New Insights into the Role of Mitochondrial Dynamics and Autophagy during Oxidative Stress and Aging in the Heart

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Yoshiyuki Ikeda

2014-01-01

Full Text Available The heart is highly sensitive to the aging process. In the elderly, the heart tends to become hypertrophic and fibrotic. Stiffness increases with ensuing systolic and diastolic dysfunction. Aging also affects the cardiac response to stress. At the molecular level, the aging process is associated with accumulation of damaged proteins and organelles, partially due to defects in protein quality control systems. The accumulation of dysfunctional and abnormal mitochondria is an important pathophysiological feature of the aging process, which is associated with excessive production of reactive oxygen species. Mitochondrial fusion and fission and mitochondrial autophagy are crucial mechanisms for maintaining mitochondrial function and preserving energy production. In particular, mitochondrial fission allows for selective segregation of damaged mitochondria, which are afterward eliminated by autophagy. Unfortunately, recent evidence indicates that mitochondrial dynamics and autophagy are progressively impaired over time, contributing to the aging process. This suggests that restoration of these mechanisms could delay organ senescence and prevent age-associated cardiac diseases. Here, we discuss the current understanding of the close relationship between mitochondrial dynamics, mitophagy, oxidative stress, and aging, with a particular focus on the heart.

VALSARTAN REGULATES MYOCARDIAL AUTOPHAGY AND MITOCHONDRIAL TURNOVER IN EXPERIMENTAL HYPERTENSION

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Zhang, Xin; Li, Zi-Lun; Crane, John A.; Jordan, Kyra L.; Pawar, Aditya S.; Textor, Stephen C.; Lerman, Amir; Lerman, Lilach O.

2014-01-01

Renovascular hypertension alters cardiac structure and function. Autophagy is activated during left ventricular hypertrophy and linked to adverse cardiac function. The Angiotensin II receptor blocker Valsartan lowers blood pressure and is cardioprotective, but whether it modulates autophagy in the myocardium is unclear. We hypothesized that Valsartan would alleviate autophagy and improve left ventricular myocardial mitochondrial turnover in swine renovascular hypertension. Domestic pigs were randomized to control, unilateral renovascular hypertension, and renovascular hypertension treated with Valsartan (320 mg/day) or conventional triple therapy (Reserpine+hydralazine+hydrochlorothiazide) for 4 weeks post 6-weeks of renovascular hypertension (n=7 each group). Left ventricular remodeling, function and myocardial oxygenation and microcirculation were assessed by multi-detector computer tomography, blood-oxygen-level-dependent magnetic resonance imaging and microcomputer tomography. Myocardial autophagy, markers for mitochondrial degradation and biogenesis, and mitochondrial respiratory-chain proteins were examined ex vivo. Renovascular hypertension induced left ventricular hypertrophy and myocardial hypoxia, enhanced cellular autophagy and mitochondrial degradation, and suppressed mitochondrial biogenesis. Valsartan and triple therapy similarly decreased blood pressure, but Valsartan solely alleviated left ventricular hypertrophy, ameliorated myocardial autophagy and mitophagy, and increased mitochondrial biogenesis. In contrast, triple therapy only slightly attenuated autophagy and preserved mitochondrial proteins, but elicited no improvement in mitophagy. These data suggest a novel potential role of Valsartan in modulating myocardial autophagy and mitochondrial turnover in renovascular hypertension-induced hypertensive heart disease, which may possibly bolster cardiac repair via a blood pressure-independent manner. PMID:24752430

PFOS prenatal exposure induce mitochondrial injury and gene expression change in hearts of weaned SD rats

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Xia, Wei; Wan, Yanjian; Li, Yuan-yuan; Zeng, Huaicai; Lv, Ziquan; Li, Gengqi; Wei, Zhengzheng; Xu, Shun-qing

2011-01-01

Xenobiotics exposure in early life may have adverse effects on animals' development through mitochondrial injury or dysfunction. The current study demonstrated the possibility of cardiac mitochondrial injury in prenatal PFOS-exposed weaned rat heart. Pregnant Sprague-Dawley (SD) rats were exposed to perfluorooctane sulfonate (PFOS) at doses of 0.1, 0.6 and 2.0 mg/kg/d and 0.05% Tween 80 as control by gavage from gestation days 2-21. The dams were allowed to give nature delivery and then heart tissues from weaned (postnatal day 21) offspring rats were analyzed for mitochondrial injury through ultrastructure observation by electron microscope, global gene expression profile by microarray, as well as related mRNA and proteins expression levels by quantitative PCR and western blot. Ultrastructural analysis revealed significant vacuolization and inner membrane injury occurred at the mitochondria of heart tissues from 2.0 mg/kg/d dosage group. Meanwhile, the global gene expression profile showed significant difference in level of some mRNA expression associated with mitochondrial function at 2.0 mg/kg/d dosage group, compared to the control. Furthermore, dose-response trends for the expression of selected genes were analyzed by quantitative PCR and western blot analysis. The selected genes were mainly focused on those encoding for proteins involved in energy production, control of ion levels, and maintenance of heart function. The down-regulation of mitochondrial ATP synthetase (ATP5E, ATP5I and ATP5O) implicated a decrease in energy supply. This was accompanied by down-regulation of gene transcripts involved in energy consumption such as ion transporting ATPase (ATP1A3 and ATP2B2) and inner membrane protein synthesis (SLC25A3, SLC25A4, SLC25A10, SLC25A29). The up-regulation of gene transcripts encoding for uncoupling proteins (UCP1 and UCP3), epidermal growth factor receptor (EGFR) and connective tissue growth factor (CTGF), was probably a protective process to maintain

3D imaging of the mitochondrial redox state of rat hearts under normal and fasting conditions

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He N. Xu

2014-03-01

Full Text Available The heart requires continuous ATP availability that is generated in the mitochondria. Although studies using the cell culture and perfused organ models have been carried out to investigate the biochemistry in the mitochondria in response to a change in substrate supply, mitochondrial bioenergetics of heart under normal feed or fasting conditions has not been studied at the tissue level with a sub-millimeter spatial resolution either in vivo or ex vivo. Oxidation of many food-derived metabolites to generate ATP in the mitochondria is realized through the NADH/NAD+ couple acting as a central electron carrier. We employed the Chance redox scanner — the low-temperature fluorescence scanner to image the three-dimensional (3D spatial distribution of the mitochondrial redox states in heart tissues of rats under normal feeding or an overnight starvation for 14.5 h. Multiple consecutive sections of each heart were imaged to map three redox indices, i.e., NADH, oxidized flavoproteins (Fp, including flavin adenine dinucleotide (FAD and the redox ratio NADH/Fp. The imaging results revealed the micro-heterogeneity and the spatial distribution of these redox indices. The quantitative analysis showed that in the fasted hearts the standard deviation of both NADH and Fp, i.e., SD_NADH and SD_Fp, significantly decreased with a p value of 0.032 and 0.045, respectively, indicating that the hearts become relatively more homogeneous after fasting. The fasted hearts contained 28.6% less NADH (p = 0.038. No significant change in Fp was found (p = 0.4. The NADH/Fp ratio decreased with a marginal p value (0.076. The decreased NADH in the fasted hearts is consistent with the cardiac cells' reliance of fatty acids consumption for energy metabolism when glucose becomes scarce. The experimental observation of NADH decrease induced by dietary restriction in the heart at tissue level has not been reported to our best knowledge. The Chance redox scanner demonstrated the

3D IMAGING OF THE MITOCHONDRIAL REDOX STATE OF RAT HEARTS UNDER NORMAL AND FASTING CONDITIONS.

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Xu, He N; Zhou, Rong; Moon, Lily; Feng, Min; Li, Lin Z

2014-03-01

The heart requires continuous ATP availability that is generated in the mitochondria. Although studies using the cell culture and perfused organ models have been carried out to investigate the biochemistry in the mitochondria in response to a change in substrate supply, mitochondrial bioenergetics of heart under normal feed or fasting conditions has not been studied at the tissue level with a sub-millimeter spatial resolution either in vivo or ex vivo . Oxidation of many food-derived metabolites to generate ATP in the mitochondria is realized through the NADH/NAD + couple acting as a central electron carrier. We employed the Chance redox scanner - the low-temperature fluorescence scanner to image the three-dimensional (3D) spatial distribution of the mitochondrial redox states in heart tissues of rats under normal feeding or an overnight starvation for 14.5 h. Multiple consecutive sections of each heart were imaged to map three redox indices, i.e., NADH, oxidized flavoproteins (Fp, including flavin adenine dinucleotide (FAD)) and the redox ratio NADH/Fp. The imaging results revealed the micro-heterogeneity and the spatial distribution of these redox indices. The quantitative analysis showed that in the fasted hearts the standard deviation of both NADH and Fp, i.e., SD_NADH and SD_Fp, significantly decreased with a p value of 0.032 and 0.045, respectively, indicating that the hearts become relatively more homogeneous after fasting. The fasted hearts contained 28.6% less NADH ( p = 0.038). No significant change in Fp was found ( p = 0.4). The NADH/Fp ratio decreased with a marginal p value (0.076). The decreased NADH in the fasted hearts is consistent with the cardiac cells' reliance of fatty acids consumption for energy metabolism when glucose becomes scarce. The experimental observation of NADH decrease induced by dietary restriction in the heart at tissue level has not been reported to our best knowledge. The Chance redox scanner demonstrated the feasibility of 3D

Over-expression of mitochondrial creatine kinase in the murine heart improves functional recovery and protects against injury following ischaemia-reperfusion.

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Whittington, Hannah J; Ostrowski, Philip J; McAndrew, Debra J; Cao, Fang; Shaw, Andrew; Eykyn, Thomas R; Lake, Hannah; Tyler, Jack; Schneider, Jurgen E; Neubauer, Stefan; Zervou, Sevasti; Lygate, Craig A

2018-03-02

Mitochondrial creatine kinase (MtCK) couples ATP production via oxidative phosphorylation to phosphocreatine in the cytosol, which acts as a mobile energy store available for regeneration of ATP at times of high demand. We hypothesised that elevating MtCK would be beneficial in ischaemia-reperfusion (I/R) injury. Mice were created overexpressing the sarcomeric MtCK gene with αMHC promoter at the Rosa26 locus (MtCK-OE) and compared with wild-type (WT) littermates. MtCK activity was 27% higher than WT, with no change in other CK isoenzymes or creatine levels. Electron microscopy confirmed normal mitochondrial cell density and mitochondrial localisation of transgenic protein. Respiration in isolated mitochondria was unaltered and metabolomic analysis by 1H-NMR suggests that cellular metabolism was not grossly affected by transgene expression. There were no significant differences in cardiac structure or function under baseline conditions by cine-MRI or LV haemodynamics. In Langendorff-perfused hearts subjected to 20min ischaemia and 30 min reperfusion, MtCK-OE exhibited less ischaemic contracture and improved functional recovery (Rate pressure product 58% above WT; P < 0.001). These hearts had reduced myocardial infarct size, which was confirmed in vivo: 55±4% in WT vs 29±4% in MtCK-OE; P < 0.0001). Isolated cardiomyocytes from MtCK-OE hearts exhibited delayed opening of the mitochondrial permeability transition pore (mPTP) compared to WT, which was confirmed by reduced mitochondrial swelling in response to calcium. There was no detectable change in the structural integrity of the mitochondrial membrane. Modest elevation of MtCK activity in the heart does not adversely affect cellular metabolism, mitochondrial or in vivo cardiac function, but modifies mPTP opening to protect against I/R injury and improve functional recovery. Our findings support MtCK as a prime therapeutic target in myocardial ischaemia.

Aging-dependent changes in rat heart mitochondrial glutaredoxins—Implications for redox regulation

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Xing-Huang Gao

2013-01-01

Full Text Available Clinical and animal studies have documented that hearts of the elderly are more susceptible to ischemia/reperfusion damage compared to young adults. Recently we found that aging-dependent increase in susceptibility of cardiomyocytes to apoptosis was attributable to decrease in cytosolic glutaredoxin 1 (Grx1 and concomitant decrease in NF-κB-mediated expression of anti-apoptotic proteins. Besides primary localization in the cytosol, Grx1 also exists in the mitochondrial intermembrane space (IMS. In contrast, Grx2 is confined to the mitochondrial matrix. Here we report that Grx1 is decreased by 50–60% in the IMS, but Grx2 is increased by 1.4–2.6 fold in the matrix of heart mitochondria from elderly rats. Determination of in situ activities of the Grx isozymes from both subsarcolemmal (SSM and interfibrillar (IFM mitochondria revealed that Grx1 was fully active in the IMS. However, Grx2 was mostly in an inactive form in the matrix, consistent with reversible sequestration of the active-site cysteines of two Grx2 molecules in complex with an iron–sulfur cluster. Our quantitative evaluations of the active/inactive ratio for Grx2 suggest that levels of dimeric Grx2 complex with iron–sulfur clusters are increased in SSM and IFM in the hearts of elderly rats. We found that the inactive Grx2 can be fully reactivated by sodium dithionite or exogenous superoxide production mediated by xanthine oxidase. However, treatment with rotenone, which generates intramitochondrial superoxide through inhibition of mitochondrial respiratory chain Complex I, did not lead to Grx2 activation. These findings suggest that insufficient ROS accumulates in the vicinity of dimeric Grx2 to activate it in situ.

Hypoxia-induced decrease of UCP3 gene expression in rat heart parallels metabolic gene switching but fails to affect mitochondrial respiratory coupling.

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Essop, M Faadiel; Razeghi, Peter; McLeod, Chris; Young, Martin E; Taegtmeyer, Heinrich; Sack, Michael N

2004-02-06

Mitochondrial uncoupling proteins 2 and 3 (UCP2 and UCP3) are postulated to contribute to antioxidant defense, nutrient partitioning, and energy efficiency in the heart. To distinguish isotype function in response to metabolic stress we measured cardiac mitochondrial function and cardiac UCP gene expression following chronic hypobaric hypoxia. Isolated mitochondrial O(2) consumption and ATP synthesis rate were reduced but respiratory coupling was unchanged compared to normoxic groups. Concurrently, left ventricular UCP3 mRNA levels were significantly decreased with hypoxia (pheart as opposed to uncoupling of mitochondria. Moreover, the divergent hypoxia-induced regulation of UCP2 and UCP3 supports distinct mitochondrial regulatory functions of these inner mitochondrial membrane proteins in the heart in response to metabolic stress.

Propofol Compared to Isoflurane Inhibits Mitochondrial Metabolism in Immature Swine Cerebral Cortex

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Kajimoto, Masaki; Atkinson, D. B.; Ledee, Dolena R.; Kayser, Ernst-Bernhard; Morgan, Phil G.; Sedensky, Margaret M.; Isern, Nancy G.; Des Rosiers, Christine; Portman, Michael A.

2014-01-08

Anesthetics used in infants and children are implicated in development of neurocognitive disorders. Although propofol induces neuroapoptosis in developing brain, the underlying mechanisms require elucidation and may have an energetic basis. We studied substrate utilization in an immature swine model anesthetized with either propofol or isoflurane for 4 hours. Piglets were infused with 13-Carbon labeled glucose and leucine in the common carotid artery in order to assess citric acid cycle (CAC) metabolism in the parietal cortex. The anesthetics produced similar systemic hemodynamics and cerebral oxygen saturation by near-infrared-spectroscopy. Compared to isoflurane, propofol depleted ATP and glycogen stores. Propofol also decreased pools of the CAC intermediates, citrate and α-ketoglutarate, while markedly increasing succinate along with decreasing mitochondrial complex II activity. Propofol also inhibited acetyl-CoA entry into the CAC through pyruvate dehydrogenase, while promoting glycolytic flux with marked accumulation of lactate. Although oxygen supply appeared similar between the anesthetic groups, propofol yielded a metabolic phenotype which resembled a hypoxic state. Propofol impairs substrate flux through the CAC in the immature cerebral cortex. These impairments occurred without systemic metabolic perturbations which typically accompany propofol infusion syndrome. These metabolic abnormalities may play a role in neurotoxity observed with propofol in the vulnerable immature brain.

Decreased mitochondrial oxidative phosphorylation capacity in the human heart with left ventricular systolic dysfunction

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Stride, Nis; Larsen, Steen; Hey-Mogensen, Martin

2013-01-01

Heart failure (HF) with left ventricular systolic dysfunction (LVSD) is associated with a shift in substrate utilization and a compromised energetic state. Whether these changes are connected with mitochondrial dysfunction is not known. We hypothesized that the cardiac phenotype in LVSD could...

Supercomplexes of the mitochondrial electron transport chain decline in the aging rat heart.

