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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. 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.

  3. Electro-acupuncture at Neiguan pretreatment alters genome-wide gene expressions and protects rat myocardium against ischemia-reperfusion.

    PubMed

    Huang, Yan; Lu, Sheng-Feng; Hu, Chen-Jun; Fu, Shu-Ping; Shen, Wei-Xing; Liu, Wan-Xin; Li, Qian; Wang, Ning; He, Su-Yun; Liang, Fan-Rong; Zhu, Bing-Mei

    2014-10-09

    This study investigated genome-wide gene expressions and the cardioprotective effects of electro-acupuncture pretreatment at the PC6 Neiguan acupoint on myocardial ischemia reperfusion (I/R) injury. Male SD rats were randomly divided into four groups: sham operation (SO), I/R, electro-acupuncture at the PC6 Neiguan acupoint pretreatment (EA) and electro-acupuncture at non-acupoint pretreatment (NA). Compared with the I/R group, the survival rate of the EA group was significantly increased, the arrhythmia score, infarction area, serum concentrations of CK, LDH and CK-Mb and plasma level of cTnT were significantly decreased. RNA-seq results showed that 725 genes were up-regulated and 861 genes were down-regulated under I/R conditions compared to the SO group; both EA and NA reversed some of these gene expression levels (592 in EA and 238 in NA group). KEGG pathway analysis indicated that these genes were involved in multiple pathways, including ECM, MAPK signaling, apoptosis, cytokine and leukocyte pathways. In addition, some pathways were uniquely regulated by EA, but not NA pretreatment, such as oxidative stress, cardiac muscle contraction, gap junction, vascular smooth muscle contraction, hypertrophic, NOD-like receptor, and P53 and B-cell receptor pathways. This study was first to reveal the gene expression signatures of acute myocardial I/R injury and electro-acupuncture pretreatment in rats.

  4. Aspirin upregulates αB-Crystallin to protect the myocardium against heat stress in broiler chickens

    PubMed Central

    Tang, Shu; Yin, Bin; Song, Erbao; Chen, Hongbo; Cheng, Yanfen; Zhang, Xiaohui; Bao, Endong; Hartung, Joerg

    2016-01-01

    We established in vivo and in vitro models to investigate the role of αB-Crystallin (CryAB) and assess the ability of aspirin (ASA) to protect the myocardium during prolonged heat stress. Thirty-day-old chickens were divided into three groups (n = 90): heat stress (HS, 40±1 °C); ASA(−)HS(+), 1 mg/kg ASA orally 2 h before heat stress; and ASA(+)HS(−), pretreated with aspirin, no heat stress (25 °C). Hearts were excised after 0, 1, 2, 3, 5, 7, 10, 15 and 24 h. Heat stress increased body temperature, though the ASA(−)HS(+) group had significantly higher temperatures than the ASA(+)HS(+) group at all time points. Compared to ASA(+)HS(+), the ASA(−)HS(+) group displayed increased sensitivity to heat stress. Pathological analysis revealed the ASA (+)HS(+) myocardium showed less severe changes (narrowed, chaotic fibers; fewer necrotic cells) than the ASA(−)HS(+) group (bleeding and extensive cell death). In vitro, ASA-pretreatment significantly increased primary chicken myocardial cell survival during heat stress. ELISAs indicated ASA induced CryAB in vivo to protect against heat stress-induced myocardial damage, but ASA did not induce CryAB in primary chicken myocardial cells. The mechanisms by which ASA induces the expression of CryAB in vivo and protects the myocardium during heat stress merit further research. PMID:27857180

  5. S100A4 protects the myocardium against ischemic stress.

    PubMed

    Doroudgar, Shirin; Quijada, Pearl; Konstandin, Mathias; Ilves, Kelli; Broughton, Kathleen; Khalafalla, Farid G; Casillas, Alexandria; Nguyen, Kristine; Gude, Natalie; Toko, Haruhiro; Ornelas, Luis; Thuerauf, Donna J; Glembotski, Christopher C; Sussman, Mark A; Völkers, Mirko

    2016-11-01

    Myocardial infarction is followed by cardiac dysfunction, cellular death, and ventricular remodeling, including tissue fibrosis. S100A4 protein plays multiple roles in cellular survival, and tissue fibrosis, but the relative role of the S100A4 in the myocardium after myocardial infarction is unknown. This study aims to investigate the role of S100A4 in myocardial remodeling and cardiac function following infarct damage. S100A4 expression is low in the adult myocardium, but significantly increased following myocardial infarction. Deletion of S100A4 increased cardiac damage after myocardial infarction, whereas cardiac myocyte-specific overexpression of S100A4 protected the infarcted myocardium. Decreased cardiac function in S100A4 Knockout mice was accompanied with increased cardiac remodeling, fibrosis, and diminished capillary density in the remote myocardium. Loss of S100A4 caused increased apoptotic cell death both in vitro and in vivo in part mediated by decreased VEGF expression. Conversely, S100A4 overexpression protected cells against apoptosis in vitro and in vivo. Increased pro-survival AKT-signaling explained reduced apoptosis in S100A4 overexpressing cells. S100A4 expression protects cardiac myocytes against myocardial ischemia and is required for stabilization of cardiac function after MI. Copyright © 2016 Elsevier Ltd. All rights reserved.

  6. 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.

  7. Plasma exosomes protect the myocardium from ischemia-reperfusion injury.

    PubMed

    Vicencio, Jose M; Yellon, Derek M; Sivaraman, Vivek; Das, Debashish; Boi-Doku, Claire; Arjun, Sapna; Zheng, Ying; Riquelme, Jaime A; Kearney, Jessica; Sharma, Vikram; Multhoff, Gabriele; Hall, Andrew R; Davidson, Sean M

    2015-04-21

    Exosomes are nanometer-sized vesicles released from cells into the blood, where they can transmit signals throughout the body. Shown to act on the heart, exosomes' composition and the signaling pathways they activate have not been explored. We hypothesized that endogenous plasma exosomes can communicate signals to the heart and provide protection against ischemia and reperfusion injury. This study sought to isolate and characterize exosomes from rats and healthy volunteers, evaluate their cardioprotective actions, and identify the molecular mechanisms involved. The exosome-rich fraction was isolated from the blood of adult rats and human volunteers and was analyzed by protein marker expression, transmission electron microscopy, and nanoparticle tracking analysis. This was then used in ex vivo, in vivo, and in vitro settings of ischemia-reperfusion, with the protective signaling pathways activated on cardiomyocytes identified using Western blot analyses and chemical inhibitors. Exosomes exhibited the expected size and expressed marker proteins CD63, CD81, and heat shock protein (HSP) 70. The exosome-rich fraction was powerfully cardioprotective in all tested models of cardiac ischemia-reperfusion injury. We identified a pro-survival signaling pathway activated in cardiomyocytes involving toll-like receptor (TLR) 4 and various kinases, leading to activation of the cardioprotective HSP27. Cardioprotection was prevented by a neutralizing antibody against a conserved HSP70 epitope expressed on the exosome surface and by blocking TLR4 in cardiomyocytes, identifying the HSP70/TLR4 communication axis as a critical component in exosome-mediated cardioprotection. Exosomes deliver endogenous protective signals to the myocardium by a pathway involving TLR4 and classic cardioprotective HSPs. Copyright © 2015 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.

  8. Picroside II protects myocardium from ischemia/reperfusion-induced injury through inhibition of the inflammatory response

    PubMed Central

    Li, Jian-Zhe; Xie, Mei-Qing; Mo, Dan; Zhao, Xiao-Fang; Yu, Shu-Yi; Liu, Li-Juan; Wu, Cheng; Yang, Yang

    2016-01-01

    The inflammatory response is important in the pathogenesis of myocardial ischemia/reperfusion (I/R) injury. Picroside II, the primary active constituent of Picrorhizae, has been reported to protect the myocardium from I/R-induced injury, however, the exact mechanism underlying these protective effects remains unclear. The aim of the present study was to investigate the mechanism underlying the protective effects of picroside II on I/R-induced myocardial injury. Adult male Sprague-Dawley rats underwent 1 h left coronary artery occlusion followed by 3 h reperfusion. Picroside II was administered (10 mg/kg) via the tail vein 30 min prior to left coronary artery occlusion. The results revealed that pretreatment of picroside II could significantly alleviate I/R-induced myocardial injury concomitantly with a decrease in inflammatory factor production. In addition, picroside II was also able to decrease high mobility group box 1 (HMGB1) expression, and release and downregulate the expression of the receptor for advanced glycation end products (RAGE), toll-like receptor (TLR)-2 and TLR-4. Furthermore, picroside II was able to inhibit nuclear factor-κB (NF-κB) activation. The results indicated that the protective effect of picroside II on I/R-induced myocardial injury was associated, at least partly, with inhibition of the inflammatory response by suppressing the HMGB1-RAGE/TLR-2/TLR-4-NF-κB signaling pathway. PMID:28105084

  9. Protective effect of methylprednisolone on ischaemic myocardium assessed by ventricular function.

    PubMed Central

    Krause, B L; Hassan, M A; McMilan, A B; Brown, A H

    1977-01-01

    Intracardiac surgical procedures are best carried out when the heart is still and bloodless. This condition, however, produces myocardial cellular damage with loss of contractility and compliance unless some protection can be provided. Myocardial contractility and compliance is best studied by isovolumic ventricular function tests, which were used to evaluate the protective effect of methylprednisolone on the isolated cross-perfused canine heart made ischaemic for 2 hours. Control experiments included 2 hours of ischaemia without methylprednisolone, and 2 hours of continuous normothermic cross-perfusion. The methylprednisolone-treated hearts had probably significantly better ventricular function after 2 hours of ischaemia than did hearts without the methylprednisolone, while the cross-perfused hearts were best overall. This work suggests that methylprednisolone may have a protective effect on the ischaemic myocardium of the intact canine heart. PMID:867332

  10. Protecting the myocardium from ischemic injury: a critical role for alpha(1)-adrenoreceptors?

    PubMed

    Salvi, S

    2001-04-01

    Ischemic preconditioning (IPC) refers to the ability of short periods of ischemia to make the myocardium more resistant to a subsequent ischemic insult. It is the most powerful form of endogenous protection against myocardial infarction and has been demonstrated in all species evaluated to date. However, the cellular mechanisms that drive IPC remain poorly understood. This hypothesis describes an important role for alpha(1)-adrenoreceptors in mediating IPC and discusses the underlying mechanisms by which this is likely achieved. alpha(1)-Adrenoreceptors are present in the myocardium of all mammalian species, and several lines of evidence suggest that they play an important role in mediating IPC. During periods of myocardial hypoxia/ischemia, cardiomyocytes have to rely solely on anaerobic glycolysis for energy production; for this, the cells have to depend on increased glucose entry inside the cell as well as increased glycolysis. Stimulation of alpha(1)-adrenoreceptors increases glucose transport inside the cardiomyocytes by translocating glucose transporter (GLUT)-1 and GLUT-4 from the cytoplasm to the plasma membrane, enhances glycogenolysis by activating phosphorylase kinase, increases the rate of glycolysis by activating the enzyme phosphofructokinase, reduces intracellular acidity produced during excessive glycolysis by activating the Na(+)/H(+) exchanger, and inhibits apoptosis by increasing the levels of the antiapoptotic protein Bcl-2. Myocardial ischemia produces an increase in the expression of alpha(1)-adrenoreceptors in cardiomyocytes, as well as increases the levels of its agonist norepinephrine by several fold. During ischemic states, upregulation of alpha(1)-adrenoreceptors and increase in norepinephrine release could be a powerful adaptive mechanism that drives IPC. An understanding into the role of alpha(1)-adrenoreceptors in mediating IPC could not only point to newer treatments for limiting myocardial damage during myocardial infarction or heart

  11. 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.

  12. Nicorandil pretreatment and improved myocardial protection during cold blood cardioplegia.

    PubMed

    Li, Y; Iguchi, A; Tsuru, Y; Nakame, T; Satou, K; Tabayashi, K

    2000-01-01

    The present study was designed to assess whether pretreatment with nicorandil enhanced myocardial protection provided by cold (15 degrees C) high-potassium (25 mmol/l) blood cardioplegia during open heart surgery. Subjects were 40 patients with a variety of acquired heart diseases undergoing cardiac surgery involved cardiopulmonary bypass. They were randomly divided into two groups, 25 pretreated nicorandil (0.3 mg/kg) 30 minutes before aortic cross clamping, 15 not pretreated. After aortic cross clamping, the initial dose of cardioplegic solution (10 ml/kg) was administered through the ascending aorta and supplemental doses of cardioplegia (5 ml/kg) given each 30 minutes thereafter. Preoperative and postoperative cardiac troponin-T, myosin light chain 1 and cardiac enzymes were measured and hemodynamic data recorded. Postoperative serum creatine kinase and myosin light chain 1 were significantly lower in the nicorandil pretreatment group than in controls. Serum glutamic oxalacetic transaminase and troponin-T were lower and cardiac output was higher after surgery in the nicorandil group, although not statistically significant. This data suggests that pretreatment with nicorandil enhances the myocardial protection achieved by cold blood cardioplegia.

  13. The protective effects of high-dose ascorbic acid on myocardium against reperfusion injury during and after cardiopulmonary bypass.

    PubMed

    Dingchao, H; Zhiduan, Q; Liye, H; Xiaodong, F

    1994-10-01

    The protective effects of high-dose ascorbic acid (250 mg/kg) on the myocardium were observed in 85 patients undergoing Cardiopulmonary Bypass (CPB). The changes in serum Malonyldialdehyde (MDA). Creatine Phosphokinase (CPK), Creatine Phosphokinase isozyme (CPK-MB) and Lactic Dehydrogenase (LDH) in group B (n = 45, receiving ascorbic acid) were lower (p < 0.05) than in group A (n = 40, no ascorbic acid) during and after CPB. The MDA remained at a higher level two days postoperatively; CPK and CPK-MB, the sensitive and specific reflectors of myocardial injury, recovered very slowly in the control group (A) after the operation. The hearts in all the patients of group B resuscitated automatically intraoperatively while five cases (12.5%) needed defibrillation in group A. The cardiac index (CI) measured in ICU in group B was higher than in group A (p < 0.05). The patients needed shorter ICU and hospital stays in group B than in group A. The results indicate that ascorbic acid can act as a scavenger of free radicals to decrease the peroxidation of the lipids present in the cell membrane and remove the radicals to protect the myocardium from ischemia-reperfusion injury effectively during and after open-heart operation.

  14. In vivo protein transduction: delivery of PEP-1-SOD1 fusion protein into myocardium efficiently protects against ischemic insult.

    PubMed

    Zhang, You-En; Wang, Jia-Ning; Tang, Jun-Ming; Guo, Ling-Yun; Yang, Jian-Ye; Huang, Yong-Zhang; Tan, Yan; Fu, Shou-Zhi; Kong, Xia; Zheng, Fei

    2009-02-28

    Myocardial ischemia-reperfusion injury is a medical problem occurring as damage to the myocardium following blood flow restoration after a critical period of coronary occlusion. Oxygen free radicals (OFR) are implicated in reperfusion injury after myocardial ischemia. The antioxidant enzyme, Cu, Zn-superoxide dismutase (Cu, Zn-SOD, also called SOD1) is one of the major means by which cells counteract the deleterious effects of OFR after ischemia. Recently, we reported that a PEP-1-SOD1 fusion protein was efficiently delivered into cultured cells and isolated rat hearts with ischemia-reperfusion injury. In the present study, we investigated the protective effects of the PEP-1-SOD1 fusion protein after ischemic insult. Immunofluorescecnce analysis revealed that the expressed and purified PEP-1-SOD1 fusion protein injected into rat tail veins was efficiently transduced into the myocardium with its native protein structure intact. When injected into Sprague-Dawley rat tail veins, the PEP-1- SOD1 fusion protein significantly attenuated myocardial ischemia-reperfusion damage; characterized by improving cardiac function of the left ventricle, decreasing infarct size, reducing the level of malondialdehyde (MDA), decreasing the release of creatine kinase (CK) and lactate dehydrogenase (LDH), and relieving cardiomyocyte apoptosis. These results suggest that the biologically active intact forms of PEP-1-SOD1 fusion protein will provide an efficient strategy for therapeutic delivery in various diseases related to SOD1 or to OFR.

  15. Involvement of Bcl-2 Signal Pathway in the Protective Effects of Apigenin on Anoxia/Reoxygenation-induced Myocardium Injury.

    PubMed

    Chen, Chuanjun; He, Huan; Luo, Yong; Zhou, Min; Yin, Dong; He, Ming

    2016-02-01

    Apigenin is a type of flavonoids, which has been demonstrated to protect myocardium against ischemia/reperfusion (I/R) injury. However, the mechanism is still unclear. We hypothesized that the mechanism of cardioprotective action of apigenin on the I/R-induced injury might be caused via B-cell lymphoma (Bcl) signaling pathway. In this study, an in vitro I/R model was replicated on Langendorff-perfused heart and H9c2 cardiomyocytes by anoxia/reoxygenation (A/R) treatment. The recovery of cardiac contractile function, infarct size, lactate dehydrogenase (LDH) and creatine kinase (CK) in the perfusate, the expression and activity of Bcl-2 and caspase-3, and cardiomyocyte apoptosis were measured in the Langendorff heart undergoing A/R injury. In addition, the cell viability, LDH release, intracellular reactive oxygen species (ROS), mitochondrial membrane potential (Δψm), expression of cytochrome c in the cytosol, and cell apoptosis were examined in the culture of H9c2 cardiomyocytes after the A/R. The results showed that apigenin significantly improved rat heart contractile function, reduced LDH release, infarct size and apoptotic rate, upregulated the expression of Bcl-2 and caspase-3, and downregulated the expression of cleaved caspase-3 after the A/R. Moreover, apigenin increased the cell viability and decreased the release of LDH, production of reactive oxygen species, release of mitochondrial cytochrome c into the cytosol, and cell apoptosis in the culture of H9c2 cardiomyocytes after the A/R. In addition, inhibition of Bcl-2 activity by ABT-737 markedly attenuated the protective effect of apigenin on the A/R-induced myocardium injury. Taken together, we firstly demonstrated that the effect of apigenin against A/R injury in cardiomyocytes involves Bcl-2 signal pathway and at least partly depends on its effect of upregulating the expression of Bcl-2.

  16. 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.

  17. Creatine pretreatment protects cortical axons from energy depletion in vitro

    PubMed Central

    Shen, Hua; Goldberg, Mark P.

    2012-01-01

    Creatine is a natural nitrogenous guanidino compound involved in bioenergy metabolism. Although creatine has been shown to protect neurons of the central nervous system (CNS) from experimental hypoxia/ischemia, it remains unclear if creatine may also protect CNS axons, and if the potential axonal protection depends on glial cells. To evaluate the direct impact of creatine on CNS axons, cortical axons were cultured in a separate compartment from their somas and proximal neurites using a modified two-compartment culture device. Axons in the axon compartment were subjected to acute energy depletion, an in vitro model of white matter ischemia, by exposure to 6 mM sodium azide for 30 min in the absence of glucose and pyruvate. Energy depletion reduced axonal ATP by 65%, depolarized axonal resting potential, and damaged 75% of axons. Application of creatine (10 mM) to both compartments of the culture at 24 h prior to energy depletion significantly reduced axonal damage by 50%. In line with the role of creatine in the bioenergy metabolism, this application also alleviated the axonal ATP loss and depolarization. Inhibition of axonal depolarization by blocking sodium influx with tetrodotoxin also effectively reduced the axonal damage caused by energy depletion. Further study revealed that the creatine effect was independent of glial cells, as axonal protection was sustained even when creatine was applied only to the axon compartment (free from somas and glial cells) for as little as 2 h. In contrast, application of creatine after energy depletion did not protect axons. The data provide the first evidence that creatine pretreatment may directly protect CNS axons from energy deficiency. PMID:22521466

  18. 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

  19. Improving the cardio protective effect of aFGF in ischemic myocardium with ultrasound-mediated cavitation of heparin modified microbubbles: preliminary experiment.

    PubMed

    Zhao, Ying-Zheng; Lu, Cui-Tao; Li, Xiao-Kun; Tang, Qin-Qin; Tian, Xin-Qiao; Zhao, Ya-Ping; Zhang, Yan; Tian, Ji-Lai; Yang, Wei; Ge, Shuping; Nair, Chandra K; Shen, Xuedong

    2012-08-01

    Ultrasound (US)-mediated cavitation of microbubbles has evolved into a new tool for organ-specific gene and drug delivery. This paper was to investigate the feasibility of acidic fibroblast growth factor (aFGF) intravenous delivery to the ischemic myocardium of rats by ultrasonic microbubbles modified with heparin. Heparin modified microbubbles (HMB) were prepared by the freeze-dried method. Acute myocardial infarction (AMI) model was established and the cardio protective effect of the aFGF combing with HMB (aFGF-HMB) under US-mediated cavitation technique was investigated. aFGF-HMB combined with US-mediated cavitation technique was examined by ECG. Ejection fraction (EF), fractional shortening (FS) and left ventricular diastolic diameter (LVDd) were measured to monitor the improvement of global myocardial contractile function. Myocardial tissue was stained with hematoxylin and eosine (HE) to evaluate the elaborate general morphology of the ischemic myocardium. From morphologic observation and echocardiography in rat heart, aFGF-HMB had suitable size distribution, physical stability and good acoustic resonance function. From AMI rat experiments, aFGF-HMB under US-mediated cavitation technique exerted aFGF cardio protective effect in ischemic myocardium. From histological evaluation, US-mediated cavitation of aFGF-HMB showed improvement of myocardial ischemia. With the visual imaging and US-triggered drug release advantages, US-mediated cavitation of aFGF-HMB might be developed as a novel technique for targeting delivery of aFGF into ischemic myocardium.

  20. Mitochondrial ferritin protects the murine myocardium from acute exhaustive exercise injury

    PubMed Central

    Wu, Wenyue; Chang, Shiyang; Wu, Qiong; Xu, Zhifang; Wang, Peina; Li, Yaru; Yu, Peng; Gao, Guofen; Shi, Zhenhua; Duan, Xianglin; Chang, Yan-Zhong

    2016-01-01

    Mitochondrial ferritin (FtMt) is a mitochondrially localized protein possessing ferroxidase activity and the ability to store iron. FtMt overexpression in cultured cells protects against oxidative damage by sequestering redox-active, intracellular iron. Here, we found that acute exhaustive exercise significantly increases FtMt expression in the murine heart. FtMt gene disruption decreased the exhaustion exercise time and altered heart morphology with severe cardiac mitochondrial injury and fibril disorganization. The number of apoptotic cells as well as the levels of apoptosis-related proteins was increased in the FtMt−/− mice, though the ATP levels did not change significantly. Concomitant to the above was a high ‘uncommitted' iron level found in the FtMt−/− group when exposed to acute exhaustion exercise. As a result of the increase in catalytic metal, reactive oxygen species were generated, leading to oxidative damage of cellular components. Taken together, our results show that the absence of FtMt, which is highly expressed in the heart, increases the sensitivity of mitochondria to cardiac injury via oxidative stress. PMID:27853170

  1. Protection of the ischemic myocardium by propionylcarnitine taurine amide. Comparison with other carnitine derivatives.

    PubMed

    Regitz, V; Paulson, D J; Noonan, J; Fleck, E; Shug, A L

    1987-01-01

    The cardioprotective effect of the two synthetic carnitine derivatives, propionylcarnitine taurine amide (PCTA) and butyrylcarnitine taurine amide (BCTA), were studied in isolated perfused rat hearts. The protective effects of PCTA and BCTA were compared with those of chemically similar compounds, which have already been investigated in part and reported on; i.e. propionylcarnitine, carnitine, taurine and the combination of propionylcarnitine and taurine. The addition of either PCTA or BCTA significantly improved the recovery of cardiac function of ischemic reperfused hearts. PCTA (0.5 mM) treated hearts regained 75%, 91% and 89% of their preischemic values for cardiac output, left ventricular pressure and dp/dt after 90 min ischemia and 15 min reperfusion. These parameters of cardiac function remained impaired in control hearts which recovered only 38% of the initial preischemic cardiac output, 73% of initial intraventricular developed pressure and 64% of initial positive dp/dt. The cardioprotective effects of PCTA, BCTA and propionylcarnitine were in the same range. However, PCTA and BCTA acted in 20-fold lower molar concentrations compared to propionylcarnitine. Carnitine (11 mM), taurine (11 mM) as well as the combination of propionylcarnitine and taurine at low concentrations had no cardioprotective effect in these experiments. Myocardial adenosine triphosphate (ATP) and creatine phosphate (CP) concentrations were significantly higher in the PCTA or BCTA treated hearts than in controls, and lactate levels were reduced.(ABSTRACT TRUNCATED AT 250 WORDS)

  2. Protecting the myocardium: a role for the beta2 adrenergic receptor in the heart.

    PubMed

    Patterson, Andrew J; Zhu, Weizhong; Chow, Amy; Agrawal, Rani; Kosek, Jon; Xiao, Rui Ping; Kobilka, Brian

    2004-04-01

    The sympathetic nervous system enhances cardiac muscle function by activating beta adrenergic receptors (betaARs). Recent studies suggest that chronic betaAR stimulation is detrimental, however, and that it may play a role in the clinical deterioration of patients with congestive heart failure. To examine the impact of chronic beta1AR and beta2AR subtype stimulation individually, we studied the cardiovascular effects of catecholamine infusions in betaAR subtype knockout mice (beta1KO, beta2KO). Prospective, randomized, experimental study. Animal research laboratory. beta1KO and beta2KO mice and wild-type controls. The animals were subjected to 2 wks of continuous infusion of the betaAR agonist isoproterenol. Analyses of cardiac function and structure were performed during and 3 days after completion of the infusions. Functional studies included graded exercise treadmill testing, in vivo assessments of left ventricular function using Mikro-Tip catheter transducers, right ventricular pressure measurements, and analyses of organ weight to body weight ratios. Structural studies included heart weight measurements, assessments of myocyte ultrastructure using electron microscopy, and in situ terminal deoxynucleotidyl transferase-mediated biotin-dUTP nick-end labeling staining to quantitate myocyte apoptosis. We found that isoproterenol-treated beta2KO mice experienced greater mortality rates (p =.001, chi-square test using Fisher's exact method) and increased myocyte apoptosis at 3- and 7-day time points (p =.04 and p =.0007, respectively, two-way analysis of variance). The results of this study suggest that in vivo beta2AR activation is antiapoptotic and contributes to myocardial protection.

  3. Rotigaptide protects the myocardium and arterial vasculature from ischaemia reperfusion injury

    PubMed Central

    Venkatasubramanian, Sowmya; Vase, Henrik; Hyldebrandt, Janus A.; Contractor, Hussain; Schmidt, Michael R.; Bøtker, Hans Erik; Cruden, Nicholas L.; Newby, David E.; Kharbanda, Rajesh K.; Lang, Ninian N.

    2016-01-01

    Aim Ischaemia‐reperfusion injury (IRI) causes impaired endothelial function and is a major component of the adverse effects of reperfusion following myocardial infarction. Rotigaptide increases gap junction conductance via connexin‐43. We tested the hypothesis that rotigaptide reduces experimental myocardial infarction size and ameliorates endothelial IRI in humans. Methods Myocardial infarction study: porcine myocardial infarction was achieved by catheter‐induced occlusion of the left anterior descending artery. In a randomized double‐blind study, rotigaptide (n = 9) or placebo (n = 10) was administered intravenously as a 10 min bolus prior to reperfusion and continuously during 2 h of reperfusion. Myocardial infarction size (IS) was assessed as proportion of the area at risk (AAR). Human translational study: forearm IRI was induced in the presence or absence of intra‐arterial rotigaptide. In a randomized double‐blind study, forearm arterial blood flow was measured at rest and during intra‐arterial infusion of acetylcholine (5–20 μg min–1; n = 11) or sodium nitroprusside (2–8 mg min–1; n = 10) before and after intra‐arterial infusion of placebo or rotigaptide, and again following IRI. Results Myocardial infarction study: Rotigaptide treatment was associated with a reduction of infarct size (IS/AAR[%]: 18.7 ± 4.1 [rotigaptide] vs. 43.6 ± 4.2 [placebo], P = 0.006). Human translational study: Endothelium‐dependent vasodilatation to acetylcholine was attenuated after ischaemia‐reperfusion in the presence of placebo (P = 0.007), but not in the presence of rotigaptide (P = NS). Endothelium‐independent vasodilatation evoked by sodium nitroprusside was unaffected by IRI or rotigaptide (P = NS). Conclusions Rotigaptide reduces myocardial infarction size in a porcine model and protects from IRI‐related endothelial dysfunction in man. Rotigaptide may have therapeutic potential in the treatment of myocardial

  4. Rotigaptide protects the myocardium and arterial vasculature from ischaemia reperfusion injury.

    PubMed

    Pedersen, Christian M; Venkatasubramanian, Sowmya; Vase, Henrik; Hyldebrandt, Janus A; Contractor, Hussain; Schmidt, Michael R; Bøtker, Hans Erik; Cruden, Nicholas L; Newby, David E; Kharbanda, Rajesh K; Lang, Ninian N

    2016-06-01

    Ischaemia-reperfusion injury (IRI) causes impaired endothelial function and is a major component of the adverse effects of reperfusion following myocardial infarction. Rotigaptide increases gap junction conductance via connexin-43. We tested the hypothesis that rotigaptide reduces experimental myocardial infarction size and ameliorates endothelial IRI in humans. Myocardial infarction study: porcine myocardial infarction was achieved by catheter-induced occlusion of the left anterior descending artery. In a randomized double-blind study, rotigaptide (n = 9) or placebo (n = 10) was administered intravenously as a 10 min bolus prior to reperfusion and continuously during 2 h of reperfusion. Myocardial infarction size (IS) was assessed as proportion of the area at risk (AAR). Human translational study: forearm IRI was induced in the presence or absence of intra-arterial rotigaptide. In a randomized double-blind study, forearm arterial blood flow was measured at rest and during intra-arterial infusion of acetylcholine (5-20 μg min(-1) ; n = 11) or sodium nitroprusside (2-8 mg min(-1) ; n = 10) before and after intra-arterial infusion of placebo or rotigaptide, and again following IRI. Myocardial infarction study: Rotigaptide treatment was associated with a reduction of infarct size (IS/AAR[%]: 18.7 ± 4.1 [rotigaptide] vs. 43.6 ± 4.2 [placebo], P = 0.006). Human translational study: Endothelium-dependent vasodilatation to acetylcholine was attenuated after ischaemia-reperfusion in the presence of placebo (P = 0.007), but not in the presence of rotigaptide (P = NS). Endothelium-independent vasodilatation evoked by sodium nitroprusside was unaffected by IRI or rotigaptide (P = NS). Rotigaptide reduces myocardial infarction size in a porcine model and protects from IRI-related endothelial dysfunction in man. Rotigaptide may have therapeutic potential in the treatment of myocardial infarction. © 2016 The British Pharmacological Society.

  5. Metabolic effects of propionate, hexanoate and propionylcarnitine in normoxia, ischaemia and reperfusion. Does an anaplerotic substrate protect the ischaemic myocardium?

    PubMed

    Sundqvist, K E; Vuorinen, K H; Peuhkurinen, K J; Hassinen, I E

    1994-04-01

    It has been suggested that propionyl-L-carnitine administration to ischaemic hearts facilitates the restoration of cardiac function upon reperfusion, but it is still a matter of dispute whether its effect is conveyed via the metabolic effect of the propionyl moiety, the carnitine moiety or other mechanisms involving membrane receptor interactions. The metabolism of propionylcarnitine involves the formation of succinyl-CoA, which causes an increase in the total amount of tricarboxylic acid cycle intermediates. According to the current paradigm, anaplerosis ensures rapid restoration of tricarboxylic acid cycle activity during reperfusion. To evaluate the contribution of anaplerosis to the protective effect of propionylcarnitine during ischaemia and reperfusion, isolated rat hearts were perfused with Krebs-Henseleit bicarbonate buffer containing 5 mM glucose+insulin (12 IU per litre), to which 1 mM propionate, 0.8 mM hexanoate or 1 mM propionylcarnitine were added. Global 20 or 24 min no-flow ischaemia was followed by 10 min reperfusion. The flavoprotein redox state, myoglobin oxygenation, oxygen consumption and mechanical functioning of the heart were recorded and metabolites determined in freeze-trapped tissue. In parallel experiments, the cellular energy state was studied with phosphorus nuclear magnetic resonance spectrometry. The addition of 1 mM propionylcarnitine failed to cause an anaplerotic effect, but did bring about an oxidation of flavins, probably due to citrate synthase inhibition. Propionate showed similar but stronger effects and a marked anaplerosis, but still failed to improve the recovery of the heart upon reperfusion. The addition of hexanoate caused marked anaplerosis upon reperfusion and flavin reduction. The results failed to demonstrate that propionylcarnitine had any beneficial effect on the ischaemic myocardium.

