was protective against the genotoxic and apoptotic effects initiated by PM[Formula: see text] oxidative stress. Vascular permeability revealed that PM[Formula: see text] only accumulated on the surface of cells after GTDE treatment; no penetration was detected. After two weeks of GTDE treatment, VEGFA secretion was significantly reduced in human umbilical vein endothelial cells (HUVEC) and endothelial cell migration was blocked. Our results suggest GTDE prevents PM

  10. Pretreatment of microbial sludges

    DOEpatents

    Rivard, Christopher J.; Nagle, Nicholas J.

    1995-01-01

    Methods are described for pretreating microbial sludges to break cells and disrupt organic matter. One method involves the use of sonication, and another method involves the use of shear forces. The pretreatment of sludge enhances bioconversion of the organic fraction. This allows for efficient dewatering of the sludge and reduces the cost for final disposal of the waste.

  11. Pretreatment of microbial sludges

    DOEpatents

    Rivard, C.J.; Nagle, N.J.

    1995-01-10

    Methods are described for pretreating microbial sludges to break cells and disrupt organic matter. One method involves the use of sonication, and another method involves the use of shear forces. The pretreatment of sludge enhances bioconversion of the organic fraction. This allows for efficient dewatering of the sludge and reduces the cost for final disposal of the waste.

  12. GREET Pretreatment Module

    SciTech Connect

    Adom, Felix K.; Dunn, Jennifer B.; Han, Jeongwoo

    2014-09-01

    A wide range of biofuels and biochemicals can be produced from biomass via different pretreatment technologies that yield sugars. This report documents the material and energy flows that occur when fermentable sugars from four lignocellulosic feedstocks (corn stover, miscanthus, switchgrass, and poplar) are produced via dilute acid pretreatment and ammonia fiber expansion. These flows are documented for inclusion in the pretreatment module of the Greenhouses Gases, Regulated Emissions, and Energy Use in Transportation (GREET) model. Process simulations of each pretreatment technology were developed in Aspen Plus. Material and energy consumption data from Aspen Plus were then compiled in the GREET pretreatment module. The module estimates the cradle-to-gate fossil energy consumption (FEC) and greenhouse gas (GHG) emissions associated with producing fermentable sugars. This report documents the data and methodology used to develop this module and the cradle-to-gate FEC and GHG emissions that result from producing fermentable sugars.

  13. Noncompaction of the ventricular myocardium associated with mitral regurgitation and preserved ventricular systolic function.

    PubMed

    Ali, Sulafa Khalid M; Omran, Ahmed S; Najm, Hani; Godman, Michael J

    2004-01-01

    Noncompaction of the ventricular myocardium is an embryonic cardiomyopathy that is increasingly being recognized. Mitral regurgitation, when present, is usually a result of the associated left ventricular systolic dysfunction. We report 4 patients with noncompaction of the ventricular myocardium in whom ventricular systolic function was preserved. Mitral regurgitation was associated with changes in the mitral valve leaflets and an abnormal coaptation pattern. This association of noncompaction of the ventricular myocardium with mitral regurgitation has not, to our knowledge, been reported.

  14. [The effect of helium-neon laser radiation on the energy metabolic indices of the myocardium].

    PubMed

    Chizhov, G K; Koval'skaia, N I; Kozlov, V I

    1991-03-01

    It was shown in experiments on white rats, that intravenous and direct myocardium helium-neon laser irradiation leads to the some activation of lactate, glucose-6-phosphate, succinate and reduced NAD degydrogenases. During direct myocardium irradiation these changes are in a less degree. It is suggested that helium-neon laser irradiation displays some active influence on the energy metabolism enzymes of the myocardium, and the mechanisms of this action are discussed. PMID:2054512

  15. Solids Control in Sludge Pretreatment

    SciTech Connect

    Beahm, E.C., Weber, C.F., Hunt, R.D., Dillow, T.A.

    1997-12-31

    Sludge pretreatment will likely involve washing, followed by caustic or acidic leaching and washing of sludge residues after leaching. The principal goal of pretreatment is to obtain a low-volume high-activity waste stream and a high-volume low-activity waste stream. Also, some waste constituents such as chromium and phosphate can be included in glass formulations only at very low concentrations; therefore, it is desirable to remove them from high-level waste streams. Two aspects of sludge treatment and subsequent separations should be well delineated and predictable: (1) the distribution of chemical species between aqueous solutions and solids and (2) potential problems due to chemical interactions that could result in process difficulties or safety concerns.Before any treatment technology is adopted, it must be demonstrated that the process can be carried out as planned. Three pretreatment methods were considered in the Tri-Party (Washington State Ecology, U.S. Environmental Protection Agency, and U.S. Department of Energy) negotiations: (1) sludge washing with corrosion- inhibiting water, (2) Enhanced Sludge Washing, and (3)acidic dissolution with separations processes. Enhanced Sludge Washing is the baseline process. In Enhanced Sludge Washing, sludge is first washed with corrosion-inhibiting water; it is then leached with caustic (sodium hydroxide solution) and washed again with corrosion- inhibiting water. The initial concern is whether a pretreatment technique is effective in separating sludge components. This can be evaluated by bench-scale tests with sludge specimens from underground storage tanks. The results give data on the distribution of important species such as aluminum, phosphate, and radionuclides between wash and leach solutions and solid sludge residues.

  16. Ethanol Promotes Arteriogenesis and Restores Perfusion to Chronically Ischemic Myocardium

    PubMed Central

    Lassaletta, Antonio D.; Elmadhun, Nassrene Y.; Liu, Yuhong; Feng, Jun; Burgess, Thomas A.; Karlson, Nicholas W.; Laham, Roger J.; Sellke, Frank W.

    2014-01-01

    Background Moderate alcohol consumption is known to be cardioprotective as compared to either heavy drinking or complete abstinence. We assessed the hypothesis that ethanol supplementation would improve myocardial function in the setting of chronic ischemia. Methods and Results Sixteen male Yorkshire swine underwent placement of an ameroid constrictor to the left circumflex artery to induce chronic myocardial ischemia. Post-operatively animals were supplemented with either 90 ml of ethanol daily (50%/V, EtOH) or 80 g of sucrose of equal caloric value (SUC) serving as controls. Seven weeks after ameroid placement, arteriolar density (1.74 ± 0.210 vs. 3.11 ± 0.368 % area of arterioles per low-powered field in SUC vs. EtOH, p = 0.004), myocardial perfusion (ratio of blood flow to the at-risk myocardium compared to the normal ventricle during demand pacing was 0.585 ± 0.107 vs. 1.08 ± 0.138 for SUC vs. EtOH, p = 0.014), and microvascular reactivity were significantly increased in the ethanol-treated animals compared to controls in the at-risk myocardium. Analysis of VEGF and NOTCH pathway signaling suggested pro-neovascular and proliferative activity in the ischemic area. The average peak blood alcohol level in the treatment group was 40 ± 4 mg/dL consistent with levels of moderate drinking in humans. Conclusions Ethanol supplementation increased arteriolar density and significantly improved myocardial perfusion and endothelium-dependent vasorelaxation in chronically ischemic myocardium. These findings suggest that at moderate doses, ethanol directly promotes vasculogenesis and improves microvascular function resulting in significant improvements in myocardial perfusion in the setting of chronic ischemia. PMID:24030397

  17. The effects of exposure to electromagnetic field on rat myocardium.

    PubMed

    Kiray, Amac; Tayefi, Hamid; Kiray, Muge; Bagriyanik, Husnu Alper; Pekcetin, Cetin; Ergur, Bekir Ugur; Ozogul, Candan

    2013-06-01

    Exposure to electromagnetic fields (EMFs) causes increased adverse effects on biological systems. The aim of this study was to investigate the effects of EMF on heart tissue by biochemical and histomorphological evaluations in EMF-exposed adult rats. In this study, 28 male Wistar rats weighing 200-250 g were used. The rats were divided into two groups: sham group (n = 14) and EMF group (n = 14). Rats in sham group were exposed to same conditions as the EMF group except the exposure to EMF. Rats in EMF group were exposed to a 50-Hz EMF of 3 mT for 4 h/day and 7 days/week for 2 months. After 2 months of exposure, rats were killed; the hearts were excised and evaluated. Determination of oxidative stress parameters was performed spectrophotometrically. To detect apoptotic cells, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining and caspase-3 immunohistochemistry were performed. In EMF-exposed group, levels of lipid peroxidation significantly increased and activities of superoxide dismutase and glutathione peroxidase decreased compared with sham group. The number of TUNEL-positive cells and caspase-3 immunoreactivity increased in EMF-exposed rats compared with sham. Under electron microscopy, there were mitochondrial degeneration, reduction in myofibrils, dilated sarcoplasmic reticulum and perinuclear vacuolization in EMF-exposed rats. In conclusion, the results show that the exposure to EMF causes oxidative stress, apoptosis and morphologic damage in myocardium of adult rats. The results of our study indicate that EMF-related changes in rat myocardium could be the result of increased oxidative stress. Further studies are needed to demonstrate whether the exposure to EMF can induce adverse effects on myocardium.

  18. [The viable myocardium: metabolic, diagnostic and therapeutic aspects].

    PubMed

    Strozzi, C; Spisani, P

    1993-01-01

    The term stunned myocardium is used to indicate a reversible post-ischemic dysfunction of the ventricular mechanism which may persist for hours, days or weeks after the restoration of coronary flow following spontaneous or pharmacological thrombolysis, transluminal coronary angioplasty, aorto-coronary bypass and ischemic attacks. Hibernating myocardium is used to describe a depression of ventricular contractility in the presence of chronic hypoperfusion which may be reversed following revascularization as a result of aorto-coronary by-pass surgery. Three biochemical and physiopathological hypotheses are currently acknowledged to explain the phenomenon of stunning: the hypothesis of free oxygen radicals, the hypothesis related to an energy deficit and that involving a calcium overload. It is possible that oxydizing stress induced by free radicals may modify the activity of one or more sarcolemmic proteins which regulate the flow of calcium or other ions. Alterations in the transport and accumulation of calcium ions due to a Na+/Ca++ pump deficit and calcium-ATPase of the sarcoplasmatic reticle appear to be responsible for contractile dysfunction. The hypothesis concerning an energy deficit appears to be least probable since even if ATP levels are low the intracellular energy status does not appear to be a factor which limits mechanical function which may be stimulated in the absence of further variations in the content of highly energetic phosphates. There is also reduced myofibrillar creatinkinase activity. In hibernating myocardium the mechanical dysfunction is due to a metabolic and therefore contractile "down-regulation' with low myocardial energy and oxygen consumption to ensure the survival of chronically hypoperfused areas.(ABSTRACT TRUNCATED AT 250 WORDS) PMID:8233008

  19. Influence of propranolol on high energy phosphate and tissue acidosis in regional ischemic myocardium of pigs: assessment with arterial pressure and respiration gated in vivo 31-phosphorus magnetic resonance spectroscopy.

    PubMed

    Tanaka, M; Fujiwara, H; Ishida, M; Kida, M; Onodera, T; Wu, D J; Matsuda, M; Kawamura, A; Takemura, G; Kawai, C

    1989-08-01

    In an attempt to define the metabolic abnormalities of the ischemic myocardium, the changes in high energy phosphates, inorganic phosphate and intracellular pH were serially and quantitatively evaluated in ischemic porcine hearts having no collateral circulation, using arterial pressure and respiration gated in vivo 31P magnetic resonance spectroscopy. The protocol was also modified for propranolol pretreatment (0.6 mg/kg intravenously) to define its effect on the metabolism of ischemic myocardium. In the non-treated group, creatine phosphate was rapidly depleted by 10 minutes after ischemia; by 40 minutes, ATP and intracellular pH gradually decreased to 10 +/- 11% of control and to 5.90 +/- 0.26, respectively, and inorganic phosphate rose to 303 +/- 43% of control. In the propranolol treated group, the concentrations of creatine phosphate and ATP were higher, and those of inorganic phosphate and tissue pH were similar compared with controls during 40 minutes of ischemia. This suggests that the beneficial effect of propranolol on the ischemic myocardium is due to the preservation of ATP, an essential energy resource for numerous enzymatic reactions in viable myocardium.

  20. Cellular compartmentation in ischemic myocardium: indirect analysis by electron probe

    SciTech Connect

    Walsh, L.G.; Tormey, J.M.

    1988-10-01

    Electron probe microanalysis (EPMA) was carried out directly on myocardial cells and on the myofibrils and the mitochondria within them. A third subcellular compartment, which contains sarcoplasmic reticulum (SR), was measured indirectly. The percent of the total cell calcium content that resides within this ''hidden'' compartment was calculated from cell data minus weighted myofibril and mitochondria data. This approach was applied to control, ischemic, and reperfused myocardium, and other elements were also quantified. We found that the calcium content of this third compartment is little changed during global ischemia but is markedly depleted after 5 min reperfusion. We conclude that these changes are ascribable to changes in SR function.

  1. Detection of viable myocardium using coronary angiography and ventriculography.

    PubMed

    Conti, C Richard

    2002-08-01

    In 2002, coronary angiography is the only way to assess precisely the combination of proximal stenoses, distal target vessels, collaterals, microcirculation, and TIMI antegrade flow. At the time of coronary angiography, global LV function is best determined using biplane ventriculography in order to correlate wall motion with coronary stenoses, distal target vessels, microcirculation, collaterals, and antegrade TIMI flow. This can be done under resting conditions after nitrates or after postextrasystolic potentiation. The absolute diagnosis of viability can only be made retrospectively. Large areas of ischemic viable myocardium should improve contraction after revascularization, decrease symptoms, and prolong survival.

  2. Remote Ischemic Postconditioning Ameliorates the Mesenchymal Stem Cells Engraftment in Reperfused Myocardium

    PubMed Central

    Jiang, Qin; Yu, Tao; Huang, Keli; Lu, Jing; Zhang, Hao; Hu, Shengshou

    2016-01-01

    Objectives Remote Ischemic postconditioning (RIPoC) is a cardioprotective strategy for alleviating the reperfusion injury. We hypothesized that RIPoC or ischemic postconditioning (IPoC) could protect the engrafted mesenchymal stem cells (MSCs) in reperfusion myocardium. Methods Female Sprague-Dawley rats were subject to 30 minutes of occlusion of left anterior descending (LAD). Ischemia reperfusion (IR) received reperfusion without interruption after ischemia. RIPoC received 3 cycles of 30 seconds reperfusion and re-occlusion on the limb at the onset of reperfusion. IPoC received 3 cycles of 30 seconds reperfusion and re-occlusion on the LAD at the same time. Male MSCs were intramyocardially administered after ischemia. Results Compared with that in IR group, ischemic myocardium in RIPoC+IPoC group, RIPoC group and IPoC group were found to have higher anti-oxidative stress and mitochondrial function level, lower lipid peroxidation and inflammational injury level, higher level of stromal cell derived factor-1 alpha and vascular endothelium growth factor gene expression at 3 days later. By immunohistochemical examination and quantitative polymerase chain reaction, more engrafted MSCs, better cardiac function and less cardiac fibrosis in RIPoC+IPoC group, RIPoC group and IPoC group were detected at 3 weeks after delivery. There were no significant differences between RIPoC and RIPoC+IPoC group. Conclusions Combination therapy using intramyocardial MSCs transplantation with RIPoC enhanced transplantation efficiency and cardiac function, and reduced cardiac fibrosis. These beneficial effects were mainly attributed to hospitable milieu for engrafted cells. IPoC could not render additional effect on MSCs engraftment elicited by RIPoC. PMID:26760781

  3. 40 CFR 445.3 - General pretreatment standards.

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... subject to this part that introduces wastewater pollutants into a publicly owned treatment works (POTW) must comply with 40 CFR part 403. ... 40 Protection of Environment 30 2011-07-01 2011-07-01 false General pretreatment standards....

  4. 40 CFR 403.20 - Pretreatment Program Reinvention Pilot Projects Under Project XL.

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... 40 Protection of Environment 29 2011-07-01 2009-07-01 true Pretreatment Program Reinvention Pilot Projects Under Project XL. 403.20 Section 403.20 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS GENERAL PRE-TREAT-MENT REGULATIONS FOR EXIST-ING AND...

  5. 40 CFR 403.13 - Variances from categorical pretreatment standards for fundamentally different factors.

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... 40 Protection of Environment 29 2011-07-01 2009-07-01 true Variances from categorical pretreatment standards for fundamentally different factors. 403.13 Section 403.13 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS GENERAL PRE-TREAT-MENT REGULATIONS FOR...

  6. 40 CFR 403.20 - Pretreatment Program Reinvention Pilot Projects Under Project XL.

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... 40 Protection of Environment 28 2010-07-01 2010-07-01 true Pretreatment Program Reinvention Pilot Projects Under Project XL. 403.20 Section 403.20 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS GENERAL PRE-TREAT-MENT REGULATIONS FOR EXIST-ING AND...

  7. 40 CFR 455.37 - Pretreatment standards for new sources (PSNS). [Reserved

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... 40 Protection of Environment 30 2011-07-01 2011-07-01 false Pretreatment standards for new sources (PSNS). 455.37 Section 455.37 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS PESTICIDE CHEMICALS Metallo-Organic Pesticide Chemicals Manufacturing Subcategory § 455.37 Pretreatment...

  8. 40 CFR 455.27 - Pretreatment standards for new sources (PSNS).

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... 40 Protection of Environment 30 2011-07-01 2011-07-01 false Pretreatment standards for new sources (PSNS). 455.27 Section 455.27 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS PESTICIDE CHEMICALS Organic Pesticide Chemicals Manufacturing Subcategory § 455.27 Pretreatment standards for...

  9. 40 CFR 455.26 - Pretreatment standards for existing sources (PSES).

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... 40 Protection of Environment 30 2011-07-01 2011-07-01 false Pretreatment standards for existing sources (PSES). 455.26 Section 455.26 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS PESTICIDE CHEMICALS Organic Pesticide Chemicals Manufacturing Subcategory § 455.26 Pretreatment standards...

  10. 40 CFR 420.26 - Pretreatment standards for new sources (PSNS).

    Code of Federal Regulations, 2012 CFR

    2012-07-01

    ... § 420.26 Pretreatment standards for new sources (PSNS). Except as provided in 40 CFR 403.7, any new... 40 Protection of Environment 30 2012-07-01 2012-07-01 false Pretreatment standards for new sources (PSNS). 420.26 Section 420.26 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY...

  11. Sundarban Honey Confers Protection against Isoproterenol-Induced Myocardial Infarction in Wistar Rats

    PubMed Central

    Karim, Nurul; Hossain, Md. Sabir; Alam, Nadia

    2016-01-01

    The present study was designed to investigate the cardioprotective effects of Sundarban honey (SH) in rats with isoproterenol- (ISO-) induced myocardial infarction. Adult male Wistar Albino rats were pretreated with Sundarban honey (5 g/kg) daily for a period of 6 weeks. After the treatment period, ISO (85 mg/kg) was subcutaneously injected into the rats at 24 h intervals for 2 days. ISO-induced myocardial damage was indicated by increased serum cardiac specific troponin I levels and cardiac marker enzyme activities including creatine kinase-MB, lactate dehydrogenase, aspartate transaminase, and alanine transaminase. Significant increases in serum total cholesterol, triglycerides, and low-density lipoprotein-cholesterol levels were also observed, along with a reduction in the serum high-density lipoprotein-cholesterol level. In addition to these diagnostic markers, the levels of lipid peroxide products were significantly increased. The activities of antioxidant enzymes such as superoxide dismutase, glutathione peroxidase, and glutathione reductase were significantly decreased in the hearts after ISO-induced myocardial infarction. However, pretreatment of ischemic rats with Sundarban honey brought the biochemical parameters to near normalcy, indicating the protective effect of Sundarban honey against ISO-induced ischemia in rats. Histopathological findings of the heart tissues further confirmed the biochemical findings, indicating that Sundarban honey confers protection against ISO-induced oxidative stress in the myocardium. PMID:27294126

  12. Pretreatment with low-dose gadolinium chloride attenuates myocardial ischemia/reperfusion injury in rats

    PubMed Central

    Chen, Min; Zheng, Yuan-yuan; Song, Yun-tao; Xue, Jing-yi; Liang, Zheng-yang; Yan, Xin-xin; Luo, Da-li

    2016-01-01

    Aim: We have shown that low-dose gadolinium chloride (GdCl3) abolishes arachidonic acid (AA)-induced increase of cytoplasmic Ca2+, which is known to play a crucial role in myocardial ischemia/reperfusion (I/R) injury. The present study sought to determine whether low-dose GdCl3 pretreatment protected rat myocardium against I/R injury in vitro and in vivo. Methods: Cultured neonatal rat ventricular myocytes (NRVMs) were treated with GdCl3 or nifedipine, followed by exposure to anoxia/reoxygenation (A/R). Cell apoptosis was detected; the levels of related signaling molecules were assessed. SD rats were intravenously injected with GdCl3 or nifedipine. Thirty min after the administration the rats were subjected to LAD coronary artery ligation followed by reperfusion. Infarction size, the release of serum myocardial injury markers and AA were measured; cell apoptosis and related molecules were assessed. Results: In A/R-treated NRVMs, pretreatment with GdCl3 (2.5, 5, 10 μmol/L) dose-dependently inhibited caspase-3 activation, death receptor-related molecules DR5/Fas/FADD/caspase-8 expression, cytochrome c release, AA release and sustained cytoplasmic Ca2+ increases induced by exogenous AA. In I/R-treated rats, pre-administration of GdCl3 (10 mg/kg) significantly reduced the infarct size, and the serum levels of CK-MB, cardiac troponin-I, LDH and AA. Pre-administration of GdCl3 also significantly decreased the number of apoptotic cells, caspase-3 activity, death receptor-related molecules (DR5/Fas/FADD) expression and cytochrome c release in heart tissues. The positive control drug nifedipine produced comparable cardioprotective effects in vitro and in vivo. Conclusion: Pretreatment with low-dose GdCl3 significantly attenuates I/R-induced myocardial apoptosis in rats by suppressing activation of both death receptor and mitochondria-mediated pathways. PMID:26948086

  13. 40 CFR 35.907 - Municipal pretreatment program.

    Code of Federal Regulations, 2014 CFR

    2014-07-01

    ... 40 Protection of Environment 1 2014-07-01 2014-07-01 false Municipal pretreatment program. 35.907 Section 35.907 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY GRANTS AND OTHER FEDERAL ASSISTANCE STATE AND LOCAL ASSISTANCE Grants for Construction of Treatment Works-Clean Water Act §...

  14. 40 CFR 35.907 - Municipal pretreatment program.

    Code of Federal Regulations, 2012 CFR

    2012-07-01

    ... 40 Protection of Environment 1 2012-07-01 2012-07-01 false Municipal pretreatment program. 35.907 Section 35.907 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY GRANTS AND OTHER FEDERAL ASSISTANCE STATE AND LOCAL ASSISTANCE Grants for Construction of Treatment Works-Clean Water Act §...

  15. 40 CFR 425.04 - Applicability of sulfide pretreatment standards.

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... 40 Protection of Environment 29 2010-07-01 2010-07-01 false Applicability of sulfide pretreatment standards. 425.04 Section 425.04 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS LEATHER TANNING AND FINISHING POINT SOURCE CATEGORY General...

  16. 40 CFR 405.66 - Pretreatment standards for new sources.

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... introduces process wastewater pollutants into a publicly owned treatment works must comply with 40 CFR part... 40 Protection of Environment 29 2011-07-01 2009-07-01 true Pretreatment standards for new sources. 405.66 Section 405.66 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED)...

  17. 40 CFR 420.48 - Pretreatment standards compliance dates.

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... 40 Protection of Environment 28 2010-07-01 2010-07-01 true Pretreatment standards compliance dates. 420.48 Section 420.48 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS IRON AND STEEL MANUFACTURING POINT SOURCE CATEGORY Steelmaking Subcategory §...

  18. 40 CFR 420.28 - Pretreatment standards compliance dates.

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... 40 Protection of Environment 29 2011-07-01 2009-07-01 true Pretreatment standards compliance dates. 420.28 Section 420.28 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS IRON AND STEEL MANUFACTURING POINT SOURCE CATEGORY Sintering Subcategory §...

  19. 40 CFR 420.18 - Pretreatment standards compliance dates.

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... 40 Protection of Environment 29 2011-07-01 2009-07-01 true Pretreatment standards compliance dates. 420.18 Section 420.18 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS IRON AND STEEL MANUFACTURING POINT SOURCE CATEGORY Cokemaking Subcategory §...

  20. 40 CFR 420.28 - Pretreatment standards compliance dates.

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... 40 Protection of Environment 28 2010-07-01 2010-07-01 true Pretreatment standards compliance dates. 420.28 Section 420.28 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS IRON AND STEEL MANUFACTURING POINT SOURCE CATEGORY Sintering Subcategory §...

  1. 40 CFR 420.18 - Pretreatment standards compliance dates.

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... 40 Protection of Environment 28 2010-07-01 2010-07-01 true Pretreatment standards compliance dates. 420.18 Section 420.18 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS IRON AND STEEL MANUFACTURING POINT SOURCE CATEGORY Cokemaking Subcategory §...

  2. 40 CFR 420.48 - Pretreatment standards compliance dates.

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... 40 Protection of Environment 29 2011-07-01 2009-07-01 true Pretreatment standards compliance dates. 420.48 Section 420.48 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS IRON AND STEEL MANUFACTURING POINT SOURCE CATEGORY Steelmaking Subcategory §...

  3. 40 CFR 406.76 - Pretreatment standards for new sources.

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... 40 Protection of Environment 29 2011-07-01 2009-07-01 true Pretreatment standards for new sources. 406.76 Section 406.76 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS GRAIN MILLS POINT SOURCE CATEGORY Animal Feed Subcategory § 406.76...

  4. 40 CFR 412.3 - General pretreatment standards.

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... 40 Protection of Environment 29 2011-07-01 2009-07-01 true General pretreatment standards. 412.3 Section 412.3 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS CONCENTRATED ANIMAL FEEDING OPERATIONS (CAFO) POINT SOURCE CATEGORY § 412.3...

  5. 40 CFR 406.76 - Pretreatment standards for new sources.

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... 40 Protection of Environment 28 2010-07-01 2010-07-01 true Pretreatment standards for new sources. 406.76 Section 406.76 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS GRAIN MILLS POINT SOURCE CATEGORY Animal Feed Subcategory § 406.76...

  6. 40 CFR 412.3 - General pretreatment standards.

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... 40 Protection of Environment 28 2010-07-01 2010-07-01 true General pretreatment standards. 412.3 Section 412.3 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS CONCENTRATED ANIMAL FEEDING OPERATIONS (CAFO) POINT SOURCE CATEGORY § 412.3...

  7. 40 CFR 428.66 - Pretreatment standards for new sources.

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... 40 Protection of Environment 29 2010-07-01 2010-07-01 false Pretreatment standards for new sources. 428.66 Section 428.66 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS RUBBER MANUFACTURING POINT SOURCE CATEGORY Medium-Sized General Molded,...

  8. 40 CFR 420.18 - Pretreatment standards compliance dates.

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ... 40 Protection of Environment 30 2013-07-01 2012-07-01 true Pretreatment standards compliance dates. 420.18 Section 420.18 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS IRON AND STEEL MANUFACTURING POINT SOURCE CATEGORY Cokemaking Subcategory §...

  9. 40 CFR 420.48 - Pretreatment standards compliance dates.

    Code of Federal Regulations, 2012 CFR

    2012-07-01

    ... 40 Protection of Environment 30 2012-07-01 2012-07-01 false Pretreatment standards compliance dates. 420.48 Section 420.48 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS IRON AND STEEL MANUFACTURING POINT SOURCE CATEGORY...

  10. 40 CFR 420.18 - Pretreatment standards compliance dates.

    Code of Federal Regulations, 2012 CFR

    2012-07-01

    ... 40 Protection of Environment 30 2012-07-01 2012-07-01 false Pretreatment standards compliance dates. 420.18 Section 420.18 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS IRON AND STEEL MANUFACTURING POINT SOURCE CATEGORY Cokemaking...

  11. 40 CFR 420.28 - Pretreatment standards compliance dates.

    Code of Federal Regulations, 2012 CFR

    2012-07-01

    ... 40 Protection of Environment 30 2012-07-01 2012-07-01 false Pretreatment standards compliance dates. 420.28 Section 420.28 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS IRON AND STEEL MANUFACTURING POINT SOURCE CATEGORY Sintering...

  12. 40 CFR 420.18 - Pretreatment standards compliance dates.

    Code of Federal Regulations, 2014 CFR

    2014-07-01

    ... 40 Protection of Environment 29 2014-07-01 2012-07-01 true Pretreatment standards compliance dates. 420.18 Section 420.18 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS IRON AND STEEL MANUFACTURING POINT SOURCE CATEGORY Cokemaking Subcategory §...

  13. 40 CFR 420.28 - Pretreatment standards compliance dates.

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ... 40 Protection of Environment 30 2013-07-01 2012-07-01 true Pretreatment standards compliance dates. 420.28 Section 420.28 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS IRON AND STEEL MANUFACTURING POINT SOURCE CATEGORY Sintering Subcategory §...

  14. 40 CFR 420.28 - Pretreatment standards compliance dates.

    Code of Federal Regulations, 2014 CFR

    2014-07-01

    ... 40 Protection of Environment 29 2014-07-01 2012-07-01 true Pretreatment standards compliance dates. 420.28 Section 420.28 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS IRON AND STEEL MANUFACTURING POINT SOURCE CATEGORY Sintering Subcategory §...

  15. 40 CFR 463.26 - Pretreatment for new sources.

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... 40 Protection of Environment 29 2010-07-01 2010-07-01 false Pretreatment for new sources. 463.26 Section 463.26 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS PLASTICS MOLDING AND FORMING POINT SOURCE CATEGORY Cleaning Water Subcategory §...

  16. 40 CFR 463.16 - Pretreatment standards for new sources.

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... 40 Protection of Environment 29 2010-07-01 2010-07-01 false Pretreatment standards for new sources. 463.16 Section 463.16 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS PLASTICS MOLDING AND FORMING POINT SOURCE CATEGORY Contact Cooling and Heating...

  17. 40 CFR 408.236 - Pretreatment standards for new sources.

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... 40 Protection of Environment 28 2010-07-01 2010-07-01 true Pretreatment standards for new sources. 408.236 Section 408.236 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS CANNED AND PRESERVED SEAFOOD PROCESSING POINT SOURCE CATEGORY Hand-Shucked...

  18. 40 CFR 408.234 - Pretreatment standards for existing sources.

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... 40 Protection of Environment 28 2010-07-01 2010-07-01 true Pretreatment standards for existing sources. 408.234 Section 408.234 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS CANNED AND PRESERVED SEAFOOD PROCESSING POINT SOURCE CATEGORY...

  19. 40 CFR 455.11 - Compliance date for pretreatment standards for existing sources (PSES).

    Code of Federal Regulations, 2014 CFR

    2014-07-01

    ... PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) PESTICIDE CHEMICALS Organic Pesticide Chemicals Manufacturing Subcategory § 455.11 Compliance date for pretreatment standards...

  20. 40 CFR 455.11 - Compliance date for pretreatment standards for existing sources (PSES).

    Code of Federal Regulations, 2012 CFR

    2012-07-01

    ... PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) PESTICIDE CHEMICALS Organic Pesticide Chemicals Manufacturing Subcategory § 455.11 Compliance date for pretreatment standards...

  1. 40 CFR 455.11 - Compliance date for pretreatment standards for existing sources (PSES).

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ... PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) PESTICIDE CHEMICALS Organic Pesticide Chemicals Manufacturing Subcategory § 455.11 Compliance date for pretreatment standards...

  2. Recapitulating maladaptive, multiscale remodeling of failing myocardium on a chip.

    PubMed

    McCain, Megan L; Sheehy, Sean P; Grosberg, Anna; Goss, Josue A; Parker, Kevin Kit

    2013-06-11

    The lack of a robust pipeline of medical therapeutic agents for the treatment of heart disease may be partially attributed to the lack of in vitro models that recapitulate the essential structure-function relationships of healthy and diseased myocardium. We designed and built a system to mimic mechanical overload in vitro by applying cyclic stretch to engineered laminar ventricular tissue on a stretchable chip. To test our model, we quantified changes in gene expression, myocyte architecture, calcium handling, and contractile function and compared our results vs. several decades of animal studies and clinical observations. Cyclic stretch activated gene expression profiles characteristic of pathological remodeling, including decreased α- to β-myosin heavy chain ratios, and induced maladaptive changes to myocyte shape and sarcomere alignment. In stretched tissues, calcium transients resembled those reported in failing myocytes and peak systolic stress was significantly reduced. Our results suggest that failing myocardium, as defined genetically, structurally, and functionally, can be replicated in an in vitro microsystem by faithfully recapitulating the structural and mechanical microenvironment of the diseased heart.

  3. Innate immune inflammatory response in the acutely ischemic myocardium.

    PubMed

    Deftereos, Spyridon; Angelidis, Christos; Bouras, Georgios; Raisakis, Konstantinos; Gerckens, Ulrich; Cleman, Michael W; Giannopoulos, Georgios

    2014-01-01

    The "holy grail" of modern interventional cardiology is the salvage of viable myocardial tissue in the distribution of an acutely occluded coronary artery. Thrombolysis and percutaneous coronary interventions, provided they can be delivered on time, can interrupt the occlusion and save tissue. At the same time restoring the patency of the coronary vessels and providing the ischemic myocardium with blood can cause additional tissue damage. A key element of ischemic and reperfusion injury and major determinant of the evolution of damage in the injured myocardium is the inflammatory response. The innate immune system initiates and directs this response which is a prerequisite for subsequent healing. The complement cascade is set in motion following the release of subcellular membrane constituents. Endogenous 'danger' signals known as danger-associated molecular patterns (DAMPs) released from ischemic and dying cells alert the innate immune system and activate several signal transduction pathways through interactions with the highly conserved Toll like receptors (TLRs). Reactive oxygen species (ROS) generation directly induces pro-inflammatory cascades and triggers formation of the inflammasome. The challenge lies into designing strategies that specifically block the inflammatory cascades responsible for tissue damage without affecting those concerned with tissue healing.

  4. Ramipril-induced delayed myocardial protection against free radical injury involves bradykinin B2 receptor-NO pathway and protein synthesis

    PubMed Central

    Jin, Zhu-Qiu; Chen, Xiu

    1998-01-01

    The aim of the present study was to examine whether ramipril induces delayed myocardial protection against free radical injuries ex vivo and to determine the possible role of the bradykinin B2–nitric oxide (NO) pathway, prostaglandins(PGs) and protein synthesis in this delayed adaptive response.Rats were pretreated with ramipril (10 or 50 μg kg−1, i.v.) and hearts were isolated after 24, 48 and 72 h. Langendorff hearts were subjected to 1,1-diphenyl-2-picryl-hydrazyl (DPPH) free radical-induced injury.Left ventricular developed pressure (LVDP) and its maximal increase velocity (+dP/dtmax), coronary flow (CF), heart rate (HR), lactate dehydrogenase (LDH) in coronary effluent and thiobarbituric acid reactive substances (TBARS) in the myocardium were measured.The results showed that in the DPPH control group, 20 min after free radical-induced injury, LVDP, +dP/dtmax, CF, HR declined, whereas TBARS and LDH increased significantly. The above cardiac function parameters were significantly improved in RAM-pretreated rats after 24 and 48 h.Pretreatment with HOE 140, the selective bradykinin B2 receptor antagonist, NG-nitro-L-arginine, the NO synthase inhibitor, and actinomycin D, the RNA transcription inhibitor, prior to ramipril injection abolished the beneficial effects of ramipril at 24 h while indomethacin, a cyclooxygenase inhibitor, pretreatment had no effect on ramipril-induced delayed protection.In conclusion, ramipril induces delayed myocardial protection against free radical injury in the rat heart. This delayed protection was sustained for 48 h, is associated with the bradykinin B2 receptor–NO pathway and depends on protein but not prostaglandin synthesis. PMID:9806340

  5. Probability mapping of scarred myocardium using texture and intensity features in CMR images

    PubMed Central

    2013-01-01

    Background The myocardium exhibits heterogeneous nature due to scarring after Myocardial Infarction (MI). In Cardiac Magnetic Resonance (CMR) imaging, Late Gadolinium (LG) contrast agent enhances the intensity of scarred area in the myocardium. Methods In this paper, we propose a probability mapping technique using Texture and Intensity features to describe heterogeneous nature of the scarred myocardium in Cardiac Magnetic Resonance (CMR) images after Myocardial Infarction (MI). Scarred tissue and non-scarred tissue are represented with high and low probabilities, respectively. Intermediate values possibly indicate areas where the scarred and healthy tissues are interwoven. The probability map of scarred myocardium is calculated by using a probability function based on Bayes rule. Any set of features can be used in the probability function. Results In the present study, we demonstrate the use of two different types of features. One is based on the mean intensity of pixel and the other on underlying texture information of the scarred and non-scarred myocardium. Examples of probability maps computed using the mean intensity of pixel and the underlying texture information are presented. We hypothesize that the probability mapping of myocardium offers alternate visualization, possibly showing the details with physiological significance difficult to detect visually in the original CMR image. Conclusion The probability mapping obtained from the two features provides a way to define different cardiac segments which offer a way to identify areas in the myocardium of diagnostic importance (like core and border areas in scarred myocardium). PMID:24053280

  6. Observations on the effects of CO/sub 2/-laser on rat myocardium

    SciTech Connect

    Owen, E.R.; Canfield, P.; Bryant, K.; Hopwood, P.R.

    1984-01-01

    The effect of CO/sub 2/-laser burn on rat myocardium was studied to evaluate a hypothesis developed by Mirhoseini and Cayton that infarcted myocardium may be revascularized by establishing an alternative circulation from a ventricle to the coronary arteries by means of laser channels burned through the myocardium. The hearts of 22 rats were examined histologically for a period ranging from a few minutes to 50 days after CO/sub 2/ laser was applied to the myocardium. The laser initiated an intense inflammatory response in the myocardium adjacent to the target site. The authors believe that the inflammatory response, observed in this study to the Biophy-Las 80 surgical laser, must be reduced if laser is to be an effective means of myocardial revascularization.

  7. Investigation of myocardial photodynamic revascularization method on ischemic rat myocardium model

    NASA Astrophysics Data System (ADS)

    Vasilchenko, S. Yu.; Stratonnikov, A. A.; Volkova, A. I.; Loschenov, V. B.; Sheptak, E. A.; Kharnas, S. S.

    2006-08-01

    Ischemic heart disease is one of the leading reasons of invalidisation and death rate of able-bodied citizens in the world. There are many various surgical and medicamentous methods of its treatment for today, however all these methods have restrictions in application. Our work was directed at initiation possibility clarification of ischemic myocardium revascularization by means of making necrosis with photodynamic therapy. The investigation was carried out in rats with the ischemia artificial made by means of left coronary artery ligation. Level of Photosense photosensitizer accumulation in ischemic and normal rat myocardium zones was defined. Myocardial photodynamic revascularization procedure of ischemic rat myocardium was carried out. Morphological analysis of the myocardium preparations showed the presence of active revascularization of ischemic myocardium after photodynamic therapy. The method of ischemia level estimation based on spectral optical definition of blood oxygen saturation was developed.

  8. Protective effects of remote ischemic preconditioning in isolated rat hearts

    PubMed Central

    Teng, Xiao; Yuan, Xin; Tang, Yue; Shi, Jingqian

    2015-01-01

    To use Langendorff model to investigate whether remote ischemic preconditioning (RIPC) attenuates post-ischemic mechanical dysfunction on isolated rat heart and to explore possible mechanisms. SD rats were randomly divided into RIPC group, RIPC + norepinephrine (NE) depletion group, RIPC + pertussis toxin (PTX) pretreatment group, ischemia/reperfusion group without treatment (ischemia group) and time control (TC) group. RIPC was achieved through interrupted occlusion of anterior mesenteric artery. Then, Langendorff model was established using routine methods. Heart function was tested; immunohistochemistry and ELISA methods were used to detect various indices related to myocardial injury. Compared with ischemia group in which the hemodynamic parameters deteriorated significantly, heart function recovered to a certain degree among the RIPC, RIPC + NE depletion, and RIPC + PTX groups (P<0.05). More apoptotic nuclei were observed in ischemia group than in the other three groups (P<0.05); more apoptotic nuclei were detected in NE depletion and PTX groups than in RIPC group (P<0.05). While, there was no significant difference between NE depletion and PTX groups. In conclusion, RIPC protection on I/R myocardium extends to the period after hearts are isolated. NE and PTX-sensitive inhibitory G protein might have a role in the protection process. PMID:26550168

  9. Physical invariant strain energy function for passive myocardium.

    PubMed

    Shariff, M H B M

    2013-04-01

    Principal axis formulations are regularly used in isotropic elasticity, but they are not often used in dealing with anisotropic problems. In this paper, based on a principal axis technique, we develop a physical invariant orthotropic constitutive equation for incompressible solids, where it contains only a one variable (general) function. The corresponding strain energy function depends on six invariants that have immediate physical interpretation. These invariants are useful in facilitating an experiment to obtain a specific constitutive equation for a particular type of materials. The explicit appearance of the classical ground-state constants in the constitutive equation simplifies the calculation for their admissible values. A specific constitutive model is proposed for passive myocardium, and the model fits reasonably well with existing simple shear and biaxial experimental data. It is also able to predict a set of data from a simple shear experiment.

  10. An analysis of the cable properties of frog ventricular myocardium.

    PubMed Central

    Chapman, R A; Fry, C H

    1978-01-01

    1. The passive and active electrical parameters of frog ventricular myocardium have been measured. 2. The cytoplasmic resistivity has been determined by following changes in the resistance of a micro-electrode on penetration of a cell. 3. Unidimensional cable analysis using direct and alternating currents revealed the presence of a single time constant attributed to the surface membrane. 4. Longitudinal impedance measurements indicate that a second time constant is present in the intracellular pathway. 5. The results indicate that the resistance between cells is low so that action potentials can propagate from cell to cell by local circuits. 6. A three-dimensional cable analysis has also been carried out and compared to a simplified mathematical model which is presented in an Appendix and which closely approximates the experimental situation. PMID:309942

  11. Monolayered mesenchymal stem cells repair scarred myocardium after myocardial infarction.

    PubMed

    Miyahara, Yoshinori; Nagaya, Noritoshi; Kataoka, Masaharu; Yanagawa, Bobby; Tanaka, Koichi; Hao, Hiroyuki; Ishino, Kozo; Ishida, Hideyuki; Shimizu, Tatsuya; Kangawa, Kenji; Sano, Shunji; Okano, Teruo; Kitamura, Soichiro; Mori, Hidezo

    2006-04-01

    Mesenchymal stem cells are multipotent cells that can differentiate into cardiomyocytes and vascular endothelial cells. Here we show, using cell sheet technology, that monolayered mesenchymal stem cells have multipotent and self-propagating properties after transplantation into infarcted rat hearts. We cultured adipose tissue-derived mesenchymal stem cells characterized by flow cytometry using temperature-responsive culture dishes. Four weeks after coronary ligation, we transplanted the monolayered mesenchymal stem cells onto the scarred myocardium. After transplantation, the engrafted sheet gradually grew to form a thick stratum that included newly formed vessels, undifferentiated cells and few cardiomyocytes. The mesenchymal stem cell sheet also acted through paracrine pathways to trigger angiogenesis. Unlike a fibroblast cell sheet, the monolayered mesenchymal stem cells reversed wall thinning in the scar area and improved cardiac function in rats with myocardial infarction. Thus, transplantation of monolayered mesenchymal stem cells may be a new therapeutic strategy for cardiac tissue regeneration. PMID:16582917

  12. [Inappropriate preservation of myocardium by topical cooling with iced slush].

    PubMed

    Takeuchi, K; Takashima, K; Munakata, M; Ono, Y; Fukui, K; Suzuki, S; del Nido, P J

    1996-09-01

    Topical cooling with iced slush has been applied as a conventional myocardial preservation in open heart surgery. However, there might be several disadvantages due to topical cooling with iced slush which melted to be liquid, because of membrane integrity decreased during ischemia. To understand more detailed mechanism of deterioration for myocardium by immersion in some liquid during ischemia, we subjected isolated crystalloid perfused rabbit hearts to a 30 minute of ischemia with immersion in Krebs-Henseleit (K-H) solution (I), K-H+hexamethlyamiloride which was Na+/H+ channel blocker (II) and histidine containing cardioplegia (HBS) designed to accelerate anaerobic glycolysis by a proton buffering (III), followed by a 30 minute of reperfusion. These groups were compared to the hearts hanging in air during ischemia (control). Phosphocreatine (PCr), ATP and intracellular pH were measured by 31 PNMR in group I, II, III. Developed pressure (Dev P) and diastolic pressure (EDP) with a intracavitary balloon were also evaluated with monitoring of 2 mmHg diastolic contracture during ischemia. Dev P declined to 46%, 54% of preischemic value in group I and group II, respectively, although % recovery of control heart was 74% after ischemia-reperfusion process. Diastolic function was severely deteriorated in group I and II, as compared to control heart. ATP and intracellular pH showed a similar decline as PCr in group I and II which was not seen in group III during ischemia. HBS prevented the deterioration of PCr, ATP and intracellular pH during ischemia along with excellent recovery of myocardial function. We therefore conclude that 1) significant deterioration of myocardium occurs with ischemia if the heart preserved in Krebs-Heseleit solution and the mechanism of injury by immersion in liquid on the heart appears to be due to proton accumulation caused by intracellular acidification and loss of high energy phosphate. PMID:8911040

  13. Pretreatment methods for bioethanol production.

    PubMed

    Xu, Zhaoyang; Huang, Fang

    2014-09-01

    Lignocellulosic biomass, such as wood, grass, agricultural, and forest residues, are potential resources for the production of bioethanol. The current biochemical process of converting biomass to bioethanol typically consists of three main steps: pretreatment, enzymatic hydrolysis, and fermentation. For this process, pretreatment is probably the most crucial step since it has a large impact on the efficiency of the overall bioconversion. The aim of pretreatment is to disrupt recalcitrant structures of cellulosic biomass to make cellulose more accessible to the enzymes that convert carbohydrate polymers into fermentable sugars. This paper reviews several leading acidic, neutral, and alkaline pretreatments technologies. Different pretreatment methods, including dilute acid pretreatment (DAP), steam explosion pretreatment (SEP), organosolv, liquid hot water (LHW), ammonia fiber expansion (AFEX), soaking in aqueous ammonia (SAA), sodium hydroxide/lime pretreatments, and ozonolysis are intensively introduced and discussed. In this minireview, the key points are focused on the structural changes primarily in cellulose, hemicellulose, and lignin during the above leading pretreatment technologies.

  14. Repetitive stimulation of autophagy-lysosome machinery by intermittent fasting preconditions the myocardium to ischemia-reperfusion injury.

    PubMed

    Godar, Rebecca J; Ma, Xiucui; Liu, Haiyan; Murphy, John T; Weinheimer, Carla J; Kovacs, Attila; Crosby, Seth D; Saftig, Paul; Diwan, Abhinav

    2015-01-01

    Autophagy, a lysosomal degradative pathway, is potently stimulated in the myocardium by fasting and is essential for maintaining cardiac function during prolonged starvation. We tested the hypothesis that intermittent fasting protects against myocardial ischemia-reperfusion injury via transcriptional stimulation of the autophagy-lysosome machinery. Adult C57BL/6 mice subjected to 24-h periods of fasting, every other day, for 6 wk were protected from in-vivo ischemia-reperfusion injury on a fed day, with marked reduction in infarct size in both sexes as compared with nonfasted controls. This protection was lost in mice heterozygous null for Lamp2 (coding for lysosomal-associated membrane protein 2), which demonstrate impaired autophagy in response to fasting with accumulation of autophagosomes and SQSTM1, an autophagy substrate, in the heart. In lamp2 null mice, intermittent fasting provoked progressive left ventricular dilation, systolic dysfunction and hypertrophy; worsening cardiomyocyte autophagosome accumulation and lack of protection to ischemia-reperfusion injury, suggesting that intact autophagy-lysosome machinery is essential for myocardial homeostasis during intermittent fasting and consequent ischemic cardioprotection. Fasting and refeeding cycles resulted in transcriptional induction followed by downregulation of autophagy-lysosome genes in the myocardium. This was coupled with fasting-induced nuclear translocation of TFEB (transcription factor EB), a master regulator of autophagy-lysosome machinery; followed by rapid decline in nuclear TFEB levels with refeeding. Endogenous TFEB was essential for attenuation of hypoxia-reoxygenation-induced cell death by repetitive starvation, in neonatal rat cardiomyocytes, in-vitro. Taken together, these data suggest that TFEB-mediated transcriptional priming of the autophagy-lysosome machinery mediates the beneficial effects of fasting-induced autophagy in myocardial ischemia-reperfusion injury.