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Gómez, Luis A; Monette, Jeffrey S; Chavez, Juan D; Maier, Claudia S; Hagen, Tory M

2009-10-01

Accumulation of mitochondrial electron transport chain (ETC) defects is a recognized hallmark of the age-associated decline in cardiac bioenergetics; however, the molecular events involved are only poorly understood. In the present work, we hypothesized that age-related ETC deterioration stemmed partly from disassociation of large solid-state macromolecular assemblies termed "supercomplexes". Mitochondrial proteins from young and old rat hearts were separated by blue native-PAGE, protein bands analyzed by LC-MALDI-MS/MS, and protein levels quantified by densitometry. Results showed that supercomplexes comprised of various stoichiometries of complexes I, III and IV were observed, and declined significantly (p<0.05, n=4) with age. Supercomplexes displaying the highest molecular masses were the most severely affected. Considering that certain diseases (e.g. Barth Syndrome) display similar supercomplex destabilization as our results for aging, the deterioration in ETC supercomplexes may be an important underlying factor for both impaired mitochondrial function and loss of cardiac bioenergetics with age.

Desmin loss and mitochondrial damage precede left ventricular systolic failure in volume overload heart failure.

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Guichard, Jason L; Rogowski, Michael; Agnetti, Giulio; Fu, Lianwu; Powell, Pamela; Wei, Chih-Chang; Collawn, James; Dell'Italia, Louis J

2017-07-01

Heart failure due to chronic volume overload (VO) in rats and humans is characterized by disorganization of the cardiomyocyte desmin/mitochondrial network. Here, we tested the hypothesis that desmin breakdown is an early and continuous process throughout VO. Male Sprague-Dawley rats had aortocaval fistula (ACF) or sham surgery and were examined 24 h and 4 and 12 wk later. Desmin/mitochondrial ultrastructure was examined by transmission electron microscopy (TEM) and immunohistochemistry (IHC). Protein and kinome analysis were performed in isolated cardiomyocytes, and desmin cleavage was assessed by mass spectrometry in left ventricular (LV) tissue. Echocardiography demonstrated a 40% decrease in the LV mass-to-volume ratio with spherical remodeling at 4 wk with ACF and LV systolic dysfunction at 12 wk. Starting at 24 h and continuing to 4 and 12 wk, with ACF there is TEM evidence of extensive mitochondrial clustering, IHC evidence of disorganization associated with desmin breakdown, and desmin protein cleavage verified by Western blot analysis and mass spectrometry. IHC results revealed that ACF cardiomyocytes at 4 and 12 wk had perinuclear translocation of αB-crystallin from the Z disk with increased α, β-unsaturated aldehyde 4-hydroxynonelal. Use of protein markers with verification by TUNEL staining and kinome analysis revealed an absence of cardiomyocyte apoptosis at 4 and 12 wk of ACF. Significant increases in protein indicators of mitophagy were countered by a sixfold increase in p62/sequestosome-1, which is indicative of an inability to complete autophagy. An early and continuous disruption of the desmin/mitochondrial architecture, accompanied by oxidative stress and inhibition of apoptosis and mitophagy, suggests its causal role in LV dilatation and systolic dysfunction in VO. NEW & NOTEWORTHY This study provides new evidence of early onset (24 h) and continuous (4-12 wk) desmin misarrangement and disruption of the normal sarcomeric and mitochondrial

Harnessing the Power of Integrated Mitochondrial Biology and Physiology: A Special Report on the NHLBI Mitochondria in Heart Diseases Initiative.

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Ping, Peipei; Gustafsson, Åsa B; Bers, Don M; Blatter, Lothar A; Cai, Hua; Jahangir, Arshad; Kelly, Daniel; Muoio, Deborah; O'Rourke, Brian; Rabinovitch, Peter; Trayanova, Natalia; Van Eyk, Jennifer; Weiss, James N; Wong, Renee; Schwartz Longacre, Lisa

2015-07-17

Mitochondrial biology is the sum of diverse phenomena from molecular profiles to physiological functions. A mechanistic understanding of mitochondria in disease development, and hence the future prospect of clinical translations, relies on a systems-level integration of expertise from multiple fields of investigation. Upon the successful conclusion of a recent National Institutes of Health, National Heart, Lung, and Blood Institute initiative on integrative mitochondrial biology in cardiovascular diseases, we reflect on the accomplishments made possible by this unique interdisciplinary collaboration effort and exciting new fronts on the study of these remarkable organelles. © 2015 American Heart Association, Inc.

Mitochondrial DNA Hypomethylation Is a Biomarker Associated with Induced Senescence in Human Fetal Heart Mesenchymal Stem Cells

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Dehai Yu

2017-01-01

Full Text Available Background. Fetal heart can regenerate to restore its normal anatomy and function in response to injury, but this regenerative capacity is lost within the first week of postnatal life. Although the specific molecular mechanisms remain to be defined, it is presumed that aging of cardiac stem or progenitor cells may contribute to the loss of regenerative potential. Methods. To study this aging-related dysfunction, we cultured mesenchymal stem cells (MSCs from human fetal heart tissues. Senescence was induced by exposing cells to chronic oxidative stress/low serum. Mitochondrial DNA methylation was examined during the period of senescence. Results. Senescent MSCs exhibited flattened and enlarged morphology and were positive for the senescence-associated beta-galactosidase (SA-β-Gal. By scanning the entire mitochondrial genome, we found that four CpG islands were hypomethylated in close association with senescence in MSCs. The mitochondrial COX1 gene, which encodes the main subunit of the cytochrome c oxidase complex and contains the differentially methylated CpG island 4, was upregulated in MSCs in parallel with the onset of senescence. Knockdown of DNA methyltransferases (DNMT1, DNMT3a, and DNMT3B also upregulated COX1 expression and induced cellular senescence in MSCs. Conclusions. This study demonstrates that mitochondrial CpG hypomethylation may serve as a critical biomarker associated with cellular senescence induced by chronic oxidative stress.

Attenuation of Ca2+ homeostasis, oxidative stress, and mitochondrial dysfunctions in diabetic rat heart: insulin therapy or aerobic exercise?

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da Silva, Márcia F; Natali, Antônio J; da Silva, Edson; Gomes, Gilton J; Teodoro, Bruno G; Cunha, Daise N Q; Drummond, Lucas R; Drummond, Filipe R; Moura, Anselmo G; Belfort, Felipe G; de Oliveira, Alessandro; Maldonado, Izabel R S C; Alberici, Luciane C

2015-07-15

We tested the effects of swimming training and insulin therapy, either alone or in combination, on the intracellular calcium ([Ca(2+)]i) homeostasis, oxidative stress, and mitochondrial functions in diabetic rat hearts. Male Wistar rats were separated into control, diabetic, or diabetic plus insulin groups. Type 1 diabetes mellitus was induced by streptozotocin (STZ). Insulin-treated groups received 1 to 4 UI of insulin daily for 8 wk. Each group was divided into sedentary or exercised rats. Trained groups were submitted to swimming (90 min/day, 5 days/wk, 8 wk). [Ca(2+)]i transient in left ventricular myocytes (LVM), oxidative stress in LV tissue, and mitochondrial functions in the heart were assessed. Diabetes reduced the amplitude and prolonged the times to peak and to half decay of the [Ca(2+)]i transient in LVM, increased NADPH oxidase-4 (Nox-4) expression, decreased superoxide dismutase (SOD), and increased carbonyl protein contents in LV tissue. In isolated mitochondria, diabetes increased Ca(2+) uptake, susceptibility to permeability transition pore (MPTP) opening, uncoupling protein-2 (UCP-2) expression, and oxygen consumption but reduced H2O2 release. Swimming training corrected the time course of the [Ca(2+)]i transient, UCP-2 expression, and mitochondrial Ca(2+) uptake. Insulin replacement further normalized [Ca(2+)]i transient amplitude, Nox-4 expression, and carbonyl content. Alongside these benefits, the combination of both therapies restored the LV tissue SOD and mitochondrial O2 consumption, H2O2 release, and MPTP opening. In conclusion, the combination of swimming training with insulin replacement was more effective in attenuating intracellular Ca(2+) disruptions, oxidative stress, and mitochondrial dysfunctions in STZ-induced diabetic rat hearts. Copyright © 2015 the American Physiological Society.

Methylene blue improves mitochondrial respiration and decreases oxidative stress in a substrate-dependent manner in diabetic rat hearts.

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Duicu, Oana M; Privistirescu, Andreea; Wolf, Adrian; Petruş, Alexandra; Dănilă, Maria D; Raţiu, Corina D; Muntean, Danina M; Sturza, Adrian

2017-11-01

Diabetic cardiomyopathy has been systematically associated with compromised mitochondrial energetics and increased generation of reactive oxygen species (ROS) that underlie its progression to heart failure. Methylene blue is a redox drug with reported protective effects mainly on brain mitochondria. The purpose of the present study was to characterize the effects of acute administration of methylene blue on mitochondrial respiration, H 2 O 2 production, and calcium sensitivity in rat heart mitochondria isolated from healthy and 2 months (streptozotocin-induced) diabetic rats. Mitochondrial respiratory function was assessed by high-resolution respirometry. H 2 O 2 production and calcium retention capacity were measured spectrofluorimetrically. The addition of methylene blue (0.1 μmol·L -1 ) elicited an increase in oxygen consumption of mitochondria energized with complex I and II substrates in both normal and diseased mitochondria. Interestingly, methylene blue elicited a significant increase in H 2 O 2 release in the presence of complex I substrates (glutamate and malate), but had an opposite effect in mitochondria energized with complex II substrate (succinate). No changes in the calcium retention capacity of healthy or diabetic mitochondria were found in the presence of methylene blue. In conclusion, in cardiac mitochondria isolated from diabetic and nondiabetic rat hearts, methylene blue improved respiratory function and elicited a dichotomic, substrate-dependent effect on ROS production.

Haloperidol aggravates transverse aortic constriction-induced heart failure via mitochondrial dysfunction.

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Shinoda, Yasuharu; Tagashira, Hideaki; Bhuiyan, Md Shenuarin; Hasegawa, Hideyuki; Kanai, Hiroshi; Fukunaga, Kohji

2016-07-01

Haloperidol is an antipsychotic drug that inhibits the dopamine D2 receptor among others. Haloperidol also binds the sigma-1 receptor (σ1R) and inhibits it irreversibly. A serious outcome of haloperidol treatment of schizophrenia patients is death due to sudden cardiac failure. Although the cause remains unclear, we hypothesized that these effects were mediated by chronic haloperidol inhibition of cardiac σ1R. To test this, we treated neonatal rat cardiomyocytes with haloperidol, exposed them to angiotensin II and assessed hypertrophy, σ1R expression, mitochondrial Ca(2+) transport and ATP levels. In this context, haloperidol treatment altered mitochondrial Ca(2+) transport resulting in decreased ATP content by inactivating cardiac σ1R and/or reducing its expression. We also performed transverse aortic constriction (TAC) and then treated mice with haloperidol. After two weeks, haloperidol-treated mice showed enhanced heart failure marked by deteriorated cardiac function, reduced ATP production and increasing mortality relative to TAC only mice. ATP supplementation via sodium pyruvate rescued phenotypes seen in haloperidol-treated TAC mice. We conclude that σ1R inactivation or downregulation in response to haloperidol treatment impairs mitochondrial Ca(2+) mobilization, depleting ATP depletion from cardiomyocytes. These findings suggest a novel approach to mitigate haloperidol-related adverse effects in schizophrenia patients by ATP supplementation. Copyright © 2016 The Authors. Production and hosting by Elsevier B.V. All rights reserved.

Haloperidol aggravates transverse aortic constriction-induced heart failure via mitochondrial dysfunction

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Yasuharu Shinoda

2016-07-01

Full Text Available Haloperidol is an antipsychotic drug that inhibits the dopamine D2 receptor among others. Haloperidol also binds the sigma-1 receptor (σ1R and inhibits it irreversibly. A serious outcome of haloperidol treatment of schizophrenia patients is death due to sudden cardiac failure. Although the cause remains unclear, we hypothesized that these effects were mediated by chronic haloperidol inhibition of cardiac σ1R. To test this, we treated neonatal rat cardiomyocytes with haloperidol, exposed them to angiotensin II and assessed hypertrophy, σ1R expression, mitochondrial Ca2+ transport and ATP levels. In this context, haloperidol treatment altered mitochondrial Ca2+ transport resulting in decreased ATP content by inactivating cardiac σ1R and/or reducing its expression. We also performed transverse aortic constriction (TAC and then treated mice with haloperidol. After two weeks, haloperidol-treated mice showed enhanced heart failure marked by deteriorated cardiac function, reduced ATP production and increasing mortality relative to TAC only mice. ATP supplementation via sodium pyruvate rescued phenotypes seen in haloperidol-treated TAC mice. We conclude that σ1R inactivation or downregulation in response to haloperidol treatment impairs mitochondrial Ca2+ mobilization, depleting ATP depletion from cardiomyocytes. These findings suggest a novel approach to mitigate haloperidol-related adverse effects in schizophrenia patients by ATP supplementation.

Altered expression of mitochondrial and extracellular matrix genes in the heart of human fetuses with chromosome 21 trisomy

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Olla Carlo

2007-08-01

Full Text Available Abstract Background The Down syndrome phenotype has been attributed to overexpression of chromosome 21 (Hsa21 genes. However, the expression profile of Hsa21 genes in trisomic human subjects as well as their effects on genes located on different chromosomes are largely unknown. Using oligonucleotide microarrays we compared the gene expression profiles of hearts of human fetuses with and without Hsa21 trisomy. Results Approximately half of the 15,000 genes examined (87 of the 168 genes on Hsa21 were expressed in the heart at 18–22 weeks of gestation. Hsa21 gene expression was globally upregulated 1.5 fold in trisomic samples. However, not all genes were equally dysregulated and 25 genes were not upregulated at all. Genes located on other chromosomes were also significantly dysregulated. Functional class scoring and gene set enrichment analyses of 473 genes, differentially expressed between trisomic and non-trisomic hearts, revealed downregulation of genes encoding mitochondrial enzymes and upregulation of genes encoding extracellular matrix proteins. There were no significant differences between trisomic fetuses with and without heart defects. Conclusion We conclude that dosage-dependent upregulation of Hsa21 genes causes dysregulation of the genes responsible for mitochondrial function and for the extracellular matrix organization in the fetal heart of trisomic subjects. These alterations might be harbingers of the heart defects associated with Hsa21 trisomy, which could be based on elusive mechanisms involving genetic variability, environmental factors and/or stochastic events.

Radiation-induced signaling results in mitochondrial impairment in mouse heart at 4 weeks after exposure to X-rays.

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Barjaktarovic, Zarko; Schmaltz, Dominik; Shyla, Alena; Azimzadeh, Omid; Schulz, Sabine; Haagen, Julia; Dörr, Wolfgang; Sarioglu, Hakan; Schäfer, Alexander; Atkinson, Michael J; Zischka, Hans; Tapio, Soile

2011-01-01

Radiation therapy treatment of breast cancer, Hodgkin's disease or childhood cancers expose the heart to high local radiation doses, causing an increased risk of cardiovascular disease in the survivors decades after the treatment. The mechanisms that underlie the radiation damage remain poorly understood so far. Previous data show that impairment of mitochondrial oxidative metabolism is directly linked to the development of cardiovascular disease. In this study, the radiation-induced in vivo effects on cardiac mitochondrial proteome and function were investigated. C57BL/6N mice were exposed to local irradiation of the heart with doses of 0.2 Gy or 2 Gy (X-ray, 200 kV) at the age of eight weeks, the control mice were sham-irradiated. After four weeks the cardiac mitochondria were isolated and tested for proteomic and functional alterations. Two complementary proteomics approaches using both peptide and protein quantification strategies showed radiation-induced deregulation of 25 proteins in total. Three main biological categories were affected: the oxidative phophorylation, the pyruvate metabolism, and the cytoskeletal structure. The mitochondria exposed to high-dose irradiation showed functional impairment reflected as partial deactivation of Complex I (32%) and Complex III (11%), decreased succinate-driven respiratory capacity (13%), increased level of reactive oxygen species and enhanced oxidation of mitochondrial proteins. The changes in the pyruvate metabolism and structural proteins were seen with both low and high radiation doses. This is the first study showing the biological alterations in the murine heart mitochondria several weeks after the exposure to low- and high-dose of ionizing radiation. Our results show that doses, equivalent to a single dose in radiotherapy, cause long-lasting changes in mitochondrial oxidative metabolism and mitochondria-associated cytoskeleton. This prompts us to propose that these first pathological changes lead to an increased

Flu and Heart Disease and Stroke

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... Seasonal Avian Swine Variant Pandemic Other Flu and Heart Disease & Stroke Language: English (US) Español Recommend on Facebook Tweet Share Compartir People with Heart Disease* and Those Who Have Had a Stroke Are ...