  6. Celastrol protects ischaemic myocardium through a heat shock response with up-regulation of haeme oxygenase-1

    PubMed Central

    Der Sarkissian, S; Cailhier, J-F; Borie, M; Stevens, L-M; Gaboury, L; Mansour, S; Hamet, P; Noiseux, N

    2014-01-01

    Background and Purpose Celastrol, a triterpene from plants, has been used in traditional oriental medicine to treat various diseases. Here, we investigated the cardioprotective effects of celastrol against ischaemia. Experimental Approach Protective pathways induced by celastrol were investigated in hypoxic cultures of H9c2 rat cardiomyoblasts and in a rat model of myocardial infarction, assessed with echocardiographic and histological analysis. Key Results In H9c2 cells, celastrol triggered reactive oxygen species (ROS) formation within minutes, induced nuclear translocation of the transcription factor heat shock factor 1 (HSF1) resulting in a heat shock response (HSR) leading to increased expression of heat shock proteins (HSPs). ROS scavenger N-acetylcysteine reduced expression of HSP70 and HSP32 (haeme oxygenase-1, HO-1). Celastrol improved H9c2 survival under hypoxic stress, and functional analysis revealed HSF1 and HO-1 as key effectors of the HSR, induced by celastrol, in promoting cytoprotection. In the rat ischaemic myocardium, celastrol treatment improved cardiac function and reduced adverse left ventricular remodelling at 14 days. Celastrol triggered expression of cardioprotective HO-1 and inhibited fibrosis and infarct size. In the peri-infarct area, celastrol reduced myofibroblast and macrophage infiltration, while attenuating up-regulation of TGF-β and collagen genes. Conclusions and Implications Celastrol treatment induced an HSR through activation of HSF1 with up-regulation of HO-1 as the key effector, promoting cardiomyocyte survival, reduction of injury and adverse remodelling with preservation of cardiac function. Celastrol may represent a novel potent pharmacological cardioprotective agent mimicking ischaemic conditioning that could have a valuable impact in the treatment of myocardial infarction. PMID:25041185

  7. 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.

  8. Attempted protection of spermatogenesis from single doses of gamma-irradiation in the androgen pretreated rat.

    PubMed

    Schlappack, O K; Delic, J I; Harwood, J R; Stanley, J A

    1987-01-01

    Spermatogenic stem-cell survival after gamma-irradiation has been investigated in the adult Wistar rat. Single doses of 4.5 and 9 Gy gamma-rays were administered to the testes of rats who received arachis oil (0.1 ml/100 g body weight) or testosterone enanthate (240 micrograms/100 g body weight) subcutaneously three times weekly for 6 weeks prior to radiation and during the week in which the radiations were given. A mean percentage of regenerating seminiferous tubule cross-sections of 32.45% and 7.26% was found in the testes of androgen-pretreated rats at 8 weeks after 4.5 and 9 Gy, respectively. Similar values (33.4% and 6.2%) were obtained in arachis oil-pretreated controls. We therefore conclude that protection of rat spermatogenesis from single doses of gamma-rays cannot be achieved by androgen pretreatment.

  9. 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

  10. 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.

  11. Docosahexaenoic acid pretreatment confers protection and functional improvements after acute spinal cord injury in adult rats.

    PubMed

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

    2012-02-10

    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.

  12. Dinitrophenol pretreatment of rat ventricular myocytes protects against damage by metabolic inhibition and reperfusion.

    PubMed

    Rodrigo, G C; Lawrence, C L; Standen, N B

    2002-05-01

    We have investigated the protective effects of pretreatment with the mitochondrial uncoupler 2,4-dinitrophenol on the cellular damage induced by metabolic inhibition (with cyanide and iodoacetic acid) and reperfusion in freshly isolated adult rat ventricular myocytes. Damage was assessed from changes in cell length and morphology measured using video microscopy. Intracellular Ca(2+), mitochondrial membrane potential, and NADH were measured using fura-2, tetramethylrhodamine ethyl ester and autofluorescence, respectively. During metabolic inhibition myocytes developed rigor, and on reperfusion 73.6+/-8.1% hypercontracted and 10.8+/-6.7% recovered contractile function in response to electrical stimulation. Intracellular Ca(2+) increased substantially, indicated by a rise in the fura-2 ratio (340/380 nm) on reperfusion from 0.86+/-0.04 to 1.93+/-0.18. Myocytes pretreated with substrate-free Tyrode containing 50 microm dinitrophenol showed reduced reperfusion injury: 29.0+/-7.4% of cells hypercontracted and 65.3+/-7.3% recovered contractile function (P<0.001 vs control). The fura-2 ratio on reperfusion was also lower at 1.01+/-0.08. Fluorescence measurements showed that dinitrophenol caused mitochondrial depolarisation, and decreased NADH. The presence of the substrates glucose and pyruvate reduced these effects, and abolished the protection against damage by metabolic inhibition and reperfusion. However protection was unaffected by block of ATP-sensitive potassium channels. Thus the protective effects of pretreatment with dinitrophenol may result from a reduction in NADH in response to mitochondrial depolarisation.

  13. 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.

  14. Protection from radiation-induced damage to spermatogenesis in the androgen pretreated rat.

    PubMed

    Schlappack, O K; Delic, J I; Harwood, J R; Stanley, J A

    1988-07-01

    Protection of spermatogenesis from radiation-induced damage has been investigated in the adult Wistar rat. Silastic tubing containing either cholesterol or testosterone was implanted subcutaneously 7 weeks before 4 equal daily fractions of either 1, 1.5, 2, and 2.5 Gy of 230 kVp X-rays locally to the testes. Implants were removed on the day following the last fraction and 8 weeks after irradiation 88.6%, 83.8%, 63.6% and 28.9% tubule cross-sections respectively were found regenerating in rats pretreated with testosterone. In contrast, 68.45%, 58.6%, 38.2% and 17.3% tubule cross-sections regenerating were obtained in rats pretreated with cholesterol. Changes in testis weight however were found to show the reverse trend (i.e. a greater weight loss was observed following androgen pretreatment). These results show that protection of spermatogenesis from fractionated irradiation may be achieved in rat testis by androgen pretreatment.

  15. Elevated levels of activated NHE1 protect the myocardium and improve metabolism following ischemia/reperfusion injury.

    PubMed

    Mraiche, Fatima; Wagg, Cory S; Lopaschuk, Gary D; Fliegel, Larry

    2011-01-01

    In the myocardium, the Na(+)/H(+) exchanger isoform 1 (NHE1) is a plasma membrane protein that regulates intracellular pH. Inhibition of NHE1 activity has been shown to be beneficial in cardiovascular disease. However, recent reports have suggested that elevation of NHE1 levels has beneficial effects in hearts subjected to ischemia/reperfusion. We determined if activated and non-activated NHE1 proteins have varying cardioprotective and metabolic effects with ischemia/reperfusion in the isolated perfused working mouse heart. We used transgenic mice hearts that specifically expressed wild type NHE1 (N-line) or activated NHE1 protein (K-line). Intact hearts 10-12 weeks of age were perfused under working conditions, with fatty acids and glucose present as substrates. Hearts were subjected to 30 min of aerobic perfusion, followed by 20 min of global no-flow ischemia and 40 min of aerobic reperfusion. We examined changes in contractility and substrate use and ATP levels. K-line hearts expressing activated NHE1, recovered to a much greater extent than N-line and control hearts recovering almost 75% of their preischemic function. In addition, K-line hearts had elevated fatty acid oxidation, increased glycolysis rates and elevated ATP levels relative to N-line mice or controls. An examination of kinase activation showed that there were no differences between controls and transgenics in ERK, p38, p90(rsk) or pGSK3β levels. The results demonstrate that elevated levels of NHE1 induce cardioprotection and alter cardiac metabolism. However, in the working heart model, with glucose and fatty acid as substrates, this required an activated NHE1 protein.

  16. Protection of the ischaemic myocardium by L-propionylcarnitine: effects on the recovery of cardiac output after ischaemia and reperfusion, carnitine transport, and fatty acid oxidation.

    PubMed

    Paulson, D J; Traxler, J; Schmidt, M; Noonan, J; Shug, A L

    1986-07-01

    The effects of L-propionylcarnitine on the recovery of cardiac contractile performance after global ischaemia and reperfusion were studied in isolated perfused rat hearts. The addition of either 5.5 or 11 mmol X litre-1 L-propionylcarnitine significantly improved the recovery of cardiac output, left ventricular pressure, and dP/dt after 90 min of ischaemia and 15 min of reperfusion. Myocardial adenosine triphosphate and creatine phosphate concentrations were significantly higher in the L-propionylcarnitine treated hearts than in controls, but the concentrations of long chain acyl carnitine and coenzyme A were unaffected. The protecting effects of L-propionylcarnitine were compared with those of L-carnitine and L-acetylcarnitine. A 11 mmol X litre-1 dose of L-propionylcarnitine and L-acetylcarnitine significantly improved the recovery of cardiac output after 90 min of ischaemia and 15 min of reperfusion, but L-carnitine did not. L-Propionylcarnitine was the most protective agent. The effects of these derivatives on L-3H-carnitine transport and 14C-palmitate oxidation were also measured. All of these derivatives competitively inhibited L-3H-carnitine transport in isolated cardiac myocytes, but L-propionylcarnitine was the most potent. Carnitine and L-propionylcarnitine stimulated palmitate oxidation in the homogenate, whereas L-acetylcarnitine inhibited it. In myocytes only L-propionylcarnitine affected palmitate oxidation. These data show that L-propionylcarnitine protects the ischaemic myocardium. Its protection is greater than that for L-carnitine or L-acetylcarnitine, and the difference in effectiveness may relate to the rate of transport into the cells and the effects on fatty acid utilisation.

  17. Assessment of membrane protection by /sup 31/P-NMR effects of lidocaine on calcium-paradox in myocardium

    SciTech Connect

    Sakai, Hirosumi; Yoshiyama, Minoru; Teragaki, Masakazu; Takeuchi, Kazuhide; Takeda, Takeda; Ikata, Mari; Ishikawa, Makoto; Miura, Iwao

    1989-01-01

    In studying calcium paradox, perfused rat hearts were used to investigate the myocardial protective effects of lidocaine. Intracellular contents of phosphates were measured using the /sup 31/P-NMR method. In hearts reexposed to calcium, following 3 minute calcium-free perfusion, a rapid contracture occurred, followed by rapid and complete disappearance of intracellular phosphates with no resumption of cardiac function. In hearts where lidocaine was administered from the onset of the calcium-free perfusion until 2 minutes following the onset of reexposure to calcium, both intracellular phosphates and cardiac contractility were maintained. Therefore, it can be said that cell membranes were protected by lidocaine.

  18. Pretreatment with a mixture of essential fatty acids protects rats from anxiogenic effects of REM deprivation.

    PubMed

    Yehuda, Shlomo; Rabinovitz, Sharon; Carasso, Ralph L; Mostofsky, David I

    2007-01-01

    Rapid eye movements (REM) deprivation induces complex deteriorating effects, which include brain morphological changes such as reduced neurogenesis processes, brain neurochemical and hormonal modifications, and cognitive decline. One of the major effects of REM deprivation is an increased anxiety level. The aim of this study was to examine the effects ofpretreatment with a specific mixture of essential fatty acids on the increased level of anxiety on the behavioral level (elevated plus maze), on the hormonal level (corticosterone level) and on the physiological level (thermoregulation). The results showed that pretreatment with a mixture of essential fatty acids protect the rats from the anxiolytic effects of REM deprivation. The effects of essential fatty acids on sleep mechanisms, on the one hand, and on anxiety levels, on the other hand, may explain the beneficial effects of the pretreatment.

  19. Study on the protective effect of shengmai san (see text) on the myocardium in the type 2 diabetic cardiomyopathy model rat.

    PubMed

    Ni, Qing; Wang, Jie; Li, En-Qing; Zhao, An-Bin; Yu, Bin; Wang, Min; Huang, Chun-Rong

    2011-09-01

    To study the effect of Shengmai San ((see text) Pulse-activating Powder) in protecting myocardium in the rat of the type 2 diabetic cardiomyopathy (DCM) model. The DCM rat model was established by combination of insulin resistance induced by a high-fat diet with intraperitoneal injection of high dose streptozotocin (50 mg/kg). And these rat models were randomly divided into three groups: a normal group (n = 12,one of them died), a model group (n = 15) and a Shengmai San group (treatment group, n = 15).The damage of the myocardium was assessed by electrocardiogram at the twelfth week after modeling, and the blood glucose, cholesterol and triglyceride levels were determined; the content of the left cardiac ventricle myocardial collagen was quantified by Masson staining test; the level of myocardial cell apoptosis was detected with TUNEL apoptosis detection kit; the damage extent of the myocardial sub-cellular structures was observed by electron microscopy; the expression levels of cardiac TSP-1 (Thrombospondin-1), TGF-beta1 (Transforming Growth F factor-beta) and TRB-3 (Tribbles homolog 3) proteins were detected by immunohistochemical method; the expression levels of cardiac TSP-1, A-TGF-beta1 and L-TGF-beta1 proteins were detected by Western blotting; and the expression levels of TSP-1 and TRB-3 mRNAs were detected by real-time quantitative PCR. Compared with the control group, the blood glucose, cholesterol, triglycerides levels in both the model groups and the Shengmai San group were significantly decreased; the myocardial tissue was less damaged and the collagen content was reduced in the Shengmai San group; the myocardial sub-cellular structure was injured to a lesser extent; the expression levels of myocardial TSP-1, TGF-beta1, TRB-3, and TSP-1, A-TGF-beta1, L-TGF-beta1 and chymase were decreased, and the expression levels of TSP-1 mRNA and TRB-3 mRNA were decreased in both the model groups and the Shengmai San group (the latter was better),. Shengmai San can

  20. Study on the protective effect of the Mixture of Shengmai Powder and Danshen Decoction on the myocardium of diabetic cardiomyopathy in the rat model.

    PubMed

    Ni, Qing; Wang, Jie; Li, En-Qing; Zhao, An-Bin; Yu, Bin; Wang, Min; Huang, Chun-Rong

    2011-02-01

    To study the protective effect of the Mixture of Shengmai Powder and Danshen Decoction (, abbreviated as the Mixture) in the rat model with type 2 diabetic cardiomyopathy in the rat model with type 2 diabetic cardiomyopathy, abbreviated as the Mixture) in the rat model with type 2 diabetic cardiomyopathy (DCM). Forty-two SD rats with DCM model, established by the combination of insulin resistance by a high-fat diet with the damage of pancreatic islet β cells by intraperitoneal injection of high dose streptozotocin (50 mg/kg) once, were evaluated in the damage of the myocardium by electrocardiogram at the end of 12 weeks of grouping and intervention administration; the extent of damage in the myocardial subcellular structure was observed by electron microscopy; the content of myocardial collagen in the left cardiac ventricle was quantified by Masson staining test; the myocardial cell apoptosis was determined by TUNEL; the changes in the mRNA expression levels of thrombospodin-1 (TSP-1) and tribbles homolog 3 (TRB-3) by real-time quantitative PCR, the expression levels of myocardial TSP-1, tumor growth factorβ1 (TGF-β1), TRB-3, and chymase were detected by immunohistochemistry, and the changes in the expression levels of myocardial TSP-1, active-TGF-β1 (A-TGF-β1) and latent-TGF-β1 (L-TGF-β1) protein were tested by Western blotting. Compared with the control group, the myocardial tissue was less damaged, and the extent of damage in the myocardial subcellular structure was less; the collagen fiber content and the cell apoptosis were reduced; the expression levels of TSP-1mRNA and TRB-3 mRNA, the expression levels of myocardial TSP-1, TGF-β1, TRB-3, and chymase, as well as the average expression levels of the myocardial TSP-1, A-TGFβ1, and L-TGF-β1 protein were decreased in the Mixture group. The Mixture of Shengmai Powder and Danshen Decoction could inhibit the process of myocardial fibrosis in the rat myocardium of DCM through multiple pathways and

  1. Laser pretreatment protects cells of broad bean from UV-B radiation damage.

    PubMed

    Qi, Z; Yue, M; Wang, X L

    2000-12-01

    In order to determine the role of lasers in the stress resistance of broad bean (Vicia faba L.) to ultraviolet-B (UV-B) radiation, the embryos in seeds were exposed to He-Ne laser or CO2 laser radiation. Afterwards they were cultivated in Petri dishes in a constant temperature incubator until the lengths of epicotyls were nearly 3 cm. The epicotyls were then exposed to 1.02, 3.03 or 4.52 kJ m(-2) UV-B radiation, respectively, under 70 micromol m(-2) s(-1) photosynthetically active radiation (PAR) in a growth cabinet. Changes in the concentration of malondialdehyde (MDA), ascorbic acid (AsA) and UV-B absorbing compounds (absorbance at 300 nm) were measured to test the effects of laser pretreatment. The results showed that laser pretreatment of embryos enhanced UV-B stress resistance in the epicotyls of the broad bean by decreasing the MDA concentration and increasing the content of AsA and UV-B absorbing compounds. We suggest that those changes in MDA, AsA and UV-B absorbing compounds were responsible for the increase in stress resistance observed in the broad bean. This is the first investigation reporting the use of laser pretreatment to protect the cells of the broad bean from UV-B-induced damage.

  2. 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

  3. 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.

  4. Systemic phosphatidylcholine pretreatment protects canine esophageal mucosa during acute experimental biliary reflux

    PubMed Central

    Eros, Gabor; Kaszaki, Jozsef; Czobel, Miklos; Boros, Mihaly

    2006-01-01

    AIM: To characterize the consequences of short-term exposure to luminal bile on mucosal mast cell reactions in a canine model, and to determine the effects of systemic phosphatidylcholine pretreatment in this condition. METHODS: Twenty mongrel dogs were used for experiments. Group 1 (n  = 5) served as a saline-treated control, while in group 2 (n = 5) the esophagus was exposed to bile for 3 h. In group 3 (n  = 5) the animals were pretreated with 7-nitroindazole to inhibit the neuronal isoform of nitric oxide synthase. In group 4 (n  = 5) phosphatidylcholine solution (50 mg/kg) was administered iv before the biliary challenge. Mucosal microcirculation was observed by intravital videomicroscopy. Myeloperoxidase and nitric oxide synthase activities, the degrees of mast cell degranulation and mucosal damage were evaluated via tissue biopsies. RESULTS: Exposure to bile evoked significant mast cell degranulation and leukocyte accumulation. The red blood cell velocity and the diameter of the postcapillary venules increased significantly. The tissue ATP content and constitutive nitric oxide synthase activity decreased, while the inducible nitric oxide synthase activity increased significantly as compared to the control values. 7-nitroindazole treatment significantly exacerbated the mucosal mast cell degranulation and tissue damage. In contrast, phosphatidylcholine pretreatment prevented the bile-induced ATP depletion, the inducible nitric oxide synthase and myeloperoxidase activity and the mast cell degranulation increased. CONCLUSION: The neuronal nitric oxide synthase - mast cell axis plays an important role in the esophageal mucosal defense system. Systemic phosphatidylcholine pretreatment affords effective protection through ameliorating the bile-induced ATP depletion and secondary inflammatory reaction. PMID:16482629

  5. Pretreatment of Ferulic Acid Protects Human Dermal Fibroblasts against Ultraviolet A Irradiation

    PubMed Central

    Hahn, Hyung Jin; Kim, Ki Bbeum; Bae, Seunghee; Choi, Byung Gon; An, Sungkwan

    2016-01-01

    Background Approximately 90%~99% of ultraviolet A (UVA) ray reaches the Earth's surface. The deeply penetrating UVA rays induce the formation of reactive oxygen species (ROS), which results in oxidative stress such as photoproducts, senescence, and cell death. Thus, UVA is considered a primary factor that promotes skin aging. Objective Researchers investigated whether pretreatment with ferulic acid protects human dermal fibroblasts (HDFs) against UVA-induced cell damages. Methods HDF proliferation was analyzed using the water-soluble tetrazolium salt assay. Cell cycle distribution and intracellular ROS levels were assessed by flow cytometric analysis. Senescence was evaluated using a senescence-associated β-galactosidase assay, while Gadd45α promoter activity was analyzed through a luciferase assay. The expression levels of superoxide dismutase 1 (SOD1), catalase (CAT), xeroderma pigmentosum complementation group A and C, matrix metalloproteinase 1 and 3, as well as p21 and p16 were measured using quantitative real-time polymerase chain reaction. Results Inhibition of proliferation and cell cycle arrest were detected in cells that were irradiated with UVA only. Pretreatment with ferulic acid significantly increased the proliferation and cell cycle progression in HDFs. Moreover, ferulic acid pretreatment produced antioxidant effects such as reduced DCF intensity, and affected SOD1 and CAT mRNA expression. These effects were also demonstrated in the analysis of cell senescence, promoter activity, expression of senescent markers, and DNA repair. Conclusion These results demonstrate that ferulic acid exerts protective effects on UVA-induced cell damages via anti-oxidant and stress-inducible cellular mechanisms in HDFs. PMID:27904274

  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. The polysulfide diallyl trisulfide protects the ischemic myocardium by preservation of endogenous hydrogen sulfide and increasing nitric oxide bioavailability

    PubMed Central

    Predmore, Benjamin L.; Kondo, Kazuhisa; Bhushan, Shashi; Zlatopolsky, Maxim A.; King, Adrienne L.; Aragon, Juan Pablo; Grinsfelder, D. Bennett; Condit, Marah E.

    2012-01-01

    Diallyl trisulfide (DATS), a polysulfide constituent found in garlic oil, is capable of the release of hydrogen sulfide (H2S). H2S is a known cardioprotective agent that protects the heart via antioxidant, antiapoptotic, anti-inflammatory, and mitochondrial actions. Here, we investigated DATS as a stable donor of H2S during myocardial ischemia-reperfusion (MI/R) injury in vivo. We investigated endogenous H2S levels, infarct size, postischemic left ventricular function, mitochondrial respiration and coupling, endothelial nitric oxide (NO) synthase (eNOS) activation, and nuclear E2-related factor (Nrf2) translocation after DATS treatment. Mice were anesthetized and subjected to a surgical model of MI/R injury with and without DATS treatment (200 μg/kg). Both circulating and myocardial H2S levels were determined using chemiluminescent gas chromatography. Infarct size was measured after 45 min of ischemia and 24 h of reperfusion. Troponin I release was measured at 2, 4, and 24 h after reperfusion. Cardiac function was measured at baseline and 72 h after reperfusion by echocardiography. Cardiac mitochondria were isolated after MI/R, and mitochondrial respiration was investigated. NO metabolites, eNOS phosphorylation, and Nrf2 translocation were determined 30 min and 2 h after DATS administration. Myocardial H2S levels markedly decreased after I/R injury but were rescued by DATS treatment (P < 0.05). DATS administration significantly reduced infarct size per area at risk and per left ventricular area compared with control (P < 0.001) as well as circulating troponin I levels at 4 and 24 h (P < 0.05). Myocardial contractile function was significantly better in DATS-treated hearts compared with vehicle treatment (P < 0.05) 72 h after reperfusion. DATS reduced mitochondrial respiration in a concentration-dependent manner and significantly improved mitochondrial coupling after reperfusion (P < 0.01). DATS activated eNOS (P < 0.05) and increased NO metabolites (P < 0

  8. Pretreatment with apoaequorin protects hippocampal CA1 neurons from oxygen-glucose deprivation.

    PubMed

    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.

  9. Intrastriatal pre-treatment with L-NAME protects rats from diquat neurotoxcity.

    PubMed

    Djukic, Mirjana; Jovanovic, Marina D; Ninkovic, Milica; Stevanovic, Ivana; Curcic, Marijana; Topic, Aleksandra; Vujanovic, Dragana; Djurdjevic, Dragan

    2012-01-01

    Contact herbicide diquat (DQ), redox cycling compound, mediates its systemic toxicity throughout the enlarged production of free radicals. Target organs are liver and kidney in humans. To-date, the mechanism of DQ-induced neurotoxicity has not been rationalized. The objectives of the study were to examine the ability of DQ to induce oxidative stress (OS) and/or nitrosative stress (NS) upon intrastriatal (i.s.) administration and to investigate the role of nitric oxide (NO(x)) using NG-nitro-L-arginine methyl ester (L-NAME), a non-selective inhibitor of nitric oxide synthase (NOS) in the pretreatment of DQ i.s. administration. The experiment was conducted on Wistar rats, randomly divided in experimental groups, receiving different treatments i.s. applied. Parameters of OS/NS such as: superoxide anion radical (O(2)(•-)), superoxide dismutase (SOD), malondialdehyde (MDA) and nitrates (NO(3)(-)) were measured in the cortex (bilaterally), at 30(th) min, 24 hours and 7 days after the treatments. Lethargy and high mortality rate were observed only in the DQ group (within 24 hours and 2-3 hours, respectively) after awakening from anesthesia. Markedly increased production of NO(x) and O(2)(•-) along with elevated lipid peroxidation altogether contributed to DQ neurotoxicity. The most importantly, the L-NAME i.s. pretreatment protected treated animals from dying and diminished OS/NS response against DQ-induced neurotoxicity. The i.s. pretreatment with L-NAME resulted in neuroprotection against DQ neurotoxity, based on animal survival and reduced LPO in the cortex.

  10. Pretreatment with glycomacropeptide reduces allergen sensitization, alleviates immediate cutaneous hypersensitivity and protects from anaphylaxis

    PubMed Central

    Jiménez, M; Chávez, N A; Salinas, E

    2012-01-01

    Allergic disorders are characterized by the involvement of allergen-specific immunoglobulin (Ig)E antibodies and T helper type 2 (Th2) cells. The search for new therapies for allergic diseases has been the primary focus of interest for many investigators in recent years. Glycomacropeptide (GMP) is a biologically active component of milk that exhibits a range of immunomodulatory functions. We examined whether oral administration of GMP could affect the development of allergic sensitization and the severity of immediate cutaneous hypersensitivity reactions and of anaphylaxis. Rats treated with or without GMP were ovalbumin (OVA)-sensitized and several indicators of allergy were evaluated. Pretreatment with GMP resulted in reduction of antigen-specific IgE titre in rats when sensitized with OVA. GMP administration also markedly suppressed the proliferative response of splenocytes to antigen and the production of interleukin (IL)-13 by splenocytes of sensitized animals. In addition, GMP pretreatment attenuated the intensity of the immediate cutaneous reaction induced by antigen and protected the sensitized rats from severe anaphylaxis. These data demonstrate, for the first time, that the administration of GMP prevents allergen sensitization and reduces the severity of the early-phase reaction induced by antigen in cutaneous hypersensitivity and in anaphylaxis. GMP may be used as a novel prophylactic agent for the control of allergic diseases. PMID:22943197

  11. Pretreatment of Gymnema sylvestre revealed the protection against acetic acid-induced ulcerative colitis in rats

    PubMed Central

    2014-01-01

    Background Overproduction of free radicals and decreased antioxidant capacity are well-known risk factors for inflammatory bowel diseases. Gymnema sylvestre (GS) leaves extract is distinguished for its anti-diabetic, antioxidant and anti-inflammatory properties. Present study is designed to evaluate the preventative activities of GS against acetic acid (AA)-induced ulcerative colitis in Wistar rats. Methods Experimentally ulcerative colitis (UC) was induced by AA in animals pretreated with three different doses of GS leaves extract (50, 100, 200 mg/kg/day) and a single dose of mesalazine (MES, 300 mg/kg/day) for seven days. Twenty four hours later, animals were sacrificed and the colonic tissues were collected. Colonic mucus content was determined using Alcian blue dye binding technique. Levels of thiobarbituric acid reactive substances (TBARS), total glutathione sulfhydryl group (T-GSH) and non-protein sulfhydryl group (NPSH) as well as the activity of the antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT) were estimated in colon tissues. Colonic nucleic acids (DNA and RNA) and total protein (TP) concentrations were also determined. Levels of pro-inflammatory cytokines including interleukin-1 beta (IL-1β), tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) as well as prostaglandin E2 (PGE2) and nitric oxide (NO) were estimated in colonic tissues. The histopathological changes of the colonic tissues were also observed. Results In AA administered group TBARS levels were increased, while colonic mucus content, T-GSH and NP-SH, SOD and CAT were reduced in colon. Pretreatment with GS inhibited TBARS elevation as well as mucus content, T-GSH and NP-SH reduction. Enzymatic activities of SOD and CAT were brought back to their normal levels in GS pretreated group. A significant reduction in DNA, RNA and TP levels was seen following AA administration and this inhibition was significantly eliminated by GS treatment. GS pretreatment also inhibited

  12. Pretreatment of Gymnema sylvestre revealed the protection against acetic acid-induced ulcerative colitis in rats.

    PubMed

    Aleisa, Abdulaziz M; Al-Rejaie, Salim S; Abuohashish, Hatem M; Ola, Mohammed S; Parmar, Mihir Y; Ahmed, Mohammed M

    2014-02-10

    Overproduction of free radicals and decreased antioxidant capacity are well-known risk factors for inflammatory bowel diseases. Gymnema sylvestre (GS) leaves extract is distinguished for its anti-diabetic, antioxidant and anti-inflammatory properties. Present study is designed to evaluate the preventative activities of GS against acetic acid (AA)-induced ulcerative colitis in Wistar rats. Experimentally ulcerative colitis (UC) was induced by AA in animals pretreated with three different doses of GS leaves extract (50, 100, 200 mg/kg/day) and a single dose of mesalazine (MES, 300 mg/kg/day) for seven days. Twenty four hours later, animals were sacrificed and the colonic tissues were collected. Colonic mucus content was determined using Alcian blue dye binding technique. Levels of thiobarbituric acid reactive substances (TBARS), total glutathione sulfhydryl group (T-GSH) and non-protein sulfhydryl group (NPSH) as well as the activity of the antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT) were estimated in colon tissues. Colonic nucleic acids (DNA and RNA) and total protein (TP) concentrations were also determined. Levels of pro-inflammatory cytokines including interleukin-1 beta (IL-1β), tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) as well as prostaglandin E2 (PGE2) and nitric oxide (NO) were estimated in colonic tissues. The histopathological changes of the colonic tissues were also observed. In AA administered group TBARS levels were increased, while colonic mucus content, T-GSH and NP-SH, SOD and CAT were reduced in colon. Pretreatment with GS inhibited TBARS elevation as well as mucus content, T-GSH and NP-SH reduction. Enzymatic activities of SOD and CAT were brought back to their normal levels in GS pretreated group. A significant reduction in DNA, RNA and TP levels was seen following AA administration and this inhibition was significantly eliminated by GS treatment. GS pretreatment also inhibited AA-induced elevation of pro

  13. Sodium tanshinone IIA sulfonate protects rat myocardium against ischemia-reperfusion injury via activation of PI3K/Akt/FOXO3A/Bim pathway

    PubMed Central

    Zhang, Mei-qi; Zheng, Yue-liang; Chen, Huan; Tu, Jian-feng; Shen, Ye; Guo, Jun-ping; Yang, Xiang-hong; Yuan, Shu-ren; Chen, Liang-zhong; Chai, Jing-jie; Lu, Jian-hong; Zhai, Chang-lin

    2013-01-01

    Aim: To investigate the mechanisms underlying the protective effects of sodium tanshinone IIA sulfonate (STS) in an ischemia-reperfusion (I/R)-induced rat myocardial injury model. Methods: Male SD rats were iv injected with STS, STS+LY294002 or saline (NS) for 15 d. Then the hearts were subjected to 30 min of global ischemia followed by 2 h of reperfusion. Cardiac function, infarction size and area at risk were assessed. Cell apoptosis was evaluated with TUNEL staining, DNA laddering and measuring caspase-3 activity. In addition, isolated cardiomyocytes of neonatal rats were pretreated with the above drugs, then exposed to H2O2 (200 mol/L) for 1 h. Cell apoptosis was detected using flow cytometric assay. The levels of p-Akt, p-FOXO3A and Bim were examined with immunoblotting. Results: Compared to NS group, administration of STS (20 mg/kg) significantly reduced myocardial infarct size (40.28%±5.36% in STS group vs 59.52%±7.28% in NS group), and improved the myocardial function as demonstrated by the increased values of dp/dtmax, LVDP and coronary flow at different reperfusion time stages. Furthermore, STS significantly decreased the rate of apoptotic cells (15.11%±3.71% in STS group vs 38.21%±7.83% in NS group), and reduced caspase-3 activity to nearly a quarter of that in NS group. Moreover, STS significantly increased the phosphorylation of Akt and its downstream target FOXO3A, and decreased the expression of pro-apoptotic gene Bim. Co-treatment with the PI3K inhibitor LY294002 (40 mg/kg) partially countered the protective effects induced by STS treatment. In isolated cardiomyocytes, STS exerted similar protective effects as shown in the ex vivo I/R model. Conclusion: STS pretreatment reduces infarct size and improves cardiac function in an I/R-induced rat myocardial injury model via activation of Akt/FOXO3A/Bim-mediated signal pathway. PMID:24077633

  14. Fracture resistance behaviour of gamma-irradiation sterilized cortical bone protected with a ribose pre-treatment

    NASA Astrophysics Data System (ADS)

    Woodside, Carman Mitchell

    Structural bone allograft reconstructions are often implemented to repair large skeletal defects. To ensure the biological safety of the patient, allograft material is routinely sterilized with gamma-irradiation prior to implantation. The sterilization process damages the tissue, specifically the collagen protein network, leading to severe losses in the mechanical properties of the bone. Our lab has begun developing a ribose pre-treatment that can protect bone from these harmful effects. The goals of the present study were to develop a method to measure the fracture toughness of bone, an important clinical failure mode, and implement it to determine the effectiveness of the ribose pre-treatment on fracture toughness. We have shown that the ribose pre-treatment is successful at protecting some of the original fracture toughness of sterilized bone, and that the connectivity of the collagen network is an important contributor to the fracture resistance of bone.