  15. Repetitive stimulation of autophagy-lysosome machinery by intermittent fasting preconditions the myocardium to ischemia-reperfusion injury

    PubMed Central

    Godar, Rebecca J; Ma, Xiucui; Liu, Haiyan; Murphy, John T; Weinheimer, Carla J; Kovacs, Attila; Crosby, Seth D; Saftig, Paul; Diwan, Abhinav

    2015-01-01

    Autophagy, a lysosomal degradative pathway, is potently stimulated in the myocardium by fasting and is essential for maintaining cardiac function during prolonged starvation. We tested the hypothesis that intermittent fasting protects against myocardial ischemia-reperfusion injury via transcriptional stimulation of the autophagy-lysosome machinery. Adult C57BL/6 mice subjected to 24-h periods of fasting, every other day, for 6 wk were protected from in-vivo ischemia-reperfusion injury on a fed day, with marked reduction in infarct size in both sexes as compared with nonfasted controls. This protection was lost in mice heterozygous null for Lamp2 (coding for lysosomal-associated membrane protein 2), which demonstrate impaired autophagy in response to fasting with accumulation of autophagosomes and SQSTM1, an autophagy substrate, in the heart. In lamp2 null mice, intermittent fasting provoked progressive left ventricular dilation, systolic dysfunction and hypertrophy; worsening cardiomyocyte autophagosome accumulation and lack of protection to ischemia-reperfusion injury, suggesting that intact autophagy-lysosome machinery is essential for myocardial homeostasis during intermittent fasting and consequent ischemic cardioprotection. Fasting and refeeding cycles resulted in transcriptional induction followed by downregulation of autophagy-lysosome genes in the myocardium. This was coupled with fasting-induced nuclear translocation of TFEB (transcription factor EB), a master regulator of autophagy-lysosome machinery; followed by rapid decline in nuclear TFEB levels with refeeding. Endogenous TFEB was essential for attenuation of hypoxia-reoxygenation-induced cell death by repetitive starvation, in neonatal rat cardiomyocytes, in-vitro. Taken together, these data suggest that TFEB-mediated transcriptional priming of the autophagy-lysosome machinery mediates the beneficial effects of fasting-induced autophagy in myocardial ischemia-reperfusion injury. PMID:26103523

  16. Repetitive stimulation of autophagy-lysosome machinery by intermittent fasting preconditions the myocardium to ischemia-reperfusion injury.

    PubMed

    Godar, Rebecca J; Ma, Xiucui; Liu, Haiyan; Murphy, John T; Weinheimer, Carla J; Kovacs, Attila; Crosby, Seth D; Saftig, Paul; Diwan, Abhinav

    2015-01-01

    Autophagy, a lysosomal degradative pathway, is potently stimulated in the myocardium by fasting and is essential for maintaining cardiac function during prolonged starvation. We tested the hypothesis that intermittent fasting protects against myocardial ischemia-reperfusion injury via transcriptional stimulation of the autophagy-lysosome machinery. Adult C57BL/6 mice subjected to 24-h periods of fasting, every other day, for 6 wk were protected from in-vivo ischemia-reperfusion injury on a fed day, with marked reduction in infarct size in both sexes as compared with nonfasted controls. This protection was lost in mice heterozygous null for Lamp2 (coding for lysosomal-associated membrane protein 2), which demonstrate impaired autophagy in response to fasting with accumulation of autophagosomes and SQSTM1, an autophagy substrate, in the heart. In lamp2 null mice, intermittent fasting provoked progressive left ventricular dilation, systolic dysfunction and hypertrophy; worsening cardiomyocyte autophagosome accumulation and lack of protection to ischemia-reperfusion injury, suggesting that intact autophagy-lysosome machinery is essential for myocardial homeostasis during intermittent fasting and consequent ischemic cardioprotection. Fasting and refeeding cycles resulted in transcriptional induction followed by downregulation of autophagy-lysosome genes in the myocardium. This was coupled with fasting-induced nuclear translocation of TFEB (transcription factor EB), a master regulator of autophagy-lysosome machinery; followed by rapid decline in nuclear TFEB levels with refeeding. Endogenous TFEB was essential for attenuation of hypoxia-reoxygenation-induced cell death by repetitive starvation, in neonatal rat cardiomyocytes, in-vitro. Taken together, these data suggest that TFEB-mediated transcriptional priming of the autophagy-lysosome machinery mediates the beneficial effects of fasting-induced autophagy in myocardial ischemia-reperfusion injury. PMID:26103523

  17. PRETREATING THORIUM FOR ELECTROPLATING

    DOEpatents

    Beach, J.G.; Schaer, G.R.

    1959-07-28

    A method is presented for pretreating a thorium surface prior to electroplating the surface. The pretreatment steps of the invention comprise cleaning by vapor blasting the surface, anodically pickling in a 5 to 15% by volume aqueous hydrochloric acid bath with a current of 125 to 250 amp/sq ft for 3 to 5 min at room temperature, chemically pickling the surface in a 5 to 15% by volume of aqueous sulfuric acid for 3 to 5 min at room temperature, and rinsing the surface with water.

  18. Effect of gadolinium-DTPA on the magnetic relaxation times of normal and infarcted myocardium. [Dogs

    SciTech Connect

    Wesbey, G.E.; Higgins, C.B.; McNamara, M.T.; Engelstad, B.L.; Lipton, M.J.; Sievers, R.; Ehman, R.L.; Lovin, J.; Brasch, R.C.

    1984-10-01

    Acute myocardial infarctions were produced in 11 dogs by ligation of the left anterior descending coronary artery. Twenty-four hours after ligation Gd-DTPA was injected intravenously, followed by cardiectomy either 90 seconds (3 dogs) or 5 minutes (5 dogs) later. The remaining 3 dogs had cardiectomy without injection of Gd-DTPA at 24 hours after coronary occlusion. The 3 dogs that did not receive Gd-DTPA had longer T1 and T2 relaxation times in infarcted myocardium than in normal myocardium. The T1 and T2 relaxation times of normal myocardium at 90 seconds postinjection of Gd-DTPA were significantly shorter than those of the normal myocardium of animals that did not receive Gd-DTPA. At five minutes postinjection, significantly greater T1 shortening was exhibited in the infarcted myocardium compared with adjacent normal myocardium in the dogs injected with Gd-DTPA. Thus, Gd-DTPA has differential and time-varying effects on relaxation times of normal and infarcted myocardium.

  19. The alteration of interelemental ratios in myocardium under the congenital heart disease (SRXRF)

    NASA Astrophysics Data System (ADS)

    Trunova, V. A.; Zvereva, V. V.; Okuneva, G. N.; Levicheva, E. N.

    2007-05-01

    It is the myocardium that bears the basic functional loading during heart working, including muscle contractility and enzyme activity. The elemental concentrations in myocardium tissue of heart were determined by SRXRF technique. Our investigation is systematical: the elemental content in each compartment (left and right ventricles, left and right auricles) of hearts of healthy and diseased children (congenital heart diseases, transposition of main vessels (TMV)) was analyzed. The elemental distribution in myocardium of four heart chambers of human fetuses was also analyzed. Following elements were determined: S, Cl, K, Ca, Cr, Mn, Fe, Ni, Cu, Zn, As, Se, Br, Rb, Sr. It was revealed that the elemental concentrations in myocardium of both ventricles are almost constant in heart of fetuses and healthy children. The transition from pre-natal study (fetus) to post-natal study is accompanied by the redistribution of chemical elements in myocardium. The higher concentrations of S, Fe, Ca, Sr and Cu in myocardium of children are observed, the content of K, Br, Rb and especially Se is lower than in heart of fetuses. The elemental distribution in myocardium of children TMV is considerably different in comparison with the healthy children: the higher levels of Cu are observed. The content of Se is lower.

  20. [Blood supply of the compact and spongy myocardium of fish, amphibia and reptiles].

    PubMed

    Romenskiĭ, O Iu

    1978-07-01

    Coronal arteries were injected with lead carbonate suspension and with Indian ink and cleared preparations 150--300 mkm thick were made in 195 hearts of fish, amphibians and reptiles and studied roentgenographically. It was stated that in Chondrichthyes (shark, skate) and in Chondrostei (beluga, stellate sturgeon, sturgeon), as well as in alligator both compact and spongy myocardium of the cardiac ventricle possess blood vessels. In teleostei, amphibians and reptiles (except alligator) spongy myocardium is avascular and receives its nutrition from the ventricle. In view of the data on the presence of blood vessels in the spongy myocardium in some vertebrates, it is impossible to accept the theory suggested by Grant and Regnier according to which vessels in the heart walls appear only in connection with compactization of the myocardium. Vascularization of the spongy myocardium is closely connected with oxygen saturation of the blood flowing through the heart. When this saturation is not satisfactory, the spongy myocardium has blood vessels. In alligator, vascularization of the spongy myocardium is connected with the fact that the heart has four chambers and there are arterial and venous blood streams.

  1. [Four-week simulated weightlessness increases the expression of atrial natriuretic peptide in the myocardium].

    PubMed

    Zhang, Wen-Cheng; Lu, Yuan-Ming; Yang, Huai-Zhang; Xu, Peng-Tao; Chang, Hui; Yu, Zhi-Bin

    2013-04-25

    One of the major circulatory changes that occur in human during space flight and simulated weightlessness is a cerebral redistribution of body fluids, which is accompanied by an increase of blood volume in the upper body. Therefore, atrial myocardium should increase the secretion of atrial natriuretic peptide (ANP), but the researches lack common conclusion until now. The present study was to investigate the expression level of ANP in simulated weightlessness rats, and to confirm the changes of ANP by observing the associated proteins of soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNAREs). The tail-suspended rat model was used to simulate weightlessness. Western blots were carried out to examine the expression levels of ANP and SNARE proteins in atrial and left ventricular myocardium. The results showed that ANP expression in atrial myocardium showed an increase in 4-week tail-suspended rats (SUS) compared with that in the synchronous control rats (CON). We only detected a trace amount of ANP in the left ventricular myocardium of the CON, but found an enhanced expression of ANP in left ventricular myocardium of the SUS. Expression of VAMP-1/2 (vesicle associated SNARE) increased significantly in both atrial and left ventricular myocardium in the SUS compared with that in the CON. There was no difference of the expression of syntaxin-4 (target compartment associated SNARE) between the CON and SUS, but the expression of SNAP-23 showed an increase in atrial myocardium of the SUS compared with that in the CON. Synip and Munc-18c as regulators of SNAREs did not show significant difference between the CON and SUS. These results suggest that the expression of ANP shows an increase in atrial and left ventricular myocardium of 4-week tail-suspended rats. Enhanced expression of VAMP-1/2 associated with ANP vesicles confirms the increased expression of ANP in atrial and left ventricular myocardium.

  2. Erythropoietin protects myocardin-expressing cardiac stem cells against cytotoxicity of tumor necrosis factor-{alpha}

    SciTech Connect

    Madonna, Rosalinda; Shelat, Harnath; Xue, Qun; Willerson, James T.; De Caterina, Raffaele; Geng, Yong-Jian

    2009-10-15

    Cardiac stem cells are vulnerable to inflammation caused by infarction or ischemic injury. The growth factor, erythropoietin (Epo), ameliorates the inflammatory response of the myocardium to ischemic injury. This study was designed to assess the role of Epo in regulation of expression and activation of the cell death-associated intracellular signaling components in cardiac myoblasts stimulated with the proinflammatory cytokine tumor necrosis factor (TNF)-{alpha}. Cardiac myoblasts isolated from canine embryonic hearts characterized by expression of myocardin A, a promyogenic transcription factor for cardiovascular muscle development were pretreated with Epo and then exposed to TNF-{alpha}. Compared to untreated cells, the Epo-treated cardiac myoblasts exhibited better morphology and viability. Immunoblotting revealed lower levels of active caspase-3 and reductions in iNOS expression and NO production in Epo-treated cells. Furthermore, Epo pretreatment reduced nuclear translocation of NF-{kappa}B and inhibited phosphorylation of inhibitor of kappa B (I{kappa}B) in TNF-{alpha}-stimulated cardiac myoblasts. Thus, Epo protects cardiac myocyte progenitors or myoblasts against the cytotoxic effects of TNF-{alpha} by inhibiting NF-{kappa}B-mediated iNOS expression and NO production and by preventing caspase-3 activation.

  3. Helium-induced cardioprotection of healthy and hypertensive rat myocardium in vivo.

    PubMed

    Oei, Gezina T M L; Huhn, Ragnar; Heinen, Andre; Hollmann, Markus W; Schlack, Wolfgang S; Preckel, Benedikt; Weber, Nina C

    2012-06-01

    Helium protects healthy myocardium against ischemia/reperfusion injury by early and late preconditioning (EPC, LPC) and postconditioning (PostC). We investigated helium-induced PostC of the hypertensive heart and enhancement by addition of LPC and EPC. We also investigated involvement of signaling kinases glycogen synthase kinase 3 beta (GSK-3β) and protein kinase C-epsilon (PKC-ε). To assess myocardial cell damage, we performed infarct size measurements in healthy Wistar Kyoto (WKY rats, n=8-9) and Spontaneous Hypertensive rats (SHR, n=8-9) subjected to 25 min ischemia and 120 min reperfusion. Rats inhaled 70% helium for 15 min after index ischemia (PostC), combined with 15 min helium 24h prior to index ischemia (LPC+PostC), a triple intervention with additional 3 short cycles of 5 min helium inhalation shortly before ischemia (EPC+LPC+PostC), or no further treatment. In WKY rats, PostC reduced infarct size from 46 ± 2% (mean ± S.E.M) in the control group to 29 ± 2%. LPC+PostC or EPC+LPC+PostC reduced infarct sizes to a similar extent (30 ± 3% and 32 ± 2% respectively). In SHR, EPC+LPC+PostC reduced infarct size from 53 ± 3% in control to 39 ± 3%, while PostC or LPC+PostC alone were not protective; infarct size 48 ± 4% and 44 ± 4%, respectively. Neither PostC in WKY rats nor EPC+LPC+PostC in SHR was associated with an increase in phosphorylation of GSK-3β and PKC-ε after 15 min of reperfusion. Concluding, a triple intervention of helium conditioning results in cardioprotection in SHR, whereas a single intervention does not. In WKY rats, the triple intervention does not further augment protection. Helium conditioning is not associated with a mechanism involving GSK-3β and PKC-ε.

  4. 40 CFR 421.65 - Pretreatment standards for existing sources.

    Code of Federal Regulations, 2014 CFR

    2014-07-01

    ... sources. 421.65 Section 421.65 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS NONFERROUS METALS MANUFACTURING POINT SOURCE CATEGORY Secondary Copper Subcategory § 421.65 Pretreatment standards for existing sources. Except as provided in 40 CFR 403.7 and...

  5. PROJECT W-551 INTERIM PRETREATMENT SYSTEM PRECONCEPTUAL CANDIDATE TECHNOLOGY DESCRIPTIONS

    SciTech Connect

    MAY TH

    2008-08-12

    The Office of River Protection (ORP) has authorized a study to recommend and select options for interim pretreatment of tank waste and support Waste Treatment Plant (WTP) low activity waste (LAW) operations prior to startup of all the WTP facilities. The Interim Pretreatment System (IPS) is to be a moderately sized system which separates entrained solids and 137Cs from tank waste for an interim time period while WTP high level waste vitrification and pretreatment facilities are completed. This study's objective is to prepare pre-conceptual technology descriptions that expand the technical detail for selected solid and cesium separation technologies. This revision includes information on additional feed tanks.

  6. Bisoprolol improves perfusion of ischaemic myocardium in anaesthetized pigs.

    PubMed Central

    Sassen, L. M.; den Boer, M. O.; Rensen, R. J.; Saxena, P. R.; Verdouw, P. D.

    1988-01-01

    1. The ability of the cardioselective beta-adrenoceptor antagonist bisoprolol ((+/-)-1-[4-(2-isopropoxyethoxymethyl)-phenoxy]-3-isopropyl-amino -2-propanol hemifumarate, EMD 33512) to suppress isoprenaline-induced increases in heart rate and maximal rate of rise in left ventricular pressure (LVdP/dtmax) was studied in 6 anaesthetized pigs given 4 cumulative doses (16, 64, 256 and 1024 micrograms kg-1). Bisoprolol was about 2 times more effective in suppressing isoprenaline-induced increases in LVdP/dtmax than those in heart rate. 2. In 8 animals which had a partial stenosis of the left anterior descending coronary artery (LADCA), the effects of 3 consecutive doses (50, 200 and 750 micrograms kg-1) of bisoprolol were studied on systemic haemodynamics, regional myocardial perfusion and function. The effects of the drug were compared with those obtained in a group of 9 animals with LADCA stenosis which did not receive any treatment. 3. The lowest dose of bisoprolol (50 micrograms kg-1) increased perfusion of the ischaemic myocardium (which had been reduced from 123 +/- 20 ml min-1 100 g-1 to 42 +/- 11 ml min-1 100 g-1) by 21 +/- 10 ml min-1 100 g-1 (P less than 0.05). In particular the subendocardial layers, which were most severely affected by the stenosis (a decrease from 128 +/- 19 ml min-1 100 g-1 to 20 +/- 6 ml min-1 100 g-1) benefited from the administration of the drug (an increase of 30 +/- 10 ml min-1 100 g-1). Perfusion of the subepicardium was not significantly affected. With the higher dose only a minor additional improvement in perfusion of the ischaemic myocardium was observed. 4. The negative chronotropic response is the most likely factor leading to the improvement in perfusion. 5. Myocardial wall thickening, which decreased from 41 +/- 2% to 9 +/- 4% (P less than 0.05) due to the hypoperfusion, did not improve after administration of the drug. This lack of improvement may possibly be due to the duration of ischaemia before and the magnitude of the

  7. Stress and vitamin D: altered vitamin D metabolism in both the hippocampus and myocardium of chronic unpredictable mild stress exposed rats.

    PubMed

    Jiang, Pei; Zhang, Wen-Yuan; Li, Huan-De; Cai, Hua-Lin; Liu, Yi-Ping; Chen, Lin-Yao

    2013-10-01

    Exposure to stressful life events is associated with the onset of major depression and increases the risk of cardiac morbidity and mortality. While recent evidence has indicated the existence of an interrelationship between local vitamin D (VD) metabolism and many aspects of human physiology including brain and heart function, much is still unknown concerning the biological link between VD signaling and stress-induced depressive behavior and cardiac dysfunction. In the present study, we observed the VD intracrine system in the hippocampus and myocardium of chronic unpredictable mild stress (CUMS) exposed rats. After 4 weeks of CUMS procedure, rats were induced to a depressive-like state and the cytochromes P450 enzymes involved in VD activating and catabolizing (CYP27B1 and CYP24A1 respectively) and VD receptor (VDR) were assessed by real time RT-PCR and western blot in the hippocampus, myocardium and kidney. In the hippocampus of depressed rats, CYP27B1, CYP24A1 and VDR expression were significantly increased and the local status of 1,25-dihydroxyvitamin D (1,25(OH)2D) was higher compared with controls. Furthermore, hippocampal mRNA levels of VD target genes (calbindin-d28k, neurotrophin-3) and RXRα (heterodimeric partner of VDR) were upregulated in response to chronic stress. Similar to the hippocampus, CUMS also induced CYP27B1/CYP24A1/VDR expression in the myocardium. However, renal metabolism of VD and serum1,25(OH)2D status were unchanged. Meanwhile, sertraline treatment could partly normalize the stress-induced alterations of VD metabolism. In conclusion, this study firstly showed a co-elevated expression of CYP27B1/CYP24A1/VDR in both the hippocampus and myocardium of CUMS rats, which suggests VD signaling may be involved in the compensatory mechanism that protect from stress-induced deteriorating effects on the brain and heart.

  8. Regional left ventricular filling: Does it reflect diastolic abnormalities in contiguous areas of myocardium

    SciTech Connect

    Brown, E.J. Jr.; Idoine, J.; Swinford, R.D.; Pollack, W.M.; Lawson, W.E.; Shatkin, B.; Oster, Z.H.; Atkins, H.L.; Cohn, P.F.

    1989-02-01

    To test the hypothesis that regional left ventricular filling reflects diastolic changes in contiguous areas of myocardium, we performed radionuclide ventriculograms on normal subjects, patients with left anterior descending coronary artery disease, and patients with anteroseptal myocardial infarctions. We reasoned that because diastolic properties of the anteroseptal myocardium should be different in the three groups of patients, regional filling in the anteroseptal area of the left ventricle should also be different, if regional filling does, indeed, reflect diastolic changes in the adjacent myocardium. While anteroseptal regional filling in the normal subjects was different than regional filling in the two patient groups, the degree of filling abnormality was similar in patients with and without myocardial infarctions. Our results suggest that regional left ventricular filling is not exclusively determined by diastolic changes in contiguous areas of myocardium.

  9. Nonhazardous Urine Pretreatment Method

    NASA Technical Reports Server (NTRS)

    Akse, James R.; Holtsnider, John T.

    2012-01-01

    A method combines solid phase acidification with two non-toxic biocides to prevent ammonia volatilization and microbial proliferation. The safe, non-oxidizing biocide combination consists of a quaternary amine and a food preservative. This combination has exhibited excellent stabilization of both acidified and unacidified urine. During pretreatment tests, composite urine collected from donors was challenged with a microorganism known to proliferate in urine, and then was processed using the nonhazardous urine pre-treatment method. The challenge microorganisms included Escherichia coli, a common gram-negative bacteria; Enterococcus faecalis, a ureolytic gram-positive bacteria; Candida albicans, a yeast commonly found in urine; and Aspergillus niger, a problematic mold that resists urine pre-treatment. Urine processed in this manner remained microbially stable for over 57 days. Such effective urine stabilization was achieved using non-toxic, non-oxidizing biocides at higher pH (3.6 to 5.8) than previous methods in use or projected for use aboard the International Space Station (ISS). ISS urine pretreatment methods employ strong oxidants including ozone and hexavalent chromium (Cr(VI)), a carcinogenic material, under very acidic conditions (pH = 1.8 to 2.4). The method described here offers a much more benign chemical environment than previous pretreatment methods, and will lower equivalent system mass (ESM) by reducing containment volume and mass, system complexity, and crew time needed to handle pre-treatment chemicals. The biocides, being non-oxidizing, minimize the potential for chemical reactions with urine constituents to produce volatile, airborne contaminants such as cyanogen chloride. Additionally, the biocides are active under significantly less acidic conditions than those used in the current system, thereby reducing the degree of required acidification. A simple flow-through solid phase acidification (SPA) bed is employed to overcome the natural buffering

  10. 40 CFR 403.11 - Approval procedures for POTW pretreatment programs and POTW granting of removal credits.

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... 40 Protection of Environment 29 2011-07-01 2009-07-01 true Approval procedures for POTW pretreatment programs and POTW granting of removal credits. 403.11 Section 403.11 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS GENERAL PRE-TREAT-MENT...

  11. Coagulating activity of the blood, vascular wall, and myocardium under hypodynamia conditions

    NASA Technical Reports Server (NTRS)

    Petrovskiy, B. V. (Editor); Chazov, E. I. (Editor); Andreyev, S. V. (Editor)

    1980-01-01

    In order to study the effects of hypodynamia on the coagulating properties of the blood, vascular wall, and myocardium, chinchilla rabbits were kept for varying periods in special cages which restricted their movements. At the end of the experiment, blood samples were taken and the animals were sacrificed. Preparations were made from the myocardium venae cavae, and layers of the aorta. Two resultant interrelated and mutually conditioned syndromes were discovered: thrombohemorrhagic in the blood and hemorrago-thrombotic in the tissues.

  12. Remodeling of the myocardium in early trabeculation and cardiac valve formation; a role for TGFβ2.

    PubMed

    Kruithof, Boudewijn P T; Kruithof-De-Julio, Marianna; Poelmann, Robert E; Gittenberger-De-Groot, Adriana C; Gaussin, Vinciane; Goumans, Marie-José

    2013-01-01

    Trabeculation and the formation of the leaflets of the mitral and tricuspid valves both involve remodeling of the embryonic myocardium. The nature and possible connection of these myocardial remodeling processes, however, are unclear. Therefore, we examined the morphogenesis of the early ventricular and atrioventricular (AV) myocardium and report for the first time that the formation of the early trabeculae and the positioning of the valve primordia (endocardial cushions) into the ventricular lumen are part of one continuous myocardial remodeling process, which involves the dissociation of the myocardial layers. For the endocardial cushions, this process results in delamination from the AV myocardium. The AV myocardium that will harbor the right lateral cushion is the exception and becomes positioned in the ventricular lumen by folding of the right ventricle. As a consequence, remodeling of the left and right AV myocardium occurs differently with implications for the formation of the mural leaflets and annulus fibrosis. At both the right and left side, the valvular myocardium harbors a distinct molecular phenotype and its removal from the cardiac leaflets involves a second wave of delamination. Interestingly, in the TGFβ2-KO mouse, which is a known model for cushion and valve defects, remodeling of the early myocardium is disturbed as indicated by defective trabeculae formation, persistence of valvular myocardium, disturbed myocardial phenotypes and differential defects at left and right side of the AV canal. Based on these results we propose a new model clarifying early trabeculae formation and AV valve formation and provide new inroads for an enhanced understanding of congenital heart defects.

  13. Probing myocardium biomechanics using quantitative optical coherence elastography

    NASA Astrophysics Data System (ADS)

    Wang, Shang; Lopez, Andrew L.; Morikawa, Yuka; Tao, Ge; Li, Jiasong; Larina, Irina V.; Martin, James F.; Larin, Kirill V.

    2015-03-01

    We present a quantitative optical coherence elastographic method for noncontact assessment of the myocardium elasticity. The method is based on shear wave imaging optical coherence tomography (SWI-OCT), where a focused air-puff system is used to induce localized tissue deformation through a low-pressure short-duration air stream and a phase-sensitive OCT system is utilized to monitor the propagation of the induced tissue displacement with nanoscale sensitivity. The 1-D scanning of M-mode OCT imaging and the application of optical phase retrieval and mapping techniques enable the reconstruction and visualization of 2-D depth-resolved shear wave propagation in tissue with ultra-high frame rate. The feasibility of this method in quantitative elasticity measurement is demonstrated on tissue-mimicking phantoms with the estimated Young's modulus compared with uniaxial compression tests. We also performed pilot experiments on ex vivo mouse cardiac muscle tissues with normal and genetically altered cardiomyocytes. Our results indicate this noncontact quantitative optical coherence elastographic method can be a useful tool for the cardiac muscle research and studies.

  14. Robust left ventricular myocardium segmentation for multi-protocol MR

    NASA Astrophysics Data System (ADS)

    Groth, A.; Weese, J.; Lehmann, H.

    2012-02-01

    For a number of cardiac procedures like the treatments of ventricular tachycardia (VT), coronary artery disease (CAD) and heart failure (HF) both anatomical as well as vitality information about the left ventricular myocardium are required. To this end, two images for the anatomical and functional information, respectively, must be acquired and analyzed, e.g. using two different 3D MR protocols. To enable automatic analysis, a workflow has been proposed1 which allows to integrate the vitality information extracted from the functional image data into a patient-specific anatomical model generated from the anatomical image. However, in the proposed workflow the extraction of accurate vitality information from the functional image depends to a large extend on the accuracy of both the anatomical model and the mapping of the model to the functional image. In this paper we propose and evaluate methods for improving these two aspects. More specifically, on one hand we aim to improve the segmentation of the often low-contrast left ventricular epicardium in the anatomical 3D MR images by introducing a patient-specific shape-bias. On the other hand, we introduce a registration approach that facilitates the mapping of the anatomical model to images acquired by different protocols and modalities, such as functional 3D MR. The new methods are evaluated on clinical MR data, for which considerable improvements can be achieved.

  15. Biochemical and subcellular distribution of arachidonic acid in rat myocardium

    SciTech Connect

    Miyazaki, Y.; Gross, R.W.; Sobel, B.E.; Saffitz, J.E. )

    1987-12-01

    Selective release of arachidonic acid from prelabeled phospholipid pools has been observed following exposure of neonatal rat cardiac myocytes to metabolic inhibitors in vitro and has been correlated temporally with the development of irreversible sarcolemmal damage. Hydrolysis of phospholipids with release of arachidonic acid may be an important mechanism in the pathogenesis of sarcolemmal damage induced by ischemia. To elucidate potential subcellular loci of arachidonic acid release in ischemic myocardium, the authors characterized the phospholipid composition of adult rat myocardial sarcolemma and delineated the biochemical and subcellular distribution of radiolabeled arachidonic acid in neonatal rat myocytes incubated with ({sup 3}H)-arachidonic acid for selected intervals. Radioactivity was located almost exclusively in mitochondria and internal cytoplasmic membranes (primarily sarcoplasmic reticulum), which collectively contained 90% of myocyte radioactivity. These results indicate that radiolabeled arachidonic acid released from prelabeled phospholipid pools on exposure of neonatal rat myocytes to oxidative inhibitors is derived from mitochondria and internal cell membranes. The diminutive labeling of the sarcolemma suggests that turnover of arachidonoyl phospholipids is slower in the sarcolemma than in other membranous organelles.

  16. Using Gabor filter banks and temporal-spatial constraints to compute 3D myocardium strain.

    PubMed

    Chen, Ting; Axel, Leon

    2006-01-01

    In this paper, we describe a new approach for reconstructing 3D strains in the myocardium using tagged MR images. We first segment the myocardium using a 3D deformable model driven by image gradients and Gabor filter responses. Tags are automatically detected and tracked as deformable thin plates during systole and early diastole. To keep the tracking results more stable and consistent, we use a combination of gradient information, an intensity probabilistic model, the phase information, and a temporal-spatial smoothness constraint. Based on the tag deformation, we compute a dense displacement in the myocardium around both ventricles. The displacements in x-, y-, and z- directions are calculated separately and are combined to form the final displacement maps. We do not use the information outside the segmented surface of the myocardium to avoid displacement errors caused by noises, artifacts, and correlations between different regions in the myocardium. The strain in the myocardium during the heart cycle is derived from the displacement. This method accepts images of either a tag grid or separate horizontal and vertical tag lines as its input. Experimental results on phantom and real data demonstrate good performance of this method in calculating the myocardial strain.

  17. Biomass shock pretreatment

    DOEpatents

    Holtzapple, Mark T.; Madison, Maxine Jones; Ramirez, Rocio Sierra; Deimund, Mark A.; Falls, Matthew; Dunkelman, John J.

    2014-07-01

    Methods and apparatus for treating biomass that may include introducing a biomass to a chamber; exposing the biomass in the chamber to a shock event to produce a shocked biomass; and transferring the shocked biomass from the chamber. In some aspects, the method may include pretreating the biomass with a chemical before introducing the biomass to the chamber and/or after transferring shocked biomass from the chamber.

  18. Structure and vascularization of the ventricular myocardium in Holocephali: their evolutionary significance.

    PubMed

    Durán, Ana C; López-Unzu, Miguel A; Rodríguez, Cristina; Fernández, Borja; Lorenzale, Miguel; Linares, Andrea; Salmerón, Francisca; Sans-Coma, Valentín

    2015-06-01

    It was generally assumed that the ventricle of the primitive vertebrate heart was composed of trabeculated, or spongy, myocardium, supplied by oxygen-poor luminal blood. In addition, it was presumed that the mixed ventricular myocardium, consisting of a compacta and a spongiosa, and its supply through coronary arteries appeared several times throughout fish evolution. Recent work has suggested, however, that a fully vascularized, mixed myocardium may be the primitive condition in gnathostomes. The present study of the heart ventricles of four holocephalan species aimed to clarify this controversy. Our observations showed that the ventricular myocardium of Chimaera monstrosa and Harriotta raleighana consists of a very thin compacta overlying a widespread spongiosa. The ventricle of Hydrolagus affinis is composed exclusively of trabeculated myocardium. In these three species there is a well-developed coronary artery system. The main coronary artery trunks run along the outflow tract, giving off subepicardial ventricular arteries. The trabeculae of the spongiosa are irrigated by branches of the subepicardial arteries and by penetrating arterial vessels arising directly from the main coronary trunks at the level of the conoventricular junction. The ventricle of Rhinochimaera atlantica has only spongy myocardium supplied by luminal blood. Small coronary arterial vessels are present in the subepicardium, but they do not enter the myocardial trabeculae. The present findings show for the first time that in a wild living vertebrate species, specifically H. affinis, an extensive coronary artery system supplying the whole cardiac ventricle exists in the absence of a well-developed compact ventricular myocardium. This is consistent with the notion derived from experimental work that myocardial cell proliferation and coronary vascular growth rely on distinct developmental programs. Our observations, together with data in the literature on elasmobranchs, support the view that

  19. [The action of short-range low-intensity infrared laser irradiation on the functional and metabolic parameters of the isolated rat myocardium in hypoxia].

    PubMed

    Luk'ianova, L D; Denisov, I M; Zamula, S V; Meller, S M

    1991-03-01

    It was found that infrared laser radiation (IRL) reduces the sparing action of acute hypoxia on ventricular transport function of low-resistant animals and accelerates the recovery of the function during the post-hypoxia period. The effect was caused by the IRL affecting directly the speed of perfusion through the myocardium and thus the latter's breathing rate. The protective effect of the IRL was practically absent in highly resistant animals, which may be indicative of the existence of basic differences in the regulatory systems which is responsible for local vasodilation and supply of oxygen to cells, and which participates in the formation of resistance of cardiomyocytes to oxygen shortage.

  20. Urine Pretreat Injection System

    NASA Technical Reports Server (NTRS)

    1995-01-01

    A new method of introducing the OXONE (Registered Trademark) Monopersulfate Compound for urine pretreat into a two-phase urine/air flow stream has been successfully tested and evaluated. The feasibility of this innovative method has been established for purposes of providing a simple, convenient, and safe method of handling a chemical pretreat required for urine processing in a microgravity space environment. Also, the Oxone portion of the urine pretreat has demonstrated the following advantages during real time collection of 750 pounds of urine in a Space Station design two-phase urine Fan/Separator: Eliminated urine precipitate buildup on internal hardware and plumbing; Minimized odor from collected urine; and Virtually eliminated airborne bacteria. The urine pretreat, as presently defined for the Space Station program for proper downstream processing of urine, is a two-part chemical treatment of 5.0 grams of Oxone and 2.3 ml of H2SO4 per liter of urine. This study program and test demonstrated only the addition of the proper ratio of Oxone into the urine collection system upstream of the Fan/Separator. This program was divided into the following three major tasks: (1) A trade study, to define and recommend the type of Oxone injection method to pursue further; (2) The design and fabrication of the selected method; and (3) A test program using high fidelity hardware and fresh urine to demonstrate the method feasibility. The trade study was conducted which included defining several methods for injecting Oxone in different forms into a urine system. Oxone was considered in a liquid, solid, paste and powered form. The trade study and the resulting recommendation were presented at a trade study review held at Hamilton Standard on 24-25 October 94. An agreement was reached at the meeting to continue the solid tablet in a bag concept which included a series of tablets suspended in the urine/air flow stream. These Oxone tablets would slowly dissolve at a controlled rate

  1. Increased expression of Dock180 protein in the noninfarcted myocardium in rats.

    PubMed

    Liu, Xiao-Lan; Li, Gang; Wang, Zhi-Hua; Zhao, Wen-Ju; Wang, Li-Ping

    2013-03-01

    The integrin β1 subunit and its downstream molecule focal adhesion kinase have been identified as critical molecules for the inhibition of postinfarction cardiac remodeling, ischemic cardiomyopathy, and heart failure. However, as a component of the integrin pathway, it is still unclear whether Dock180 (dedicator of cytokinesis 1) protein is expressed in the noninfarcted myocardium of the peri-infarct zones. In this study, experimental myocardial infarction (MI) and sham-operation (sham) models were established in Sprague Dawley rats and the expression of Dock180 protein in the myocardium of the sham group and in the noninfarcted myocardium of the peri-infarct zones of the MI group was detected by Western blot technique. The Dock180 protein expression in the myocardium was as follows: postsham 24-hour group, 0.10 ± 0.04 (n = 8); post-MI 24-hour group, 0.13 ± 0.03 (n = 8); postsham 12-week group, 0.11 ± 0.05 (n = 8); and post-MI 12-week group 0.17 ± 0.04 (n = 8). The Dock180 protein expression in the myocardium in the post-MI 12-week group was significantly higher than that in the postsham 12-week group (p = 0.019), in the postsham 24-hour group (p = 0.004), and in the post-MI 24-hour group (p = 0.040). We conclude that Dock180 protein is expressed in the myocardium in rats. Furthermore, its expression is significantly increased in the noninfarcted myocardium of the peri-infarct zones.

  2. Distinct microRNA expression signatures in human right atrial and ventricular myocardium.

    PubMed

    Zhang, Yangyang; Wang, Xiaowei; Xu, Xiaohan; Wang, Jun; Liu, Xiang; Chen, Yijiang

    2012-12-01

    Human atrial and ventricular myocardium has distinct structure and physiology. MicroRNAs (miRNAs) are the central players in the regulation of gene expression, participating in many physiological processes. A comprehensive knowledge of miRNA expression in the human heart is essential for the understanding of myocardial function. The aim of this study was to compare the miRNA signature in human right atrial and ventricular myocardium. Agilent human miRNA arrays were used to indicate the miRNA expression signatures of the right atrial (n = 8) and ventricular (n = 9) myocardium of healthy individuals. Quantitative reverse transcription-polymerase chain reactions (qRT-PCRs) were used to validate the array results. DIANA-mirPath was used to incorporate the miRNAs into pathways. MiRNA arrays showed that 169 miRNAs were expressed at different levels in human right atrial and ventricular myocardium. The unsupervised hierarchical clustering analysis based on the 169 dysregulated miRNAs showed that miRNA expression categorized two well-defined clusters that corresponded to human right atrial and ventricular myocardium. The qRT-PCR results correlated well with the microarray data. Bioinformatic analysis indicated the potential miRNA targets and molecular pathways. This study indicates that distinct miRNA expression signatures in human right atrial and ventricular myocardium. The findings provide a novel understanding of the molecular differences between human atrial and ventricular myocardium and may establish a framework for an anatomically detailed evaluation of cardiac function regulation.

  3. Harnessing the potential of ligninolytic enzymes for lignocellulosic biomass pretreatment.

    PubMed

    Masran, Ruqayyah; Zanirun, Zuraidah; Bahrin, Ezyana Kamal; Ibrahim, Mohamad Faizal; Lai Yee, Phang; Abd-Aziz, Suraini

    2016-06-01

    Abundant lignocellulosic biomass from various industries provides a great potential feedstock for the production of value-added products such as biofuel, animal feed, and paper pulping. However, low yield of sugar obtained from lignocellulosic hydrolysate is usually due to the presence of lignin that acts as a protective barrier for cellulose and thus restricts the accessibility of the enzyme to work on the cellulosic component. This review focuses on the significance of biological pretreatment specifically using ligninolytic enzymes as an alternative method apart from the conventional physical and chemical pretreatment. Different modes of biological pretreatment are discussed in this paper which is based on (i) fungal pretreatment where fungi mycelia colonise and directly attack the substrate by releasing ligninolytic enzymes and (ii) enzymatic pretreatment using ligninolytic enzymes to counter the drawbacks of fungal pretreatment. This review also discusses the important factors of biological pretreatment using ligninolytic enzymes such as nature of the lignocellulosic biomass, pH, temperature, presence of mediator, oxygen, and surfactant during the biodelignification process. PMID:27115758

  4. [Possible reasons for the variability of the inotropic insulin effect in papillary muscles of ground squirrel myocardium].

    PubMed

    Nakipova, O V; Chumaeva, L A; Andreeva, L A; Anufriev, A I; Kukushkin, N I

    2012-01-01

    The effects of insulin (0.1-50 nM) on isometric twitch force (0.1 to 1.0 Hz; 30 +/- 1 degree C; 1.8 mM Ca(2+)) were studied in right ventricular papillary muscles from active ground squirrels of different seasons (summer, n = 14; autumn, n = 16 and winter interbout, n = 16) in control conditions and after one-hour pretreatment of PM with 2 mkM nifedipine (an L-type Ca(2+)-channel inhibitor) and 1.0 mM orthovanadate (a tyrosine phosphatase inhibitor). In active animals of different seasonal periods insulin causes both positive and negative inotropic effects. At low frequencies (0.1-0.5 Hz), insulin of low concentrations (0.1-1.0 nM) induces a transient (within the first 20 min after application) positive effect (about 15-25%). Application of high hormone concentration (10 nM) in a low range of stimulation frequencies causes a biphasic effect (a small initial positive inotropic effect followed by a marked negative one). At frequencies above 0.5-Hz stimulation, insulin of 10 nM concentration causes presumably a negative inotropic effect. It was proposed that ICaL is possibly involved in the insulin-induced negative inotropy in ground squirrels hearts. Alteration of protein phosphorylation in tyrosine residues is known to be a major link in the mechanism of insulin action. We performed a study on orthovanadate action (a known inhibitor of tyrosine phosphatase) on the inotropic insulin effect. In the group of summer animals the pretreatment of papillary muscles with orthovanadate (100 mkM) does not change the negative inotropic effect of insulin in a low range of stimulation frequencies but almost completely removes this effect at stimulation frequencies above 0.3 Hz (n = 4). Nifedipine (1-1.5 hr pretreatment), a blocker of L-type calcium channel, reduces the inhibitory effect of insulin in autumn and winter animals, and on the contrary intensifies it in summer animals. This fact indicates that different mechanisms must be involved in insulin actions in animals of

  5. [Possible reasons for the variability of the inotropic insulin effect in papillary muscles of ground squirrel myocardium].

    PubMed

    Nakipova, O V; Chumaeva, L A; Andreeva, L A; Anufriev, A I; Kukushkin, N I

    2012-01-01

    The effects of insulin (0.1-50 nM) on isometric twitch force (0.1 to 1.0 Hz; 30 +/- 1 degree C; 1.8 mM Ca(2+)) were studied in right ventricular papillary muscles from active ground squirrels of different seasons (summer, n = 14; autumn, n = 16 and winter interbout, n = 16) in control conditions and after one-hour pretreatment of PM with 2 mkM nifedipine (an L-type Ca(2+)-channel inhibitor) and 1.0 mM orthovanadate (a tyrosine phosphatase inhibitor). In active animals of different seasonal periods insulin causes both positive and negative inotropic effects. At low frequencies (0.1-0.5 Hz), insulin of low concentrations (0.1-1.0 nM) induces a transient (within the first 20 min after application) positive effect (about 15-25%). Application of high hormone concentration (10 nM) in a low range of stimulation frequencies causes a biphasic effect (a small initial positive inotropic effect followed by a marked negative one). At frequencies above 0.5-Hz stimulation, insulin of 10 nM concentration causes presumably a negative inotropic effect. It was proposed that ICaL is possibly involved in the insulin-induced negative inotropy in ground squirrels hearts. Alteration of protein phosphorylation in tyrosine residues is known to be a major link in the mechanism of insulin action. We performed a study on orthovanadate action (a known inhibitor of tyrosine phosphatase) on the inotropic insulin effect. In the group of summer animals the pretreatment of papillary muscles with orthovanadate (100 mkM) does not change the negative inotropic effect of insulin in a low range of stimulation frequencies but almost completely removes this effect at stimulation frequencies above 0.3 Hz (n = 4). Nifedipine (1-1.5 hr pretreatment), a blocker of L-type calcium channel, reduces the inhibitory effect of insulin in autumn and winter animals, and on the contrary intensifies it in summer animals. This fact indicates that different mechanisms must be involved in insulin actions in animals of

  6. Pre-treatment of synthetic elastomeric scaffolds by cardiac fibroblasts improves engineered heart tissue.

    PubMed

    Radisic, Milica; Park, Hyoungshin; Martens, Timothy P; Salazar-Lazaro, Johanna E; Geng, Wenliang; Wang, Yadong; Langer, Robert; Freed, Lisa E; Vunjak-Novakovic, Gordana

    2008-09-01

    Native myocardium consists of several cell types, of which approximately one-third are myocytes and most of the nonmyocytes are fibroblasts. By analogy with monolayer culture in which fibroblasts were removed to prevent overgrowth, early attempts to engineer myocardium utilized cell populations enriched for cardiac myocytes (CMs; approximately 80-90% of total cells). We hypothesized that the pre-treatment of synthetic elastomeric scaffolds with cardiac fibroblasts (CFs) will enhance the functional assembly of the engineered cardiac constructs by creating an environment supportive of cardiomyocyte attachment and function. Cells isolated from neonatal rat ventricles were prepared to form three distinct populations: rapidly plating cells identified as CFs, slowly plating cells identified as CMs, and unseparated initial population of cells (US). The cell fractions (3 x 10(6) cells total) were seeded into poly(glycerol sebacate) scaffolds (highly porous discs, 5 mm in diameter x 2-mm thick) using Matrigeltrade mark, either separately (CM or CF), concurrently (US), or sequentially (CF pre-treatment followed by CM culture, CF + CM), and cultured in spinner flasks. The CF + CM group had the highest amplitude of contraction and the lowest excitation threshold, superior DNA content, and higher glucose consumption rate. The CF + CM group exhibited compact 100- to 200-mum thick layers of elongated myocytes aligned in parallel over layers of collagen-producing fibroblasts, while US and CM groups exhibited scattered and poorly elongated myocytes. The sequential co-culture of CF and CM on a synthetic elastomer scaffold thus created an environment supportive of cardiomyocyte attachment, differentiation, and contractile function, presumably due to scaffold conditioning by cultured fibroblasts. When implanted over the infarcted myocardium in a nude rat model, cell-free poly(glycerol sebacate) remained at the ventricular wall after 2 weeks of in vivo, and was vascularized. PMID

  7. Electrolytic pretreatment of urine

    NASA Technical Reports Server (NTRS)

    1977-01-01

    Electrolysis has been under evaluation for several years as a process to pretreat urine for ultimate recovery of potable water in manned spacecraft applications. The conclusions that were drawn from this investigation are the following: (1) A platinum alloy containing 10 percent rhodium has been shown to be an effective, corrosion-resistant anode material for the electrolytic pretreatment of urine. Black platinum has been found to be suitable as a cathode material. (2) The mechanism of the reactions occurring during the electrolysis of urine is two-stage: (a) a total Kjeldahl nitrogen and total organic carbon (TOC) removal in the first stage is the result of electrochemical oxidation of urea to CO2, H2O, and ammonia followed by chloride interaction to produce N2 from ammonia, (b) after the urea has been essentially removed and the chloride ions have no more ammonia to interact with, the chloride ions start to oxidize to higher valence states, thus producing perchlorates. (3) Formation of perchlorates can be suppressed by high/low current operation, elevated temperature, and pH adjustment. (4) UV-radiation showed promise in assisting electrolytic TOC removal in beaker tests, but was not substantiated in limited single cell testing. This may have been due to non-optimum configurations of the single cell test rig and the light source.

  8. [The application of hemoreologic indicators in prognosis of complications of acute myocardium infarction].