Swine Influenza (Swine Flu) in Pigs

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... Address What's this? Submit What's this? Submit Button Influenza Types Seasonal Avian Swine Variant Pandemic Other Key Facts about Swine Influenza (Swine Flu) in Pigs Language: English (US) Español ...

Novel remodeling of the mouse heart mitochondrial proteome in response to acute insulin stimulation

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Pedersen, Brian A; Yazdi, Puya G; Taylor, Jared F; Khattab, Omar S; Chen, Yu-Han; Chen, Yumay; Wang, Ping H

2015-01-01

Mitochondrial dysfunction contributes to the pathophysiology of diabetic cardiomyopathy. The aim of this study was to investigate the acute changes in the mitochondrial proteome in response to insulin stimulation. Cardiac mitochondria from C57BL/6 mice after insulin stimulation were analyzed using two-dimensional fluorescence difference gel electrophoresis. MALDI-TOF MS/MS was utilized to identify differences. Two enzymes involved in metabolism and four structural proteins were identified. Succinyl-CoA ligase [ADP forming] subunit beta was identified as one of the differentially regulated proteins. Upon insulin stimulation, a relatively more acidic isoform of this protein was increased by 53% and its functional activity was decreased by ∼32%. This proteomic remodeling in response to insulin stimulation may play an important role in the normal and diabetic heart. PMID:26610654

Maintaining ancient organelles: mitochondrial biogenesis and maturation.

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Vega, Rick B; Horton, Julie L; Kelly, Daniel P

2015-05-22

The ultrastructure of the cardiac myocyte is remarkable for the high density of mitochondria tightly packed between sarcomeres. This structural organization is designed to provide energy in the form of ATP to fuel normal pump function of the heart. A complex system comprised of regulatory factors and energy metabolic machinery, encoded by both mitochondrial and nuclear genomes, is required for the coordinate control of cardiac mitochondrial biogenesis, maturation, and high-capacity function. This process involves the action of a transcriptional regulatory network that builds and maintains the mitochondrial genome and drives the expression of the energy transduction machinery. This finely tuned system is responsive to developmental and physiological cues, as well as changes in fuel substrate availability. Deficiency of components critical for mitochondrial energy production frequently manifests as a cardiomyopathic phenotype, underscoring the requirement to maintain high respiration rates in the heart. Although a precise causative role is not clear, there is increasing evidence that perturbations in this regulatory system occur in the hypertrophied and failing heart. This review summarizes current knowledge and highlights recent advances in our understanding of the transcriptional regulatory factors and signaling networks that serve to regulate mitochondrial biogenesis and function in the mammalian heart. © 2015 American Heart Association, Inc.

Short term exercise induces PGC-1α, ameliorates inflammation and increases mitochondrial membrane proteins but fails to increase respiratory enzymes in aging diabetic hearts.

Science.gov (United States)

Botta, Amy; Laher, Ismail; Beam, Julianne; Decoffe, Daniella; Brown, Kirsty; Halder, Swagata; Devlin, Angela; Gibson, Deanna L; Ghosh, Sanjoy

2013-01-01

PGC-1α, a transcriptional coactivator, controls inflammation and mitochondrial gene expression in insulin-sensitive tissues following exercise intervention. However, attributing such effects to PGC-1α is counfounded by exercise-induced fluctuations in blood glucose, insulin or bodyweight in diabetic patients. The goal of this study was to investigate the role of PGC-1α on inflammation and mitochondrial protein expressions in aging db/db mice hearts, independent of changes in glycemic parameters. In 8-month-old db/db mice hearts with diabetes lasting over 22 weeks, short-term, moderate-intensity exercise upregulated PGC-1α without altering body weight or glycemic parameters. Nonetheless, such a regimen lowered both cardiac (macrophage infiltration, iNOS and TNFα) and systemic (circulating chemokines and cytokines) inflammation. Curiously, such an anti-inflammatory effect was also linked to attenuated expression of downstream transcription factors of PGC-1α such as NRF-1 and several respiratory genes. Such mismatch between PGC-1α and its downstream targets was associated with elevated mitochondrial membrane proteins like Tom70 but a concurrent reduction in oxidative phosphorylation protein expressions in exercised db/db hearts. As mitochondrial oxidative stress was predominant in these hearts, in support of our in vivo data, increasing concentrations of H2O2 dose-dependently increased PGC-1α expression while inhibiting expression of inflammatory genes and downstream transcription factors in H9c2 cardiomyocytes in vitro. We conclude that short-term exercise-induced oxidative stress may be key in attenuating cardiac inflammatory genes and impairing PGC-1α mediated gene transcription of downstream transcription factors in type 2 diabetic hearts at an advanced age.

Mitochondrial phospholipase A2 activated by reactive oxygen species in heart mitochondria induces mild uncoupling

Czech Academy of Sciences Publication Activity Database

Ježek, Jan; Jabůrek, Martin; Zelenka, Jaroslav; Ježek, Petr

2010-01-01

Roč. 59, č. 5 (2010), s. 737-747 ISSN 0862-8408 R&D Projects: GA ČR(CZ) GA303/07/0105; GA MŠk ME09018; GA AV ČR(CZ) KJB500110902 Institutional research plan: CEZ:AV0Z50110509 Keywords : Heart mitochondrial phospholipase A2 * Fatty Acids * Adenine nucleotide translocase Subject RIV: ED - Physiology Impact factor: 1.646, year: 2010

Critical role of mitochondrial ROS is dependent on their site of production on the electron transport chain in ischemic heart.

Science.gov (United States)

Madungwe, Ngonidzashe B; Zilberstein, Netanel F; Feng, Yansheng; Bopassa, Jean C

2016-01-01

Reactive oxygen species (ROS) generation has been implicated in many pathologies including ischemia/reperfusion (I/R) injury. This led to multiple studies on antioxidant therapies to treat cardiovascular diseases but paradoxically, results have so far been mixed as ROS production can be beneficial as a signaling mechanism and in cardiac protection via preconditioning interventions. We investigated whether the differential impact of increased ROS in injury as well as in protection could be explained by their site of production on the mitochondrial electron transport chain. Using amplex red to measure ROS production, we found that mitochondria isolated from hearts after I/R produced more ROS than non-ischemic when complex I substrate (glutamate/malate) was used. Interestingly, the substrates of complex II (succinate) and ubiquinone (sn-glycerol 3-phosphate, G3P) produced less ROS in mitochondria from I/R hearts compared to normal healthy hearts. The inhibitors of complex I (rotenone) and complex III (antimycin A) increased ROS production when glutamate/malate and G3P were used; in contrast, they reduced ROS production when the complex II substrate was used. Mitochondrial calcium retention capacity required to induce mitochondrial permeability transition pore (mPTP) opening was measured using calcium green fluorescence and was found to be higher when mitochondria were treated with G3P and succinate compared to glutamate/malate. Furthermore, Langendorff hearts treated with glutamate/malate exhibited reduced cardiac functional recovery and increased myocardial infarct size compared to hearts treated with G3P. Thus, ROS production by the stimulated respiratory chain complexes I and III has opposite roles: cardio-deleterious when produced in complex I and cardio-protective when produced in complex III. The mechanism of these ROS involves the inhibition of the mPTP opening, a key event in cell death following ischemia/reperfusion injury.

Reducing mitochondrial bound hexokinase II mediates transition from non-injurious into injurious ischemia/reperfusion of the intact heart

NARCIS (Netherlands)

R. Nederlof (Rianne); Gürel-Gurevin, E. (Ebru); O. Eerbeek (Otto); C. Xie (Chaoqin); Deijs, G.S.; Konkel, M. (Moritz); Hu, J. (Jun); N.C. Weber (Nina); C. Schumacher (Cees); A. Baartscheer (Antonius); E.G. Mik (Egbert); M.W. Hollmann (Markus); F.G. Akar (Fadi); C.J. Zuurbier (Coert J.)

2016-01-01

textabstractIschemia/reperfusion (I/R) of the heart becomes injurious when duration of the ischemic insult exceeds a certain threshold (approximately ≥20 min). Mitochondrial bound hexokinase II (mtHKII) protects against I/R injury, with the amount of mtHKII correlating with injury. Here, we examine

Compensatory role of the NBCn1 sodium/bicarbonate cotransporter on Ca2+-induced mitochondrial swelling in hypertrophic hearts.

Science.gov (United States)

Vargas, Lorena A; Velasquez, Fernanda Carrizo; Alvarez, Bernardo V

2017-03-01

NBC Na + /HCO 3 - cotransporter (NBCn1) and NHE1 Na + /H + exchanger have been associated with cardiac disorders and recently located in coronary endothelial cells (CEC) and cardiomyocytes mitochondria, respectively. Mitochondrial NHE1 blockade delays permeability transition pore (MPTP) opening and reduces superoxide levels, two critical events exacerbated in cells of diseased hearts. Conversely, activation of NBCn1 prevented apoptosis in CEC subjected to ischemic stress. We characterized the role of the NHE1 and NBCn1 transporters in heart mitochondria from hypertrophic (SHR) and control (Wistar) rats. Expression of NHE1 was analyzed in left ventricular mitochondrial lysates (LVML), by immunoblots. NHE1 expression increased by ~40% in SHR compared to control (P < 0.05, n = 4). To examine NHE1-mediated Na + /H + exchange activity in cardiac hypertrophy, mitochondria were loaded with BCECF-AM dye and the maximal rate of pHm change measured after the addition of 50 mM NaCl. SHR mitochondria had greater changes in pHm compared to Wistar, 0.10 ± 0.01 vs. 0.06 ± 0.01, respectively (P < 0.05, n = 5). In addition, mitochondrial suspensions from SHR and control myocardium were exposed to 200 μM CaCl 2 to induce MPTP opening (light-scattering decrease, LSD) and swelling. Surprisingly, SHR rats showed smaller LSD and a reduction in mitochondrial swelling, 67 ± 10% (n = 15), compared to control, 100 ± 8% (n = 13). NBC inhibition with S0859 (1 μM) significantly increased swelling in both control 139 ± 10% (n = 8) and SHR 115 ± 10% (n = 4). Finally, NBCn1 Na + /HCO 3 - cotransporter increased by twofold its expression in SHR LVML, compared to normal (P < 0.05, n = 5). We conclude that increased NBCn1 activity may play a compensatory role in hypertrophic hearts, protecting mitochondria from Ca 2+ -induced MPTP opening and swelling.

Development of swine-specific DNA markers for biosensor-based halal authentication.

Science.gov (United States)

Ali, M E; Hashim, U; Kashif, M; Mustafa, S; Che Man, Y B; Abd Hamid, S B

2012-06-29

The pig (Sus scrofa) mitochondrial genome was targeted to design short (15-30 nucleotides) DNA markers that would be suitable for biosensor-based hybridization detection of target DNA. Short DNA markers are reported to survive harsh conditions in which longer ones are degraded into smaller fragments. The whole swine mitochondrial-genome was in silico digested with AluI restriction enzyme. Among 66 AluI fragments, five were selected as potential markers because of their convenient lengths, high degree of interspecies polymorphism and intraspecies conservatism. These were confirmed by NCBI blast analysis and ClustalW alignment analysis with 11 different meat-providing animal and fish species. Finally, we integrated a tetramethyl rhodamine-labeled 18-nucleotide AluI fragment into a 3-nm diameter citrate-tannate coated gold nanoparticle to develop a swine-specific hybrid nanobioprobe for the determination of pork adulteration in 2.5-h autoclaved pork-beef binary mixtures. This hybrid probe detected as low as 1% pork in deliberately contaminated autoclaved pork-beef binary mixtures and no cross-species detection was recorded, demonstrating the feasibility of this type of probe for biosensor-based detection of pork adulteration of halal and kosher foods.

Myocardial mitochondrial and contractile function are preserved in mice lacking adiponectin.

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Martin Braun

Full Text Available Adiponectin deficiency leads to increased myocardial infarct size following ischemia reperfusion and to exaggerated cardiac hypertrophy following pressure overload, entities that are causally linked to mitochondrial dysfunction. In skeletal muscle, lack of adiponectin results in impaired mitochondrial function. Thus, it was our objective to investigate whether adiponectin deficiency impairs mitochondrial energetics in the heart. At 8 weeks of age, heart weight-to-body weight ratios were not different between adiponectin knockout (ADQ-/- mice and wildtypes (WT. In isolated working hearts, cardiac output, aortic developed pressure and cardiac power were preserved in ADQ-/- mice. Rates of fatty acid oxidation, glucose oxidation and glycolysis were unchanged between groups. While myocardial oxygen consumption was slightly reduced (-24% in ADQ-/- mice in isolated working hearts, rates of maximal ADP-stimulated mitochondrial oxygen consumption and ATP synthesis in saponin-permeabilized cardiac fibers were preserved in ADQ-/- mice with glutamate, pyruvate or palmitoyl-carnitine as a substrate. In addition, enzymatic activity of respiratory complexes I and II was unchanged between groups. Phosphorylation of AMP-activated protein kinase and SIRT1 activity were not decreased, expression and acetylation of PGC-1α were unchanged, and mitochondrial content of OXPHOS subunits was not decreased in ADQ-/- mice. Finally, increasing energy demands due to prolonged subcutaneous infusion of isoproterenol did not differentially affect cardiac contractility or mitochondrial function in ADQ-/- mice compared to WT. Thus, mitochondrial and contractile function are preserved in hearts of mice lacking adiponectin, suggesting that adiponectin may be expendable in the regulation of mitochondrial energetics and contractile function in the heart under non-pathological conditions.

9 CFR 85.10 - Interstate movement of swine semen and swine embryos for insemination of or implantation into swine.

Science.gov (United States)

2010-01-01

... 9 Animals and Animal Products 1 2010-01-01 2010-01-01 false Interstate movement of swine semen and... ANIMALS (INCLUDING POULTRY) AND ANIMAL PRODUCTS PSEUDORABIES § 85.10 Interstate movement of swine semen and swine embryos for insemination of or implantation into swine. Swine semen and swine embryos moved...

A single intracoronary injection of midkine reduces ischemia/reperfusion injury in swine hearts: a novel therapeutic approach for acute coronary syndrome

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Hisaaki eIshiguro

2011-06-01

Full Text Available Several growth factors are effective for salvaging myocardium and limiting infarct size in experimental studies with small animals. Their benefit in large animals and feasibility in clinical practice remains to be elucidated. We investigate the cardioprotective effect of midkine (MK in swine subjected to ischemia/reperfusion (I/R. I/R was created in swine by left anterior descending coronary artery occlusion for 45 min using a percutaneous over-the-wire balloon catheter. MK protein was injected as a bolus through the catheter at the initiation of reperfusion (midkine injected group; MKT. Saline was injected in controls (CONT. Survival rate 24h after I/R was significantly higher in MKT than in CONT, whereas infarct size/area at risk was almost 5 times smaller. Echocardiography in MKT revealed a significantly higher percent wall thickening of the interventricular septum, a higher % fractional shortening and a lower E/e’ compared with CONT. LV catheterization in MKT showed a lower LVEDP, and a higher dP/dtmax compared with CONT. TUNEL-positive myocytes and CD45-positive cell infiltration in the peri-infarct area were significantly less in MKT than in CONT. Here, we showed that a single intracoronary injection of MK protein in swine hearts at the onset of reperfusion dramatically reduces infarct size and mortality and ameliorates systolic/diastolic LV function. This beneficial effect is associated with a reduction of apoptotic and inflammatory reactions. MK application during percutaneous coronary intervention may become a promising adjunctive therapy in acute coronary syndromes.