  15. Cobalt protoporphyrin pretreatment protects human embryonic stem cell-derived cardiomyocytes from hypoxia/reoxygenation injury in vitro and increases graft size and vascularization in vivo.

    PubMed

    Luo, Jun; Weaver, Matthew S; Cao, Baohong; Dennis, James E; Van Biber, Benjamin; Laflamme, Michael A; Allen, Margaret D

    2014-06-01

    Human embryonic stem cell-derived cardiomyocytes (hESC-CMs) can regenerate infarcted myocardium. However, when implanted into acutely infarcted hearts, few cells survive the first week postimplant. To improve early graft survival, hESC-CMs were pretreated with cobalt protoporphyrin (CoPP), a transcriptional activator of cytoprotective heme oxygenase-1 (HO-1). When hESC-CMs were challenged with an in vitro hypoxia/reoxygenation injury, mimicking cell transplantation into an ischemic site, survival was significantly greater among cells pretreated with CoPP versus phosphate-buffered saline (PBS)-pretreated controls. Compared with PBS-pretreated cells, CoPP-pretreated hESC-CM preparations exhibited higher levels of HO-1 expression, Akt phosphorylation, and vascular endothelial growth factor production, with reduced apoptosis, and a 30% decrease in intracellular reactive oxygen species. For in vivo translation, 1 × 10(7) hESC-CMs were pretreated ex vivo with CoPP or PBS and then injected intramyocardially into rat hearts immediately following acute infarction (permanent coronary ligation). At 1 week, hESC-CM content, assessed by quantitative polymerase chain reaction for human Alu sequences, was 17-fold higher in hearts receiving CoPP- than PBS-pretreated cells. On histomorphometry, cardiomyocyte graft size was 2.6-fold larger in hearts receiving CoPP- than PBS-pretreated cells, occupying up to 12% of the ventricular area. Vascular density of host-perfused human-derived capillaries was significantly greater in grafts composed of CoPP- than PBS-pretreated cells. Taken together, these experiments demonstrate that ex vivo pretreatment of hESC-CMs with a single dose of CoPP before intramyocardial implantation more than doubled resulting graft size and improved early graft vascularization in acutely infarcted hearts. These findings open the door for delivery of these, or other, stem cells during acute interventional therapy following myocardial infarction or ischemia.

  16. DNA damage in leukocytes from pretreatment mucopolysaccharidosis type II patients; protective effect of enzyme replacement therapy.

    PubMed

    Filippon, Letícia; Wayhs, Carlos A Y; Atik, Diana M; Manfredini, Vanusa; Herber, Silvani; Carvalho, Clarissa G; Schwartz, Ida V D; Giugliani, Roberto; Vargas, Carmen R

    2011-04-03

    Mucopolysaccharidosis type II (MPS II) is an X-linked recessive disease caused by deficiency of the lysosomal enzyme iduronate-2-sulfatase, leading to progressive accumulation of glycosaminoglycans in nearly all cell types, tissues and organs. Enzyme replacement therapy reduces the storage of these substances in the lysosomes. Oxidative stress is related to the pathophysiology of many disorders, including inborn errors of metabolism. Oxidative damage to protein and lipid has been described in MPS types I and III. The aim of this study was to analyze DNA damage, as determined by the alkaline comet assay using silver staining, in peripheral leukocytes from MPS II patients before treatment and during the first six months of enzyme replacement therapy. We also correlated DNA damage with lipid and protein oxidative damages, analyzed by plasma malondialdehyde levels and carbonyl group content, respectively. We found a significant increase in lipid and protein damage in MPS II patients before treatment when compared to controls. Also, our results showed greater DNA damage in terms of damage index (DI) in pretreatment MPS II patients (DI=18.0 ± 2.4) when compared to controls (DI=66.0 ± 2.0). Enzyme replacement therapy led to a significant decrease in levels of malondialdehyde and DNA damage when compared to pretreatment, but did not reach control values. Significant positive correlations between DNA damage and malondialdehyde levels, as well as carbonyl group content, were observed. Our findings indicate that MPS II patients are subject to DNA damage and that enzyme replacement therapy is able to protect against this process.

  17. L-carnitine pretreatment protects slow-twitch skeletal muscles in a rat model of ischemia-reperfusion injury.

    PubMed

    Demirel, Mert; Kaya, Burak; Cerkez, Cem; Ertunc, Mert; Sara, Yildirim

    2013-10-01

    Ischemia-reperfusion (I/R) injury negatively affects the outcome of surgical interventions for amputated or severely traumatized extremities. This study aimed to evaluate the protective role of l-carnitine on the contractile properties of fast-twitch (extensor digitorum longus [EDL]) and slow-twitch (soleus [SOL]) skeletal muscles following I/R-induced injury in a rat model. Rats were divided into 4 groups (1) saline pretreatment, (2) l-carnitine pretreatment, (3) saline pretreatment and I/R, and (4) l-carnitine pretreatment and I/R. Twitch and tetanic contractions in the EDL and SOL muscles in each group were recorded. Additionally, a fatigue protocol was performed in these muscles. Twitch and tetanic contraction amplitudes were lower in the EDL and SOL muscles in which I/R was induced (P < .01). l-Carnitine pretreatment significantly increased tetanic contraction amplitude in the SOL muscles following I/R (P < .01) but not in the EDL muscles. l-Carnitine pretreatment did not alter the fatigue response in any of the muscles.

  18. 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

  19. Protective Effect of Eupatilin Pretreatment Against Hepatic Ischemia-Reperfusion Injury in Mice.

    PubMed

    Lee, H M; Jang, H J; Kim, S S; Kim, H J; Lee, S Y; Oh, M Y; Kwan, H C; Jang, D S; Eom, D W

    2016-05-01

    Eupatilin, a pharmacologically active flavone derived from Artemisia species, is known to have antioxidant and antiinflammatory activities. Ischemia-reperfusion injury (IRI) is a major critical event that commonly occurs after liver transplantation and resection. Furthermore, inflammatory responses to IRI exacerbate the resultant hepatic injury. In this study, we investigated whether eupatilin protects against IR-induced acute liver injury in mice. Partial (70%) hepatic IRI was induced in male C57BL/6 mice by portal triad pedicle occlusion for 90 minutes followed by reperfusion for 6 hours. Eupatilin (10 mg/kg body weight, oral) was administered 4 days before the IRI. Treatment with eupatilin significantly decreased serum alanine aminotransferase and serum aspartate aminotransferase as well as liver histologic changes. Eupatilin also prevented hepatic glutathione depletion and increased malondialdehyde levels induced by IRI. Western blotting indicated that eupatilin significantly increased the levels of heat shock protein and B-cell lymphoma 2 protein, attenuated inducible nitric oxide synthase, and cleaved caspase-3 levels 6 hours after IRI. The expression of the Toll-like receptor 2/4, and phosphorylated nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor was significantly decreased in the eupatilin pretreatment group. Eupatilin improved the acute hepatic IRI by reducing inflammation and apoptosis. These findings suggest that eupatilin is a promising therapeutic agent against acute IR-induced hepatic damage. Copyright © 2016 Elsevier Inc. All rights reserved.

  20. Carnosine pretreatment protects against hypoxia-ischemia brain damage in the neonatal rat model.

    PubMed

    Zhang, Xiangmin; Song, Lili; Cheng, Xiuyong; Yang, Yi; Luan, Bin; Jia, Liting; Xu, Falin; Zhang, Zhan

    2011-09-30

    Perinatal hypoxia-ischemia brain injury is a major cause of mortality and morbidity in neonates and lacks an effective treatment thus far. Carnosine has been demonstrated to play a neuroprotective role in the adult brain injuries. However, there is no information available concerning its neuroprotective role in the immature brains after hypoxia-ischemia insults. Therefore, we investigated whether carnosine could also confer neuroprotective effects in a neonatal rat hypoxia-ischemia model. Hypoxia-ischemia was induced in rats on postnatal day 7 (P7). Carnosine (250 mg/kg) was administered intraperitoneally, 30 min prior to hypoxia-ischemia induction. Morphological brain injury and biochemical markers of apoptosis and oxidative stress were evaluated 24 h after hypoxia-ischemia induction. Cognitive performance was evaluated by the Morris Water Maze test on P28-P33. We found that pretreatment with carnosine significantly reduced the infarct volume and the number of terminal-deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL)-positive cells in the hypoxia-ischemia brain. Carnosine also inhibited mRNA expression of apoptosis-inducing factor(AIF) and caspase-3, which was accompanied by an increase in superoxide dismutase(SOD)activity and a decrease in the malondialdehyde(MDA)level in carnosine-treated rats. Furthermore, carnosine also improved the spatial learning and memory abilities of rats declined due to hypoxia-ischemia. These results demonstrate that carnosine can protect rats against hypoxia-ischemia-induced brain damage by antioxidation.

  1. Insulin pretreatment protects the liver from ischemic damage during Pringle's maneuver.

    PubMed

    Morimoto, Y; Nishida, T; Kamiike, W; Mizuno, H; Kazuo, H; Furuya, E; Matsuda, H

    1996-11-01

    Although maintenance of adenosine triphosphate (ATP) levels is important to restore liver functions during anoxia, ATP production by oxidative phosphorylation is inhibited during Pringle's maneuver, and only a little ATP can be supplied by glycolysis. The glycolytic activity of the liver is controlled by the nutritional condition and hormones. Enhancement of glycolytic activity by insulin may increase ATP production and thus may protect the liver from ischemia. Rats were divided into three groups: fasted group, food was withheld for 24 hours; fed group, food was provided ad libitum; and insulin group, fed rats were administered insulin (12 units/kg during a 30-minute period) before portal triad clamping (PTC) was performed. After laparotomy was performed, PTC was performed for 30 minutes. The fructose 2,6-bisphosphate (F-2,6-BP) level, the hepatic levels of lactate and ATP, the bile flow rate, the plasma levels of aspartate transaminase and lactate dehydrogenase, and the indocyanine green clearance were measured at appropriate times. The hepatic F-2,6-BP levels before PTC in the fasted, fed, and insulin groups were 6.2 +/- 3.8, 55.6 +/- 10.6, and 122.2 +/- 31.3 nmol/gm dry weight liver, respectively. The glycolytic activity of the insulin group before PTC was significantly enhanced compared with that of the other groups. Lactate was more rapidly accumulated in livers of the insulin group during PTC than in those of the other groups. The ATP level and energy charge during PTC of the insulin group were higher than those of the other groups. The bile flow rate and indocyanine green clearance after PTC were restored in the order of the insulin, fed, and fasted groups. Insulin administration before PTC increased the hepatic F-2,6-BP content and enhanced glycolytic activity. Insulin pretreatment combined with feeding improved the hepatic energy metabolism during PTC and restored the liver functions after PTC. Insulin has protective effects on the liver during PTC.

  2. Pretreatment with scutellaria baicalensis stem-leaf total flavonoid protects against cerebral ischemia/reperfusion injury in hippocampal neurons

    PubMed Central

    Kong, Xiangyu; Kong, Wei; Miao, Guangxin; Zhao, Shumin; Chen, Meng; Zheng, Xiaoying; Bai, Jiangtao

    2014-01-01

    Previous experimental studies have shown that cerebral infarction can be effectively reduced following treatment with scutellaria baicalensis stem-leaf total flavonoid (SSTF). However, the mechanism of action of SSTF as a preventive drug to treat cerebral infarction remains unclear. In this study, Sprague-Dawley rats were pretreated with 50, 100, 200 mg/kg SSTF via intragastric administration for 1 week prior to the establishment of focal cerebral ischemia/reperfusion injury. The results showed that pretreatment with SSTF effectively improved neurological function, reduced brain water content and the permeability of blood vessels, ameliorated ischemia-induced morphology changes in hippocampal microvessels, down-regulated Fas and FasL protein expression, elevated the activity of superoxide dismutase and glutathione peroxidase, and decreased malondialdehyde content. In contrast to low-dose SSTF pretreatment, the above changes were most obvious after pretreatment with moderate- and high-doses of SSTF. Experimental findings indicate that SSTF pretreatment can exert protective effects on the brain against cerebral ischemia/reperfusion injury. The underlying mechanisms may involve reducing brain water content, increasing microvascular recanalization, inhibiting the apoptosis of hippocampal neurons, and attenuating free radical damage. PMID:25657723

  3. Antioxidative Peptides Derived from Enzyme Hydrolysis of Bone Collagen after Microwave Assisted Acid Pre-Treatment and Nitrogen Protection

    PubMed Central

    Lin, Yun-Jian; Le, Guo-Wei; Wang, Jie-Yun; Li, Ya-Xin; Shi, Yong-Hui; Sun, Jin

    2010-01-01

    This study focused on the preparation method of antioxidant peptides by enzymatic hydrolysis of bone collagen after microwave assisted acid pre-treatment and nitrogen protection. Phosphoric acid showed the highest ability of hydrolysis among the four other acids tested (hydrochloric acid, sulfuric acid and/or citric acid). The highest degree of hydrolysis (DH) was 9.5% using 4 mol/L phosphoric acid with a ratio of 1:6 under a microwave intensity of 510 W for 240 s. Neutral proteinase gave higher DH among the four protease tested (Acid protease, neutral protease, Alcalase and papain), with an optimum condition of: (1) ratio of enzyme and substrate, 4760 U/g; (2) concentration of substrate, 4%; (3) reaction temperature, 55 °C and (4) pH 7.0. At 4 h, DH increased significantly (P < 0.01) under nitrogen protection compared with normal microwave assisted acid pre-treatment hydrolysis conditions. The antioxidant ability of the hydrolysate increased and reached its maximum value at 3 h; however DH decreased dramatically after 3 h. Microwave assisted acid pre-treatment and nitrogen protection could be a quick preparatory method for hydrolyzing bone collagen. PMID:21151439

  4. Antioxidative peptides derived from enzyme hydrolysis of bone collagen after microwave assisted acid pre-treatment and nitrogen protection.

    PubMed

    Lin, Yun-Jian; Le, Guo-Wei; Wang, Jie-Yun; Li, Ya-Xin; Shi, Yong-Hui; Sun, Jin

    2010-11-01

    This study focused on the preparation method of antioxidant peptides by enzymatic hydrolysis of bone collagen after microwave assisted acid pre-treatment and nitrogen protection. Phosphoric acid showed the highest ability of hydrolysis among the four other acids tested (hydrochloric acid, sulfuric acid and/or citric acid). The highest degree of hydrolysis (DH) was 9.5% using 4 mol/L phosphoric acid with a ratio of 1:6 under a microwave intensity of 510 W for 240 s. Neutral proteinase gave higher DH among the four protease tested (Acid protease, neutral protease, Alcalase and papain), with an optimum condition of: (1) ratio of enzyme and substrate, 4760 U/g; (2) concentration of substrate, 4%; (3) reaction temperature, 55 °C and (4) pH 7.0. At 4 h, DH increased significantly (P < 0.01) under nitrogen protection compared with normal microwave assisted acid pre-treatment hydrolysis conditions. The antioxidant ability of the hydrolysate increased and reached its maximum value at 3 h; however DH decreased dramatically after 3 h. Microwave assisted acid pre-treatment and nitrogen protection could be a quick preparatory method for hydrolyzing bone collagen.

  5. Protection of rhesus monkeys against Soman and prevention of performance decrement by pretreatment with acetylcholinesterase. (Reannouncement with new availability information)

    SciTech Connect

    Maxwell, D.M.; Castro, C.A.; De La Hoz, D.M.; Gentry, M.K.; Gold, M.B.

    1992-12-31

    The ability of acetylcholinesterase from fetal bovine serum (FBS AChE) to protect against soman, a highly toxic organophosphorus (OP) compound, was tested in rhesus monkeys. Intravenous administration of FBS AChE produced a minimal behavioral effect on the serial probe recognition task, a sensitive test of cognitive function and short-term memory. Pharmacokinetic studies of injected FBS AChE indicated a plasma half-life of 40 hr for FBS AChE in monkeys. Both in vitro and in vivo titration of FBS AChE with soman produced a 1:1 stoichiometry between organophosphate-inhibited FBS AChE and the cumulative dose of the toxic stereoisomers of soman. Administration of FBS AChE protected monkeys against the lethal effects of up to 2.7 LD50 of soman and prevented any signs of organophosphate intoxication, e.g., excessive secretions, respiratory depression, muscle fasciculations, or convulsions. In addition, monkeys pretreated with FBS AChE were devoid of any behavioral incapacitation after soman challenge, as measured by the serial probe recognition task. Compared to the current multicomponent drug treatment against soman, which does not prevent the signs or the behavioral deficits resulting from OP intoxication, use of FBS AChE as a single pretreatment drug provides significantly effective protection against both the lethal and the behavioral effects of soman.... Pretreatment, Nonhuman primate, Performance decrements, Acetylcholinesterase, Soman, Nerve agents.

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

    PubMed

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

    2016-10-12

    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.

  7. Hyperbaric Oxygen Preconditioning Attenuates Myocardium Ischemia-Reperfusion Injury Through Upregulation of Heme Oxygenase 1 Expression: PI3K/Akt/Nrf2 Pathway Involved.

    PubMed

    Yin, Xuesong; Wang, Xiaofeng; Fan, Zhixin; Peng, Chenghai; Ren, Zhongqiao; Huang, Le; Liu, Zhuang; Zhao, Kan

    2015-07-01

    With the rise of the burden of ischemic heart disease, both clinical and economic evidence show a desperate need to protect the heart against myocardium ischemia-reperfusion injury-related complications following cardiac surgery or percutaneous coronary intervention. However, there is no effective intervention for myocardium ischemia-reperfusion injury as yet. We pretreated mice with 4 daily 2.0 absolute atmosphere (ATA) hyperbaric oxygen, then observed its effects on heart function parameters and infarct size following in situ ischemia-reperfusion. Multiple oxidative and inflammation products were measured in the myocardium. Next, we investigated the expression of heme oxygenase 1 (HO-1), phosphatidylinositol 3-kinase (PI3K)/serine/threonine protein kinase (Akt) pathway, and NF-E2-related factor 2 (Nrf2) in the presence of myocardium ischemia-reperfusion injury, hyperbaric oxygen preconditioning, and their inhibitors and their effects on heart function parameters. Hyperbaric oxygen preconditioning ameliorated the cardiac function and histological alterations induced by myocardium ischemia-reperfusion injury, decreased oxidative products and proinflammatory cytokine. Hyperbaric oxygen preconditioning increased expression of HO-1, which was suppressed by PI3K inhibitor LY294002, Nrf2 knockout, and Akt inhibitor triciribine. The expression of Nrf2 was enhanced by hyperbaric oxygen preconditioning, but decreased by LY294002 and triciribine. The Akt was also activated by hyperbaric oxygen preconditioning but suppressed by LY294002. The hemodynamic assays showed that cardiac function was suppressed by LY294002, Nrf2 knockout, and triciribine. These data present a novel signaling mechanism by which hyperbaric oxygen preconditioning protects myocardium ischemia-reperfusion injury via PI3K/Akt/Nrf2-dependent antioxidant defensive system. © The Author(s) 2015.

  8. Amiodarone pretreatment of organ donors exerts anti-oxidative protection but induces excretory dysfunction in liver preservation and reperfusion.

    PubMed

    Moussavian, Mohammed Reza; Kollmar, Otto; Schmidt, Michael; Scheuer, Claudia; Wagner, Matthias; Slotta, Jan Erik; Gronow, Gernot; Justinger, Christoph; Menger, Michael Dieter; Schilling, Martin Karl

    2009-07-01

    The continuous shortage of organs necessitates the use of marginal organs from donors with various diseases, including arrhythmia-associated cardiac failure. One of the most frequently used anti-arrhythmic drugs is amiodarone (AM), which is given in particular in emergency situations. Apart from its anti-arrhythmic actions, AM provides anti-oxidative properties in cardiomyocytes. Thus, we were interested in whether AM donor pretreatment affects the organ quality and function of livers procured for preservation and transplantation. Donor rats were pretreated with AM (5 mg/kg of body weight) 10 minutes before flush-out of the liver with a cold (4 degrees C) histidine-tryptophan-ketoglutarate solution (n = 8). Livers were then stored for 24 hours at 4 degrees C before ex situ reperfusion with a 37 degrees C Krebs-Henseleit solution for 60 minutes in a nonrecirculating system. At the end of reperfusion, tissue samples were taken for histology and Western blot analysis. Animals with vehicle only (0.9% NaCl) served as ischemia/reperfusion controls (n = 8). Additionally, livers of untreated animals (n = 8) not subjected to 24 hours of cold ischemia served as sham controls. AM pretreatment effectively attenuated lipid peroxidation, stress protein expression, and apoptotic cell death. This was indicated by an AM-mediated reduction of malondialdehyde, heme oxygenase-1, and caspase-3 activation. However, AM treatment also induced mitochondrial damage and hepatocellular excretory dysfunction, as indicated by a significantly increased glutamate dehydrogenase concentration in the effluate and decreased bile production. In conclusion, AM donor pretreatment exerts anti-oxidative actions in liver preservation and reperfusion. However, these protective AM actions are counteracted by an induction of mitochondrial damage and hepatocellular dysfunction. Accordingly, AM pretreatment of donors for anti-arrhythmic therapy should be performed with caution.

  9. [Neurogenic stunned myocardium].

    PubMed

    Ruiz Bailén, M; Rucabado Aguilar, L; López Martínez, A

    2006-01-01

    The existence of stunned myocardium and reversible myocardial dysfunction is widely described and accepted in patients suffering ischemic heart disease. However, it cannot be exclusive to coronary disease. Classically, the appearance of electrocardiographic changes in the critical neurological disease has been described. However, at present, it seems to be observed that some of these patients with critical neurological disease could have variable grades of myocardial dysfunction, which is generally reversible in the surviving patients. This myocardial dysfunction, which could affect critically ill neurological patients, has traits similar to stunned myocardium generated in coronary patients since: a) it is generally associated to electrocardiographic changes, b) it can be accompanied by segmental contractility disorders and even c) it may be accompanied by a certain increase of cardiac biomarkers. Although its etiopathogeny is unknown, it could be related with the severity of the primary neurological disease. Its prophylaxis and prognosis are also unknown. It could be related with neurogenic edema, with hemodynamic instability, and could also play a very important role in brain death and in organ donation.

  10. Donor pretreatment with adenosine monophosphate-activated protein kinase activator protects cardiac grafts from cold ischaemia/reperfusion injury.

    PubMed

    Yang, Chao; Xu, Honglai; Cai, Lanjun; Du, Xiaoxiao; Jiang, Yinan; Zhang, Yong; Zhou, Hongmin; Chen, Zhonghua Klaus

    2016-05-01

    Adenosine monophosphate-activated protein kinase (AMPK) is a master regulator of energy metabolism and has been shown to be protective in ischaemia/reperfusion injury (IRI). We hypothesized that preactivation of AMPK with an activator before donor heart procurement could protect heart grafts from cold IRI. Donor Sprague-Dawley rats were injected intravenously with AMPK activator 5-amino-imidazole-4-carboxamide ribonucleotide (AICAR) or vehicle 30 min before heart procurement. Heart grafts were then preserved in histidine-tryptophan-ketoglutarate (HTK) solution at 4°C for 8 h. After preservation, grafts were immediately mounted on the Langendorff perfusion system and perfused with Krebs-Henseleit buffer at 37°C for 1 h. Adenosine triphosphate (ATP) and malondialdehyde (MDA) content in graft tissue were quantified post-preservation and post-reperfusion. After reperfusion, isolated heart function was assessed using a pressure transducer; cumulative release of creatine kinase (CK) and lactate dehydrogenase (LDH) into the perfusate was measured to assess cardiomyocyte necrosis; ultrastructural changes in the mitochondria of the grafts were examined using transmission electron microscopy (TEM). After preservation, myocardial ATP content in the pretreated hearts was significantly higher than in the control hearts (3.247 ± 0.3034 vs 1.817 ± 0.2533 µmol/g protein; P < 0.05). AICAR-pretreated heart grafts exhibited significantly higher coronary flow (9.667 ± 0.3159 vs 8.033 ± 0.2459 ml/min; P < 0.05) and left ventricular developing pressure (58.67 ± 2.894 vs 42.67 ± 3.333 mmHg; P < 0.05) than the vehicle treated after reperfusion. Cumulative release of CK (300.0 ± 25.30 vs 431.7 ± 42.39 U/l; P < 0.05) and LDH (228.0 ± 16.68 vs 366.8 ± 57.41 U/l; P < 0.05) in the perfusate was significantly lower in the AICAR-pretreated group than that in the control group. Myocardial MDA content was also reduced in the pretreated group (0.5167 ± 0.1046 vs 0.9333 ± 0.1333 nmol

  11. 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.

  12. 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. © 2014 Society for the Study of Addiction.

  13. 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

  14. Noble gases without anesthetic properties protect myocardium against infarction by activating prosurvival signaling kinases and inhibiting mitochondrial permeability transition in vivo.

    PubMed

    Pagel, Paul S; Krolikowski, John G; Shim, Yon Hee; Venkatapuram, Suneetha; Kersten, Judy R; Weihrauch, Dorothee; Warltier, David C; Pratt, Phillip F

    2007-09-01

    The anesthetic noble gas, xenon, produces cardioprotection. We hypothesized that other noble gases without anesthetic properties [helium (He), neon (Ne), argon (Ar)] also produce cardioprotection, and further hypothesized that this beneficial effect is mediated by activation of prosurvival signaling kinases [including phosphatidylinositol-3-kinase, extracellular signal-regulated kinase, and 70-kDa ribosomal protein s6 kinase] and inhibition of mitochondrial permeability transition pore (mPTP) opening in vivo. Rabbits (n = 98) instrumented for hemodynamic measurement and subjected to a 30-min left anterior descending coronary artery (LAD) occlusion and 3 h reperfusion received 0.9% saline (control), three cycles of 70% He-, Ne-, or Ar-30% O2 administered for 5 min interspersed with 5 min of 70% N2-30% O2 before LAD occlusion, or three cycles of brief (5 min) ischemia interspersed with 5 min reperfusion before prolonged LAD occlusion and reperfusion (ischemic preconditioning). Additional groups of rabbits received selective inhibitors of phosphatidylinositol-3-kinase (wortmannin; 0.6 mg/kg), extracellular signal-regulated kinase (PD 098059; 2 mg/kg), or 70-kDa ribosomal protein s6 kinase (rapamycin; 0.25 mg/kg) or mPTP opener atractyloside (5 mg/kg) in the absence or presence of He pretreatment. He, Ne, Ar, and ischemic preconditioning significantly (P < 0.05) reduced myocardial infarct size [23% +/- 4%, 20% +/- 3%, 22% +/- 2%, 17% +/- 3% of the left ventricular area at risk (mean +/- sd); triphenyltetrazolium chloride staining] versus control (45% +/- 5%). Wortmannin, PD 098059, rapamycin, and atractyloside alone did not affect infarct size, but these drugs abolished He-induced cardioprotection. The results indicate that noble gases without anesthetic properties produce cardioprotection by activating prosurvival signaling kinases and inhibiting mPTP opening in rabbits.

  15. Glibenclamide pretreatment protects against chronic memory dysfunction and glial activation in rat cranial blast traumatic brain injury.

    PubMed

    Stokum, Jesse A; Keledjian, Kaspar; Hayman, Erik; Karimy, Jason K; Pampori, Adam; Imran, Ziyan; Woo, Seung Kyoon; Gerzanich, Volodymyr; Simard, J Marc

    2017-08-30

    Blast traumatic brain injury (bTBI) affects both military and civilian populations, and often results in chronic deficits in cognition and memory. Chronic glial activation after bTBI has been linked with cognitive decline. Pharmacological inhibition of sulfonylurea receptor 1 (SUR1) with glibenclamide was shown previously to reduce glial activation and improve cognition in contusive models of CNS trauma, but has not been examined in bTBI. We postulated that glibenclamide would reduce chronic glial activation and improve long-term memory function after bTBI. Using a rat direct cranial model of bTBI (dc-bTBI), we evaluated the efficacy of two glibenclamide treatment paradigms: glibenclamide prophylaxis (pre-treatment), and treatment with glibenclamide starting after dc-bTBI (post-treatment). Our results show that dc-bTBI caused hippocampal astrocyte and microglial/macrophage activation that was associated with hippocampal memory dysfunction (rapid place learning paradigm) at 28days, and that glibenclamide pre-treatment, but not post-treatment, effectively protected against glial activation and memory dysfunction. We also report that a brief transient time-window of blood-brain barrier (BBB) disruption occurs after dc-bTBI, and we speculate that glibenclamide, which is mostly protein bound and does not normally traverse the intact BBB, can undergo CNS delivery only during this brief transient opening of the BBB. Together, our findings indicate that prophylactic glibenclamide treatment may help to protect against chronic cognitive sequelae of bTBI in warfighters and other at-risk populations. Copyright © 2017 Elsevier B.V. All rights reserved.