    PubMed

    Pakhrova, O A; Kudriashova, M V; Grineva, M R; Mishina, I E

    2015-02-01

    The sampling of 60 patients with acute myocardium infarction underwent a complex study of hemoreologic indicators with purpose to establish predictors of development of early complications of diseases to substantiate additions to algorithm of examination and to differentiate treatment regimens. It is established that under acute myocardium infarction the blood viscosity increases on low velocity of shifting and plasma. Also, the process of aggregation of erythrocytes increases and number of normocytes decreases without significant alterations of blood viscosity on high velocity of shift and capacity of erythrocytes to be distorted. At the same time, the mentioned above alterations in patients with acute myocardium infarction does not result in decreasing of effectiveness oftransportation of oxygen to tissues. Against the background of development the hemoreologic disorders have more apparent character and result in progressive decreasing of tissue perfusion. The most significant prognostic indicator concerning complications of acute myocardium infarction is a time parameter of increment of aggregation of erythrocytes surpassing 2.80 in 89% of patients with complications. The expedience of inclusion of detection of reologic blood indicators fir their subsequent correction in the complex of examination ofpatients with acute myocardium infarction.

  9. Exendin-4 pretreated adipose derived stem cells are resistant to oxidative stress and improve cardiac performance via enhanced adhesion in the infarcted heart.

    PubMed

    Liu, Jianfeng; Wang, Haibin; Wang, Yan; Yin, Yujing; Wang, Liman; Liu, Zhiqiang; Yang, Junjie; Chen, Yundai; Wang, Changyong

    2014-01-01

    Reactive oxygen species (ROS), which were largely generated after myocardial ischemia, severely impaired the adhesion and survival of transplanted stem cells. In this study, we aimed to determine whether Exendin-4 pretreatment could improve the adhesion and therapeutic efficacy of transplanted adipose derived stem cells (ADSCs) in ischemic myocardium. In vitro, H2O2 was used to provide ROS environments, in which ADSCs pretreated with Exendin-4 were incubated. ADSCs without pretreatment were used as control. Then, cell adhesion and viability were analyzed with time. Compared with control ADSCs, Exendin-4 treatment significantly increased the adhesion of ADSCs in ROS environment, while reduced intracellular ROS and cell injury as determined by dihydroethidium (DHE) staining live/Dead staining, lactate dehydrogenase-release assay and MTT assay. Western Blotting demonstrated that ROS significantly decreased the expression of adhesion-related integrins and integrin-related focal adhesion proteins, which were significantly reversed by Exendin-4 pretreatment and followed by decreases in caspase-3, indicating that Exendin-4 may facilitate cell survival through enhanced adhesion. In vivo, myocardial infarction (MI) was induced by the left anterior descending artery ligation in SD rats. Autologous ADSCs with or without Exendin-4 pretreatment were injected into the border area of infarcted hearts, respectively. Multi-techniques were used to assess the beneficial effects after transplantation. Longitudinal bioluminescence imaging and histological staining revealed that Exendin-4 pretreatment enhanced the survival and differentiation of engrafted ADSCs in ischemic myocardium, accompanied with significant benefits in cardiac function, matrix remodeling, and angiogenesis compared with non-pretreated ADSCs 4 weeks post-transplantation. In conclusion, transplantation of Exendin-4 pretreated ADSCs significantly improved cardiac performance and can be an innovative approach in the

  10. SERCA overexpression reduces hydroxyl radical injury in murine myocardium.

    PubMed

    Hiranandani, Nitisha; Bupha-Intr, Tepmanas; Janssen, Paul M L

    2006-12-01

    Hydroxyl radicals (*OH) are involved in the pathogenesis of ischemia-reperfusion injury and are observed in clinical situations, including acute heart failure, stroke, and myocardial infarction. Acute transient exposure to *OH causes an intracellular Ca(2+) overload and leads to impaired contractility. We investigated whether upregulation of sarcoplasmic reticulum Ca(2+)-ATPase function (SERCA) can attenuate *OH-induced dysfunction. Small, contracting right ventricular papillary muscles from wild-type (WT) SERCA1a-overexpressing (transgenic, TG) and SERCA2a heterogeneous knockout (HET) mice were directly exposed to *OH. This brief 2-min exposure led to a transient elevation of diastolic force (F(dia)) and depression of developed force (F(dev)). In WT mice, F(dia) increased to 485 +/- 49% and F(dev) decreased to 11 +/- 3%. In sharp contrast, in TG mice F(dia) increased only to 241 +/- 17%, whereas F(dev) decreased only to 51 +/- 5% (P < 0.05 vs. WT). In HET mice, F(dia) rose more than WT (to 597 +/- 20%, P < 0.05), whereas F(dev) was reduced in a similar amount. After approximately 45 min after *OH exposure, a new steady state was reached: F(dev) returned to 37 +/- 6% and 32 +/- 6%, whereas F(dia) came back to 238 +/- 28% and 292 +/- 17% in WT and HET mice, respectively. In contrast, the sustained dysfunction was significantly less in TG mice: F(dia) and F(dev) returned to 144 +/- 20% and 67 +/- 6%, respectively. Before exposure to *OH, there is decrease in phospholamban (PLB) phosphorylation at Ser16 (pPLBSer16) and PLB phosphorylation at Thr17 (pPLBThr17) in TG mice and an increase in pPLBSer16 and pPLBThr17 in HET mice versus WT. After exposure to *OH there is decrease in pPLBSer16 in WT, TG, and HET mice but no significant change in the level of pPLBThr17 in any group. The results indicate that SERCA overexpression can reduce the *OH-induced contractile dysfunction in murine myocardium, whereas a reduced SR Ca(2+)-ATPase activity aggravates this injury. Loss of

  11. Unique Transcriptional Profile of Sustained Ligand-Activated Preconditioning in Pre- and Post-Ischemic Myocardium

    PubMed Central

    Ashton, Kevin J.; Tupicoff, Amanda; Williams-Pritchard, Grant; Kiessling, Can J.; See Hoe, Louise E.; Headrick, John P.; Peart, Jason N.

    2013-01-01

    Background Opioidergic SLP (sustained ligand-activated preconditioning) induced by 3–5 days of opioid receptor (OR) agonism induces persistent protection against ischemia-reperfusion (I-R) injury in young and aged hearts, and is mechanistically distinct from conventional preconditioning responses. We thus applied unbiased gene-array interrogation to identify molecular effects of SLP in pre- and post-ischemic myocardium. Methodology/Principal Findings Male C57Bl/6 mice were implanted with 75 mg morphine or placebo pellets for 5 days. Resultant SLP did not modify cardiac function, and markedly reduced dysfunction and injury in perfused hearts subjected to 25 min ischemia/45 min reperfusion. Microarray analysis identified 14 up- and 86 down-regulated genes in normoxic hearts from SLP mice (≥1.3-fold change, FDR≤5%). Induced genes encoded sarcomeric/contractile proteins (Myh7, Mybpc3,Myom2,Des), natriuretic peptides (Nppa,Nppb) and stress-signaling elements (Csda,Ptgds). Highly repressed genes primarily encoded chemokines (Ccl2,Ccl4,Ccl7,Ccl9,Ccl13,Ccl3l3,Cxcl3), cytokines (Il1b,Il6,Tnf) and other proteins involved in inflammation/immunity (C3,Cd74,Cd83, Cd86,Hla-dbq1,Hla-drb1,Saa1,Selp,Serpina3), together with endoplasmic stress proteins (known: Dnajb1,Herpud1,Socs3; putative: Il6, Gadd45g,Rcan1) and transcriptional controllers (Egr2,Egr3, Fos,Hmox1,Nfkbid). Biological themes modified thus related to inflammation/immunity, together with cellular/cardiovascular movement and development. SLP also modified the transcriptional response to I-R (46 genes uniquely altered post-ischemia), which may influence later infarction/remodeling. This included up-regulated determinants of cellular resistance to oxidant (Mgst3,Gstm1,Gstm2) and other forms of stress (Xirp1,Ankrd1,Clu), and repression of stress-response genes (Hspa1a,Hspd1,Hsp90aa,Hsph1,Serpinh1) and Txnip. Conclusions Protection via SLP is associated with transcriptional repression of inflammation/immunity, up

  12. Protective Effects of Cardamom in Isoproterenol-Induced Myocardial Infarction in Rats

    PubMed Central

    Goyal, Sameer N.; Sharma, Charu; Mahajan, Umesh B.; Patil, Chandragouda R.; Agrawal, Yogeeta O.; Kumari, Santosh; Arya, Dharamvir Singh; Ojha, Shreesh

    2015-01-01

    Cardamom is a popular spice that has been commonly used in cuisines for flavor since ancient times. It has copious health benefits such as improving digestion, stimulating metabolism, and exhibits antioxidant and anti-inflammatory effects. The current study investigated the effect of cardamom on hemodynamic, biochemical, histopathological and ultrastructural changes in isoproterenol (ISO)-induced myocardial infarction. Wistar male albino rats were randomly divided and treated with extract of cardamom (100 and 200 mg/kg per oral) or normal saline for 30 days with concomitant administration of ISO (85 mg/kg, subcutaneous) on 29th and 30th days, at 24 h interval. ISO injections to rats caused cardiac dysfunction evidenced by declined arterial pressure indices, heart rate, contractility and relaxation along with increased preload. ISO also caused a significant decrease in endogenous antioxidants, superoxide dismutase, catalase, glutathione peroxidase, depletion of cardiomyocytes enzymes, creatine kinase-MB, lactate dehydrogenase and increase in lipid peroxidation. All these changes in cardiac and left ventricular function as well as endogenous antioxidants, lipid peroxidation and myocyte enzymes were ameliorated when the rats were pretreated with cardamom. Additionally, the protective effects were strengthened by improved histopathology and ultrastructural changes, which specifies the salvage of cardiomyocytes from the deleterious effects of ISO. The present study findings demonstrate that cardamom significantly protects the myocardium and exerts cardioprotective effects by free radical scavenging and antioxidant activities. PMID:26593900

  13. Protective Effects of Cardamom in Isoproterenol-Induced Myocardial Infarction in Rats.

    PubMed

    Goyal, Sameer N; Sharma, Charu; Mahajan, Umesh B; Patil, Chandragouda R; Agrawal, Yogeeta O; Kumari, Santosh; Arya, Dharamvir Singh; Ojha, Shreesh

    2015-01-01

    Cardamom is a popular spice that has been commonly used in cuisines for flavor since ancient times. It has copious health benefits such as improving digestion, stimulating metabolism, and exhibits antioxidant and anti-inflammatory effects. The current study investigated the effect of cardamom on hemodynamic, biochemical, histopathological and ultrastructural changes in isoproterenol (ISO)-induced myocardial infarction. Wistar male albino rats were randomly divided and treated with extract of cardamom (100 and 200 mg/kg per oral) or normal saline for 30 days with concomitant administration of ISO (85 mg/kg, subcutaneous) on 29th and 30th days, at 24 h interval. ISO injections to rats caused cardiac dysfunction evidenced by declined arterial pressure indices, heart rate, contractility and relaxation along with increased preload. ISO also caused a significant decrease in endogenous antioxidants, superoxide dismutase, catalase, glutathione peroxidase, depletion of cardiomyocytes enzymes, creatine kinase-MB, lactate dehydrogenase and increase in lipid peroxidation. All these changes in cardiac and left ventricular function as well as endogenous antioxidants, lipid peroxidation and myocyte enzymes were ameliorated when the rats were pretreated with cardamom. Additionally, the protective effects were strengthened by improved histopathology and ultrastructural changes, which specifies the salvage of cardiomyocytes from the deleterious effects of ISO. The present study findings demonstrate that cardamom significantly protects the myocardium and exerts cardioprotective effects by free radical scavenging and antioxidant activities. PMID:26593900

  14. Protective Effects of Cardamom in Isoproterenol-Induced Myocardial Infarction in Rats.

    PubMed

    Goyal, Sameer N; Sharma, Charu; Mahajan, Umesh B; Patil, Chandragouda R; Agrawal, Yogeeta O; Kumari, Santosh; Arya, Dharamvir Singh; Ojha, Shreesh

    2015-11-17

    Cardamom is a popular spice that has been commonly used in cuisines for flavor since ancient times. It has copious health benefits such as improving digestion, stimulating metabolism, and exhibits antioxidant and anti-inflammatory effects. The current study investigated the effect of cardamom on hemodynamic, biochemical, histopathological and ultrastructural changes in isoproterenol (ISO)-induced myocardial infarction. Wistar male albino rats were randomly divided and treated with extract of cardamom (100 and 200 mg/kg per oral) or normal saline for 30 days with concomitant administration of ISO (85 mg/kg, subcutaneous) on 29th and 30th days, at 24 h interval. ISO injections to rats caused cardiac dysfunction evidenced by declined arterial pressure indices, heart rate, contractility and relaxation along with increased preload. ISO also caused a significant decrease in endogenous antioxidants, superoxide dismutase, catalase, glutathione peroxidase, depletion of cardiomyocytes enzymes, creatine kinase-MB, lactate dehydrogenase and increase in lipid peroxidation. All these changes in cardiac and left ventricular function as well as endogenous antioxidants, lipid peroxidation and myocyte enzymes were ameliorated when the rats were pretreated with cardamom. Additionally, the protective effects were strengthened by improved histopathology and ultrastructural changes, which specifies the salvage of cardiomyocytes from the deleterious effects of ISO. The present study findings demonstrate that cardamom significantly protects the myocardium and exerts cardioprotective effects by free radical scavenging and antioxidant activities.

  15. Intravenous administration of atorvastatin-pretreated mesenchymal stem cells improves cardiac performance after acute myocardial infarction: role of CXCR4

    PubMed Central

    Li, Na; Yang, Yue-Jin; Qian, Hai-Yan; Li, Qing; Zhang, Qian; Li, Xiang-Dong; Dong, Qiu-Ting; Xu, Hui; Song, Lei; Zhang, Hao

    2015-01-01

    Background: The interaction between stromal cell-derived factor 1 (SDF-1) and its receptor CXC chemokine receptor 4 (CXCR4) plays an important role in mesenchymal stem cells (MSCs) migration and engraftment. Statins can increase the survival of MSCs. However, whether statins could enhance MSCs migration and engraftment is still unknown. Therefore, we designed the study to investigate whether atorvastatin (ATV) could enhance CXCR4 expression of MSCs and promote them homing toward the injured myocardium. Methods and results: Expression of CXCR4 was evaluated by flow cytometry and real time PCR. A transwell system was used to assess MSCs migration ability. Recruitment of systematically delivered MSCs to the infarcted heart was evaluated in Sprague-Dawley rats with acute myocardial infarction (AMI). ATV pretreatment enhanced the expression of CXCR4 and stimulated MSCs migration in vitro. However, the effect was largely abolished by CXCR4 neutralizing antibody. In AMI models, we found much more ATV-pretreated MSCs homing toward the infarcted myocardium than non-treated cells and this was accompanied by improved cardiac performance. Conclusions: ATV increases the migration ability of MSCs and improves cardiac performance due to up-regulated expression of CXCR4. These results suggest that ATV pretreatment of donor MSCs is an effective way to promote cell therapeutic potential for AMI. PMID:26279750

  16. [Structural-metabolic characteristics of the myocardium in acute hemorrhage and hyperbaric oxygenation].

    PubMed

    Berkutskaia, T S; Bykov, E G; Leonov, A N

    1975-01-01

    Histochemical and pathomorphological changes in the myocardium in acute loss of blood and hyperbaric oxygenation were investigated in experiments on 130 white rats. It was established that acute loss of blood brought about an activation of phosphorylase, a decrease in the content of glycogen, an inhibition of the activity of cytochrome oxidase and succinic dehydrogenase in the myocardium. Foci of dystrophy were formed in the subendocaridal zone of the two ventricles and septum. Oxygenobarotherapy contributed to normalization of the level of activity of enzymes, preservation of glycogen, reduced the extent of manifestation of dystrophic changes in myocardiocytes. Hyperbaric oxygenation of healthy animals led to changes in the enzymatic activity in the myocardium. Dystrophic changes were noted in individual myocardiocytes. The data obtained testify to a direct influence of oxygen on metabolism of the myocardial cells.

  17. Diabetes and the heart: could the diabetic myocardium be protected by preconditioning?

    PubMed

    Vinokur, Vladimir; Leibowitz, Gil; Grinberg, Leonid; Eliashar, Ron; Berenshtein, Eduard; Chevion, Mordechai

    2007-01-01

    Both type 1 and type 2 diabetes (insulin-dependent and non-insulin dependent diabetes, respectively) are associated with increased risk for microvascular and macrovascular complications including retinopathy, neuropathy, nephropathy and atherosclerosis. Type 2 diabetes markedly increases the risk for cardiovascular morbidity and mortality, which has major public health implications. In this review, molecular mechanisms pertaining to diabetes-induced heart pathology are addressed. PMID:17961296

  18. 40 CFR 412.26 - Pretreatment standards for new sources (PSNS).

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ...) EFFLUENT GUIDELINES AND STANDARDS CONCENTRATED ANIMAL FEEDING OPERATIONS (CAFO) POINT SOURCE CATEGORY Ducks § 412.26 Pretreatment standards for new sources (PSNS). (a) Except as provided in 40 CFR 403.7 and in... 40 Protection of Environment 28 2010-07-01 2010-07-01 true Pretreatment standards for new...

  19. 40 CFR 415.86 - Pretreatment standards for new sources (PSNS).

    Code of Federal Regulations, 2014 CFR

    2014-07-01

    ...) EFFLUENT GUIDELINES AND STANDARDS INORGANIC CHEMICALS MANUFACTURING POINT SOURCE CATEGORY Hydrofluoric Acid Production Subcategory § 415.86 Pretreatment standards for new sources (PSNS). Except as provided in 40 CFR... 40 Protection of Environment 29 2014-07-01 2012-07-01 true Pretreatment standards for new...

  20. 40 CFR 415.666 - Pretreatment standards for new sources (PSNS).

    Code of Federal Regulations, 2014 CFR

    2014-07-01

    ...) EFFLUENT GUIDELINES AND STANDARDS INORGANIC CHEMICALS MANUFACTURING POINT SOURCE CATEGORY Sodium Chlorate Production Subcategory § 415.666 Pretreatment standards for new sources (PSNS). Except as provided in 40 CFR... 40 Protection of Environment 29 2014-07-01 2012-07-01 true Pretreatment standards for new...

  1. 40 CFR 415.546 - Pretreatment standards for new sources (PSNS).

    Code of Federal Regulations, 2014 CFR

    2014-07-01

    ...) EFFLUENT GUIDELINES AND STANDARDS INORGANIC CHEMICALS MANUFACTURING POINT SOURCE CATEGORY Sodium Bisulfite Production Subcategory § 415.546 Pretreatment standards for new sources (PSNS). Except as provided in 40 CFR... 40 Protection of Environment 29 2014-07-01 2012-07-01 true Pretreatment standards for new...

  2. 40 CFR 415.546 - Pretreatment standards for new sources (PSNS).

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ...) EFFLUENT GUIDELINES AND STANDARDS INORGANIC CHEMICALS MANUFACTURING POINT SOURCE CATEGORY Sodium Bisulfite Production Subcategory § 415.546 Pretreatment standards for new sources (PSNS). Except as provided in 40 CFR... 40 Protection of Environment 28 2010-07-01 2010-07-01 true Pretreatment standards for new...

  3. 40 CFR 415.206 - Pretreatment standards for new sources (PSNS).

    Code of Federal Regulations, 2014 CFR

    2014-07-01

    ...) EFFLUENT GUIDELINES AND STANDARDS INORGANIC CHEMICALS MANUFACTURING POINT SOURCE CATEGORY Sodium Sulfite Production Subcategory § 415.206 Pretreatment standards for new sources (PSNS). Except as provided in 40 CFR... 40 Protection of Environment 29 2014-07-01 2012-07-01 true Pretreatment standards for new...

  4. 40 CFR 415.546 - Pretreatment standards for new sources (PSNS).

    Code of Federal Regulations, 2012 CFR

    2012-07-01

    ...) EFFLUENT GUIDELINES AND STANDARDS INORGANIC CHEMICALS MANUFACTURING POINT SOURCE CATEGORY Sodium Bisulfite Production Subcategory § 415.546 Pretreatment standards for new sources (PSNS). Except as provided in 40 CFR... 40 Protection of Environment 30 2012-07-01 2012-07-01 false Pretreatment standards for new...

  5. Sewage sludge pretreatment and disposal. (Latest citations from the NTIS bibliographic database). Published Search

    SciTech Connect

    1995-06-01

    The bibliography contains citations concerning techniques and equipment used in the pretreatment and disposal of sewage sludges. Citations discuss sludge digestion, dewatering, disinfection, stabilization, chlorination, and desulfurization. Topics include pretreatment programs, land disposal, incineration, and waste utilization. Environmental monitoring and protection, federal regulations, and legal aspects are examined. (Contains 50-250 citations and includes a subject term index and title list.)

  6. Impact of Denervated Myocardium on Improving Risk Stratification for Sudden Cardiac Death

    PubMed Central

    Cain, Michael E.

    2014-01-01

    Between 184,000 and 462,000 Americans die suddenly each year. Fifty percent to 70% of these deaths are due to ventricular tachycardia/fibrillation (VT/VF). We tested whether hibernating myocardium or myocardial sympathetic denervation identifies patients at high-risk for developing VT/VF independently of ejection fraction (EF). Positron emission tomography (PET) was used to quantify myocardial sympathetic denervation (11C-meta-hydroxyephedrine [11C-HED]), perfusion (13N-ammonia), and viability (insulin-stimulated 18F-2-deoxyglucose [18FDG]) in patients with ischemic cardiomyopathy (EF < 35%) eligible for a primary prevention implantable cardioverter defibrillator (ICD). The primary end-point was sudden cardiac arrest (SCA) defined as arrhythmic death or ICD discharge for VT/VF > 240 bpm. Volumes of total denervated (P = .001) and viable denervated myocardium (11C-HED-18FDG mismatch, P = .03) predicted SCA, whereas hibernating and infarcted myocardium did not. Multivariate analysis identified four independent predictors of SCA: denervated myocardium > 37.6% of left ventricule (LV), LV end-diastolic volume > 98 mL/m2, creatinine level > 1.49 mg/dL, and no angiotensin- inhibition therapy. Denervated myocardium had a hazard ratio of 3.5 for SCA (10.3%/year vs. 3.0%/year, p=0.001). Absence of all four factors predicted low risk (44% of cohort; SCA <1%/y) whereas two or more factors identified subjects at high-risk (20% of cohort; SCA 12%/y). Denervated myocardium quantified using PET strongly predicts risk of SCA, and is independent of EF, infarct volume, and other clinical variables. PMID:25125727

  7. Impact of denervated myocardium on improving risk stratification for sudden cardiac death.

    PubMed

    Cain, Michael E

    2014-01-01

    Between 184,000 and 462,000 Americans die suddenly each year. Fifty percent to 70% of these deaths are due to ventricular tachycardia/fibrillation (VT/VF). We tested whether hibernating myocardium or myocardial sympathetic denervation identifies patients at high-risk for developing VT/VF independently of ejection fraction (EF). Positron emission tomography (PET) was used to quantify myocardial sympathetic denervation ((11)C-meta-hydroxyephedrine [(11)C-HED]), perfusion ((13)N-ammonia), and viability (insulin-stimulated (18)F-2-deoxyglucose [(18)FDG]) in patients with ischemic cardiomyopathy (EF < 35%) eligible for a primary prevention implantable cardioverter defibrillator (ICD). The primary end-point was sudden cardiac arrest (SCA) defined as arrhythmic death or ICD discharge for VT/VF > 240 bpm. Volumes of total denervated (P = .001) and viable denervated myocardium ((11)C-HED-(18)FDG mismatch, P = .03) predicted SCA, whereas hibernating and infarcted myocardium did not. Multivariate analysis identified four independent predictors of SCA: denervated myocardium > 37.6% of left ventricule (LV), LV end-diastolic volume > 98 mL/m(2), creatinine level > 1.49 mg/dL, and no angiotensin- inhibition therapy. Denervated myocardium had a hazard ratio of 3.5 for SCA (10.3%/year vs. 3.0%/year, p=0.001). Absence of all four factors predicted low risk (44% of cohort; SCA <1%/y) whereas two or more factors identified subjects at high-risk (20% of cohort; SCA 12%/y). Denervated myocardium quantified using PET strongly predicts risk of SCA, and is independent of EF, infarct volume, and other clinical variables.

  8. VEGF-C/VEGFR-3 pathway promotes myocyte hypertrophy and survival in the infarcted myocardium

    PubMed Central

    Zhao, Tieqiang; Zhao, Wenyuan; Meng, Weixin; Liu, Chang; Chen, Yuanjian; Gerling, Ivan C; Weber, Karl T; Bhattacharya, Syamal K; Kumar, Rahul; Sun, Yao

    2015-01-01

    Background: Numerous studies have shown that in addition to angio/lymphangiogenesis, the VEGF family is involved in other cellular actions. We have recently reported that enhanced VEGF-C and VEGFR-3 in the infarcted rat myocardium, suggesting the paracrine/autocrine function of VEGF-C on cardiac remodeling. The current study was designed to test the hypothesis that VEGF-C regulates cardiomyocyte growth and survival in the infarcted myocardium. Methods and results: Gene profiling and VEGFR-3 expression of cardiomyocytes were assessed by laser capture microdissection/microarray and immunohistochemistry in the normal and infarcted myocardium. The effect of VEGF-C on myocyte hypertrophy and apoptosis during normoxia and hypoxia was detected by RT-PCR and western blotting in cultured rat neonatal cardiomyocytes. VEGFR-3 was minimally expressed in cardiomyocytes of the normal and noninfarcted myocardium, while markedly elevated in the surviving cardiomyocytes of the infarcted myocardium and border zone. Genes altered in the surviving cardiomyocytes were associated with the networks regulating cellular growth and survival. VEGF-C significantly increased the expression of atrial natriuretic factor (ANP), brain natriuretic factor (BNP), and β-myosin heavy chain (MHC), markers of hypertrophy, in neonatal cardiomyocytes. Hypoxia caused neonatal cardiomyocyte atrophy, which was prevented by VEGF-C treatment. Hypoxia significantly enhanced apoptotic mediators, including cleaved caspase 3, 8, and 9, and Bax in neonatal cardiomyocytes, which were abolished by VEGF-C treatment. Conclusion: Our findings indicate that VEGF-C/VEGFR-3 pathway exerts a beneficial role in the infarcted myocardium by promoting compensatory cardiomyocyte hypertrophy and survival. PMID:26064438

  9. [Effect of allergic damage on plastic metabolism of the myocardium in rabbits].

    PubMed

    Grozdova, M D; Starostina, L K

    1975-12-01

    The plastic metabolism of the myocardium in rabbits was studied after varying periods of allergic damage induced by repeated injections of normal horse serum. An accelerated decompostion of the myofibril proteins was demomstrated to occur during the acute phase. During the reparation phase, an activation of the protein synthesis in the myocardium occurred. The newly synthesized myofibril proteins had a longer turnover in the tissues, than under normal conditions. The turnover time of the mitochondrial proteins did not differ from the normal one. PMID:1223362

  10. Statistical and fractal analysis of autofluorescent myocardium images in posthumous diagnostics of acute coronary insufficiency

    NASA Astrophysics Data System (ADS)

    Boichuk, T. M.; Bachinskiy, V. T.; Vanchuliak, O. Ya.; Minzer, O. P.; Garazdiuk, M.; Motrich, A. V.

    2014-08-01

    This research presents the results of investigation of laser polarization fluorescence of biological layers (histological sections of the myocardium). The polarized structure of autofluorescence imaging layers of biological tissues was detected and investigated. Proposed the model of describing the formation of polarization inhomogeneous of autofluorescence imaging biological optically anisotropic layers. On this basis, analytically and experimentally tested to justify the method of laser polarimetry autofluorescent. Analyzed the effectiveness of this method in the postmortem diagnosis of infarction. The objective criteria (statistical moments) of differentiation of autofluorescent images of histological sections myocardium were defined. The operational characteristics (sensitivity, specificity, accuracy) of these technique were determined.

  11. Scale-selective analysis of myocardium polarization images in problems of diagnostic of necrotic changes

    NASA Astrophysics Data System (ADS)

    Ushenko, O. G.; Dubolazov, O. V.; Ushenko, Yu. O.; Gorsky, M. P.

    2015-11-01

    This research presents the results of investigation of laser polarization fluorescence of biological layers (histological sections of the myocardium). The polarized structure of autofluorescence imaging layers of biological tissues was detected and investigated. Proposed the model of describing the formation of polarization inhomogeneous of autofluorescence imaging biological optically anisotropic layers. On this basis, analytically and experimentally tested to justify the method of laser polarimetry autofluorescent. Analyzed the effectiveness of of this method in the postmortem diagnosis of infarction. The objective criteria (statistical moments) of differentiation of autofluorescent images of histological sections myocardium were defined. The operational characteristics (sensitivity, specificity, accuracy) of these technique were determined.

  12. [Protein fractions and their enzyme activity in rat myocardium after a 22-hour space flight].

    PubMed

    Gaevskaia, M S; Veresotskaia, N A; Kolganova, N S; Kolchina, E V; Kurkina, L M

    1976-01-01

    No significant changes in the content of sarcoplasmatic and myofibrillar proteins were found in the myocardium of rats that made a 22-day flight onboard the biosatellite. On the 2nd and 26th postflight days the activity of aspartate and alanine aminotransferases of sarcoplasmatic proteins was increased and the total activity of lactate dehydrogenase and its isoenzyme spectrum remained unchanged. On the 2nd postflight day the ATPase activity of myosin of the myocardium was substantially lowered and on the 26th postflight day it returned to the normal. This decline in the ATPase activity of myosin can be regarded as an adaptive reaction to weightlessness.

  13. Effects of subacute pretreatment with carbamate together with acute adjunct pretreatment against nerve agent exposure. (Reannouncement with new availability information)

    SciTech Connect

    Anderson, D.R.; Harris, L.W.; Lennox, W.J.; Solana, R.P.

    1991-12-31

    Acute carbamate pretreatment, in conjunction with atropine pretreatment or followed by atropine and oxime therapy has been shown to protect rabbits, rats, guinea pigs and monkeys against multiple lethal doses of soman. In those experiments, pretreated animals were usually challenged with soman at the time of peak whole blood acetylcholinesterase (AChE) inhibition by the carbamate or when the concentration of carbamate in the blood was expected to be rapidly diminishing. However, soldiers in a chemical environment, having taken carbamate orally might well be exposed to nerve agent shortly thereafter. Thus, both active carbamate and nerve agent would be entering the blood simultaneously. In a recent study it was reported that subacute administration of physostigmine (Phy), via subcutaneously implanted 28 day osmotic minipump, afforded protection against an iv challenge of soman on the 27th day.

  14. 40 CFR 442.3 - General pretreatment standards.

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... standards. Any source subject to this part that introduces process wastewater pollutants into a publicly owned treatment works (POTW) must comply with 40 CFR part 403. ... 40 Protection of Environment 30 2011-07-01 2011-07-01 false General pretreatment standards....

  15. 40 CFR 439.3 - General pretreatment standards.

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... standards. Any source subject to this part that introduces process wastewater pollutants into a publicly owned treatment works (POTW) must comply with 40 CFR part 403. ... 40 Protection of Environment 30 2011-07-01 2011-07-01 false General pretreatment standards....

  16. 40 CFR 437.3 - General pretreatment standards.

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... owned treatment works (POTW) must comply with 40 CFR part 403. ... 40 Protection of Environment 30 2011-07-01 2011-07-01 false General pretreatment standards. 437.3... AND STANDARDS THE CENTRALIZED WASTE TREATMENT POINT SOURCE CATEGORY § 437.3 General...

  17. 40 CFR 403.9 - POTW pretreatment programs and/or authorization to revise pretreatment standards: Submission for...

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... with any approved water quality management plan developed in accordance with 40 CFR parts 130, 131, as... Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS GENERAL PRE-TREAT... applied to individual Industrial Users (e.g., by order, permit, ordinance, etc.); and, (iii) Identify...

  18. Effects of Cordyceps sinensis on the Expressions of NF-κB and TGF-β1 in Myocardium of Diabetic Rats.

    PubMed

    Gu, You-You; Wang, Huan; Wang, Su; Gao, Hua; Qiu, Ming-Cai

    2015-01-01

    Objective. To investigate the effect of Cordyceps sinensis (CS) on the expressions of NF-κB and TGF-β1 in myocardium of streptozotocin-induced diabetic rats. Methods. A total of 53 healthy male SD rats, mice age of 8 weeks and weight of 220 ± 20 g, were randomly divided into five groups by randomized block design: normal control group (n = 10), diabetic group (n = 10), low dose of CS group (n = 12; CS 0.6 g·kg(-1)·d(-1)), middle dose of CS group (n = 11; CS 2.5 g·kg(-1)·d(-1)), and high dose of CS group (n = 10; CS 5 g·kg(-1)·d(-1)). The diabetic models with tail intravenous injection by streptozotocin (45 mg·kg(-1)). Diabetic rats were sacrificed after 8 weeks; the expressions of NF-κB and TGF-β1 proteins and mRNA in the cardiac muscle were determined by using immunohistochemistry staining and reverse transcription polymerase chain reaction (RT-PCR) method. The data were analyzed using one factor analysis of variance. Result. The expressions of NF-κB and TGF-β1 proteins and mRNA in the cardiac muscle of diabetic rats were significantly raised (P < 0.05), which could be decreased by CS (P < 0.05). Conclusions. The changes on the expressions of NF-κB and TGF-β1 in myocardium may be involved in the occurrence of diabetic cardiomyopathy (DC). CS may play its role on myocardial protection by regulating the expressions of NF-κB and TGF-β1 in myocardium. PMID:26697096

  19. 40 CFR 429.66 - Pretreatment standards for new sources (PSNS).

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... which introduces process wastewater pollutants into a publicly owned treatment works must comply with 40 CFR part 403. ... 40 Protection of Environment 30 2011-07-01 2011-07-01 false Pretreatment standards for new...

  20. 40 CFR 429.115 - Pretreatment standards for existing sources (PSES).

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... subpart which introduces process wastewater pollutants into a publicly owned treatment works must comply with 40 CFR part 403. ... 40 Protection of Environment 30 2011-07-01 2011-07-01 false Pretreatment standards for...

  1. 40 CFR 429.45 - Pretreatment standards for existing sources (PSES).

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... which introduces process wastewater pollutants into a publicly owned treatment works must comply with 40 CFR part 403. ... 40 Protection of Environment 30 2011-07-01 2011-07-01 false Pretreatment standards for...

  2. 40 CFR 429.25 - Pretreatment standards for existing sources (PSES).

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... which introduces process wastewater pollutants into a publicly owned treatment works must comply with 40 CFR part 403. ... 40 Protection of Environment 30 2011-07-01 2011-07-01 false Pretreatment standards for...

  3. 40 CFR 429.155 - Pretreatment standards for existing sources (PSES).

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... subject to this subpart which introduces process wastewater pollutants into publicly owned treatment works must comply with 40 CFR part 403. ... 40 Protection of Environment 30 2011-07-01 2011-07-01 false Pretreatment standards for...

  4. 40 CFR 429.146 - Pretreatment standards for new sources (PSNS).

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... this subpart which introduce process wastewater pollutants into a publicly owned treatment works must comply with 40 CFR part 403. ... 40 Protection of Environment 30 2011-07-01 2011-07-01 false Pretreatment standards for new...

  5. 40 CFR 429.56 - Pretreatment standards for new sources (PSNS).

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... which introduces process wastewater pollutants into a publicly owned treatment works must comply with 40 CFR part 403. ... 40 Protection of Environment 30 2011-07-01 2011-07-01 false Pretreatment standards for new...

  6. 40 CFR 429.135 - Pretreatment standards for existing sources (PSES).

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... subpart which introduces process wastewater pollutants into a publicly owned treatment works must comply with 40 CFR part 403. ... 40 Protection of Environment 30 2011-07-01 2011-07-01 false Pretreatment standards for...

  7. 40 CFR 429.126 - Pretreatment standards for new sources (PSNS).

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... this subpart which introduces process wastewater pollutants into a publicly owned treatment works must comply with 40 CFR part 403. ... 40 Protection of Environment 30 2011-07-01 2011-07-01 false Pretreatment standards for new...

  8. 40 CFR 429.65 - Pretreatment standards for existing sources (PSES).

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... subpart which introduces process wastewater pollutants into a publicly owned treatment works must comply with 40 CFR part 403. ... 40 Protection of Environment 30 2011-07-01 2011-07-01 false Pretreatment standards for...

  9. 40 CFR 429.145 - Pretreatment standards for existing sources (PSES).

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... subject to this subpart which introduces process wastewater pollutants into a publicly owned treatment works must comply with 40 CFR part 403. ... 40 Protection of Environment 30 2011-07-01 2011-07-01 false Pretreatment standards for...

  10. 40 CFR 429.125 - Pretreatment standards for existing sources (PSES).

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... source subject to this subpart which introduces process wastewater pollutants into a publicly owned treatment works must comply with 40 CFR part 403. ... 40 Protection of Environment 30 2011-07-01 2011-07-01 false Pretreatment standards for...

  11. 40 CFR 429.156 - Pretreatment standards for new sources (PSNS).

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... which introduces process wastewater pollutants into publicly owned treatment works must comply with 40 CFR part 403. ... 40 Protection of Environment 30 2011-07-01 2011-07-01 false Pretreatment standards for new...

  12. 40 CFR 429.55 - Pretreatment standards for existing sources (PSES).

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... subpart which introduces process wastewater pollutants into a publicly owned treatment works must comply with 40 CFR part 403. ... 40 Protection of Environment 30 2011-07-01 2011-07-01 false Pretreatment standards for...

  13. 40 CFR 429.35 - Pretreatment standards for existing sources (PSES).

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... which introduces process wastewater pollutants into a publicly owned treatment works must comply with 40 CFR part 403. ... 40 Protection of Environment 30 2011-07-01 2011-07-01 false Pretreatment standards for...

  14. 40 CFR 429.105 - Pretreatment standards for existing sources (PSES).

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... subpart which introduces process wastewater pollutants into a publicly owned treatment works must comply with 40 CFR part 403. ... 40 Protection of Environment 30 2011-07-01 2011-07-01 false Pretreatment standards for...

  15. Rewarming Rate of the Myocardium During the Aortic Cross-Clamp Time: Variations with Different Levels of Body Hypothermia

    PubMed Central

    Juffé, Alberto; Burgos, Raul; Montero, Carlos Garcia; Tellez, Gaberiel; Prades, Gonzalo; Lloves, Eduardo; Figuera, Diego

    1985-01-01

    Twenty patients underwent elective cardiac valve replacement at 20° C of body hypothermia. Temperatures of the ventricles of both walls were monitored on 12 different sites. Distribution of myocardial temperature ranged between 24.3 and 29.3° C for patients of Group I before cardioplegia delivery and 13.2° C in the septum after cardioplegic infusion. Average temperatures for the anterior and posterior wall were 13.6 C and 15° C in the left ventricle and 14.7 and 15° C in the right ventricle. Myocardial temperatures ranged from 26 to 28.7° C for patients of Group II. After cardioplegic arrest, septal temperatures averaged 14.9° C. The recorded sites of the anterior and posterior left ventricle were 14.1 and 13.1° C. The effects of rewarming on the different myocardial areas occurred according to a logarithmic equation, which is faster in the first 10 minutes. The data suggest that the myocardium can be adequately protected with 25° C hypothermia when the cross-clamp period is shorter than 60 minutes. When longer ischemic periods are expected, myocardial protection is best accomplished with 20° C hypothermia. PMID:15227003

  16. In Vivo Cardiac Cellular Reprogramming Efficacy Is Enhanced by Angiogenic Preconditioning of the Infarcted Myocardium With Vascular Endothelial Growth Factor

    PubMed Central

    Mathison, Megumi; P. Gersch, Robert; Nasser, Ahmed; Lilo, Sarit; Korman, Mallory; Fourman, Mitchell; Hackett, Neil; Shroyer, Kenneth; Yang, Jianchang; Ma, Yupo; Crystal, Ronald G.; Rosengart, Todd K.

    2012-01-01

    Background In situ cellular reprogramming offers the possibility of regenerating functional cardiomyocytes directly from scar fibroblasts, obviating the challenges of cell implantation. We hypothesized that pretreating scar with gene transfer of the angiogenic vascular endothelial growth factor (VEGF) would enhance the efficacy of this strategy. Methods and Results Gata4, Mef2c, and Tbx5 (GMT) administration via lentiviral transduction was demonstrated to transdifferentiate rat fibroblasts into (induced) cardiomyocytes in vitro by cardiomyocyte marker studies. Fisher 344 rats underwent coronary ligation and intramyocardial administration of an adenovirus encoding all 3 major isoforms of VEGF (AdVEGF‐All6A+) or an AdNull control vector (n=12/group). Lentivirus encoding GMT or a GFP control was administered to each animal 3 weeks later, followed by histologic and echocardiographic analyses. GMT administration reduced the extent of fibrosis by half compared with GFP controls (12±2% vs 24±3%, P<0.01) and reduced the number of myofibroblasts detected in the infarct zone by 4‐fold. GMT‐treated animals also demonstrated greater density of cardiomyocyte‐specific marker beta myosin heavy chain 7+ cells compared with animals receiving GFP with or without VEGF (P<0.01). Ejection fraction was significantly improved after GMT vs GFP administration (12±3% vs −7±3%, P<0.01). Eight (73%) GFP animals but no GMT animals demonstrated decreased ejection fraction during this interval (P<0.01). Also, improvement in ejection fraction was 4‐fold greater in GMT/VEGF vs GMT/null animals (17±2% vs 4±1%, P<0.05). Conclusions VEGF administration to infarcted myocardium enhances the efficacy of GMT‐mediated cellular reprogramming in improving myocardial function and reducing the extent of myocardial fibrosis compared with the use of GMT or VEGF alone. PMID:23316332

  17. Luteolin Limits Infarct Size and Improves Cardiac Function after Myocardium Ischemia/Reperfusion Injury in Diabetic Rats

    PubMed Central

    Gao, Haokao; Li, Jiayi; Shen, Min; Cao, Feng; Wang, Haichang

    2012-01-01

    Background The present study was to investigate the effects and mechanism of Luteolin on myocardial infarct size, cardiac function and cardiomyocyte apoptosis in diabetic rats with myocardial ischemia/reperfusion (I/R) injury. Methodology/Principal Findings Diabetic rats underwent 30 minutes of ischemia followed by 3 h of reperfusion. Animals were pretreated with or without Luteolin before coronary artery ligation. The severity of myocardial I/R induced LDH release, arrhythmia, infarct size, cardiac function impairment, cardiomyocyte apoptosis were compared. Western blot analysis was performed to elucidate the target proteins of Luteolin. The inflammatory cytokine production were also examined in ischemic myocardium underwent I/R injury. Our results revealed that Luteolin administration significantly reduced LDH release, decreased the incidence of arrhythmia, attenuated myocardial infarct size, enhanced left ventricular ejection fraction and decreased myocardial apoptotic death compared with I/R group. Western blot analysis showed that Luteolin treatment up-regulated anti-apoptotic proteins FGFR2 and LIF expression, increased BAD phosphorylation while decreased the ratio of Bax to Bcl-2. Luteolin treatment also inhibited MPO expression and inflammatory cytokine production including IL-6, IL-1a and TNF-a. Moreover, co-administration of wortmannin and Luteolin abolished the beneficial effects of Luteolin. Conclusions/Significance This study indicates that Luteolin preserves cardiac function, reduces infarct size and cardiomyocyte apoptotic rate after I/R injury in diabetic rats. Luteolin exerts its action by up-regulating of anti-apoptotic proteins FGFR2 and LIF expression, activating PI3K/Akt pathway while increasing BAD phosphorylation and decreasing ratio of Bax to Bcl-2. PMID:22432030

  18. Chronic intermittent hypobaric hypoxia protects the heart against ischemia/reperfusion injury through upregulation of antioxidant enzymes in adult guinea pigs

    PubMed Central

    Guo, Hui-cai; Zhang, Zhe; Zhang, Li-nan; Xiong, Chen; Feng, Chen; Liu, Qian; Liu, Xu; Shi, Xiao-lu; Wang, Yong-li

    2009-01-01

    Aim: To investigate the protection and the anti-oxidative mechanism afforded by chronic intermittent hypobaric hypoxia (CIHH) against ischemia/reperfusion (I/R) injury in guinea pig hearts. Methods: Adult male guinea pigs were exposed to CIHH by mimicking a 5000 m high altitude (pB=404 mmHg, pO2=84 mmHg) in a hypobaric chamber for 6 h/day for 28 days. Langendorff-perfused isolated guinea pig hearts were used to measure variables of left ventricular function during baseline perfusion, ischemia and the reperfusion period. The activity and protein expression of antioxidant enzymes in the left myocardium were evaluated using biochemical methods and Western blotting, respectively. Intracellular reactive oxygen species (ROS) were assessed using ROS-sensitive fluorescence. Results: After 30 min of global no-flow ischemia followed by 60 min of reperfusion, myocardial function had better recovery rates in CIHH guinea pig hearts than in control hearts. The activity and protein expression of superoxide dismutase (SOD) and catalase (CAT) were significantly increased in the myocardium of CIHH guinea pigs. Pretreatment of control hearts with an antioxidant mixture containing SOD and CAT exerted cardioprotective effects similar to CIHH. The irreversible CAT inhibitor aminotriazole (ATZ) abolished the cardioprotection of CIHH. Cardiac contractile dysfunction and oxidative stress induced by exogenous hydrogen peroxide (H2O2) were attenuated by CIHH and CAT. Conclusions: These data suggest that CIHH protects the heart against I/R injury through upregulation of antioxidant enzymes in guinea pig. PMID:19543301

  19. First report on application of diode laser for photocoagulation of canine myocardium

    NASA Astrophysics Data System (ADS)

    Ware, David L.; Motamedi, Massoud; Pohl, John; Bell, Brent A.; Boor, Paul

    1994-07-01

    Ventricular tachycardia (VT) is a rapid heart rhythm which is often life threatening. Several surgical and percutaneous ways to destroy the myocardium responsible for VT have been studied. It has been postulated that laser therapy may be ideal for this purpose because it can heat a large volume of tissue. Recent developments in diode lasers have prompted us to evaluate this source (810 nm) for photocoagulation of myocardial tissue. Its size, ease of maintenance, and cost make diode laser suitable for clinical practice in general, and for percutaneous photoablation in particular. Lesions were created in myocardium with contact irradiation using a 600 micron bare tipped optical fiber both in vitro and in vivo. Exposures of 2 to 3 W over 30 to 60 seconds created lesions with no or minimal char formations. In vivo lesions tended to be larger than in vitro, with better defined border zones. Animals tolerated laser irradiation well without significant ventricular ectopy. Diode laser irradiation is a promising means to percutaneously coagulate ventricular myocardium and for cure of VT. Further investigation of the dosimetry and healing response in both healthy and diseased myocardium is warranted.

  20. The sinus venosus myocardium contributes to the atrioventricular canal: potential role during atrioventricular node development?

    PubMed

    Kelder, Tim P; Vicente-Steijn, Rebecca; Harryvan, Tom J; Kosmidis, Georgios; Gittenberger-de Groot, Adriana C; Poelmann, Rob E; Schalij, Martin J; DeRuiter, Marco C; Jongbloed, Monique R M

    2015-06-01

    The presence of distinct electrophysiological pathways within the atrioventricular node (AVN) is a prerequisite for atrioventricular nodal reentrant tachycardia to occur. In this study, the different cell contributions that may account for the anatomical and functional heterogeneity of the AVN were investigated. To study the temporal development of the AVN, the expression pattern of ISL1, expressed in cardiac progenitor cells, was studied in sequential stages performing co-staining with myocardial markers (TNNI2 and NKX2-5) and HCN4 (cardiac conduction system marker). An ISL1+/TNNI2+/HCN4+ continuity between the myocardium of the sinus venosus and atrioventricular canal was identified in the region of the putative AVN, which showed a pacemaker-like phenotype based on single cell patch-clamp experiments. Furthermore, qPCR analysis showed that even during early development, different cell populations can be identified in the region of the putative AVN. Fate mapping was performed by in ovo vital dye microinjection. Embryos were harvested and analysed 24 and 48 hrs post-injection. These experiments showed incorporation of sinus venosus myocardium in the posterior region of the atrioventricular canal. The myocardium of the sinus venosus contributes to the atrioventricular canal. It is postulated that the myocardium of the sinus venosus contributes to nodal extensions or transitional cells of the AVN since these cells are located in the posterior region of the AVN. This finding may help to understand the origin of atrioventricular nodal reentrant tachycardia.