Cardioprotection by modulation of mitochondrial respiration during ischemia–reperfusion: Role of apoptosis-inducing factor

Energy Technology Data Exchange (ETDEWEB)

Xu, Aijun [Department of Internal Medicine (Division of Cardiology), Virginia Commonwealth University, Richmond, VA 23298 (United States); Department of Anesthesiology, Tongji Hospital, Huazhong University of Science and Technology, Wuhan 430030 (China); Szczepanek, Karol; Hu, Ying [Department of Internal Medicine (Division of Cardiology), Virginia Commonwealth University, Richmond, VA 23298 (United States); Lesnefsky, Edward J. [Department of Internal Medicine (Division of Cardiology), Virginia Commonwealth University, Richmond, VA 23298 (United States); Department of Biochemistry and Molecular Biology, Virginia Commonwealth University, Richmond, VA 23298 (United States); Department of Physiology and Biophysics, Virginia Commonwealth University, Richmond, VA 23298 (United States); McGuire Department of Veterans Affairs Medical Center, Richmond, VA 23249 (United States); Chen, Qun, E-mail: qchen8@vcu.edu [Department of Internal Medicine (Division of Cardiology), Virginia Commonwealth University, Richmond, VA 23298 (United States)

2013-06-14

Highlights: •Blockade of electron transport prevents the loss of AIF from mitochondria during IR. •Blockade of electron transport decreases caspase-independent cell death during IR. •Mitochondrial AIF content is down-regulated in Harlequin mice. •Blockade of electron transport protects Harlequin mouse hearts during IR. •Amobarbital protection is partially dependent on mitochondrial AIF content. -- Abstract: The transient, reversible blockade of electron transport (BET) during ischemia or at the onset of reperfusion protects mitochondria and decreases cardiac injury. Apoptosis inducing factor (AIF) is located within the mitochondrial intermembrane space. A release of AIF from mitochondria into cytosol and nucleus triggers caspase-independent cell death. We asked if BET prevents the loss of AIF from mitochondria as a mechanism of protection in the buffer perfused heart. BET during ischemia with amobarbital, a rapidly reversible inhibitor of mitochondrial complex I, attenuated a release of AIF from mitochondria into cytosol, in turn decreasing the formation of cleaved and activated PARP-1. These results suggest that BET-mediated protection may occur through prevention of the loss of AIF from mitochondria during ischemia–reperfusion. In order to further clarify the role of mitochondrial AIF in BET-mediated protection, Harlequin (Hq) mice, a genetic model with mitochondrial AIF deficiency, were used to test whether BET could still decrease cell injury in Hq mouse hearts during reperfusion. BET during ischemia protected Hq mouse hearts against ischemia–reperfusion injury and improved mitochondrial function in these hearts during reperfusion. Thus, cardiac injury can still be decreased in the presence of down-regulated mitochondrial AIF content. Taken together, BET during ischemia protects both hearts with normal mitochondrial AIF content and hearts with mitochondrial AIF deficiency. Although preservation of mitochondrial AIF content plays a key role in

Cardioprotection by modulation of mitochondrial respiration during ischemia–reperfusion: Role of apoptosis-inducing factor

International Nuclear Information System (INIS)

Xu, Aijun; Szczepanek, Karol; Hu, Ying; Lesnefsky, Edward J.; Chen, Qun

2013-01-01

Highlights: •Blockade of electron transport prevents the loss of AIF from mitochondria during IR. •Blockade of electron transport decreases caspase-independent cell death during IR. •Mitochondrial AIF content is down-regulated in Harlequin mice. •Blockade of electron transport protects Harlequin mouse hearts during IR. •Amobarbital protection is partially dependent on mitochondrial AIF content. -- Abstract: The transient, reversible blockade of electron transport (BET) during ischemia or at the onset of reperfusion protects mitochondria and decreases cardiac injury. Apoptosis inducing factor (AIF) is located within the mitochondrial intermembrane space. A release of AIF from mitochondria into cytosol and nucleus triggers caspase-independent cell death. We asked if BET prevents the loss of AIF from mitochondria as a mechanism of protection in the buffer perfused heart. BET during ischemia with amobarbital, a rapidly reversible inhibitor of mitochondrial complex I, attenuated a release of AIF from mitochondria into cytosol, in turn decreasing the formation of cleaved and activated PARP-1. These results suggest that BET-mediated protection may occur through prevention of the loss of AIF from mitochondria during ischemia–reperfusion. In order to further clarify the role of mitochondrial AIF in BET-mediated protection, Harlequin (Hq) mice, a genetic model with mitochondrial AIF deficiency, were used to test whether BET could still decrease cell injury in Hq mouse hearts during reperfusion. BET during ischemia protected Hq mouse hearts against ischemia–reperfusion injury and improved mitochondrial function in these hearts during reperfusion. Thus, cardiac injury can still be decreased in the presence of down-regulated mitochondrial AIF content. Taken together, BET during ischemia protects both hearts with normal mitochondrial AIF content and hearts with mitochondrial AIF deficiency. Although preservation of mitochondrial AIF content plays a key role in

The purification and steady-state kinetic behaviour of rabbit heart mitochondrial NAD(P)+ malic enzyme.

OpenAIRE

Davisson, V J; Schulz, A R

1985-01-01

The mitochondrial NAD(P)+ malic enzyme [EC 1.1.1.39, L-malate:NAD+ oxidoreductase (decarboxylating)] was purified from rabbit heart to a specific activity of 7 units (mumol/min)/mg at 23 degrees C. A study of the reductive carboxylation reaction indicates that this enzymic reaction is reversible. The rate of the reductive carboxylation reaction appears to be completely inhibited at an NADH concentration of 0.92 mM. A substrate saturation curve of this reaction with NADH as the varied substrat...

Mitochondrial DNA analysis of the putative heart of Louis XVII, son of Louis XVI and Marie-Antoinette.

Science.gov (United States)

Jehaes, E; Pfeiffer, H; Toprak, K; Decorte, R; Brinkmann, B; Cassiman, J J

2001-03-01

According to official historiography, the 10-year-old Louis XVII died in the Temple of Paris on June 8, 1795. However, public rumour spread the theory that Louis XVII escaped and that his descendants would be alive today. One such putative 'Louis XVII' was Carl Wilhelm Naundorff, who died in 1845 in Delft (the Netherlands). Comparative mitochondrial DNA (mtDNA) analysis gave evidence that his remains could not be identified as those of Louis XVII. In the present study, mtDNA analysis was performed on the heart of the young boy who died in the prison of Paris in 1795. In order to obtain the strongest evidence possible, two laboratories independently analysed the heart. The results showed that the consensus mtDNA sequence of the heart was identical to that of the maternal relatives of Louis XVII.

Padronização de modelo de coração isolado "working heart" com circulação parabiótica Development of isolated swine "working heart model" with parabiotic circulation

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Lindemberg da Mota Silveira Filho

2008-03-01

Full Text Available OBJETIVO: Desenvolver modelo de coração isolado de suíno "working heart" sob suporte por circulação parabiótica e verificar se o mesmo é estável e se possibilitou de forma efetiva a mensuração dos dados propostos. MÉTODOS: O modelo foi padronizado durante preparação para estudo de associação de agente à solução cardioplégica. Foram realizados 18 experimentos com um animal suporte e um animal doador em cada. O coração do animal doador foi perfundido como coração isolado pelo animal suporte em modo de execução de trabalho ("coração ejetante". O coração isolado foi submetido à isquemia regional por pinçamento da artéria interventricular anterior seguido de isquemia global. Durante reperfusão, com o coração ejetante (em modo "working heart", aos 30, 60 e 90 minutos foram medidos parâmetros hemodinâmicos de contratilidade e metabólicos, obtendo-se assim a elastância máxima (Emáx, o trabalho sistólico pré-recrutável (PRSW, rigidez do ventrículo (EDPRV, fluxo coronariano, consumo de oxigênio e dosagens de lactato e glicose. RESULTADOS: Os animais suporte ficaram estáveis durante todo o experimento. O pH, a pressão parcial de oxigênio e o hematócrito foram mantidos estáveis e dentro da faixa fisiológica. O coração isolado foi perfundido de forma adequada durante todo o experimento. Os dados hemodinâmicos e metabólicos propostos puderam ser mensurados adequadamente e sempre com o coração ejetante, em modo de execução de trabalho ("working heart". CONCLUSÃO: O modelo de coração isolado desenvolvido tipo "working heart" se manteve estável durante todo o experimento, sem a administração de drogas cardiotônicas e possibilitou a mensuração de todos os dados propostos de forma efetiva com o coração executando trabalho.OBJECTIVE: To develop an isolated working heart model with parabiotic circulaton in swines and verify its stability and possibility to allow effective measurements of

Magnetic resonance imaging guided transatrial electrophysiological studies in swine using active catheter tracking - experience with 14 cases

Energy Technology Data Exchange (ETDEWEB)

Grothoff, Matthias; Gutberlet, Matthias [University of Leipzig - Heart Center, Department of Radiology, Leipzig (Germany); Hindricks, Gerhard; Sommer, Philipp; Hilbert, Sebastian [University of Leipzig - Heart Center, Department of Electrophysiology, Leipzig (Germany); Fleiter, Christian [Helios Klinikum Berlin-Buch, Department of Orthopaedic Surgery, Berlin (Germany); Schnackenburg, Bernhard [Philips Healthcare, Hamburg (Germany); Weiss, Steffen; Krueger, Sascha [Philips Innovative Technologies, Hamburg (Germany); Piorkowski, Christopher; Gaspar, Thomas [University of Dresden - Heart Center, Department of Electrophysiology, Dresden (Germany); Wedan, Steve; Lloyd, Thomas [Imricor Medical Systems, Burnsville, MN (United States)

2017-05-15

To evaluate the feasibility of performing comprehensive Cardiac Magnetic resonance (CMR) guided electrophysiological (EP) interventions in a porcine model encompassing left atrial access. After introduction of two femoral sheaths 14 swine (41 ± 3.6 kg) were transferred to a 1.5 T MR scanner. A three-dimensional whole-heart sequence was acquired followed by segmentation and the visualization of all heart chambers using an image-guidance platform. Two MR conditional catheters were inserted. The interventional protocol consisted of intubation of the coronary sinus, activation mapping, transseptal left atrial access (n = 4), generation of ablation lesions and eventually ablation of the atrioventricular (AV) node. For visualization of the catheter tip active tracking was used. Catheter positions were confirmed by passive real-time imaging. Total procedure time was 169 ± 51 minutes. The protocol could be completed in 12 swine. Two swine died from AV-ablation induced ventricular fibrillation. Catheters could be visualized and navigated under active tracking almost exclusively. The position of the catheter tips as visualized by active tracking could reliably be confirmed with passive catheter imaging. Comprehensive CMR-guided EP interventions including left atrial access are feasible in swine using active catheter tracking. (orig.)

Normalization of NAD+ Redox Balance as a Therapy for Heart Failure.

Science.gov (United States)

Lee, Chi Fung; Chavez, Juan D; Garcia-Menendez, Lorena; Choi, Yongseon; Roe, Nathan D; Chiao, Ying Ann; Edgar, John S; Goo, Young Ah; Goodlett, David R; Bruce, James E; Tian, Rong

2016-09-20

Impairments of mitochondrial function in the heart are linked intricately to the development of heart failure, but there is no therapy for mitochondrial dysfunction. We assessed the reduced/oxidized ratio of nicotinamide adenine dinucleotide (NADH/NAD(+) ratio) and protein acetylation in the failing heart. Proteome and acetylome analyses were followed by docking calculation, mutagenesis, and mitochondrial calcium uptake assays to determine the functional role of specific acetylation sites. The therapeutic effects of normalizing mitochondrial protein acetylation by expanding the NAD(+) pool also were tested. Increased NADH/NAD(+) and protein hyperacetylation, previously observed in genetic models of defective mitochondrial function, also are present in human failing hearts as well as in mouse hearts with pathologic hypertrophy. Elevation of NAD(+) levels by stimulating the NAD(+) salvage pathway suppressed mitochondrial protein hyperacetylation and cardiac hypertrophy, and improved cardiac function in responses to stresses. Acetylome analysis identified a subpopulation of mitochondrial proteins that was sensitive to changes in the NADH/NAD(+) ratio. Hyperacetylation of mitochondrial malate-aspartate shuttle proteins impaired the transport and oxidation of cytosolic NADH in the mitochondria, resulting in altered cytosolic redox state and energy deficiency. Furthermore, acetylation of oligomycin-sensitive conferring protein at lysine-70 in adenosine triphosphate synthase complex promoted its interaction with cyclophilin D, and sensitized the opening of mitochondrial permeability transition pore. Both could be alleviated by normalizing the NAD(+) redox balance either genetically or pharmacologically. We show that mitochondrial protein hyperacetylation due to NAD(+) redox imbalance contributes to the pathologic remodeling of the heart via 2 distinct mechanisms. Our preclinical data demonstrate a clear benefit of normalizing NADH/NAD(+) imbalance in the failing hearts

Sinclair swine melanoma

International Nuclear Information System (INIS)

Hook, R.R.; Berkelhammer, J.; Hamby, C.V.

1986-01-01

Sinclair(S-1) miniature swine spontaneously develop melanomas which have many biologic and histologic features in common with human superficial spreading melanoma. Host control of this neoplasm was indicated by the high incidence of spontaneous regression, a decrease in tumor development with age and a decrease in progressive growth of the tumor as age of tumor development increases. Immunologic mechanisms were implicated in host control by histologic observation of a mononuclear inflammatory infiltration of tumors which lead to depigmentation and fibrosis. In vitro immunologic studies revealed that leukocytes from melanoma swine were sensitized specifically to a tumor associated antigen like substance present in extracts of cutaneous melanomas and cultured swine melanoma cells and that melanoma swine leukocytes were cytotoxic for swine melanoma cells. Furthermore, these studies suggested the existence of a common cross reactive, melanoma associated antigen shared by human and swine melanomas. Antigenic analyses of swine melanomas with mouse monoclonal antibodies developed to a single swine melanoma cell culture and with rabbit antisera developed to pooled extracts of cutaneous melanomas demonstrated the presence of tumor associated antigens in swine melanoma cell culture and cutaneous melanomas. The failure of mouse monoclonal antibodies to detect antigens in cutaneous melanoma extracts and the failure of rabbit antisera to detect antigens in melanoma cell culture extracts suggested a differential in antigen expression between swine melanoma cells grown in vitro and in vivo

Characterization of canine mitochondrial protein expression in natural and induced forms of idiopathic dilated cardiomyopathy.

Science.gov (United States)

Lopes, Rosana; Solter, Philip F; Sisson, D David; Oyama, Mark A; Prosek, Robert

2006-06-01

To map canine mitochondrial proteins and identify qualitative and quantitative differences in heart mitochondrial protein expression between healthy dogs and dogs with naturally occurring and induced dilated cardiomyopathy (DCM). Left ventricle samples were obtained from 7 healthy dogs, 7 Doberman Pinschers with naturally occurring DCM, and 7 dogs with induced DCM. Fresh and frozen mitochondrial fractions were isolated from the left ventricular free wall and analyzed by 2-dimensional electrophoresis. Protein spots that increased or decreased in density by >or= 2-fold between groups were analyzed by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry or quadrupole selecting, quadrupole collision cell, time-of-flight mass spectrometry. Within narrow pH gradients of control canine heart mitochondrial samples, a total of 1,528 protein spots were revealed. Forty subunits of heart mitochondrial proteins that differ significantly from control tissues were altered in tissue specimens from dogs with naturally occurring and induced forms of DCM. The most affected heart mitochondrial proteins in both groups were those of oxidative phosphorylation (55%). Upregulation of manganese superoxide dismutase was suggestive of heart oxidative injury in tissue specimens from dogs with both forms of DCM. Evidence of apoptosis was associated with overexpression of the heart mitochondrial voltage-dependent anion channel-2 protein and endonuclease G in tissue specimens from dogs with induced DCM. Alterations of heart mitochondrial proteins related to oxidative phosphorylation dysfunction were more prevalent in tissue specimens from dogs with induced or naturally occurring DCM, compared with those of control dogs.

Initiation of electron transport chain activity in the embryonic heart coincides with the activation of mitochondrial complex 1 and the formation of supercomplexes.

Science.gov (United States)

Beutner, Gisela; Eliseev, Roman A; Porter, George A

2014-01-01

Mitochondria provide energy in form of ATP in eukaryotic cells. However, it is not known when, during embryonic cardiac development, mitochondria become able to fulfill this function. To assess this, we measured mitochondrial oxygen consumption and the activity of the complexes (Cx) 1 and 2 of the electron transport chain (ETC) and used immunoprecipitation to follow the generation of mitochondrial supercomplexes. We show that in the heart of mouse embryos at embryonic day (E) 9.5, mitochondrial ETC activity and oxidative phosphorylation (OXPHOS) are not coupled, even though the complexes are present. We show that Cx-1 of the ETC is able to accept electrons from the Krebs cycle, but enzyme assays that specifically measure electron flow to ubiquinone or Cx-3 show no activity at this early embryonic stage. At E11.5, mitochondria appear functionally more mature; ETC activity and OXPHOS are coupled and respond to ETC inhibitors. In addition, the assembly of highly efficient respiratory supercomplexes containing Cx-1, -3, and -4, ubiquinone, and cytochrome c begins at E11.5, the exact time when Cx-1 becomes functional activated. At E13.5, ETC activity and OXPHOS of embryonic heart mitochondria are indistinguishable from adult mitochondria. In summary, our data suggest that between E9.5 and E11.5 dramatic changes occur in the mitochondria of the embryonic heart, which result in an increase in OXPHOS due to the activation of complex 1 and the formation of supercomplexes.