  16. Tert-Butylhydroquinone pretreatment protects kidney from ischemia-reperfusion injury.

    PubMed

    Guerrero-Beltrán, Carlos E; Tapia, Edilia; Sánchez-González, Dolores J; Martínez-Martínez, Claudia M; Cristobal-García, Magdalena; Pedraza-Chaverri, José

    2012-01-01

    It is generally accepted that an excessive production of reactive oxygen species plays an important role in acute renal failure secondary to ischemia and reperfusion. tert-Butylhydroquinone (tBHQ) is a well-known antioxidant. In this study, we evaluated whether tBHQ pretreatment prevented renal damage induced by ischemia and reperfusion (I/R). Four groups of rats were studied: (a) control-sham (CT), (b) tBHQ-sham (tBHQ), (c) I/R and (d) tBHQ + I/R. Intraperitoneal (i.p.) injections of tBHQ (50 mg/kg) were given to the tBHQ and tBHQ + I/R groups and 3% ethanol/isotonic saline solution to the CT and I/R groups. Animals were killed 24 hours after I/R. tBHQ attenuated I/R-induced renal dysfunction, structural damage, oxidative/nitrosative stress, glutathione depletion and the decrease in several antioxidant enzymes. The renoprotective effect of tBHQ on I/R injury was associated with the attenuation in oxidative/nitrosative stress and the preservation of antioxidant enzymes.

  17. 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.

  18. Effect of glutathion pretreatment on hypothermic ischemic cardioplegia.

    PubMed

    Amano, J; Sunamori, M; Okamura, T; Suzuki, A

    1982-01-01

    Glutathion (GSH) plays an important role in maintenance of the redox state of the myocardium and acts as the membrane stabilizer. Seventeen patients who underwent cardiac surgery were subjected to cardiopulmonary bypass (CPB) and ischemic cardioplegia. The effect of GSH on ischemic myocardium was evaluated by serum lysosomal enzymes (acid phosphatase, beta-glucuronidase), isoenzymes of creatine phosphokinase (MB-CPK) and aspartate aminotransferase (m-GOT). standard CPB was instituted and systemic hypothermia was employed. GSH was administered to 8 patients in a dose of 200 mg/kg i.v. prior to institution of CPB. Mixed venous blood was sampled before administration of GSH, 10 min after institution of CPB and 0, 1, 6, 24 and 48 hr of reperfusion period following cardioplegia. Activity of acid phosphatase and beta-glucuronidase were significantly suppressed in the GSH-treated group compared to the non-treated group at 24 hours of reperfusion and immediately after aortic unclamping, respectively. Serum MB-CPK levels remained stable during reperfusion, but in the non-treated group, the level increased significantly at 6 hours of reperfusion. Increment of serum m-GOT levels was significantly suppressed at 1, 6 and 24 hours of reperfusion, compared to the non-treated group. These data suggest that pretreatment of GSH can protect the myocardium subjected to CPB from ischemic insult.

  19. 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

  20. [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.

  1. Anoxia pretreatment protects soybean cells against H(2)O(2)-induced cell death: possible involvement of peroxidases and of alternative oxidase.

    PubMed

    Amora, Y; Chevionb, M; Levinea, A

    2000-07-21

    Anoxia followed by reoxygenation causes extensive damage to cellular components through generation of reactive oxygen intermediates. We examined cellular responses to oxidative stress after anoxia in cultured soybean or human fibroblast cells. Anoxia pretreatment protected soybean but not fibroblasts against H(2)O(2) concentrations that induced programmed cell death in normoxic cells. H(2)O(2) removal in anoxia-pretreated soybean cultures was faster. Protection was associated with increased action of alternative oxidase (AOX) and peroxidases. AOX inhibitors abolished the protective effect, while induction of AOX protected normoxic cells against H(2)O(2). We propose that during anoxia, plant cells can prepare for reoxygenation injury by up-regulating their antioxidant capacity, and that AOX is involved in this process.

  2. Pretreatment of Adipose Derived Stem Cells with Curcumin Facilitates Myocardial Recovery via Antiapoptosis and Angiogenesis.

    PubMed

    Liu, Jianfeng; Zhu, Ping; Song, Peng; Xiong, Weiping; Chen, Haixu; Peng, Wenhui; Wang, Shuxia; Li, Shan; Fu, Zhiqing; Wang, Yutang; Wang, Haibin

    2015-01-01

    The poor survival rate of transplanted stem cells in ischemic myocardium has limited their therapeutic efficacy. Curcumin has potent antioxidant property. This study investigates whether prior curcumin treatment protects stem cells from oxidative stress injury and improves myocardial recovery following cells transplantation. Autologous Sprague-Dawley rat adipose derived mesenchymal stem cells (ADSCs) were pretreated with or without curcumin. The hydrogen peroxide/serum deprivation (H2O2/SD) medium was used to mimic the ischemic condition in vitro. Cytoprotective effects of curcumin on ADSCs were evaluated. Curcumin pretreatment significantly increased cell viability and VEGF secretion, and decreased cell injury and apoptosis via regulation of PTEN/Akt/p53 and HO-1 signal proteins expression. The therapeutic potential of ADSCs implantation was investigated in myocardial ischemia-reperfusion injury (IRI) model. Transplantation of curcumin pretreated ADSCs not only resulted in better heart function, higher cells retention, and smaller infarct size, but also decreased myocardial apoptosis, promoted neovascularization, and increased VEGF level in ischemic myocardium. Together, priming of ADSCs with curcumin improved tolerance to oxidative stress injury and resulted in enhancement of their therapeutic potential of ADSCs for myocardial repair. Curcumin pretreatment is a promising adjuvant strategy for stem cells transplantation in myocardial restoration.

  3. Microleakage in Resin Composite Restoration following Antimicrobial Pre-treatments with 2% Chlorhexidine and Clearfil Protect Bond

    PubMed Central

    Hameed, Hisham; Babu, Biju P; Sagir, V M Mohammed; Chiriyath, Kennet J; Mathias, Jones; Shaji, A P

    2015-01-01

    Aim: To evaluate microleakage in resin composite restorations after antimicrobial pre – treatments Materials and Methods: Forty freshly extracted non carious human premolars were procured. In all forty premolar specimens, class V preparation of standard dimension were prepared and were randomly divided into three experimental and one control group. In all control and experimental groups the class V preparations were restored with FILTEK Z350 composite restorative material. The experimental groups included different self etching primers and 2% Chlorhexidine gluconate. The control group included Xeno III and no antimicrobial pre-treatment was done for the control group. Thereafter these specimens were thermocycled, dried and sealed with nail varnish, leaving 1mm around the restoration and immersed in 0.5% basic fuchsin for 24 hours and then the specimens were subjected for microleakage evaluation. The results were statistically analyzed by Kruskal Wallis Test and Mann Whitney ‘U’ test. Results: Results indicate that group II (2% chlorhexidine gluconate group) had the minimum mean value (15.05) and group III(Clearfil protect Bond group) and IV(control group) had the maximum mean microleakage at the enamel margin (23.00). At the gingival margin the lowest mean microleakage values were obtained with group I (Clearfil SE bond group) and group II (2% chlorhexidine gluconate) (20.25) and highest with group III and group IV (20.85). The difference was not statistically significant both at the enamel margin and the dentin margin (p>0.05). Interpretation & Conclusions: Within the limitations of this in-vitro study, we conclude that: None of the materials tested in this study completely eliminated microleakage at the enamel and at the gingival margin.All of the tested materials provided better sealing at the enamel margin than at the gingival margin. PMID:26229374

  4. 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.

  5. 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

  6. Examination of Spray-Applied Oxsilan 9810/2 Steel Pretreatment on a Mine Resistant Ambush Protected (MRAP) Vehicle

    DTIC Science & Technology

    2013-10-01

    HHA, MRAP, steel pretreatments 16. SECURITY CLASSIFICATION OF: 17. LIMITATION OF ABSTRACT UU 18. NUMBER OF PAGES 28 19a. NAME OF...a limited scope. The MRAP PMO has agreed to provide one set of two rear doors off of an MRAP variant for pretreatment using Oxsilan 9810/2. The...Primer, Epoxy Coating, Corrosion Inhibiting, Lead and Chromate Free, U.S. Department of Defense, Washington DC, January 2007. 4. MIL-DTL-53030C

  7. Pretreated quercetin protects gerbil hippocampal CA1 pyramidal neurons from transient cerebral ischemic injury by increasing the expression of antioxidant enzymes

    PubMed Central

    Chen, Bai Hui; Park, Joon Ha; Ahn, Ji Hyeon; Cho, Jeong Hwi; Kim, In Hye; Lee, Jae Chul; Won, Moo-Ho; Lee, Choong-Hyun; Hwang, In Koo; Kim, Jong-Dai; Kang, Il Jun; Cho, Jun Hwi; Shin, Bich Na; Kim, Yang Hee; Lee, Yun Lyul; Park, Seung Min

    2017-01-01

    Quercetin (QE; 3,5,7,3′,4′-pentahydroxyflavone), a well-known flavonoid, has been shown to prevent against neurodegenerative disorders and ischemic insults. However, few studies are reported regarding the neuroprotective mechanisms of QE after ischemic insults. Therefore, in this study, we investigated the effects of QE on ischemic injury and the expression of antioxidant enzymes in the hippocampal CA1 region of gerbils subjected to 5 minutes of transient cerebral ischemia. QE was pre-treated once daily for 15 days before ischemia. Pretreatment with QE protected hippocampal CA1 pyramidal neurons from ischemic injury, which was confirmed by neuronal nuclear antigen immunohistochemistry and Fluoro-Jade B histofluorescence staining. In addition, pretreatment with QE significantly increased the expression levels of endogenous antioxidant enzymes Cu/Zn superoxide dismutase, Mn superoxide dismutase, catalase and glutathione peroxidase in the hippocampal CA1 pyramidal neurons of animals with ischemic injury. These findings demonstrate that pretreated QE displayed strong neuroprotective effects against transient cerebral ischemia by increasing the expression of antioxidant enzymes. PMID:28400803

  8. [Protective effects of sufentanil pretreatment against acute gastric mucosal lesion in rats and its relationship with acid-sensing ion channels].

    PubMed

    Jiang, Qun; Tu, Wei-feng

    2010-05-01

    To investigate the effects of sufentanil pretreatment on acute gastric mucosal lesion and its impact on the expression of acid-sensing ion channel 3 (ASIC3) in thoracic dorsal root ganglia (DRG) neurons in rats with water immersion-restraint stress (WIRS). Twenty-four Wistar rats were randomly assigned into 3 groups, namely the normal control group (n=6), WIRS group (n=12) and sufentanil pretreatment group (n=6). Gastric mucosal lesion was induced by WIRS, and after 6 h of WIRS, the gastric tissues were excised and observed under microscope, with the ulcer index (UI) calculated. The expression of ASIC3 in the DRG neurons was detected by immunofluorescence assay, and the ASIC3 mRNA expression by quantitative real-time RT-PCR. Compared with the normal control group, the rats in the WIRS group showed obvious gastric injury with increased UI and extensive expression of ASIC3 in the DRG neurons. Sufentanil pretreatment of the rats subjected to WIRS significantly alleviated the gastric mucosal injury, lowered the UI, and reduced ASIC3 mRNA expression in thoracic DRG neurons. ASIC3 is involved in the development of acute gastric mucosal lesion, and sufentanil pretreatment offers protection of gastric mucosa by inhibiting the expression of ASIC3.

  9. 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. Copyright © 2016. Published by Elsevier Taiwan.

  10. 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.

  11. Hypoxia pretreatment and EPO-modification enhance the protective effects of MSC on neuron-like PC12 cells in a similar way.

    PubMed

    Feng, Jinli; Wang, Wei

    2017-01-08

    Mesenchymal stem cells (MSC) based cell transplantation therapy is proved to be an attractive strategy with great potential for improvement of hypoxia induced neural damage. In the present study, MSCs were co-culture with PC12 to investigate its protective effects against hypoxia pretreatment, and the Lactate dehydrogenase (LDH) release assay, MTT and Anexin V staining were performed to analysis the cellular damage or apoptotic. RT-PCR and Western blotting were further used to investigate the underlying mechanism. The results indicate that hypoxia treatment results in the decrease of PC12 cell viability, yet co-culture with MSC could protect the PC12 from hypoxia induced damage. Hypoxia pre-activated or EPO transduced MSC with up-regulated erythropoietin (EPO) expression could further enhance MSC's protective effect against hypoxia induced cell damage, which was associated with high level of anti-apoptotic p-Akt and ration Bcl-2/Bax, and decreased Caspase 3 in PC12. Taken together, these data suggests high levels of MSC-mediated cyto-protection is closely tied to high gene expression levels of EPO. The up-regulation of EPO for enhanced MSC-mediated cyto-protection may has great potential for the MSC cellular therapy of neural or neuronal injuries induced by hypoxia. Copyright © 2016 Elsevier Inc. All rights reserved.

  12. Prophylactic pretreatment of mice with hematopoietic growth factors induces expansion of primitive cell compartments and results in protection against 5-fluorouracil-induced toxicity.

    PubMed

    de Haan, G; Donte, B; Engel, C; Loeffler, M; Nijhof, W

    1996-06-01

    second dose of 5-FU given respectively after 7 or 10 days. To assess whether chemoprotection in this setting could be ascribed to protection of the hematopoietic system, we transplanted a high number of normal bone marrow cells (sufficient to compensate for any hematopoietic deficiency) to normal and pretreated mice after they had been administered 2 doses of 5-FU, given 7 days apart. Bone marrow transplantation (BMT) could only rescue 50% of mice not pretreated, showing that a significant part of the mortality was because of nonhematologic toxicity. However, a BMT given to growth factor pretreated mice saved all mice, indicating that in this setting SCF + IL-11 had additional protective effects on cell systems other than hematopoiesis. In conclusion, our study showed fundamental knowledge about the behavior of primitive cells in vivo and has shown that manipulation of these and other cell compartments with appropriate growth factors may confer resistance against cytotoxic drugs.

  13. Spirulina maxima pretreatment partially protects against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine neurotoxicity.

    PubMed

    Chamorro, Germán; Pérez-Albiter, Mónica; Serrano-García, Norma; Mares-Sámano, José J; Rojas, Patricia

    2006-01-01

    Spirulina is an alga that has a high nutritional value and some of its biological activities are attributed to the presence of antioxidants. Oxidative stress is involved in Parkinson's disease. This study aims at evaluating the neuroprotective role of Spirulina maxima (Sp.) against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) neurotoxicity, used as a model of Parkinson's disease. Ninety-six male C-57 black mice were pretreated with Spirulina for 14 days (25, 50, 100, 150 or 200 mg/kg, oral), followed by three MPTP administrations (30 mg/kg, intraperitoneal, i.p.). Animals were given Sp. for 8 additional days. After the treatment, the striatal dopamine (DA) content was analysed by high performance liquid chromatography, and lipid peroxidation was studied as an index of oxidative stress. Sp. pretreatment at 150 mg/kg partially prevented (51%) the DA-depleting effect of MPTP and blocked oxidative stress. Spirulina partially prevents MPTP neurotoxicity and oxidative stress, suggesting it could be a possible alternative in experimental therapy.

  14. [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.

  15. 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

  16. 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

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

    PubMed

    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 30mg/kg orally for two weeks, starting one week before giving a single nephrotoxic dose of cisplatin (7mg/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

  18. 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).

  19. Lime pretreatment.

    PubMed

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

    2009-01-01

    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 degrees C, and can be applied with or without oxygen (pressure approximately 200 psig); (2) long-term pretreatment taking up to 8 weeks, requiring only 55-65 degrees 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 approximately 18% lignin), whereas oxidative conditions are required for high lignin contents (above approximately 18% lignin).

  20. Gypenosides pre-treatment protects the brain against cerebral ischemia and increases neural stem cells/progenitors in the subventricular zone.

    PubMed

    Wang, Xiao-Jing; Sun, Tao; Kong, Liang; Shang, Zhen-Hua; Yang, Kun-Qi; Zhang, Qing-Yu; Jing, Fang-Miao; Dong, Lun; Xu, Xu-Feng; Liu, Jia-Xin; Xin, Hua; Chen, Zhe-Yu

    2014-04-01

    Gypenosides (GPs) have been reported to have neuroprotective effects in addition to other bioactivities. The protective activity of GPs during stroke and their effects on neural stem cells (NSCs) in the ischemic brain have not been fully elucidated. Here, we test the effects of GPs during stroke and on the NSCs within the subventricular zone (SVZ) of middle cerebral artery occlusion (MCAO) rats. Our results show that pre-treatment with GPs can reduce infarct volume and improve motor function following MCAO. Pre-treatment with GPs significantly increased the number of BrdU-positive cells in the ipsilateral and contralateral SVZ of MCAO rats. The proliferating cells in both sides of the SVZ were glial fibrillary acidic protein (GFAP)/nestin-positive type B cells and doublecortin (DCX)/nestin-positive type A cells. Our data indicate that GPs have neuroprotective effects during stroke which might be mediated through the enhancement of neurogenesis within the SVZ. These findings provide new evidence for a potential therapy involving GPs for the treatment of stroke.

  1. Angiogenesis in the Infarcted Myocardium

    PubMed Central

    Cochain, Clement; Channon, Keith M.

    2013-01-01

    Abstract Significance: Proangiogenic therapy appeared a promising strategy for the treatment of patients with acute myocardial infarction (MI), as de novo formation of microvessels, has the potential to salvage ischemic myocardium at early stages after MI, and is also essential to prevent the transition to heart failure through the control of cardiomyocyte hypertrophy and contractility. Recent Advances: Exciting preclinical studies evaluating proangiogenic therapies for MI have prompted the initiation of numerous clinical trials based on protein or gene transfer delivery of growth factors and administration of stem/progenitor cells, mainly from bone marrow origin. Nonetheless, these clinical trials showed mixed results in patients with acute MI. Critical Issues: Even though methodological caveats, such as way of delivery for angiogenic growth factors (e.g., protein vs. gene transfer) and stem/progenitor cells or isolation/culture procedure for regenerative cells might partially explain the failure of such trials, it appears that delivery of a single growth factor or cell type does not support angiogenesis sufficiently to promote cardiac repair. Future Directions: Optimization of proangiogenic therapies might include stimulation of both angiogenesis and vessel maturation and/or the use of additional sources of stem/progenitor cells, such as cardiac progenitor cells. Experimental unraveling of the mechanisms of angiogenesis, vessel maturation, and endothelial cell/cardiomyocyte cross talk in the ischemic heart, analysis of emerging pathways, as well as a better understanding of how cardiovascular risk factors impact endogenous and therapeutically stimulated angiogenesis, would undoubtedly pave the way for the development of novel and hopefully efficient angiogenesis targeting therapeutics for the treatment of acute MI. Antioxid. Redox Signal. 18, 1100–1113. PMID:22870932

  2. 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.

  3. 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

  4. Immunomodulatory pretreatment with Kalanchoe pinnata extract and its quercitrin flavonoid effectively protects mice against fatal anaphylactic shock.

    PubMed

    Cruz, E A; Da-Silva, S A G; Muzitano, M F; Silva, P M R; Costa, S S; Rossi-Bergmann, B

    2008-12-10

    Previously, we reported the immunosuppressive action of the aqueous extract of Kalanchoe pinnata (Kp) in mice. In the present study, we report on the protective effect of Kp in fatal anaphylactic shock, likewise a Th2-driven immunopathology, and the identification of its active component. Mice daily treated with oral Kp during hypersensitization with ovalbumin were all protected against death when challenged with the allergen, as compared with the 100% mortality in the untreated group. A single intraperitoneal dose 3 h prior to challenge was partially effective. Oral protection was accompanied by a reduced production of OVA-specific IgE antibodies, reduced eosinophilia, and impaired production of the IL-5, IL-10 and TNF-alpha cytokines. In vitro, Kp prevented antigen-induced mast cell degranulation and histamine release. Oral treatment with the quercitrin flavonoid isolated from Kp prevented fatal anaphylaxis in 75% of the animals. These findings indicate that oral treatment with Kp effectively downmodulates pro-anaphylactic inducing immune responses. Protection achieved with quercitrin, although not maximal, suggests that this flavonoid is a critical component of Kp extract against this extreme allergic reaction.

  5. 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.

  6. Involvement of protein kinase C in the delayed cytoprotection following sublethal ischaemia in rabbit myocardium.

    PubMed Central

    Baxter, G. F.; Goma, F. M.; Yellon, D. M.

    1995-01-01

    Rabbit hearts were preconditioned with four 5 min coronary artery occlusions 24 h before 30 min coronary occlusion with 120 min reperfusion. Preconditioning significantly reduced the percentage of myocardium infarcting within the risk zone from 49.1 +/- 4.3% to 31.8 +/- 3.5% (P < 0.05). When the protein kinase C (PKC) inhibitor, chelerythrine, was administered just before preconditioning, the delayed protection against infarction 24 h later was abolished. We conclude that the delayed cytoprotective response associated with ischaemic preconditioning of myocardium is likely to involve the early activation of one or more PKC subtypes. PMID:7545515

  7. Acute Pre-/Post-Treatment with 8th Day SOD-Like Supreme (a Free Radical Scavenging Health Product) Protects against Oxidant-Induced Injury in Cultured Cardiomyocytes and Hepatocytes In Vitro as Well as in Mouse Myocardium and Liver In Vivo.

    PubMed

    Leong, Pou Kuan; Chen, Jihang; Chan, Wing Man; Leung, Hoi Yan; Chan, Lincoln; Ko, Kam Ming

    2017-04-10

    8th Day superoxide dismutase (SOD)-Like Supreme (SOD-Like Supreme, a free radical scavenging health product) is an antioxidant-enriched fermentation preparation with free radical scavenging properties. In the present study, the cellular/tissue protective actions of SOD-Like Supreme against menadione toxicity in cultured H9c2 cardiomyocytes and in AML12 hepatocytes as well as oxidant-induced injury in the mouse myocardium and liver were investigated. SOD-Like Supreme was found to possess potent free radical scavenging activity in vitro as assessed by an oxygen radical absorbance capacity assay. Incubation with SOD-Like Supreme (0.5-3% (v/v)) was shown to protect against menadione-induced toxicity in H9c2 and AML12 cells, as evidenced by increases in cell viability. The ability of SOD-Like Supreme to protect against menadione cytotoxicity was associated with an elevation in the cellular reduced glutathione (GSH)/oxidized glutathione (GSSG) ratio in menadione-challenged cells. Consistent with the cell-based studies, pre-/post-treatment with SOD-Like Supreme (0.69 and 2.06 mL/kg, three intermittent doses per day for two consecutive days) was found to protect against isoproterenol-induced myocardial injury and carbon tetrachloride hepatotoxicity in mice. The cardio/hepatoprotection afforded by SOD-Like Supreme was also paralleled by increases in myocardial/hepatic mitochondrial GSH/GSSG ratios in the SOD-Like Supreme-treated/oxidant-challenged mice. In conclusion, incubation/treatment with SOD-Like Supreme was found to protect against oxidant-induced injury in vitro and in vivo, presumably by virtue of its free radical scavenging activity.

  8. 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.

  9. Periodic 17β-estradiol pretreatment protects rat brain from cerebral ischemic damage via estrogen receptor-β.

    PubMed

    Raval, Ami P; Borges-Garcia, Raquel; Javier Moreno, William; Perez-Pinzon, Miguel A; Bramlett, Helen

    2013-01-01

    Although chronic 17β-estradiol (E2) has been shown to be a cognition-preserving and neuroprotective agent in animal brain injury models, concern regarding its safety was raised by the failed translation of this phenomenon to the clinic. Previously, we demonstrated that a single bolus of E2 48 hr prior to ischemia protected the hippocampus from damage in ovariectomized rats via phosphorylation of cyclic-AMP response element binding protein, which requires activation of estrogen receptor subtype beta (ER-β). The current study tests the hypothesis that long-term periodic E2-treatment improves cognition and reduces post-ischemic hippocampal injury by means of ER-β activation. Ovariectomized rats were given ten injections of E2 at 48 hr intervals for 21 days. Hippocampal-dependent learning, memory and ischemic neuronal loss were monitored. Results demonstrated that periodic E2 treatments improved spatial learning, memory and ischemic neuronal survival in ovariectomized rats. Additionally, periodic ER-β agonist treatments every 48 hr improved post-ischemic cognition. Silencing of hippocampal ER-β attenuated E2-mediated ischemic protection suggesting that ER-β plays a key role in mediating the beneficial effects of periodic E2 treatments. This study emphasizes the need to investigate a periodic estrogen replacement regimen to reduce cognitive decline and cerebral ischemia incidents/impact in post-menopausal women.

  10. Periodic 17β-Estradiol Pretreatment Protects Rat Brain from Cerebral Ischemic Damage via Estrogen Receptor-β

    PubMed Central

    Raval, Ami P.; Borges-Garcia, Raquel; Javier Moreno, William; Perez-Pinzon, Miguel A.; Bramlett, Helen

    2013-01-01

    Although chronic 17β-estradiol (E2) has been shown to be a cognition-preserving and neuroprotective agent in animal brain injury models, concern regarding its safety was raised by the failed translation of this phenomenon to the clinic. Previously, we demonstrated that a single bolus of E2 48 hr prior to ischemia protected the hippocampus from damage in ovariectomized rats via phosphorylation of cyclic-AMP response element binding protein, which requires activation of estrogen receptor subtype beta (ER-β). The current study tests the hypothesis that long-term periodic E2-treatment improves cognition and reduces post-ischemic hippocampal injury by means of ER-β activation. Ovariectomized rats were given ten injections of E2 at 48 hr intervals for 21 days. Hippocampal-dependent learning, memory and ischemic neuronal loss were monitored. Results demonstrated that periodic E2 treatments improved spatial learning, memory and ischemic neuronal survival in ovariectomized rats. Additionally, periodic ER-β agonist treatments every 48 hr improved post-ischemic cognition. Silencing of hippocampal ER-β attenuated E2-mediated ischemic protection suggesting that ER-β plays a key role in mediating the beneficial effects of periodic E2 treatments. This study emphasizes the need to investigate a periodic estrogen replacement regimen to reduce cognitive decline and cerebral ischemia incidents/impact in post-menopausal women. PMID:23593292

  11. L-propionylcarnitine and myocardial performance in stunned porcine myocardium.

    PubMed

    Sassen, L M; Duncker, D J; Hogendoorn, A; McFalls, E O; Krams, R; Bezstarosti, K; Lamers, J M; Verdouw, P D

    1992-10-21

    Recently, we showed that L-propionylcarnitine did not affect recovery of regional contractile function of porcine myocardium subjected to 1 h of low-flow ischemia followed by 2 hr of reperfusion. In that study, ischemia may have been too severe and/or the duration of reperfusion too short to detect a beneficial effect of the compound. Therefore, in the present study we investigated the effects of saline (control group; n = 14) or pretreatment with L-propionyl-carnitine (3 days of 50 mg/kg p.o. b.i.d. + 50 mg/kg i.v. prior to the experiment; n = 13) on recovery of regional contractile function of the myocardium in open-chest anesthetized pigs, subjected to two cycles of 10 min of left anterior descending coronary artery (LADCA) occlusion, each followed by 30 min of reperfusion. In the control animals, at the end of the second reperfusion period, systemic vascular resistance had increased by 18%, which, however, was not observed in the L-propionylcarnitine-treated pigs. In the control group, during the first occlusion, systolic segment length shortening (SSLS) of the LADCA-perfused area decreased from 18.5 +/- 5.5% to -3.7 = 3.2%. After 30 min of reperfusion, SSLS of the LADCA-perfused area had only partially recovered to 6.2 +/- 5.9%. During the second occlusion-reperfusion cycle similar values for SSLS were observed. In the treated animals, SSLS of the LADCA-perfused area was slightly improved after the second occlusion-reperfusion cycle (p = 0.056). This effect did not result in an overall improvement in cardiac pump function.(ABSTRACT TRUNCATED AT 250 WORDS)

  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. 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.

  14. Neurogenic stunned myocardium in subarachnoid hemorrhage.

    PubMed

    Kerro, Ali; Woods, Timothy; Chang, Jason J

    2017-04-01

    "Stunned myocardium," characterized by reversible left ventricular dysfunction, was first described via animal models using transient coronary artery occlusion. However, this phenomenon has also been noted with neurologic pathologies and collectively been labeled "neurogenic stunned myocardium" (NSM). Neurogenic stunned myocardium resulting from subarachnoid hemorrhage (SAH) is a challenging pathology due to its diagnostic uncertainty. Traditional diagnostic criteria for NSM after SAH focus on electrocardiographic and echocardiographic abnormalities and troponemia. However, tremendous heterogeneity still exists. Traditional pathophysiological mechanisms for NSM encompassed hypothalamic and myocardial perivascular lesions. More recently, research on pathophysiology has centered on myocardial microvascular dysfunction and genetic polymorphisms. Catecholamine surging as a mechanism has also gained attention with particular focus placed on the role of adrenergic blockade in both the prehospital and acute settings. Management remains largely supportive with case reports acknowledging the utility of inotropes such as dobutamine and milrinone and intra-aortic balloon pump when NSM is accompanied by cardiogenic shock. Neurogenic stunned myocardium that follows SAH can result in many complications such as arrhythmias, pulmonary edema, and prolonged intubation, which can negatively impact long-term recovery from SAH and increase morbidity and mortality. This necessitates the need to accurately diagnose and treat NSM.

  15. 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

  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

    NASA Astrophysics Data System (ADS)

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

    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. 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.

  20. Vegfa Impacts Early Myocardium Development in Zebrafish

    PubMed Central

    Zhu, Diqi; Fang, Yabo; Gao, Kun; Shen, Jie; Zhong, Tao P.; Li, Fen

    2017-01-01

    Vascular endothelial growth factor A (Vegfa) signaling regulates cardiovascular development. However, the cellular mechanisms of Vegfa signaling in early cardiogenesis remain poorly understood. The present study aimed to understand the differential functions and mechanisms of Vegfa signaling in cardiac development. A loss-of-function approach was utilized to study the effect of Vegfa signaling in cardiogenesis. Both morphants and mutants for vegfaa display defects in cardiac looping and chamber formation, especially the ventricle. Vegfa regulates the heart morphogenesis in a dose-dependent manner. Furthermore, the initial fusion of the bilateral myocardium population is delayed rather than endocardium. The results demonstrate that Vegfa signaling plays a direct impact on myocardium fusion, indicating that it is the initial cause of the heart defects. The heart morphogenesis is regulated by Vegfa in a dose-dependent manner, and later endocardium defects may be secondary to impaired myocardium–endocardium crosstalk. PMID:28230770

  1. Automatic cardiac MRI myocardium segmentation using graphcut

    NASA Astrophysics Data System (ADS)

    Kedenburg, Gunnar; Cocosco, Chris A.; Köthe, Ullrich; Niessen, Wiro J.; Vonken, Evert-jan P. A.; Viergever, Max A.

    2006-03-01

    Segmentation of the left myocardium in four-dimensional (space-time) cardiac MRI data sets is a prerequisite of many diagnostic tasks. We propose a fully automatic method based on global minimization of an energy functional by means of the graphcut algorithm. Starting from automatically obtained segmentations of the left and right ventricles and a cardiac region of interest, a spatial model is constructed using simple and plausible assumptions. This model is used to learn the appearance of different tissue types by non parametric robust estimation. Our method does not require previously trained shape or appearance models. Processing takes 30-40s on current hardware. We evaluated our method on 11 clinical cardiac MRI data sets acquired using cine balanced fast field echo. Linear regression of the automatically segmented myocardium volume against manual segmentations (performed by a radiologist) showed an RMS error of about 12ml.

  2. Mechanisms of myocardium-coronary vessel interaction

    PubMed Central

    Algranati, Dotan; Kassab, Ghassan S.

    2010-01-01

    The mechanisms by which the contracting myocardium exerts extravascular forces (intramyocardial pressure, IMP) on coronary blood vessels and by which it affects the coronary flow remain incompletely understood. Several myocardium-vessel interaction (MVI) mechanisms have been proposed, but none can account for all the major flow features. In the present study, we hypothesized that only a specific combination of MVI mechanisms can account for all observed coronary flow features. Three basic interaction mechanisms (time-varying elasticity, myocardial shortening-induced intracellular pressure, and ventricular cavity-induced extracellular pressure) and their combinations were analyzed based on physical principles (conservation of mass and force equilibrium) in a realistic data-based vascular network. Mechanical properties of both vessel wall and myocardium were coupled through stress analysis to simulate the response of vessels to internal blood pressure and external (myocardial) mechanical loading. Predictions of transmural dynamic vascular pressure, diameter, and flow velocity were determined under each MVI mechanism and compared with reported data. The results show that none of the three basic mechanisms alone can account for the measured data. Only the combined effect of the cavity-induced extracellular pressure and the shortening-induced intramyocyte pressure provides good agreement with the majority of measurements. These findings have important implications for elucidating the physical basis of IMP and for understanding coronary phasic flow and coronary artery and microcirculatory disease. PMID:19966048

  3. Butyrate pretreatment attenuates heart depression in a mice model of endotoxin-induced sepsis via anti-inflammation and anti-oxidation.