  1. Effects of dietary magnesium deficiency on thallium-201 kinetics and distribution in rat myocardium: concise communication

    SciTech Connect

    Llaurado, J.G.; Madden, J.A.; Smith, G.A.

    1983-05-01

    Kinetics and distribution of TI-201 were studied in myocardium of rats with chronic dietary induced Mg deficiency. Rats were fed the Mg-deficient diet for 30 days and were then injected intravenously with 0.2 mCi of TI-201. Comparable control animals were fed a standard laboratory diet. One-half hour after injection, rats were killed and a segment of myocardium was washed with nonradioactive Krebs solution in a special chamber. Radioactivity in the tissue was recorded continuously for 1 hr. A three-compartment model (extracellular, main intracellular, and subcellular) was found to describe adequately the kinetics of TI-201. In myocardium of Mg-deficient animals, significant changes in values of transport rate constants and compartment sizes for TI-201 indicated a moderate decrease in extracellular compartment and a threefold enlargement in subcellular compartment (presumably mitochondrial) at the expense of the main intracellular compartment, which underwent a marked reduction. Bulk TI-201 uptake in myocardium of Mg-deficient rats was unchanged. The findings are interpreted as being consistent with mitochondrial alterations reported in Mg-deficient animals. Clinical implications are discussed.

  2. Isolated noncompaction of the myocardium: multiplane transesophageal echocardiography diagnosis in an adult.

    PubMed

    Maltagliati, A; Pepi, M

    2000-11-01

    We describe a case of isolated noncompaction of the myocardium in a 66-year-old patient. Peculiar anatomic features of this disease were clearly suspected on transthoracic echocardiography and precisely recognized through transesophageal echocardiography. The role of transthoracic and transesophageal echocardiography in the detection of this rare disease is described in this report.

  3. Concentration of digoxin, methyldigoxin, digitoxin and ouabain in the myocardium of the dog following coronary occulsion.

    PubMed

    Kuhlmann, J; Kötter, V; von Leitner, E; Arbeiter, G; Schröder, R

    1975-01-01

    26 mongrel dogs were given a single dose of 0.03mg/kg tritium-labelled digoxin, beta-methyldigoxin, digitoxin or ouabain 2 hrs or 95 hrs following experimental coronary occlusion. Examination of the epicardial ECG was performed by moving from intact to ischemic or necrotic zones. 60 min after glycoside administration the animals were sacrificed and tissue samples from the marked heart muscles areas and from the skeletal muscle were analysed for glycoside content. The early glycoside uptake in acute ischemic or necrotic myocardium was diminished independently of the physicochemical properties of the glycoside. Significantly higher glycoside concentrations (ng/g wet weight) were measured in the injured myocardium 3 hrs after coronary occlusion than 96 hrs afterward (p less than 0.005). The values in acute ischemic myocardium varied considerably. This nonhomogeneity of glycoside uptake in the acute ischemic heart muscle may partly explain the increased sensitivity to glycosides in myocardial infarction. The decline of glycoside concentration correlates with the alterations in the epicardial ECG. The cardiac effects of cardenolides 60 min after intravenous administration was caused by the unchanged glycoside. In contrast to the myocardium, glycoside accumulation could not be found in the skeletal muscle. The concentrations of digoxin, beta-methyldigoxin and digitoxin in the skeletal muscle were significantly higher than the concentration of ouabain, which was rapidly eliminated via the urine.

  4. A murine experimental model for the mechanical behaviour of viable right-ventricular myocardium

    PubMed Central

    Valdez-Jasso, Daniela; Simon, Marc A; Champion, Hunter C; Sacks, Michael S

    2012-01-01

    Although right-ventricular function is an important determinant of cardio-pulmonary performance in health and disease, right ventricular myocardium mechanical behaviour has received relatively little attention. We present a novel experimental method for quantifying the mechanical behaviour of transmurally intact, viable right-ventricular myocardium. Seven murine right ventricular free wall (RVFW) specimens were isolated and biaxial mechanical behaviour measured, along with quantification of the local transmural myofibre and collagen fibre architecture. We developed a complementary strain energy function based method to capture the average biomechanical response. Overall, murine RVFW revealed distinct mechanical anisotropy. The preferential alignment of the myofibres and collagen fibres to the apex-to-outflow-tract direction was consistent with this also being the mechanically stiffer axis. We also observed that the myofibre and collagen fibre orientations were remarkably uniform throughout the entire RVFW thickness. Thus, our findings indicate a close correspondence between the tissue microstructure and biomechanical behaviour of the RVFW myocardium, and are a first step towards elucidating the structure–function of non-contracted murine RVFW myocardium in health and disease. PMID:22848044

  5. Collaborative processing to extract myocardium from a sequence of two-dimensional echocardiograms

    NASA Astrophysics Data System (ADS)

    Revankar, Shriram V.; Sher, David B.; Rosenthal, Steven

    1991-06-01

    Echocardiography is an important clinical method for identification and assessment of the entire spectrum of cardiac diseases. Visual assessment of the echocardiograms is tedious and subjective, but on the other hand, owing to the poor quality of the data, the automatic techniques are unreliable. One can minimize these drawbacks through collaborative processing. The authors describe a collaborative method to extract the myocardium from a sequence of two-dimensional echocardiograms. Initially, a morphologically adaptive thresholding scheme generates a rough estimate of the myocardium, and then a collaborative scheme refines the estimate. The threshold is computed at each pixel as a function of the local morphology and a default threshold. The points that have echodensities greater than the threshold form a rough estimate of the myocardium. This is collaboratively refined in accordance with the corrections specified by the operator, through mouse gestures. The gestures are mapped on to an image processing scheme that decides the precise boundaries of the intended regions that are to be added to or deleted from the estimated myocardium.

  6. Scrib:Rac1 interactions are required for the morphogenesis of the ventricular myocardium

    PubMed Central

    Boczonadi, Veronika; Gillespie, Rachel; Keenan, Iain; Ramsbottom, Simon A.; Donald-Wilson, Charlotte; Al Nazer, Mariana; Humbert, Patrick; Schwarz, Robert J.; Chaudhry, Bill; Henderson, Deborah J.

    2014-01-01

    Aims The organization and maturation of ventricular cardiomyocytes from the embryonic to the adult form is crucial for normal cardiac function. We have shown that a polarity protein, Scrib, may be involved in regulating the early stages of this process. Our goal was to establish whether Scrib plays a cell autonomous role in the ventricular myocardium, and whether this involves well-known polarity pathways. Methods and results Deletion of Scrib in cardiac precursors utilizing Scribflox mice together with the Nkx2.5-Cre driver resulted in disruption of the cytoarchitecture of the forming trabeculae and ventricular septal defects. Although the majority of mice lacking Scrib in the myocardium survived to adulthood, they developed marked cardiac fibrosis. Scrib did not physically interact with the planar cell polarity (PCP) protein, Vangl2, in early cardiomyocytes as it does in other tissues, suggesting that the anomalies did not result from disruption of PCP signalling. However, Scrib interacted with Rac1 physically in embryonic cardiomyocytes and genetically to result in ventricular abnormalities, suggesting that this interaction is crucial for the development of the early myocardium. Conclusions The Scrib–Rac1 interaction plays a crucial role in the organization of developing cardiomyocytes and formation of the ventricular myocardium. Thus, we have identified a novel signalling pathway in the early, functioning, heart muscle. These data also show that the foetus can recover from relatively severe abnormalities in prenatal ventricular development, although cardiac fibrosis can be a long-term consequence. PMID:25139745

  7. Seabuckthorn Pulp Oil Protects against Myocardial Ischemia-Reperfusion Injury in Rats through Activation of Akt/eNOS.

    PubMed

    Suchal, Kapil; Bhatia, Jagriti; Malik, Salma; Malhotra, Rajiv Kumar; Gamad, Nanda; Goyal, Sameer; Nag, Tapas C; Arya, Dharamvir S; Ojha, Shreesh

    2016-01-01

    Seabuckthorn (SBT) pulp oil obtained from the fruits of seabuckthorn [Hippophae rhamnoides L. (Elaeagnaceae)] has been used traditionally for its medicinal and nutritional properties. However, its role in ischemia-reperfusion (IR) injury of myocardium in rats has not been elucidated so far. The present study reports the cardioprotective effect of SBT pulp oil in IR-induced model of myocardial infarction in rats and underlying mechanism mediating activation of Akt/eNOS signaling pathway. Male albino Wistar rats were orally administered SBT pulp oil (5, 10, and 20 ml/kg/day) or saline for 30 days. On the day 31, ischemia was induced by one-stage ligation of left anterior descending coronary artery for 45 min followed by reperfusion for 60 min. SBT pulp oil pretreatment at the dose of 20 ml/kg observed to stabilize cardiac function and myocardial antioxidants such as glutathione, superoxide dismutase, catalase, and inhibited lipid peroxidation evidenced by reduced malondialdehyde levels as compared to IR-control group. SBT pulp oil also improved hemodynamic and contractile function and decreased tumor necrosis factor and activities of myocyte injury marker enzymes; lactate dehydrogenase and creatine kinase-MB. Additionally, a remarkable rise in expression of pAkt-eNOS, Bcl-2 and decline in expression of IKKβ/NF-κB and Bax was observed in the myocardium. The histopathological and ultrastructural salvage of cardiomyocytes further supports the cardioprotective effect of SBT pulp oil. Based on findings, it can be concluded that SBT pulp oil protects against myocardial IR injury mediating favorable modulation of Akt-eNOS and IKKβ/NF-κB expression. PMID:27445803

  8. Seabuckthorn Pulp Oil Protects against Myocardial Ischemia–Reperfusion Injury in Rats through Activation of Akt/eNOS

    PubMed Central

    Suchal, Kapil; Bhatia, Jagriti; Malik, Salma; Malhotra, Rajiv Kumar; Gamad, Nanda; Goyal, Sameer; Nag, Tapas C.; Arya, Dharamvir S.; Ojha, Shreesh

    2016-01-01

    Seabuckthorn (SBT) pulp oil obtained from the fruits of seabuckthorn [Hippophae rhamnoides L. (Elaeagnaceae)] has been used traditionally for its medicinal and nutritional properties. However, its role in ischemia–reperfusion (IR) injury of myocardium in rats has not been elucidated so far. The present study reports the cardioprotective effect of SBT pulp oil in IR-induced model of myocardial infarction in rats and underlying mechanism mediating activation of Akt/eNOS signaling pathway. Male albino Wistar rats were orally administered SBT pulp oil (5, 10, and 20 ml/kg/day) or saline for 30 days. On the day 31, ischemia was induced by one-stage ligation of left anterior descending coronary artery for 45 min followed by reperfusion for 60 min. SBT pulp oil pretreatment at the dose of 20 ml/kg observed to stabilize cardiac function and myocardial antioxidants such as glutathione, superoxide dismutase, catalase, and inhibited lipid peroxidation evidenced by reduced malondialdehyde levels as compared to IR-control group. SBT pulp oil also improved hemodynamic and contractile function and decreased tumor necrosis factor and activities of myocyte injury marker enzymes; lactate dehydrogenase and creatine kinase-MB. Additionally, a remarkable rise in expression of pAkt–eNOS, Bcl-2 and decline in expression of IKKβ/NF-κB and Bax was observed in the myocardium. The histopathological and ultrastructural salvage of cardiomyocytes further supports the cardioprotective effect of SBT pulp oil. Based on findings, it can be concluded that SBT pulp oil protects against myocardial IR injury mediating favorable modulation of Akt-eNOS and IKKβ/NF-κB expression. PMID:27445803

  9. Bone marrow transplantation across major histocompatibility barriers. V. Protection of mice from lethal graft-vs. -host disease by pretreatment of donor cells with monoclonal anti-Thy-1. 2 coupled to the toxin ricin

    SciTech Connect

    Vallera, D.A.; Youle, R.J.; Neville, D.M. Jr.; Kersey, J.H.

    1982-03-01

    A new method has been devised to eliminate T cells from murine bone marrow grafts across major histocompatibility barriers and thus prevent graft-vs.-host disease (GVHD). The method utilizes a monoclonal antibody directed at the Thy-1.2 antigen but is complement independent. To make anti-Thy-1.2 toxic, the antibody is covalently linked to the toxin ricin. Ricin ordinarily binds, enters, and kills cells through receptors containing galactose. The hybrid protein, anti-Thy-1.2-ricin, can enter and kill cells via the Thy-1.2 receptor. In the presence of lactose the usual entry route for ricin is largely blocked and the hybrid is shown to be a highly selective reagent that is T cell specific in its inhibition of mitogen-stimulated splenocytes. We have used a model of severe and fatal GVHD where BALB/c splenocytes and bone marrow cells are given to irradiated C57BL/6 recipients. Over 90% of these mice die by day 70, exhibiting signs of GVHD. When donor cells are pretreated with 0.5 microgram/ml of anti-Thy-1.2-ricin plus 200 mM lactose before injection, 10 of 11 animals survive through day 70 without signs of GVHD. These studies demonstrate that ricin linked to monoclonal antibodies may have utility related to the prevention of GVHD in human bone marrow transplantation.

  10. 40 CFR 432.16 - Pretreatment standards for new sources (PSNS). [Reserved

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... 40 Protection of Environment 30 2011-07-01 2011-07-01 false Pretreatment standards for new sources (PSNS). 432.16 Section 432.16 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS MEAT AND POULTRY PRODUCTS POINT SOURCE CATEGORY Simple...

  11. 40 CFR 432.24 - Pretreatment standards for existing sources (PSES). [Reserved

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... 40 Protection of Environment 30 2011-07-01 2011-07-01 false Pretreatment standards for existing sources (PSES). 432.24 Section 432.24 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS MEAT AND POULTRY PRODUCTS POINT SOURCE CATEGORY Complex...

  12. 40 CFR 432.14 - Pretreatment standards for existing sources (PSES). [Reserved

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... 40 Protection of Environment 30 2011-07-01 2011-07-01 false Pretreatment standards for existing sources (PSES). 432.14 Section 432.14 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS MEAT AND POULTRY PRODUCTS POINT SOURCE CATEGORY Simple...

  13. 40 CFR 432.26 - Pretreatment standards for new sources (PSNS). [Reserved

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... 40 Protection of Environment 30 2011-07-01 2011-07-01 false Pretreatment standards for new sources (PSNS). 432.26 Section 432.26 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS MEAT AND POULTRY PRODUCTS POINT SOURCE CATEGORY Complex...

  14. 40 CFR 471.84 - Pretreatment standards for existing sources (PSES). [Reserved

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... 40 Protection of Environment 30 2011-07-01 2011-07-01 false Pretreatment standards for existing sources (PSES). 471.84 Section 471.84 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS NONFERROUS METALS FORMING AND METAL POWDERS POINT SOURCE CATEGORY...

  15. 40 CFR 414.12 - Compliance date for pretreatment standards for existing sources (PSES).

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ... 40 Protection of Environment 30 2013-07-01 2012-07-01 true Compliance date for pretreatment standards for existing sources (PSES). 414.12 Section 414.12 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS ORGANIC CHEMICALS, PLASTICS, AND...

  16. 40 CFR 455.36 - Pretreatment standards for existing sources (PSES). [Reserved

    Code of Federal Regulations, 2012 CFR

    2012-07-01

    ... 40 Protection of Environment 31 2012-07-01 2012-07-01 false Pretreatment standards for existing sources (PSES). 455.36 Section 455.36 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) PESTICIDE CHEMICALS Metallo-Organic Pesticide...

  17. 40 CFR 455.37 - Pretreatment standards for new sources (PSNS). [Reserved

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ... 40 Protection of Environment 31 2013-07-01 2013-07-01 false Pretreatment standards for new sources (PSNS). 455.37 Section 455.37 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) PESTICIDE CHEMICALS Metallo-Organic Pesticide...

  18. 40 CFR 455.37 - Pretreatment standards for new sources (PSNS). [Reserved

    Code of Federal Regulations, 2014 CFR

    2014-07-01

    ... 40 Protection of Environment 30 2014-07-01 2014-07-01 false Pretreatment standards for new sources (PSNS). 455.37 Section 455.37 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) PESTICIDE CHEMICALS Metallo-Organic Pesticide...

  19. 40 CFR 455.11 - Compliance date for pretreatment standards for existing sources (PSES).

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... 40 Protection of Environment 30 2011-07-01 2011-07-01 false Compliance date for pretreatment standards for existing sources (PSES). 455.11 Section 455.11 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS PESTICIDE CHEMICALS Organic Pesticide Chemicals Manufacturing Subcategory §...

  20. 40 CFR 455.36 - Pretreatment standards for existing sources (PSES). [Reserved

    Code of Federal Regulations, 2014 CFR

    2014-07-01

    ... 40 Protection of Environment 30 2014-07-01 2014-07-01 false Pretreatment standards for existing sources (PSES). 455.36 Section 455.36 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) PESTICIDE CHEMICALS Metallo-Organic Pesticide...

  1. 40 CFR 455.36 - Pretreatment standards for existing sources (PSES). [Reserved

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ... 40 Protection of Environment 31 2013-07-01 2013-07-01 false Pretreatment standards for existing sources (PSES). 455.36 Section 455.36 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) PESTICIDE CHEMICALS Metallo-Organic Pesticide...

  2. 40 CFR 455.36 - Pretreatment standards for existing sources (PSES). [Reserved

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... 40 Protection of Environment 30 2011-07-01 2011-07-01 false Pretreatment standards for existing sources (PSES). 455.36 Section 455.36 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS PESTICIDE CHEMICALS Metallo-Organic Pesticide Chemicals Manufacturing Subcategory § 455.36...

  3. 40 CFR 455.36 - Pretreatment standards for existing sources (PSES). [Reserved

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... 40 Protection of Environment 29 2010-07-01 2010-07-01 false Pretreatment standards for existing sources (PSES). 455.36 Section 455.36 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS PESTICIDE CHEMICALS Metallo-Organic Pesticide Chemicals...

  4. 40 CFR 455.37 - Pretreatment standards for new sources (PSNS). [Reserved

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... 40 Protection of Environment 29 2010-07-01 2010-07-01 false Pretreatment standards for new sources (PSNS). 455.37 Section 455.37 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS PESTICIDE CHEMICALS Metallo-Organic Pesticide Chemicals...

  5. 40 CFR 455.37 - Pretreatment standards for new sources (PSNS). [Reserved

    Code of Federal Regulations, 2012 CFR

    2012-07-01

    ... 40 Protection of Environment 31 2012-07-01 2012-07-01 false Pretreatment standards for new sources (PSNS). 455.37 Section 455.37 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) PESTICIDE CHEMICALS Metallo-Organic Pesticide...

  6. 40 CFR 430.87 - Pretreatment standards for new sources (PSNS). [Reserved

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... 40 Protection of Environment 29 2010-07-01 2010-07-01 false Pretreatment standards for new sources (PSNS). 430.87 Section 430.87 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS THE PULP, PAPER, AND PAPERBOARD POINT SOURCE CATEGORY Non-Wood...

  7. 40 CFR 430.86 - Pretreatment standards for existing sources (PSES). [Reserved

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... 40 Protection of Environment 29 2010-07-01 2010-07-01 false Pretreatment standards for existing sources (PSES). 430.86 Section 430.86 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS THE PULP, PAPER, AND PAPERBOARD POINT SOURCE CATEGORY Non-Wood...

  8. 40 CFR 471.84 - Pretreatment standards for existing sources (PSES). [Reserved

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... 40 Protection of Environment 29 2010-07-01 2010-07-01 false Pretreatment standards for existing sources (PSES). 471.84 Section 471.84 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS NONFERROUS METALS FORMING AND METAL POWDERS POINT SOURCE CATEGORY...

  9. 40 CFR 435.47 - Pretreatment standards of performance for new sources (PSNS).

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ... 40 Protection of Environment 31 2013-07-01 2013-07-01 false Pretreatment standards of performance for new sources (PSNS). 435.47 Section 435.47 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) OIL AND GAS EXTRACTION POINT SOURCE CATEGORY Coastal Subcategory § 435.47...

  10. 40 CFR 435.46 - Pretreatment standards of performance for existing sources (PSES).

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ... 40 Protection of Environment 31 2013-07-01 2013-07-01 false Pretreatment standards of performance for existing sources (PSES). 435.46 Section 435.46 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) OIL AND GAS EXTRACTION POINT SOURCE CATEGORY Coastal Subcategory §...

  11. 40 CFR 432.14 - Pretreatment standards for existing sources (PSES). [Reserved

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... 40 Protection of Environment 29 2010-07-01 2010-07-01 false Pretreatment standards for existing sources (PSES). 432.14 Section 432.14 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS MEAT AND POULTRY PRODUCTS POINT SOURCE CATEGORY Simple...

  12. 40 CFR 432.16 - Pretreatment standards for new sources (PSNS). [Reserved

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... 40 Protection of Environment 29 2010-07-01 2010-07-01 false Pretreatment standards for new sources (PSNS). 432.16 Section 432.16 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS MEAT AND POULTRY PRODUCTS POINT SOURCE CATEGORY Simple...

  13. 40 CFR 429.136 - Pretreatment standards for new sources (PSNS).

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... introduces process wastewater pollutants into a publicly owned treatment works must comply with 40 CFR part... 40 Protection of Environment 30 2011-07-01 2011-07-01 false Pretreatment standards for new sources (PSNS). 429.136 Section 429.136 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY...

  14. 40 CFR 429.26 - Pretreatment standards for new sources (PSNS).

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... introduces process wastewater pollutants into a publicly owned treatment works must comply with 40 CFR part... 40 Protection of Environment 30 2011-07-01 2011-07-01 false Pretreatment standards for new sources (PSNS). 429.26 Section 429.26 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY...

  15. 40 CFR 429.36 - Pretreatment standards for new sources (PSNS).

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... introduces process wastewater pollutants into a publicly owned treatment works must comply with 40 CFR part... 40 Protection of Environment 30 2011-07-01 2011-07-01 false Pretreatment standards for new sources (PSNS). 429.36 Section 429.36 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY...

  16. 40 CFR 429.46 - Pretreatment standards for new sources (PSNS).

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... introduces process wastewater pollutants into a publicly owned treatment works must comply with 40 CFR part... 40 Protection of Environment 30 2011-07-01 2011-07-01 false Pretreatment standards for new sources (PSNS). 429.46 Section 429.46 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY...

  17. 40 CFR 429.116 - Pretreatment standards for new sources (PSNS).

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... introduces process wastewater pollutants into a publicly owned treatment works must comply with 40 CFR part... 40 Protection of Environment 30 2011-07-01 2011-07-01 false Pretreatment standards for new sources (PSNS). 429.116 Section 429.116 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY...

  18. 40 CFR 429.106 - Pretreatment standards for new sources (PSNS).

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... introduces process wastewater pollutants into a publicly owned treatment works must comply with 40 CFR part... 40 Protection of Environment 30 2011-07-01 2011-07-01 false Pretreatment standards for new sources (PSNS). 429.106 Section 429.106 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY...

  19. 40 CFR 432.24 - Pretreatment standards for existing sources (PSES). [Reserved

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... 40 Protection of Environment 29 2010-07-01 2010-07-01 false Pretreatment standards for existing sources (PSES). 432.24 Section 432.24 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS MEAT AND POULTRY PRODUCTS POINT SOURCE CATEGORY Complex...

  20. 40 CFR 432.26 - Pretreatment standards for new sources (PSNS). [Reserved

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... 40 Protection of Environment 29 2010-07-01 2010-07-01 false Pretreatment standards for new sources (PSNS). 432.26 Section 432.26 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS MEAT AND POULTRY PRODUCTS POINT SOURCE CATEGORY Complex...

  1. 40 CFR 432.76 - Pretreatment standards for new sources (PSNS). [Reserved

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... 40 Protection of Environment 29 2010-07-01 2010-07-01 false Pretreatment standards for new sources (PSNS). 432.76 Section 432.76 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS MEAT AND POULTRY PRODUCTS POINT SOURCE CATEGORY Sausage and...

  2. 40 CFR 432.74 - Pretreatment standards for existing sources (PSES). [Reserved

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... 40 Protection of Environment 29 2010-07-01 2010-07-01 false Pretreatment standards for existing sources (PSES). 432.74 Section 432.74 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS MEAT AND POULTRY PRODUCTS POINT SOURCE CATEGORY Sausage and...

  3. 40 CFR 414.66 - Pretreatment standards for new sources (PSNS).

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... 40 Protection of Environment 28 2010-07-01 2010-07-01 true Pretreatment standards for new sources (PSNS). 414.66 Section 414.66 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS ORGANIC CHEMICALS, PLASTICS, AND SYNTHETIC FIBERS Commodity...

  4. 40 CFR 414.36 - Pretreatment standards for new sources (PSNS).

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... 40 Protection of Environment 28 2010-07-01 2010-07-01 true Pretreatment standards for new sources (PSNS). 414.36 Section 414.36 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS ORGANIC CHEMICALS, PLASTICS, AND SYNTHETIC FIBERS Other Fibers §...

  5. 40 CFR 414.85 - Pretreatment standards for existing sources (PSES).

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... 40 Protection of Environment 28 2010-07-01 2010-07-01 true Pretreatment standards for existing sources (PSES). 414.85 Section 414.85 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS ORGANIC CHEMICALS, PLASTICS, AND SYNTHETIC FIBERS Specialty...

  6. 40 CFR 414.65 - Pretreatment standards for existing sources (PSES).

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... 40 Protection of Environment 28 2010-07-01 2010-07-01 true Pretreatment standards for existing sources (PSES). 414.65 Section 414.65 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS ORGANIC CHEMICALS, PLASTICS, AND SYNTHETIC FIBERS Commodity...

  7. 40 CFR 414.35 - Pretreatment standards for existing sources (PSES).

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... 40 Protection of Environment 28 2010-07-01 2010-07-01 true Pretreatment standards for existing sources (PSES). 414.35 Section 414.35 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS ORGANIC CHEMICALS, PLASTICS, AND SYNTHETIC FIBERS Other Fibers §...

  8. 40 CFR 414.86 - Pretreatment standards for new sources (PSNS).

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... 40 Protection of Environment 28 2010-07-01 2010-07-01 true Pretreatment standards for new sources (PSNS). 414.86 Section 414.86 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS ORGANIC CHEMICALS, PLASTICS, AND SYNTHETIC FIBERS Specialty...

  9. 40 CFR 414.56 - Pretreatment standards for new sources (PSNS).

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... 40 Protection of Environment 28 2010-07-01 2010-07-01 true Pretreatment standards for new sources (PSNS). 414.56 Section 414.56 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS ORGANIC CHEMICALS, PLASTICS, AND SYNTHETIC FIBERS Thermosetting...

  10. 40 CFR 414.12 - Compliance date for pretreatment standards for existing sources (PSES).

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... 40 Protection of Environment 28 2010-07-01 2010-07-01 true Compliance date for pretreatment standards for existing sources (PSES). 414.12 Section 414.12 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS ORGANIC CHEMICALS, PLASTICS, AND...

  11. 40 CFR 414.76 - Pretreatment standards for new sources (PSNS).

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... 40 Protection of Environment 28 2010-07-01 2010-07-01 true Pretreatment standards for new sources (PSNS). 414.76 Section 414.76 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS ORGANIC CHEMICALS, PLASTICS, AND SYNTHETIC FIBERS Bulk Organic...

  12. 40 CFR 414.55 - Pretreatment standards for existing sources (PSES).

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... 40 Protection of Environment 28 2010-07-01 2010-07-01 true Pretreatment standards for existing sources (PSES). 414.55 Section 414.55 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS ORGANIC CHEMICALS, PLASTICS, AND SYNTHETIC FIBERS Thermosetting...

  13. 40 CFR 414.75 - Pretreatment standards for existing sources (PSES).

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... 40 Protection of Environment 28 2010-07-01 2010-07-01 true Pretreatment standards for existing sources (PSES). 414.75 Section 414.75 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS ORGANIC CHEMICALS, PLASTICS, AND SYNTHETIC FIBERS Bulk Organic...

  14. 40 CFR 471.74 - Pretreatment standards for existing sources (PSES). [Reserved

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... 40 Protection of Environment 30 2011-07-01 2011-07-01 false Pretreatment standards for existing sources (PSES). 471.74 Section 471.74 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS NONFERROUS METALS FORMING AND METAL POWDERS POINT SOURCE CATEGORY...

  15. 40 CFR 471.74 - Pretreatment standards for existing sources (PSES). [Reserved

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... 40 Protection of Environment 29 2010-07-01 2010-07-01 false Pretreatment standards for existing sources (PSES). 471.74 Section 471.74 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS NONFERROUS METALS FORMING AND METAL POWDERS POINT SOURCE CATEGORY...

  16. 40 CFR 432.66 - Pretreatment standards for new sources (PSNS). [Reserved

    Code of Federal Regulations, 2012 CFR

    2012-07-01

    ... 40 Protection of Environment 31 2012-07-01 2012-07-01 false Pretreatment standards for new sources (PSNS). 432.66 Section 432.66 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) MEAT AND POULTRY PRODUCTS POINT SOURCE CATEGORY Meat...

  17. 40 CFR 432.64 - Pretreatment standards for existing sources (PSES). [Reserved

    Code of Federal Regulations, 2012 CFR

    2012-07-01

    ... 40 Protection of Environment 31 2012-07-01 2012-07-01 false Pretreatment standards for existing sources (PSES). 432.64 Section 432.64 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) MEAT AND POULTRY PRODUCTS POINT SOURCE CATEGORY Meat...

  18. 40 CFR 432.96 - Pretreatment standards for new sources (PSNS). [Reserved

    Code of Federal Regulations, 2012 CFR

    2012-07-01

    ... 40 Protection of Environment 31 2012-07-01 2012-07-01 false Pretreatment standards for new sources (PSNS). 432.96 Section 432.96 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) MEAT AND POULTRY PRODUCTS POINT SOURCE CATEGORY Canned...

  19. 40 CFR 432.94 - Pretreatment standards for existing sources (PSES). [Reserved

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ... 40 Protection of Environment 31 2013-07-01 2013-07-01 false Pretreatment standards for existing sources (PSES). 432.94 Section 432.94 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) MEAT AND POULTRY PRODUCTS POINT SOURCE CATEGORY Canned...

  20. 40 CFR 432.94 - Pretreatment standards for existing sources (PSES). [Reserved

    Code of Federal Regulations, 2014 CFR

    2014-07-01

    ... 40 Protection of Environment 30 2014-07-01 2014-07-01 false Pretreatment standards for existing sources (PSES). 432.94 Section 432.94 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) MEAT AND POULTRY PRODUCTS POINT SOURCE CATEGORY Canned...

  1. 40 CFR 432.96 - Pretreatment standards for new sources (PSNS). [Reserved

    Code of Federal Regulations, 2014 CFR

    2014-07-01

    ... 40 Protection of Environment 30 2014-07-01 2014-07-01 false Pretreatment standards for new sources (PSNS). 432.96 Section 432.96 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) MEAT AND POULTRY PRODUCTS POINT SOURCE CATEGORY Canned...

  2. 40 CFR 432.66 - Pretreatment standards for new sources (PSNS). [Reserved

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... 40 Protection of Environment 30 2011-07-01 2011-07-01 false Pretreatment standards for new sources (PSNS). 432.66 Section 432.66 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS MEAT AND POULTRY PRODUCTS POINT SOURCE CATEGORY Meat Cutters §...

  3. 40 CFR 432.94 - Pretreatment standards for existing sources (PSES). [Reserved

    Code of Federal Regulations, 2012 CFR

    2012-07-01

    ... 40 Protection of Environment 31 2012-07-01 2012-07-01 false Pretreatment standards for existing sources (PSES). 432.94 Section 432.94 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) MEAT AND POULTRY PRODUCTS POINT SOURCE CATEGORY Canned...

  4. 40 CFR 432.94 - Pretreatment standards for existing sources (PSES). [Reserved

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... 40 Protection of Environment 30 2011-07-01 2011-07-01 false Pretreatment standards for existing sources (PSES). 432.94 Section 432.94 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS MEAT AND POULTRY PRODUCTS POINT SOURCE CATEGORY Canned Meats...

  5. 40 CFR 432.64 - Pretreatment standards for existing sources (PSES). [Reserved

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ... 40 Protection of Environment 31 2013-07-01 2013-07-01 false Pretreatment standards for existing sources (PSES). 432.64 Section 432.64 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) MEAT AND POULTRY PRODUCTS POINT SOURCE CATEGORY Meat...

  6. 40 CFR 432.96 - Pretreatment standards for new sources (PSNS). [Reserved

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ... 40 Protection of Environment 31 2013-07-01 2013-07-01 false Pretreatment standards for new sources (PSNS). 432.96 Section 432.96 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) MEAT AND POULTRY PRODUCTS POINT SOURCE CATEGORY Canned...

  7. 40 CFR 432.64 - Pretreatment standards for existing sources (PSES). [Reserved

    Code of Federal Regulations, 2014 CFR

    2014-07-01

    ... 40 Protection of Environment 30 2014-07-01 2014-07-01 false Pretreatment standards for existing sources (PSES). 432.64 Section 432.64 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) MEAT AND POULTRY PRODUCTS POINT SOURCE CATEGORY Meat...

  8. 40 CFR 432.96 - Pretreatment standards for new sources (PSNS). [Reserved

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... 40 Protection of Environment 30 2011-07-01 2011-07-01 false Pretreatment standards for new sources (PSNS). 432.96 Section 432.96 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS MEAT AND POULTRY PRODUCTS POINT SOURCE CATEGORY Canned Meats...

  9. 40 CFR 432.94 - Pretreatment standards for existing sources (PSES). [Reserved

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... 40 Protection of Environment 29 2010-07-01 2010-07-01 false Pretreatment standards for existing sources (PSES). 432.94 Section 432.94 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS MEAT AND POULTRY PRODUCTS POINT SOURCE CATEGORY Canned Meats...

  10. 40 CFR 432.66 - Pretreatment standards for new sources (PSNS). [Reserved

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... 40 Protection of Environment 29 2010-07-01 2010-07-01 false Pretreatment standards for new sources (PSNS). 432.66 Section 432.66 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS MEAT AND POULTRY PRODUCTS POINT SOURCE CATEGORY Meat Cutters §...

  11. 40 CFR 432.66 - Pretreatment standards for new sources (PSNS). [Reserved

    Code of Federal Regulations, 2014 CFR

    2014-07-01

    ... 40 Protection of Environment 30 2014-07-01 2014-07-01 false Pretreatment standards for new sources (PSNS). 432.66 Section 432.66 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) MEAT AND POULTRY PRODUCTS POINT SOURCE CATEGORY Meat...

  12. 40 CFR 432.66 - Pretreatment standards for new sources (PSNS). [Reserved

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ... 40 Protection of Environment 31 2013-07-01 2013-07-01 false Pretreatment standards for new sources (PSNS). 432.66 Section 432.66 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) MEAT AND POULTRY PRODUCTS POINT SOURCE CATEGORY Meat...

  13. 40 CFR 432.64 - Pretreatment standards for existing sources (PSES). [Reserved

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... 40 Protection of Environment 30 2011-07-01 2011-07-01 false Pretreatment standards for existing sources (PSES). 432.64 Section 432.64 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS MEAT AND POULTRY PRODUCTS POINT SOURCE CATEGORY Meat Cutters §...

  14. 40 CFR 432.64 - Pretreatment standards for existing sources (PSES). [Reserved

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... 40 Protection of Environment 29 2010-07-01 2010-07-01 false Pretreatment standards for existing sources (PSES). 432.64 Section 432.64 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS MEAT AND POULTRY PRODUCTS POINT SOURCE CATEGORY Meat Cutters §...

  15. 40 CFR 432.96 - Pretreatment standards for new sources (PSNS). [Reserved

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... 40 Protection of Environment 29 2010-07-01 2010-07-01 false Pretreatment standards for new sources (PSNS). 432.96 Section 432.96 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS MEAT AND POULTRY PRODUCTS POINT SOURCE CATEGORY Canned Meats...

  16. Cellulose pretreatments of lignocellulosic substrates

    NASA Technical Reports Server (NTRS)

    Weil, J.; Westgate, P.; Kohlmann, K.; Ladisch, M. R.; Mitchell, C. A. (Principal Investigator)

    1994-01-01

    Cellulose in inedible plant materials, forestry residues, and municipal wastes must be pretreated to disrupt its physical structure, thereby making its hydrolysis to glucose practical. Developments since 1991 are summarized.

  17. Myocardial kinetics of fluorine-18 misonidazole: A marker of hypoxic myocardium

    SciTech Connect

    Shelton, M.E.; Dence, C.S.; Hwang, D.R.; Welch, M.J.; Bergmann, S.R.

    1989-03-01

    Fluoromisonidazole, a member of a class of compounds referred to as ''hypoxic sensitizers,'' accumulates in hypoxic, viable tumor cells. We hypothesized that it might therefore accumulate also in ischemic, but non-necrotic myocardium potentially salvageable by interventional therapy. To evaluate the myocardial kinetics of (18F)fluoromisonidazole (FM), 20 isolated perfused rabbit hearts were used to characterize the uptake and binding of tracer under control conditions (n = 6), or with ischemia (flow 10% of control, n = 5), hypoxia without low flow (control flow rates with hypoxic medium, n = 5), or with reperfusion (n = 4). Myocardial retention of tracer detected externally with gamma scintillation probes after 20 min of constant (18F)FM infusion followed by 20 min of washout with nonradioactive buffer was 41 +/- 7% and 46 +/- 8% of peak activity in hearts subjected to ischemia or hypoxia, respectively, and significantly higher than in hearts subjected to either control perfusion or to ischemia followed by reperfusion (18 +/- 6 and 16 +/- 5% of peak activity, respectively, p less than 0.01). The biologic half-time of retained tracer was 40 hr in all hearts indicating essentially irreversible binding. Based on these findings, we measured uptake of (18F)FM using positron emission tomography in five dogs subjected to acute coronary occlusion. Five to thirteen millicuries of tracer were injected within 3 hr of occlusion. Within 30 min after administration of tracer, 18F accumulation in ischemic myocardium was greater than that observed in normal myocardium. The results indicate that (18F)FM accumulates in ischemic myocardium in relation to diminished tissue oxygen content and not simply because of diminished flow. Thus, this class of compounds may be potentially useful to help identify hypoxic myocardium.

  18. Decline of Phosphotransfer and Substrate Supply Metabolic Circuits Hinders ATP Cycling in Aging Myocardium.

    PubMed

    Nemutlu, Emirhan; Gupta, Anu; Zhang, Song; Viqar, Maria; Holmuhamedov, Ekhson; Terzic, Andre; Jahangir, Arshad; Dzeja, Petras

    2015-01-01

    Integration of mitochondria with cytosolic ATP-consuming/ATP-sensing and substrate supply processes is critical for muscle bioenergetics and electrical activity. Whether age-dependent muscle weakness and increased electrical instability depends on perturbations in cellular energetic circuits is unknown. To define energetic remodeling of aged atrial myocardium we tracked dynamics of ATP synthesis-utilization, substrate supply, and phosphotransfer circuits through adenylate kinase (AK), creatine kinase (CK), and glycolytic/glycogenolytic pathways using 18O stable isotope-based phosphometabolomic technology. Samples of intact atrial myocardium from adult and aged rats were subjected to 18O-labeling procedure at resting basal state, and analyzed using the 18O-assisted HPLC-GC/MS technique. Characteristics for aging atria were lower inorganic phosphate Pi[18O], γ-ATP[18O], β-ADP[18O], and creatine phosphate CrP[18O] 18O-labeling rates indicating diminished ATP utilization-synthesis and AK and CK phosphotransfer fluxes. Shift in dynamics of glycolytic phosphotransfer was reflected in the diminished G6P[18O] turnover with relatively constant glycogenolytic flux or G1P[18O] 18O-labeling. Labeling of G3P[18O], an indicator of G3P-shuttle activity and substrate supply to mitochondria, was depressed in aged myocardium. Aged atrial myocardium displayed reduced incorporation of 18O into second (18O2), third (18O3), and fourth (18O4) positions of Pi[18O] and a lower Pi[18O]/γ-ATP[18 O]-labeling ratio, indicating delayed energetic communication and ATP cycling between mitochondria and cellular ATPases. Adrenergic stress alleviated diminished CK flux, AK catalyzed β-ATP turnover and energetic communication in aging atria. Thus, 18O-assisted phosphometabolomics uncovered simultaneous phosphotransfer through AK, CK, and glycolytic pathways and G3P substrate shuttle deficits hindering energetic communication and ATP cycling, which may underlie energetic vulnerability of aging

  19. [Separate evaluation of beta-methyl fatty acid uptake and perfusion in rat myocardium].

    PubMed

    Taniguchi, M; Bunkou, H; Nakajima, K; Taki, J; Muramori, A; Matsunari, I; Nambu, I; Shiirei, Y; Tonami, N; Hisada, K

    1989-12-01

    The kinetics and distribution of I-125 beta-methyl iodophenyl pentadecanoic acid (BMIPP) in rat's heart were studied for separate evaluation of perfusion and metabolism. Tl-201 and BMIPP were simultaneously injected. The experimental groups consisted of control (C), glucose (G) and sodium lactate loaded group (L). In C, myocardial uptake at 5 minutes after BMIPP injection was 3.60% ID/g and remained constant up to 60 minutes. The myocardium/lung ratio (2.44) and the myocardium/muscle ratio (4.55) of BMIPP were almost equal to those of Tl-201. But myocardium/liver ratio was low (1.31). In G, myocardial uptake of BMIPP (1.94 +/- 0.36% ID/g) and g-BMIPP/Tl (0.31 +/- 0.03) at 15 minutes after injection were significantly decreased (p less than 0.001) than those of C (3.16 +/- 0.18% ID/g and 0.48 +/- 0.05). In L. myocardial perfusion was decreased and g-BMIPP/Tl (0.73 +/- 0.14) was significantly higher (p less than 0.01) than those of C. Coefficient of variance of the density within a myocardium, and the ratio of inner to outer layer of myocardium (I/O ratio) were calculated from autoradiogram by videodensitometry. The myocardial distribution of BMIPP was more inhomogeneous, and the I/O ratio was lower than that of Tl-201, although these were not specific for metabolic interventions. In conclusion BMIPP is suitable for SPECT imaging and dual nuclide imaging by BMIPP and Tl-201 will provide informations about myocardial fatty acid metabolism and perfusion. PMID:2622083

  20. Decline of Phosphotransfer and Substrate Supply Metabolic Circuits Hinders ATP Cycling in Aging Myocardium.

    PubMed

    Nemutlu, Emirhan; Gupta, Anu; Zhang, Song; Viqar, Maria; Holmuhamedov, Ekhson; Terzic, Andre; Jahangir, Arshad; Dzeja, Petras

    2015-01-01

    Integration of mitochondria with cytosolic ATP-consuming/ATP-sensing and substrate supply processes is critical for muscle bioenergetics and electrical activity. Whether age-dependent muscle weakness and increased electrical instability depends on perturbations in cellular energetic circuits is unknown. To define energetic remodeling of aged atrial myocardium we tracked dynamics of ATP synthesis-utilization, substrate supply, and phosphotransfer circuits through adenylate kinase (AK), creatine kinase (CK), and glycolytic/glycogenolytic pathways using 18O stable isotope-based phosphometabolomic technology. Samples of intact atrial myocardium from adult and aged rats were subjected to 18O-labeling procedure at resting basal state, and analyzed using the 18O-assisted HPLC-GC/MS technique. Characteristics for aging atria were lower inorganic phosphate Pi[18O], γ-ATP[18O], β-ADP[18O], and creatine phosphate CrP[18O] 18O-labeling rates indicating diminished ATP utilization-synthesis and AK and CK phosphotransfer fluxes. Shift in dynamics of glycolytic phosphotransfer was reflected in the diminished G6P[18O] turnover with relatively constant glycogenolytic flux or G1P[18O] 18O-labeling. Labeling of G3P[18O], an indicator of G3P-shuttle activity and substrate supply to mitochondria, was depressed in aged myocardium. Aged atrial myocardium displayed reduced incorporation of 18O into second (18O2), third (18O3), and fourth (18O4) positions of Pi[18O] and a lower Pi[18O]/γ-ATP[18 O]-labeling ratio, indicating delayed energetic communication and ATP cycling between mitochondria and cellular ATPases. Adrenergic stress alleviated diminished CK flux, AK catalyzed β-ATP turnover and energetic communication in aging atria. Thus, 18O-assisted phosphometabolomics uncovered simultaneous phosphotransfer through AK, CK, and glycolytic pathways and G3P substrate shuttle deficits hindering energetic communication and ATP cycling, which may underlie energetic vulnerability of aging

  1. Processes for pretreating lignocellulosic biomass: A review

    SciTech Connect

    McMillan, J.D.

    1992-11-01

    This paper reviews existing and proposed pretreatment processes for biomass. The focus is on the mechanisms by which the various pretreatments act and the influence of biomass structure and composition on the efficacy of particular pretreatment techniques. This analysis is used to identify pretreatment technologies and issues that warrant further research.

  2. Reduced expression of CRHR2 and Sp-1 in myocardium of ovariectomized rats is improved by exercise training.

    PubMed

    Tang, Zhiping; Wang, Yujun; Zhu, Xiaoyan; Ni, Xin; Cong, Binhai; Lu, Jianqiang

    2015-01-01

    Exercise training has been looked on as a non-pharmacologic approach to treating ovariectomy (OVX)-induced dysfunctions. In this study, we investigated whether chronic exercise impacts on expression of urocortins (UCNs) and corticotropin-releasing hormone receptor type 2 (CRHR2) in myocardium of OVX rats. Bilateral OVX or sham-operation was performed under anesthesia. Both groups were then divided into two subgroups, with or without treadmill training for 8 weeks. It was found that OVX as well as exercise did not affect the mRNA levels of UCN, UCN2 and UCN3 in myocardium. OVX caused down-regulation of CRHR2 in myocardium. Exercise training reversed the OVX-induced reduction of CRHR2, but had no influence on CRHR2 level in sham rats. OVX resulted in a decrease in estrogen receptor α (ERα) expression in myocardium, which was restored by exercise. Moreover, exercise training also reversed OVX-induced down-regulation of specific protein-1 (Sp-1) expression in myocardium. CRHR2 expression level correlated with Sp-1 and ERα level in myocardium. These results indicate that exercise training can restore the CRHR2 level in myocardium of OVX rats, which is associated with ERα and Sp-1 expression.

  3. Steam pretreatment for coal liquefaction

    NASA Astrophysics Data System (ADS)

    Ivanenko, Olga

    The objectives of this work are to test the application of steam pretreatment to direct coal liquefaction, to investigate the reaction of model compounds with water, and to explore the use of zeolites in these processes. Previous work demonstrated the effectiveness of steam pretreatment in a subsequent flash pyrolysis. Apparently, subcritical steam ruptures nearly all of the ether cross links, leaving a partially depolymerized structure. It was postulated that very rapid heating of the pretreated coal to liquefaction conditions would be required to preserve the effects of such treatment. Accordingly, a method was adopted in which coal slurry is injected into a hot autoclave containing solvent. Since oxygen is capable of destroying the pretreatment effect, precautions were taken for its rigorous exclusion. Tests were conducted with Illinois No. 6 coal steam treated at 340sp°C, 750 psia for 15 minutes. Both raw and pretreated samples were liquified in deoxygenated tetralin at high severity (400sp°C, 30 min.) and low severity (a: 350sp°C, 30 min., and b: 385sp°C, 15 min.) conditions under 1500 psia hydrogen. Substantial improvement in liquid product quality was obtained and the need for rapid heating and oxygen exclusion demonstrated. Under low severity conditions, the oil yield was more than doubled, going from 12.5 to 29 wt%. Also chemistry of the pretreatment process was studied using aromatic ethers as model compounds. alpha-Benzylnaphthyl ether (alpha-BNE), alpha-naphthylmethyl phenyl (alpha-NMPE), and 9-phenoxyphenanthrene were exposed to steam and inert gas at pretreatment conditions and in some cases to liquid water at 315sp°C. alpha-BNE and alpha-NMPE showed little difference in conversion in inert gas and in steam. Hence, these compounds are poor models for coal in steam pretreatment. Thermally stable 9-phenoxyphenanthrene, however, was completely converted in one hour by liquid water at 315sp°C. At pretreatment conditions mostly rearranged starting

  4. [CHANGES BLOOD GAS AND OF FREE RADICAL OXIDATION OF LIPIDS IN THE MYOCARDIUM DURING ADAPTATION TO PHYSICAL STRESS].