Mitochondrial and genomic ancestry are associated with etiology of heart failure in Brazilian patients.

Science.gov (United States)

Cardena, M M S G; Ribeiro-Dos-Santos, A K; Santos, S E B; Mansur, A J; Bernardez-Pereira, S; Santos, P C J L; Pereira, A C; Fridman, C

2016-02-01

There is a high prevalence of heart failure (HF) in the general population, but it is more common in black people. We evaluated the association between genomic ancestry and mitochondrial haplogroups (mt-haplogroups) with HF etiology in 503 Brazilian patients. We elicited Mt-haplogroups by analyzing the control region of mitochondrial DNA, and genomic ancestry, by using 48 autosomal insertion-deletion ancestry informative markers. Hypertensive (28.6%, n=144) and ischemic (28.4%, n=143) etiologies of HF were the most prevalent herein. Our results showed that 233 individuals (46.3%) presented African mitochondrial (mt)-haplogroups, and the major contribution in the genomic ancestry analysis was the European ancestry (57.5% (±22.1%)). African mt-haplogroups were positively associated with a diagnosis of hypertensive cardiomyopathy (odds ratio, OR 1.55, confidence interval, CI 95% 1.04-2.44, P=0.04) when compared with European mt-haplogroups. Regarding the genomic ancestry, the African ancestry variant had higher risks (OR 7.84, 95% CI 2.81-21.91, Pancestry variant had lower risks (OR 0.14, 95% CI 0.04-5.00, Pancestry showed an OR of 4.05 (CI 95% 1.53-10.74, P=0.005), whereas African ancestry showed an OR of 0.17 (CI 95% 0.06-0.48, P=0.001) for developing ischemic etiology. In conclusion, this study supports the importance of using ancestry informative markers and mitochondrial DNA to study the genetics of complex diseases in admixed populations to improve the management, treatment and prevention of these illnesses. Therefore, the ancestry informative markers and mt-haplogroups could provide new biomarkers to be associated with HF etiologies and be used as a premise for more specific management.

Mitochondrial cardiomyopathies

Directory of Open Access Journals (Sweden)

Ayman W. El-Hattab

2016-07-01

Full Text Available Mitochondria are found in all nucleated human cells and perform a variety of essential functions, including the generation of cellular energy. Mitochondria are under dual genome control. Only a small fraction of their proteins are encoded by mitochondrial DNA (mtDNA while more than 99% of them are encoded by nuclear DNA (nDNA. Mutations in mtDNA or mitochondria-related nDNA genes result in mitochondrial dysfunction leading to insufficient energy production required to meet the needs of various organs, particularly those with high energy requirements, including the central nervous system, skeletal and cardiac muscles, kidneys, liver, and endocrine system. Because cardiac muscles are one of the high energy demanding tissues, cardiac involvement occurs in mitochondrial diseases with cardiomyopathies being one of the most frequent cardiac manifestations found in these disorders. Cardiomyopathy is estimated to occur in 20-40% of children with mitochondrial diseases. Mitochondrial cardiomyopathies can vary in severity from asymptomatic status to severe manifestations including heart failure, arrhythmias, and sudden cardiac death. Hypertrophic cardiomyopathy is the most common type; however, mitochondrial cardiomyopathies might also present as dilated, restrictive, left ventricular noncompaction, and histiocytoid cardiomyopathies. Cardiomyopathies are frequent manifestations of mitochondrial diseases associated with defects in electron transport chain (ETC complexes subunits and their assembly factors, mitochondrial tRNAs, rRNAs, ribosomal proteins, and translation factors, mtDNA maintenance, and coenzyme Q10 synthesis. Other mitochondrial diseases with cardiomyopathies include Barth syndrome, Sengers syndrome, TMEM70-related mitochondrial complex V deficiency, and Friedreich ataxia.

Echinococcus canadensis (G7) and Echinococcus granulosus sensu stricto (G1) in swine of southern Brazil.

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Monteiro, D U; Botton, S A; Tonin, A A; Azevedo, M I; Graichen, D A S; Noal, C B; de la Rue, M L

2014-05-28

The cystic echinococcosis (CE) is an important zoonotic disease caused by the parasite Echinococcus spp. In Brazil, this parasite is present in Rio Grande do Sul (RS) state, border with Argentina and Uruguay, causing several damages to human and animal health. This study aimed to identify Echinococcus spp. in hydatid cysts of swine and evaluate the similarity of the genotypes through the phylogenetic analysis. A total of 3,101,992 swine were slaughtered in the central/northern region of RS/Brazil, during 2008-2012. Five isolates were characterized as hydatid cyst by molecular analysis, based on the mitochondrial gene cytochrome c oxidase subunit I (cox-I). The genotypes E. granulosus sensu stricto (G1) (n=2) and E. canadensis (G7) (n=3) were identified in the hydatid cysts. The swine represents a potential intermediate host for different genotypes of Echinococcus spp., besides it can contribute to the perpetuation of the parasite's life cycle in rural areas. Copyright © 2014 Elsevier B.V. All rights reserved.

Troxerutin attenuates diet-induced oxidative stress, impairment of mitochondrial biogenesis and respiratory chain complexes in mice heart.

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Rajagopalan, Geetha; Chandrasekaran, Sathiya Priya; Carani Venkatraman, Anuradha

2017-01-01

Mitochondrial abnormality is thought to play a key role in cardiac disease originating from the metabolic syndrome (MS). We evaluated the effect of troxerutin (TX), a semi-synthetic derivative of the natural bioflavanoid rutin, on the respiratory chain complex activity, oxidative stress, mitochondrial biogenesis and dynamics in heart of high fat, high fructose diet (HFFD) -induced mouse model of MS. Adult male Mus musculus mice of body weight 25-30 g were fed either control diet or HFFD for 60 days. Mice from each dietary regimen were divided into two groups on the 16th day and were treated or untreated with TX (150 mg/kg body weight [bw], per oral) for the next 45 days. At the end of experimental period, respiratory chain complex activity, uncoupling proteins (UCP)-2 and -3, mtDNA content, mitochondrial biogenesis and dynamics, oxidative stress markers and reactive oxygen species (ROS) generation were analyzed. Reduced mtDNA abundance with alterations in the expression of genes related to mitochondrial biogenesis and fission and fusion processes were observed in HFFD-fed mice. Disorganized and smaller mitochondria, reduction in complexes I, III and IV activities (by about 55%) and protein levels of UCP-2 (52%) and UCP-3 (46%) were noted in these mice. TX administration suppressed oxidative stress, improved the oxidative capacity and biogenesis and restored fission/fusion imbalance in the cardiac mitochondria of HFFD-fed mice. TX protects the myocardium by modulating the putative molecules of mitochondrial biogenesis and dynamics and by its anti-oxidant function in a mouse model of MS. © 2016 John Wiley & Sons Australia, Ltd.

Improvement of heart function in postinfarct heart failure swine models after hepatocyte growth factor gene transfer: comparison of low-, medium- and high-dose groups.

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Yang, Zhi-jian; Chen, Bo; Sheng, Zhang; Zhang, Ding-guo; Jia, En-zhi; Wang, Wei; Ma, Dong-chao; Zhu, Tie-bing; Wang, Lian-sheng; Li, Chun-jian; Wang, Hui; Cao, Ke-jiang; Ma, Wen-zhu

2010-04-01

Despite advances in surgical and reperfusion therapy, there is no effective therapy currently exists to prevent the progressive decline in cardiac function following myocardial infarction. Hepatocyte growth factor has potent angiogenic and anti-apoptotic activities. The aim of this study was to investigate the therapeutic effect and dose-effect relationship on postinfarction heart failure with different doses of adenovirus-mediated human hepatocyte growth factor (Ad(5)-HGF) transference in swine models. Totally twenty swine were randomly divided into four groups: (a) control group (null- Ad(5), 1 ml); (b) low-dose group (1 x 10(9) Pfu/ml Ad(5)-HGF, 1 ml); (c) medium-dose group (5 x 10(9) Pfu/ml Ad(5)-HGF, 1 ml); (d) high-dose group (1 x 10(10) Pfu/ml Ad(5)-HGF, 1 ml). Four weeks after left anterior descending coronary artery (LAD) ligation, different doses of Ad(5)-HGF were transferred in three therapeutic groups via right coronary artery. Four and seven weeks after LAD ligation, gate cardiac perfusion imaging was performed to evaluate cardiac perfusion and left ventricular ejection fraction (LVEF). Seven weeks after surgery, the apoptotic index of cardiocyte was observed by TUNEL, the expression of Bcl-2, Bax, alpha-SMA and Factor VIII in the border zones were evaluated by immunohistochemistry, respectively. Four weeks after myocardial infarction, no significant difference was observed among four groups. Three weeks after Ad(5)-HGF transfer, the improvement of cardiac perfusion and LVEF was obviously observed, especially after 1 x 10(10) Pfu Ad(5)-HGF transfer. TUNEL assay showed that 5 x 10(9) Pfu and 1 x 10(10) Pfu Ad(5)-HGF treatment had a obvious reduction in the apoptotic index compared with the null-Ad(5) group, especially after 1 x 10(10) Pfu Ad(5)-HGF treatment. The expression of Bcl-2 protein was increased and the expression of Bax protein was inhibited in the 5 x 10(9) Pfu and 1 x 10(10) Pfu Ad(5)-HGF groups compared with the null-Ad(5) group. The vessel

Mitochondrial apoptotic pathway activation in the atria of heart failure patients due to mitral and tricuspid regurgitation.

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Chang, Jen-Ping; Chen, Mien-Cheng; Liu, Wen-Hao; Lin, Yu-Sheng; Huang, Yao-Kuang; Pan, Kuo-Li; Ho, Wan-Chun; Fang, Chih-Yuan; Chen, Chien-Jen; Chen, Huang-Chung

2015-08-01

Apoptosis occurs in atrial cardiomyocytes in mitral and tricuspid valve disease. The purpose of this study was to examine the respective roles of the mitochondrial and tumor necrosis factor-α receptor associated death domain (TRADD)-mediated death receptor pathways for apoptosis in the atrial cardiomyocytes of heart failure patients due to severe mitral and moderate-to-severe tricuspid regurgitation. This study comprised eighteen patients (7 patients with persistent atrial fibrillation and 11 in sinus rhythm). Atrial appendage tissues were obtained during surgery. Three purchased normal human left atrial tissues served as normal controls. Moderately-to-severely myolytic cardiomyocytes comprised 59.7±22.1% of the cardiomyocytes in the right atria and 52.4±12.9% of the cardiomyocytes in the left atria of mitral and tricuspid regurgitation patients with atrial fibrillation group and comprised 58.4±24.8% of the cardiomyocytes in the right atria of mitral and tricuspid regurgitation patients with sinus rhythm. In contrast, no myolysis was observed in the normal human adult left atrial tissue samples. Immunohistochemical analysis showed expression of cleaved caspase-9, an effector of the mitochondrial pathways, in the majority of right atrial cardiomyocytes (87.3±10.0%) of mitral and tricuspid regurgitation patients with sinus rhythm, and right atrial cardiomyocytes (90.6±31.4%) and left atrial cardiomyocytes (70.7±22.0%) of mitral and tricuspid regurgitation patients with atrial fibrillation. In contrast, only 5.7% of cardiomyocytes of the normal left atrial tissues showed strongly positive expression of cleaved caspase-9. Of note, none of the atrial cardiomyocytes in right atrial tissue in sinus rhythm and in the fibrillating right and left atria of mitral and tricuspid regurgitation patients, and in the normal human adult left atrial tissue samples showed cleaved caspase-8 expression, which is a downstream effector of TRADD of the death receptor pathway

Antibody levels to hepatitis E virus in North Carolina swine workers, non-swine workers, swine, and murids.

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Withers, Mark R; Correa, Maria T; Morrow, Morgan; Stebbins, Martha E; Seriwatana, Jitvimol; Webster, W David; Boak, Marshall B; Vaughn, David W

2002-04-01

In a cross-sectional serosurvey, eastern North Carolina swine workers (n = 165) were compared with non-swine workers (127) for the presence of antibodies to hepatitis E virus as measured by a quantitative immunoglobulin enzyme-linked immunosorbent assay. Using a cutoff of 20 Walter Reed U/ml, swine-exposed subjects had a 4.5-fold higher antibody prevalence (10.9%) than unexposed subjects (2.4%). No evidence of past clinical hepatitis E or unexplained jaundice could be elicited. Swine (84) and mice (61), from farm sites in the same region as exposed subjects, were also tested. Antibody prevalence in swine (overall = 34.5%) varied widely (10.0-91.7%) according to site, but no antibody was detected in mice. Our data contribute to the accumulating evidence that hepatitis E may be a zoonosis and specifically to the concept of it as an occupational infection of livestock workers.

Nanoparticle sensor for label free detection of swine DNA in mixed biological samples

Energy Technology Data Exchange (ETDEWEB)

Ali, M E; Hashim, U [Institute of Nano Electronic Engineering (INNE), Universiti Malaysia Perlis, Lot 104-108, Tingkat 1, Block A, Taman Pertiwi Indah, Jalan Kangar-Alor Star, Seriab, 01000 Kangar, Perlis (Malaysia); Mustafa, S; Che Man, Y B; Yusop, M H M [Halal Products Research Institute, Universiti Putra Malaysia, 43400 UPM Serdang, Selangor (Malaysia); Bari, M F [School of Materials Engineering, University Malaysia Perlis, Seriab 01000, Kangar, Perlis (Malaysia); Islam, Kh N [Department of Preclinical Sciences, Faculty of Veterinary Medicine, Universiti Putra Malaysia, 43400 UPM Serdang, Selangor (Malaysia); Hasan, M F, E-mail: uda@unimap.edu.my [Department of Crop Science, Faculty of Agriculture, Universiti Putra Malaysia, 43400 UPM Serdang, Selangor (Malaysia)

2011-05-13

We used 40 {+-} 5 nm gold nanoparticles (GNPs) as colorimetric sensor to visually detect swine-specific conserved sequence and nucleotide mismatch in PCR-amplified and non-amplified mitochondrial DNA mixtures to authenticate species. Colloidal GNPs changed color from pinkish-red to gray-purple in 2 mM PBS. Visually observed results were clearly reflected by the dramatic reduction of surface plasmon resonance peak at 530 nm and the appearance of new features in the 620-800 nm regions in their absorption spectra. The particles were stabilized against salt-induced aggregation upon the adsorption of single-stranded DNA. The PCR products, without any additional processing, were hybridized with a 17-base probe prior to exposure to GNPs. At a critical annealing temperature (55 {sup 0}C) that differentiated matched and mismatched base pairing, the probe was hybridized to pig PCR product and dehybridized from the deer product. The dehybridized probe stuck to GNPs to prevent them from salt-induced aggregation and retained their characteristic red color. Hybridization of a 27-nucleotide probe to swine mitochondrial DNA identified them in pork-venison, pork-shad and venison-shad binary admixtures, eliminating the need of PCR amplification. Thus the assay was applied to authenticate species both in PCR-amplified and non-amplified heterogeneous biological samples. The results were determined visually and validated by absorption spectroscopy. The entire assay (hybridization plus visual detection) was performed in less than 10 min. The LOD (for genomic DNA) of the assay was 6 {mu}g ml{sup -1} swine DNA in mixed meat samples. We believe the assay can be applied for species assignment in food analysis, mismatch detection in genetic screening and homology studies between closely related species.

Nanoparticle sensor for label free detection of swine DNA in mixed biological samples

International Nuclear Information System (INIS)

Ali, M E; Hashim, U; Mustafa, S; Che Man, Y B; Yusop, M H M; Bari, M F; Islam, Kh N; Hasan, M F

2011-01-01

We used 40 ± 5 nm gold nanoparticles (GNPs) as colorimetric sensor to visually detect swine-specific conserved sequence and nucleotide mismatch in PCR-amplified and non-amplified mitochondrial DNA mixtures to authenticate species. Colloidal GNPs changed color from pinkish-red to gray-purple in 2 mM PBS. Visually observed results were clearly reflected by the dramatic reduction of surface plasmon resonance peak at 530 nm and the appearance of new features in the 620-800 nm regions in their absorption spectra. The particles were stabilized against salt-induced aggregation upon the adsorption of single-stranded DNA. The PCR products, without any additional processing, were hybridized with a 17-base probe prior to exposure to GNPs. At a critical annealing temperature (55 0 C) that differentiated matched and mismatched base pairing, the probe was hybridized to pig PCR product and dehybridized from the deer product. The dehybridized probe stuck to GNPs to prevent them from salt-induced aggregation and retained their characteristic red color. Hybridization of a 27-nucleotide probe to swine mitochondrial DNA identified them in pork-venison, pork-shad and venison-shad binary admixtures, eliminating the need of PCR amplification. Thus the assay was applied to authenticate species both in PCR-amplified and non-amplified heterogeneous biological samples. The results were determined visually and validated by absorption spectroscopy. The entire assay (hybridization plus visual detection) was performed in less than 10 min. The LOD (for genomic DNA) of the assay was 6 μg ml -1 swine DNA in mixed meat samples. We believe the assay can be applied for species assignment in food analysis, mismatch detection in genetic screening and homology studies between closely related species.