    PubMed

    Wang, Fangyan; Jin, Zengyou; Shen, Kaiyi; Weng, Tingting; Chen, Zhisong; Feng, Jiahui; Zhang, Zhengzheng; Liu, Jiaming; Zhang, Xiaolong; Chu, Maoping

    2017-03-01

    The depressed heart function is the main complication to cause death of septic patients in clinic. It is urgent to find effective interventions for this intractable disease. In this study, we investigated whether butyrate could be protective for heart against sepsis and the underlying mechanism. Mice were randomly divided into three groups. Model group challenged with LPS (30 mg/kg, i.p.) only. Butyrate group received butyrate (200 mg/kg·d) for 3days prior to LPS administration (30 mg/kg). Normal group received saline only. 6h and 12h after LPS administration were chosen for detection the parameters to estimate the effects or mechanism of butyrate pretreatment on heart of sepsis. The data showed that septic heart depression was attenuated by butyrate pretreatment through improvement of heart function depression (P<0.01) and reduction of morphological changes of myocardium. The overexpression of proinflammatory factors, TNF-α, IL-6 and LTB4, in heart tissues induced by sepsis was significantly alleviated by butyrate pretreatment (P<0.01). As oxidative stress indicators, SOD and CAT activity, and MDA content in heart were deteriorated by LPS challenge, which was noticeably ameliorated by butyrate pretreatment (P<0.01 or P<0.05). In conclusion, pretreatment with butyrate attenuated septic heart depression via anti-inflammation and anti-oxidation. Copyright © 2016 Elsevier Inc. All rights reserved.

  4. 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

  5. The endothelial nitric oxide synthase cofactor tetrahydrobiopterin shields the remote myocardium from apoptosis after experimental myocardial infarction in vivo.

    PubMed

    Heidrich, Felix M; Jercke, Marcel C; Ritzkat, Anna; Ebner, Annette; Poitz, David M; Pfluecke, Christian; Quick, Silvio; Speiser, Uwe; Simonis, Gregor; Wäßnig, Nadine K; Strasser, Ruth H; Wiedemann, Stephan

    2017-08-23

    Following myocardial infarction (MI), apoptosis occurs early in the remote myocardium and contributes to the processes of myocardial remodeling. Increased nitrosative stress is a well-known and potent inductor of myocardial apoptosis. Excess activation of endothelial nitric oxide synthase (eNOS) increases its uncoupling potential and results in nitrosative stress via formation of peroxynitrite. However, the pathophysiologic role of eNOS signaling in the remote myocardium after MI is as yet undefined. The impact of eNOS activation on pro- and anti-apoptotic signaling in the remote myocardium and the influence of pretreatment with the eNOS cofactor tetrahydrobiopterin (BH4) on eNOS activation, nitrosative stress level and apoptosis induction and execution were studied in a rat myocardial infarction model in vivo. 24 hours after anterior MI, eNOS activity in animals treated with left anterior descending coronary artery ligation (LIG) significantly increased in the posterior left ventricular myocardium as did protein nitrosylation when compared to sham treatment. This was paralleled by induction of apoptosis via both, the extrinsic and intrinsic pathways. Moreover, anti-apoptotic signaling via protein kinase B/Akt and glycogen synthase-kinase 3 beta was suppressed. Notably, pretreatment with the eNOS cofactor BH4 reduced eNOS activation, prevented excess protein nitrosylation, blunted apoptosis induction, facilitated anti-apoptotic signaling and eventually prevented apoptosis execution. Here we showed that 24 hours after experimental MI in rats in vivo, apoptosis was induced in the posterior non-infarcted LV wall. Evidence is presented that pretreatment with the eNOS cofactor BH4 resulted in less nitrosative stress and weakened apoptotic processes, although stabilizers contained did participate in this phenomenon. Because apoptosis is a crucial component of myocardial remodeling, influencing eNOS signaling might be an interesting pharmacological target for the

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

    PubMed Central

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

    2015-01-01

    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. Lastly, we discuss the pathophysiology of neurogenic stunned myocardium, as well as its implications for anesthesiologists caring for neurosurgical patients. PMID:26462162

  7. 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.

  8. Portland, Maine Industrial Pretreatment Program Recognized for Excellence

    EPA Pesticide Factsheets

    The City of Portland Maine's Industrial Pretreatment Program was recently honored with a 2015 Regional Industrial Pretreatment Program Excellence Award by the US Environmental Protection Agency's New England regional office.

  9. [Functional state of myocardium in polisher colourers of automobile factory].

    PubMed

    Vlasov, V N

    2007-01-01

    The article covers influence of combined occupational chemical and physical factors on functional state of myocardium in polisher colourers of automobile factory painting shop. The authors detected dependence of myocardium functional state on work conditions and on duration of exposure to occupational factors.

  10. 2-Aminobutyric acid modulates glutathione homeostasis in the myocardium

    PubMed Central

    Irino, Yasuhiro; Toh, Ryuji; Nagao, Manabu; Mori, Takeshige; Honjo, Tomoyuki; Shinohara, Masakazu; Tsuda, Shigeyasu; Nakajima, Hideto; Satomi-Kobayashi, Seimi; Shinke, Toshiro; Tanaka, Hidekazu; Ishida, Tatsuro; Miyata, Okiko; Hirata, Ken-ichi

    2016-01-01

    A previous report showed that the consumption of glutathione through oxidative stress activates the glutathione synthetic pathway, which is accompanied by production of ophthalmic acid from 2-aminobutyric acid (2-AB). We conducted a comprehensive quantification of serum metabolites using gas chromatography-mass spectrometry in patients with atrial septal defect to find clues for understanding myocardial metabolic regulation, and demonstrated that circulating 2-AB levels reflect hemodynamic changes. However, the metabolism and pathophysiological role of 2-AB remains unclear. We revealed that 2-AB is generated by an amino group transfer reaction to 2-oxobutyric acid, a byproduct of cysteine biosynthesis from cystathionine. Because cysteine is a rate-limiting substrate for glutathione synthesis, we hypothesized that 2-AB reflects glutathione compensation against oxidative stress. A murine cardiomyopathy model induced by doxorubicin supported our hypothesis, i.e., increased reactive oxygen species are accompanied by 2-AB accumulation and compensatory maintenance of myocardial glutathione levels. Intriguingly, we also found that 2-AB increases intracellular glutathione levels by activating AMPK and exerts protective effects against oxidative stress. Finally, we demonstrated that oral administration of 2-AB efficiently raises both circulating and myocardial glutathione levels and protects against doxorubicin-induced cardiomyopathy in mice. This is the first study to demonstrate that 2-AB modulates glutathione homeostasis in the myocardium. PMID:27827456

  11. Sestrin2 protects the myocardium against radiation-induced damage.

    PubMed

    Zeng, Yue-Can; Chi, Feng; Xing, Rui; Zeng, Jing; Gao, Song; Chen, Jia-Jia; Wang, Hong-Mei; Duan, Qiong-Yu; Sun, Yu-Nan; Niu, Nan; Tang, Mei-Yue; Wu, Rong

    2016-05-01

    The purpose of this study was to investigate the role of Sestrin2 in response to radiation-induced injury to the heart and on the cardiomyopathy development in the mouse. Mice with genetic deletion of the Sestrin2 (Sestrin2 knockout mice [Sestrin2 KO]) and treatment with irradiation (22 or 15 Gy) were used as independent approaches to determine the role of Sestrin2. Echocardiography (before and after isoproterenol challenge) and left ventricular (LV) catheterization were performed to evaluate changes in LV dimensions and function. Masson's trichrome was used to assess myocardial fibrosis. Immunohistochemistry and Western blot were used to detect the capillary density. After 22 or 15 Gy irradiation, the LV ejection fraction (EF) was impaired in wt mice at 1 week and 4 months after irradiation when compared with sham irradiation. Compared to wt mice, Sestrin2 KO mice had significant reduction in reduced LVEF at 1 week and 4 months after irradiation. A significant increase in LV end-diastolic pressure and myocardial fibrosis and a significant decrease in capillary density were observed in irradiation-wt mice, as well as in irradiation-Sestrin2 KO mice. Sestrin2 involved in the regulation of cardiomyopathy (such as myocardial fibrosis) after irradiation. Overexpression of Sestrin2 might be useful in limiting radiation-induced myocardial injury.

  12. Response of the human myocardium to ischemic injury and preconditioning: The role of cardiac and comorbid conditions, medical treatment, and basal redox status

    PubMed Central

    Casós, Kelly; Ferrer-Curriu, Gemma; Soler-Ferrer, Paula; Pérez, María L; Permanyer, Eduard; Blasco-Lucas, Arnau; Gracia-Baena, Juan Manuel; Castro, Miguel A; Sureda, Carlos; Barquinero, Jordi

    2017-01-01

    Background The diseased human myocardium is highly susceptible to ischemia/reoxygenation (I/R)-induced injury but its response to protective interventions such as ischemic preconditioning (IPreC) is unclear. Cardiac and other pre-existing clinical conditions as well as previous or ongoing medical treatment may influence the myocardial response to I/R injury and protection. This study investigated the effect of both on myocardial susceptibility to I/R-induced injury and the protective effects of IPreC. Methods and results Atrial myocardium from cardiac surgery patients (n = 300) was assigned to one of three groups: aerobic control, I/R alone, and IPreC. Lactate dehydrogenase leakage, as a marker of cell injury, and cell viability were measured. The basal redox status was determined in samples from 90 patients. The response to I/R varied widely. Myocardium from patients with aortic valve disease was the most susceptible to injury whereas myocardium from dyslipidemia patients was the least susceptible. Tissue from females was better protected than tissue from males. Myocardium from patients with mitral valve disease was the least responsive to IPreC. The basal redox status was altered in the myocardium from patients with mitral and aortic valve disease. Conclusions The response of the myocardium to I/R and IPreC is highly variable and influenced by the underlying cardiac pathology, dyslipidemia, sex, and the basal redox status. These results should be taken into account in the design of future clinical studies on the prevention of I/R injury and protection. PMID:28380047

  13. Response of the human myocardium to ischemic injury and preconditioning: The role of cardiac and comorbid conditions, medical treatment, and basal redox status.

    PubMed

    Casós, Kelly; Ferrer-Curriu, Gemma; Soler-Ferrer, Paula; Pérez, María L; Permanyer, Eduard; Blasco-Lucas, Arnau; Gracia-Baena, Juan Manuel; Castro, Miguel A; Sureda, Carlos; Barquinero, Jordi; Galiñanes, Manuel

    2017-01-01

    The diseased human myocardium is highly susceptible to ischemia/reoxygenation (I/R)-induced injury but its response to protective interventions such as ischemic preconditioning (IPreC) is unclear. Cardiac and other pre-existing clinical conditions as well as previous or ongoing medical treatment may influence the myocardial response to I/R injury and protection. This study investigated the effect of both on myocardial susceptibility to I/R-induced injury and the protective effects of IPreC. Atrial myocardium from cardiac surgery patients (n = 300) was assigned to one of three groups: aerobic control, I/R alone, and IPreC. Lactate dehydrogenase leakage, as a marker of cell injury, and cell viability were measured. The basal redox status was determined in samples from 90 patients. The response to I/R varied widely. Myocardium from patients with aortic valve disease was the most susceptible to injury whereas myocardium from dyslipidemia patients was the least susceptible. Tissue from females was better protected than tissue from males. Myocardium from patients with mitral valve disease was the least responsive to IPreC. The basal redox status was altered in the myocardium from patients with mitral and aortic valve disease. The response of the myocardium to I/R and IPreC is highly variable and influenced by the underlying cardiac pathology, dyslipidemia, sex, and the basal redox status. These results should be taken into account in the design of future clinical studies on the prevention of I/R injury and protection.

  14. A Review of Neurogenic Stunned Myocardium

    PubMed Central

    Wongrakpanich, Supakanya; Agrawal, Akanksha; Yadlapati, Sujani; Kishlyansky, Marina; Figueredo, Vincent

    2017-01-01

    Neurologic stunned myocardium (NSM) is a phenomenon where neurologic events give rise to cardiac abnormalities. Neurologic events like stroke and seizures cause sympathetic storm and autonomic dysregulation that result in myocardial injury. The clinical presentation can involve troponin elevation, left ventricular dysfunction, and ECG changes. These findings are similar to Takotsubo cardiomyopathy and acute coronary syndrome. It is difficult to distinguish NSM from acute coronary syndrome based on clinical presentation alone. Because of this difficulty, a patient with NSM who is at high risk for coronary heart disease may undergo cardiac catheterization to rule out coronary artery disease. The objective of this review of literature is to enhance physician's awareness of NSM and its features to help tailor management according to the patient's clinical profile. PMID:28875040

  15. 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. Copyright © 2015 Elsevier Inc. All rights reserved.

  16. 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.

  17. Mutagenic and morphologic impacts of 1.8GHz radiofrequency radiation on human peripheral blood lymphocytes (hPBLs) and possible protective role of pre-treatment with Ginkgo biloba (EGb 761).

    PubMed

    Esmekaya, Meric Arda; Aytekin, Ebru; Ozgur, Elcin; Güler, Göknur; Ergun, Mehmet Ali; Omeroğlu, Suna; Seyhan, Nesrin

    2011-12-01

    The mutagenic and morphologic effects of 1.8GHz Global System for Mobile Communications (GSM) modulated RF (radiofrequency) radiation alone and in combination with Ginkgo biloba (EGb 761) pre-treatment in human peripheral blood lymphocytes (hPBLs) were investigated in this study using Sister Chromatid Exchange (SCE) and electron microscopy. Cell viability was assessed with 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) reduction assay. The lymphocyte cultures were exposed to GSM modulated RF radiation at 1.8GHz for 6, 8, 24 and 48h with and without EGb 761. We observed morphological changes in pulse-modulated RF radiated lymphocytes. Longer exposure periods led to destruction of organelle and nucleus structures. Chromatin change and the loss of mitochondrial crista occurred in cells exposed to RF for 8h and 24h and were more pronounced in cells exposed for 48h. Cytoplasmic lysis and destruction of membrane integrity of cells and nuclei were also seen in 48h RF exposed cells. There was a significant increase (p<0.05) in SCE frequency in RF exposed lymphocytes compared to sham controls. EGb 761 pre-treatment significantly decreased SCE from RF radiation. RF radiation also inhibited cell viability in a time dependent manner. The inhibitory effects of RF radiation on the growth of lymphoctes were marked in longer exposure periods. EGb 761 pre-treatment significantly increased cell viability in RF+EGb 761 treated groups at 8 and 24h when compared to RF exposed groups alone. The results of our study showed that RF radiation affects cell morphology, increases SCE and inhibits cell proliferation. However, EGb 761 has a protective role against RF induced mutagenity. We concluded that RF radiation induces chromosomal damage in hPBLs but this damage may be reduced by EGb 761 pre-treatment. Copyright © 2011 Elsevier B.V. All rights reserved.

  18. 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.

  19. 40 CFR 403.18 - Modification of POTW pretreatment programs.

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... 40 Protection of Environment 28 2010-07-01 2010-07-01 true Modification of POTW pretreatment programs. 403.18 Section 403.18 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS GENERAL PRE-TREAT-MENT REGULATIONS FOR EXIST-ING AND NEW SOURCES...

  20. 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...

  1. 40 CFR 463.35 - Pretreatment standards for existing sources.

    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. 463.35 Section 463.35 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED... Water Subcategory § 463.35 Pretreatment standards for existing sources. (a) PSES for bis(2-ethylhexyl...

  2. 40 CFR 465.35 - Pretreatment standards for new sources.

    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. 465.35 Section 465.35 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT... § 465.35 Pretreatment standards for new sources. Except as provided in 40 CFR 403.7, any new source...

  3. 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...

  4. 40 CFR 403.18 - Modification of POTW pretreatment programs.

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... 40 Protection of Environment 29 2011-07-01 2009-07-01 true Modification of POTW pretreatment programs. 403.18 Section 403.18 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS GENERAL PRE-TREAT-MENT REGULATIONS FOR EXIST-ING AND NEW SOURCES...

  5. 40 CFR 406.26 - 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. 406.26 Section 406.26 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS GRAIN MILLS POINT SOURCE CATEGORY Corn Dry Milling Subcategory § 406.26 Pretreatment...

  6. 40 CFR 406.26 - Pretreatment standards for new sources.

    Code of Federal Regulations, 2012 CFR

    2012-07-01

    ... 40 Protection of Environment 30 2012-07-01 2012-07-01 false Pretreatment standards for new sources. 406.26 Section 406.26 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS GRAIN MILLS POINT SOURCE CATEGORY Corn Dry Milling Subcategory § 406.26 Pretreatment...

  7. 40 CFR 406.26 - Pretreatment standards for new sources.

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ... 40 Protection of Environment 30 2013-07-01 2012-07-01 true Pretreatment standards for new sources. 406.26 Section 406.26 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS GRAIN MILLS POINT SOURCE CATEGORY Corn Dry Milling Subcategory § 406.26 Pretreatment...

  8. 40 CFR 406.26 - Pretreatment standards for new sources.

    Code of Federal Regulations, 2014 CFR

    2014-07-01

    ... 40 Protection of Environment 29 2014-07-01 2012-07-01 true Pretreatment standards for new sources. 406.26 Section 406.26 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS GRAIN MILLS POINT SOURCE CATEGORY Corn Dry Milling Subcategory § 406.26 Pretreatment...

  9. 40 CFR 406.26 - 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. 406.26 Section 406.26 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS GRAIN MILLS POINT SOURCE CATEGORY Corn Dry Milling Subcategory § 406.26 Pretreatment...

  10. 40 CFR 403.18 - Modification of POTW pretreatment programs.

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ... 40 Protection of Environment 30 2013-07-01 2012-07-01 true Modification of POTW pretreatment programs. 403.18 Section 403.18 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS GENERAL PRETREATMENT REGULATIONS FOR EXISTING AND NEW SOURCES...

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

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ... 40 Protection of Environment 30 2013-07-01 2012-07-01 true Objectives of general pretreatment regulations. 403.2 Section 403.2 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED... POLLUTION § 403.2 Objectives of general pretreatment regulations. By establishing the responsibilities of...

  12. 40 CFR 403.5 - National pretreatment standards: Prohibited discharges.

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ... 40 Protection of Environment 30 2013-07-01 2012-07-01 true National pretreatment standards: Prohibited discharges. 403.5 Section 403.5 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY... OF POLLUTION § 403.5 National pretreatment standards: Prohibited discharges. (a)(1) General...

  13. 40 CFR 445.3 - General pretreatment standards.

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... 40 Protection of Environment 30 2011-07-01 2011-07-01 false General pretreatment standards. 445.3 Section 445.3 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS LANDFILLS POINT SOURCE CATEGORY § 445.3 General pretreatment standards. Any...

  14. 40 CFR 445.3 - General pretreatment standards.

    Code of Federal Regulations, 2014 CFR

    2014-07-01

    ... 40 Protection of Environment 30 2014-07-01 2014-07-01 false General pretreatment standards. 445.3 Section 445.3 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) LANDFILLS POINT SOURCE CATEGORY § 445.3 General pretreatment standards....

  15. 40 CFR 439.3 - General pretreatment standards.

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... 40 Protection of Environment 30 2011-07-01 2011-07-01 false General pretreatment standards. 439.3 Section 439.3 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS PHARMACEUTICAL MANUFACTURING POINT SOURCE CATEGORY General § 439.3 General pretreatment...

  16. 40 CFR 439.3 - General pretreatment standards.

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... 40 Protection of Environment 29 2010-07-01 2010-07-01 false General pretreatment standards. 439.3 Section 439.3 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS PHARMACEUTICAL MANUFACTURING POINT SOURCE CATEGORY General § 439.3 General pretreatment...

  17. 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

  18. 40 CFR 403.11 - Approval procedures for POTW pretreatment programs and POTW granting of removal credits.

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ... ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS GENERAL PRETREATMENT REGULATIONS FOR EXISTING AND NEW SOURCES OF POLLUTION § 403.11 Approval procedures for POTW pretreatment programs...

  19. 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.

  20. Genetic modification of mesenchymal stem cells overexpressing CCR1 increases cell viability, migration, engraftment, and capillary density in the injured myocardium.

    PubMed

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

    2010-06-11

    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 because of 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 (eg, CCR1, CXCR2) in MSCs are very low. We hypothesized that this discordance may account for the poor MSC engraftment and survival. 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. 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 3 days postmyocardial infarction (MI). CCR1-MSC-injected hearts exhibited a significant reduction in infarct size, reduced cardiomyocytes apoptosis and increased capillary density in injured myocardium 3 days after MI. Furthermore, intramyocardial injection of CCR1-MSCs prevented cardiac remodeling and restored cardiac function 4 weeks after MI. 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.

  1. Temperature measurement within myocardium during in vitro RF catheter ablation.

    PubMed

    Cao, H; Vorperian, V R; Tsai, J Z; Tungjitkusolmun, S; Woo, E J; Webster, J G

    2000-11-01

    While most commercial ablation units and research systems can provide catheter tip temperature during ablation, they do not provide information about the temperature change inside the myocardium, which determines the lesion size. We present the details of a flow simulation and temperature measurement system, which allows the monitoring of the temperature change inside the myocardium during in vitro radio frequency (RF) cardiac catheter ablation at different blood flow rates to which the catheter site may be exposed. We set up a circulation system that simulated different blood flow rates of 0 to 5 L/min at 37 degrees C. We continuously measured the temperature at the catheter tip using the built-in thermistor and inside the myocardium using a three-thermocouple probe. The system provides a means for further study of the temperature inside myocardium during RF catheter ablation under different flow conditions and at different penetration depths.

  2. 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.

  3. Impaired oxidative phosphorylation in overtrained rat myocardium

    PubMed Central

    Kadaja, Lumme; Eimre, Margus; Paju, Kalju; Roosimaa, Mart; Põdramägi, Taavi; Kaasik, Priit; Pehme, Ando; Orlova, Ehte; Mudist, Margareeta; Peet, Nadezhda; Piirsoo, Andres; Seene, Teet; Gellerich, Frank N; Seppet, Enn K

    2010-01-01

    The present study was undertaken to characterize and review the changes in energy metabolism in rat myocardium in response to chronic exhaustive exercise. It was shown that a treadmill exercise program applied for six weeks led the rats into a state characterized by decreased performance, loss of body weight and enhanced muscle catabolism, indicating development of overtraining syndrome. Electron microscopy revealed disintegration of the cardiomyocyte structure, cellular swelling and appearance of peroxisomes. Respirometric assessment of mitochondria in saponin-permeabilized cells in situ revealed a decreased rate of oxidative phosphorylation (OXPHOS) due to diminished control over it by ADP and impaired functional coupling of adenylate kinase to OXPHOS. In parallel, reduced tissue content of cytochrome c was observed, which could limit the maximal rate of OXPHOS. The results are discussed with respect to relationships between the volume of work and corresponding energy metabolism. It is concluded that overtraining syndrome is not restricted to skeletal muscle but can affect cardiac muscle as well. PMID:21264069

  4. Severe stunned myocardium after lightning strike.

    PubMed

    Rivera, Jaime; Romero, Karla Alejandra; González-Chon, Octavio; Uruchurtu, Eduardo; Márquez, Manlio Fabio; Guevara, Milton

    2007-01-01

    To report the development of myocardial stunning and severe heart failure after lightning strike with total recovery of function. Case report. Coronary care unit at Medica Sur Clinic, Mexico. A 42-yr-old woman who was hit by lightning developed rapid and progressive hemodynamic deterioration manifested by cardiogenic shock that required invasive monitoring. Twenty-four hours after the strike, intravenous levosimendan and intra-aortic balloon pump were initiated because the patient demonstrated no significant response to management with conventional inotropic agents. Two days later, echocardiographic signs of systolic and diastolic dysfunction improved markedly. Dual-isotope-imaging myocardial perfusion testing with technetium-99m-sestamibi and thallium-201, performed 9 days after admission, showed normal perfusion and normal left ventricular systolic function. The patient exhibited complete recovery of function. The exact mechanism of abnormal contractility in the absence of direct electrofulguration is unknown but may be explained by release of oxygen free radicals, proteolysis of the contractile apparatus, and cytosolic overload of intracellular calcium, followed by reduced myofilament sensitivity to calcium. These abnormalities are consistent with stunned myocardium. Lightning strike may cause serious contractile dysfunction in the absence of irreversible myocardial injury, but the exact mechanism of this phenomenon remains unknown. We propose that lighting strike can cause myocardial stunning resulting in severe but reversible left ventricular dysfunction. The patient's recovery was facilitated by support treatment including administration of levosimendan, which increases the intracellular sensitivity to calcium, a mechanism disturbed in patients with myocardial stunning.

  5. 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.

  6. Cardiac Telocytes in Regeneration of Myocardium After Myocardial Infarction.

    PubMed

    Zhaofu, Liao; Dongqing, Cai

    2016-01-01

    Recent research progress has revealed that a novel type of interstitial cells termed cardiac telocytes (CTs) is found in the interstitium of the heart. We demonstrated that CTs are distributed both longitudinally and within the cross network in the myocardium and that the density of CTs in the atrium-atria and base of the myocardium is higher than that in the middle of the myocardium, while the density of CTs in the epicardium is higher than that in the endocardium. In addition, we documented, for the first time, that the network of CTs in the infarct zone of the myocardium is destroyed during myocardial infarction (MI). This fact shows that, in addition to the death of cardiac myocytes, the previously unrecognized death of CTs is an important mechanism that contributes to the structural damage and poor healing and regeneration observed in the infarcted myocardium. Furthermore, we demonstrated, for the first time, that transplantation of CTs in cases of MI decreases the infarct size and improves myocardial function. The mechanisms behind the beneficial effects of CT transplantation are increased angiogenesis at the infarct site and the border zone, decreased fibrosis in the infarct and non-infarct zones, improved pathological reconstruction of the left ventricle, and increased regeneration of CTs in the infarct zone. Our findings reveal that CTs can be specifically identified by the following characteristics: very small cell bodies, extreme prolongation with some dilation, predisposition to cell death under ischemia, and expression of molecular markers such as c-Kit, CD34, vimentin, and PDGFR-β. CTs act as a structural and functional niche microenvironment in the myocardium and play an essential role in maintaining the integrity of the myocardium and in the regeneration of damaged myocardium.

  7. 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.

  8. 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.

  9. Myocardial blood flow in patients with hibernating myocardium.

    PubMed

    Camici, Paolo G; Rimoldi, Ornella E

    2003-02-01

    The debate on whether resting myocardial blood flow (MBF) to hibernating myocardium is reduced or not has attracted a lot of interest and has contributed to stimulate new research on heart failure in patients with coronary artery disease (CAD). Positron emission tomography with oxygen-15 labeled water (H(2)(15)O) or nitrogen-13 labeled ammonia (13NH(3)) has been used for the absolute quantification of regional MBF in human hibernating myocardium. When hibernating myocardium is properly identified, i.e. a dysfunctional segment subtended by a stenotic coronary artery that improves function upon reperfusion, the following conclusions can be reached based on the available literature: (a) in the majority of these studies resting MBF in hibernating myocardium is not different from either flow in remote tissue in the same patient or MBF in normal healthy volunteers; (b) a reduction in MBF of approximately 20% compared to MBF in remote myocardium or age matched normal subjects has been demonstrated in a minority of truly hibernating segments; (c) hibernating myocardium is characterized by a severely impaired coronary flow reserve which improves after revascularization in parallel with contractile function. Thus, the pathophysiology of hibernation in humans is more complex than initially postulated. The recent evidence that repetitive ischemia in patients with coronary artery disease can be cumulative and lead to more severe and prolonged stunning, lends further support to the hypothesis that, at least initially, stunning and hibernation are two facets of the same coin.

  10. [Antihypoxic effects of various derivatives of 3-hydroxypyridine on isolated rat myocardium].

    PubMed

    Luk'ianova, L D; Atabaeva, R E; Shepeleva, S Iu

    1993-04-01

    Antihypoxic effect of a succinate-containing derivative of hydroxypyridine = --mexidol and its analog--emoxipin on contractile function and energy exchange of rats' myocard was investigated. It was shown reliably that mexidole have more expressed protective properties in myocardium of low-resistant (but not high-resistant) rats. In case of antihypoxant emoxipin prohypoxic properties prevail. It have been proposed that antihypoxic activity of mexidol was linked with presence of succinate in composition of the substance, which can be oxidated in this conditions.

  11. Bioengineering Human Myocardium on Native Extracellular Matrix

    PubMed Central

    Guyette, Jacques P.; Charest, Jonathan M; Mills, Robert W; Jank, Bernhard J.; Moser, Philipp T.; Gilpin, Sarah E.; Gershlak, Joshua R.; Okamoto, Tatsuya; Gonzalez, Gabriel; Milan, David J.; Gaudette, Glenn R.; Ott, Harald C.

    2015-01-01

    Rationale More than 25 million individuals suffer from heart failure worldwide, with nearly 4,000 patients currently awaiting heart transplantation in the United States. Donor organ shortage and allograft rejection remain major limitations with only about 2,500 hearts transplanted each year. As a theoretical alternative to allotransplantation, patient-derived bioartificial myocardium could provide functional support and ultimately impact the treatment of heart failure. Objective The objective of this study is to translate previous work to human scale and clinically relevant cells, for the bioengineering of functional myocardial tissue based on the combination of human cardiac matrix and human iPS-derived cardiac myocytes. Methods and Results To provide a clinically relevant tissue scaffold, we translated perfusion-decellularization to human scale and obtained biocompatible human acellular cardiac scaffolds with preserved extracellular matrix composition, architecture, and perfusable coronary vasculature. We then repopulated this native human cardiac matrix with cardiac myocytes derived from non-transgenic human induced pluripotent stem cells (iPSCs) and generated tissues of increasing three-dimensional complexity. We maintained such cardiac tissue constructs in culture for 120 days to demonstrate definitive sarcomeric structure, cell and matrix deformation, contractile force, and electrical conduction. To show that functional myocardial tissue of human scale can be built on this platform, we then partially recellularized human whole heart scaffolds with human iPSC-derived cardiac myocytes. Under biomimetic culture, the seeded constructs developed force-generating human myocardial tissue, showed electrical conductivity, left ventricular pressure development, and metabolic function. Conclusions Native cardiac extracellular matrix scaffolds maintain matrix components and structure to support the seeding and engraftment of human iPS-derived cardiac myocytes, and enable

  12. 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.

  13. Diffusion of water in cat ventricular myocardium

    PubMed Central

    1978-01-01

    The rates of diffusion of tritiated water (THO) and [14C]sucrose across cat right ventricular myocardium were studied at 23 degrees C in an Ussing-type diffusion cell, recording the time-course of increase in concentration of tracer in one chamber over 4--6 h after adding tracers to the other. Sucrose data were fitted with a model for a homogeneous sheet of uneven thickness in which the tissue is considered to be an array of parallel independent pathways (parallel pathway model) of varying length. The volume of the sucrose diffusion space, presumably a wholly extracellular pathway, was 23% of the tissue or 27.4 +/-1.7% (mean +/- SEM; n=11) of the tissue water. The effective intramyocardial sucrose diffusion coefficient, D8, was 1.51 +/- 0.19 X 10(-6)cm2.s-1 (n=11). Combining these data with earlier data, D8 was 22.6 +/- 1.1% (n=95) of the free diffusion coefficient in aqueous solution D degrees 8. The parallel pathway model and a dead-end pore model, which might have accounted for intracellular sequestration of water, gave estimates of DW/D degrees W (observed/free) of 15%. Because hindrance to water diffusion must be less than for sucrose (where D8/D degrees 8=22.6%), this showed the inadequacy of these models to account simultaneously for the diffusional resistance and the tissue water content. The third or cell-matrix model, a heterogeneous system of permeable cells arrayed in the extracellular matrix, allowed logical and geometrically reasonable interpretations of the steady-state data and implied estimates of DW in the cellular and extracellular fluid of approximately 25% of the aqueous diffusion coefficient. PMID:722277

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

    PubMed Central

    Fernandez, Stanley F.; Ovchinnikov, Vladislav; Canty, John M.