    PubMed

    Balykin, M V; Sagidova, S A; Zharkov, A V

    2015-09-01

    The article considers the changes of gas composition, acid-base blood balance, lipid peroxidation processes, and activity of the antioxidant defense system in rat myocardium in the course of adaptation to physical activity (swimming). It has been found out that during the first five days physical activity is accompanied by hypoxia, acidotic blood changes, and increase of lipid peroxidation processes in myocardium. Adaptation to swimming activity (15-30 days) leads to hypoxic and acidotic blood changes, and increases antioxidant defense system in myocardium.

  5. [Catecholamines and their metabolic enzymes in the rat myocardium after a flight on the Kosmos-936 biosatellite].

    PubMed

    Kwetncanski, R; Tigranian, R A; Torda, T

    1982-01-01

    In the myocardium of the weightless and centrifuged rats flown for 18.5 days onboard the biosatellite Cosmos-936 the catecholamine concentration and activity of enzymes involved in their synthesis and degradation--dopamine-beta-hydroxylase, monoamine oxidase and catechol-O-methyl transferase--were measured. The catecholamine concentration in the myocardium of both flight groups significantly increased, and the enzyme activity did not change. These results suggest that an exposure to space flight increases the catecholamine concentration and exerts no effect on their synthesis and degradation in the rat myocardium.

  6. Effects of ischemic preconditioning on myocardium Caspase-3, SOCS-1, SOCS-3, TNF-α and IL-6 mRNA expression levels in myocardium IR rats.

    PubMed

    Ma, Jiangwei; Qiao, Zengyong; Xu, Biao

    2013-10-01

    The aim of this study was to characterise the effects of ischemic preconditioning (IP) on heart function parameters (ΔST and ΔT), activities of serum creatine kinase (CK), lactate dehydrogenase (LDH), and levels of serum nitric oxide (NO), malondialdehyde (MDA), and myocardium Caspase-3 mRNA, SOCS-1, SOCS-3, tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) expression levels and Apoptosis index in myocardium IR rats. Results showed that ΔST and ΔST values in IP group were markedly lower than those in IR group. Compared with IR group, IP significantly (p < 0.01) decreased serum CK (0.83 ± 0.09 vs 1.36 ± 0.15), LDH (5613 ± 462 vs 7106 ± 492) activities and MDA (11.32 ± 1.05 vs 15.49 ± 1.26) level, increased the serum NO (86.39 ± 7.03 vs 53.77 ± 4.27) level in IR group. The IP induced a significant decreased in myocardium Caspase-3 mRNA (0.303 ± 0.021 vs 0.515 ± 0.022) gene expression (p < 0.01) compared to IR model group. The IP induced a significant decreased in myocardium SOCS-1 (0.241 ± 0.031 vs 0.596 ± 0.036), SOCS-3 (0.258 ± 0.031 vs 0.713 ± 0.057), TNF-α (0.137 ± 0.011 vs 0.427 ± 0.035) and IL-6 (0.314 ± 0.021 vs 0.719 ± 0.064) mRNA gene expression (p < 0.01) compared to IR model group. We conclude that IP is effective in the therapy of heart disease. These findings may have implications for the clinical development of preconditioning-based therapies for ischemic heart disease.

  7. Exenatide exerts a PKA-dependent positive inotropic effect in human atrial myocardium: GLP-1R mediated effects in human myocardium.

    PubMed

    Wallner, Markus; Kolesnik, Ewald; Ablasser, Klemens; Khafaga, Mounir; Wakula, Paulina; Ljubojevic, Senka; Thon-Gutschi, Eva Maria; Sourij, Harald; Kapl, Martin; Edmunds, Nicholas J; Kuzmiski, J Brent; Griffith, David A; Knez, Igor; Pieske, Burkert; von Lewinski, Dirk

    2015-12-01

    Glucagon-like peptide-1 receptor (GLP-1R) agonists are a rapidly growing class of drugs developed for treating type-2 diabetes mellitus. Patients with diabetes carry an up to 5-fold greater mortality risk compared to non-diabetic patients, mainly as a result of cardiovascular diseases. Although beneficial cardiovascular effects have been reported, exact mechanisms of GLP-1R-agonist action in the heart, especially in human myocardium, are poorly understood. The effects of GLP-1R-agonists (exenatide, GLP-1(7-36)NH2, PF-06446009, PF-06446667) on cardiac contractility were tested in non-failing atrial and ventricular trabeculae from 72 patients. The GLP-1(7-36)NH2 metabolite, GLP-1(9-36)NH2, was also examined. In electrically stimulated trabeculae, the effects of compounds on isometric force were measured in the absence and presence of pharmacological inhibitors of signal transduction pathways. The role of β-arrestin signaling was examined using a β-arrestin partial agonist, PF-06446667. Expression levels were tested by immunoblots. Translocation of GLP-1R downstream molecular targets, Epac2, GLUT-1 and GLUT-4, were assessed by fluorescence microscopy. All tested GLP-1R-agonists significantly increased developed force in human atrial trabeculae, whereas GLP-1(9-36)NH2 had no effect. Exendin(9-39)NH2, a GLP-1R-antagonist, and H-89 blunted the inotropic effect of exenatide. In addition, exenatide increased PKA-dependent phosphorylation of phospholamban (PLB), GLUT-1 and Epac2 translocation, but not GLUT-4 translocation. Exenatide failed to enhance contractility in ventricular myocardium. Quantitative real-time PCR (qRT-PCR) revealed a significant higher GLP-1R expression in the atrium compared to ventricle. Exenatide increased contractility in a dose-dependent manner via GLP-1R/cAMP/PKA pathway and induced GLUT-1 and Epac2 translocation in human atrial myocardium, but had no effect in ventricular myocardium. Therapeutic use of GLP-1R-agonists may therefore impart

  8. Quantification of Shear Deformations and Corresponding Stresses in the Biaxially Tested Human Myocardium.

    PubMed

    Sommer, Gerhard; Haspinger, Daniel Ch; Andrä, Michaela; Sacherer, Michael; Viertler, Christian; Regitnig, Peter; Holzapfel, Gerhard A

    2015-10-01

    One goal of cardiac research is to perform numerical simulations to describe/reproduce the mechanoelectrical function of the human myocardium in health and disease. Such simulations are based on a complex combination of mathematical models describing the passive mechanical behavior of the myocardium and its electrophysiology, i.e., the activation of cardiac muscle cells. The problem in developing adequate constitutive models is the shortage of experimental data suitable for detailed parameter estimation in specific functional forms. A combination of shear and biaxial extension tests with different loading protocols on different specimen orientations is necessary to capture adequately the direction-dependent (orthotropic) response of the myocardium. In most experimental animal studies, where planar biaxial extension tests on the myocardium have been conducted, the generated shear stresses were neither considered nor discussed. Hence, in this study a method is presented which allows the quantification of shear deformations and related stresses. It demonstrates an approach for experimenters as to how the generation of these shear stresses can be minimized during mechanical testing. Experimental results on 14 passive human myocardial specimens, obtained from nine human hearts, show the efficiency of this newly developed method. Moreover, the influence of the clamping technique of the specimen, i.e., the load transmission between the testing device and the tissue, on the stress response is determined by testing an isotropic material (Latex). We identified that the force transmission between the testing device and the specimen by means of hooks and cords does not influence the performed experiments. We further showed that in-plane shear stresses definitely exist in biaxially tested human ventricular myocardium, but can be reduced to a minimum by preparing the specimens in an appropriate manner. Moreover, we showed whether shear stresses can be neglected when performing

  9. The effect of a heparin-based coacervate of fibroblast growth factor-2 on scarring in the infarcted myocardium.

    PubMed

    Chu, Hunghao; Chen, Chien-Wen; Huard, Johnny; Wang, Yadong

    2013-02-01

    Effective delivery of exogenous angiogenic growth factors can provide a new therapy for ischemic diseases. However, clinical translation of growth factor therapies faces multiples challenges; the most significant one is the short half-life of the naked protein. We use heparin and a nontoxic polycation to form an injectable coacervate that protects growth factors and preserves their bioactivities. Here we report the effectiveness of fibroblast growth factor-2 (FGF2) coacervate in reducing scar burden in a mouse myocardial infarction model. The coacervate provides spatial and temporal control of the release of heparin-binding proteins. Coacervate treated animals show lower level of inflammation, fibrosis and cardiomyocyte death in the infarcted myocardium. Histological evaluation indicates that FGF2 coacervate significantly increases the number of endothelial and mural cells and results in stable capillaries and arterioles to at least 6 weeks post injection. Echocardiographic assessment shows that FGF2 coacervate promotes cardiac contractibility and inhibits ventricular dilation, suggesting that the improvement at the tissue level leads to better cardiac functions. On the contrary, identical dosage of free FGF2 shows no statistical difference from saline or vehicle control in histological or functional assessment. Overall, injection of FGF2 coacervate ameliorated the ischemic injury caused by myocardial infarction. The promising data in rodent warrant further examination of the potential of clinical translation of this technology.

  10. Cellulose Aggregation under Hydrothermal Pretreatment Conditions.

    PubMed

    Silveira, Rodrigo L; Stoyanov, Stanislav R; Kovalenko, Andriy; Skaf, Munir S

    2016-08-01

    Cellulose, the most abundant biopolymer on Earth, represents a resource for sustainable production of biofuels. Thermochemical treatments make lignocellulosic biomaterials more amenable to depolymerization by exposing cellulose microfibrils to enzymatic or chemical attacks. In such treatments, the solvent plays fundamental roles in biomass modification, but the molecular events underlying these changes are still poorly understood. Here, the 3D-RISM-KH molecular theory of solvation has been employed to analyze the role of water in cellulose aggregation under different thermodynamic conditions. The results show that, under ambient conditions, highly structured hydration shells around cellulose create repulsive forces that protect cellulose microfibrils from aggregating. Under hydrothermal pretreatment conditions, however, the hydration shells lose structure, and cellulose aggregation is favored. These effects are largely due to a decrease in cellulose-water interactions relative to those at ambient conditions, so that cellulose-cellulose attractive interactions become prevalent. Our results provide an explanation to the observed increase in the lateral size of cellulose crystallites when biomass is subject to pretreatments and deepen the current understanding of the mechanisms of biomass modification. PMID:27301535

  11. Tank Focus Area pretreatment activities

    SciTech Connect

    McGinnis, C.P.; Welch, T.D.; Manke, K.L.

    1997-03-01

    Plans call for the high-level wastes to be retrieved from the tanks and immobilized in a stable waste form suitable for long-term isolation. Chemistry and chemical engineering operations are required to retrieve the wastes, to condition the wastes for subsequent steps, and to reduce the costs of the waste management enterprise. Pretreatment includes those processes between retrieval and immobilization, and includes preparation of suitable feed material for immobilization and separations to partition the waste into streams that yield lower life-cycle costs. Some of the technologies being developed by the Tank Focus Area (TFA) to process these wastes are described. These technologies fall roughly into three areas: (1) solid/liquid separation (SLS), (2) sludge pretreatment, and (3) supernate pretreatment.

  12. Segmentation of scarred and non-scarred myocardium in LG enhanced CMR images using intensity-based textural analysis.

    PubMed

    Kotu, Lasya Priya; Engan, Kjersti; Eftestøl, Trygve; Ørn, Stein; Woie, Leik

    2011-01-01

    The Late Gadolinium (LG) enhancement in Cardiac Magnetic Resonance (CMR) imaging is used to increase the intensity of scarred area in myocardium for thorough examination. Automatic segmentation of scar is important because scar size is largely responsible in changing the size, shape and functioning of left ventricle and it is a preliminary step required in exploring the information present in scar. We have proposed a new technique to segment scar (infarct region) from non-scarred myocardium using intensity-based texture analysis. Our new technique uses dictionary-based texture features and dc-values to segment scarred and non-scarred myocardium using Maximum Likelihood Estimator (MLE) based Bayes classification. Texture analysis aided with intensity values gives better segmentation of scar from myocardium with high sensitivity and specificity values in comparison to manual segmentation by expert cardiologists.

  13. Enhanced infarct myocardium repair mediated by thermosensitive copolymer hydrogel-based stem cell transplantation

    PubMed Central

    Xia, Yu; Zhu, Kai; Lai, Hao; Lang, Meidong; Xiao, Yan; Lian, Sheng

    2015-01-01

    Mesenchymal stem cell (MSC) transplantation by intramyocardial injection has been proposed as a promising therapy strategy for cardiac repair after myocardium infarction. However, low retention and survival of grafted MSCs hinder its further application. In this study, copolymer with N-isopropylacrylamide/acrylic acid/2-hydroxylethyl methacrylate-poly(ɛ-caprolactone) ratio of 88:9.6:2.4 was bioconjugated with type I collagen to construct a novel injectable thermosensitive hydrogel. The injectable and biocompatible hydrogel-mediated MSC transplantation could enhance the grafted cell survival in the myocardium, which contributed to the increased neovascularization, decreased interstitial fibrosis, and ultimately improved heart function to a significantly greater degree than regular MSC transplantation. We suggest that this novel hydrogel has the potential for future stem cell transplantation. PMID:25432986

  14. [CHANGES IN THE METABOLISM IN THE MYOCARDIUM OF RATS WITH ARTERIAL HYPERTENSION].

    PubMed

    Dovgan, R S; Zagorodnyi, M I

    2015-01-01

    In the myocardium of the rats with arterial hypertension marked increase in the amount of unsaturated fatty acids and polyunsaturated fatty acids. Reducing the concentration of palmitic acid and increased levels of arachidonic acid is considered as one of the factors that lead to the development of energy deficit and oxidative stress. In rats, with hypertension myocardial lactate concentration increases in the cytoplasmic fraction and reducing the amount of ATP. The level in the cytoplasmic and mitochondrial fractions above benchmarks, indicating about the change of antioxidant systems of the body In the cytoplasm and mitochondria of cardiomyocytes of the rats with arterial hypertension marked decrease in the activity of antioxidant enzymes: NO-synthase, catalase, glutathione reductase, which causes metabolic changes of the myocardium. PMID:27491168

  15. [Hibernating and stunned myocardium. Pathogenetic mechanisms during and after myocardial ischemia].

    PubMed

    Carella, Giovanni; Mazzone, Marinella; Forte, Paola; Buccelletti, Francesco; Portale, Grazia

    2002-10-01

    In this paper the Authors consider the concept of stunning/hibernating myocardium, analizing the most recent articles and reviews in literature, until April 2002 (database PubMed). Dysfunctional segments with normal perfusion and normal glucose utilization are considered to be "stunned", and dysfunctional segments with reduced perfusion and preserved glucose utilization are considered to be "hibernated". Together with the two major hypothesis (generation of oxygen-derived free radicals and transient calcium overload) in developing of dysfunctional myocardium after ischaemia, recent studies have demonstrated an important role in down-regulation of beta-adrenergic receptors both in the stunned and in the hibernated segments. Moreover, the increase of negatively inotropic cytokines TNF-alpha and NOS2 has been observed in dysfunctional segments. The number of copies of mRNA has been quantified by reverse transcription-polymerase chain reaction (reverse-PCR).

  16. A structurally based viscoelastic model for passive myocardium in finite deformation

    NASA Astrophysics Data System (ADS)

    Shen, Jing Jin

    2016-09-01

    This paper discusses the finite-deformation viscoelastic modeling for passive myocardium tissue. The formulations established can also be applied to model other fiber-reinforced soft tissue. Based on the morphological structure of the myocardium, a specific free-energy function is constructed to reflect its orthotropicity. After deriving the stress-strain relationships in the simple shear deformation, a genetic algorithm is used to optimally estimate the material parameters of the myocardial constitutive equation. The results show that the proposed myocardial model can well fit the shear experimental data. To validate the viscoelastic model, it is used to predict the creep and the dynamic responses of a cylindrical model of the left ventricle. Upon comparing the results calculated by the proven myocardial elastic model with those by the viscoelastic model, the merits of the latter are discussed.

  17. Age-dependent changes in expression of alpha/sub 1/-adrenergic receptors in rat myocardium

    SciTech Connect

    Schaffer, W.; Williams, R.S.

    1986-07-16

    The expression of alpha/sub 1/-adrenergic receptors within ventricular myocardium of rats ranging in age from 21 days of fetal life to 24 months after birth was measured from (/sup 125/I) 2-(..beta.. hydroxy phenyl) ethylaminomethyl tetralone binding isotherms. No difference was observed in binding affinity between any of the age groups studied. The number of alpha/sub 1/-adrenergic receptors was found to be 60-120% higher in membranes from fetal or immature rats up to 25 days of age when compared with adult animals. The increased expression of alpha/sub 1/-adrenergic receptors in the developing heart relative to that observed in adult heart is consistent with the hypothesis that alpha/sub 1/-adrenergic receptor stimulation may modulate protein synthesis and growth in mammalian myocardium.

  18. Motion estimation and compensation for coronary artery and myocardium in cardiac CT

    NASA Astrophysics Data System (ADS)

    Tang, Qiulin; Matthews, James; Razeto, Marco; Linde, Jesper J.; Nakanishi, Satoru

    2015-03-01

    Motion blurring is still a challenge for cardiac CT imaging. A new motion estimation (ME) and motion compensation method is developed for cardiac CT. The proposed method estimates motion of entire heart, and then applies motion compensation. Therefore, the proposed method reduces motion artifacts not only in coronary artery region as most other methods did, but also reduces motion blurring in myocardium region. In motion compensated reconstruction, we use the Fourier transfer method proposed by Pack et al to obtain a series of partial images, and then warp and sum together to obtain final motion compensated images. The robustness and performance of the proposed method was verified with data from 10 patients and improvements in sharpness of both coronary arteries and myocardium were obtained.

  19. Second harmonic generation imaging of the collagen in myocardium for atrial fibrillation diagnosis

    NASA Astrophysics Data System (ADS)

    Tsai, Ming-Rung; Chiou, Yu-We; Sun, Chi-Kuang

    2009-02-01

    Myocardial fibrosis, a common sequela of cardiac hypertrophy, has been shown to be associated with arrhythmias in experimental models. Some research has indicated that myocardial fibrosis plays an important role in predisposing patients to atrial fibrillation. Second harmonic generation (SHG) is an optically nonlinear coherent process to image the collagen network. In this presentation, we observe the SHG images of the collagen matrix in atrial myocardium and we analyzed of collagen fibers arrangement by using Fourier-transform analysis. Moreover, comparing the SHG images of the collagen fibers in atrial myocardium between normal sinus rhythm (NSR) and atrial fibrillation (AF), our result indicated that it is possible to realize the relation between myocardial fibrosis and AF.

  20. Myoblasts transplanted into rat infarcted myocardium are functionally isolated from their host

    PubMed Central

    Léobon, Bertrand; Garcin, Isabelle; Menasché, Philippe; Vilquin, Jean-Thomas; Audinat, Etienne; Charpak, Serge

    2003-01-01

    Survival and differentiation of myogenic cells grafted into infarcted myocardium have raised the hope that cell transplantation becomes a new therapy for cardiovascular diseases. The approach was further supported by transplantation of skeletal myoblasts, which was shown to improve cardiac performance in several animal species. Despite the success of myoblast transplantation and its recent trial in human, the mechanism responsible for the functional improvement remains unclear. Here, we used intracellular recordings coupled to video and fluorescence microscopy to establish whether myoblasts, genetically labeled with enhanced GFP and transplanted into rat infarcted myocardium, retain excitable and contractile properties, and participate actively to cardiac function. Our results indicate that grafted myoblasts differentiate into peculiar hyperexcitable myotubes with a contractile activity fully independent of neighboring cardiomyocytes. We conclude that mechanisms other than electromechanical coupling between grafted and host cells are involved in the improvement of cardiac function. PMID:12805561

  1. Effect of ethanol and the catalase inhibitor aminotriazole on lipid peroxidation in the rat myocardium

    SciTech Connect

    Panchenko, L.F.; Pirozhkov, S.V.; Popova, S.V.; Antonenkov, V.D.

    1987-09-01

    The authors study the effect of chronic administration of ethanol and aminotriazole on the level of lipid peroxidation in the ray myocardium. The action of natural and artificial antioxidants on alcohol-induced lipid peroxidation also was studied. To determine the level of chemiluminescence, 1 ml of a sample of nuclear free homogenate or of the total fraction of particles was introduced for radioactivity measurement. After incubation the spontaneous weak luminescence was measured.

  2. Influence of mechanical ventilation and sepsis on redox balance in diaphragm, myocardium, limb muscles, and lungs.

    PubMed

    Chacon-Cabrera, Alba; Rojas, Yeny; Martínez-Caro, Leticia; Vila-Ubach, Monica; Nin, Nicolas; Ferruelo, Antonio; Esteban, Andrés; Lorente, José A; Barreiro, Esther

    2014-12-01

    Mechanical ventilation (MV), using high tidal volumes (V(T)), causes lung (ventilator-induced lung injury [VILI]) and distant organ injury. Additionally, sepsis is characterized by increased oxidative stress. We tested whether MV is associated with enhanced oxidative stress in sepsis, the commonest underlying condition in clinical acute lung injury. Protein carbonylation and nitration, antioxidants, and inflammation (immunoblotting) were evaluated in diaphragm, gastrocnemius, soleus, myocardium, and lungs of nonseptic and septic (cecal ligation and puncture 24 hours before MV) rats undergoing MV (n = 7 per group) for 150 minutes using 3 different strategies (low V(T) [V(T) = 9 mL/kg], moderate V(T) [V(T) = 15 mL/kg], and high V(T) [V(T) = 25 mL/kg]) and in nonventilated control animals. Compared with nonventilated control animals, in septic and nonseptic rodents (1) diaphragms, limb muscles, and myocardium of high-V(T) rats exhibited a decrease in protein oxidation and nitration levels, (2) antioxidant levels followed a specific fiber-type distribution in slow- and fast-twitch muscles, (3) tumor necrosis factor α (TNF-α) levels were higher in respiratory and limb muscles, whereas no differences were observed in myocardium, and (4) in lungs, protein oxidation was increased, antioxidants were rather decreased, and TNF-α remained unmodified. In this model of VILI, oxidative stress does not occur in distant organs or skeletal muscles of rodents after several hours of MV with moderate-to-high V(T), whereas protein oxidation levels were increased in the lungs of the animals. Inflammatory events were moderately expressed in skeletal muscles and lungs of the MV rats. Concomitant sepsis did not strongly affect the MV-induced effects on muscles, myocardium, or lungs in the rodents.

  3. Imaging necrotic myocardium: Detection with 99mTc-pyrophosphate and radiolabeled antimyosin

    SciTech Connect

    Khaw, B.A.; Haber, E. )

    1989-08-01

    The major value of hot-spot imaging of the myocardium is its ability to define areas of necrosis rather than areas of diminished blood flow or cellular function. Applications of hot-spot imaging include the diagnosis and quantitation of myocardial infarction, myocarditis, and cardiac transplant rejection. The two agents in clinical use, 99mTc-Pyrophosphate and radiolabeled antimyosin, are discussed. 52 references.

  4. Regulation of acetylation restores proteolytic function of diseased myocardium in mouse and human.

    PubMed

    Wang, Ding; Fang, Caiyun; Zong, Nobel C; Liem, David A; Cadeiras, Martin; Scruggs, Sarah B; Yu, Hongxiu; Kim, Allen K; Yang, Pengyuan; Deng, Mario; Lu, Haojie; Ping, Peipei

    2013-12-01

    Proteasome complexes play essential roles in maintaining cellular protein homeostasis and serve fundamental roles in cardiac function under normal and pathological conditions. A functional detriment in proteasomal activities has been recognized as a major contributor to the progression of cardiovascular diseases. Therefore, approaches to restore proteolytic function within the setting of the diseased myocardium would be of great clinical significance. In this study, we discovered that the cardiac proteasomal activity could be regulated by acetylation. Histone deacetylase (HDAC) inhibitors (suberoylanilide hydroxamic acid and sodium valproate) enhanced the acetylation of 20S proteasome subunits in the myocardium and led to an elevation of proteolytic capacity. This regulatory paradigm was present in both healthy and acutely ischemia/reperfusion (I/R) injured murine hearts, and HDAC inhibition in vitro restored proteolytic capacities to baseline sham levels in injured hearts. This mechanism of regulation was also viable in failing human myocardium. With 20S proteasomal complexes purified from murine myocardium treated with HDAC inhibitors in vivo, we confirmed that acetylation of 20S subunits directly, at least in part, presents a molecular explanation for the improvement in function. Furthermore, using high-resolution LC-MS/MS, we unraveled the first cardiac 20S acetylome, which identified the acetylation of nine N-termini and seven internal lysine residues. Acetylation on four lysine residues and four N-termini on cardiac proteasomes were novel discoveries of this study. In addition, the acetylation of five lysine residues was inducible via HDAC inhibition, which correlated with the enhancement of 20S proteasomal activity. Taken as a whole, our investigation unveiled a novel mechanism of proteasomal function regulation in vivo and established a new strategy for the potential rescue of compromised proteolytic function in the failing heart using HDAC inhibitors.

  5. Effects of myocardial infarction on the distribution and transport of nutrients and oxygen in porcine myocardium.

    PubMed

    Davis, Bryce H; Morimoto, Yoshihisa; Sample, Chris; Olbrich, Kevin; Leddy, Holly A; Guilak, Farshid; Taylor, Doris A

    2012-10-01

    One of the primary limitations of cell therapy for myocardial infarction is the low survival of transplanted cells, with a loss of up to 80% of cells within 3 days of delivery. The aims of this study were to investigate the distribution of nutrients and oxygen in infarcted myocardium and to quantify how macromolecular transport properties might affect cell survival. Transmural myocardial infarction was created by controlled cryoablation in pigs. At 30 days post-infarction, oxygen and metabolite levels were measured in the peripheral skeletal muscle, normal myocardium, the infarct border zone, and the infarct interior. The diffusion coefficients of fluorescein or FITC-labeled dextran (0.3-70 kD) were measured in these tissues using fluorescence recovery after photobleaching. The vascular density was measured via endogenous alkaline phosphatase staining. To examine the influence of these infarct conditions on cells therapeutically used in vivo, skeletal myoblast survival and differentiation were studied in vitro under the oxygen and glucose concentrations measured in the infarct tissue. Glucose and oxygen concentrations, along with vascular density were significantly reduced in infarct when compared to the uninjured myocardium and infarct border zone, although the degree of decrease differed. The diffusivity of molecules smaller than 40 kD was significantly higher in infarct center and border zone as compared to uninjured heart. Skeletal myoblast differentiation and survival were decreased stepwise from control to hypoxia, starvation, and ischemia conditions. Although oxygen, glucose, and vascular density were significantly reduced in infarcted myocardium, the rate of macromolecular diffusion was significantly increased, suggesting that diffusive transport may not be inhibited in infarct tissue, and thus the supply of nutrients to transplanted cells may be possible. in vitro studies mimicking infarct conditions suggest that increasing nutrients available to

  6. Wave propagation simulation in normal and infarcted myocardium: computational and modelling issues.

    PubMed

    Maglaveras, N; Van Capelle, F J; De Bakker, J M

    1998-01-01

    Simulation of propagating action potentials (PAP) in normal and abnormal myocardium is used for the understanding of mechanisms responsible for eliciting dangerous arrhythmias. One- and two-dimensional models dealing with PAP properties are reviewed in this paper viewed both from the computational and mathematical aspects. These models are used for linking theoretical and experimental results. The discontinuous nature of the PAP is demonstrated through the combination of experimental and theoretically derived results. In particular it can be shown that for increased intracellular coupling resistance the PAP upstroke phase properties (Vmax, dV/dtmax and tau foot) change considerably, and in some cases non-monotonically with increased coupling resistance. It is shown that tau foot) is a parameter that is very sensitive to the cell's distance to the stimulus site, the stimulus strength and the coupling resistance. In particular it can be shown that in a one-dimensional structure the tau foot value can increase dramatically for lower coupling resistance values near the stimulus site and subsequently can be reduced as we move to distances larger than five resting length constants from the stimulus site. The tau foot variability is reduced with increased coupling resistance, rendering the lower coupling resistance structures, under abnormal excitation sequences, more vulnerable to conduction block and arrhythmias. Using the theory of discontinuous propagation of the PAP in the myocardium it is demonstrated that for specific abnormal situations in the myocardium, such as infarcted tissue, one- and two-dimensional models can reliably simulate propagation characteristics and explain complex phenomena such as propagation at bifurcation sites and mechanisms of block and re-entry. In conclusion it is shown that applied mathematics and informatics can help in elucidating electrophysiologically complex mechanisms such as arrhythmias and conduction disturbances in the myocardium

  7. Function of remote non-infarcted myocardium after STEMI: analysis with cardiovascular magnetic resonance.

    PubMed

    Husser, Oliver; Chaustre, Fabian; Sanchis, Juan; Nunez, Julio; Monmeneu, Jose V; Lopez-Lereu, Maria P; Bonanad, Clara; Gomez, Cristina; Oltra, Ricardo; Llacer, Angel; Riegger, Günter A J; Chorro, Francisco J; Bodi, Vicente

    2012-12-01

    To evaluate remote myocardial function after ST-elevation myocardial infarction (STEMI) and the impact of infarct size (IS) using cardiovascular magnetic resonance (CMR). 161 patients and 15 controls underwent CMR at 1st week and 6th month after STEMI. Using the 17-segments model, segments were categorized into infarcted, adjacent and remote myocardium. Relative systolic wall thickening (SWT, %) was assessed using the centerline method. IS (% of left ventricular mass) was determined in late enhancement imaging. Overall, in remote myocardium, SWT was comparable (83 ± 32) to controls (77 ± 25, P = .5) and did not increase significantly (P = .2) at the 6th month (88 ± 35, P = .3 vs. control). When IS was categorized into tertiles (<13.6%, (n = 49), 13.7-28.2%, (n = 60), >28.2%, (n = 52)), SWT in the remote area at the 1st week was not different from controls, regardless of infarct size (p between .2 and .8 for all tertiles). At 6 months, SWT was larger compared to controls only in small infarctions (98 ± 34 vs. 77 ± 25, P = .03). In medium and large infarctions there was no difference in SWT of the remote area compared to controls (87 ± 33 and 79 ± 34, P = .3 and P = .09) and there was no significant increase at 6 months (P between .2 and .9). In remote myocardium there was no difference in contractility compared to controls after STEMI. After 6 month a slight hypercontractility can only be observed in small infarctions. In medium and large infarctions no difference of SWT in remote myocardium compared to controls can be observed.

  8. Effect of hyperbaric oxygenation on carbohydrate metabolism protein synthesis in the myocardium during sustained hypodynamia

    NASA Technical Reports Server (NTRS)

    Makarov, G. A.

    1980-01-01

    Glycolysis and the intensity of protein synthesis were studied in 140 white male rats in subcellular fractions of the myocardium during 45 day hypodynamia and hyperbaric oxygenation. Hypodynamia increased: (1) the amount of lactic acids; (2) the amount of pyruvic acid; (3) the lactate/pyruvate coefficient; and (4) the activities of aldolase and lactate dehydrogenase. Hyperbaric oxygenation was found to have a favorable metabolic effect on the animals with hypodynamia.

  9. Postcountershock myocardial damage after pretreatment with adrenergic and calcium channel antagonists in halothane-anesthetized dogs

    SciTech Connect

    Gaba, D.M.; Metz, S.; Maze, M.

    1985-05-01

    Transthoracic electric countershock can cause necrotic myocardial lesions in humans as well as experimental animals. The authors investigated the effect on postcountershock myocardial damage of pretreatment with prazosin, an alpha-1 antagonist; L-metoprolol, a beta-1 antagonist, and verapamil, a calcium channel-blocking agent. Twenty dogs were anesthetized with halothane and given two transthoracic countershocks of 295 delivered joules each after drug or vehicle treatment. Myocardial injury was quantitated 24 h following countershock by measuring the uptake of technetium-99m pyrophosphate in the myocardium. Elevated technetium-99m pyrophosphate uptake occurred in visible lesions in most dogs regardless of drug treatment. For each of four parameters of myocardial damage there was no statistically significant difference between control animals and those treated with prazosin, metoprolol, or verapamil. These data suggest that adrenergic or calcium channel-mediated mechanisms are not involved in the pathogenesis of postcountershock myocardial damage.

  10. Study on the Mechanism of mTOR-Mediated Autophagy during Electroacupuncture Pretreatment against Cerebral Ischemic Injury

    PubMed Central

    Wu, Zhou-Quan; Cui, Su-yang; Zhu, Liang

    2016-01-01

    This study is aimed at investigating the association between the electroacupuncture (EA) pretreatment-induced protective effect against early cerebral ischemic injury and autophagy. EA pretreatment can protect cerebral ischemic and reperfusion injuries, but whether the attenuation of early cerebral ischemic injury by EA pretreatment was associated with autophagy is not yet clear. This study used the middle cerebral artery occlusion model to monitor the process of ischemic injury. For rats in the EA pretreatment group, EA pretreatment was conducted at Baihui acupoint before ischemia for 30 min for 5 consecutive days. The results suggested that EA pretreatment significantly increased the expression of autophagy in the cerebral cortical area on the ischemic side of rats. But the EA pretreatment-induced protective effects on the brain could be reversed by the specific inhibitor 3-methyladenine of autophagy. Additionally, the Pearson correlation analysis indicated that the impact of EA pretreatment on p-mTOR (2481) was negatively correlated with its impact on autophagy. In conclusion, the mechanism of EA pretreatment at Baihui acupoint against cerebral ischemic injury is mainly associated with the upregulation of autophagy expression, and its regulation of autophagy may depend on mTOR-mediated signaling pathways. PMID:27547233

  11. Unsupervised 4D myocardium segmentation with a Markov Random Field based deformable model.

    PubMed

    Cordero-Grande, L; Vegas-Sánchez-Ferrero, G; Casaseca-de-la-Higuera, P; San-Román-Calvar, J Alberto; Revilla-Orodea, Ana; Martín-Fernández, M; Alberola-López, C

    2011-06-01

    A stochastic deformable model is proposed for the segmentation of the myocardium in Magnetic Resonance Imaging. The segmentation is posed as a probabilistic optimization problem in which the optimal time-dependent surface is obtained for the myocardium of the heart in a discrete space of locations built upon simple geometric assumptions. For this purpose, first, the left ventricle is detected by a set of image analysis tools gathered from the literature. Then, the segmentation solution is obtained by the Maximization of the Posterior Marginals for the myocardium location in a Markov Random Field framework which optimally integrates temporal-spatial smoothness with intensity and gradient related features in an unsupervised way by the Maximum Likelihood estimation of the parameters of the field. This scheme provides a flexible and robust segmentation method which has been able to generate results comparable to manually segmented images for some derived cardiac function parameters in a set of 43 patients affected in different degrees by an Acute Myocardial Infarction.

  12. Imaging of the myocardium using (18)F-FDG-PET/MRI.

    PubMed

    Ferda, Jiří; Hromádka, Milan; Baxa, Jan

    2016-10-01

    The introduction of the integrated hybrid PET/MRI equipment creates the possibility to perform PET and MRI simultaneously. Depending on the clinical question, the metabolic conversion to glycolytic activity or beta-oxidation is performed before the application of FDG. Since FDG aids to evaluate the energetic metabolism of the myocytes and myocardial MRI reaches the imaging capabilities of perfusion and tissue characterization in the daily routine, FDG-PET/MRI looks to be a promising method of PET/MRI exploitation in cardiac imaging. When myocardial FDG uptake should be evaluated in association with the perfusion distribution, the cross-evaluation of FDG accumulation distribution and perfusion distribution pattern is necessary. The different scenarios may be used in the assessment of myocardium, the conversion to glycolytic activity is used in the imaging of the viable myocardium, but the glycolytic activity suppression might be used in the indications of the identification of injured myocardium by ischemia or inflammation. FDG-PET/MRI might aid to answer the clinical tasks according to the structure, current function and possibilities to improve the function in ischemic heart disease or to display the extent or activity of myocardial inflammation in sarcoidosis. The tight coupling between metabolism, perfusion and contractile function offers an opportunity for the simultaneous assessment of cardiac performance using one imaging modality. PMID:27470994

  13. The endoderm and myocardium join forces to drive early heart tube assembly.

    PubMed

    Aleksandrova, Anastasiia; Czirok, Andras; Kosa, Edina; Galkin, Oleksandr; Cheuvront, Tracey J; Rongish, Brenda J

    2015-08-01

    Formation of the muscular layer of the heart, the myocardium, involves the medial movement of bilateral progenitor fields; driven primarily by shortening of the endoderm during foregut formation. Using a combination of time-lapse imaging, microsurgical perturbations and computational modeling, we show that the speed of the medial-ward movement of the myocardial progenitors is similar, but not identical to that of the adjacent endoderm. Further, the extracellular matrix microenvironment separating the two germ layers also moves with the myocardium, indicating that collective tissue motion and not cell migration drives tubular heart assembly. Importantly, as myocardial cells approach the midline, they perform distinct anterior-directed movements relative to the endoderm. Based on the analysis of microincision experiments and computational models, we propose two characteristic, autonomous morphogenetic activities within the early myocardium: 1) an active contraction of the medial portion of the heart field and 2) curling- the tendency of the unconstrained myocardial tissue to form a spherical surface with a concave ventral side. In the intact embryo, these deformations are constrained by the endoderm and the adjacent mesoderm, nevertheless the corresponding mechanical stresses contribute to the proper positioning of myocardial primordia.

  14. Neutrophil depletion suppresses In-labeled platelet accumulation in infarcted myocardium

    SciTech Connect

    Bednar, M.; Smith, B.; Pinto, A.; Mullane, K.M.

    1985-09-01

    Platelets and neutrophils accumulate rapidly in infarcted myocardium. Although antineutrophil agents reduce the size of the infarcted area, this is not observed with antiplatelet drugs. The possibility that myocardial ischemia-induced platelet deposition was secondary to a neutrophil-mediated event was assessed by injecting prostacyclin-washed autologous In-labeled platelets and measuring the amount of radioactivity in different regions of the heart following 90-min occlusion of the left anterior descending coronary artery followed by reperfusion for periods up to 5 h. Platelet deposition during the reperfusion phase was linear with time and similar to the time course of neutrophil accumulation. There was a transmural distribution of radioactivity across the myocardium where the ''zone'' between infarcted and risk regions, called the ''interface,'' greater than infarct greater than risk greater than normal. Neutropenia, had minimal effects on platelet aggregation ex vivo, but significantly reduced platelet accumulation in the ischemic myocardium following 5-h reperfusion and abolished the transmural platelet distribution. These results suggest that myocardial platelet deposition is secondary to a neutrophil-mediated event in this occlusion-reperfusion model of myocardial injury. Interactions between platelets and neutrophils at the site of tissue damage may influence the process of myocardial ischemic injury.

  15. Differentiation of viable and nonviable myocardium after acute reperfusion using serial thallium-201 imaging

    SciTech Connect

    Okada, R.D.; Boucher, C.A.

    1987-02-01

    This study was performed to determine if differences in regional myocardial thallium clearance rates could differentiate salvaged from nonsalvaged myocardium after reperfusion. Twenty-one dogs underwent 2 hours of left anterior descending coronary artery ligation followed by reperfusion. Thallium was administered 5 minutes later and serial images were acquired over 3 hours. Of the 21 dogs, 15 had infarctions of which nine had initially reduced anterior wall thallium activity (group 1) and six had normal or increased activity (group 2). Six dogs did not have an infarction (group 3). All group 1 dogs demonstrated reduced clearance rates in the anterior wall (T1/2 = 15.0 +/- 4.7 hours, SD) compared to the posterior wall (T1/2 = 9.0 +/- 4.4 hours; p less than 0.001). Group 2 dogs demonstrated increased clearance rates in the anterior wall (T1/2 = 5.7 +/- 2.0 hours) compared to the posterior wall (T1/2 = 10.5 +/- 4.6 hours; p less than 0.001). Group 3 dogs demonstrated no difference in clearance rates. In conclusion, although thallium uptake is frequently reduced in nonsalvaged myocardium, tracer uptake can be normal or increased if perfusion has been completely restored. However, an increased clearance rate from the reperfused zone compared to the normal zone is a reliable indicator of nonsalvaged myocardium, despite normal initial thallium uptake.

  16. Activation of neutrophils in the microvasculature of the ischaemic and reperfused myocardium.

    PubMed

    Tillmanns, H; Neumann, F J; Tiefenbacher, C; Dorigo, O; Parekh, N; Waas, W; Zimmermann, R; Steinhausen, M; Kuebler, W

    1993-11-01

    In 11 rats, the microcirculation of the repeatedly ischaemic (stunned) left ventricular myocardium was studied using in vivo fluorescence microscopy. Stunning was provoked by six subsequent 10 min ligations of the left anterior descending coronary artery, each of them followed by a 20 min reperfusion period. In the stunned myocardium showing hypokinetic wall motion, myocardial blood flow dropped by 55%; in this region, leukocytes often appeared in slow-flow capillaries plugging capillary branches. Closely linking to leukocyte adherence, a rise of microvascular permeability was documented by extravascular clouds of fluorescent dextran. After nifedipine treatment, in ischaemic regions marked dilatation of larger A1 and A2 arterioles was noted, in addition to the ischaemia-induced dilatation of smaller A3 and A4 arterioles. Furthermore nifedipine and nisoldipine reduced the number of adherent leukocytes in post-capillary venules and capillaries of the repeatedly ischaemic myocardium. In 12 patients with coronary one-vessel disease and without previous transmural myocardial infarction, elective coronary angioplasty (PTCA) was performed (balloon inflation for 2 min). After elective PTCA of the LAD, a significant rise in the proportion of activated neutrophils was noted. After elective 2 min PTCA of the LAD, coronary sinus blood samples showed a marked rise of FMLC stimulated superoxide anion production, whereas passive deformability decreased considerably. Furthermore, an increase in chemotactic activity in coronary sinus blood samples was observed.

  17. Functional Differences in Engineered Myocardium from Embryonic Stem Cell-Derived versus Neonatal Cardiomyocytes

    PubMed Central

    Feinberg, Adam W.; Ripplinger, Crystal M.; van der Meer, Peter; Sheehy, Sean P.; Domian, Ibrahim; Chien, Kenneth R.; Parker, Kevin Kit

    2013-01-01

    Summary Stem cell-derived cardiomyocytes represent unique tools for cell- and tissue-based regenerative therapies, drug discovery and safety, and studies of fundamental heart-failure mechanisms. However, the degree to which stem cell-derived cardiomyocytes compare to mature cardiomyocytes is often debated. We reasoned that physiological metrics of engineered cardiac tissues offer a means of comparison. We built laminar myocardium engineered from cardiomyocytes that were differentiated from mouse embryonic stem cell-derived cardiac progenitors or harvested directly from neonatal mouse ventricles, and compared their anatomy and physiology in vitro. Tissues assembled from progenitor-derived myocytes and neonate myocytes demonstrated similar cytoskeletal architectures but different gap junction organization and electromechanical properties. Progenitor-derived myocardium had significantly less contractile stress and slower longitudinal conduction velocity than neonate-derived myocardium, indicating that the developmental state of the cardiomyocytes affects the electromechanical function of the resultant engineered tissue. These data suggest a need to establish performance metrics for future stem cell applications. PMID:24286027

  18. Imaging of the myocardium using (18)F-FDG-PET/MRI.

    PubMed

    Ferda, Jiří; Hromádka, Milan; Baxa, Jan

    2016-10-01

    The introduction of the integrated hybrid PET/MRI equipment creates the possibility to perform PET and MRI simultaneously. Depending on the clinical question, the metabolic conversion to glycolytic activity or beta-oxidation is performed before the application of FDG. Since FDG aids to evaluate the energetic metabolism of the myocytes and myocardial MRI reaches the imaging capabilities of perfusion and tissue characterization in the daily routine, FDG-PET/MRI looks to be a promising method of PET/MRI exploitation in cardiac imaging. When myocardial FDG uptake should be evaluated in association with the perfusion distribution, the cross-evaluation of FDG accumulation distribution and perfusion distribution pattern is necessary. The different scenarios may be used in the assessment of myocardium, the conversion to glycolytic activity is used in the imaging of the viable myocardium, but the glycolytic activity suppression might be used in the indications of the identification of injured myocardium by ischemia or inflammation. FDG-PET/MRI might aid to answer the clinical tasks according to the structure, current function and possibilities to improve the function in ischemic heart disease or to display the extent or activity of myocardial inflammation in sarcoidosis. The tight coupling between metabolism, perfusion and contractile function offers an opportunity for the simultaneous assessment of cardiac performance using one imaging modality.

  19. Interleukin-8 gene induction in the myocardium after ischemia and reperfusion in vivo.

    PubMed Central

    Kukielka, G L; Smith, C W; LaRosa, G J; Manning, A M; Mendoza, L H; Daly, T J; Hughes, B J; Youker, K A; Hawkins, H K; Michael, L H

    1995-01-01

    Neutrophil adhesion and direct cytotoxicity for cardiac myocytes require chemotactic stimulation and are dependent upon CD18-ICAM-1 binding. To characterize the potential role of IL-8 in this interaction, canine IL-8 cDNA was cloned and the mature recombinant protein expressed in Escherichia coli BL21 cells. Recombinant canine IL-8 markedly increased adhesion of neutrophils to isolated canine cardiac myocytes. This adhesion resulted in direct cytotoxicity for cardiac myocytes. Both processes were specifically blocked by antibodies directed against CD18 and IL-8. In vivo, after 1 h of coronary occlusion, IL-8 mRNA was markedly and consistently induced in reperfused segments of myocardium. IL-8 mRNA was not induced in control (normally perfused) myocardial segments. Minimal amounts of IL-8 mRNA were detected after 3 or 4 h of ischemia without reperfusion. Highest levels of induction were evident in the most ischemic myocardial segments. IL-8 mRNA peaked in the first 3 h of reperfusion and persisted at high levels beyond 24 h. IL-8 staining was present in the inflammatory infiltrate near the border between necrotic and viable myocardium, as well as in small veins in the same area. These findings provide the first direct evidence for regulation of IL-8 in ischemic and reperfused canine myocardium and support the hypothesis that IL-8 participates in neutrophil-mediated myocardial injury. Images PMID:7814650

  20. Genetic modification of stem cells for improved therapy of the infarcted myocardium.

    PubMed

    Haider, Husnain Kh; Mustafa, Anique; Feng, Yuliang; Ashraf, Muhammad

    2011-10-01

    The conventional treatment modalities for ischemic heart disease only provide symptomatic relief to the patient without repairing and regenerating the damaged myocardium. Stem cell transplantation has emerged as a promising alternative therapeutic approach for cardiovascular diseases. Stem cells possess the potential of differentiation to adopt morphofunctional cardiac and vasculogenic phenotypes to repopulate the scar tissue and restore regional blood flow in the ischemic myocardium. These beneficial therapeutic effects make stem cell transplantation the method of choice for the treatment of ischemic heart disease. The efficacy of stem cell transplantation may be augmented by genetic manipulation of the cells prior to transplantation. Not only will insertion of therapeutic transgene(s) into the stem cells support the survival and differentiation of cells in the unfavorable microenvironment of the ischemic myocardium, but also the genetically manipulated stem cells will serve as a source of the transgene expression product in the heart for therapeutic benefits. We provide an overview of the extensively studied stem cell types for cardiac regeneration, the various methods in which these cells have been genetically manipulated and rationale of genetic modification of stem cells for use in regenerative cardiovascular therapeutics.