Loss of PINK1 increases the heart's vulnerability to ischemia-reperfusion injury.

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Hilary K Siddall

Full Text Available Mutations in PTEN inducible kinase-1 (PINK1 induce mitochondrial dysfunction in dopaminergic neurons resulting in an inherited form of Parkinson's disease. Although PINK1 is present in the heart its exact role there is unclear. We hypothesized that PINK1 protects the heart against acute ischemia reperfusion injury (IRI by preventing mitochondrial dysfunction.Over-expressing PINK1 in HL-1 cardiac cells reduced cell death following simulated IRI (29.2±5.2% PINK1 versus 49.0±2.4% control; N = 320 cells/group P5 animals/group; P<0.05. Cardiomyocytes isolated from PINK1-/- hearts had a lower resting mitochondrial membrane potential, had inhibited mitochondrial respiration, generated more oxidative stress during simulated IRI, and underwent rigor contracture more rapidly in response to an uncoupler when compared to PINK1+/+ cells suggesting mitochondrial dysfunction in hearts deficient in PINK1.We show that the loss of PINK1 increases the heart's vulnerability to ischemia-reperfusion injury. This may be due, in part, to increased mitochondrial dysfunction. These findings implicate PINK1 as a novel target for cardioprotection.

Feral Swine in the United States Have Been Exposed to both Avian and Swine Influenza A Viruses.

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Martin, Brigitte E; Sun, Hailiang; Carrel, Margaret; Cunningham, Fred L; Baroch, John A; Hanson-Dorr, Katie C; Young, Sean G; Schmit, Brandon; Nolting, Jacqueline M; Yoon, Kyoung-Jin; Lutman, Mark W; Pedersen, Kerri; Lager, Kelly; Bowman, Andrew S; Slemons, Richard D; Smith, David R; DeLiberto, Thomas; Wan, Xiu-Feng

2017-10-01

Influenza A viruses (IAVs) in swine can cause sporadic infections and pandemic outbreaks among humans, but how avian IAV emerges in swine is still unclear. Unlike domestic swine, feral swine are free ranging and have many opportunities for IAV exposure through contacts with various habitats and animals, including migratory waterfowl, a natural reservoir for IAVs. During the period from 2010 to 2013, 8,239 serum samples were collected from feral swine across 35 U.S. states and tested against 45 contemporary antigenic variants of avian, swine, and human IAVs; of these, 406 (4.9%) samples were IAV antibody positive. Among 294 serum samples selected for antigenic characterization, 271 cross-reacted with ≥1 tested virus, whereas the other 23 did not cross-react with any tested virus. Of the 271 IAV-positive samples, 236 cross-reacted with swine IAVs, 1 with avian IAVs, and 16 with avian and swine IAVs, indicating that feral swine had been exposed to both swine and avian IAVs but predominantly to swine IAVs. Our findings suggest that feral swine could potentially be infected with both avian and swine IAVs, generating novel IAVs by hosting and reassorting IAVs from wild birds and domestic swine and facilitating adaptation of avian IAVs to other hosts, including humans, before their spillover. Continued surveillance to monitor the distribution and antigenic diversities of IAVs in feral swine is necessary to increase our understanding of the natural history of IAVs. IMPORTANCE There are more than 5 million feral swine distributed across at least 35 states in the United States. In contrast to domestic swine, feral swine are free ranging and have unique opportunities for contact with wildlife, livestock, and their habitats. Our serological results indicate that feral swine in the United States have been exposed to influenza A viruses (IAVs) consistent with those found in both domestic swine and wild birds, with the predominant infections consisting of swine-adapted IAVs

Effects of vildagliptin versus sitagliptin, on cardiac function, heart rate variability and mitochondrial function in obese insulin-resistant rats

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Apaijai, Nattayaporn; Pintana, Hiranya; Chattipakorn, Siriporn C; Chattipakorn, Nipon

2013-01-01

Background and Purpose Long-term high-fat diet (HFD) consumption has been shown to cause insulin resistance, which is characterized by hyperinsulinaemia with metabolic inflexibility. Insulin resistance is associated with cardiac sympathovagal imbalance, cardiac dysfunction and cardiac mitochondrial dysfunction. Dipeptidyl peptidase-4 (DPP-4) inhibitors, vildagliptin and sitagliptin, are oral anti-diabetic drugs often prescribed in patients with cardiovascular disease. Therefore, in this study, we sought to determine the effects of vildagliptin and sitagliptin in a murine model of insulin resistance. Experimental Approach Male Wistar rats weighing 180–200 g, were fed either a normal diet (20% energy from fat) or a HFD (59% energy from fat) for 12 weeks. These rats were then divided into three subgroups to receive vildagliptin (3 mg·kg−1·day−1), sitagliptin (30 mg·kg−1·day−1) or vehicle for another 21 days. Metabolic parameters, oxidative stress, heart rate variability (HRV), cardiac function and cardiac mitochondrial function were determined. Key Results Rats that received HFD developed insulin resistance characterized by increased body weight, plasma insulin, total cholesterol and oxidative stress levels along with a decreased high-density lipoprotein (HDL) level. Moreover, cardiac dysfunction, depressed HRV, cardiac mitochondrial dysfunction and cardiac mitochondrial morphology changes were observed in HFD rats. Both vildagliptin and sitagliptin decreased plasma insulin, total cholesterol and oxidative stress as well as increased HDL level. Furthermore, vildagliptin and sitagliptin attenuated cardiac dysfunction, prevented cardiac mitochondrial dysfunction and completely restored HRV. Conclusions and Implications Both vildagliptin and sitagliptin share similar efficacy in cardioprotection in obese insulin-resistant rats. PMID:23488656

9 CFR 85.6 - Interstate movement of pseudorabies vaccinate swine, except swine from qualified negative gene...

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2010-01-01

... vaccinate swine, except swine from qualified negative gene-altered vaccinated herds, not known to be..., except swine from qualified negative gene-altered vaccinated herds, not known to be infected with or exposed to pseudorabies. Pseudorabies vaccinate swine, except swine from qualified negative gene-altered...

Paraoxonase 2 prevents the development of heart failure.

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Li, Wei; Kennedy, David; Shao, Zhili; Wang, Xi; Kamdar, Andre Klaassen; Weber, Malory; Mislick, Kayla; Kiefer, Kathryn; Morales, Rommel; Agatisa-Boyle, Brendan; Shih, Diana M; Reddy, Srinivasa T; Moravec, Christine S; Tang, W H Wilson

2018-05-02

Mitochondrial oxidation is a major source of reactive oxygen species (ROS) and mitochondrial dysfunction plays a central role in development of heart failure (HF). Paraoxonase 2 deficient (PON2-def) mitochondria are impaired in function. In this study, we tested whether PON2-def aggravates HF progression. Using qPCR, immunoblotting and lactonase activity assay, we demonstrate that PON2 activity was significantly decreased in failing hearts despite increased PON2 expression. To determine the cardiac-specific function of PON2, we performed heart transplantations in which PON2-def and wild type (WT) donor hearts were implanted into WT recipient mice. Beating scores of the donor hearts, assessed at 4 weeks post-transplantation, were significantly decreased in PON2-def hearts when compared to WT donor hearts. By using a transverse aortic constriction (TAC) model, we found PON2 deficiency significantly exacerbated left ventricular remodeling and cardiac fibrosis post-TAC. We further demonstrated PON2 deficiency significantly enhanced ROS generation in heart tissues post-TAC. ROS generation was measured through dihydroethidium (DHE) using high-pressure liquid chromatography (HPLC) with a fluorescent detector. By using neonatal cardiomyocytes treated with CoCl 2 to mimic hypoxia, we found PON2 deficiency dramatically increased ROS generation in the cardiomyocytes upon CoCl 2 treatment. In response to a short CoCl 2 exposure, cell viability and succinate dehydrogenase (SDH) activity assessed by MTT assay were significantly diminished in PON2-def cardiomyocytes compared to those in WT cardiomyocytes. PON2-def cardiomyocytes also had lower baseline SDH activity. By using adult mouse cardiomyocytes and mitochondrial ToxGlo assay, we found impaired cellular ATP generation in PON2-def cells compared to that in WT cells, suggesting that PON2 is necessary for proper mitochondrial function. Our study suggests a cardioprotective role for PON2 in both experimental and human heart

Mitochondrial Bioenergetics During Ischemia and Reperfusion.

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Consolini, Alicia E; Ragone, María I; Bonazzola, Patricia; Colareda, Germán A

2017-01-01

During ischemia and reperfusion (I/R) mitochondria suffer a deficiency to supply the cardiomyocyte with chemical energy, but also contribute to the cytosolic ionic alterations especially of Ca 2+ . Their free calcium concentration ([Ca 2+ ]m) mainly depends on mitochondrial entrance through the uniporter (UCam) and extrusion in exchange with Na + (mNCX) driven by the electrochemical gradient (ΔΨm). Cardiac energetic is frequently estimated by the oxygen consumption, which determines metabolism coupled to ATP production and to the maintaining of ΔΨm. Nevertheless, a better estimation of heart energy consumption is the total heat release associated to ATP hydrolysis, metabolism, and binding reactions, which is measurable either in the presence or the absence of oxygenation or perfusion. Consequently, a mechano-calorimetrical approach on isolated hearts gives a tool to evaluate muscle economy. The mitochondrial role during I/R depends on the injury degree. We investigated the role of the mitochondrial Ca 2+ transporters in the energetic of hearts stunned by a model of no-flow I/R in rat hearts. This chapter explores an integrated view of previous and new results which give evidences to the mitochondrial role in cardiac stunning by ischemia o hypoxia, and the influence of thyroid alterations and cardioprotective strategies, such as cardioplegic solutions (high K-low Ca, pyruvate) and the phytoestrogen genistein in both sex. Rat ventricles were perfused in a flow-calorimeter at either 30 °C or 37 °C to continuously measure the left ventricular pressure (LVP) and total heat rate (Ht). A pharmacological treatment was done before exposing to no-flow I and R. The post-ischemic contractile (PICR as %) and energetical (Ht) recovery and muscle economy (Eco: P/Ht) were determined during stunning. The functional interaction between mitochondria (Mit) and sarcoplasmic reticulum (SR) was evaluated with selective mitochondrial inhibitors in hearts reperfused with Krebs-10 m

Protocol: Transmission and prevention of influenza in Hutterites: Zoonotic transmission of influenza A: swine & swine workers

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Loeb Mark

2009-11-01

Full Text Available Abstract Background Among swine, reassortment of influenza virus genes from birds, pigs, and humans could generate influenza viruses with pandemic potential. Humans with acute infection might also be a source of infection for swine production units. This article describes the study design and methods being used to assess influenza A transmission between swine workers and pigs. We hypothesize that transmission of swine influenza viruses to humans, transmission of human influenza viruses to swine, and reassortment of human and swine influenza A viruses is occurring. The project is part of a Team Grant; all Team Grant studies include active surveillance for influenza among Hutterite swine farmers in Alberta, Canada. This project also includes non-Hutterite swine farms that are experiencing swine respiratory illness. Methods/Design Nurses conduct active surveillance for influenza-like-illness (ILI, visiting participating communally owned and operated Hutterite swine farms twice weekly. Nasopharyngeal swabs and acute and convalescent sera are obtained from persons with any two such symptoms. Swabs are tested for influenza A and B by a real time RT-PCR (reverse transcriptase polymerase chain reaction at the Alberta Provincial Laboratory for Public Health (ProvLab. Test-positive participants are advised that they have influenza. The occurrence of test-positive swine workers triggers sampling (swabbing, acute and convalescent serology of the swine herd by veterinarians. Specimens obtained from swine are couriered to St. Jude Children's Research Hospital, Memphis, TN for testing. Veterinarians and herd owners are notified if animal specimens are test-positive for influenza. If swine ILI occurs, veterinarians obtain samples from the pigs; test-positives from the animals trigger nurses to obtain specimens (swabbing, acute and convalescent serology from the swine workers. ProvLab cultures influenza virus from human specimens, freezes these cultures and

Control of African swine fever epidemics in industrialized swine populations

DEFF Research Database (Denmark)

Hisham Beshara Halasa, Tariq; Bøtner, Anette; Mortensen, Sten

2016-01-01

, it is important to explore strategies that can effectively control an epidemic of ASF. In this study, the epidemiological and economic effects of strategies to control the spread of ASF between domestic swine herds were examined using a published model (DTU-DADS-ASF). The control strategies were the basic EU...... and national strategy (Basic), the basic strategy plus pre-emptive depopulation of neighboring swine herds, and intensive surveillance of herds in the control zones, including testing live or dead animals. Virus spread via wild boar was not modelled. Under the basic control strategy, the median epidemic......African swine fever (ASF) is a notifiable infectious disease with a high impact on swine health. The disease is endemic in certain regions in the Baltic countries and has spread to Poland constituting a risk of ASF spread toward Western Europe. Therefore, as part of contingency planning...

POSSIBLE ROLE OF MITOCHONDRIAL GENOME MUTATIONS IN CORONARY HEART DISEASE

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L. A. Egorova

2013-01-01

Full Text Available Mitochondria are not only the major producers of adenosine triphosphate, but also an endogenous source of reactive oxygen species. Mitochondrialdysfunction plays a key role in the trigger and progression of atherosclerotic lesion. Impaired function in the mitochondria due to their elevated level of oxidized oxygen species, the accumulation of mitochondrial DNA damages, and the exhaustion of respiratory chains induces dysfunction and apoptosis in the endothelial cells; activation of matrix metalloproteinases; growth of vascular smooth muscle cells and their migration into the intima; expression of adhesion molecules, and oxidation of low-density lipoproteins. Mitochondrial dysfunction may be an important unifying mechanism that accounts for the atherogenic effect of major cardiovascular risk factors. Small clinical pilot studies have shown an association of different mitochondrial genome mutations with atherosclerotic lesion in the artery. Taking into account the available data on the possible role of mitochondria in atherogenesis, novel drugs are now being designed to affect mitochondrial function.

POSSIBLE ROLE OF MITOCHONDRIAL GENOME MUTATIONS IN CORONARY HEART DISEASE

Directory of Open Access Journals (Sweden)

L. A. Egorova

2014-07-01

Full Text Available Mitochondria are not only the major producers of adenosine triphosphate, but also an endogenous source of reactive oxygen species. Mitochondrialdysfunction plays a key role in the trigger and progression of atherosclerotic lesion. Impaired function in the mitochondria due to their elevated level of oxidized oxygen species, the accumulation of mitochondrial DNA damages, and the exhaustion of respiratory chains induces dysfunction and apoptosis in the endothelial cells; activation of matrix metalloproteinases; growth of vascular smooth muscle cells and their migration into the intima; expression of adhesion molecules, and oxidation of low-density lipoproteins. Mitochondrial dysfunction may be an important unifying mechanism that accounts for the atherogenic effect of major cardiovascular risk factors. Small clinical pilot studies have shown an association of different mitochondrial genome mutations with atherosclerotic lesion in the artery. Taking into account the available data on the possible role of mitochondria in atherogenesis, novel drugs are now being designed to affect mitochondrial function.

Electrophysiological effects of Chinese medicine Shen song Yang xin (SSYX) on Chinese miniature swine heart and isolated guinea pig ventricular myocytes.