    2013-01-01

    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. PMID:23125211

  15. 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.

  16. 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.

  17. Cellular cardiomyoplasty: a new therapeutic approach for regenerating the myocardium.

    PubMed

    Piano, Mariann R; Carrigan, Timothy M

    2003-01-01

    One of the most promising new therapeutic techniques for the augmentation and regeneration of the myocardium is cellular cardiomyoplasty. Reports from animal and clinical investigations indicate that the transplant of different cell types, such as autologous skeletal myoblasts and adult stem cells, into injured myocardium results in the generation of new cardiac myocytes and improvement in myocardial performance. Although there is no consensus with regard to the best cell type to transplant or the extent of myocardial renewal and regeneration, the technique of cardiac cellular myoplasty may become one of the most important advancements in the treatment of cardiovascular diseases such as myocardial infarction and heart failure.

  18. 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.

  19. [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.

  20. 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

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

    2015-12-01

    To investigate the potential mechanisms underlying the protective effects of recombinant human erythropoietin (rhEPO) and carbamylated EPO (CEPO) against myocardial cell apoptosis in epilepsy. 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. 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. 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.

  1. 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

  2. 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.

  3. 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.

  4. 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.

  5. Stereology of the myocardium in Leontopithecus (Lesson, 1840) callitrichidae - primates.

    PubMed

    Pissinatti, A; Burity, C H F; Mandarim-de-Lacerda, C A

    2003-06-01

    Rare morphological features of the Leontopithecus cardiovascular system have been reported in the literature. The samples analyzed in this study came from 33 specimens of Leontopithecus from the collection of the Center of Primatology of Rio de Janeiro-FEEMA (CPRJ-FEEMA). Morphometry and stereological data were obtained from all animals. Adult body weights of L. rosalia were the lowest, the greatest being those of L. chrysopygus caissara; body weights of L. chrysomelas and L. c. chrysopygus were similar and in between those of the two former species. Cardiomyocytes (left ventricular myocardium) were bigger in adults than in infants. The myocardium of L. rosalia showed focal fibrosis, fatty vacuoles, and hyalinization. In L. chrysomelas the myocardium showed areas of fibrosis and presence of mononuclear cells. Fibrosis and areas of congestion were observed in L. c. chrysopygus; areas of disorganization and vascular congestion were found in L. c. caissara. In L. rosalia infants, a greater density of vessels per myocardial area and a greater length density of vessels were observed as compared with those of L. chrysomelas. In adults, L. chrysomelas showed greater density of connective tissue in the myocardium than L. c. chrysopygus and L. c. caissara did. In L. rosalia, cardiomyocyte nuclei had a greater area density than those of the other forms of Leontopithecus. These characteristics may explain the faster development of L. rosalia infants as compared with that of L. chrysomelas and L. c. chrysopygus kept under the same handling conditions at the CPRJ-FEEMA.

  6. [Morphological signs of impaired excitation conduction in the myocardium].

    PubMed

    Kapustin, A V

    2005-01-01

    The article describes morphological changes in cardiac muscular fibers and cardiomyocytes secondary to disorders in conduction of excitation in the myocardium. These changes may indicate cardiac arrest as a result of reflex impacts including cases of damage which is not lethal.

  7. Engineering and Visualization of Bacteria for Targeting Infarcted Myocardium

    PubMed Central

    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

    2011-01-01

    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 (PBAD), selectively targeted and delivered RLuc8 in the infarcted myocardium only upon injection of -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. PMID:21364539

  8. Protection against acute lung injury by intravenous or intratracheal pretreatment with EPI-HNE-4, a new potent neutrophil elastase inhibitor.

    PubMed

    Delacourt, Christophe; Hérigault, Sabine; Delclaux, Christophe; Poncin, Alain; Levame, Micheline; Harf, Alain; Saudubray, François; Lafuma, Chantal

    2002-03-01

    Excessive accumulation of active neutrophil elastase (NE) in pulmonary fluids and tissues of patients with cystic fibrosis (CF) is thought to act on the lungs, compromising their structure and function. The aim of this study was to investigate the in vitro and in vivo protective effect of a new, rapidly acting, potent (Ki = 5.45 x 10(-12) M and Kon = 8 x 10(6) M(-1) s(-1)) and specific human NE inhibitor, EPI-HNE-4, engineered from the Kunitz domain. The results demonstrated that this inhibitor was able to (i) effectively inhibit in vitro the high levels of active NE present in a medium as complex as sputum from children with CF, with a measured IC(50) equal or close to the calculated IC(50) in 60% of cases, and (ii) almost completely block (91%) the N-formyl-methionine-leucine-phenylalanine-induced migration of purified human neutrophils across a Matrigel basement membrane. Intratracheal administration (250, 175, or 100 microg per rat) of the inhibitor 5 min before instillation of pure human NE (HNE) (150 microg per rat) to rats induced effective, dose-dependent protection of the lungs, 4 h later, from hemorrhage, serum albumin leakage, residual active NE, and discrete neutrophil influx in air spaces induced by instillation of pure HNE. Intravenous administration (3 mg per rat) of EPI-HNE-4, 15 min before instillation of the soluble fraction of pooled sputum (delivering 120 microg of active NE per rat) from children with CF, effectively reduced (64%), 4 h later, the massive neutrophil influx induced by sputum instillation. Overall, these data strongly suggest that associated aerosol and systemic administration of EPI-HNE-4 would be beneficial in the treatment of CF.

  9. Myocardial protection after monophosphoryl lipid A: studies of delayed anti-ischaemic properties in rabbit heart.

    PubMed Central

    Baxter, G. F.; Goodwin, R. W.; Wright, M. J.; Kerac, M.; Heads, R. J.; Yellon, D. M.

    1996-01-01

    1. Monophosphoryl lipid A (MLA) is a non-pyrogenic derivative of Salmonella lipopolysaccharide. Administration of this agent at high doses to rats and at low doses to dogs was previously shown to confer marked protection against ischaemia-reperfusion 24 h later, although the cellular mechanisms of this delayed protection are obscure. We hypothesized that MLA pretreatment causes the induction of the 70 kDa cytoprotective stress protein HSP70i in the myocardium. If this were the case, protection against ischaemia-reperfusion injury would be observed both in vitro and in vivo. 2. Rabbits were pretreated with MLA 0.035 mg kg-1, i.v. or vehicle solution. For the in vitro study, hearts were isolated 24 h later and Langendorff-perfused with Krebs-Henseleit buffer at 37 degrees C. Global ischaemia was induced for 20 min followed by 120 min reperfusion. Recovery of post-ischaemic left ventricular function and lactate dehydrogenase efflux was similar in MLA and vehicle pretreated hearts and there was no significant difference in the percentage of infarction of the left ventricle determined by triphenyltetrazolium staining (MLA 22.4 +/- 5.2%, vehicle 24.8 +/- 5.1%). 3. When 30 min regional ischaemia and 120 min reperfusion was instituted in pentobarbitone-anaesthetized rabbits 24 h after pretreatment with MLA or vehicle, the percentage infarction within the risk zone was reduced from 42.6 +/- 5.7% in vehicle pretreated animals to 19.6 +/- 4.4% in MLA pretreated animals (P < 0.01). 4. Determination of myocardial HSP70i content by Western blot analysis showed that MLA treatment did not increase HSP70i immunoreactivity. 5. We conclude that MLA at this dose confers protection only against ischaemia-reperfusion injury in vivo and that this protection is not related to induction of HSP70i. Because protection was observed only in vivo it seems possible that the delayed protection conferred by MLA is mediated by effects on humoral or blood-borne factors. Images Figure 1 Figure 2

  10. 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.

  11. Methods for pretreating biomass

    DOEpatents

    Balan, Venkatesh; Dale, Bruce E; Chundawat, Shishir; Sousa, Leonardo

    2017-05-09

    A method for pretreating biomass is provided, which includes, in a reactor, allowing gaseous ammonia to condense on the biomass and react with water present in the biomass to produce pretreated biomass, wherein reactivity of polysaccharides in the biomass is increased during subsequent biological conversion as compared to the reactivity of polysaccharides in biomass which has not been pretreated. A method for pretreating biomass with a liquid ammonia and recovering the liquid ammonia is also provided. Related systems which include a biochemical or biofuel production facility are also disclosed.

  12. Body mass index and myocardium at risk in patients with acute coronary syndrome.

    PubMed

    Arrebola-Moreno, A L; Marfil-Alvarez, R; Catena, A; García-Retamero, R; Arrebola, J P; Melgares-Moreno, R; Ramirez-Hernández, J A; Kaski, J C

    2014-04-01

    Whilst traditional studies have shown that obese individuals are at a higher risk of cardiovascular events compared to lean subjects, recent studies in patients with acute myocardial infarction (AMI) have suggested that obesity may exert protective effects (the "obesity paradox"). We sought to assess the relationship between body mass index (BMI) and the BARI score (BARIsc), a validated tool used to assess myocardium at risk, in patients with acute coronary syndrome. Participants were 116 consecutive patients (mean age, 60.6 years; 97 men) with AMI (68 ST elevated myocardial infarction, STEMI; 48 non-ST elevated myocardial infarction, NSTEMI). Demographics, BMI, risk factors, biochemistry data, left ventricular function, angiographic data and the BARIsc were assessed in every patient. Multiple linear regression analyses showed that BMI significantly correlated with BARIsc; β=.23, p<0.02. This was found only in the overweight/obese patients, β=.27, p<0.01, but not in patients with normal BMIs, β=0.08, p=0.71. An increased body weight is associated with an increased area of myocardium at risk in patients with ACS. Copyright © 2013 Elsevier España, S.L. All rights reserved.

  13. Functional antagonism of β-adrenoceptor subtypes in the catecholamine-induced automatism in rat myocardium

    PubMed Central

    Boer, DC; Bassani, JWM; Bassani, RA

    2011-01-01

    BACKGROUND AND PURPOSE Myocardial automatism and arrhythmias may ensue during strong sympathetic stimulation. We sought to investigate the relevant types of adrenoceptor, as well as the role of phosphodiesterase (PDE) activity, in the production of catecholaminergic automatism in atrial and ventricular rat myocardium. EXPERIMENTAL APPROACH The effects of adrenoceptor agonists on the rate of spontaneous contractions (automatic response) and the amplitude of electrically evoked contractions (inotropic response) were determined in left atria and ventricular myocytes isolated from Wistar rats. KEY RESULTS Catecholaminergic automatism was Ca2+-dependent, as it required a functional sarcoplasmic reticulum to be exhibited. Although both α- and β-adrenoceptor activation caused inotropic stimulation, only β1-adrenoceptors seemed to mediate the induction of spontaneous activity. Catecholaminergic automatism was enhanced and suppressed by β2-adrenoceptor blockade and stimulation respectively. Inhibition of either PDE3 or PDE4 (by milrinone and rolipram, respectively) potentiated the automatic response of myocytes to catecholamines. However, only rolipram abolished the attenuation of automatism produced by β2-adrenoceptor stimulation. CONCLUSIONS AND IMPLICATIONS α- and β2-adrenoceptors do not seem to be involved in the mediation of catecholaminergic stimulation of spontaneous activity in atrial and ventricular myocardium. However, a functional antagonism of β1- and β2-adrenoceptor activation was identified, the former mediating catecholaminergic myocardial automatism and the latter attenuating this effect. Results suggest that hydrolysis of cAMP by PDE4 is involved in the protective effect mediated by β2-adrenoceptor stimulation. PMID:21091648

  14. 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

  15. 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

  16. 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.

  17. 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.

  18. Blockade of spinal nerves inhibits expression of neural growth factor in the myocardium at an early stage of acute myocardial infarction in rats.

    PubMed

    Yue, W; Guo, Z

    2012-09-01

    Neural growth factor (NGF) is required for healing and sprouting of cardiac sympathetic and sensory nerves and plays important roles in cardiac protection, sustaining cardiac function and regeneration in ischaemic heart disease. The overexpression or lack of the NGF could be harmful to the heart. In this study, we examined the role of spinal nerves in the modulation of expression of the NGF in the myocardium at risk of ischaemia soon after acute myocardial infarction in rats. Coronary artery occlusion (CAO) was carried out in anaesthetized rats with and without preconditioning of blockade of the spinal nerves. The expression of the NGF protein and mRNA in the myocardium at risk of ischaemia was examined using immunohistochemical assay, enzyme-linked immunosorbent assay, and real-time quantitative reverse transcription polymerase chain reaction assay. In the left ventricle, immunoreactive cells and fibre-like structures were mainly located in the myocardium and in the epicardium. The NGF protein expression was increased by two-fold in the myocardium at risk of ischaemia during the 60 min of CAO, while the NGF mRNA was up-regulated three-fold, at 360 min after acute myocardial infarction. The blockade of the spinal nerves completely abolished the up-regulation of the NGF in the myocardium (P<0.05). The spinal nerves innervating the heart may play an important role in sustaining the up-regulation of the NGF in the myocardium early after acute myocardial infarction, an effect which can be inhibited by the blockade of these nerves.

  19. 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.

  20. [Regulation by opiod peptides of the antioxidant enzyme activity and the prostanoid system in myocardium during stress].

    PubMed

    Rebrova, T Iu; Maslov, L N; Lishmanov, Iu B

    2005-01-01

    The six hour stress in rats was modeled by the method of O. Desiderato. Cardiac damage was estimated by myocardial uptace of radioactive 99Tc-pyrophosphate. Intravenous administration of mixed mu and delta opioid receptor agonist, D- Ala2, Leu5, Arg6-enkephalin (dalargin), (non-penetrating through the blood brain barrier) at a dose of 0.1 mg/kg before stress decreased stress-induced 99Tc-pyroposphate uptake. Pretreatment with dalargin completely abolished the stress-induced increase in conjugated dienes and malondialdehyde levels in myocardium and prevented a decrease in total lipid soluble antioxidant levels in the heart after stress exposure. Stress is accompanied by an increase in activity of catalase, glutathione peroxidase, glutathione reductase and a decrease in activity of superoxide dismutase (SOD). Pretreatment with dalargin completely reversed stress-induced decrease in SOD activity but had minor effect on the activity of other antioxidant enzymes. Stress also resulted in an increase in myocardial content of thromboxane and a decrease in prostacycline and prostaglandin E levels in the heart. Pretreatment with dalargin completely eliminated these stress-induced changes in myocardial prostanoid levels. We propose that stress-induced heart injury depends on the activation of lipid peroxidation processes and changes in the prostanoid levels in the heart. Cardioprotective effect of dalargin during stress may be mediated via peripheral mu and delta opioid receptor stimulation and an inhibition of lipid peroxidation processes through SOD activation and also a recovery, of normal prostanoid levels in the heart.

  1. [Neurogenic stunned myocardium in Pediatrics. A case report].

    PubMed

    Alados Arboledas, F J; Millán-Miralles, L; Millán-Bueno, M P; Expósito-Montes, J F; Santiago-Gutierrez, C; Martínez Padilla, M C

    2015-10-01

    Neurogenic stunned myocardium is an unusual clinical entity. It mimics an acute coronary syndrome with electrocardiographic abnormalities, cardiac dysfunction and elevated cardiac enzymes with absence of obstructive coronary disease. It may occur after a neurosurgical procedure. A case is presented of neurogenic stunned myocardium occurring in a child after removal of a posterior fossa medulloblastoma. The patient developed nodal tachycardia with hemodynamic impairment. The clinical course was satisfactory due to antiarrhythmic therapy, with biochemical, echocardiographic, and clinical improvement within a week. Copyright © 2014 Sociedad Española de Anestesiología, Reanimación y Terapéutica del Dolor. Publicado por Elsevier España, S.L.U. All rights reserved.

  2. 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.

  3. 40 CFR 125.65 - Urban area pretreatment program.

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... 40 Protection of Environment 22 2011-07-01 2011-07-01 false Urban area pretreatment program. 125... Modifying the Secondary Treatment Requirements Under Section 301(h) of the Clean Water Act § 125.65 Urban... this section shall demonstrate that it either: (i) Has an applicable pretreatment requirement in effect...

  4. 40 CFR 125.65 - Urban area pretreatment program.

    Code of Federal Regulations, 2014 CFR

    2014-07-01

    ... 40 Protection of Environment 22 2014-07-01 2013-07-01 true Urban area pretreatment program. 125.65... Secondary Treatment Requirements Under Section 301(h) of the Clean Water Act § 125.65 Urban area... section shall demonstrate that it either: (i) Has an applicable pretreatment requirement in effect in...

  5. 40 CFR 125.65 - Urban area pretreatment program.

    Code of Federal Regulations, 2012 CFR

    2012-07-01

    ... 40 Protection of Environment 23 2012-07-01 2012-07-01 false Urban area pretreatment program. 125... Modifying the Secondary Treatment Requirements Under Section 301(h) of the Clean Water Act § 125.65 Urban... this section shall demonstrate that it either: (i) Has an applicable pretreatment requirement in effect...

  6. 40 CFR 424.16 - Pretreatment standards for new sources.

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... GUIDELINES AND STANDARDS FERROALLOY MANUFACTURING POINT SOURCE CATEGORY Open Electric Furnaces With Wet Air Pollution Control Devices Subcategory § 424.16 Pretreatment standards for new sources. Any new source... 40 Protection of Environment 28 2010-07-01 2010-07-01 true Pretreatment standards for new sources...

  7. 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.

  8. Erythropoietin pretreatment suppresses inflammation by activating the PI3K/Akt signaling pathway in myocardial ischemia-reperfusion injury

    PubMed Central

    RONG, REN; XIJUN, XIAO

    2015-01-01

    Erythropoietin (EPO), a glycoprotein originally known for its important role in the stimulation of erythropoiesis, has recently been shown to have significant protective effects in animal models of kidney and intestinal ischemia-reperfusion injury (IRI). However, the mechanism underlying these protective effects remains unclear. The aim of the current study was to evaluate the effects of EPO on myocardial IRI and to investigate the mechanism underlying these effects. A total of 18 male Sprague Dawley rats were randomly divided into three groups, namely the sham, IRI-saline and IRI-EPO groups. Rats in the IRI-EPO group were administered 5,000 U/kg EPO intraperitoneally 24 h prior to the induction of IRI. IRI was induced by ligating the left descending coronary artery for 30 min, followed by reperfusion for 3 h. Pathological changes in the myocardial tissue were observed and scored. The levels of the proinflammatory cytokines, interleukin (IL)-6, IL-1β and tumor necrosis factor (TNF)-α, were evaluated in the serum and myocardial tissue. Furthermore, the effects of EPO on phosphoinositide 3-kinase/protein kinase B (PI3K/Akt) signaling and EPO receptor (EPOR) phosphorylation were measured. Pathological changes in the myocardial tissue, increased expression levels of TNF-α, IL-6 and IL-1β in the myocardium, and increased serum levels of these mediators, as a result of IRI, were significantly decreased by EPO pretreatment. The effects of EPO were found to be associated with the activation of PI3K/Akt signaling, which suppressed the inflammatory responses, following the initiation of EPOR activation by EPO. Therefore, EPO pretreatment was demonstrated to decrease myocardial IRI, which was associated with activation of EPOR, subsequently increasing PI3K/Akt signaling to inhibit the production and release of inflammatory mediators. Thus, the results of the present study indicated that EPO may be useful for preventing myocardial IRI. PMID:26622330

  9. 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.

  10. Ischemic postconditioning of the isolated human myocardium: Role of the applied protocol.

    PubMed

    Casós, Kelly; Pérez, María-Llanos; Blasco-Lucas, Arnau; Ferrer-Curriu, Gemma; Gracia-Baena, Juan Manuel; Sureda, Carlos; Permanyer, Eduard; Igual, Alberto; Galiñanes, Manuel

    2015-09-01

    Ischemic postconditioning (IPostC), has been proposed as a useful approach to reduce infarct size in all species, but its clinical utility remains unclear. To investigate the role played by the protocol used on the efficacy of IPostC in protecting the diseased human myocardium. Myocardial atrial samples from patients were subjected to a 90 min ischemia/120 min reoxygenation followed by different IPostC protocols to investigate the role of the time of ischemia (30, 60, 90 and 120 s) and the number of cycles (1, 2, 3 and 4) with 60 and 120 s of total ischemic time. Muscles were also subjected to ischemic preconditioning (IPreC). The release of lactate dehydrogenase (LDH) and the measurement of tetrazolium bromide (MTT) were determined. IPostC increased the LDH and decreased the MTT values from those of control, independently of the duration of the conditioning ischemia. LDH and MTT values also worsened by augmenting the number of IPostC cycles whereas they were significantly improved by IPreC. However, analysis of individual results indicated that in approximately 1/3 of the cases IPostC exhibited some degree of protection especially in the presence of increased ischemic injury. The present findings show that IPostC of the human myocardium may be influenced by the protocol used and also by the degree of the preceding ischemic injury. IPostC was beneficial in approximately 1/3 of the cases; however in the remaining cases it increased ischemic damage and, therefore, these results raise a word of caution on its broad clinical use.

  11. A biochemical, electrocardiographic, electrophoretic, histopathological and in vitro study on the protective effects of (-)epicatechin in isoproterenol-induced myocardial infarcted rats.

    PubMed

    Prince, Ponnian Stanely Mainzen

    2011-12-05

    (-) Epicatechin rich foods and (-) epicatechin improve cardiovascular function. Consumption of diets rich in flavonoids is associated with reduced risk of cardiovascular diseases. Oxidative stress resulting from increased production of free radicals associated with decreased levels of antioxidants in the myocardium plays a major role in the pathogenesis of myocardial infarction. This study aims to evaluate the preventive effects of (-) epicatechin on oxidative stress in isoproterenol-induced myocardial infarcted rats. Male Wistar rats were pretreated with (-) epicatechin (20mg/kg body weight) daily for 21 days. After pretreatment, isoproterenol (100mg/kg body weight) was injected into the rats at an interval of 24h for two days to induce myocardial infarction. Isoproterenol induced rat's electrocardiogram showed elevated ST segments and significant increase in the activity of serum creatine kinase-MB, level of serum troponin-T and increased intensities of serum lactate dehydrogenase 1 and 2-isoenzymes. The rats also showed significant increased levels of heart lipid peroxidation products and significant decreased activities of heart superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and levels of reduced glutathione. Pretreatment with (-) epicatechin revealed significant protective effects on all the biochemical parameters and electrocardiogram investigated. Histopathology of myocardium confirmed the present findings. The in vitro study on the effects of (-) epicatechin on scavenging free radical 1,1-diphenyl-2-picrylhydrazyl revealed the free radical scavenging potential of (-) epicatechin. Thus, (-) epicatechin exerts protective effects against isoproterenol-induced oxidative stress thereby reducing cardiac tissue damage by its free radical scavenging and antioxidant effects. Copyright © 2011 Elsevier B.V. All rights reserved.

  12. Efficacy of coronary angioplasty for the treatment of hibernating myocardium

    PubMed Central

    Fath-Ordoubadi, F; Beatt, K; Spyrou, N; Camici, P

    1999-01-01

    OBJECTIVES—To determine the efficacy of coronary angioplasty as the sole method of revascularisation in patients with coronary artery disease and chronically dysfunctional but viable myocardium (hibernating myocardium), and to assess the effect of restenosis on functional outcome.
DESIGN AND PATIENTS—24 consecutive patients with hibernating myocardium were studied. Positron emission tomography was used to assess myocardial viability, blood flow, and flow reserve. One patient refused angioplasty, one had bypass surgery, and one died while waiting for an elective procedure. The procedure failed in three patients. The remaining 18 patients had repeat echocardiography, 15 had repeat coronary angiography, and nine had repeat assessments of blood flow and flow reserve at mean (SD) 17 (2) weeks after angioplasty. In three patients restenosis was documented.
RESULTS—The wall motion score index in the revascularised territories improved from 1.71 (0.37) to 1.34 (0.47) (p = 0.008). Thirty of 51 dysfunctional segments improved in territories without restenosis compared with three of 14 in restenosed territories (p = 0.001). Hibernating and normal segments had comparable flows (0.82 (0.26) v 0.89 (0.24) ml/min/g; NS) while flow reserve was lower in hibernating segments (1.55 (0.68) v 2.07 (1.08); p = 0.03). In segments without restenosis flow reserve improved from 2.03 (1.25) to 2.33 (1.4) (p = 0.03). Sensitivity, specificity, and positive and negative predictive accuracy of the viability study were 97%, 77%, 82%, and 96%, respectively. After excluding patients with restenosis, specificity and positive predictive accuracy improved to 90% and 93%.
CONCLUSIONS—Angioplasty improves function in hibernating myocardium, and restenosis prevents recovery; hibernating myocardium is characterised by an impairment of flow reserve; restenosis affects the diagnostic accuracy of viability studies.


Keywords: coronary artery disease; percutaneous

  13. Atlantic salmon endothelial cells from the heart were more susceptible than fibroblasts from the bulbus arteriosus to four RNA viruses but protected from two viruses by dsRNA pretreatment.

    PubMed

    Pham, Phuc H; Tong, Winnie W L; Misk, Ehab; Jones, Ginny; Lumsden, John S; Bols, Niels C

    2017-09-04

    Heart diseases caused by viruses are major causes of Atlantic salmon aquaculture loss. Two Atlantic salmon cardiovascular cell lines, an endothelial cell line (ASHe) from the heart and a fibroblast cell line (BAASf) from the bulbus arteriosus, were evaluated for their response to four fish viruses, CSV, IPNV, VHSV IVa and VHSV IVb, and the innate immune agonist, double-stranded RNA mimic poly IC. All four viruses caused cytopathic effects in ASHe and BAASf. However, ASHe was more susceptible to all four viruses than BAASf. When comparing between the viruses, ASHe cells were found to be moderately susceptible to CSV and VHSV IVb, but highly susceptible to IPNV and VHSV IVa induced cell death. All four viruses were capable of propagating in the ASHe cell line, leading to increases in virus titre over time. In BAASf, CSV and IPNV produced more than one log increase in titre from initial infection, but VHSV IVb and IVa did not. When looking at the antiviral response of both cell lines, Mx proteins were induced in ASHe and BAASf by poly IC. All four viruses induced Mx proteins in BAASf, while only CSV and VHSV IVb induced Mx proteins in ASHe. IPNV and VHSV IVa suppressed Mx proteins expression in ASHe. Pretreatment of ASHe with poly IC to allow for Mx proteins accumulation protected the culture from subsequent infections with IPNV and VHSV IVa, resulting in delayed cell death, reduced virus titres and reduced viral proteins expression. These data suggest that endothelial cells potentially can serve as points of infections for viruses in the heart and that two of the four viruses, IPNV and VHSV IVa, have mechanisms to avoid or downregulate antiviral responses in ASHe cells. Furthermore, the high susceptibility of the ASHe cell line to IPNV and VHSV IVa can make it a useful tool for studying antiviral compounds against these viruses and for general detection of fish viruses. Copyright © 2017 Elsevier Ltd. All rights reserved.

  14. Pretreatment and Enzymatic Hydrolysis

    SciTech Connect

    2006-06-01

    Activities in this project are aimed at overcoming barriers associated with high capital and operating costs and sub-optimal sugar yields resulting from pretreatment and subsequent enzymatic hydrolysis of biomass.

  15. 40 CFR 403.10 - Development and submission of NPDES State pretreatment programs.

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... 40 Protection of Environment 28 2010-07-01 2010-07-01 true Development and submission of NPDES State pretreatment programs. 403.10 Section 403.10 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS GENERAL PRE-TREAT-MENT REGULATIONS FOR EXIST-ING...

  16. 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...

  17. 40 CFR 429.35 - Pretreatment standards for existing sources (PSES).

    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). 429.35 Section 429.35 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED... Subcategory § 429.35 Pretreatment standards for existing sources (PSES). Any existing source subject to this...

  18. 40 CFR 437.35 - Pretreatment standards for existing sources (PSES).

    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). 437.35 Section 437.35 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED... Organics Treatment and Recovery § 437.35 Pretreatment standards for existing sources (PSES). Except as...

  19. 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...

  20. 40 CFR 403.10 - Development and submission of NPDES State pretreatment programs.

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... 40 Protection of Environment 29 2011-07-01 2009-07-01 true Development and submission of NPDES State pretreatment programs. 403.10 Section 403.10 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS GENERAL PRE-TREAT-MENT REGULATIONS FOR EXIST-ING...

  1. 40 CFR 403.10 - Development and submission of NPDES State pretreatment programs.

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ... 40 Protection of Environment 30 2013-07-01 2012-07-01 true Development and submission of NPDES State pretreatment programs. 403.10 Section 403.10 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS GENERAL PRETREATMENT REGULATIONS FOR EXISTING...

  2. 40 CFR 403.20 - Pretreatment Program Reinvention Pilot Projects Under Project XL.

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ... 40 Protection of Environment 30 2013-07-01 2012-07-01 true Pretreatment Program Reinvention Pilot Projects Under Project XL. 403.20 Section 403.20 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY... OF POLLUTION § 403.20 Pretreatment Program Reinvention Pilot Projects Under Project XL. The Approval...

  3. 40 CFR 437.15 - Pretreatment standards for existing sources (PSES).

    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). 437.15 Section 437.15 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED... subject to this subpart must achieve the following pretreatment standards: Standards for antimony,...

  4. 40 CFR 444.18 - Pretreatment standards for new sources (PSNS).

    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). 444.18 Section 444.18 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED... part 403 and achieve the following pretreatment standards: Standards for arsenic, cadmium,...

  5. 40 CFR 407.46 - 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. 407.46 Section 407.46 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS CANNED AND PRESERVED FRUITS AND VEGETABLES PROCESSING POINT SOURCE CATEGORY...

  6. 40 CFR 426.56 - Pretreatment standards for new sources.

    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. 426.56 Section 426.56 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS GLASS MANUFACTURING POINT SOURCE CATEGORY Float Glass Manufacturing Subcategory...

  7. 40 CFR 426.106 - Pretreatment standards for new sources.

    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. 426.106 Section 426.106 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) GLASS MANUFACTURING POINT SOURCE CATEGORY Glass Tubing (Danner...

  8. 40 CFR 426.64 - Pretreatment standards for existing sources.

    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. 426.64 Section 426.64 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS GLASS MANUFACTURING POINT SOURCE CATEGORY Automotive Glass Tempering...

  9. 40 CFR 426.26 - Pretreatment standards for new sources.

    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. 426.26 Section 426.26 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) GLASS MANUFACTURING POINT SOURCE CATEGORY Sheet Glass Manufacturing...

  10. 40 CFR 426.56 - Pretreatment standards for new sources.

    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. 426.56 Section 426.56 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) GLASS MANUFACTURING POINT SOURCE CATEGORY Float Glass Manufacturing...

  11. 40 CFR 426.76 - Pretreatment standards for new sources.

    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. 426.76 Section 426.76 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS GLASS MANUFACTURING POINT SOURCE CATEGORY Automotive Glass Laminating Subcategory...

  12. 40 CFR 426.24 - Pretreatment standards for existing sources.

    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. 426.24 Section 426.24 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) GLASS MANUFACTURING POINT SOURCE CATEGORY Sheet Glass...

  13. 40 CFR 426.64 - Pretreatment standards for existing sources.

    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. 426.64 Section 426.64 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) GLASS MANUFACTURING POINT SOURCE CATEGORY Automotive Glass...

  14. 40 CFR 426.34 - Pretreatment standards for existing sources.

    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. 426.34 Section 426.34 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) GLASS MANUFACTURING POINT SOURCE CATEGORY Rolled Glass...

  15. 40 CFR 426.136 - Pretreatment standards for new sources.

    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. 426.136 Section 426.136 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS GLASS MANUFACTURING POINT SOURCE CATEGORY Hand Pressed and Blown Glass Manufacturing...