  1. Polarization birefringence measurements for characterizing the myocardium, including healthy, infarcted, and stem-cell-regenerated tissues

    NASA Astrophysics Data System (ADS)

    Wood, Michael F. G.; Ghosh, Nirmalya; Wallenburg, Marika A.; Li, Shu-Hong; Weisel, Richard D.; Wilson, Brian C.; Li, Ren-Ke; Vitkin, I. Alex

    2010-07-01

    Myocardial infarction leads to structural remodeling of the myocardium, in particular to the loss of cardiomyocytes due to necrosis and an increase in collagen with scar formation. Stem cell regenerative treatments have been shown to alter this remodeling process, resulting in improved cardiac function. As healthy myocardial tissue is highly fibrous and anisotropic, it exhibits optical linear birefringence due to the different refractive indices parallel and perpendicular to the fibers. Accordingly, changes in myocardial structure associated with infarction and treatment-induced remodeling will alter the anisotropy exhibited by the tissue. Polarization-based linear birefringence is measured on the myocardium of adult rat hearts after myocardial infarction and compared with hearts that had received mesenchymal stem cell treatment. Both point measurement and imaging data show a decrease in birefringence in the region of infarction, with a partial rebound back toward the healthy values following regenerative treatment with stem cells. These results demonstrate the ability of optical polarimetry to characterize the micro-organizational state of the myocardium via its measured anisotropy, and the potential of this approach for monitoring regenerative treatments of myocardial infarction.

  2. [An improved method for microdialysis study of noradrenaline level in rat myocardium].

    PubMed

    Gilinskiĭ, M A; Faĭbushevich, A A; Lunte, C E

    1998-01-01

    A level of myocardial norepinephrine (NE) is considered as one of the meaningful parameters in the estimation of myocardium functioning. Long lasting changes of myocardial NE appear to be not only a sequence of pathologic processes in myocardium, but could also be a factor responsible for some diseases. An improved microdialysis sampling technique with HPLC-ED analysis was developed to measure in vivo NE content in a rat myocardial interstitium. Linear polyacrylonitryl 5 mm probes were flushed with methanol while being immersed in water. In vitro NE recovery with the flow rate of perfusate was found at the level 67.9 + 0.4%. Probes were implanted into the rat myocardium under the general anaesthesia. Myocardial dialysate was collected during 20 min into plastic vials, containing 10 microliters of 0.1 M perchloric acid. Low noise, high sensitivity dual electrochemical detection was used for the determination of NE amount in the samples. Overall sensitivity threshold was found about 0.3 pg of NE in 20 microliters. Steady state concentration of NE in myocardial dialysate was found 54 + 7 pg/ml. 20 min before cardiac arrest the concentration of NE in myocardial dialysate was found to be increased 4-5 times. 40 min after cardiac arrest further increase in NE content was registered up to 1-4 ng per ml of perfusate. It is suggested that the method will be useful for routine study of myocardial NE.

  3. Impaired translocation and activation of mitochondrial Akt1 mitigated mitochondrial oxidative phosphorylation Complex V activity in diabetic myocardium.

    PubMed

    Yang, Jia-Ying; Deng, Wu; Chen, Yumay; Fan, Weiwei; Baldwin, Kenneth M; Jope, Richard S; Wallace, Douglas C; Wang, Ping H

    2013-06-01

    Insulin can translocate Akt to mitochondria in cardiac muscle. The goals of this study were to define sub-mitochondrial localization of the translocated Akt, to dissect the effects of insulin on Akt isoform translocation, and to determine the direct effect of mitochondrial Akt activation on Complex V activity in normal and diabetic myocardium. The translocated Akt sequentially localized to the mitochondrial intermembrane space, inner membrane, and matrix. To confirm Akt translocation, in vitro import assay showed rapid entry of Akt into mitochondria. Akt isoforms were differentially regulated by insulin stimulation, only Akt1 translocated into mitochondria. In the insulin-resistant Type 2 diabetes model, Akt1 translocation was blunted. Mitochondrial activation of Akt1 increased Complex V activity by 24% in normal myocardium in vivo and restored Complex V activity in diabetic myocardium. Basal mitochondrial Complex V activity was lower by 22% in the Akt1(-/-) myocardium. Insulin-stimulated Complex V activity was not impaired in the Akt1(-/-) myocardium, due to compensatory translocation of Akt2 to mitochondria. Akt1 is the primary isoform that relayed insulin signaling to mitochondria and modulated mitochondrial Complex V activity. Activation of mitochondrial Akt1 enhanced ATP production and increased phosphocreatine in cardiac muscle cells. Dysregulation of this signal pathway might impair mitochondrial bioenergetics in diabetic myocardium.

  4. Carbonic Acid Pretreatment of Biomass

    SciTech Connect

    G. Peter van Walsum; Kemantha Jayawardhana; Damon Yourchisin; Robert McWilliams; Vanessa Castleberry

    2003-05-31

    This project sought to address six objectives, outlined below. The objectives were met through the completion of ten tasks. 1) Solidify the theoretical understanding of the binary CO2/H2O system at reaction temperatures and pressures. The thermodynamics of pH prediction have been improved to include a more rigorous treatment of non-ideal gas phases. However it was found that experimental attempts to confirm theoretical pH predictions were still off by a factor of about 1.8 pH units. Arrhenius experiments were carried out and the activation energy for carbonic acid appears to be substantially similar to sulfuric acid. Titration experiments have not yet confirmed or quantified the buffering or acid suppression effects of carbonic acid on biomass. 2) Modify the carbonic acid pretreatment severity function to include the effect of endogenous acid formation and carbonate buffering, if necessary. It was found that the existing severity functions serve adequately to account for endogenous acid production and carbonate effects. 3) Quantify the production of soluble carbohydrates at different reaction conditions and severity. Results show that carbonic acid has little effect on increasing soluble carbohydrate concentrations for pretreated aspen wood, compared to pretreatment with water alone. This appears to be connected to the release of endogenous acids by the substrate. A less acidic substrate such as corn stover would derive benefit from the use of carbonic acid. 4) Quantify the production of microbial inhibitors at selected reaction conditions and severity. It was found that the release of inhibitors was correlated to reaction severity and that carbonic acid did not appear to increase or decrease inhibition compared to pretreatment with water alone. 5) Assess the reactivity to enzymatic hydrolysis of material pretreated at selected reaction conditions and severity. Enzymatic hydrolysis rates increased with severity, but no advantage was detected for the use of carbonic

  5. Gain or loss? Sunscreen efficiency after cosmetic pretreatment of the skin.

    PubMed

    Kluschke, F; Weigmann, H J; Schanzer, S; Meinke, M; Vergou, T; Sterry, W; Lademann, J

    2014-01-01

    Sunscreens are a key pillar of the multimodal protection strategy against short- and long-term impacts of intermittent and continuous UV exposure. Hitherto, an unanswered part of current scientific discourse is the question whether a cosmetic pretreatment has an impact on distribution and adhesiveness of sunscreens on the skin and therefore affects UV protection. In order to evaluate the homogeneity of sunscreen filter distribution, water resistance as a parameter of adhesiveness and effective UV protection of sunscreens after a pretreatment with cream or lotion was investigated in 18 volunteers who were examined before and after swimming, using the established combination of the tape stripping procedure and UV/VIS spectroscopy. It was shown that a cosmetic skin pretreatment affects neither filter homogeneity nor effective UV protection prior to water contact. However, compared to nonpretreated skin, a considerable loss of water resistance is caused. Therefore, using a cream or lotion before application of sunscreens is not to be recommended.

  6. 40 CFR 442.25 - Pretreatment standards for existing sources (PSES).

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ... sources (PSES). 442.25 Section 442.25 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED... Tank Cars Transporting Chemical and Petroleum Cargos § 442.25 Pretreatment standards for existing sources (PSES). (a) Except as provided in 40 CFR 403.7 and 403.13 or in paragraph (b) of this section,...

  7. 40 CFR 442.26 - Pretreatment standards for new sources (PSNS).

    Code of Federal Regulations, 2012 CFR

    2012-07-01

    ... (PSNS). 442.26 Section 442.26 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED... Tank Cars Transporting Chemical and Petroleum Cargos § 442.26 Pretreatment standards for new sources (PSNS). (a) Except as provided in 40 CFR 403.7 and 403.13 or in paragraph (b) of this section, any...

  8. 40 CFR 442.25 - Pretreatment standards for existing sources (PSES).

    Code of Federal Regulations, 2012 CFR

    2012-07-01

    ... sources (PSES). 442.25 Section 442.25 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED... Tank Cars Transporting Chemical and Petroleum Cargos § 442.25 Pretreatment standards for existing sources (PSES). (a) Except as provided in 40 CFR 403.7 and 403.13 or in paragraph (b) of this section,...

  9. 40 CFR 442.26 - Pretreatment standards for new sources (PSNS).

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ... (PSNS). 442.26 Section 442.26 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED... Tank Cars Transporting Chemical and Petroleum Cargos § 442.26 Pretreatment standards for new sources (PSNS). (a) Except as provided in 40 CFR 403.7 and 403.13 or in paragraph (b) of this section, any...

  10. 40 CFR 415.344 - Pretreatment standards for existing sources (PSES).

    Code of Federal Regulations, 2014 CFR

    2014-07-01

    ... sources (PSES). 415.344 Section 415.344 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS INORGANIC CHEMICALS MANUFACTURING POINT SOURCE CATEGORY Chrome Pigments Production Subcategory § 415.344 Pretreatment standards for existing sources (PSES). (a)...

  11. Efficacy evaluation of physostigmine and anticholinergic adjuncts as a pretreatment for nerve agent intoxication. (Reannouncement with new availability information)

    SciTech Connect

    von Bredow, J.; Corcoran, K.; Maitland, G.; Kaminskis, A.; Adams, N.

    1991-12-31

    Pretreatment of nonhuman primates with physostigmine (Phy) and scopolamine or physostigmine and trihexyphenidyl 25 min before exposure to 2 LD50 soman im resulted in complete survival without convulsions or loss of consciousness. When identically pretreated animals were challenged with 5 LD50s of soman followed by atropine and 2-PAM therapy 1 min later, all animals experienced a loss of consciousness for approximately 10 min followed by functional recovery within an additional 20 min. These findings indicated that a pretreatment regimen composed of Phy and cholinolytic is capable of protecting primates from an absolute lethal dose of soman with rapid recovery from incapacitation. Physostigmine, nerve agent pretreatment, cynomolgus monkeys soman (GD).

  12. Lime pretreatment of lignocellulosic biomass

    NASA Astrophysics Data System (ADS)

    Chang, Shushien

    Lignocellulose is a valuable alternative energy source. The susceptibility of lignocellulosic biomass to enzymatic hydrolysis is constrained due to its structural features, so pretreatment is essential to enhance enzymatic digestibility. Of the chemicals used as pretreatment agents, it has been reported that alkalis improve biomass digestibility significantly. In comparison with other alkalis such as NaOH and ammonia, lime (calcium hydroxide) has many advantages; it is very inexpensive, is safe, and can be recovered by carbonating wash water. The effects of lime pretreatment were explored on switchgrass and poplar wood, representing herbaceous and woody biomass, respectively. The effects of pretreatment conditions (time, temperature, lime loading, water loading, particle size, and oxygen pressure) have been systematically studies. Lime alone enhances the digestibility of switchgrass significantly; under the recommended conditions, the 3-d total sugar (glucose + xylose) yields of lime-treated switchgrass were 7 times that of untreated sample. When treating poplar wood, lime must be combined with oxygen to achieve high digestibility; oxidative lime pretreatment increased the 3-d total sugar yield of poplar wood to 12 times that of untreated sample. In a fundamental study, to determine why lime pretreatment is effective, the effects of three structural features on enzymatic digestibility were studied: lignin content, acetyl content, and crystallinity index (CrI). Poplar wood was treated with peracetic acid, potassium hydroxide, and ball milling to produce model lignocelluloses with a broad spectrum of lignin contents, acetyl contents, and CrI, respectively. Enzymatic hydrolysis was performed on the model lignocelluloses to determine the digestibility. Correlations between lignin/carbohydrate ratio, acetyl/carbohydrate ratio, CrI and digestibility were developed. The 95% prediction intervals show that the correlations predict the 1-h and 3-d total sugar conversions of

  13. In-vivo assessment of normal T1 values of the right-ventricular myocardium by cardiac MRI.

    PubMed

    Kawel-Boehm, N; Dellas Buser, T; Greiser, A; Bieri, O; Bremerich, J; Santini, F

    2014-02-01

    To test feasibility of myocardial T1 mapping of the right ventricle (RV) at systole when myocardium is more compact and to determine the most appropriate imaging plane. 20 healthy volunteers (11 men; 33 ± 8 years) were imaged on a 1.5T scanner (MAGNETOM Avanto, Siemens AG, Erlangen, Germany). A modified look-locker inversion-recovery sequence was acquired at mid-ventricular short axis (SAX), as horizontal long-axis view and as transversal view at systole (mean trigger time 363 ± 37 ms). Myocardial T1 time of the left-ventricular and RV myocardium was measured within a region of interest (ROI) on generated T1-maps. The most appropriate imaging plane for the RV was determined by the ability to draw a ROI including the largest amount of myocardium without including adjacent tissue or blood. At systole, when myocardium is thicker, measurements of the RV myocardium were feasible in 18/20 subjects. Average size of the ROI was 0.42 ± 0.28 cm(2). In 10/18 subjects, short axis was the most appropriate imaging plane to obtain measurements (p = 0.034). Average T1 time of the RV myocardium was 1,016 ± 61 ms, and average T1 of the left-ventricular (LV) was 956 ± 25 ms (p < 0.001). T1 mapping of the RV myocardium is feasible during systole in the majority of healthy subjects but with a small ROI only. SAX plane was the optimal imaging plane in the majority of subjects. Native myocardial T1 time of the RV is significantly longer compared to the LV, which might be explained by the naturally higher collagen content of the RV.

  14. Nerve Growth Factor Protects the Ischemic Heart via Attenuation of the Endoplasmic Reticulum Stress Induced Apoptosis by Activation of Phosphatidylinositol 3-Kinase

    PubMed Central

    Wei, Ke; Liu, Li; Xie, Fei; Hao, Xuechao; Luo, Jie; Min, Su

    2015-01-01

    Background: Increased expression of nerve growth factor (NGF) has been found in the myocardium suffered from ischemia and reperfusion (I/R). The pro-survival activity of NGF on ischemic heart has been supposed to be mediated by phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) signaling pathway. Endoplasmic reticulum (ER) stress, which is activated initially as a defensive response to eliminate the accumulated unfolded proteins, has shown a critical involvement in the ischemia induced myocardial apoptosis. This study was aimed to investigate whether NGF induced heart protection against I/R injury includes a mechanism of attenuation of ER stress-induced myocardial apoptosis by activation of PI3K/Akt pathway. Methods: Isolated adult rat hearts were perfused with a Langendörff perfusion system. Hearts in the Sham group were subjected to 225 min of continuous Krebs-Henseleit buffer (KHB) perfusion without ischemia. Hearts in I/R group were perfused with KHB for a 75-min of equilibration period followed by 30 min of global ischemia and 120 min of KHB reperfusion. Hearts in the NGF group accepted 45 min of euilibration perfusion and 30 min of NGF pretreatment (with a final concentration of 100 ng/ml in the KHB) before 30 min of global ischemia and 120 min of reperfusion. Hearts in K252a and LY294002 groups were pretreated with either a TrkA inhibitor, K252a or a phosphatidyl inositol 3-kinase inhibitor, LY294002 for 30 min before NGF (100 ng/ml) administration. Cardiac hemodynamics were measured from the beginning of the perfusion. Cardiac enzymes and cardiac troponin I (cTnI) were assayed before ischemia and at the end of reperfusion. Myocardial apoptosis rate was measured by TUNEL staining, and expression of glucose-related protein 78 (GRP78), CCAAT/enhancer-binding protein homologous protein (CHOP), caspase-12, total- and phospho-(Ser473)-Akt were assessed by Western blot analyses. Results: NGF pretreatment significantly improved the recovery of post

  15. Pretreatment of CO oxidation catalysts

    NASA Technical Reports Server (NTRS)

    Vannorman, John D.

    1988-01-01

    CO oxidation catalysts with high activity in the range of 25 C to 100 C are important for long-life, closed-cycle operation of pulsed carbon dioxide 2 lasers. A reductive pretreatment with either CO or H sub 2 was shown to significantly enhance the activity of a commerically-available platinum on tin (IV) oxide (Pt/SnO2) catalyst relative to an oxidative or inert pretreatment or no pretreatment. Pretreatment at temperatures of 175 C and above caused an initial dip in observed CO or O sub 2 loss or CO sub 2 formation in a test gas mixture of 1 percent CO and 0.5 percent O sub 2 in a He gas matrix before a steady-state yield was obtained. This dip was found to be caused by dehydration of the surface of the catalyst and was readily eliminated by humidifying the catalyst or the test gas mixture. It was also found that too much moisture resulted in a lower overall yield of CO sub 2. Under similar conditions, it is hypothesized that the effect of the humidification is to increase the concentration of OH groups on the surface of the catalyst. The effect of having high concentration of CO sub 2 in the test gas mixture upon the loss of CO and O sub 2 as well as the effect of periods of relaxation of the catalyst under non-test gas conditions was studied. The purpose of these studies was to gain an insight into the mechanism of CO oxidation on this type of catalyst.

  16. Dilute Acid and Autohydrolysis Pretreatment

    NASA Astrophysics Data System (ADS)

    Yang, Bin; Wyman, Charles E.

    Exposure of cellulosic biomass to temperatures of about 120-210°C can remove most of the hemicellulose and produce cellulose-rich solids from which high glucose yields are possible with cellulase enzymes. Furthermore, the use of dilute sulfuric acid in this pretreatment operation can increase recovery of hemicellulose sugars substantially to about 85-95% of the maximum possible versus only about 65% if no acid is employed. The use of small-diameter tubes makes it possible to employ high solids concentrations similar to those preferred for commercial operations, with rapid heat-up, good temperature control, and accurate closure of material balances. Mixed reactors can be employed to pretreat larger amounts of biomass than possible in such small-diameter tubes, but solids concentrations are limited to about 15% or less to provide uniform temperatures. Pretreatment of large amounts of biomass at high solids concentrations is best carried out using direct steam injection and rapid pressure release, but closure of material balances in such “steam gun” devices is more difficult. Although flow of water alone or containing dilute acid is not practical commercially, such flow-through configurations provide valuable insight into biomass deconstruction kinetics not possible in the batch tubes, mixed reactors, or steam gun systems.

  17. Intracoronary thallium 201 scintigraphy as an immediate predictor of salvaged myocardium following intracoronary lysis

    SciTech Connect

    Krebber, H.J.; Schofer, J.; Mathey, D.; Montz, R.; Kalmar, P.; Rodewald, G.

    1984-01-01

    Since February of 1980, 157 patients who had had symptoms of acute myocardial infarction for less than 3 hours underwent intracoronary lysis. Forty-six patients required early aorta-coronary revascularization. However, operation was believed to be indicated only when intracoronary lysis was successful and myocardium was salvaged. Since left ventricular angiography proved unreliable in assessing the viability of the myocardium in the acute stage, starting in March of 1981 intracoronary thallium 201 scintiscans were obtained in 23 patients before and after intracoronary lysis. Patients in whom there was a significant reduction in the initial /sup 201/Th defect were considered ideal candidates for operation (Group 3). Patients with poor or unimproved /sup 201/Th uptake after successful intracoronary lysis were treated medically (Group 2), as were patients in whom intracoronary lysis was unsuccessful (Group 1). In order to validate this new approach, a comparison was made of the change in the regional wall motion of the ''infarcted area,'' as shown in the early and follow-up left ventricular angiograms in all three groups. In the acute stage, the mean regional ejection fraction was 19.9% in Group 1, 19.1% in Group 2, and 20.1% in Group 3. Only in Group 3 was there a significant increase in regional ejection fraction to a mean of 51%. The mean ejection fraction obtained at follow-up in Groups 1 and 2 was 16.5% and 17.3%, respectively. From these findings, it was concluded that /sup 201/Th scintigraphy is a valuable predictor of the salvageability of myocardium immediately following intracoronary lysis. To date, it has been the most valuable tool in assessing those patients suitable for early coronary revascularization.

  18. Sustained nonoxidative glucose utilization and depletion of glycogen in reperfused canine myocardium

    SciTech Connect

    Schwaiger, M.; Neese, R.A.; Araujo, L.; Wyns, W.; Wisneski, J.A.; Sochor, H.; Swank, S.; Kulber, D.; Selin, C.; Phelps, M.

    1989-03-01

    Ischemically injured reperfused myocardium is characterized by increased 18F-fluorodeoxyglucose uptake as demonstrated by positron emission tomography. To elucidate the metabolic fate of exogenous glucose entering reperfused myocardium, D-(6-14C) glucose and L-(U-13C) lactate were used to determine glucose uptake, glucose oxidation and the contribution of exogenous glucose to lactate production. The pathologic model under investigation consisted of a 3 h balloon occlusion of the left anterior descending coronary artery followed by 24 h of reperfusion in canine myocardium. The extent and severity of myocardial injury after the ischemia and reperfusion were assessed by histochemical evaluation (triphenyltetrazolium chloride and periodic acid-Schiff stains). Thirteen intervention and four control dogs were studied. The glucose uptake in the occluded/reperfused area was significantly enhanced compared with that in control dogs (0.40 +/- 0.14 versus 0.15 +/- 0.10 mumol/ml, respectively). In addition, a significantly greater portion of the glucose extracted immediately entered glycolysis in the intervention group (75%) than in the control dogs (33%). The activity of the nonoxidative glycolytic pathway was markedly increased in the ischemically injured reperfused area, as evidenced by the four times greater lactate release in this area compared with the control value. The dual carbon-labeled isotopes showed that 57% of the exogenous glucose entering glycolysis was being converted to lactate. Exogenous glucose contributed to greater than 90% of the observed lactate production. This finding was confirmed by the histochemical finding of sustained glycogen depletion in the occlusion/reperfusion area. The average area of glycogen depletion (37%) significantly exceeded the average area of necrosis (17%).

  19. Nonoxidative ethanol metabolism in rabbit myocardium: purification to homogeneity of fatty acyl ethyl ester synthase

    SciTech Connect

    Mogelson, S.; Lange, L.G.

    1984-08-28

    Fatty acyl ethyl esters arise from an esterification of free fatty acids with ethanol in the absence of ATP and coenzyme A. This study was designed to purify the enzyme(s) in rabbit myocardium that catalyze(s) this reaction. Enzyme activity in homogenates of myocardium, as assayed by the rate of synthesis of ethyl (/sup 14/C)oleate from 0.4 mM (/sup 14/C)oleic acid and 0.2 M ethanol, was 31 nmol/ (g x h), and was recovered in the 48400g supernatant. This soluble ethyl ester synthase activity bound to DEAE-cellulose at pH 8, and elution with a NaCl gradient (0-0.25 M0 separated two enzyme activities accounting for 13 and 87% of recovered synthase activity. The major enzyme activity was purified over 5000-fold to homogeneity. Gel electrophoresis showed a single polypeptide with M/sub r/ 26,000, and gel permeation chromatography under nondenaturing conditions indicated a M/sub r/ of 50,000 for the active enzyme. Kinetic analyses indicated that greatest rates of synthesis were observed with unsaturated octadecanoic fatty acid substrates. K/sub m/'s for these fatty acids were essentially identical and equal to 0.2 mM; substrate specificity resulted from varying K/sub m/'s for methanol, ethanol, 1-propanol, and 1-butanol, while V/sub max/ was constant at approximately 1.5 nmol/(mg x s). The amino acid analysis of this synthase distinguishes it from typical cholesterol esterases. When the enzyme is maximally active with respect to ethyl ester synthesis, it does not hydrolyze cholesterol oleate. Fatty acid ethyl esters are synthesized in myocardium primarily by a soluble dimeric enzyme comprised of two nearly identical subunits which esterifies free fatty acids with ethanol to produce a nonoxidative metabolite.

  20. Spacial and temporal profiles of neutrophil accumulation in the reperfused ischemic myocardium

    SciTech Connect

    de Lorgeril, M.; Rousseau, G.; Basmadjian, A.; St-Jean, G.; Tran, D.C.; Latour, J.G. )

    1990-01-01

    To elucidate further the pathogenic role of neutrophils in evolving reperfused myocardial infarction, we investigated the dynamics of their accumulation and distribution in the ischemic myocardium. The left anterior descending coronary artery was occluded in dogs for 2 hours followed by reperfusion for 0, 3, 6, or 24 hours. 111In-labeled neutrophils were injected at the time of occlusion or after 16 hours of reperfusion. The area at risk was similar among groups. Infarct size expressed in percent of the area at risk was identical between groups reperfused for 6 (35.2 +/- 4.4%) or 24 (32.3 +/- 3.9%) hours but smaller (22.0 +/- 4.4%; p less than 0.05) after 3 hours of reperfusion. 111In-neutrophils accumulation quantified by scintigraphy correlated positively with infarct size (r = 0.64, p less than 0.005); accumulation rates (cells/h/cm2MI) were high during the first 3 (2288 +/- 754) and 6 hours (1953 +/- 463) but low (490 +/- 192) between 16 and 24 hours of reperfusion. Cells accumulating during reperfusion (12,566 +/- 2307 cells/g at 3 hours) were found within the borders of the necrotic area, and the cell counts (2420 +/- 724 cells/g, p less than 0.05) in the live tissue located within the area at risk after 3 hours of reperfusion were similar to those found in the subepicardium at the onset of reperfusion: (2240 +/- 571 cells/g). Only a few cells were detected in the normally perfused myocardium (67 +/- 33 cells/g). We conclude that reperfusion accumulation in the ischemic myocardium; the reaction takes place within 3-6 hours of reperfusion, a period of time where infarct size is growing by about 40%. These results support the concept that leukocytes may play a pathogenic role on infarct size in models with brief ischemia followed by reperfusion.

  1. Effects of acute and chronic uremia on active cation transport in rat myocardium

    SciTech Connect

    Druml, W.; Kelly, R.A.; England, B.K.; O'Hara, D.S.; Mitch, W.E. )

    1990-12-01

    As abnormalities of active cation transport could contribute to the genesis of uremic cardiomyopathy, we investigated myocardial sodium pump function in rats with acute renal failure (ARF) and with a model of experimental chronic renal failure (CRF) that has metabolic similarities to advanced chronic uremia in humans. CRF rats were hypertensive and had left ventricular hypertrophy (33% higher heart:body weight ratio; P less than 0.01) at four weeks compared to pair-fed sham-operated rats. Importantly, both ouabain- and furosemide-sensitive 86Rb uptake rates were unchanged in left ventricular myocardial slices from CRF, and the intracellular sodium concentration was not different from that of control rats even though skeletal muscle sodium was increased, as we found previously. Insulin-stimulated, ouabain-sensitive 86Rb influx was also preserved. There also were no abnormalities in myocardium cation transport in rats with ARF. However, (3H)ouabain binding was decreased 45% in CRF rats (P less than 0.01); it was unchanged in acute uremia. Decreased ouabain binding in chronic uremia was due entirely to fewer low affinity (3H)ouabain binding sites (the binding affinity for ouabain was unaffected). We conclude that in chronic, (but not acute) renal failure, sodium pump number is reduced in myocardium but intracellular sodium is unchanged and active cation flux rates are maintained. These results emphasize that in rats with chronic uremia, intracellular sodium homeostasis is preserved in myocardium, despite the presence of marked abnormalities of active cation transport in skeletal muscle that are characteristic of chronic uremia.

  2. Kinetics of thallium-201 in reperfused canine myocardium after coronary artery occlusion

    SciTech Connect

    Okada, R.D.

    1984-05-01

    To study the kinetics of thallium-201 in nonsalvaged acutely infarcted myocardium and salvaged myocardium, the tracer was administered after experimental left anterior descending coronary artery reperfusion 2 hours after occlusion. In 19 dogs, thallium activity was then monitored for 4 hours in the reperfused anterior wall and normal posterior wall using miniature cadmium telluride radiation detectors. After sacrifice, 13 of the dogs were found to have an infarcted anterior wall by triphenyltetrazolium-chloride staining. In these dogs, mean (+/- standard deviation) fractional 4 hour thallium clearance was 0.33 +/- 0.08 for the infarct zone and 0.15 +/- 0.06 for the normal control zone (p less than 0.001). When computer-modeled, the clearance curve from the infarct zone was biexponential. The second exponential clearance curve from the infarct zone began 19.1 +/- 3.2 minutes after tracer administration, and was indistinguishable from the monoexponential clearance curve from the normal control zone. Thallium clearance from the blood pool was triexponential, the final exponential clearance curve being indistinguishable from the normal control zone clearance curve. Six dogs were found to have a salvaged noninfarcted anterior wall by triphenyltetrazolium-chloride staining. In these dogs, mean fractional 4 hour thallium clearance was 0.20 +/- 0.07 for the reperfused zone, and 0.19 +/- 0.08 for the normal control zone (p . NS). When computer-modeled, clearance curves for the reperfused and control zones were monoexponential. The monoexponential clearance curve for the salvaged reperfused zone was indistinguishable from the monoexponential clearance curve for normal myocardium.

  3. In vivo mechanical study of helical cardiac pacing electrode interacting with canine myocardium

    NASA Astrophysics Data System (ADS)

    Zhang, Xiangming; Ma, Nianke; Fan, Hualin; Niu, Guodong; Yang, Wei

    2007-06-01

    Cardiac pacing is a medical device to help human to overcome arrhythmia and to recover the regular beats of heart. A helical configuration of electrode tip is a new type of cardiac pacing lead distal tip. The helical electrode attaches itself to the desired site of heart by screwing its helical tip into the myocardium. In vivo experiments on anesthetized dogs were carried out to measure the acute interactions between helical electrode and myocardium during screw-in and pull-out processes. These data would be helpful for electrode tip design and electrode/myocardium adherence safety evaluation. They also provide reliability data for clinical site choice of human heart to implant and to fix the pacing lead. A special design of the helical tip using strain gauges is instrumented for the measurement of the screw-in and pull-out forces. We obtained the data of screw-in torques and pull-out forces for five different types of helical electrodes at nine designed sites on ten canine hearts. The results indicate that the screw-in torques increased steplike while the torque time curves presente saw-tooth fashion. The maximum torque has a range of 0.3 1.9 N mm. Obvious differences are observed for different types of helical tips and for different test sites. Large pull-out forces are frequently obtained at epicardium of left ventricle and right ventricle lateral wall, and the forces obtained at right ventricle apex and outflow tract of right ventricle are normally small. The differences in pull-out forces are dictated by the geometrical configuration of helix and regional structures of heart muscle.

  4. Anisotropic physical properties of myocardium characterized by ultrasonic measurements of backscatter, attenuation, and velocity

    NASA Astrophysics Data System (ADS)

    Baldwin, Steven L.

    The goal of elucidating the physical mechanisms underlying the propagation of ultrasonic waves in anisotropic soft tissue such as myocardium has posed an interesting and largely unsolved problem in the field of physics for the past 30 years. In part because of the vast complexity of the system being studied, progress towards understanding and modeling the mechanisms that underlie observed acoustic parameters may first require the guidance of careful experiment. Knowledge of the causes of observed ultrasonic properties in soft tissue including attenuation, speed of sound, and backscatter, and how those properties are altered with specific pathophysiologies, may lead to new noninvasive approaches to the diagnosis of disease. The primary aim of this Dissertation is to contribute to an understanding of the physics that underlies the mechanisms responsible for the observed interaction of ultrasound with myocardium. To this end, through-transmission and backscatter measurements were performed by varying acoustic properties as a function of angle of insonification relative to the predominant myofiber direction and by altering the material properties of myocardium by increased protein cross-linking induced by chemical fixation as an extreme form of changes that may occur in certain pathologies such as diabetes. Techniques to estimate acoustic parameters from backscatter were broadened and challenges to implementing these techniques in vivo were addressed. Provided that specific challenges identified in this Dissertation can be overcome, techniques to estimate attenuation from ultrasonic backscatter show promise as a means to investigate the physical interaction of ultrasound with anisotropic biological media in vivo. This Dissertation represents a step towards understanding the physics of the interaction of ultrasonic waves with anisotropic biological media.

  5. Metabolic Syndrome Impairs Notch Signaling and Promotes Apoptosis in Chronically Ischemic Myocardium

    PubMed Central

    Elmadhun, Nassrene Y.; Sabe, Ashraf A.; Lassaletta, Antonio D.; Chu, Louis M.; Kondra, Katelyn; Sturek, Michael; Sellke, Frank W.

    2014-01-01

    Objective Impaired angiogenesis is a known consequence of metabolic syndrome (MetS), however, the mechanism is not fully understood. Recent studies have shown that the Notch signaling pathway is an integral component of cardiac angiogenesis. We tested in a clinically relevant swine model the effects of MetS on Notch and apoptosis signaling in chronically ischemic myocardium. Methods Ossabaw swine were fed either a regular diet (CTL, n=8) or a high-cholesterol diet (MetS, n=8) to induce MetS. An ameroid constrictor was placed to induce chronic myocardial ischemia. Eleven weeks later, animals underwent cardiac harvest of the ischemic myocardium. Results There was down-regulation of pro-angiogenesis proteins Notch2, Notch4, Jagged2, Ang1 and ENOS in the MetS group compared to CTL. There was also up-regulation of pro-apoptosis protein Caspase8, and down-regulation of anti-angiogenesis protein pFOX03, and pro-survival proteins pP38 and HSP90 in the MetS group. Cell death was increased in the MetS group compared to CTL. Both CTL and MetS groups had similar arteriolar count and capillary density, and Notch3 and Jagged1 were both similarly concentrated in the smooth muscle wall in both groups. Conclusions MetS in chronic myocardial ischemia significantly impairs Notch signaling by down regulating Notch receptors, ligands and pro-angiogenesis proteins. MetS also increases apoptosis signaling, decreases survival signaling and increases cell death in chronically ischemic myocardium. Although short-term angiogenesis appears unaffected in this model of early MetS, the molecular signals for angiogenesis are impaired, thus suggesting that inhibition of Notch signaling may underlie decreased angiogenesis in later stages of MetS. PMID:25037620

  6. The effects of prenatal and neonatal exposure to electromagnetic fields on infant rat myocardium

    PubMed Central

    Tayefi, Hamid; Kiray, Amac; Ergur, Bekir Ugur; Bagriyanik, Husnu Alper; Pekcetin, Cetin; Fidan, Mustafa; Ozogul, Candan

    2010-01-01

    Introduction Electromagnetic fields (EMF) have adverse effects as a result of widespread use of electromagnetic energy on biological systems. The aim of this study was to investigate the effects of prenatal exposure to EMF on rat myocardium by biochemical and histopathological evaluations. Material and methods In this study, 10 pregnant Wistar rats were used. Half of the pregnant rats were exposed to EMF of 3 mT, and the other half to sham conditions during gestation. After parturition, rat pups in the 5 EMF-exposed litters from birth until postnatal day 20 were exposed to EMF of 3 mT for 4 h/day (EMF-exposed group, n = 30). Rat pups in sham litters from birth until postnatal day 20 were exposed to sham conditions (sham group, n= 20). Results In the EMF-exposed group, lipid peroxidation levels significantly increased compared to sham. Superoxide dismutase activities decreased significantly in the EMF-exposed group compared to sham. TUNEL staining showed that the number of TUNEL-positive cells increased significantly in EMF-exposed rats compared with sham. Under electron microscopy, there were mitochondrial degeneration, reduction in myofibrils, dilated sarcoplasmic reticulum and perinuclear vacuolization in EMF-exposed rats. Conclusions In conclusion, the results show that prenatal exposure to EMF causes oxidative stress, apoptosis and morphological pathology in myocardium of rat pups. The results of our study indicate a probable role of free radicals in the adverse effects of prenatal exposure to EMF. Further studies are needed to demonstrate whether the EMF exposure can induce adverse effects on the myocardium. PMID:22427754

  7. Flow into ischemic myocardium and across coronary collateral vessels is modulated by a waterfall mechanism.

    PubMed

    Eng, C; Kirk, E S

    1984-07-01

    If a coronary artery is ligated and the distal end cannulated, blood flows retrograde from the cannula when vented to the atmosphere. By varying the height of the outflow tubing, and thereby changing the outflow pressure, pressure-flow relationships can be constructed. We used this technique in eight dogs to assess the characteristics of blood flow into ischemic myocardium. Above a back pressure of 10 mm Hg, increasing back pressure resulted in a decrease of retrograde blood flow. However, below a back pressure of about 10 mm Hg (10.7 +/- 2.7 mm Hg), alterations in back pressure did not result in changes in retrograde blood flow (back pressure-independent region). The transition at 10 mm Hg is interpreted as the critical waterfall pressure in ischemic myocardium. In another group of eight dogs, the ischemic bed was completely embolized with 25-micron sized microspheres to prevent RBF from entering the tissue as back pressure was raised. Pressure-flow relationships performed in this group revealed a back pressure-independent region that extended to approximately 20 mm Hg (23.0 +/- 2.5 mm Hg). This behavior of the pressure-flow relationship is consistent with a waterfall phenomenon on the collateral vessels. To the extent that collateral vessels in the dog are mainly epicardial in location, the findings suggest that extravascular pressures of 20 mm Hg can occur in the more superficial layers of the heart. In addition, the waterfall on the collaterals indicates that this mechanism can operate on nonvenous vessels. Our results suggest separate waterfall phenomena operating on the collateral vessels (20 mm Hg) and on the vessels in the ischemic myocardium (10 mm Hg).

  8. [Intramural chronotopography of depolarization of myocardium of heart ventricles of pig (Sus scrofa domesticus)].

    PubMed

    Gulyaeva, A S; Roshchecskaya, I M; Roshchevsky, M P

    2014-01-01

    Sequence of depolarization of myocardium of pig heart ventricles was studied by the method of multichannel synchronous cardioelectrotopography. There is established formation of areas of early depolarization in subendocardium of interventricular septum and in the base of left ventricle papillary muscles; of multiple foci--in the depth of walls; of areas of late depolarization--in subepicardium of the left ventricle dorsolateral side. As compared with other species of ungulate animals (reindeer and sheep, in pig heart ventricles, differences are revealed in locations of early and late depolarization, a breakdown of the excitation wave into subepicardium.

  9. Regional Stress-Induced Ischemia in Non-fibrotic Hypertrophied Myocardium in Young HCM Patients.

    PubMed

    Jablonowski, Robert; Fernlund, Eva; Aletras, Anthony H; Engblom, Henrik; Heiberg, Einar; Liuba, Petru; Arheden, Håkan; Carlsson, Marcus

    2015-12-01

    The relationship between hypertrophy, perfusion abnormalities and fibrosis is unknown in young patients with hypertrophic cardiomyopathy (HCM). Since mounting evidence suggests causal relationship between myocardial ischemia and major adverse cardiac events, we sought to investigate whether (1) regional myocardial perfusion is decreased in young HCM patients and in individuals at risk of HCM, and (2) hypoperfused areas are larger than areas with fibrosis. HCM patients (n = 12), HCM-risk subjects (n = 15) and controls (n = 9) were imaged on a 1.5 T MRI scanner. Myocardial hypertrophy was assessed on cine images. Perfusion images were acquired during adenosine hyperemia and at rest. Maximum upslope ratios of perfusion (stress/rest) were used for semiquantitative analysis. Fibrosis was assessed by late gadolinium enhancement (LGE). Results are presented as median and range. Perfusion in HCM-risk subjects and in non-hypertrophied segments in HCM patients showed no difference compared to controls (P = ns). Hypertrophic segments in HCM patients without LGE showed decreased perfusion compared to segments without hypertrophy [1.5 (1.1-2.3) vs. 2.0 (1.8-2.6), P < 0.001], and hypertrophic segments with LGE showed even lower perfusion using a segmental analysis [0.9 (0.6-1.8), P < 0.05]. The extent of hypoperfused myocardium in HCM patients during adenosine exceeded the extent of fibrosis on LGE [20 (0-48) vs. 4 (0-7) % slice area, P < 0.05] and hypoperfused areas at rest (P < 0.001). Regional perfusion is decreased in hypertrophied compared to non-hypertrophied myocardium and is lowest in fibrotic myocardium in young HCM patients but does not discriminate HCM-risk subjects from controls. The stress-induced hypoperfused regions exceed regions with LGE, indicating that hypoperfusion precedes fibrosis and may be a more sensitive marker of diseased myocardium in HCM.

  10. Effects of hypodynamia on the hemocoagulative properties of the vascular wall and myocardium

    NASA Technical Reports Server (NTRS)

    Inchina, V. I.

    1980-01-01

    The hemocoagulative properties of the aorta (laminar), myocardium, hollow veins, and fibrinolytic capacity of tissues were studied in 14 rabbits subjected to 7 days of restricted mobility and compared to those of 10 control animals. Two tables of results show that, as a result of hypodynamia, the thromboplastic activity of the inner and middle layers of the aorta together with the destruction of endothelium increases the hemocoagulative potential and creates the threat of thrombogenesis. There is also an increase in fibrin-stabilizing activity for all tissues.

  11. Two-dimensional strain combined with adenosine stress echocardiography assessment of viable myocardium.

    PubMed

    Fang, Ling-Ling; Zhang, Ping-Yang; Wang, Chong; Wang, Li-Ming; Ma, Xiao-Wu; Shi, Hong-Wei; Feng, Xue-Hong

    2011-03-01

    The objective of this study was to explore a new method for the identification of viable myocardium by means of two-dimensional (2D) strain imaging combined with adenosine stress echocardiography. A total of 15 anesthetized open-chest healthy mongrel dogs underwent left anterior descending coronary artery occlusion for 90 min followed by 120-min reperfusion. Adenosine was infused at 140 μg kg(-1) min(-1) over a period of 6 min. Images were acquired at baseline (when pericardial cradle was made), after reperfusion (when reperfusion finished) and after adenosine administration (while administration stopped). Measurements of the regional peak-systolic strain in radial, circumferential, and longitudinal motion on anterior wall and anterior septum were, respectively, performed under different conditions. The dogs were killed after the echocardiographic studies finished and then the area of infracted myocardium was defined by triphenyltetrazolium chloride histology. A segment with equal or less than 50% area of infracted myocardium was considered to be viable. As a result, 37 regions were viable whereas 53 were non-viable among 90 regions in 15 dogs. At baseline, there was no significant difference in peak-systolic radial strain (Rs), circumferential strain (Cs), and longitudinal strain (Ls) between the viable and non-viable groups. After reperfusion, Rs, Cs, and Ls in absolute value decreased compared to those at baseline in both groups, although there was no significant difference between these groups. Rs and Ls increased after adenosine administration compared to reperfusion (p < 0.01; p < 0.05) in viable group while there were no changes in non-viable group. Compared with non-viable group Rs, Cs and Ls in viable group increased significantly (p < 0.01; 0.05) after adenosine administration. There was a negative correlation between Rs and infarct size (r = -0.72). Cs and Ls correlated well with infarct size, respectively (r = 0.40; 0.67). A change of Rs more than 13

  12. MRI monitoring of function, perfusion and viability in microembolized moderately ischemic myocardium.

    PubMed

    Do, Loi; Wilson, Mark W; Krug, Roland; Hetts, Steven W; Saeed, Maythem

    2015-08-01

    Assessment of microembolization after coronary interventions is clinically challenging, thus we longitudinally investigated microemboli effects on moderately ischemic myocardium using MRI and histopathology. Twenty-four pigs (8/group) were divided into: group I (no intervention), group II (45 min LAD occlusion) and group III (45 min LAD occlusion with microembolization). Cine, perfusion and delayed contrast enhanced MRI (DE-MRI), using 1.5T MRI, were used for assessment at 3 days and 5 weeks. Triphenyltetrazolium-chloride (TTC) and Masson-trichrome were used as gold standard references for macro and microscopic quantification of myocardial infarction (MI). Cine MRI showed differential increase in end systolic volume (1.3 ± 0.08 ml/kg group II and 1.6 ± 0.1 ml/kg group III) and decrease in ejection fraction (45 ± 2 and 36 ± 2%, respectively) compared with controls at 3 days (2.1 ± 0.1 ml ESV and 50 ± 1% EF, P < 0.05). At 5 weeks group III, but not II, showed persistent perfusion deficits, wall thinning in the LAD territory and compensatory hypertrophy in remote myocardium. DE-MRI MI at 3 days was significantly smaller in group II (3.3 ± 2.2 g) than III (9.8 ± 0.6 g), at 5 weeks, MI were smaller by 60% (1.3 ± 0.9 g) and 22% (7.7 ± 0.5 g), respectively. TTC MI was similar to DE-MRI in group II (1.6 ± 1.0 g) and III (9.2 ± 1.6 g), but not microscopy (2.8 ± 0.4 and 10.5 ± 1.5 g, respectively). The effects of moderate ischemia with and without microembolization on myocardium could be differentiated using multiple MRI sequences. MRI demonstrated that microemboli in moderately ischemic myocardium, but not solely ischemia, prolonged ventricular dysfunction, created perfusion deficits, poor infarct resorption and enhanced compensatory hypertrophy, while moderate ischemia alone caused minor LV changes.

  13. Viscoelastic properties of pressure overload hypertrophied myocardium: effect of serine protease treatment

    NASA Technical Reports Server (NTRS)

    Stroud, Jason D.; Baicu, Catalin F.; Barnes, Mary A.; Spinale, Francis G.; Zile, Michael R.

    2002-01-01

    To determine whether and to what extent one component of the extracellular matrix, fibrillar collagen, contributes causally to abnormalities in viscoelasticity, collagen was acutely degraded by activation of endogenous matrix metalloproteinases (MMPs) with the serine protease plasmin. Papillary muscles were isolated from normal cats and cats with right ventricular pressure overload hypertrophy (POH) induced by pulmonary artery banding. Plasmin treatment caused MMP activation, collagen degradation, decreased the elastic stiffness constant, and decreased the viscosity constant in both normal and POH muscles. Thus, whereas many mechanisms may contribute to the abnormalities in myocardial viscoelasticity in the POH myocardium, changes in fibrillar collagen appear to play a predominant role.

  14. [Intramural chronotopography of depolarization of myocardium of heart ventricles of pig (Sus scrofa domesticus)].

    PubMed

    2014-01-01

    Sequence of depolarization of myocardium of pig heart ventricles was studied by the method of multichannel synchronous cardioelectrotopography. There is established formation of areas of early depolarization in subendocardium of interventricular septum and in the base of left ventricle papillary muscles; of multiple foci--in the depth of walls; of areas of late depolarization--in subepicardium of the left ventricle dorsolateral side. As compared with other species of ungulate animals (reindeer and sheep, in pig heart ventricles, differences are revealed in locations of early and late depolarization, a breakdown of the excitation wave into subepicardium. PMID:25508945

  15. [Intramural chronotopography of depolarization of myocardium of heart ventricles of pig (Sus scrofa domesticus)].

    PubMed

    Gulyaeva, A S; Roshchecskaya, I M; Roshchevsky, M P

    2014-01-01

    Sequence of depolarization of myocardium of pig heart ventricles was studied by the method of multichannel synchronous cardioelectrotopography. There is established formation of areas of early depolarization in subendocardium of interventricular septum and in the base of left ventricle papillary muscles; of multiple foci--in the depth of walls; of areas of late depolarization--in subepicardium of the left ventricle dorsolateral side. As compared with other species of ungulate animals (reindeer and sheep, in pig heart ventricles, differences are revealed in locations of early and late depolarization, a breakdown of the excitation wave into subepicardium. PMID:25486814

  16. Arrangements of multiple images of human myocardium for information for the surgeon during open heart surgery

    NASA Astrophysics Data System (ADS)

    Kessler, Manfred D.; Cristea, Paul D.; Hiller, Michael; Trinks, Tobias

    2002-06-01

    The feasibility to obtain visualized information of myocardium by imaging is a new dimension. However, during heart surgery the surgeon does not need all data of images continuously. Therefore, development of strategies able to reduce flux of information transiently in between images might become important. Arrangements of images in 3-dimensional structures can produce better outlines. Images often contain information of several parameters. Therefore, a selection of important parts of the pictures might be helpful. Optical sensors will have the ability to detect dangerous situations in tissues which can release optical or acoustic signals.