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Feng, Li; Gong, Jing; Jin, Zhen-yi; Li, Ning; Sun, Li-ping; Wu, Yi-ling; Pu, Jie-lin

2009-07-05

Shen song Yang xin (SSYX) is a compound of Chinese medicine with the effect of increasing heart rate (HR). This study aimed to evaluate its electrophysiological properties at heart and cellular levels. The Chinese miniature swines were randomly assigned to two groups, administered with SSYX or placebo for 4 weeks (n = 8 per group). Cardiac electrophysiological study (EPS) was performed before and after drug administration. The guinea pig ventricular myocytes were enzymatically isolated and whole cell voltage-clamp technique was used to evaluate the effect of SSYX on cardiac action potential (AP). SSYX treatment accelerated the HR from (141.8 +/- 36.0) beats per minute to (163.0 +/- 38.0) beats per minute (P = 0.013) without changing the other parameters in surface electrocardiogram. After blockage of the autonomic nervous system with metoprolol and atropin, SSYX had no effect on intrinsic HR (IHR), but decreased corrected sinus node recovery time (CSNRT) and sinus atrium conducting time (SACT). Intra cardiac EPS showed that SSYX significantly decreased the A-H and A-V intervals as well as shortened the atrial (A), atrioventricular node (AVN) and ventricular (V) effective refractory period (ERP). In isolated guinea pig ventricular myocytes, the most obvious effect of SSYX on action potential was a shortening of the action potential duration (APD) without change in shape of action potential. The shortening rates of APD(30), APD(50) and APD(90) were 19.5%, 17.8% and 15.3%, respectively. The resting potential (Em) and the interval between the end of APD(30) and APD(90) did not significantly change. The present study demonstrates that SSYX increases the HR and enhances the conducting capacity of the heart in the condition of the intact autonomic nervous system. SSYX homogenously decreases the ERP of the heart and shortens the APD of the myocytes, suggesting its antiarrhythmic effect without proarrhythmia.

Impaired cardiac mitochondrial oxidative phosphorylation and enhanced mitochondrial oxidative stress in feline hypertrophic cardiomyopathy

DEFF Research Database (Denmark)

Christiansen, Liselotte Bruun; Dela, Flemming; Koch, Jørgen

2015-01-01

respiration with complex I-linked nonfatty acid substrates and with fatty acid substrates, respectively, was significantly lower in the hearts of HCM cats compared with control cats. Mitochondrial ROS release during state 3 with complex I-linked substrates and thiobarbituric acid-reactive substances...

Mitochondrial events responsible for morphine's cardioprotection against ischemia/reperfusion injury

International Nuclear Information System (INIS)

He, Haiyan; Huh, Jin; Wang, Huihua; Kang, Yi; Lou, Jianshi; Xu, Zhelong

2016-01-01

Morphine may induce cardioprotection by targeting mitochondria, but little is known about the exact mitochondrial events that mediate morphine's protection. We aimed to address the role of the mitochondrial Src tyrosine kinase in morphine's protection. Isolated rat hearts were subjected to 30 min ischemia and 2 h of reperfusion. Morphine was given before the onset of ischemia. Infarct size and troponin I release were measured to evaluate cardiac injury. Oxidative stress was evaluated by measuring mitochondrial protein carbonylation and mitochondrial ROS generation. HL-1 cells were subjected to simulated ischemia/reperfusion and LDH release and mitochondrial membrane potential (ΔΨm) were measured. Morphine reduced infarct size as well as cardiac troponin I release which were aborted by the selective Src tyrosine kinase inhibitors PP2 and Src-I1. Morphine also attenuated LDH release and prevented a loss of ΔΨm at reperfusion in a Src tyrosine kinase dependent manner in HL-1 cells. However, morphine failed to reduce LDH release in HL-1 cells transfected with Src siRNA. Morphine increased mitochondrial Src phosphorylation at reperfusion and this was abrogated by PP2. Morphine attenuated mitochondrial protein carbonylation and mitochondrial superoxide generation at reperfusion through Src tyrosine kinase. The inhibitory effect of morphine on the mitochondrial complex I activity was reversed by PP2. These data suggest that morphine induces cardioprotection by preventing mitochondrial oxidative stress through mitochondrial Src tyrosine kinase. Inhibition of mitochondrial complex I at reperfusion by Src tyrosine kinase may account for the prevention of mitochondrial oxidative stress by morphine. - Highlights: • Morphine induced mito-Src phosphorylation and reduced infarct size in rat hearts. • Morphine failed to reduce I/R-induced LDH release in Src-silencing HL-1 cells. • Morphine prevented mitochondria damage caused by I/R through Src. • Morphine reduced

Parkinson's disease proteins: Novel mitochondrial targets for cardioprotection

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Mukherjee, Uma A.; Ong, Sang-Bing; Ong, Sang-Ging; Hausenloy, Derek J.

2015-01-01

Ischemic heart disease (IHD) is the leading cause of death and disability worldwide. Therefore, novel therapeutic targets for protecting the heart against acute ischemia/reperfusion injury (IRI) are required to attenuate cardiomyocyte death, preserve myocardial function, and prevent the onset of heart failure. In this regard, a specific group of mitochondrial proteins, which have been linked to familial forms of Parkinson's disease (PD), may provide novel therapeutic targets for cardioprotect...

Cardioprotective effect of hyperthyroidism on the stunned rat heart during ischaemia-reperfusion: energetics and role of mitochondria.

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Ragone, María Inés; Bonazzola, Patricia; Colareda, Germán A; Consolini, Alicia E

2015-06-01

What is the central question of this study? Hyperthyroidism is a cardiac risk factor, but thyroid therapy is used on myocardial stunning. What is the consequence of hyperthyroidism for mitochondrial metabolism and Ca(2+) handling of the postischaemic stunned heart? What is the main finding and its importance? Hyperthyroidism reduced stunning and improved muscle economy of the postischaemic rat heart. The activities of the mitochondrial sodium-calcium exchanger and mitochondrial K(+) channel in hyperthyroid rat hearts were different from those in the euthyroid rat hearts. These findings contribute to the understanding of mitochondrial bioenergetics in pathology and support thyroid therapy in the stunning induced by ischaemia. Transient ischaemia and hyperthyroidism are cardiovascular risk factors. Nevertheless, 3,5,3'-triiodothyronine/thyroxine therapy has been used to revert myocardial stunning. We studied the influence of hyperthyroidism on the role played by mitochondria in myocardial stunning consequent to ischaemia-reperfusion. Rats were injected s.c. daily with 20 μg kg(-1) triiodothyronine for 15 days (HpT group). Isolated ventricles from either HpT or euthyroid (EuT) rats were perfused in a calorimeter, and left intraventricular pressure (in millimetres of mercury) and heat release (Ht; in milliwatts per gram) were measured. Stunning was evoked by 20 min of no-flow ischaemia and 45 min reperfusion. The HpT hearts developed higher postischaemic contractile recovery (PICR) and improved total muscle economy (P/Ht) with lower diastolic contracture (ΔLVEDP) than EuT hearts. Release of Ca(2+) from the sarcoplasmic reticulum during reperfusion with 10 mm caffeine in low-[Na(+) ] Krebs solution evoked a higher contracture in EuT than in HpT hearts. Blockade of the mitochondrial sodium-calcium exchanger with clonazepam increased ΔLVEDP and reduced P/Ht and PICR in HpT but not in EuT hearts. The clonazepam-induced dysfunction in HpT hearts was reduced by

Ischemic preconditioning improves mitochondrial tolerance to experimental calcium overload.

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Crestanello, Juan A; Doliba, Nicolai M; Babsky, Andriy M; Doliba, Natalia M; Niibori, Koki; Whitman, Glenn J R; Osbakken, Mary D

2002-04-01

Ca(2+) overload leads to mitochondrial uncoupling, decreased ATP synthesis, and myocardial dysfunction. Pharmacologically opening of mitochondrial K(ATP) channels decreases mitochondrial Ca(2+) uptake, improving mitochondrial function during Ca(2+) overload. Ischemic preconditioning (IPC), by activating mitochondrial K(ATP) channels, may attenuate mitochondrial Ca(2+) overload and improve mitochondrial function during reperfusion. The purpose of these experiments was to study the effect of IPC (1) on mitochondrial function and (2) on mitochondrial tolerance to experimental Ca(2+) overload. Rat hearts (n = 6/group) were subjected to (a) 30 min of equilibration, 25 min of ischemia, and 30 min of reperfusion (Control) or (b) two 5-min episodes of ischemic preconditioning, 25 min of ischemia, and 30 min of reperfusion (IPC). Developed pressure (DP) was measured. Heart mitochondria were isolated at end-Equilibration (end-EQ) and at end-Reperfusion (end-RP). Mitochondrial respiratory function (state 2, oxygen consumption with substrate only; state 3, oxygen consumption stimulated by ADP; state 4, oxygen consumption after cessation of ADP phosphorylation; respiratory control index (RCI, state 3/state 4); rate of oxidative phosphorylation (ADP/Deltat), and ADP:O ratio) was measured with polarography using alpha-ketoglutarate as a substrate in the presence of different Ca(2+) concentrations (0 to 5 x 10(-7) M) to simulate Ca(2+) overload. IPC improved DP at end-RP. IPC did not improve preischemic mitochondrial respiratory function or preischemic mitochondrial response to Ca(2+) loading. IPC improved state 3, ADP/Deltat, and RCI during RP. Low Ca(2+) levels (0.5 and 1 x 10(-7) M) stimulated mitochondrial function in both groups predominantly in IPC. The Control group showed evidence of mitochondrial uncoupling at lower Ca(2+) concentrations (1 x 10(-7) M). IPC preserved state 3 at high Ca(2+) concentrations. The cardioprotective effect of IPC results, in part, from

Cardiomyocyte specific deletion of Crif1 causes mitochondrial cardiomyopathy in mice.

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Juhee Shin

Full Text Available Mitochondria are key organelles dedicated to energy production. Crif1, which interacts with the large subunit of the mitochondrial ribosome, is indispensable for the mitochondrial translation and membrane insertion of respiratory subunits. To explore the physiological function of Crif1 in the heart, Crif1(f/f mice were crossed with Myh6-cre/Esr1 transgenic mice, which harbor cardiomyocyte-specific Cre activity in a tamoxifen-dependent manner. The tamoxifen injections were given at six weeks postnatal, and the mutant mice survived only five months due to hypertrophic heart failure. In the mutant cardiac muscles, mitochondrial mass dramatically increased, while the inner structure was altered with lack of cristae. Mutant cardiac muscles showed decreased rates of oxygen consumption and ATP production, suggesting that Crif1 plays a critical role in the maintenance of both mitochondrial structure and respiration in cardiac muscles.

Preventing phrenic nerve stimulation by a patch insulation in an intact swine heart model.

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Jin-Long Huang

Full Text Available Phrenic nerve stimulation (PNS could be prevented by a silastic patch over the epicardial lead. We studied the effects in preventing PNS by placing a silastic patch directly over an epicardial lead or placing a graft around the phrenic nerve (PN.Fourteen Lanyu swine were enrolled. A bipolar lead was placed epicardially on the left ventricle (LV inferior to the PN. An implantable cardioverter-defibrillator (ICD lead was placed into the right ventricle (RV. The maximal influential distance (MID was measured under 3 pacing configurations to express the influential electrical field on the PN. The threshold of the LV and PN were evaluated epicardially. Then, PTFE patches of different sizes (10×10 mm, 20×20 mm and 30×30 mm were placed between the LV lead and PN to study the rise in PN threshold in 7 swine. On the other hand, the PN were surrounded by a PTFE graft of different lengths (10 mm, 20 mm, and 30 mm in the remaining 7 swine. LV-bipolar pacing showed the shortest MID when compared to the other 2 unipolar pacing configurations at pacing voltage of 10 V. The patch was most effective in preventing PNS during LV-bipolar pacing. PNS was prevented under all circumstances with a larger PTFE patch (30×30 mm or long graft (30 mm.PNS was avoided by placing a PTFE patch over the LV lead or a graft around the PN despite pacing configurations. Hence if PNS persisted during CRT implantation, a PTFE patch on the LV lead or a graft around the PN could be considered.

Garlic activates SIRT-3 to prevent cardiac oxidative stress and mitochondrial dysfunction in diabetes.

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Sultana, Md Razia; Bagul, Pankaj K; Katare, Parameshwar B; Anwar Mohammed, Soheb; Padiya, Raju; Banerjee, Sanjay K

2016-11-01

Cardiac complications are major contributor in the mortality of diabetic people. Mitochondrial dysfunctioning is a crucial contributor for the cardiac complications in diabetes, and SIRT-3 remains the major mitochondrial deacetylase. We hypothesized whether garlic has any role on SIRT-3 to prevent mitochondrial dysfunction in diabetic heart. Rats with developed hyperglycemia after STZ injection were divided into two groups; diabetic (Dia) and diabetic+garlic (Dia+Garl). Garlic was administered at a dose of 250mg/kg/day, orally for four weeks. An additional group was maintained to evaluate the effect of raw garlic administration on control rat heart. We have observed altered functioning of cardiac mitochondrial enzymes involved in metabolic pathways, and increased levels of cardiac ROS with decreased activity of catalase and SOD in diabetic rats. Cardiac mRNA expression of TFAM, PGC-1α, and CO1 was also altered in diabetes. In addition, reduced levels of electron transport chain complexes that observed in Dia group were normalized with garlic administration. This indicates the presence of increased oxidative stress with mitochondrial dysfunctioning in diabetic heart. We have observed reduced activity of SIRT3 and increased acetylation of MnSOD. Silencing SIRT-3 in cells also revealed the same. However, administration of garlic improved the SIRT-3 and MnSOD activity, by deacetylating MnSOD. Increased SOD activity was correlated with reduced levels of ROS in garlic-administered rat hearts. Collectively, our results provide an insight into garlic's protection to T1DM heart through activation of SIRT3-MnSOD pathway. Copyright © 2016 Elsevier Inc. All rights reserved.

Inhibition of NAPDH Oxidase 2 (NOX2 Prevents Oxidative Stress and Mitochondrial Abnormalities Caused by Saturated Fat in Cardiomyocytes.

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Leroy C Joseph

Full Text Available Obesity and high saturated fat intake increase the risk of heart failure and arrhythmias. The molecular mechanisms are poorly understood. We hypothesized that physiologic levels of saturated fat could increase mitochondrial reactive oxygen species (ROS in cardiomyocytes, leading to abnormalities of calcium homeostasis and mitochondrial function. We investigated the effect of saturated fat on mitochondrial function and calcium homeostasis in isolated ventricular myocytes. The saturated fatty acid palmitate causes a decrease in mitochondrial respiration in cardiomyocytes. Palmitate, but not the monounsaturated fatty acid oleate, causes an increase in both total cellular ROS and mitochondrial ROS. Palmitate depolarizes the mitochondrial inner membrane and causes mitochondrial calcium overload by increasing sarcoplasmic reticulum calcium leak. Inhibitors of PKC or NOX2 prevent mitochondrial dysfunction and the increase in ROS, demonstrating that PKC-NOX2 activation is also required for amplification of palmitate induced-ROS. Cardiomyocytes from mice with genetic deletion of NOX2 do not have palmitate-induced ROS or mitochondrial dysfunction. We conclude that palmitate induces mitochondrial ROS that is amplified by NOX2, causing greater mitochondrial ROS generation and partial depolarization of the mitochondrial inner membrane. The abnormal sarcoplasmic reticulum calcium leak caused by palmitate could promote arrhythmia and heart failure. NOX2 inhibition is a potential therapy for heart disease caused by diabetes or obesity.

ROS-mediated PARP activity undermines mitochondrial function after permeability transition pore opening during myocardial ischemia-reperfusion.

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Schriewer, Jacqueline M; Peek, Clara Bien; Bass, Joseph; Schumacker, Paul T

2013-04-18

Ischemia-reperfusion (I/R) studies have implicated oxidant stress, the mitochondrial permeability transition pore (mPTP), and poly(ADP-ribose) polymerase (PARP) as contributing factors in myocardial cell death. However, the interdependence of these factors in the intact, blood-perfused heart is not known. We therefore wanted to determine whether oxidant stress, mPTP opening, and PARP activity contribute to the same death pathway after myocardial I/R. A murine left anterior descending coronary artery (LAD) occlusion (30 minutes) and release (1 to 4 hours) model was employed. Experimental groups included controls and antioxidant-treated, mPTP-inhibited, or PARP-inhibited hearts. Antioxidant treatment prevented oxidative damage, mPTP opening, ATP depletion, and PARP activity, placing oxidant stress as the proximal death trigger. Genetic deletion of cyclophilin D (CypD(-/-)) prevented loss of total NAD(+) and PARP activity, and mPTP-mediated loss of mitochondrial function. Control hearts showed progressive mitochondrial depolarization and loss of ATP from 1.5 to 4 hours of reperfusion, but not outer mitochondrial membrane rupture. Neither genetic deletion of PARP-1 nor its pharmacological inhibition prevented the initial mPTP-mediated depolarization or loss of ATP, but PARP ablation did allow mitochondrial recovery by 4 hours of reperfusion. These results indicate that oxidant stress, the mPTP, and PARP activity contribute to a single death pathway after I/R in the heart. PARP activation undermines cell survival by preventing mitochondrial recovery after mPTP opening early in reperfusion. This suggests that PARP-mediated prolongation of mitochondrial depolarization contributes significantly to cell death via an energetic crisis rather than by mitochondrial outer membrane rupture.