  16. 40 CFR 426.36 - Pretreatment standards for new sources.

    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. 426.36 Section 426.36 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) GLASS MANUFACTURING POINT SOURCE CATEGORY Rolled Glass Manufacturing...

  17. 40 CFR 426.76 - Pretreatment standards for new sources.

    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. 426.76 Section 426.76 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) GLASS MANUFACTURING POINT SOURCE CATEGORY Automotive Glass Laminating...

  18. 40 CFR 426.34 - Pretreatment standards for existing sources.

    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. 426.34 Section 426.34 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS GLASS MANUFACTURING POINT SOURCE CATEGORY Rolled Glass Manufacturing...

  19. 40 CFR 426.24 - Pretreatment standards for existing sources.

    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. 426.24 Section 426.24 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS GLASS MANUFACTURING POINT SOURCE CATEGORY Sheet Glass Manufacturing...

  20. 40 CFR 426.76 - Pretreatment standards for new sources.

    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. 426.76 Section 426.76 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) GLASS MANUFACTURING POINT SOURCE CATEGORY Automotive Glass Laminating...

  1. 40 CFR 426.106 - Pretreatment standards for new sources.

    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. 426.106 Section 426.106 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS GLASS MANUFACTURING POINT SOURCE CATEGORY Glass Tubing (Danner) Manufacturing...

  2. 40 CFR 426.26 - Pretreatment standards for new sources.

    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. 426.26 Section 426.26 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS GLASS MANUFACTURING POINT SOURCE CATEGORY Sheet Glass Manufacturing Subcategory...

  3. 40 CFR 426.34 - Pretreatment standards for existing sources.

    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. 426.34 Section 426.34 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) GLASS MANUFACTURING POINT SOURCE CATEGORY Rolled Glass...

  4. 40 CFR 426.34 - Pretreatment standards for existing sources.

    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. 426.34 Section 426.34 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) GLASS MANUFACTURING POINT SOURCE CATEGORY Rolled Glass...

  5. 40 CFR 426.66 - Pretreatment standards for new sources.

    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. 426.66 Section 426.66 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS GLASS MANUFACTURING POINT SOURCE CATEGORY Automotive Glass Tempering Subcategory...

  6. 40 CFR 426.64 - Pretreatment standards for existing sources.

    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. 426.64 Section 426.64 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) GLASS MANUFACTURING POINT SOURCE CATEGORY Automotive Glass...

  7. 40 CFR 426.56 - Pretreatment standards for new sources.

    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. 426.56 Section 426.56 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) GLASS MANUFACTURING POINT SOURCE CATEGORY Float Glass Manufacturing...

  8. 40 CFR 426.36 - Pretreatment standards for new sources.

    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. 426.36 Section 426.36 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS GLASS MANUFACTURING POINT SOURCE CATEGORY Rolled Glass Manufacturing Subcategory...

  9. 40 CFR 426.26 - Pretreatment standards for new sources.

    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. 426.26 Section 426.26 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) GLASS MANUFACTURING POINT SOURCE CATEGORY Sheet Glass Manufacturing...

  10. 40 CFR 426.76 - Pretreatment standards for new sources.

    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. 426.76 Section 426.76 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) GLASS MANUFACTURING POINT SOURCE CATEGORY Automotive Glass Laminating...

  11. 40 CFR 426.26 - Pretreatment standards for new sources.

    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. 426.26 Section 426.26 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) GLASS MANUFACTURING POINT SOURCE CATEGORY Sheet Glass Manufacturing...

  12. 40 CFR 426.66 - Pretreatment standards for new sources.

    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. 426.66 Section 426.66 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) GLASS MANUFACTURING POINT SOURCE CATEGORY Automotive Glass Tempering...

  13. 40 CFR 426.36 - Pretreatment standards for new sources.

    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. 426.36 Section 426.36 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) GLASS MANUFACTURING POINT SOURCE CATEGORY Rolled Glass Manufacturing...

  14. 40 CFR 426.66 - Pretreatment standards for new sources.

    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. 426.66 Section 426.66 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) GLASS MANUFACTURING POINT SOURCE CATEGORY Automotive Glass Tempering...

  15. 40 CFR 426.24 - Pretreatment standards for existing sources.

    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. 426.24 Section 426.24 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) GLASS MANUFACTURING POINT SOURCE CATEGORY Sheet Glass...

  16. 40 CFR 426.56 - Pretreatment standards for new sources.

    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. 426.56 Section 426.56 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) GLASS MANUFACTURING POINT SOURCE CATEGORY Float Glass Manufacturing...

  17. 40 CFR 426.106 - Pretreatment standards for new sources.

    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. 426.106 Section 426.106 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) GLASS MANUFACTURING POINT SOURCE CATEGORY Glass Tubing (Danner...

  18. 40 CFR 426.66 - Pretreatment standards for new sources.

    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. 426.66 Section 426.66 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) GLASS MANUFACTURING POINT SOURCE CATEGORY Automotive Glass Tempering...

  19. 40 CFR 426.106 - Pretreatment standards for new sources.

    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. 426.106 Section 426.106 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) GLASS MANUFACTURING POINT SOURCE CATEGORY Glass Tubing (Danner...

  20. 40 CFR 426.64 - Pretreatment standards for existing sources.

    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. 426.64 Section 426.64 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) GLASS MANUFACTURING POINT SOURCE CATEGORY Automotive Glass...

  1. 40 CFR 426.24 - Pretreatment standards for existing sources.

    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. 426.24 Section 426.24 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) GLASS MANUFACTURING POINT SOURCE CATEGORY Sheet Glass...

  2. 40 CFR 426.36 - Pretreatment standards for new sources.

    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. 426.36 Section 426.36 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) GLASS MANUFACTURING POINT SOURCE CATEGORY Rolled Glass Manufacturing...

  3. 40 CFR 424.16 - Pretreatment standards for new sources.

    Code of Federal Regulations, 2014 CFR

    2014-07-01

    ... 40 Protection of Environment 29 2014-07-01 2012-07-01 true Pretreatment standards for new sources. 424.16 Section 424.16 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS FERROALLOY MANUFACTURING POINT SOURCE CATEGORY Open Electric Furnaces With Wet Air...

  4. 40 CFR 458.16 - Pretreatment standards for new sources.

    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. 458.16 Section 458.16 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) CARBON BLACK MANUFACTURING POINT SOURCE CATEGORY Carbon Black Furnace...

  5. 40 CFR 458.16 - Pretreatment standards for new sources.

    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. 458.16 Section 458.16 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS CARBON BLACK MANUFACTURING POINT SOURCE CATEGORY Carbon Black Furnace Process...

  6. 40 CFR 458.16 - Pretreatment standards for new sources.

    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. 458.16 Section 458.16 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) CARBON BLACK MANUFACTURING POINT SOURCE CATEGORY Carbon Black Furnace...

  7. 40 CFR 424.26 - Pretreatment standards for new sources.

    Code of Federal Regulations, 2014 CFR

    2014-07-01

    ... 40 Protection of Environment 29 2014-07-01 2012-07-01 true Pretreatment standards for new sources. 424.26 Section 424.26 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS FERROALLOY MANUFACTURING POINT SOURCE CATEGORY Covered Electric Furnaces and Other...

  8. 40 CFR 424.16 - Pretreatment standards for new sources.

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ... 40 Protection of Environment 30 2013-07-01 2012-07-01 true Pretreatment standards for new sources. 424.16 Section 424.16 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS FERROALLOY MANUFACTURING POINT SOURCE CATEGORY Open Electric Furnaces With Wet Air...

  9. 40 CFR 424.26 - Pretreatment standards for new sources.

    Code of Federal Regulations, 2012 CFR

    2012-07-01

    ... 40 Protection of Environment 30 2012-07-01 2012-07-01 false Pretreatment standards for new sources. 424.26 Section 424.26 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS FERROALLOY MANUFACTURING POINT SOURCE CATEGORY Covered Electric Furnaces and Other...

  10. 40 CFR 424.26 - Pretreatment standards for new sources.

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ... 40 Protection of Environment 30 2013-07-01 2012-07-01 true Pretreatment standards for new sources. 424.26 Section 424.26 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS FERROALLOY MANUFACTURING POINT SOURCE CATEGORY Covered Electric Furnaces and Other...

  11. 40 CFR 424.16 - Pretreatment standards for new sources.

    Code of Federal Regulations, 2012 CFR

    2012-07-01

    ... 40 Protection of Environment 30 2012-07-01 2012-07-01 false Pretreatment standards for new sources. 424.16 Section 424.16 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS FERROALLOY MANUFACTURING POINT SOURCE CATEGORY Open Electric Furnaces With Wet Air...

  12. 40 CFR 424.26 - 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. 424.26 Section 424.26 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS FERROALLOY MANUFACTURING POINT SOURCE CATEGORY Covered Electric Furnaces and Other...

  13. 40 CFR 424.16 - 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. 424.16 Section 424.16 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS FERROALLOY MANUFACTURING POINT SOURCE CATEGORY Open Electric Furnaces With Wet Air...

  14. 40 CFR 458.16 - Pretreatment standards for new sources.

    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. 458.16 Section 458.16 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) CARBON BLACK MANUFACTURING POINT SOURCE CATEGORY Carbon Black Furnace...

  15. 40 CFR 405.46 - 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. 405.46 Section 405.46 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS DAIRY PRODUCTS PROCESSING POINT SOURCE CATEGORY Butter Subcategory §...

  16. 40 CFR 405.44 - Pretreatment standards for existing 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 existing sources. 405.44 Section 405.44 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS DAIRY PRODUCTS PROCESSING POINT SOURCE CATEGORY Butter Subcategory §...

  17. 40 CFR 408.36 - Pretreatment standards for new sources.

    Code of Federal Regulations, 2014 CFR

    2014-07-01

    ... 40 Protection of Environment 29 2014-07-01 2012-07-01 true Pretreatment standards for new sources. 408.36 Section 408.36 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS CANNED AND PRESERVED SEAFOOD PROCESSING POINT SOURCE CATEGORY Mechanized Blue...

  18. 40 CFR 408.26 - Pretreatment standards for new sources.

    Code of Federal Regulations, 2012 CFR

    2012-07-01

    ... 40 Protection of Environment 30 2012-07-01 2012-07-01 false Pretreatment standards for new sources. 408.26 Section 408.26 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS CANNED AND PRESERVED SEAFOOD PROCESSING POINT SOURCE CATEGORY Conventional Blue...

  19. 40 CFR 408.26 - Pretreatment standards for new sources.

    Code of Federal Regulations, 2014 CFR

    2014-07-01

    ... 40 Protection of Environment 29 2014-07-01 2012-07-01 true Pretreatment standards for new sources. 408.26 Section 408.26 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS CANNED AND PRESERVED SEAFOOD PROCESSING POINT SOURCE CATEGORY Conventional Blue...

  20. 40 CFR 408.36 - 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. 408.36 Section 408.36 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS CANNED AND PRESERVED SEAFOOD PROCESSING POINT SOURCE CATEGORY Mechanized Blue...

  1. 40 CFR 408.36 - Pretreatment standards for new sources.

    Code of Federal Regulations, 2012 CFR

    2012-07-01

    ... 40 Protection of Environment 30 2012-07-01 2012-07-01 false Pretreatment standards for new sources. 408.36 Section 408.36 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS CANNED AND PRESERVED SEAFOOD PROCESSING POINT SOURCE CATEGORY Mechanized Blue...

  2. 40 CFR 408.26 - 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. 408.26 Section 408.26 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS CANNED AND PRESERVED SEAFOOD PROCESSING POINT SOURCE CATEGORY Conventional Blue...

  3. 40 CFR 408.36 - 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. 408.36 Section 408.36 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS CANNED AND PRESERVED SEAFOOD PROCESSING POINT SOURCE CATEGORY Mechanized Blue...

  4. 40 CFR 408.26 - Pretreatment standards for new sources.

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ... 40 Protection of Environment 30 2013-07-01 2012-07-01 true Pretreatment standards for new sources. 408.26 Section 408.26 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS CANNED AND PRESERVED SEAFOOD PROCESSING POINT SOURCE CATEGORY Conventional Blue...

  5. 40 CFR 408.26 - 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. 408.26 Section 408.26 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS CANNED AND PRESERVED SEAFOOD PROCESSING POINT SOURCE CATEGORY Conventional Blue...

  6. 40 CFR 408.36 - Pretreatment standards for new sources.

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ... 40 Protection of Environment 30 2013-07-01 2012-07-01 true Pretreatment standards for new sources. 408.36 Section 408.36 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS CANNED AND PRESERVED SEAFOOD PROCESSING POINT SOURCE CATEGORY Mechanized Blue...

  7. 40 CFR 406.34 - 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. 406.34 Section 406.34 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS GRAIN MILLS POINT SOURCE CATEGORY Normal Wheat Flour Milling...

  8. 40 CFR 406.44 - 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. 406.44 Section 406.44 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS GRAIN MILLS POINT SOURCE CATEGORY Bulgur Wheat Flour Milling...

  9. 40 CFR 406.36 - 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. 406.36 Section 406.36 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS GRAIN MILLS POINT SOURCE CATEGORY Normal Wheat Flour Milling Subcategory §...

  10. 40 CFR 406.46 - 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. 406.46 Section 406.46 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS GRAIN MILLS POINT SOURCE CATEGORY Bulgur Wheat Flour Milling Subcategory §...

  11. 40 CFR 427.106 - Pretreatment standards for new sources.

    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. 427.106 Section 427.106 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) ASBESTOS MANUFACTURING POINT SOURCE CATEGORY Vapor...

  12. 40 CFR 427.106 - Pretreatment standards for new sources.

    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. 427.106 Section 427.106 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) ASBESTOS MANUFACTURING POINT SOURCE CATEGORY Vapor...

  13. 40 CFR 427.106 - 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. 427.106 Section 427.106 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS ASBESTOS MANUFACTURING POINT SOURCE CATEGORY Vapor Absorption Subcategory §...

  14. 40 CFR 427.106 - Pretreatment standards for new sources.

    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. 427.106 Section 427.106 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS ASBESTOS MANUFACTURING POINT SOURCE CATEGORY Vapor Absorption Subcategory §...

  15. 40 CFR 427.106 - Pretreatment standards for new sources.

    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. 427.106 Section 427.106 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) ASBESTOS MANUFACTURING POINT SOURCE CATEGORY Vapor...

  16. 40 CFR 412.3 - General pretreatment standards.

    Code of Federal Regulations, 2014 CFR

    2014-07-01

    ... 40 Protection of Environment 29 2014-07-01 2012-07-01 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 General...

  17. 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 General...

  18. 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 General...

  19. 40 CFR 412.3 - General pretreatment standards.

    Code of Federal Regulations, 2012 CFR

    2012-07-01

    ... 40 Protection of Environment 30 2012-07-01 2012-07-01 false 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 General...

  20. 40 CFR 412.3 - General pretreatment standards.

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ... 40 Protection of Environment 30 2013-07-01 2012-07-01 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 General...

  1. 40 CFR 458.16 - 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. 458.16 Section 458.16 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS CARBON BLACK MANUFACTURING POINT SOURCE CATEGORY Carbon Black Furnace...

  2. 40 CFR 424.26 - 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. 424.26 Section 424.26 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS FERROALLOY MANUFACTURING POINT SOURCE CATEGORY Covered Electric Furnaces and...

  3. 40 CFR 411.26 - 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. 411.26 Section 411.26 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS CEMENT MANUFACTURING POINT SOURCE CATEGORY Leaching Subcategory §...

  4. 40 CFR 411.34 - 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. 411.34 Section 411.34 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS CEMENT MANUFACTURING POINT SOURCE CATEGORY Materials Storage Piles...

  5. 40 CFR 411.16 - 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. 411.16 Section 411.16 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS CEMENT MANUFACTURING POINT SOURCE CATEGORY Nonleaching Subcategory §...

  6. 40 CFR 411.14 - 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. 411.14 Section 411.14 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS CEMENT MANUFACTURING POINT SOURCE CATEGORY Nonleaching Subcategory §...

  7. 40 CFR 411.36 - 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. 411.36 Section 411.36 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS CEMENT MANUFACTURING POINT SOURCE CATEGORY Materials Storage Piles...

  8. 40 CFR 411.24 - 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. 411.24 Section 411.24 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS CEMENT MANUFACTURING POINT SOURCE CATEGORY Leaching Subcategory §...

  9. 40 CFR 427.36 - Pretreatment standards for new sources.

    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. 427.36 Section 427.36 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS ASBESTOS MANUFACTURING POINT SOURCE CATEGORY Asbestos Paper (Starch Binder...

  10. 40 CFR 427.36 - Pretreatment standards for new sources.

    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. 427.36 Section 427.36 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) ASBESTOS MANUFACTURING POINT SOURCE CATEGORY Asbestos Paper (Starch...

  11. 40 CFR 427.34 - Pretreatment standards for existing sources.

    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. 427.34 Section 427.34 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS ASBESTOS MANUFACTURING POINT SOURCE CATEGORY Asbestos Paper (Starch...

  12. 40 CFR 427.36 - 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. 427.36 Section 427.36 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS ASBESTOS MANUFACTURING POINT SOURCE CATEGORY Asbestos Paper (Starch Binder...

  13. 40 CFR 427.34 - Pretreatment standards for existing 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 existing sources. 427.34 Section 427.34 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS ASBESTOS MANUFACTURING POINT SOURCE CATEGORY Asbestos Paper (Starch...

  14. 40 CFR 427.36 - Pretreatment standards for new sources.

    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. 427.36 Section 427.36 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) ASBESTOS MANUFACTURING POINT SOURCE CATEGORY Asbestos Paper (Starch...

  15. 40 CFR 427.36 - Pretreatment standards for new sources.

    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. 427.36 Section 427.36 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) ASBESTOS MANUFACTURING POINT SOURCE CATEGORY Asbestos Paper (Starch...

  16. 40 CFR 407.24 - Pretreatment standards for existing sources.

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ... 40 Protection of Environment 30 2013-07-01 2012-07-01 true Pretreatment standards for existing sources. 407.24 Section 407.24 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS CANNED AND PRESERVED FRUITS AND VEGETABLES PROCESSING POINT...

  17. 40 CFR 407.14 - Pretreatment standards for existing sources.

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ... 40 Protection of Environment 30 2013-07-01 2012-07-01 true Pretreatment standards for existing sources. 407.14 Section 407.14 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS CANNED AND PRESERVED FRUITS AND VEGETABLES PROCESSING POINT...

  18. 40 CFR 409.16 - Pretreatment standards for new sources.

    Code of Federal Regulations, 2012 CFR

    2012-07-01

    ... 40 Protection of Environment 30 2012-07-01 2012-07-01 false Pretreatment standards for new sources. 409.16 Section 409.16 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS SUGAR PROCESSING POINT SOURCE CATEGORY Beet Sugar Processing Subcategory § 409.16...

  19. 40 CFR 409.34 - Pretreatment standards for existing sources.

    Code of Federal Regulations, 2014 CFR

    2014-07-01

    ... 40 Protection of Environment 29 2014-07-01 2012-07-01 true Pretreatment standards for existing sources. 409.34 Section 409.34 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS SUGAR PROCESSING POINT SOURCE CATEGORY Liquid Cane Sugar Refining...

  20. 40 CFR 409.34 - Pretreatment standards for existing sources.

    Code of Federal Regulations, 2012 CFR

    2012-07-01

    ... 40 Protection of Environment 30 2012-07-01 2012-07-01 false Pretreatment standards for existing sources. 409.34 Section 409.34 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS SUGAR PROCESSING POINT SOURCE CATEGORY Liquid Cane Sugar Refining...

  1. 40 CFR 409.14 - Pretreatment standards for existing sources.

    Code of Federal Regulations, 2014 CFR

    2014-07-01

    ... 40 Protection of Environment 29 2014-07-01 2012-07-01 true Pretreatment standards for existing sources. 409.14 Section 409.14 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS SUGAR PROCESSING POINT SOURCE CATEGORY Beet Sugar Processing Subcategory...

  2. 40 CFR 409.26 - Pretreatment standards for new sources.

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ... 40 Protection of Environment 30 2013-07-01 2012-07-01 true Pretreatment standards for new sources. 409.26 Section 409.26 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS SUGAR PROCESSING POINT SOURCE CATEGORY Crystalline Cane Sugar Refining Subcategory...

  3. 40 CFR 409.24 - Pretreatment standards for existing sources.

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ... 40 Protection of Environment 30 2013-07-01 2012-07-01 true Pretreatment standards for existing sources. 409.24 Section 409.24 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS SUGAR PROCESSING POINT SOURCE CATEGORY Crystalline Cane Sugar Refining...

  4. 40 CFR 409.24 - Pretreatment standards for existing sources.

    Code of Federal Regulations, 2014 CFR

    2014-07-01

    ... 40 Protection of Environment 29 2014-07-01 2012-07-01 true Pretreatment standards for existing sources. 409.24 Section 409.24 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS SUGAR PROCESSING POINT SOURCE CATEGORY Crystalline Cane Sugar Refining...

  5. 40 CFR 409.36 - Pretreatment standards for new sources.

    Code of Federal Regulations, 2012 CFR

    2012-07-01

    ... 40 Protection of Environment 30 2012-07-01 2012-07-01 false Pretreatment standards for new sources. 409.36 Section 409.36 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS SUGAR PROCESSING POINT SOURCE CATEGORY Liquid Cane Sugar Refining Subcategory § 409...

  6. 40 CFR 409.16 - Pretreatment standards for new sources.

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ... 40 Protection of Environment 30 2013-07-01 2012-07-01 true Pretreatment standards for new sources. 409.16 Section 409.16 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS SUGAR PROCESSING POINT SOURCE CATEGORY Beet Sugar Processing Subcategory § 409.16...

  7. 40 CFR 409.26 - Pretreatment standards for new sources.

    Code of Federal Regulations, 2012 CFR

    2012-07-01

    ... 40 Protection of Environment 30 2012-07-01 2012-07-01 false Pretreatment standards for new sources. 409.26 Section 409.26 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS SUGAR PROCESSING POINT SOURCE CATEGORY Crystalline Cane Sugar Refining Subcategory...

  8. 40 CFR 409.24 - Pretreatment standards for existing sources.

    Code of Federal Regulations, 2012 CFR

    2012-07-01

    ... 40 Protection of Environment 30 2012-07-01 2012-07-01 false Pretreatment standards for existing sources. 409.24 Section 409.24 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS SUGAR PROCESSING POINT SOURCE CATEGORY Crystalline Cane Sugar Refining...

  9. 40 CFR 409.34 - Pretreatment standards for existing sources.

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ... 40 Protection of Environment 30 2013-07-01 2012-07-01 true Pretreatment standards for existing sources. 409.34 Section 409.34 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS SUGAR PROCESSING POINT SOURCE CATEGORY Liquid Cane Sugar Refining...

  10. 40 CFR 409.16 - 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. 409.16 Section 409.16 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS SUGAR PROCESSING POINT SOURCE CATEGORY Beet Sugar Processing Subcategory § 409.16...

  11. 40 CFR 409.26 - Pretreatment standards for new sources.

    Code of Federal Regulations, 2014 CFR

    2014-07-01

    ... 40 Protection of Environment 29 2014-07-01 2012-07-01 true Pretreatment standards for new sources. 409.26 Section 409.26 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS SUGAR PROCESSING POINT SOURCE CATEGORY Crystalline Cane Sugar Refining Subcategory...

  12. 40 CFR 409.36 - Pretreatment standards for new sources.

    Code of Federal Regulations, 2014 CFR

    2014-07-01

    ... 40 Protection of Environment 29 2014-07-01 2012-07-01 true Pretreatment standards for new sources. 409.36 Section 409.36 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS SUGAR PROCESSING POINT SOURCE CATEGORY Liquid Cane Sugar Refining Subcategory § 409...

  13. 40 CFR 409.16 - 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. 409.16 Section 409.16 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS SUGAR PROCESSING POINT SOURCE CATEGORY Beet Sugar Processing Subcategory § 409.16...

  14. 40 CFR 409.36 - Pretreatment standards for new sources.

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ... 40 Protection of Environment 30 2013-07-01 2012-07-01 true Pretreatment standards for new sources. 409.36 Section 409.36 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS SUGAR PROCESSING POINT SOURCE CATEGORY Liquid Cane Sugar Refining Subcategory § 409...

  15. 40 CFR 409.14 - Pretreatment standards for existing sources.

    Code of Federal Regulations, 2012 CFR

    2012-07-01

    ... 40 Protection of Environment 30 2012-07-01 2012-07-01 false Pretreatment standards for existing sources. 409.14 Section 409.14 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS SUGAR PROCESSING POINT SOURCE CATEGORY Beet Sugar Processing Subcategory...

  16. 40 CFR 409.14 - Pretreatment standards for existing 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 existing sources. 409.14 Section 409.14 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS SUGAR PROCESSING POINT SOURCE CATEGORY Beet Sugar Processing Subcategory...

  17. 40 CFR 409.14 - Pretreatment standards for existing sources.

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ... 40 Protection of Environment 30 2013-07-01 2012-07-01 true Pretreatment standards for existing sources. 409.14 Section 409.14 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS SUGAR PROCESSING POINT SOURCE CATEGORY Beet Sugar Processing Subcategory...

  18. 40 CFR 409.16 - Pretreatment standards for new sources.

    Code of Federal Regulations, 2014 CFR

    2014-07-01

    ... 40 Protection of Environment 29 2014-07-01 2012-07-01 true Pretreatment standards for new sources. 409.16 Section 409.16 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS SUGAR PROCESSING POINT SOURCE CATEGORY Beet Sugar Processing Subcategory § 409.16...

  19. 40 CFR 409.14 - 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. 409.14 Section 409.14 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS SUGAR PROCESSING POINT SOURCE CATEGORY Beet Sugar Processing Subcategory...

  20. 40 CFR 447.16 - Pretreatment standards for new sources.

    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. 447.16 Section 447.16 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) INK FORMULATING POINT SOURCE CATEGORY Oil-Base Solvent Wash Ink...

  1. 40 CFR 447.16 - Pretreatment standards for new sources.

    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. 447.16 Section 447.16 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) INK FORMULATING POINT SOURCE CATEGORY Oil-Base Solvent Wash Ink...

  2. 40 CFR 447.16 - Pretreatment standards for new sources.

    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. 447.16 Section 447.16 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) INK FORMULATING POINT SOURCE CATEGORY Oil-Base Solvent Wash Ink...

  3. 40 CFR 408.156 - 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. 408.156 Section 408.156 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS CANNED AND PRESERVED SEAFOOD PROCESSING POINT SOURCE CATEGORY Fish Meal...

  4. 40 CFR 408.154 - 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. 408.154 Section 408.154 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS CANNED AND PRESERVED SEAFOOD PROCESSING POINT SOURCE CATEGORY Fish...

  5. 40 CFR 408.206 - 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. 408.206 Section 408.206 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS CANNED AND PRESERVED SEAFOOD PROCESSING POINT SOURCE CATEGORY Alaskan Bottom...

  6. 40 CFR 413.54 - Pretreatment standards for existing 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 existing sources. 413.54 Section 413.54 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS ELECTROPLATING POINT SOURCE CATEGORY Coatings Subcategory § 413.54...

  7. 40 CFR 413.44 - Pretreatment standards for existing 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 existing sources. 413.44 Section 413.44 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS ELECTROPLATING POINT SOURCE CATEGORY Anodizing Subcategory § 413.44...

  8. 40 CFR 463.26 - Pretreatment for new sources.

    Code of Federal Regulations, 2014 CFR

    2014-07-01

    ... 40 Protection of Environment 30 2014-07-01 2014-07-01 false Pretreatment for new sources. 463.26 Section 463.26 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) PLASTICS MOLDING AND FORMING POINT SOURCE CATEGORY Cleaning...

  9. 40 CFR 463.26 - Pretreatment for new sources.

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ... 40 Protection of Environment 31 2013-07-01 2013-07-01 false Pretreatment for new sources. 463.26 Section 463.26 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) PLASTICS MOLDING AND FORMING POINT SOURCE CATEGORY Cleaning...

  10. 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 Steelmaking...

  11. 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 § 420.28...

  12. 40 CFR 420.05 - Pretreatment standards compliance date.

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... 40 Protection of Environment 28 2010-07-01 2010-07-01 true Pretreatment standards compliance date. 420.05 Section 420.05 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS IRON AND STEEL MANUFACTURING POINT SOURCE CATEGORY General Provisions § 420.05...

  13. 40 CFR 420.04 - Calculation of pretreatment standards.

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ... 40 Protection of Environment 30 2013-07-01 2012-07-01 true Calculation of pretreatment standards. 420.04 Section 420.04 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS IRON AND STEEL MANUFACTURING POINT SOURCE CATEGORY General Provisions § 420.04...

  14. 40 CFR 420.05 - Pretreatment standards compliance date.

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... 40 Protection of Environment 29 2011-07-01 2009-07-01 true Pretreatment standards compliance date. 420.05 Section 420.05 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS IRON AND STEEL MANUFACTURING POINT SOURCE CATEGORY General Provisions § 420.05...

  15. 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 § 420.18...

  16. 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 § 420.28...

  17. 40 CFR 420.05 - Pretreatment standards compliance date.

    Code of Federal Regulations, 2014 CFR

    2014-07-01

    ... 40 Protection of Environment 29 2014-07-01 2012-07-01 true Pretreatment standards compliance date. 420.05 Section 420.05 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS IRON AND STEEL MANUFACTURING POINT SOURCE CATEGORY General Provisions § 420.05...

  18. 40 CFR 420.05 - Pretreatment standards compliance date.

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ... 40 Protection of Environment 30 2013-07-01 2012-07-01 true Pretreatment standards compliance date. 420.05 Section 420.05 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS IRON AND STEEL MANUFACTURING POINT SOURCE CATEGORY General Provisions § 420.05...

  19. 40 CFR 466.25 - Pretreatment standards for new sources.

    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. 466.25 Section 466.25 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) PORCELAIN ENAMELING POINT SOURCE CATEGORY Cast Iron Basis Material...

  20. 40 CFR 420.04 - Calculation of pretreatment standards.

    Code of Federal Regulations, 2014 CFR

    2014-07-01

    ... 40 Protection of Environment 29 2014-07-01 2012-07-01 true Calculation of pretreatment standards. 420.04 Section 420.04 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS IRON AND STEEL MANUFACTURING POINT SOURCE CATEGORY General Provisions § 420.04...

  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 § 420.18...

  2. 40 CFR 420.04 - Calculation of pretreatment standards.

    Code of Federal Regulations, 2012 CFR

    2012-07-01

    ... 40 Protection of Environment 30 2012-07-01 2012-07-01 false Calculation of pretreatment standards. 420.04 Section 420.04 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS IRON AND STEEL MANUFACTURING POINT SOURCE CATEGORY General Provisions § 420.04...

  3. 40 CFR 420.04 - Calculation of pretreatment standards.

    Code of Federal Regulations, 2010 CFR

    2010-07-01

    ... 40 Protection of Environment 28 2010-07-01 2010-07-01 true Calculation of pretreatment standards. 420.04 Section 420.04 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS IRON AND STEEL MANUFACTURING POINT SOURCE CATEGORY General Provisions § 420.04...

  4. 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 § 420.18...

  5. 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 Subcategory...

  6. 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 § 420.28...

  7. 40 CFR 466.24 - Pretreatment standards for existing sources.

    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. 466.24 Section 466.24 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) PORCELAIN ENAMELING POINT SOURCE CATEGORY Cast Iron Basis...

  8. 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 Subcategory...

  9. 40 CFR 420.05 - Pretreatment standards compliance date.

    Code of Federal Regulations, 2012 CFR

    2012-07-01

    ... 40 Protection of Environment 30 2012-07-01 2012-07-01 false Pretreatment standards compliance date. 420.05 Section 420.05 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS IRON AND STEEL MANUFACTURING POINT SOURCE CATEGORY General Provisions § 420.05...

  10. 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 § 420.28...

  11. 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 § 420.18...

  12. 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 § 420.48...

  13. 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 § 420.48...