  17. Amelioration of Cardiac Function and Activation of Anti-Inflammatory Vasoactive Peptides Expression in the Rat Myocardium by Low Level Laser Therapy

    PubMed Central

    Manchini, Martha Trindade; Serra, Andrey Jorge; Feliciano, Regiane dos Santos; Santana, Eduardo Tadeu; Antônio, Ednei Luis; de Tarso Camillo de Carvalho, Paulo; Montemor, Jairo; Crajoinas, Renato Oliveira; Girardi, Adriana Castello Costa; Tucci, Paulo José Ferreira; Silva, José Antônio

    2014-01-01

    Low-level laser therapy (LLLT) has been used as an anti-inflammatory treatment in several disease conditions, even when inflammation is a secondary consequence, such as in myocardial infarction (MI). However, the mechanism by which LLLT is able to protect the remaining myocardium remains unclear. The present study tested the hypothesis that LLLT reduces inflammation after acute MI in female rats and ameliorates cardiac function. The potential participation of the Renin-Angiotensin System (RAS) and Kallikrein-Kinin System (KKS) vasoactive peptides was also evaluated. LLLT treatment effectively reduced MI size, attenuated the systolic dysfunction after MI, and decreased the myocardial mRNA expression of interleukin-1 beta and interleukin-6 in comparison to the non-irradiated rat tissue. In addition, LLLT treatment increased protein and mRNA levels of the Mas receptor, the mRNA expression of kinin B2 receptors and the circulating levels of plasma kallikrein compared to non-treated post-MI rats. On the other hand, the kinin B1 receptor mRNA expression decreased after LLLT. No significant changes were found in the expression of vascular endothelial growth factor (VEGF) in the myocardial remote area between laser-irradiated and non-irradiated post-MI rats. Capillaries density also remained similar between these two experimental groups. The mRNA expression of the inducible nitric oxide synthase (iNOS) was increased three days after MI, however, this effect was blunted by LLLT. Moreover, endothelial NOS mRNA content increased after LLLT. Plasma nitric oxide metabolites (NOx) concentration was increased three days after MI in non-treated rats and increased even further by LLLT treatment. Our data suggest that LLLT diminishes the acute inflammation in the myocardium, reduces infarct size and attenuates left ventricle dysfunction post-MI and increases vasoactive peptides expression and nitric oxide (NO) generation. PMID:24991808

  18. Amelioration of cardiac function and activation of anti-inflammatory vasoactive peptides expression in the rat myocardium by low level laser therapy.

    PubMed

    Manchini, Martha Trindade; Serra, Andrey Jorge; Feliciano, Regiane dos Santos; Santana, Eduardo Tadeu; Antônio, Ednei Luis; de Tarso Camillo de Carvalho, Paulo; Montemor, Jairo; Crajoinas, Renato Oliveira; Girardi, Adriana Castello Costa; Tucci, Paulo José Ferreira; Silva, José Antônio

    2014-01-01

    Low-level laser therapy (LLLT) has been used as an anti-inflammatory treatment in several disease conditions, even when inflammation is a secondary consequence, such as in myocardial infarction (MI). However, the mechanism by which LLLT is able to protect the remaining myocardium remains unclear. The present study tested the hypothesis that LLLT reduces inflammation after acute MI in female rats and ameliorates cardiac function. The potential participation of the Renin-Angiotensin System (RAS) and Kallikrein-Kinin System (KKS) vasoactive peptides was also evaluated. LLLT treatment effectively reduced MI size, attenuated the systolic dysfunction after MI, and decreased the myocardial mRNA expression of interleukin-1 beta and interleukin-6 in comparison to the non-irradiated rat tissue. In addition, LLLT treatment increased protein and mRNA levels of the Mas receptor, the mRNA expression of kinin B2 receptors and the circulating levels of plasma kallikrein compared to non-treated post-MI rats. On the other hand, the kinin B1 receptor mRNA expression decreased after LLLT. No significant changes were found in the expression of vascular endothelial growth factor (VEGF) in the myocardial remote area between laser-irradiated and non-irradiated post-MI rats. Capillaries density also remained similar between these two experimental groups. The mRNA expression of the inducible nitric oxide synthase (iNOS) was increased three days after MI, however, this effect was blunted by LLLT. Moreover, endothelial NOS mRNA content increased after LLLT. Plasma nitric oxide metabolites (NOx) concentration was increased three days after MI in non-treated rats and increased even further by LLLT treatment. Our data suggest that LLLT diminishes the acute inflammation in the myocardium, reduces infarct size and attenuates left ventricle dysfunction post-MI and increases vasoactive peptides expression and nitric oxide (NO) generation. PMID:24991808

  19. The myocardium.

    PubMed

    Langer, G A; Frank, J S; Brady, A J

    1976-01-01

    A comparison of some of the mechanical properties of cardiac with other types of muscle has been made, showing that, except for the speed of some responses, cardiac muscle is similar to other types of muscle. Furthermore, the techniques used in both living and glycerol-extracted insect fibrillar and vertebrate skeletal muscle are applicable to heart muscle, where the focus of the technique is now on cross-bridge mechanics and energetics. It is particularly encouraging to see many well known phenomena such as inactivation with shortening, stress related increases in active force, and the Fenn effect begin to find some more specific relation to cross-bridge mechanical and chemical activity. The high compliance of cardiac preparations still clouds the interpretation of data obtained from whole muscle preparations; however, the reduced compliance of glycerol-extracted cardiac muscle offers some hope of obviating some series compliance. Indeed, the correspondence in mechanical responses of living and glycerol-extracted preparations shows that glycerol preparations are of great utility since the time dependence of activation also can be removed in these studies. A more complete analysis of muscle models, in which the cross-bridge contribution to muscle elasticity is more realistically evaluated, should help in relating muscle measurements to cross-bridge activity. Furthermore, studies on both living and glycerol-extracted cardiac muscle, particularly if sarcomere length can be controlled, offer new hope of closing the perpetual gap in our understanding of cardiac muscle physiology relative to skeletal muscle.

  20. Pretreatment Engineering Platform Phase 1 Final Test Report

    SciTech Connect

    Kurath, Dean E.; Hanson, Brady D.; Minette, Michael J.; Baldwin, David L.; Rapko, Brian M.; Mahoney, Lenna A.; Schonewill, Philip P.; Daniel, Richard C.; Eslinger, Paul W.; Huckaby, James L.; Billing, Justin M.; Sundar, Parameshwaran S.; Josephson, Gary B.; Toth, James J.; Yokuda, Satoru T.; Baer, Ellen BK; Barnes, Steven M.; Golovich, Elizabeth C.; Rassat, Scot D.; Brown, Christopher F.; Geeting, John GH; Sevigny, Gary J.; Casella, Amanda J.; Bontha, Jagannadha R.; Aaberg, Rosanne L.; Aker, Pamela M.; Guzman-Leong, Consuelo E.; Kimura, Marcia L.; Sundaram, S. K.; Pires, Richard P.; Wells, Beric E.; Bredt, Ofelia P.

    2009-12-23

    Pacific Northwest National Laboratory (PNNL) was tasked by Bechtel National Inc. (BNI) on the River Protection Project, Hanford Tank Waste Treatment and Immobilization Plant (RPP-WTP) project to conduct testing to demonstrate the performance of the WTP Pretreatment Facility (PTF) leaching and ultrafiltration processes at an engineering-scale. In addition to the demonstration, the testing was to address specific technical issues identified in Issue Response Plan for Implementation of External Flowsheet Review Team (EFRT) Recommendations - M12, Undemonstrated Leaching Processes.( ) Testing was conducted in a 1/4.5-scale mock-up of the PTF ultrafiltration system, the Pretreatment Engineering Platform (PEP). Parallel laboratory testing was conducted in various PNNL laboratories to allow direct comparison of process performance at an engineering-scale and a laboratory-scale. This report presents and discusses the results of those tests.

  1. Fetal myocardium in the kidney capsule: an in vivo model of repopulation of myocytes by bone marrow cells.

    PubMed

    Zhang, Eric Y; Xiong, Qiang; Ye, Lei; Suntharalingam, Piradeep; Wang, Xiaohong; Astle, C Michael; Zhang, Jianyi; Harrison, David E

    2012-01-01

    Debate surrounds the question of whether the heart is a post-mitotic organ in part due to the lack of an in vivo model in which myocytes are able to actively regenerate. The current study describes the first such mouse model--a fetal myocardial environment grafted into the adult kidney capsule. Here it is used to test whether cells descended from bone marrow can regenerate cardiac myocytes. One week after receiving the fetal heart grafts, recipients were lethally irradiated and transplanted with marrow from green fluorescent protein (GFP)-expressing C57Bl/6J (B6) donors using normal B6 recipients and fetal donors. Levels of myocyte regeneration from GFP marrow within both fetal myocardium and adult hearts of recipients were evaluated histologically. Fetal myocardium transplants had rich neovascularization and beat regularly after 2 weeks, continuing at checkpoints of 1, 2, 4, 6, 8 and12 months after transplantation. At each time point, GFP-expressing rod-shaped myocytes were found in the fetal myocardium, but only a few were found in the adult hearts. The average count of repopulated myocardium with green rod-shaped myocytes was 996.8 cells per gram of fetal myocardial tissue, and 28.7 cells per adult heart tissue, representing a thirty-five fold increase in fetal myocardium compared to the adult heart at 12 months (when numbers of green rod-shaped myocytes were normalized to per gram of myocardial tissue). Thus, bone marrow cells can differentiate to myocytes in the fetal myocardial environment. The novel in vivo model of fetal myocardium in the kidney capsule appears to be valuable for testing repopulating abilities of potential cardiac progenitors.

  2. Alterations in vasomotor control of coronary resistance vessels in remodelled myocardium of swine with a recent myocardial infarction.

    PubMed

    Duncker, Dirk J; de Beer, Vincent J; Merkus, Daphne

    2008-05-01

    The mechanism underlying the progressive deterioration of left ventricular (LV) dysfunction after myocardial infarction (MI) towards overt heart failure remains incompletely understood, but may involve impairments in coronary blood flow regulation within remodelled myocardium leading to intermittent myocardial ischemia. Blood flow to the remodelled myocardium is hampered as the coronary vasculature does not grow commensurate with the increase in LV mass and because extravascular compression of the coronary vasculature is increased. In addition to these factors, an increase in coronary vasomotor tone, secondary to neurohumoral activation and endothelial dysfunction, could also contribute to the impaired myocardial oxygen supply. Consequently, we explored, in a series of studies, the alterations in regulation of coronary resistance vessel tone in remodelled myocardium of swine with a 2 to 3-week-old MI. These studies indicate that myocardial oxygen balance is perturbed in remodelled myocardium, thereby forcing the myocardium to increase its oxygen extraction. These perturbations do not appear to be the result of blunted beta-adrenergic or endothelial NO-mediated coronary vasodilator influences, and are opposed by an increased vasodilator influence through opening of K(ATP) channels. Unexpectedly, we observed that despite increased circulating levels of noradrenaline, angiotensin II and endothelin-1, alpha-adrenergic tone remained negligible, while the coronary vasoconstrictor influences of endogenous endothelin and angiotensin II were virtually abolished. We conclude that, early after MI, perturbations in myocardial oxygen balance are observed in remodelled myocardium. However, adaptive alterations in coronary resistance vessel control, consisting of increased vasodilator influences in conjunction with blunted vasoconstrictor influences, act to minimize the impairments of myocardial oxygen balance.

  3. Pre-Clinical Evaluation of Biopolymer Delivered Circulating Angiogenic Cells in Hibernating Myocardium

    NASA Astrophysics Data System (ADS)

    Giordano, Celine

    Vasculogenic cell-based therapy combined with tissue engineering is a promising revascularization strategy for patients with hibernating myocardium, a common clinical condition. We used a clinically relevant swine model of hibernating myocardium to examine the benefits of biopolymer-supported delivery of circulating angiogenic cells (CACs) in this context. Twenty-five swine underwent placement of an ameroid constrictor on the left circumflex artery (LCx). After 2 weeks, positron emission tomography measures of myocardial blood flow (MBF) and myocardial flow reserve (MFR) were reduced in the affected region (both p<0.001). Hibernation (mismatch) was specific to the LCx territory. Swine were randomized to receive intramyocardial injections of PBS control (n=10), CACs (n=8), or CACs + a collagen-based matrix (n=7). At follow-up, stress MBF and MFR were increased only in the cells+matrix group (p<0.01), and mismatch was lower in the cells+matrix treated animals (p=0.02) compared to controls. Similar results were found using microsphere-measured MBF. Wall motion abnormalities and ejection fraction improved only in the cells+matrix group. This preclinical swine model demonstrated ischemia and hibernation, which was improved by the combined delivery of CACs and a collagen-based matrix. To our knowledge, this is the first demonstration of the mechanisms and effects of combining progenitor cells and biopolymers in the setting of myocardial hibernation, a common clinical condition in patients with advanced coronary artery disease.

  4. Ruptured spinal arteriovenous malformation: Presenting as stunned myocardium and neurogenic shock

    PubMed Central

    Mehesry, Tasneem H.; Shaikh, Nissar; Malmstrom, Mohammad F.; Marcus, Marco A. E.; Khan, Adnan

    2015-01-01

    Background: Neurogenic pulmonary edema (NPE) is a clinical syndrome usually defined as an acute pulmonary edema occurring shortly after a central neurologic insult. NPE was identified 100 years ago, but it is still underappreciated in the clinical setup. NPE usually appears within minutes to hours after the injury. It has a high mortality rate if not recognized early and treated appropriately. Similarly, neurogenic shock is a known complication of spinal cord injury reported incidence is more than 20% in isolated upper cervical spinal injury. But NPE is rare to occur, and stunned myocardium (SM) is not reported in spinal arteriovenous malformation (AVM) rupture. SM is a reversible cardiomyopathy resulting in transient left ventricular dysfunction which has been described to occur in the setting of catecholamine release during situations of physiologic stress. We report a case of high spinal AVM rupture presenting as SM, NPE, and neurogenic shock. Case Description: A 32-year-old male who presented with sudden onset of pain and weakness in upper limbs. Imaging studies showed AVM rupture by imaging techniques. Initially, the patient had severe hypertension, respiratory distress requiring intubation and ventilation, then he developed hypotension, bradycardia, and asystole, which required immediate cardiopulmonary resuscitation and atropine. He remained with quadriplegia and suffered from frequent episodes of bradycardia and asystole. Conclusions: Spinal AVM rupture can present as neurogenic shock, stunned myocardium, and pulmonary edema. Early recognition of AVM rupture and prompt surgical intervention, as well as aggressive treatment of shock, may enhance recovery and decrease the long-term morbidity. PMID:26539315

  5. [A STUDY OF IMPACT OF MERCURY CHLORIDE ON MYOCARDIUM IN EXPERIMENT].

    PubMed

    Kamynsky, R; Primachenko, V; Sokurenko, L; Chaikovsky, Y

    2016-02-01

    The article is devoted to the study of the myocardium structural reorganization features under the action of 0,01 LD50 of mercury chloride (II) rats when comparing chronic (30 injections) and subchronic (10 injections) exposures. Structural-metabolic reorganization of the myocardium was studied using histological, histochemical and electron microscopic methods. Computer morphometric analysis with subsequent statistical processing was applied. It was established that the main mechanisms of cardiotoxic effect of mercuric chloride are: hypoxia (due to damage to micro vessels; disorder of myogenic regulation at the expense of damage intercalated discs) and the appearance of cell detrits and abnormal proteins as a result of the destruction of cardiomyocytes. Sensitive to the toxic effects of chloride mercuric in low doses are myofibrils, sarcoplasmic network and the energy apparatus of cardiomyocytes - the mitochondria. It was found that chronic exposure to low doses of mercuric chloride causes non-specific qualitative and quantitative changes in all structural components of the heart, damage to the tissue barrier is ongoing and dynamic and resorptive insufficiency hemomicrocirculatory bed of the heart that leads to chronic swelling that causes the development of diffuse fibrosis and enhances cardiac decompensation activities.

  6. Subendocardial segment length shortening at lateral margins of ischemic myocardium in dogs

    SciTech Connect

    Gallagher, K.P.; Gerren, R.A.; Choy, M.; Stirling, M.C.; Dysko, R.C. )

    1987-10-01

    The lateral borders of an infarcted area are sharply delineated in terms of perfusion, but functional impairment extends a limited distance into adjacent nonischemic myocardium. To determine the distribution of functional impairment the authors arrayed three ultrasonic dimension gauges to measure two subendocardial segment lengths in series. The center crystal, placed at the perfusion boundary (PB) between left anterior descending and circumflex arteries, radiated ultrasound to receiver crystals 7-17 mm to either side of the PB. The locations of the functional measurements relative to the PB were determined with myocardial blood flow (tracer-labeled microsphere) maps constructed from multiple small tissue samples obtained circumferentially. On the ischemic side of the PB, dL decreased from 2.24 {plus minus} 0.54 to 0.42 {plus minus} 0.39 mm. By adding the data from the two segments in series, a combined measurement of dL across heterogeneously perfused myocardium was derived that decreased by 38% from control. The level of shortening represented an integral of normal and abnormal motion that was proportional to the mean reduction in blood flow ({minus}44%) in all of the muscle spanned by the crystals. They conclude that subendocardial segment lengths average shortening in the muscle they subtend when arrayed across the perfusion boundary.

  7. Molecular imaging of induced pluripotent stem cell immunogenicity with in vivo development in ischemic myocardium.

    PubMed

    Liu, Zhiqiang; Wen, Xinyu; Wang, Haibin; Zhou, Jin; Zhao, Mengge; Lin, Qiuxia; Wang, Yan; Li, Junjie; Li, Dexue; Du, Zhiyan; Yao, Anning; Cao, Feng; Wang, Changyong

    2013-01-01

    Whether differentiation of induced pluripotent stem cells (iPSCs) in ischemic myocardium enhances their immunogenicity, thereby increasing their chance for rejection, is unclear. Here, we dynamically demonstrated the immunogenicity and rejection of iPSCs in ischemic myocardium using bioluminescent imaging (BLI). Murine iPSCs were transduced with a tri-fusion (TF) reporter gene consisting of firefly luciferase-red fluorescent protein-truncated thymidine kinase (fluc-mrfp-tTK). Ascorbic acid (Vc) were used to induce iPSCs to differentiate into cardiomyocytes (CM). iPSCs and iPS-CMs were intramyocardially injected into immunocompetent or immunosuppressed allogenic murine with myocardial infarction. BLI was performed to track transplanted cells. Immune cell infiltration was evaluated by immunohistochemistry. Syngeneic iPSCs were also injected and evaluated. The results demonstrated that undifferentiated iPSCs survived and proliferated in allogenic immunocompetent recipients early post-transplantation, accompanying with mild immune cell infiltration. With in vivo differentiation, a progressive immune cell infiltration could be detected. While transplantation of allogenic iPSC-CMs were observed an acute rejection from receipts. In immune-suppressed recipients, the proliferation of iPSCs could be maintained and intramyocardial teratomas were formed. Transplantation of syngeneic iPSCs and iPSC-CMs were also observed progressive immune cell infiltration. This study demonstrated that iPSC immunogenicity increases with in vivo differentiation, which will increase their chance for rejection in iPSC-based therapy.

  8. Beneficial actions of bevantolol on subendocardial blood flow and contractile function in ischemic myocardium.

    PubMed

    Gross, G J; Buck, J D; Warltier, D C; Hardman, H F

    1979-01-01

    The effect of a new cardioselective beta adrenergic antagonist, bevantolol (CI-775), on regional myocardial blood flow and contractile function distal to a severe flow-limiting stenosis of the left circumflex coronary artery was studied in open-chest dogs. Bevantolol (1 mg/kg, i.v.) or saline was administered 30 min after production of left circumflex stenosis sufficient to reduce resting coronary blood flow and contractile force approximately 40%. Regional myocardial blood flow and contractile force were measured with radiolabeled microspheres and Brodie-Walton strain gauge arches, respectively. No significant changes were observed in the saline-treated group. Following bevantolol treatment subendocardial blood flow (1.30 +/- 0.29 to 0.93 +/- 0.19 ml/min/g) and contractile force decreased (11.4 +/- 4.4%) significantly (p less than 0.05) in nonischemic myocardium. Subendocardial blood flow (0.59 +/- 0.14 to 0.81 +/- 0.14 ml/min/g) and contractile force increased (29.3 +/- 3.6%) significantly (p less than 0.05) in ischemic myocardium. These results suggest that bevantolol produces a favorable redistribution of flow to ischemic subendocardium. The increase in flow results in an improvement of contractile function in the ischemic region.

  9. Anisotropic engineered heart tissue made from laser-cut decellularized myocardium.

    PubMed

    Schwan, Jonas; Kwaczala, Andrea T; Ryan, Thomas J; Bartulos, Oscar; Ren, Yongming; Sewanan, Lorenzo R; Morris, Aaron H; Jacoby, Daniel L; Qyang, Yibing; Campbell, Stuart G

    2016-08-30

    We have developed an engineered heart tissue (EHT) system that uses laser-cut sheets of decellularized myocardium as scaffolds. This material enables formation of thin muscle strips whose biomechanical characteristics are easily measured and manipulated. To create EHTs, sections of porcine myocardium were laser-cut into ribbon-like shapes, decellularized, and mounted in specialized clips for seeding and culture. Scaffolds were first tested by seeding with neonatal rat ventricular myocytes. EHTs beat synchronously by day five and exhibited robust length-dependent activation by day 21. Fiber orientation within the scaffold affected peak twitch stress, demonstrating its ability to guide cells toward physiologic contractile anisotropy. Scaffold anisotropy also made it possible to probe cellular responses to stretch as a function of fiber angle. Stretch that was aligned with the fiber direction increased expression of brain natriuretic peptide, but off-axis stretches (causing fiber shear) did not. The method also produced robust EHTs from cardiomyocytes derived from human embryonic stem cells and induced pluripotent stem cells (hiPSC). hiPSC-EHTs achieved maximum peak stress of 6.5 mN/mm(2) and twitch kinetics approaching reported values from adult human trabeculae. We conclude that laser-cut EHTs are a viable platform for novel mechanotransduction experiments and characterizing the biomechanical function of patient-derived cardiomyoctyes.

  10. Clonal analysis reveals a common origin between nonsomite-derived neck muscles and heart myocardium.

    PubMed

    Lescroart, Fabienne; Hamou, Wissam; Francou, Alexandre; Théveniau-Ruissy, Magali; Kelly, Robert G; Buckingham, Margaret

    2015-02-01

    Neck muscles constitute a transition zone between somite-derived skeletal muscles of the trunk and limbs, and muscles of the head, which derive from cranial mesoderm. The trapezius and sternocleidomastoid neck muscles are formed from progenitor cells that have expressed markers of cranial pharyngeal mesoderm, whereas other muscles in the neck arise from Pax3-expressing cells in the somites. Mef2c-AHF-Cre genetic tracing experiments and Tbx1 mutant analysis show that nonsomitic neck muscles share a gene regulatory network with cardiac progenitor cells in pharyngeal mesoderm of the second heart field (SHF) and branchial arch-derived head muscles. Retrospective clonal analysis shows that this group of neck muscles includes laryngeal muscles and a component of the splenius muscle, of mixed somitic and nonsomitic origin. We demonstrate that the trapezius muscle group is clonally related to myocardium at the venous pole of the heart, which derives from the posterior SHF. The left clonal sublineage includes myocardium of the pulmonary trunk at the arterial pole of the heart. Although muscles derived from the first and second branchial arches also share a clonal relationship with different SHF-derived parts of the heart, neck muscles are clonally distinct from these muscles and define a third clonal population of common skeletal and cardiac muscle progenitor cells within cardiopharyngeal mesoderm. By linking neck muscle and heart development, our findings highlight the importance of cardiopharyngeal mesoderm in the evolution of the vertebrate heart and neck and in the pathophysiology of human congenital disease.

  11. Anisotropic engineered heart tissue made from laser-cut decellularized myocardium

    PubMed Central

    Schwan, Jonas; Kwaczala, Andrea T.; Ryan, Thomas J.; Bartulos, Oscar; Ren, Yongming; Sewanan, Lorenzo R.; Morris, Aaron H.; Jacoby, Daniel L.; Qyang, Yibing; Campbell, Stuart G.

    2016-01-01

    We have developed an engineered heart tissue (EHT) system that uses laser-cut sheets of decellularized myocardium as scaffolds. This material enables formation of thin muscle strips whose biomechanical characteristics are easily measured and manipulated. To create EHTs, sections of porcine myocardium were laser-cut into ribbon-like shapes, decellularized, and mounted in specialized clips for seeding and culture. Scaffolds were first tested by seeding with neonatal rat ventricular myocytes. EHTs beat synchronously by day five and exhibited robust length-dependent activation by day 21. Fiber orientation within the scaffold affected peak twitch stress, demonstrating its ability to guide cells toward physiologic contractile anisotropy. Scaffold anisotropy also made it possible to probe cellular responses to stretch as a function of fiber angle. Stretch that was aligned with the fiber direction increased expression of brain natriuretic peptide, but off-axis stretches (causing fiber shear) did not. The method also produced robust EHTs from cardiomyocytes derived from human embryonic stem cells and induced pluripotent stem cells (hiPSC). hiPSC-EHTs achieved maximum peak stress of 6.5 mN/mm2 and twitch kinetics approaching reported values from adult human trabeculae. We conclude that laser-cut EHTs are a viable platform for novel mechanotransduction experiments and characterizing the biomechanical function of patient-derived cardiomyoctyes. PMID:27572147

  12. Clonal analysis reveals a common origin between nonsomite-derived neck muscles and heart myocardium.

    PubMed

    Lescroart, Fabienne; Hamou, Wissam; Francou, Alexandre; Théveniau-Ruissy, Magali; Kelly, Robert G; Buckingham, Margaret

    2015-02-01

    Neck muscles constitute a transition zone between somite-derived skeletal muscles of the trunk and limbs, and muscles of the head, which derive from cranial mesoderm. The trapezius and sternocleidomastoid neck muscles are formed from progenitor cells that have expressed markers of cranial pharyngeal mesoderm, whereas other muscles in the neck arise from Pax3-expressing cells in the somites. Mef2c-AHF-Cre genetic tracing experiments and Tbx1 mutant analysis show that nonsomitic neck muscles share a gene regulatory network with cardiac progenitor cells in pharyngeal mesoderm of the second heart field (SHF) and branchial arch-derived head muscles. Retrospective clonal analysis shows that this group of neck muscles includes laryngeal muscles and a component of the splenius muscle, of mixed somitic and nonsomitic origin. We demonstrate that the trapezius muscle group is clonally related to myocardium at the venous pole of the heart, which derives from the posterior SHF. The left clonal sublineage includes myocardium of the pulmonary trunk at the arterial pole of the heart. Although muscles derived from the first and second branchial arches also share a clonal relationship with different SHF-derived parts of the heart, neck muscles are clonally distinct from these muscles and define a third clonal population of common skeletal and cardiac muscle progenitor cells within cardiopharyngeal mesoderm. By linking neck muscle and heart development, our findings highlight the importance of cardiopharyngeal mesoderm in the evolution of the vertebrate heart and neck and in the pathophysiology of human congenital disease. PMID:25605943

  13. Anisotropic engineered heart tissue made from laser-cut decellularized myocardium.

    PubMed

    Schwan, Jonas; Kwaczala, Andrea T; Ryan, Thomas J; Bartulos, Oscar; Ren, Yongming; Sewanan, Lorenzo R; Morris, Aaron H; Jacoby, Daniel L; Qyang, Yibing; Campbell, Stuart G

    2016-01-01

    We have developed an engineered heart tissue (EHT) system that uses laser-cut sheets of decellularized myocardium as scaffolds. This material enables formation of thin muscle strips whose biomechanical characteristics are easily measured and manipulated. To create EHTs, sections of porcine myocardium were laser-cut into ribbon-like shapes, decellularized, and mounted in specialized clips for seeding and culture. Scaffolds were first tested by seeding with neonatal rat ventricular myocytes. EHTs beat synchronously by day five and exhibited robust length-dependent activation by day 21. Fiber orientation within the scaffold affected peak twitch stress, demonstrating its ability to guide cells toward physiologic contractile anisotropy. Scaffold anisotropy also made it possible to probe cellular responses to stretch as a function of fiber angle. Stretch that was aligned with the fiber direction increased expression of brain natriuretic peptide, but off-axis stretches (causing fiber shear) did not. The method also produced robust EHTs from cardiomyocytes derived from human embryonic stem cells and induced pluripotent stem cells (hiPSC). hiPSC-EHTs achieved maximum peak stress of 6.5 mN/mm(2) and twitch kinetics approaching reported values from adult human trabeculae. We conclude that laser-cut EHTs are a viable platform for novel mechanotransduction experiments and characterizing the biomechanical function of patient-derived cardiomyoctyes. PMID:27572147

  14. Remodeling in myocardium adjacent to an infarction in the pig left ventricle.

    PubMed

    Zimmerman, Scott D; Criscione, John; Covell, James W

    2004-12-01

    Changes in the structure of the "normal" ventricular wall adjacent to an infarcted area involve all components of the myocardium (myocytes, fibroblasts and the extracellular matrix, and the coronary vasculature) and their three-dimensional structural relationship. Assessing changes in these components requires tracking material markers in the remodeling tissue over long periods of time with a three-dimensional approach as well as a detailed histological evaluation of the remodeled structure. The purpose of the present study was to examine the hypotheses that changes in the tissue adjacent to an infarct are related to myocyte elongation, myofiber rearrangement, and changes in the laminar architecture of the adjacent tissue. Three weeks after myocardial infarction, noninfarcted tissue adjacent to the infarct remodeled by expansion along the direction of the fibers and in the cross fiber direction. These changes are consistent with myocyte elongation and myofiber rearrangement (slippage), as well as a change in cell shape to a more elliptical cross section with the major axis in the epicardial tangent plane, and indicate that reorientation of fibers either via "cell slippage" or changes in orientation of the laminar structure of the ventricular wall are quantitatively important aspects of the remodeling of the normally perfused myocardium.

  15. Myocardium-derived angiopoietin-1 is essential for coronary vein formation in the developing heart

    PubMed Central

    Arita, Yoh; Nakaoka, Yoshikazu; Matsunaga, Taichi; Kidoya, Hiroyasu; Yamamizu, Kohei; Arima, Yuichiro; Kataoka-Hashimoto, Takahiro; Ikeoka, Kuniyasu; Yasui, Taku; Masaki, Takeshi; Yamamoto, Kaori; Higuchi, Kaori; Park, Jin-Sung; Shirai, Manabu; Nishiyama, Koichi; Yamagishi, Hiroyuki; Otsu, Kinya; Kurihara, Hiroki; Minami, Takashi; Yamauchi-Takihara, Keiko; Koh, Gou Y.; Mochizuki, Naoki; Takakura, Nobuyuki; Sakata, Yasushi; Yamashita, Jun K.; Komuro, Issei

    2014-01-01

    The origin and developmental mechanisms underlying coronary vessels are not fully elucidated. Here we show that myocardium-derived angiopoietin-1 (Ang1) is essential for coronary vein formation in the developing heart. Cardiomyocyte-specific Ang1 deletion results in defective formation of the subepicardial coronary veins, but had no significant effect on the formation of intramyocardial coronary arteries. The endothelial cells (ECs) of the sinus venosus (SV) are heterogeneous population, composed of APJ-positive and APJ-negative ECs. Among these, the APJ-negative ECs migrate from the SV into the atrial and ventricular myocardium in Ang1-dependent manner. In addition, Ang1 may positively regulate venous differentiation of the subepicardial APJ-negative ECs in the heart. Consistently, in vitro experiments show that Ang1 indeed promotes venous differentiation of the immature ECs. Collectively, our results indicate that myocardial Ang1 positively regulates coronary vein formation presumably by promoting the proliferation, migration and differentiation of immature ECs derived from the SV. PMID:25072663

  16. Effects of allocryptopine on outward potassium current and slow delayed rectifier potassium current in rabbit myocardium

    PubMed Central

    Fu, Yi-Cheng; Zhang, Yu; Tian, Liu-Yang; Li, Nan; Chen, Xi; Cai, Zhong-Qi; Zhu, Chao; Li, Yang

    2016-01-01

    Objective Allocryptopine (ALL) is an effective alkaloid of Corydalis decumbens (Thunb.) Pers. Papaveraceae and has proved to be anti-arrhythmic. The purpose of our study is to investigate the effects of ALL on transmural repolarizing ionic ingredients of outward potassium current (Ito) and slow delayed rectifier potassium current (IKs). Methods The monophasic action potential (MAP) technique was used to record the MAP duration of the epicardium (Epi), myocardium (M) and endocardium (Endo) of the rabbit heart and the whole cell patch clamp was used to record Ito and IKs in cardiomyocytes of Epi, M and Endo layers that were isolated from rabbit ventricles. Results The effects of ALL on MAP of Epi, M and Endo layers were disequilibrium. ALL could effectively reduce the transmural dispersion of repolarization (TDR) in rabbit transmural ventricular wall. ALL decreased the current densities of Ito and IKs in a voltage and concentration dependent way and narrowed the repolarizing differences among three layers. The analysis of gating kinetics showed ALL accelerated the channel activation of Ito in M layers and partly inhibit the channel openings of Ito in Epi, M and Endo cells. On the other hand, ALL mainly slowed channel deactivation of IKs channel in Epi and Endo layers without affecting its activation. Conclusions Our study gives partially explanation about the mechanisms of transmural inhibition of Ito and IKs channels by ALL in rabbit myocardium. These findings provide novel perspective regarding the anti-arrhythmogenesis application of ALL in clinical settings. PMID:27403141

  17. Anisotropic engineered heart tissue made from laser-cut decellularized myocardium

    PubMed Central

    Schwan, Jonas; Kwaczala, Andrea T.; Ryan, Thomas J.; Bartulos, Oscar; Ren, Yongming; Sewanan, Lorenzo R.; Morris, Aaron H.; Jacoby, Daniel L.; Qyang, Yibing; Campbell, Stuart G.

    2016-01-01

    We have developed an engineered heart tissue (EHT) system that uses laser-cut sheets of decellularized myocardium as scaffolds. This material enables formation of thin muscle strips whose biomechanical characteristics are easily measured and manipulated. To create EHTs, sections of porcine myocardium were laser-cut into ribbon-like shapes, decellularized, and mounted in specialized clips for seeding and culture. Scaffolds were first tested by seeding with neonatal rat ventricular myocytes. EHTs beat synchronously by day five and exhibited robust length-dependent activation by day 21. Fiber orientation within the scaffold affected peak twitch stress, demonstrating its ability to guide cells toward physiologic contractile anisotropy. Scaffold anisotropy also made it possible to probe cellular responses to stretch as a function of fiber angle. Stretch that was aligned with the fiber direction increased expression of brain natriuretic peptide, but off-axis stretches (causing fiber shear) did not. The method also produced robust EHTs from cardiomyocytes derived from human embryonic stem cells and induced pluripotent stem cells (hiPSC). hiPSC-EHTs achieved maximum peak stress of 6.5 mN/mm2 and twitch kinetics approaching reported values from adult human trabeculae. We conclude that laser-cut EHTs are a viable platform for novel mechanotransduction experiments and characterizing the biomechanical function of patient-derived cardiomyoctyes. PMID:27572147

  18. Protective effect of low dose gadolinium chloride against isoproterenol-induced myocardial injury in rat.

    PubMed

    Zheng, Yuan-Yuan; Zhang, Hai-Hong; Yan, Xin-Xin; Chen, Min; Qi, Tian-Yu; Zhang, Lan-E; Luo, Da-Li

    2015-09-01

    Acute myocardial injury remains a leading cause of morbidity and mortality worldwide, and large amount of released arachidonic acid (AA) is found to be related to cardiomyocyte apoptosis and necrosis. Previous study suggested that GdCl3 completely abolished AA-induced Ca(2+) response. Thus, this study aims to investigate possible cardioprotection effect of GdCl3 on isoproterenol (ISO)-induced myocardial injury and its underlying mechanism(s). Rats that were randomly allocated to five groups: control, GdCl3, ISO, ISO + GdCl3, and ISO + verapamil. Serum levels of AA and cardiac markers, infarct area, and cell apoptosis in heart were measured by ELISA assay, TTC and TUNEL staining, respectively. Chemical interaction between AA and GdCl3 was evaluated by mass and UV spectrometry. The expressions and translocations of death receptor related molecules into lipid rafts were detected in neonatal rat ventricular myocytes by Western blots. Compared with ISO-administered rats, GdCl3 significantly ameliorated the myocardium injury, demonstrated by restoring serum cardiac troponin I, lactate dehydrogenase, creatine kinase MB and AA to near normal levels, and decreasing infarct area and cell apoptosis. In addition, an activation of AA-Fas pathway was found in ISO-induced myocardial injury, which was abrogated by GdCl3. Furthermore, AA induced cell apoptosis through clustering and activating death receptor related molecules TNFR1, Fas and FADD in lipid rafts, a process significantly prevented by the pretreatment with GdCl3. Finally, GdCl3 at the molar ratio of 1/3 (GdCl3/AA) was mostly effective in abolishing AA-induced Ca(2+) response and cell apoptosis, because an obvious change in the chemical identity of AA was obtained by GdCl3 according to this molar ratio. In conclusion, this study demonstrates for the first time that GdCl3 protects myocardium against ISO-induced cell apoptosis through, at least partly, serving as a scavenger of AA, therefore abolishing its downstream

  19. Method for pretreating lignocellulosic biomass

    DOEpatents

    Kuzhiyil, Najeeb M.; Brown, Robert C.; Dalluge, Dustin Lee

    2015-08-18

    The present invention relates to a method for pretreating lignocellulosic biomass containing alkali and/or alkaline earth metal (AAEM). The method comprises providing a lignocellulosic biomass containing AAEM; determining the amount of the AAEM present in the lignocellulosic biomass; identifying, based on said determining, the amount of a mineral acid sufficient to completely convert the AAEM in the lignocellulosic biomass to thermally-stable, catalytically-inert salts; and treating the lignocellulosic biomass with the identified amount of the mineral acid, wherein the treated lignocellulosic biomass contains thermally-stable, catalytically inert AAEM salts.

  20. Manifestation of automaticity in the pulmonary-vein myocardium of rats with abdominal aorto-venocaval shunt.

    PubMed

    Hamaguchi, Shogo; Tsuneoka, Yayoi; Tanaka, Ayumi; Irie, Masahiko; Tsuruta, Masato; Nakayama, Takahiro; Namekata, Iyuki; Nada, Mizuki; Aimoto, Megumi; Takahara, Akira; Tanaka, Hikaru

    2015-08-01

    Effect of abdominal aorto-venocaval shunt (AVS) on the automaticity of the pulmonary-vein myocardium was studied in the rat. Spontaneous electrical activity was observed in one third of the isolated pulmonary-vein preparations from the AVS rats, but scarcely in those from sham-operated rats; the activity was induced by tertiapin and suppressed by carbachol or chelation of intracellular Ca(2+). The evoked action potentials in AVS rats had less negative resting membrane potential and longer action potential duration than those in sham-operated rats. These results suggest that the automaticity of the rat pulmonary-vein myocardium is manifested under chronic volume overload.

  1. Mechanisms of intracellular defense and activity of free radical oxidation in rat myocardium in the dynamics of chronic fluorine intoxication.

    PubMed

    Zhukova, A G; Alekhina, D A; Sazontova, T G; Prokop'ev, Yu A; Gorokhova, L G; Stryapko, N V; Mikhailova, N N

    2013-12-01

    The mechanisms of intracellular defense and activity of free radical oxidation in the myocardium were studied in the dynamics of chronic fluorine intoxication. At the early stages of fluorine intoxication (day 3-week 3), the concentrations of defense proteins HIF-1α, HSC73, and HOx-2 and activity of the main metabolic enzymes increased, which promoted maintenance of cardiomyocyte structure and function at the normal physiological level. At late stages of fluorine intoxication (weeks 6 and 9), metabolic changes in the myocardium attest to high strain of the adaptive mechanisms.

  2. Pretreatment of rapeseed straw by sodium hydroxide.

    PubMed

    Kang, Kyeong Eop; Jeong, Gwi-Taek; Park, Don-Hee

    2012-06-01

    Pretreatment method for rapeseed straw by sodium hydroxide was investigated for production of bioethanol and biobutanol. Various pretreatment parameters, including temperature, time, and sodium hydroxide concentration were optimized using a statistical method which is a central composite design of response surface methodology. In the case of sodium hydroxide pretreatment, optimal pretreatment conditions were found to be 7.9% sodium hydroxide concentration, 5.5 h of reaction time, and 68.4 °C of reaction temperature. The maximum glucose yield which can be recovered by enzymatic hydrolysis at the optimum conditions was 95.7% and the experimental result was 94.0 ± 4.8%. This experimental result was in agreement with the model prediction. An increase of surface area and pore size in pretreated rapeseed straw by sodium hydroxide pretreatment was observed by scanning electron microscope.

  3. Supercritical ammonia pretreatment of lignocellulosic materials

    SciTech Connect

    Chou, Y.C.T.; Scott, C.D.

    1986-01-01

    A pretreatment technique using ammonia in a supercritical or near-critical fluid state was shown to substantially enhance the susceptibility of polysaccharides in lignocellulosics to subsequent hydrolysis by Trichoderma reesei cellulase. Near-theoretical conversion of cellulose and 70-80% conversion of hemicellulose to sugars from supercritical ammonia pretreated hardwoods or agricultural byproducts were obtained with a small dosage of cellulase. This technique was less effective toward softwoods. The pretreatment results are discussed in light of the properties of supercritical fluids.

  4. Hydrothermal pre-treatment of rapeseed straw.

    PubMed

    Díaz, Manuel J; Cara, Cristóbal; Ruiz, Encarnación; Romero, Inmaculada; Moya, Manuel; Castro, Eulogio

    2010-04-01

    As a first step for ethanol production from alternative raw materials, rapeseed straw was studied for fermentable sugar production. Liquid hot water was used as a pre-treatment method and the influence of the main pre-treatment variables was assessed. Experimental design and response surface methodology were applied using pre-treatment temperature and process time as factors. The pretreated solids were further submitted to enzymatic hydrolysis and the corresponding yields were used as pre-treatment performance evaluation. Liquid fractions obtained from pre-treatment were also characterized in terms of sugars and no-sugar composition. A mathematical model describing pre-treatment effects is proposed. Results show that enzymatic hydrolysis yields near to 100% based on pretreated materials can be achieved at 210-220 degrees C for 30-50 min, equivalent to near 70% of glucose present in the raw material. According to the mathematical model, a softer pre-treatment at 193 degrees C for 27 min results in 65% of glucose and 39% of xylose available for fermentation.

  5. Cadmium-induced oxidative stress and histological damage in the myocardium. Effects of a soy-based diet

    SciTech Connect

    Ferramola, Mariana L.; Pérez Díaz, Matías F.F.; Honoré, Stella M.; Sánchez, Sara S.; Antón, Rosa I.; Anzulovich, Ana C.; Giménez, María S.

    2012-12-15

    Cd exposure has been associated to an augmented risk for cardiovascular disease. We investigated the effects of 15 and 100 ppm of Cd on redox status as well as histological changes in the rat heart and the putative protective effect of a soy-based diet. Male Wistar rats were separated into 6 groups and treated during 60 days as follows: groups (1), (2) and (3) were fed a casein-based diet; groups (4), (5) and (6), a soy-based diet; (1) and (4) were given tap water; (2) and (5) tap water containing 15 ppm of Cd{sup 2+}; and (3) and (6) tap water containing 100 ppm of Cd{sup 2+}. Serum lipid peroxides increased and PON-1 activity decreased in group (3). Lipoperoxidation also increased in the heart of all intoxicated groups; however protein oxidation only augmented in (3) and reduced glutathione levels diminished in (2) and (3). Catalase activity increased in groups (3) and (6) while superoxide dismutase activity increased only in (6). Glutathione peroxidase activity decreased in groups (3) and (6). Nrf2 expression was higher in groups (3) and (6), and MTI expression augmented in (3). Histological examination of the heart tissue showed the development of hypertrophic and fusion of cardiomyocytes along with foci of myocardial fiber necrosis. The transmission electron microscopy analysis showed profound ultra-structural damages. No protection against tissue degeneration was observed in animals fed the soy-based diet. Our findings indicate that even though the intake of a soy-based diet is capable of ameliorating Cd induced oxidative stress, it failed in preventing cardiac damage. -- Highlights: ► Cd intoxication produces extracellular and ultrastructural damage in the myocardium. ► The intake of a soy-based diet ameliorated Cd-induced oxidative stress. ► Cd-induced myocardial damage wasn't prevented by the intake of a soy-based diet. ► Cd-induced myocardial degeneration may not be caused by oxidative stress generation. ► Histology evaluation is needed to

  6. Suppression of Bim by microRNA-19a may protect cardiomyocytes against hypoxia-induced cell death via autophagy activation.

    PubMed

    Gao, Yan-Hua; Qian, Ju-Ying; Chen, Zhang-Wei; Fu, Ming-Qiang; Xu, Jian-Feng; Xia, Yan; Ding, Xue-Feng; Yang, Xiang-Dong; Cao, Yuan-Yuan; Zou, Yun-Zeng; Ren, Jun; Sun, Ai-Jun; Ge, Jun-Bo

    2016-08-22

    Microvascular obstruction (MO), one of unfavorable complications of percutaneous coronary intervention (PCI), is responsible for the lost benefit of reperfusion therapy. Determination of microRNA-19a, a member of the miR-17-92 cluster, using quantitative real-time polymerase chain reaction (PCR) revealed notably down-regulated microRNA-19a, in myocardium with MO. Nonetheless, the role of miR-19a in MO and the underlying mechanism remains to be elucidated. To this end, an in vitro microembolization model in cardiomyocytes was used. Our data revealed that hypoxic exposure prompted cardiomyocyte apoptosis in a time-dependent manner accompanied by reduced miR-19a. miR-19a overexpression clearly ameliorated hypoxia-induced cell death (necrosis and apoptosis), at least in part, through switching on autophagy. Further dual-luciferase reporter assay and immunoblotting studies demonstrated that miR-19a-induced cytoprotection might be achieved in part through modulation of the specific target Bcl-2 interacting mediator of cell death, Bim, an apoptotic activator. Bim sufficiently interfered with miR-19a-induced LC3 conversion and increased cardiomyocyte apoptosis under hypoxia. Moreover, cardiomyocytes pretreated with 3-methyladenine conferred resistance to the cytoprotective effect of miR-19a and displayed notably increased TUNEL staining and caspase-3 activity. In conclusion, miR-19a protected cardiomyocytes against hypoxia-induced lethality at least in part via Bim suppression and subsequently autophagy activation.

  7. Electrophysiological alternans and restitution during acute regional ischaemia in myocardium of anaesthetized pig.

    PubMed Central

    Dilly, S G; Lab, M J

    1988-01-01

    1. Alternate long and short action potential durations, or electrical alternans, has only been sporadically observed in ischaemic myocardium in situ. We systematically studied alternans in the latter to characterize the phenomenon, relate it to ventricular arrhythmia and suggest possible mechanisms. 2. Sixteen Landrace pigs were anaesthetized (Azaperone, N2O and O2), ventilated and the hearts exposed. A branch of the left coronary artery was ligated. Left intraventricular and systemic pressures were monitored. Monophasic action potentials were recorded simultaneously with up to five suction electrodes in and around the proposed ischaemia area. 3. A computer measured the duration of every action potential, at several phases of repolarization, throughout the first hour of ischaemia. This allowed the systematic study of the alternans. Measurements during defined stimulus protocols were also made for the construction of electrical restitution curves. 4. Alternans was found in all recordings within the ischaemic area and in two-thirds of those in the 'border' area. There was no alternans in non-ischaemic areas. 5. The alternans, when action potential duration was plotted for every beat, appeared as an oscillation which was pleomorphic. It could be: (a) stable for hundreds of beats; (b) switched or triggered (by one extraneous beat having a different cycle length) between one stable state with high and one with low or absent alternans; (c) damped; (d) undamped to take a crescendo form, sometimes preceding ventricular fibrillation. 6. The alternans in general showed an ill-defined peak incidence between about 200 to 1500 beats after the onset of ischaemia, and a clearer late peak at about 3000 beats. These periods occurred at about 2-7 min and 15-40 min, corresponding to so-called phase 1A and 1B arrhythmia respectively. Only the late peak was seen with triggered alternans. 7. The electrical restitution curve for the action potential duration during ischaemia when

  8. Collagen XIV is important for growth and structural integrity of the myocardium

    PubMed Central

    Tao, Ge; Levay, Agata K.; Peacock, Jacqueline D.; Huk, Danielle J.; Both, Sarah N.; Purcell, Nicole H.; Pinto, Jose R.; Galantowicz, Maarten L.; Koch, Manuel; Lucchesi, Pamela A.; Birk, David E.; Lincoln, Joy

    2012-01-01

    Collagen XIV is a fibril-associated collagen with an interrupted triple helix (FACIT). Previous studies have shown that this collagen type regulates early stages of fibrillogenesis in connective tissues of high mechanical demand. Mice null for Collagen XIV are viable, however formation of the interstitial collagen network is defective in tendons and skin leading to reduced biomechanical function. The assembly of a tightly regulated collagen network is also required in the heart, not only for structural support but also for controlling cellular processes. Collagen XIV is highly expressed in the embryonic heart, notably within the cardiac interstitium of the developing myocardium, however its role has not been elucidated. To test this, we examined cardiac phenotypes in embryonic and adult mice devoid of Collagen XIV. From as early as E11.5, Col14a1−/− mice exhibit significant perturbations in mRNA levels of many other collagen types and remodeling enzymes (MMPs, TIMPs) within the ventricular myocardium. By post natal stages, collagen fibril organization is in disarray and the adult heart displays defects in ventricular morphogenesis. In addition to the extracellular matrix, Col14a1−/− mice exhibit increased cardiomyocyte proliferation at post natal, but not E11.5 stages, leading to increased cell number, yet cell size is decreased by 3 months of age. In contrast to myocytes, the number of cardiac fibroblasts is reduced after birth associated with increased apoptosis. As a result of these molecular and cellular changes during embryonic development and post natal maturation, cardiac function is diminished in Col14a1−/− mice from 3 months of age; associated with dilation in the absence of hypertrophy, and reduced ejection fraction. Further, Col14a1 deficiency leads to a greater increase in left ventricular wall thickening in response to pathological pressure overload compared to wild type animals. Collectively, these studies identify a new role for type XIV

  9. Collagen XIV is important for growth and structural integrity of the myocardium.

    PubMed

    Tao, Ge; Levay, Agata K; Peacock, Jacqueline D; Huk, Danielle J; Both, Sarah N; Purcell, Nicole H; Pinto, Jose R; Galantowicz, Maarten L; Koch, Manuel; Lucchesi, Pamela A; Birk, David E; Lincoln, Joy

    2012-11-01

    Collagen XIV is a fibril-associated collagen with an interrupted triple helix (FACIT). Previous studies have shown that this collagen type regulates early stages of fibrillogenesis in connective tissues of high mechanical demand. Mice null for Collagen XIV are viable, however formation of the interstitial collagen network is defective in tendons and skin leading to reduced biomechanical function. The assembly of a tightly regulated collagen network is also required in the heart, not only for structural support but also for controlling cellular processes. Collagen XIV is highly expressed in the embryonic heart, notably within the cardiac interstitium of the developing myocardium, however its role has not been elucidated. To test this, we examined cardiac phenotypes in embryonic and adult mice devoid of Collagen XIV. From as early as E11.5, Col14a1(-/-) mice exhibit significant perturbations in mRNA levels of many other collagen types and remodeling enzymes (MMPs, TIMPs) within the ventricular myocardium. By post natal stages, collagen fibril organization is in disarray and the adult heart displays defects in ventricular morphogenesis. In addition to the extracellular matrix, Col14a1(-/-) mice exhibit increased cardiomyocyte proliferation at post natal, but not E11.5 stages, leading to increased cell number, yet cell size is decreased by 3 months of age. In contrast to myocytes, the number of cardiac fibroblasts is reduced after birth associated with increased apoptosis. As a result of these molecular and cellular changes during embryonic development and post natal maturation, cardiac function is diminished in Col14a1(-/-) mice from 3 months of age; associated with dilation in the absence of hypertrophy, and reduced ejection fraction. Further, Col14a1 deficiency leads to a greater increase in left ventricular wall thickening in response to pathological pressure overload compared to wild type animals. Collectively, these studies identify a new role for type XIV

  10. Gradient of integrin alpha 6A distribution in the myocardium during early heart development.

    PubMed

    Collo, G; Domanico, S Z; Klier, G; Quaranta, V

    1995-05-01

    The interactions of cells with extracellular matrices (ECM)1 are likely to be key determinants of embryonic development. Integrin adhesion receptors are ideally positioned to mediate some of these interactions since, in addition to mechanical adhesion, they transduce signals affecting cell proliferation and differentiation. We investigated expression of the integrin alpha 6 beta 1, a receptor for the ECM component, laminin in the early mouse embryo. An intriguing feature of this integrin is the existence of alpha 6 subunit isoforms. The A and B isoforms, which differ in the cytoplasmic tails, are expressed in cell-type specific fashion, and are likely to implement distinct cellular interactions with laminin. By RT-PCR, alpha 6B but not alpha 6A mRNA was detectable in embryo extracts from fertilized oocytes to 6.5 d.p.c. In subsequent stages, up to 11.5 d.p.c., alpha 6A mRNA was observed in mRNA extracts from whole embryos, but still in significantly lower amounts than alpha 6B. However, in extracts from isolated heart (9.5 to 11.5 d.p.c.), alpha 6A was the predominant alpha 6 isoform, while in extracts from other embryo parts no alpha 6A mRNA was detectable. At the protein level, immunostaining with specific antibodies showed alpha 6A protein in myocardial cells, at the early stage of heart tube development (8.5 d.p.c.). Localization to the myocardium was tightly restricted, since other structures of the embryonic heart, e.g., endocardium, or of the remaining embryo did not stain with anti-alpha 6A antibody. In the ventricular myocardium, expression of alpha 6A appeared more intense than in the subendocardial layer. Quantitation by confocal microscopy unveiled a gradient of expression of alpha 6A, increasing from the outer to the inner layers of the myocardium. This is the first demonstration of a gradient distribution of integrin molecules in a tissue, which appears to be directly connected with the process of organogenesis. The mechanism underlying our

  11. Volume of myocardium perfused by coronary artery branches as estimated from 3D micro-CT images of rat hearts

    NASA Astrophysics Data System (ADS)

    Lund, Patricia E.; Naessens, Lauren C.; Seaman, Catherine A.; Reyes, Denise A.; Ritman, Erik L.

    2000-04-01

    Average myocardial perfusion is remarkably consistent throughout the heart wall under resting conditions and the velocity of blood flow is fairly reproducible from artery to artery. Based on these observations, and the fact that flow through an artery is the product of arterial cross-sectional area and blood flow velocity, we would expect the volume of myocardium perfused to be proportional to the cross-sectional area of the coronary artery perfusing that volume of myocardium. This relationship has been confirmed by others in pigs, dogs and humans. To test the body size-dependence of this relationship we used the hearts from rats, 3 through 25 weeks of age. The coronary arteries were infused with radiopaque microfil polymer and the hearts scanned in a micro- CT scanner. Using these 3D images we measured the volume of myocardium and the arterial cross-sectional area of the artery that perfused that volume of myocardium. The average constant of proportionality was found to be 0.15 +/- 0.08 cm3/mm2. Our data showed no statistically different estimates of the constant of proportionality in the rat hearts of different ages nor between the left and right coronary arteries. This constant is smaller than that observed in large animals and humans, but this difference is consistent with the body mass-dependence on metabolic rate.

  12. [THE EFFECT OF SEROTONIN ON THE INOTROPIC FUNCTION OF MYOCARDIUM OF THE LEFT VENTRICLE OF IMMATURE SPONTANEOUSLY HYPERTENSIVE RATS].

    PubMed

    Aflyatumova, G N; Nedorezova, R S; Nigmatullina, R R; Sadykova, D I; Mateeva, V L; Chibireva, M D

    2015-08-01

    The mechanisms of the serotonin effect on the inotropic function of the myocardium of the left ventricle of immature spontaneously hypertensive rats (SHR) are unexplored. It was found that systolic arterial blood pressure of 5-6 weeks SHR rats is 147.5 mm Hg, which is statistically significantly higher (more than 25 mm Hg) than in the same age of normotensive control Wistar- Kyoto rats. The weight of the heart, of the left ventricle myocardium, of the ventricular septum, of the aorta and the force of contraction of the left ventricle of 5-6-week-old SHR rats are increased significantly compared with the control. 0.1 pM serotonin increases and 1.0 pM and 10.0 AM serotonin reduce the force of contraction of the left ventricular myocardium in hypertensive rats, but there is a dose-dependent increase of the force of contraction in the control. Serotonin reduces the time of contraction of the myocardium of the left ventricular of SHR rats, these reactions are less pronounced as compared to the control.

  13. Acute Exercise-Induced Mitochondrial Stress Triggers an Inflammatory Response in the Myocardium via NLRP3 Inflammasome Activation with Mitophagy.

    PubMed

    Li, Haiying; Miao, Weiguo; Ma, Jingfen; Xv, Zhen; Bo, Hai; Li, Jianyu; Zhang, Yong; Ji, Li Li

    2016-01-01

    Increasing evidence has indicated that acute strenuous exercise can induce a range of adverse reactions including oxidative stress and tissue inflammation. However, little is currently known regarding the mechanisms that underlie the regulation of the inflammatory response in the myocardium during acute heavy exercise. This study evaluated the mitochondrial function, NLRP3 inflammasome activation, and mitochondrial autophagy-related proteins to investigate the regulation and mechanism of mitochondrial stress regarding the inflammatory response of the rat myocardium during acute heavy exercise. The results indicated that the mitochondrial function of the myocardium was adaptively regulated to meet the challenge of stress during acute exercise. The exercise-induced mitochondrial stress also enhanced ROS generation and triggered an inflammatory reaction via the NLRP3 inflammasome activation. Moreover, the mitochondrial autophagy-related proteins including Beclin1, LC3, and Bnip3 were all significantly upregulated during acute exercise, which suggests that mitophagy was stimulated in response to the oxidative stress and inflammatory response in the myocardium. Taken together, our data suggest that, during acute exercise, mitochondrial stress triggers the rat myocardial inflammatory response via NLRP3 inflammasome activation and activates mitophagy to minimize myocardial injury.

  14. A HPLC-fluorescence detection method for determination of phosphatidic acid phosphohydrolase activity: application in human myocardium.

    PubMed

    Burgdorf, Christof; Prey, Antje; Richardt, Gert; Kurz, Thomas

    2008-03-15

    Phosphatidic acid phosphohydrolase (PAP) catalyzes the dephosphorylation of phosphatidic acid (PA) to diacylglycerol, the second messenger responsible for activation of protein kinase C. Despite the crucial role of PAP lipid signaling, there are no data on PAP signaling function in the human heart. Here we present a nonradioactive assay for the investigation of PAP activity in human myocardium using a fluorescent derivative of PA, 2-(4,4-difluoro-5,7-dimethyl-4-bora-3a,4a-diaza-s-indacene-3-pentanoyl)-1-hexadecanoyl-sn-glycero-3-phosphate (BODIPY-PA), as substrate in an in vitro PAP-catalyzed reaction. Unreacted BODIPY-PA was resolved from the PAP products by a binary gradient HPLC system and BODIPY-diacylglycerol was detected by fluorimetry. The reaction proceeded at a linear rate for up to 60 min and increased linearly with increasing amounts of cardiac protein in a range of 0.25 to 8.0 microg. This assay proved to be sensitive for accurate quantitation of total PAP activity, PAP-1 activity, and PAP-2 activity in human atrial tissue and right ventricular endomyocardial biopsies. Total PAP activity was approximately fourfold higher in ventricular myocardium than in atrial tissue. There was negligible PAP-1 activity in atrial myocardium compared with ventricular myocardium, indicating regional differences in activities and distribution pattern of PAP-1 and PAP-2 in the human heart. PMID:18023403

  15. Collateral circulation as a marker of the presence of viable myocardium in patients with recent myocardial infarction

    SciTech Connect

    Fujita, M.; Ohno, A.; Wada, O.; Miwa, K.; Nozawa, T.; Yamanishi, K.; Sasayama, S. )

    1991-08-01

    The relationship between the presence of viable myocardium and the extent of coronary collateral circulation to the infarct area was evaluated in 20 patients with a recent anterior myocardial infarction who had complete obstruction of the left anterior descending coronary artery. The viability of myocardial tissue was assessed by exercise thallium-201 myocardial scintigraphy, and the collateral circulation was angiographically evaluated by means of a collateral index ranging from 0 to 3. Patients were divided into two groups according to the presence (group 1, n = 10) or absence (group 2, n = 10) of viable myocardium in the perfusion territory of the infarct-related artery. The collateral index in group 1 was 2.5 {plus minus} 0.5 (SD), which was significantly higher than the 0.7 {plus minus} 0.8 in group 2. These findings indicate that the presence of ischemic but viable myocardium is intimately related to the development of collateral circulation in patients with myocardial infarction, and the existence of well-developed collateral channels predicts the presence of viable myocardium in the infarct area.

  16. Effects of antiarrhythmic drugs on ventricular fibrillation thresholds of normal and ischaemic myocardium in the anaesthetized rat.

    PubMed Central

    Marshall, R. J.; Muir, A. W.; Winslow, E.

    1983-01-01

    1 The effects of agents which produce membrane stabilization (class I), beta 1-adrenoceptor blockade (class II), prolongation of the cardiac action potential (class III) or inhibition of the slow inward current (class IV) were investigated for their ability to increase the ventricular fibrillation threshold (VFT) or to modify the fall in VFT consequent upon coronary artery ligation in the anaesthetized rat. 2 The class I agent, Org6001, increased VFT of normal myocardium and in lower doses reduced the postligation fall in VFT. 3 The class II agent, metoprolol, failed to increase VFT of normal myocardium but reduced the postligation fall. 4 The class III agent, melperone, increased VFT of both normal and ischaemic myocardium whereas the class IV agent, nifedipine failed to influence VFT in either region. 5 Bepridil (class I and IV) was similar to Org6001 and sotalol (class II and III) in that it increased VFT of normal myocardium and in lower doses reduced the postligation fall in VFT. 6 Measurement of VFT before and after coronary artery ligation in the rat constitutes a rapid and reproducible screen to detect antifibrillatory activity. 7 The results also suggest that in the rat, the low currents used (approximately 400 microA) do not release substantial quantities of catecholamines whereas these may be released by coronary artery ligation. PMID:6824812

  17. A HPLC-fluorescence detection method for determination of phosphatidic acid phosphohydrolase activity: application in human myocardium.

    PubMed

    Burgdorf, Christof; Prey, Antje; Richardt, Gert; Kurz, Thomas

    2008-03-15

    Phosphatidic acid phosphohydrolase (PAP) catalyzes the dephosphorylation of phosphatidic acid (PA) to diacylglycerol, the second messenger responsible for activation of protein kinase C. Despite the crucial role of PAP lipid signaling, there are no data on PAP signaling function in the human heart. Here we present a nonradioactive assay for the investigation of PAP activity in human myocardium using a fluorescent derivative of PA, 2-(4,4-difluoro-5,7-dimethyl-4-bora-3a,4a-diaza-s-indacene-3-pentanoyl)-1-hexadecanoyl-sn-glycero-3-phosphate (BODIPY-PA), as substrate in an in vitro PAP-catalyzed reaction. Unreacted BODIPY-PA was resolved from the PAP products by a binary gradient HPLC system and BODIPY-diacylglycerol was detected by fluorimetry. The reaction proceeded at a linear rate for up to 60 min and increased linearly with increasing amounts of cardiac protein in a range of 0.25 to 8.0 microg. This assay proved to be sensitive for accurate quantitation of total PAP activity, PAP-1 activity, and PAP-2 activity in human atrial tissue and right ventricular endomyocardial biopsies. Total PAP activity was approximately fourfold higher in ventricular myocardium than in atrial tissue. There was negligible PAP-1 activity in atrial myocardium compared with ventricular myocardium, indicating regional differences in activities and distribution pattern of PAP-1 and PAP-2 in the human heart.

  18. Neuroprotective effect of pretreatment with ganoderma lucidum in cerebral ischemia/reperfusion injury in rat hippocampus.

    PubMed

    Zhang, Wangxin; Zhang, Quiling; Deng, Wen; Li, Yalu; Xing, Guoqing; Shi, Xinjun; Du, Yifeng

    2014-08-01

    Ganoderma lucidum is a traditional Chinese medicine, which has been shown to have both anti-oxidative and anti-inflammatory effects, and noticeably decreases both the infarct area and neuronal apoptosis of the ischemic cortex. This study aimed to investigate the protective effects and mechanisms of pretreatment with ganoderma lucidum (by intragastric administration) in cerebral ischemia/reperfusion injury in rats. Our results showed that pretreatment with ganoderma lucidum for 3 and 7 days reduced neuronal loss in the hippocampus, diminished the content of malondialdehyde in the hippocampus and serum, decreased the levels of tumor necrosis factor-α and interleukin-8 in the hippocampus, and increased the activity of superoxide dismutase in the hippocampus and serum. These results suggest that pretreatment with ganoderma lucidum was protective against cerebral ischemia/reperfusion injury through its anti-oxidative and anti-inflammatory actions.

  19. Neuroprotective effect of pretreatment with ganoderma lucidum in cerebral ischemia/reperfusion injury in rat hippocampus

    PubMed Central

    Zhang, Wangxin; Zhang, Quiling; Deng, Wen; Li, Yalu; Xing, Guoqing; Shi, Xinjun; Du, Yifeng

    2014-01-01

    Ganoderma lucidum is a traditional Chinese medicine, which has been shown to have both anti-oxidative and anti-inflammatory effects, and noticeably decreases both the infarct area and neuronal apoptosis of the ischemic cortex. This study aimed to investigate the protective effects and mechanisms of pretreatment with ganoderma lucidum (by intragastric administration) in cerebral ischemia/reperfusion injury in rats. Our results showed that pretreatment with ganoderma lucidum for 3 and 7 days reduced neuronal loss in the hippocampus, diminished the content of malondialdehyde in the hippocampus and serum, decreased the levels of tumor necrosis factor-α and interleukin-8 in the hippocampus, and increased the activity of superoxide dismutase in the hippocampus and serum. These results suggest that pretreatment with ganoderma lucidum was protective against cerebral ischemia/reperfusion injury through its anti-oxidative and anti-inflammatory actions. PMID:25317156

  20. Microwave Pretreatment For Hydrolysis Of Cellulose

    NASA Technical Reports Server (NTRS)

    Cullingford, Hatice S.; George, Clifford E.; Lightsey, George R.

    1993-01-01

    Microwave pretreatment enhances enzymatic hydrolysis of cellulosic wastes into soluble saccharides used as feedstocks for foods, fuels, and other products. Low consumption of energy, high yield, and low risk of proposed hydrolysis process incorporating microwave pretreatment makes process viable alternative to composting.

  1. Wash water waste pretreatment system

    NASA Technical Reports Server (NTRS)

    1977-01-01

    Investigations were completed on wash waters based on each candidate personal cleansing agent. Evaluations of coagulants, antifoam agents, and the effect of promising antifoams on the chemical precipitation were included. Based on these evaluations two candidate soaps as well as their companion antifoam agents were selected for further work. Operating parameters included the effect of soap concentration, ferric chloride concentration, duration of mixing, and pore size of depth filters on the degree of soap removal. The effect of pressure on water flow through filter cartridges and on the rate of decline of water flow was also investigated. The culmination of the program was the recommendation of a pretreatment concept based on chemical precipitation followed by pressure filtration.

  2. Exploratory analysis of the spatio-temporal deformation of the myocardium during systole from tagged MRI.

    PubMed

    Clarysse, Patrick; Han, Meimei; Croisille, Pierre; Magnin, Isabelle E

    2002-11-01

    Myocardial contractile function is, with perfusion, one of the main affected factors in ischemic heart diseases. In this paper, we propose an original framework based on functional data analysis for the quantitative study of spatio-temporal parameters related to the myocardial contraction mechanics. The mechanical strains in the left-ventricular (LV) myocardium are computed from tagged magnetic resonance imaging cardiac sequences. A statistical functional model of the normal contractile function of the LV is build from the study of eight examinations on healthy subjects. We show that it is possible to detect abnormal strain patterns comparatively to this model, by generating distance maps at rest and under pharmacological stress. We demonstrate the consistency of the results for the circumferential deformation parameter on healthy and pathological data sets. PMID:12450363

  3. Successful Nd:Yag Laser Photocoagulation Of Arrhythmogenic Myocardium: Potential Limitations Of Current Optical Delivery Systems.

    NASA Astrophysics Data System (ADS)

    Svenson, Robert H.; Marroum, Marie-Claire; Frank, Frank; Selle, Jay G.; Gallagher, John J.; Bou-Saba, George; Seifert, Kathleen T.; Linder, Kathy; Tatsis, George P.

    1987-04-01

    Canine myocardial lesions of predictable dimensions can be achieved with Nd:YAG laser photocoagulation. These lesions are well demarcated from surrounding normal tissue and heal with homogeneous scar formation. Intraoperative Nd:YAG laser photocoagulation successfully ablated 52 of 55 ventricular tachycardias in 17 patients. Histologic examination of tissues from these arrhythmogenic areas showed differences from lesions produced on canine epicardium. Lesions from the human cases were less predictable and not well circumscribed. These differences are felt to be due to optical inhomogeneities present in diseased, scarred human myocardium, geometric irregularities of the endocardial surface, anatomical constraints on tissue-fiber distance, and the angle of incidence of the beam with the tissue. Modifications of current delivery systems may overcome some of these limitations. Ablation of ventricular tachycardia arising deeper than 4.0 to 6.0 mm. from the irradiated surface may require interstitial probes coupled to the fiberoptic.

  4. Difference in molecular pathology of natriuretic peptides in the myocardium between acute asphyxial and cardiac deaths.

    PubMed

    Chen, Jian-Hua; Michiue, Tomomi; Ishikawa, Takaki; Maeda, Hitoshi

    2012-07-01

    In investigating death due to mechanical asphyxiation and drowning, a cardiac attack is important for discriminating between possible causes of death and as a contributory factor in death processes; however, general pathologies involving visceral congestion are often similar. The present study compared terminal cardiac dysfunction in these fatalities using the molecular pathology of atrial and brain natriuretic peptides (ANP and BNP) in the myocardium as markers of cardiac strain. Both mechanical asphyxiation (n=27) and drowning (n=23) showed significantly lower ANP and BNP mRNA expressions in bilateral ventricular walls than sudden cardiac deaths (n=36). In addition, right atrial wall BNP mRNA expression was lower in asphyxiation; however, immunostaining did not demonstrate any difference among these fatalities. Differences among the subtypes of asphyxiation or between fresh- and saltwater drowning were insignificant. These observations suggest a difference between primary heart failure in sudden cardiac death and terminal cardiac dysfunction secondary to fatal asphyxiation or drowning.

  5. In situ electrostimulation drives a regenerative shift in the zone of infarcted myocardium.

    PubMed

    Spadaccio, Cristiano; Rainer, Alberto; De Marco, Federico; Lusini, Mario; Gallo, Paolo; Sedati, Pietro; Muda, Andrea Onetti; De Porcellinis, Stefano; Gregorj, Chiara; Avvisati, Giuseppe; Trombetta, Marcella; Chello, Massimo; Covino, Elvio; Bull, David A; Patel, Amit N; Genovese, Jorge A

    2013-01-01

    Electrostimulation represents a well-known trophic factor for different tissues. In vitro electrostimulation of non-stem and stem cells induces myogenic predifferentiation and may be a powerful tool to generate cells with the capacity to respond to local areas of injury. We evaluated the effects of in vivo electrostimulation on infarcted myocardium using a miniaturized multiparameter implantable stimulator in rats. Parameters of electrostimulation were organized to avoid a direct driving or pacing of native heart rhythm. Electrical stimuli were delivered for 14 days across the scar site. In situ electrostimulation used as a cell-free, cytokine-free stimulation system, improved myocardial function, and increased angiogenesis through endothelial progenitor cell migration and production of vascular endothelial growth factor (VEGF). In situ electrostimulation represents a novel means to stimulate repair of the heart and other organs, as well as to precondition tissues for treatment with cell-based therapies.

  6. Noncompaction of the Ventricular Myocardium and Polycystic Kidney Disease: A Case Report.

    PubMed

    Fukino, Keiko; Ishiwata, Junpei; Shinohara, Hiroki; Oshima, Tsukasa; Kozaki, Tsunashi; Ikutomi, Masayasu; Amaki, Toshihiro; Nakamura, Fumitaka

    2016-06-01

    Autosomal dominant polycystic kidney disease (ADPKD) is one of the most common hereditary disorders, characterized by the formation of multiple cysts in the kidneys and other organs, as well as noncystic manifestations such as cerebral aneurysm. The most common cardiovascular disorders associated with ADPKD include valvular abnormalities and aortic aneurysm. An association between ADPKD and impaired left ventricular function has occasionally been reported. We describe a 74-year-old woman with ADPKD and exertional dyspnea. Impaired left ventricular function resulting from noncompaction of the ventricular myocardium (NVM) and secondary left ventricular aneurysm were diagnosed. Cardiac sarcoidosis and ischemic heart disease were ruled out. Myocardial ischemia resulting from NVM was the presumptive cause of the ventricular aneurysm. To our knowledge, this is the first report of concurrent isolated NVM and left ventricular aneurysm in a patient with ADPKD. ADPKD and various cardiomyopathies, including NVM, are all reported to involve mutations of sarcomere genes, suggesting a possible link between the conditions. PMID:26873255

  7. Passive targeting of ischemic-reperfused myocardium with adenosine-loaded silica nanoparticles

    PubMed Central

    Galagudza, Michael; Korolev, Dmitry; Postnov, Viktor; Naumisheva, Elena; Grigorova, Yulia; Uskov, Ivan; Shlyakhto, Eugene

    2012-01-01

    Pharmacological agents suggested for infarct size limitation have serious side effects when used at cardioprotective doses which hinders their translation into clinical practice. The solution to the problem might be direct delivery of cardioprotective drugs into ischemic-reperfused myocardium. In this study, we explored the potential of silica nanoparticles for passive delivery of adenosine, a prototype cardioprotective agent, into ischemic-reperfused heart tissue. In addition, the biodegradation of silica nanoparticles was studied both in vitro and in vivo. Immobilization of adenosine on the surface of silica nanoparticles resulted in enhancement of adenosine-mediated infarct size limitation in the rat model. Furthermore, the hypotensive effect of adenosine was attenuated after its adsorption on silica nanoparticles. We conclude that silica nanoparticles are biocompatible materials that might potentially be used as carriers for heart-targeted drug delivery. PMID:22619519

  8. [Morphofunctional aspects of the experimental effect of hyperbaric oxygenation on the myocardium of the healthy organism].

    PubMed

    Rossinskaia, V V; Shliapnikov, V N; Uglova, M V

    1978-01-01

    Changes in the myocardium arter numerous treatments with hyperbaric oxygenation (HBO) (PO2 3 technical atmospheres, time of saturation--45 min) were studied by morphological, histochemical and enzymohistochemical methods in 50 rabbits. Three stages were found to occur in the development of these changes: 1) functional-morphological changes (1--3 seanses of HBO), 2) early morphological changes (4--5 seanses), 3) marked morphological lesions (6--8 seanses). The first three treatments produce reversible changes on the part of metabolic processes (a reduction in the content of glycogen and changes in the activity of oxidoreductases: succinate-, malate- and lactate dehydrogenase). Morphological signs of oxygen toxicity in the form of disorders in hemodynamics and microcirculation, and dystrophy of cardiomyocytes appear after 4 seanses of HBO and increase with further treatment. The experimental data permit to recommend short HBO courses (1--3 seanses) for therapeutic application.

  9. A cellular automaton model for the ventricular myocardium considering the layer structure

    NASA Astrophysics Data System (ADS)

    Deng, Min-Yi; Dai, Jing-Yu; Zhang, Xue-Liang

    2015-09-01

    A cellular automaton model for the ventricular myocardium considering the layer structure has been established. The three types of cells in this model differ principally in the repolarization characteristics. For the normal travelling waves in this model, the computer simulation results show the R, S, and T waves and they are qualitatively in agreement with the standard electrocardiograph. Phenomena such as the potential decline of point J and segment ST and the rise of the potential line after the T wave appear when the ischemia occurs in the endocardium. The spiral wave has also been simulated, and the corresponding potential has a lower amplitude, higher frequency, and wider R wave, which accords with the distinguishing feature of the clinical electrocardiograph. Mechanisms underlying the above phenomena are analyzed briefly. Project supported by the National Natural Science Foundation of China (Grant Nos. 11365003 and 11165004).

  10. Anisotropic Elastography for Local Passive Properties and Active Contractility of Myocardium from Dynamic Heart Imaging Sequence

    PubMed Central

    Wang, Ge; Sun, L. Z.

    2006-01-01

    Major heart diseases such as ischemia and hypertrophic myocardiopathy are accompanied with significant changes in the passive mechanical properties and active contractility of myocardium. Identification of these changes helps diagnose heart diseases, monitor therapy, and design surgery. A dynamic cardiac elastography (DCE) framework is developed to assess the anisotropic viscoelastic passive properties and active contractility of myocardial tissues, based on the chamber pressure and dynamic displacement measured with cardiac imaging techniques. A dynamic adjoint method is derived to enhance the numerical efficiency and stability of DCE. Model-based simulations are conducted using a numerical left ventricle (LV) phantom with an ischemic region. The passive material parameters of normal and ischemic tissues are identified during LV rapid/reduced filling and artery contraction, and those of active contractility are quantified during isovolumetric contraction and rapid/reduced ejection. It is found that quasistatic simplification in the previous cardiac elastography studies may yield inaccurate material parameters. PMID:23165032

  11. The effects of digitalis on intracellular calcium transients in mammalian working myocardium as detected with aequorin.

    PubMed

    Morgan, J P

    1985-11-01

    The effects of positive inotropic agents on the amplitude and time course of the light signal and corresponding tension response were studied in cat and human working myocardium microinjected with the bioluminescent Ca2+ indicator aequorin. Distinctive patterns of light and tension responses were identified that are consistent with known actions of the various agents on the release of Ca2+ from intracellular stores, rate of uptake of Ca2+ by the sarcoplasmic reticulum and sensitivity of the myofilaments to Ca2+. In common with most other inotropic drugs, the cardiotonic steroid, acetylstrophanthidin, in doses of 4 X 10(-7) to 2 X 10(-6)M increases the amount of Ca2+ available for excitation-contraction coupling in the heart. However, in contrast to most other agents, acetylstrophanthidin does not affect the time course of the calcium transient. In common with changes in [Ca2+]o, acetylstrophanthidin does not alter the relationship between the amplitude of the aequorin light signal and developed tension, which, in contrast to caffeine and isoproterenol, indicates that the increase in tension is fully accounted for by the increase in systolic free calcium. These findings suggest that the cardiotonic steroids increase loading of intracellular calcium stores without affecting the kinetics of subcellular handling of Ca2+. In doses of 8 X 10(-7) to 2 X 10(-6)M, acetylstrophanthidin produces a calcium-overload state characterized by 'after-contractions' and 'after-glimmers' that are associated with the development of automatic and triggerable dysrhythmias. These studies provide direct evidence that the inotropic and toxic effects of digitalis on animal and human working myocardium are produced by changes in intracellular Ca2+.

  12. Identification of Angiogenesis Rich-Viable Myocardium using RGD Dimer based SPECT after Myocardial Infarction

    PubMed Central

    Lee, Min Su; Park, Hyun Soo; Lee, Byung Chul; Jung, Jae Ho; Yoo, Jung Sun; Kim, Sang Eun

    2016-01-01

    Cardiac healing after myocardial ischemia is a complex biological process. Advances in understanding of wound healing response have paved the way for clinical testing of novel molecular imaging to improve clinical outcomes. A key factor for assessing myocardial viability after ischemic injury is the evaluation of angiogenesis accompanying increased expression of integrin αvβ3. Here, we describe the capability of an αvβ3 integrin-targeting SPECT agent, 99mTc-IDA-D-[c(RGDfK)]2, for identification of ischemic but viable myocardium, i.e., hibernating myocardium which is crucial to predict functional recovery after revascularization, the standard care of cardiovascular medicine. In vivo SPECT imaging of rat models with transient coronary occlusion showed significantly high uptake of 99mTc-IDA-D-[c(RGDfK)]2 in the ischemic region. Comparative measurements with 201Tl SPECT and 18F-FDG PET, then, proved that such prominent uptake of 99mTc-IDA-D-[c(RGDfK)]2 exactly matched the hallmark of hibernation, i.e., the perfusion-metabolism mismatch pattern. The uptake of 99mTc-IDA-D-[c(RGDfK)]2 was non-inferior to that of 18F-FDG, confirmed by time-course variation analysis. Immunohistochemical characterization revealed that an intense signal of 99mTc-IDA-D-[c(RGDfK)]2 corresponded to the vibrant angiogenic events with elevated expression of αvβ3 integrin. Together, these results establish that 99mTc-IDA-D-[c(RGDfK)]2 SPECT can serve as a sensitive clinical measure for myocardial salvage to identify the patients who might benefit most from revascularization. PMID:27283041

  13. Mesenchymal stem cells conditioned with glucose depletion augments their ability to repair-infarcted myocardium

    PubMed Central

    Choudhery, Mahmood S; Khan, Mohsin; Mahmood, Ruhma; Mohsin, Sadia; Akhtar, Shoaib; Ali, Fatima; Khan, Shaheen N; Riazuddin, Sheikh

    2012-01-01

    Mesenchymal stem cells (MSCs) are an attractive candidate for autologous cell therapy, but their ability to repair damaged myocardium is severely compromised with advanced age. Development of viable autologous cell therapy for treatment of heart failure in the elderly requires the need to address MSC ageing. In this study, MSCs from young (2 months) and aged (24 months) C57BL/6 mice were characterized for gene expression of IGF-1, FGF-2, VEGF, SIRT-1, AKT, p16INK4a, p21 and p53 along with measurements of population doubling (PD), superoxide dismutase (SOD) activity and apoptosis. Aged MSCs displayed senescent features compared with cells isolated from young animals and therefore were pre-conditioned with glucose depletion to enhance age affected function. Pre-conditioning of aged MSCs led to an increase in expression of IGF-1, AKT and SIRT-1 concomitant with enhanced viability, proliferation and delayed senescence. To determine the myocardial repair capability of pre-conditioned aged MSCs, myocardial infarction (MI) was induced in 24 months old C57BL/6 wild type mice and GFP expressing untreated and pre-conditioned aged MSCs were transplanted. Hearts transplanted with pre-conditioned aged MSCs showed increased expression of paracrine factors, such as IGF-1, FGF-2, VEGF and SDF-1α. This was associated with significantly improved cardiac performance as measured by dp/dtmax, dp/dtmin, LVEDP and LVDP, declined left ventricle (LV) fibrosis and apoptosis as measured by Masson's Trichrome and TUNEL assays, respectively, after 30 days of transplantation. In conclusion, pre-conditioning of aged MSCs with glucose depletion can enhance proliferation, delay senescence and restore the ability of aged cells to repair senescent infarcted myocardium. PMID:22435530

  14. Furosemide modifies heart hypertrophy and glycosaminoglycan myocardium content in a rat model of neurogenic hypertension.

    PubMed

    Pourzitaki, Chryssa; Tsaousi, Georgia; Manthou, Maria Eleni; Karakiulakis, Georgios; Kouvelas, Dimitrios; Papakonstantinou, Eleni

    2016-08-01

    Hypertension is a major risk factor for atherogenesis and heart hypertrophy, both of which are associated with specific morphological and functional changes of the myocardium. Glycosaminoglycans (GAGs) are complex molecules involved both in tissue morphology and function. In the present study, we investigated the effects of neurogenic hypertension and subsequent antihypertensive treatment with furosemide, on heart hypertrophy and the content of GAGs in the myocardium. Neurogenic hypertension was achieved in male Wistar rats by bilateral aortic denervation (bAD). At days 2, 7 and 15 after surgery, animals were sacrificed and the hearts were dissected away, weighted, and homogenized. Total GAGs were assessed by measuring the uronic acid content colorimetrically and individual GAGs were isolated and characterized by enzymatic treatment, with GAG-degrading enzymes, using electrophoresis on polyacrylamide gradient gels and cellulose acetate membranes. In bAD-animals blood pressure, blood pressure lability, heart rate and heart weight were significantly increased 15 days postoperatively. These effects were prevented by treatment with furosemide. Major GAGs identified in the heart were chondroitin sulphates, heparin (H), heparan sulphate (HS) and hyaluronic acid. The content of uronic and the relative content of H and HS in the heart in bAD animals significantly decreased from day 2 to day 15 postoperatively. Furosemide prevented the bAD induced decrease in GAG content. Considering that H and HS are potent inhibitors of cardiomyocyte hypertrophy, our results indicate that heart hypertrophy induced by neurogenic hypertension may be associated with decreases in the relative content of heparin and heparan sulphate in the heart. PMID:27221775

  15. Enhanced Electrical Integration of Engineered Human Myocardium via Intramyocardial versus Epicardial Delivery in Infarcted Rat Hearts

    PubMed Central

    Gerbin, Kaytlyn A.; Yang, Xiulan; Murry, Charles E.; Coulombe, Kareen L. K.

    2015-01-01

    Cardiac tissue engineering is a promising approach to provide large-scale tissues for transplantation to regenerate the heart after ischemic injury, however, integration with the host myocardium will be required to achieve electromechanical benefits. To test the ability of engineered heart tissues to electrically integrate with the host, 10 million human embryonic stem cell (hESC)-derived cardiomyocytes were used to form either scaffold-free tissue patches implanted on the epicardium or micro-tissue particles (~1000 cells/particle) delivered by intramyocardial injection into the left ventricular wall of the ischemia/reperfusion injured athymic rat heart. Results were compared to intramyocardial injection of 10 million dispersed hESC-cardiomyocytes. Graft size was not significantly different between treatment groups and correlated inversely with infarct size. After implantation on the epicardial surface, hESC-cardiac tissue patches were electromechanically active, but they beat slowly and were not electrically coupled to the host at 4 weeks based on ex vivo fluorescent imaging of their graft-autonomous GCaMP3 calcium reporter. Histologically, scar tissue physically separated the patch graft and host myocardium. In contrast, following intramyocardial injection of micro-tissue particles and suspended cardiomyocytes, 100% of the grafts detected by fluorescent GCaMP3 imaging were electrically coupled to the host heart at spontaneous rate and could follow host pacing up to a maximum of 300–390 beats per minute (5–6.5 Hz). Gap junctions between intramyocardial graft and host tissue were identified histologically. The extensive coupling and rapid response rate of the human myocardial grafts after intramyocardial delivery suggest electrophysiological adaptation of hESC-derived cardiomyocytes to the rat heart’s pacemaking activity. These data support the use of the rat model for studying electromechanical integration of human cardiomyocytes, and they identify lack of

  16. HIRA Gene is Lower Expressed in the Myocardium of Patients with Tetralogy of Fallot

    PubMed Central

    Ju, Zhao-Ru; Wang, Hui-Jun; Ma, Xiao-Jing; Ma, Duan; Huang, Guo-Ying

    2016-01-01

    Background: The most typical cardiac abnormality is conotruncal defects (CTDs) in patients with 22q11 deletion syndrome (22q11DS). HIRA (histone cell cycle regulator) gene, as one of the candidate genes located at the critical region of 22q11DS, was reported as possibly relevant to CTD in animal models. This study aimed to analyze the level of expression of the HIRA gene in tetralogy of Fallot (TOF) patients and the potential DNA sequence variations in the promoter region. Methods: The messenger RNA (mRNA) expression was examined with quantitative real-time polymerase chain reaction in 39 myocardial tissues of the right ventricular outflow tract (RVOT) from TOF patients and 4 myocardial tissues of RVOT from noncardiac death children. The protein expression was detected using immunohistochemistry in 12 TOF patients and 4 controls. A total of 100 TOF cases and 200 healthy controls were recruited for DNA sequencing. Results: The mRNA and protein expressions of the HIRA gene in the myocardium of the TOF patients were both significantly lower as compared to the controls (P < 0.05). Five single nucleotide polymorphisms (SNPs), including g.4111A>G (rs1128399), g.4265C>A (rs4585115), g.4369T>G (rs2277837), g.4371C>A (rs148516780), and g.4543T>C (rs111802956), were found in the promoter region of the HIRA gene. There were no significant differences of frequencies in these SNPs between the TOF patients and the controls (P > 0.05). Conclusion: The abnormal lower expression of the HIRA gene in the myocardium may participate in the pathogenesis of TOF. PMID:27748330

  17. Characterization of the structural and functional changes in the myocardium following focal ischemia-reperfusion injury.

    PubMed

    Ojha, Navdeep; Roy, Sashwati; Radtke, Jared; Simonetti, Orlando; Gnyawali, Surya; Zweier, Jay L; Kuppusamy, Periannan; Sen, Chandan K

    2008-06-01

    High-resolution (11.7 T) cardiac magnetic resonance imaging (MRI) and histological approaches have been employed in tandem to characterize the secondary damage suffered by the murine myocardium following the initial insult caused by ischemia-reperfusion (I/R). I/R-induced changes in the myocardium were examined in five separate groups at the following time points after I/R: 1 h, day 1, day 3, day 7, and day 14. The infarct volume increased from 1 h to day 1 post-I/R. Over time, the loss of myocardial function was observed to be associated with increased infarct volume and worsened regional wall motion. In the infarct region, I/R caused a decrease in end-systolic thickness coupled with small changes in end-diastolic thickness, leading to massive wall thickening abnormalities. In addition, compromised wall thickening was also observed in left ventricular regions adjacent to the infarct region. A tight correlation (r2 = 0.85) between measured MRI and triphenyltetrazolium chloride (TTC) infarct volumes was noted. Our observation that until day 3 post-I/R the infarct size as measured by TTC staining and MRI was much larger than that of the myocyte-silent regions in trichrome- or hematoxylin-eosin-stained sections is consistent with the literature and leads to the conclusion that at such an early phase, the infarct site contains structurally intact myocytes that are functionally compromised. Over time, such affected myocytes were noted to structurally disappear, resulting in consistent infarct sizes obtained from MRI and TTC as well as trichrome and hematoxylin-eosin analyses on day 7 following I/R. Myocardial remodeling following I/R includes secondary myocyte death followed by the loss of cardiac function over time.

  18. Quantitative shear wave imaging optical coherence tomography for noncontact mechanical characterization of myocardium

    NASA Astrophysics Data System (ADS)

    Wang, Shang; Lopez, Andrew L.; Morikawa, Yuka; Tao, Ge; Li, Jiasong; Larina, Irina V.; Martin, James F.; Larin, Kirill V.

    2015-03-01

    Optical coherence elastography (OCE) is an emerging low-coherence imaging technique that provides noninvasive assessment of tissue biomechanics with high spatial resolution. Among various OCE methods, the capability of quantitative measurement of tissue elasticity is of great importance for tissue characterization and pathology detection across different samples. Here we report a quantitative OCE technique, termed quantitative shear wave imaging optical coherence tomography (Q-SWI-OCT), which enables noncontact measurement of tissue Young's modulus based on the ultra-fast imaging of the shear wave propagation inside the sample. A focused air-puff device is used to interrogate the tissue with a low-pressure short-duration air stream that stimulates a localized displacement with the scale at micron level. The propagation of this tissue deformation in the form of shear wave is captured by a phase-sensitive OCT system running with the scan of the M-mode imaging over the path of the wave propagation. The temporal characteristics of the shear wave is quantified based on the cross-correlation of the tissue deformation profiles at all the measurement locations, and linear regression is utilized to fit the data plotted in the domain of time delay versus wave propagation distance. The wave group velocity is thus calculated, which results in the quantitative measurement of the Young's modulus. As the feasibility demonstration, experiments are performed on tissuemimicking phantoms with different agar concentrations and the quantified elasticity values with Q-SWI-OCT agree well with the uniaxial compression tests. For functional characterization of myocardium with this OCE technique, we perform our pilot experiments on ex vivo mouse cardiac muscle tissues with two studies, including 1) elasticity difference of cardiac muscle under relaxation and contract conditions and 2) mechanical heterogeneity of the heart introduced by the muscle fiber orientation. Our results suggest the

  19. Functional recovery of hibernating myocardium after coronary bypass surgery: Does it coincide with improvement in perfusion

    SciTech Connect

    Takeishi, Y.; Tono-oka, I.; Kubota, I.; Ikeda, K.; Masakane, I.; Chiba, J.; Abe, S.; Tsuiki, K.; Komatani, A.; Yamaguchi, I. )

    1991-09-01

    To determine the relationship between functional recovery and improvement in perfusion after coronary artery bypass graft surgery (CABG), 49 patients were studied. Radionuclide angiography was performed before, 1 month after, and 6 to 12 months after CABG to evaluate regional wall motion. Exercise thallium-201 myocardial perfusion imaging was done before and 1 month after CABG to assess regional perfusion. Preoperative asynergy was observed in 108 segments, and 74 of them showed an improvement in wall motion 1 month after CABG (segment A). Sixty-six of these segments (89%) were associated with an improvement in perfusion. Eight segments that had not improved 1 month after CABG demonstrated a delayed recovery of wall motion 6 to 12 months after CABG (segment B). However, seven of eight segments (88%) already showed an improvement in perfusion 1 month after CABG. A total of 82 segments exhibited functional recovery after CABG and were considered hibernating segments. In the preoperative study segment B more frequently had areas of akinesis or dyskinesis than segment A (75% vs 34%, p less than 0.05). The mean percent thallium-201 uptake in segment B was lower than that in segment A (74% {plus minus} 9% vs 83% {plus minus} 8%, p less than 0.05). Functional recovery of hibernating myocardium usually coincided with an improvement in perfusion. However, delayed functional recovery after reperfusion was observed in some instances. Severe asynergy and severe thallium-201 defects were more frequently observed in these segments with delayed recovery. Hibernating myocardium might remain stunned during those recovery periods.

  20. Identification of Angiogenesis Rich-Viable Myocardium using RGD Dimer based SPECT after Myocardial Infarction.

    PubMed

    Lee, Min Su; Park, Hyun Soo; Lee, Byung Chul; Jung, Jae Ho; Yoo, Jung Sun; Kim, Sang Eun

    2016-06-10

    Cardiac healing after myocardial ischemia is a complex biological process. Advances in understanding of wound healing response have paved the way for clinical testing of novel molecular imaging to improve clinical outcomes. A key factor for assessing myocardial viability after ischemic injury is the evaluation of angiogenesis accompanying increased expression of integrin αvβ3. Here, we describe the capability of an αvβ3 integrin-targeting SPECT agent, (99m)Tc-IDA-D-[c(RGDfK)]2, for identification of ischemic but viable myocardium, i.e., hibernating myocardium which is crucial to predict functional recovery after revascularization, the standard care of cardiovascular medicine. In vivo SPECT imaging of rat models with transient coronary occlusion showed significantly high uptake of (99m)Tc-IDA-D-[c(RGDfK)]2 in the ischemic region. Comparative measurements with (201)Tl SPECT and (18)F-FDG PET, then, proved that such prominent uptake of (99m)Tc-IDA-D-[c(RGDfK)]2 exactly matched the hallmark of hibernation, i.e., the perfusion-metabolism mismatch pattern. The uptake of (99m)Tc-IDA-D-[c(RGDfK)]2 was non-inferior to that of (18)F-FDG, confirmed by time-course variation analysis. Immunohistochemical characterization revealed that an intense signal of (99m)Tc-IDA-D-[c(RGDfK)]2 corresponded to the vibrant angiogenic events with elevated expression of αvβ3 integrin. Together, these results establish that (99m)Tc-IDA-D-[c(RGDfK)]2 SPECT can serve as a sensitive clinical measure for myocardial salvage to identify the patients who might benefit most from revascularization.