  14. 40 CFR 420.04 - Calculation of pretreatment standards.

    Code of Federal Regulations, 2011 CFR

    2011-07-01

    ... 40 Protection of Environment 29 2011-07-01 2009-07-01 true Calculation of pretreatment standards. 420.04 Section 420.04 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS IRON AND STEEL MANUFACTURING POINT SOURCE CATEGORY General Provisions § 420.04...

  15. 40 CFR 428.116 - 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. 428.116 Section 428.116 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS RUBBER MANUFACTURING POINT SOURCE CATEGORY Latex Foam Subcategory §...

  16. 40 CFR 408.56 - 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. 408.56 Section 408.56 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS CANNED AND PRESERVED SEAFOOD PROCESSING POINT SOURCE CATEGORY Remote Alaskan Crab...

  17. 40 CFR 408.56 - Pretreatment standards for new sources.

    Code of Federal Regulations, 2012 CFR

    2012-07-01

    ... 40 Protection of Environment 30 2012-07-01 2012-07-01 false Pretreatment standards for new sources. 408.56 Section 408.56 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS CANNED AND PRESERVED SEAFOOD PROCESSING POINT SOURCE CATEGORY Remote Alaskan Crab...

  18. 40 CFR 408.56 - Pretreatment standards for new sources.

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ... 40 Protection of Environment 30 2013-07-01 2012-07-01 true Pretreatment standards for new sources. 408.56 Section 408.56 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS CANNED AND PRESERVED SEAFOOD PROCESSING POINT SOURCE CATEGORY Remote Alaskan Crab...

  19. 40 CFR 408.56 - Pretreatment standards for new sources.

    Code of Federal Regulations, 2014 CFR

    2014-07-01

    ... 40 Protection of Environment 29 2014-07-01 2012-07-01 true Pretreatment standards for new sources. 408.56 Section 408.56 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS CANNED AND PRESERVED SEAFOOD PROCESSING POINT SOURCE CATEGORY Remote Alaskan Crab...

  20. 40 CFR 408.56 - 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. 408.56 Section 408.56 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS CANNED AND PRESERVED SEAFOOD PROCESSING POINT SOURCE CATEGORY Remote Alaskan Crab...

  1. 40 CFR 426.26 - 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. 426.26 Section 426.26 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS GLASS MANUFACTURING POINT SOURCE CATEGORY Sheet Glass Manufacturing...

  2. 40 CFR 426.56 - 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. 426.56 Section 426.56 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS GLASS MANUFACTURING POINT SOURCE CATEGORY Float Glass Manufacturing...

  3. 40 CFR 426.46 - 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. 426.46 Section 426.46 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS GLASS MANUFACTURING POINT SOURCE CATEGORY Plate Glass Manufacturing...

  4. 40 CFR 426.34 - Pretreatment standards for existing 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 existing sources. 426.34 Section 426.34 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS GLASS MANUFACTURING POINT SOURCE CATEGORY Rolled Glass...

  5. 40 CFR 426.76 - 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. 426.76 Section 426.76 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS GLASS MANUFACTURING POINT SOURCE CATEGORY Automotive Glass Laminating...

  6. 40 CFR 426.66 - 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. 426.66 Section 426.66 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS GLASS MANUFACTURING POINT SOURCE CATEGORY Automotive Glass Tempering...

  7. 40 CFR 426.44 - Pretreatment standards for existing 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 existing sources. 426.44 Section 426.44 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS GLASS MANUFACTURING POINT SOURCE CATEGORY Plate Glass...

  8. 40 CFR 426.106 - 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. 426.106 Section 426.106 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS GLASS MANUFACTURING POINT SOURCE CATEGORY Glass Tubing (Danner)...

  9. 40 CFR 426.36 - 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. 426.36 Section 426.36 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS GLASS MANUFACTURING POINT SOURCE CATEGORY Rolled Glass Manufacturing...

  10. 40 CFR 426.24 - Pretreatment standards for existing 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 existing sources. 426.24 Section 426.24 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS GLASS MANUFACTURING POINT SOURCE CATEGORY Sheet Glass...

  11. 40 CFR 458.26 - Pretreatment standards for new sources.

    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. 458.26 Section 458.26 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) CARBON BLACK MANUFACTURING POINT SOURCE CATEGORY Carbon Black Thermal...

  12. 40 CFR 458.26 - Pretreatment standards for new sources.

    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. 458.26 Section 458.26 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS CARBON BLACK MANUFACTURING POINT SOURCE CATEGORY Carbon Black Thermal Process...

  13. 40 CFR 458.26 - Pretreatment standards for new sources.

    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. 458.26 Section 458.26 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) CARBON BLACK MANUFACTURING POINT SOURCE CATEGORY Carbon Black Thermal...

  14. 40 CFR 466.35 - Pretreatment standards for new sources.

    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. 466.35 Section 466.35 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) PORCELAIN ENAMELING POINT SOURCE CATEGORY Aluminum Basis Material...

  15. 40 CFR 467.05 - Removal allowances for pretreatment standards.

    Code of Federal Regulations, 2014 CFR

    2014-07-01

    ... 40 Protection of Environment 30 2014-07-01 2014-07-01 false Removal allowances for pretreatment standards. 467.05 Section 467.05 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) ALUMINUM FORMING POINT SOURCE CATEGORY General Provisions...

  16. 40 CFR 464.15 - Pretreatment standards for existing sources.

    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. 464.15 Section 464.15 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) METAL MOLDING AND CASTING POINT SOURCE CATEGORY Aluminum...

  17. 40 CFR 465.35 - Pretreatment standards for new sources.

    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. 465.35 Section 465.35 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) COIL COATING POINT SOURCE CATEGORY Aluminum Basis Material Subcategory...

  18. 40 CFR 465.34 - Pretreatment standards for existing sources.

    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. 465.34 Section 465.34 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) COIL COATING POINT SOURCE CATEGORY Aluminum Basis Material...

  19. 40 CFR 464.16 - Pretreatment standards for new sources.

    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. 464.16 Section 464.16 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) METAL MOLDING AND CASTING POINT SOURCE CATEGORY Aluminum Casting...

  20. 40 CFR 466.34 - Pretreatment standards for existing sources.

    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. 466.34 Section 466.34 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) PORCELAIN ENAMELING POINT SOURCE CATEGORY Aluminum Basis...

  1. 40 CFR 426.136 - Pretreatment standards for new sources.

    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. 426.136 Section 426.136 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) GLASS MANUFACTURING POINT SOURCE CATEGORY Hand Pressed and Blown...

  2. 40 CFR 426.136 - Pretreatment standards for new sources.

    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. 426.136 Section 426.136 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) GLASS MANUFACTURING POINT SOURCE CATEGORY Hand Pressed and Blown...

  3. 40 CFR 426.136 - 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. 426.136 Section 426.136 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS GLASS MANUFACTURING POINT SOURCE CATEGORY Hand Pressed and Blown Glass...

  4. 40 CFR 426.136 - Pretreatment standards for new sources.

    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. 426.136 Section 426.136 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) GLASS MANUFACTURING POINT SOURCE CATEGORY Hand Pressed and Blown...

  5. 40 CFR 426.16 - Pretreatment standards for new sources.

    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. 426.16 Section 426.16 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS GLASS MANUFACTURING POINT SOURCE CATEGORY Insulation Fiberglass Subcategory § 426.16...

  6. 40 CFR 426.16 - Pretreatment standards for new sources.

    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. 426.16 Section 426.16 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) GLASS MANUFACTURING POINT SOURCE CATEGORY Insulation Fiberglass...

  7. 40 CFR 405.76 - 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. 405.76 Section 405.76 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS DAIRY PRODUCTS PROCESSING POINT SOURCE CATEGORY Fluid Mix for Ice Cream and...

  8. 40 CFR 405.86 - 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. 405.86 Section 405.86 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS DAIRY PRODUCTS PROCESSING POINT SOURCE CATEGORY Ice Cream, Frozen...

  9. 40 CFR 405.84 - 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. 405.84 Section 405.84 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS DAIRY PRODUCTS PROCESSING POINT SOURCE CATEGORY Ice Cream,...

  10. 40 CFR 405.74 - 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. 405.74 Section 405.74 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS DAIRY PRODUCTS PROCESSING POINT SOURCE CATEGORY Fluid Mix for Ice...

  11. 40 CFR 417.196 - 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. 417.196 Section 417.196 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS SOAP AND DETERGENT MANUFACTURING POINT SOURCE CATEGORY Manufacture of Detergent Bars...

  12. 40 CFR 417.196 - 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. 417.196 Section 417.196 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS SOAP AND DETERGENT MANUFACTURING POINT SOURCE CATEGORY Manufacture of Detergent Bars...

  13. 40 CFR 417.176 - Pretreatment standards for new sources.

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ... 40 Protection of Environment 30 2013-07-01 2012-07-01 true Pretreatment standards for new sources. 417.176 Section 417.176 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS SOAP AND DETERGENT MANUFACTURING POINT SOURCE CATEGORY Manufacture of Detergents by...

  14. 40 CFR 417.196 - Pretreatment standards for new sources.

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ... 40 Protection of Environment 30 2013-07-01 2012-07-01 true Pretreatment standards for new sources. 417.196 Section 417.196 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS SOAP AND DETERGENT MANUFACTURING POINT SOURCE CATEGORY Manufacture of Detergent Bars...

  15. 40 CFR 417.196 - Pretreatment standards for new sources.

    Code of Federal Regulations, 2014 CFR

    2014-07-01

    ... 40 Protection of Environment 29 2014-07-01 2012-07-01 true Pretreatment standards for new sources. 417.196 Section 417.196 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS SOAP AND DETERGENT MANUFACTURING POINT SOURCE CATEGORY Manufacture of Detergent Bars...

  16. 40 CFR 417.196 - Pretreatment standards for new sources.

    Code of Federal Regulations, 2012 CFR

    2012-07-01

    ... 40 Protection of Environment 30 2012-07-01 2012-07-01 false Pretreatment standards for new sources. 417.196 Section 417.196 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS SOAP AND DETERGENT MANUFACTURING POINT SOURCE CATEGORY Manufacture of Detergent Bars...

  17. 40 CFR 417.176 - 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. 417.176 Section 417.176 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS SOAP AND DETERGENT MANUFACTURING POINT SOURCE CATEGORY Manufacture of Detergents by...

  18. 40 CFR 417.176 - Pretreatment standards for new sources.

    Code of Federal Regulations, 2012 CFR

    2012-07-01

    ... 40 Protection of Environment 30 2012-07-01 2012-07-01 false Pretreatment standards for new sources. 417.176 Section 417.176 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS SOAP AND DETERGENT MANUFACTURING POINT SOURCE CATEGORY Manufacture of Detergents by...

  19. 40 CFR 417.176 - Pretreatment standards for new sources.

    Code of Federal Regulations, 2014 CFR

    2014-07-01

    ... 40 Protection of Environment 29 2014-07-01 2012-07-01 true Pretreatment standards for new sources. 417.176 Section 417.176 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS SOAP AND DETERGENT MANUFACTURING POINT SOURCE CATEGORY Manufacture of Detergents by...

  20. 40 CFR 417.176 - 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. 417.176 Section 417.176 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS SOAP AND DETERGENT MANUFACTURING POINT SOURCE CATEGORY Manufacture of Detergents by...

  1. 40 CFR 428.86 - Pretreatment standards for new sources.

    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. 428.86 Section 428.86 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) RUBBER MANUFACTURING POINT SOURCE CATEGORY Wet Digestion...

  2. 40 CFR 428.86 - Pretreatment standards for new sources.

    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. 428.86 Section 428.86 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS RUBBER MANUFACTURING POINT SOURCE CATEGORY Wet Digestion Reclaimed...

  3. 40 CFR 428.86 - Pretreatment standards for new sources.

    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. 428.86 Section 428.86 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) RUBBER MANUFACTURING POINT SOURCE CATEGORY Wet Digestion...

  4. 40 CFR 428.86 - 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. 428.86 Section 428.86 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS RUBBER MANUFACTURING POINT SOURCE CATEGORY Wet Digestion Reclaimed...

  5. 40 CFR 428.86 - Pretreatment standards for new sources.

    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. 428.86 Section 428.86 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) RUBBER MANUFACTURING POINT SOURCE CATEGORY Wet Digestion...

  6. 40 CFR 428.16 - Pretreatment standards for new sources.

    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. 428.16 Section 428.16 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) RUBBER MANUFACTURING POINT SOURCE CATEGORY Tire and Inner Tube...

  7. 40 CFR 428.16 - Pretreatment standards for new sources.

    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. 428.16 Section 428.16 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) RUBBER MANUFACTURING POINT SOURCE CATEGORY Tire and Inner Tube...

  8. 40 CFR 428.116 - Pretreatment standards for new sources.

    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. 428.116 Section 428.116 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) RUBBER MANUFACTURING POINT SOURCE CATEGORY Latex Foam Subcategory §...

  9. 40 CFR 428.46 - Pretreatment standards for new sources.

    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. 428.46 Section 428.46 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) RUBBER MANUFACTURING POINT SOURCE CATEGORY Latex Rubber...

  10. 40 CFR 428.46 - Pretreatment standards for new sources.

    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. 428.46 Section 428.46 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) RUBBER MANUFACTURING POINT SOURCE CATEGORY Latex Rubber...

  11. 40 CFR 428.16 - Pretreatment standards for new sources.

    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. 428.16 Section 428.16 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS RUBBER MANUFACTURING POINT SOURCE CATEGORY Tire and Inner Tube Plants...

  12. 40 CFR 428.116 - Pretreatment standards for new sources.

    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. 428.116 Section 428.116 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) RUBBER MANUFACTURING POINT SOURCE CATEGORY Latex Foam Subcategory §...

  13. 40 CFR 428.116 - Pretreatment standards for new sources.

    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. 428.116 Section 428.116 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS RUBBER MANUFACTURING POINT SOURCE CATEGORY Latex Foam Subcategory §...

  14. 40 CFR 428.46 - Pretreatment standards for new sources.

    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. 428.46 Section 428.46 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS RUBBER MANUFACTURING POINT SOURCE CATEGORY Latex Rubber Subcategory §...

  15. 40 CFR 428.46 - 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. 428.46 Section 428.46 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS RUBBER MANUFACTURING POINT SOURCE CATEGORY Latex Rubber Subcategory §...

  16. 40 CFR 428.46 - Pretreatment standards for new sources.

    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. 428.46 Section 428.46 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) RUBBER MANUFACTURING POINT SOURCE CATEGORY Latex Rubber...

  17. 40 CFR 428.116 - Pretreatment standards for new sources.

    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. 428.116 Section 428.116 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) RUBBER MANUFACTURING POINT SOURCE CATEGORY Latex Foam Subcategory §...

  18. 40 CFR 428.16 - Pretreatment standards for new sources.

    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. 428.16 Section 428.16 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) RUBBER MANUFACTURING POINT SOURCE CATEGORY Tire and Inner Tube...

  19. 40 CFR 406.86 - Pretreatment standards for new sources.

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ... 40 Protection of Environment 30 2013-07-01 2012-07-01 true Pretreatment standards for new sources. 406.86 Section 406.86 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS GRAIN MILLS POINT SOURCE CATEGORY Hot Cereal Subcategory § 406.86...

  20. 40 CFR 406.86 - Pretreatment standards for new sources.

    Code of Federal Regulations, 2012 CFR

    2012-07-01

    ... 40 Protection of Environment 30 2012-07-01 2012-07-01 false Pretreatment standards for new sources. 406.86 Section 406.86 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS GRAIN MILLS POINT SOURCE CATEGORY Hot Cereal Subcategory § 406.86...

  1. 40 CFR 406.96 - Pretreatment standards for new sources.

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ... 40 Protection of Environment 30 2013-07-01 2012-07-01 true Pretreatment standards for new sources. 406.96 Section 406.96 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS GRAIN MILLS POINT SOURCE CATEGORY Ready-to-Eat Cereal Subcategory §...

  2. 40 CFR 406.96 - Pretreatment standards for new sources.

    Code of Federal Regulations, 2012 CFR

    2012-07-01

    ... 40 Protection of Environment 30 2012-07-01 2012-07-01 false Pretreatment standards for new sources. 406.96 Section 406.96 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS GRAIN MILLS POINT SOURCE CATEGORY Ready-to-Eat Cereal Subcategory §...

  3. 40 CFR 406.96 - Pretreatment standards for new sources.

    Code of Federal Regulations, 2014 CFR

    2014-07-01

    ... 40 Protection of Environment 29 2014-07-01 2012-07-01 true Pretreatment standards for new sources. 406.96 Section 406.96 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS GRAIN MILLS POINT SOURCE CATEGORY Ready-to-Eat Cereal Subcategory §...

  4. 40 CFR 406.86 - Pretreatment standards for new sources.

    Code of Federal Regulations, 2014 CFR

    2014-07-01

    ... 40 Protection of Environment 29 2014-07-01 2012-07-01 true Pretreatment standards for new sources. 406.86 Section 406.86 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS GRAIN MILLS POINT SOURCE CATEGORY Hot Cereal Subcategory § 406.86...

  5. 40 CFR 421.16 - Pretreatment standards for new sources.

    Code of Federal Regulations, 2014 CFR

    2014-07-01

    ... 40 Protection of Environment 29 2014-07-01 2012-07-01 true Pretreatment standards for new sources. 421.16 Section 421.16 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS NONFERROUS METALS MANUFACTURING POINT SOURCE CATEGORY Bauxite Refining...

  6. 40 CFR 421.16 - 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. 421.16 Section 421.16 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS NONFERROUS METALS MANUFACTURING POINT SOURCE CATEGORY Bauxite Refining...

  7. 40 CFR 421.16 - Pretreatment standards for new sources.

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ... 40 Protection of Environment 30 2013-07-01 2012-07-01 true Pretreatment standards for new sources. 421.16 Section 421.16 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS NONFERROUS METALS MANUFACTURING POINT SOURCE CATEGORY Bauxite Refining...

  8. 40 CFR 421.16 - 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. 421.16 Section 421.16 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS NONFERROUS METALS MANUFACTURING POINT SOURCE CATEGORY Bauxite Refining...

  9. 40 CFR 421.16 - Pretreatment standards for new sources.

    Code of Federal Regulations, 2012 CFR

    2012-07-01

    ... 40 Protection of Environment 30 2012-07-01 2012-07-01 false Pretreatment standards for new sources. 421.16 Section 421.16 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS NONFERROUS METALS MANUFACTURING POINT SOURCE CATEGORY Bauxite Refining...

  10. 40 CFR 446.16 - Pretreatment standards for new sources.

    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. 446.16 Section 446.16 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) PAINT FORMULATING POINT SOURCE CATEGORY Oil-Base Solvent Wash...

  11. 40 CFR 446.16 - 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. 446.16 Section 446.16 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS PAINT FORMULATING POINT SOURCE CATEGORY Oil-Base Solvent Wash Paint...

  12. 40 CFR 446.16 - Pretreatment standards for new sources.

    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. 446.16 Section 446.16 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) PAINT FORMULATING POINT SOURCE CATEGORY Oil-Base Solvent Wash...

  13. 40 CFR 446.16 - Pretreatment standards for new sources.

    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. 446.16 Section 446.16 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) PAINT FORMULATING POINT SOURCE CATEGORY Oil-Base Solvent Wash...

  14. 40 CFR 446.16 - Pretreatment standards for new sources.

    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. 446.16 Section 446.16 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS PAINT FORMULATING POINT SOURCE CATEGORY Oil-Base Solvent Wash Paint...

  15. 40 CFR 406.54 - 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. 406.54 Section 406.54 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS GRAIN MILLS POINT SOURCE CATEGORY Normal Rice Milling Subcategory § 406...

  16. 40 CFR 406.56 - 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. 406.56 Section 406.56 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS GRAIN MILLS POINT SOURCE CATEGORY Normal Rice Milling Subcategory § 406.56...

  17. 40 CFR 411.26 - Pretreatment standards for new sources.

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ... 40 Protection of Environment 30 2013-07-01 2012-07-01 true Pretreatment standards for new sources. 411.26 Section 411.26 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS CEMENT MANUFACTURING POINT SOURCE CATEGORY Leaching Subcategory § 411.26...

  18. 40 CFR 411.36 - Pretreatment standards for new sources.

    Code of Federal Regulations, 2014 CFR

    2014-07-01

    ... 40 Protection of Environment 29 2014-07-01 2012-07-01 true Pretreatment standards for new sources. 411.36 Section 411.36 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS CEMENT MANUFACTURING POINT SOURCE CATEGORY Materials Storage Piles Runoff...

  19. 40 CFR 411.14 - Pretreatment standards for existing sources.

    Code of Federal Regulations, 2014 CFR

    2014-07-01

    ... 40 Protection of Environment 29 2014-07-01 2012-07-01 true Pretreatment standards for existing sources. 411.14 Section 411.14 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS CEMENT MANUFACTURING POINT SOURCE CATEGORY Nonleaching Subcategory § 411...

  20. 40 CFR 427.26 - 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. 427.26 Section 427.26 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS ASBESTOS MANUFACTURING POINT SOURCE CATEGORY Asbestos-Cement Sheet Subcategory § 427...

  1. 40 CFR 427.16 - Pretreatment standards for new sources.

    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. 427.16 Section 427.16 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) ASBESTOS MANUFACTURING POINT SOURCE CATEGORY Asbestos-Cement Pipe...

  2. 40 CFR 411.24 - Pretreatment standards for existing sources.

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ... 40 Protection of Environment 30 2013-07-01 2012-07-01 true Pretreatment standards for existing sources. 411.24 Section 411.24 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS CEMENT MANUFACTURING POINT SOURCE CATEGORY Leaching Subcategory § 411.24...

  3. 40 CFR 411.16 - Pretreatment standards for new sources.

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ... 40 Protection of Environment 30 2013-07-01 2012-07-01 true Pretreatment standards for new sources. 411.16 Section 411.16 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS CEMENT MANUFACTURING POINT SOURCE CATEGORY Nonleaching Subcategory § 411.16...

  4. 40 CFR 411.24 - Pretreatment standards for existing 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 existing sources. 411.24 Section 411.24 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS CEMENT MANUFACTURING POINT SOURCE CATEGORY Leaching Subcategory § 411.24...

  5. 40 CFR 411.36 - Pretreatment standards for new sources.

    Code of Federal Regulations, 2012 CFR

    2012-07-01

    ... 40 Protection of Environment 30 2012-07-01 2012-07-01 false Pretreatment standards for new sources. 411.36 Section 411.36 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS CEMENT MANUFACTURING POINT SOURCE CATEGORY Materials Storage Piles Runoff...

  6. 40 CFR 427.24 - Pretreatment standards for existing 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 existing sources. 427.24 Section 427.24 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS ASBESTOS MANUFACTURING POINT SOURCE CATEGORY Asbestos-Cement Sheet...

  7. 40 CFR 427.14 - Pretreatment standards for existing sources.

    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. 427.14 Section 427.14 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS ASBESTOS MANUFACTURING POINT SOURCE CATEGORY Asbestos-Cement Pipe...

  8. 40 CFR 411.26 - Pretreatment standards for new sources.

    Code of Federal Regulations, 2014 CFR

    2014-07-01

    ... 40 Protection of Environment 29 2014-07-01 2012-07-01 true Pretreatment standards for new sources. 411.26 Section 411.26 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS CEMENT MANUFACTURING POINT SOURCE CATEGORY Leaching Subcategory § 411.26...

  9. 40 CFR 411.16 - Pretreatment standards for new sources.

    Code of Federal Regulations, 2012 CFR

    2012-07-01

    ... 40 Protection of Environment 30 2012-07-01 2012-07-01 false Pretreatment standards for new sources. 411.16 Section 411.16 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS CEMENT MANUFACTURING POINT SOURCE CATEGORY Nonleaching Subcategory § 411.16...

  10. 40 CFR 411.26 - 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. 411.26 Section 411.26 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS CEMENT MANUFACTURING POINT SOURCE CATEGORY Leaching Subcategory § 411.26...

  11. 40 CFR 411.16 - Pretreatment standards for new sources.

    Code of Federal Regulations, 2014 CFR

    2014-07-01

    ... 40 Protection of Environment 29 2014-07-01 2012-07-01 true Pretreatment standards for new sources. 411.16 Section 411.16 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS CEMENT MANUFACTURING POINT SOURCE CATEGORY Nonleaching Subcategory § 411.16...

  12. 40 CFR 411.34 - Pretreatment standards for existing sources.

    Code of Federal Regulations, 2012 CFR

    2012-07-01

    ... 40 Protection of Environment 30 2012-07-01 2012-07-01 false Pretreatment standards for existing sources. 411.34 Section 411.34 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS CEMENT MANUFACTURING POINT SOURCE CATEGORY Materials Storage Piles Runoff...

  13. 40 CFR 411.26 - Pretreatment standards for new sources.

    Code of Federal Regulations, 2012 CFR

    2012-07-01

    ... 40 Protection of Environment 30 2012-07-01 2012-07-01 false Pretreatment standards for new sources. 411.26 Section 411.26 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS CEMENT MANUFACTURING POINT SOURCE CATEGORY Leaching Subcategory § 411.26...

  14. 40 CFR 411.14 - Pretreatment standards for existing 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 existing sources. 411.14 Section 411.14 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS CEMENT MANUFACTURING POINT SOURCE CATEGORY Nonleaching Subcategory § 411...

  15. 40 CFR 427.26 - Pretreatment standards for new sources.

    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. 427.26 Section 427.26 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) ASBESTOS MANUFACTURING POINT SOURCE CATEGORY Asbestos-Cement Sheet...

  16. 40 CFR 427.16 - Pretreatment standards for new sources.

    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. 427.16 Section 427.16 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) ASBESTOS MANUFACTURING POINT SOURCE CATEGORY Asbestos-Cement Pipe...

  17. 40 CFR 427.26 - Pretreatment standards for new sources.

    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. 427.26 Section 427.26 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) ASBESTOS MANUFACTURING POINT SOURCE CATEGORY Asbestos-Cement Sheet...

  18. 40 CFR 427.14 - Pretreatment standards for existing sources.

    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. 427.14 Section 427.14 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) ASBESTOS MANUFACTURING POINT SOURCE CATEGORY Asbestos-Cement...

  19. 40 CFR 427.24 - Pretreatment standards for existing sources.

    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. 427.24 Section 427.24 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS ASBESTOS MANUFACTURING POINT SOURCE CATEGORY Asbestos-Cement Sheet...

  20. 40 CFR 411.24 - Pretreatment standards for existing sources.

    Code of Federal Regulations, 2014 CFR

    2014-07-01

    ... 40 Protection of Environment 29 2014-07-01 2012-07-01 true Pretreatment standards for existing sources. 411.24 Section 411.24 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS CEMENT MANUFACTURING POINT SOURCE CATEGORY Leaching Subcategory § 411.24...

  1. 40 CFR 427.16 - Pretreatment standards for new sources.

    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. 427.16 Section 427.16 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS ASBESTOS MANUFACTURING POINT SOURCE CATEGORY Asbestos-Cement Pipe Subcategory § 427...

  2. 40 CFR 427.24 - Pretreatment standards for existing sources.

    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. 427.24 Section 427.24 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) ASBESTOS MANUFACTURING POINT SOURCE CATEGORY Asbestos-Cement...

  3. 40 CFR 427.16 - 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. 427.16 Section 427.16 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS ASBESTOS MANUFACTURING POINT SOURCE CATEGORY Asbestos-Cement Pipe Subcategory § 427...

  4. 40 CFR 427.26 - Pretreatment standards for new sources.

    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. 427.26 Section 427.26 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) ASBESTOS MANUFACTURING POINT SOURCE CATEGORY Asbestos-Cement Sheet...

  5. 40 CFR 411.34 - Pretreatment standards for existing sources.

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ... 40 Protection of Environment 30 2013-07-01 2012-07-01 true Pretreatment standards for existing sources. 411.34 Section 411.34 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS CEMENT MANUFACTURING POINT SOURCE CATEGORY Materials Storage Piles Runoff...

  6. 40 CFR 411.34 - Pretreatment standards for existing sources.

    Code of Federal Regulations, 2014 CFR

    2014-07-01

    ... 40 Protection of Environment 29 2014-07-01 2012-07-01 true Pretreatment standards for existing sources. 411.34 Section 411.34 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS CEMENT MANUFACTURING POINT SOURCE CATEGORY Materials Storage Piles Runoff...

  7. 40 CFR 411.14 - Pretreatment standards for existing sources.

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ... 40 Protection of Environment 30 2013-07-01 2012-07-01 true Pretreatment standards for existing sources. 411.14 Section 411.14 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS CEMENT MANUFACTURING POINT SOURCE CATEGORY Nonleaching Subcategory § 411...

  8. 40 CFR 411.34 - Pretreatment standards for existing 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 existing sources. 411.34 Section 411.34 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS CEMENT MANUFACTURING POINT SOURCE CATEGORY Materials Storage Piles Runoff...

  9. 40 CFR 427.24 - Pretreatment standards for existing sources.

    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. 427.24 Section 427.24 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) ASBESTOS MANUFACTURING POINT SOURCE CATEGORY Asbestos-Cement...

  10. 40 CFR 411.36 - 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. 411.36 Section 411.36 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS CEMENT MANUFACTURING POINT SOURCE CATEGORY Materials Storage Piles Runoff...

  11. 40 CFR 427.26 - Pretreatment standards for new sources.

    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. 427.26 Section 427.26 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS ASBESTOS MANUFACTURING POINT SOURCE CATEGORY Asbestos-Cement Sheet Subcategory § 427...

  12. 40 CFR 411.14 - Pretreatment standards for existing sources.

    Code of Federal Regulations, 2012 CFR

    2012-07-01

    ... 40 Protection of Environment 30 2012-07-01 2012-07-01 false Pretreatment standards for existing sources. 411.14 Section 411.14 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS CEMENT MANUFACTURING POINT SOURCE CATEGORY Nonleaching Subcategory § 411...

  13. 40 CFR 427.14 - Pretreatment standards for existing sources.

    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. 427.14 Section 427.14 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) ASBESTOS MANUFACTURING POINT SOURCE CATEGORY Asbestos-Cement...

  14. 40 CFR 411.24 - Pretreatment standards for existing sources.

    Code of Federal Regulations, 2012 CFR

    2012-07-01

    ... 40 Protection of Environment 30 2012-07-01 2012-07-01 false Pretreatment standards for existing sources. 411.24 Section 411.24 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS CEMENT MANUFACTURING POINT SOURCE CATEGORY Leaching Subcategory § 411.24...

  15. 40 CFR 411.36 - Pretreatment standards for new sources.

    Code of Federal Regulations, 2013 CFR

    2013-07-01

    ... 40 Protection of Environment 30 2013-07-01 2012-07-01 true Pretreatment standards for new sources. 411.36 Section 411.36 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS CEMENT MANUFACTURING POINT SOURCE CATEGORY Materials Storage Piles Runoff...

  16. 40 CFR 427.16 - Pretreatment standards for new sources.

    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. 427.16 Section 427.16 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) ASBESTOS MANUFACTURING POINT SOURCE CATEGORY Asbestos-Cement Pipe...

  17. 40 CFR 427.24 - Pretreatment standards for existing sources.

    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. 427.24 Section 427.24 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) ASBESTOS MANUFACTURING POINT SOURCE CATEGORY Asbestos-Cement...

  18. 40 CFR 427.14 - Pretreatment standards for existing 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 existing sources. 427.14 Section 427.14 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS ASBESTOS MANUFACTURING POINT SOURCE CATEGORY Asbestos-Cement Pipe...

  19. 40 CFR 411.16 - 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. 411.16 Section 411.16 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS CEMENT MANUFACTURING POINT SOURCE CATEGORY Nonleaching Subcategory § 411.16...

  20. 40 CFR 427.14 - Pretreatment standards for existing sources.

    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. 427.14 Section 427.14 Protection of Environment ENVIRONMENTAL PROTECTION AGENCY (CONTINUED) EFFLUENT GUIDELINES AND STANDARDS (CONTINUED) ASBESTOS MANUFACTURING POINT SOURCE CATEGORY Asbestos-Cement...