Antimicrobial use in swine production and its effect on the swine gut microbiota and antimicrobial resistance.

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Holman, Devin B; Chénier, Martin R

2015-11-01

Antimicrobials have been used in swine production at subtherapeutic levels since the early 1950s to increase feed efficiency and promote growth. In North America, a number of antimicrobials are available for use in swine. However, the continuous administration of subtherapeutic, low concentrations of antimicrobials to pigs also provides selective pressure for antimicrobial-resistant bacteria and resistance determinants. For this reason, subtherapeutic antimicrobial use in livestock remains a source of controversy and concern. The swine gut microbiota demonstrates a number of changes in response to antimicrobial administration depending on the dosage, duration of treatment, age of the pigs, and gut location that is sampled. Both culture-independent and -dependent studies have also shown that the swine gut microbiota contains a large number of antimicrobial resistance determinants even in the absence of antimicrobial exposure. Heavy metals, such as zinc and copper, which are often added at relatively high doses to swine feed, may also play a role in maintaining antimicrobial resistance and in the stability of the swine gut microbiota. This review focuses on the use of antimicrobials in swine production, with an emphasis on the North American regulatory context, and their effect on the swine gut microbiota and on antimicrobial resistance determinants in the gut microbiota.

Swine flu

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Manish Sinha

Full Text Available Summary: The recent outbreak of human infection with a novel Swine-Origin Influenza A (H1N1 virus is spreading rapidly through sustained human-to-human transmission in multiple countries. Human-to-human transmission occurs by inhalation of infectious droplets and droplet nuclei, and by direct contact, which is facilitated by air and land travel and social gatherings. The most frequently reported symptoms are fever, cough, myalgia, and sore throat. Detailed contact and travel histories and knowledge of viral activity in community are essential for prompt case detection by the health personnel. Real-time Reverse Transcriptase-Polymerase Chain Reaction analysis of throat swabs or lower respiratory samples is a sensitive means of diagnosis. Use of oral oseltamivir may be warranted for the treatment of severe illness. Keywords: Swine influenza, H1N1, Swine flu, Oseltamivir

Transgenic overexpression of adenine nucleotide translocase 1 protects ischemic hearts against oxidative stress.

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Klumpe, Inga; Savvatis, Konstantinos; Westermann, Dirk; Tschöpe, Carsten; Rauch, Ursula; Landmesser, Ulf; Schultheiss, Heinz-Peter; Dörner, Andrea

2016-06-01

Ischemia impairs the adenine nucleotide translocase (ANT), which transports ADP and ATP across the inner mitochondrial membrane. We investigated whether ANT1 overexpression has protective effects on ischemic hearts. Myocardial infarction was induced in wild-type (WT) and heart-specific ANT1-transgenic (ANT1-TG) rats, and hypoxia was set in isolated cardiomyocytes. ANT1 overexpression reduced the myocardial infarct area and increased the survival rate of infarcted rats. Reduced ANT1 expression and increased 4-hydroxynonenal modification of ANT paralleled to impaired ANT function in infarcted WT hearts. ANT1 overexpression improved ANT expression and function. This was accompanied by reduced mitochondrial cytochrome C release and caspase-3 activation. ANT1-TG hearts suffered less from oxidative stress, as shown by lower protein carbonylation and 4-hydroxynonenal modification of ANT. ANT1 overexpression also increased cell survival of hypoxic cardiomyocytes and attenuated reactive oxygen species (ROS) production. This was linked to higher stability of mitochondrial membrane potential and lower activity of ROS detoxifying catalase. ANT1-TG cardiomyocytes also showed higher resistance against H2O2 treatment, which was independent of catalase activity. In conclusion, ANT1 overexpression compensates impaired ANT activity under oxygen-restricted conditions. It reduces ROS production and oxidative stress, stabilizes mitochondrial integrity, and increases survival, making ANT1 a component in ROS management and heart protection during ischemia. ANT1 overexpression reduces infarct size and increases survival after infarction. ANT1 overexpression compensates restricted ANT expression and function in infarcted hearts. Increased ANT1 expression enhances mitochondrial integrity. ANT1-overexpressing hearts reduce oxidative stress by decreasing ROS generation. ANT1 is a component in ROS management and heart protection.

In vitro effects of toxaphene on mitochondrial calcium ATPase and calcium uptake in selected rat tissues

International Nuclear Information System (INIS)

Trottman, C.H.; Rao, K.S.P.; Morrow, W.; Uzodinma, J.E.; Desaiah, D.

1985-01-01

In vitro effects of toxaphene on Ca 2+ -ATPase activity and 45 Ca 2+ -uptake were studied in mitochondrial fractions of heart, kidney and liver tissues of rat. Mitochondrial fractions were prepared by the conventional centrifugation method. Ca 2+ -ATPase activity was determined by measuring the inorganic phosphate liberated during ATP hydrolysis. Toxaphene inhibited Ca 2+ -ATPase in a concentration dependent manner in all the three tissues. Substrate activation kinetics, with heart, kidney and liver tissue fractions, revealed that toxaphene inhibited Ca 2+ -ATPase activity non-competetively by decreasing the maximum velocity of the enzyme without affecting the enzyme-substrate affinity. Toxaphene also inhibited mitochondrial 45 Ca 2+ -uptake in the three selected tissues in a concentration dependent manner. These results indicate that toxaphene is an inhibitor of mitochondrial Ca 2+ -ATPase and calcium transport in heart, kidney and liver tissues of rat. 19 references, 5 figures

Swine brucellosis: current perspectives

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Olsen SC

2016-12-01

Full Text Available SC Olsen, FM Tatum Infectious Bacterial Diseases of Livestock Research Unit, National Animal Disease Center, Agricultural Research Service, United States Department of Agriculture, Ames, IA, USA Abstract: Brucella suis is a significant zoonotic species that is present in domestic livestock and wildlife in many countries worldwide. Transmission from animal reservoirs is the source of human infection as human-to-human transmission is very rare. Although swine brucellosis causes economic losses in domestic livestock, preventing human infection is the primary reason for its emphasis in disease control programs. Although disease prevalence varies worldwide, in areas outside of Europe, swine brucellosis is predominantly caused by B. suis biovars 1 and 3. In Europe, swine are predominantly infected with biovar 2 which is much less pathogenic in humans. In many areas worldwide, feral or wild populations of swine are important reservoir hosts. Like other Brucella spp. in their natural host, B. suis has developed mechanisms to survive in an intracellular environment and evade immune detection. Limitations in sensitivity and specificity of current diagnostics require use at a herd level, rather for individual animals. There is currently no commercial vaccine approved for preventing brucellosis in swine. Although not feasible in all situations, whole-herd depopulation is the most effective regulatory mechanism to control swine brucellosis. Keywords: livestock, transmission, pathogenicity, vaccine, host, infection

Possible X linked congenital mitochondrial cardiomyopathy in three families.

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Orstavik, K H; Skjörten, F; Hellebostad, M; Hågå, P; Langslet, A

1993-01-01

Familial cases of childhood congestive cardiomyopathy with X linked recessive inheritance and abnormalities of heart muscle mitochondria have been previously reported. We report here three families with possible X linked congestive cardiomyopathy and specific mitochondrial abnormalities. The heart disorder presented as endocardial fibroelastosis with neonatal death in two brothers in one family, and as heart failure and death in infancy in two brothers in the other two families. In one family...

Source tracking swine fecal waste in surface water proximal to swine concentrated animal feeding operations.

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Heaney, Christopher D; Myers, Kevin; Wing, Steve; Hall, Devon; Baron, Dothula; Stewart, Jill R

2015-04-01

Swine farming has gone through many changes in the last few decades, resulting in operations with a high animal density known as confined animal feeding operations (CAFOs). These operations produce a large quantity of fecal waste whose environmental impacts are not well understood. The purpose of this study was to investigate microbial water quality in surface waters proximal to swine CAFOs including microbial source tracking of fecal microbes specific to swine. For one year, surface water samples at up- and downstream sites proximal to swine CAFO lagoon waste land application sites were tested for fecal indicator bacteria (fecal coliforms, Escherichia coli and Enterococcus) and candidate swine-specific microbial source-tracking (MST) markers (Bacteroidales Pig-1-Bac, Pig-2-Bac, and Pig-Bac-2, and methanogen P23-2). Testing of 187 samples showed high fecal indicator bacteria concentrations at both up- and downstream sites. Overall, 40%, 23%, and 61% of samples exceeded state and federal recreational water quality guidelines for fecal coliforms, E. coli, and Enterococcus, respectively. Pig-1-Bac and Pig-2-Bac showed the highest specificity to swine fecal wastes and were 2.47 (95% confidence interval [CI]=1.03, 5.94) and 2.30 times (95% CI=0.90, 5.88) as prevalent proximal down- than proximal upstream of swine CAFOs, respectively. Pig-1-Bac and Pig-2-Bac were also 2.87 (95% CI=1.21, 6.80) and 3.36 (95% CI=1.34, 8.41) times as prevalent when 48 hour antecedent rainfall was greater than versus less than the mean, respectively. Results suggest diffuse and overall poor sanitary quality of surface waters where swine CAFO density is high. Pig-1-Bac and Pig-2-Bac are useful for tracking off-site conveyance of swine fecal wastes into surface waters proximal to and downstream of swine CAFOs and during rain events. Copyright © 2014 Elsevier B.V. All rights reserved.

Proteomic analysis of swine serum following highly virulent classical swine fever virus infection

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Guo Huan-cheng

2011-03-01

Full Text Available Abstract Background Classical swine fever virus (CSFV belongs to the genus Pestivirus within the family Flaviviridae. Virulent strains of classical swine fever virus (CSFV cause severe disease in pigs characterized by immunosuppression, thrombocytopenia and disseminated intravascular coagulation, which causes significant economic losses to the pig industry worldwide. Methods To reveal proteomic changes in swine serum during the acute stage of lethal CSFV infection, 5 of 10 pigs were inoculated with the virulent CSFV Shimen strain, the remainder serving as uninfected controls. A serum sample was taken at 3 days post-infection from each swine, at a stage when there were no clinical symptoms other than increased rectal temperatures (≥40°C. The samples were treated to remove serum albumin and immunoglobulin (IgG, and then subjected to two-dimension differential gel electrophoresis. Results Quantitative intensity analysis revealed 17 protein spots showing at least 1.5-fold quantitative alteration in expression. Ten spots were successfully identified by MALDI-TOF MS or LTQ MS. Expression of 4 proteins was increased and 6 decreased in CSFV-infected pigs. Functions of these proteins included blood coagulation, anti-inflammatory activity and angiogenesis. Conclusion These proteins with altered expression may have important implications in the pathogenesis of classical swine fever and provide a clue for identification of biomarkers for classical swine fever early diagnosis.

Abnormal mitochondrial respiration in failed human myocardium.

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Sharov, V G; Todor, A V; Silverman, N; Goldstein, S; Sabbah, H N

2000-12-01

Chronic heart failure (HF) is associated with morphologic abnormalities of cardiac mitochondria including hyperplasia, reduced organelle size and compromised structural integrity. In this study, we examined whether functional abnormalities of mitochondrial respiration are also present in myocardium of patients with advanced HF. Mitochondrial respiration was examined using a Clark electrode in an oxygraph cell containing saponin-skinned muscle bundles obtained from myocardium of failed explanted human hearts due to ischemic (ICM, n=9) or idiopathic dilated (IDC, n=9) cardiomyopathy. Myocardial specimens from five normal donor hearts served as controls (CON). Basal respiratory rate, respiratory rate after addition of the substrates glutamate and malate (V(SUB)), state 3 respiration (after addition of ADP, V(ADP)) and respiration after the addition of atractyloside (V(AT)) were measured in scar-free muscle bundles obtained from the subendocardial (ENDO) and subepicardial (EPI) thirds of the left ventricular (LV) free wall, interventricular septum and right ventricular (RV) free wall. There were no differences in basal and substrate-supported respiration between CON and HF regardless of etiology. V(ADP)was significantly depressed both in ICM and IDC compared to CON in all the regions studied. The respiratory control ratio, V(ADP)/V(AT), was also significantly decreased in HF compared to CON. In both ICM and IDC, V(ADP)was significantly lower in ENDO compared to EPI. The results indicate that mitochondrial respiration is abnormal in the failing human heart. The findings support the concept of low myocardial energy production in HF via oxidative phosphorylation, an abnormality with a potentially impact on global cardiac performance. Copyright 2000 Academic Press.

Mitochondrial oxidative stress and cardiac ageing.

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Martín-Fernández, Beatriz; Gredilla, Ricardo

According with different international organizations, cardiovascular diseases are becoming the first cause of death in western countries. Although exposure to different risk factors, particularly those related to lifestyle, contribute to the etiopathogenesis of cardiac disorders, the increase in average lifespan and aging are considered major determinants of cardiac diseases events. Mitochondria and oxidative stress have been pointed out as relevant factors both in heart aging and in the development of cardiac diseases such as heart failure, cardiac hypertrophy and diabetic cardiomyopathy. During aging, cellular processes related with mitochondrial function, such as bioenergetics, apoptosis and inflammation are altered leading to cardiac dysfunction. Increasing our knowledge about the mitochondrial mechanisms related with the aging process, will provide new strategies in order to improve this process, particularly the cardiovascular ones. Copyright © 2017 Sociedad Española de Arteriosclerosis. Publicado por Elsevier España, S.L.U. All rights reserved.

MANAGEMENT PATIENT OF SWINE INFLUENZA

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Endra Gunawan

2015-05-01

Full Text Available Influenza is an acute respiratory diseases caused by various influenza virus which infect the upper and lower respiratory tract and often accompanied by systemic symptoms such as fever, headache and muscle pain. Influenza spreads through the air. Swine influenza comes from swine and can cause an outbreaks in pig flocks. Even this is a kind of a rare case but the swine influenza could be transmitted to human by direct contact with infected swine or through environment that already being contaminated by swine influenza virus. There are 3 types of swine influenza virus namely H1N1, H3N2 and H1N2. Type H1N1 swine-virus had been known since 1918. Avian influenza virus infection is transmitted from one person to another through secret containing virus. Virus is binded into the mucous cells of respiratory tract before it is finally infecting the cells itself. Management patients with H1N1 influenza is based on the complications and the risk. Besides, it is also need to consider the clinical criteria of the patient. Therapy medicamentosa is applied to the patients by giving an antiviral, antibiotics and symptomatic therapy. Prevention can be done by avoid contact with infected animal or environment, having antiviral prophylaxis and vaccination.

Swine influenza virus: zoonotic potential and vaccination strategies for the control of avian and swine influenzas.

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Thacker, Eileen; Janke, Bruce

2008-02-15

Influenza viruses are able to infect humans, swine, and avian species, and swine have long been considered a potential source of new influenza viruses that can infect humans. Swine have receptors to which both avian and mammalian influenza viruses bind, which increases the potential for viruses to exchange genetic sequences and produce new reassortant viruses in swine. A number of genetically diverse viruses are circulating in swine herds throughout the world and are a major cause of concern to the swine industry. Control of swine influenza is primarily through the vaccination of sows, to protect young pigs through maternally derived antibodies. However, influenza viruses continue to circulate in pigs after the decay of maternal antibodies, providing a continuing source of virus on a herd basis. Measures to control avian influenza in commercial poultry operations are dictated by the virulence of the virus. Detection of a highly pathogenic avian influenza (HPAI) virus results in immediate elimination of the flock. Low-pathogenic avian influenza viruses are controlled through vaccination, which is done primarily in turkey flocks. Maintenance of the current HPAI virus-free status of poultry in the United States is through constant surveillance of poultry flocks. Although current influenza vaccines for poultry and swine are inactivated and adjuvanted, ongoing research into the development of newer vaccines, such as DNA, live-virus, or vectored vaccines, is being done. Control of influenza virus infection in poultry and swine is critical to the reduction of potential cross-species adaptation and spread of influenza viruses, which will minimize the risk of animals being the source of the next pandemic.

Roles of mitochondrial fragmentation and reactive oxygen species in mitochondrial dysfunction and myocardial insulin resistance

International Nuclear Information System (INIS)

Watanabe, Tomoyuki; Saotome, Masao; Nobuhara, Mamoru; Sakamoto, Atsushi; Urushida, Tsuyoshi; Katoh, Hideki; Satoh, Hiroshi; Funaki, Makoto; Hayashi, Hideharu

2014-01-01

Purpose: Evidence suggests an association between aberrant mitochondrial dynamics and cardiac diseases. Because myocardial metabolic deficiency caused by insulin resistance plays a crucial role in heart disease, we investigated the role of dynamin-related protein-1 (DRP1; a mitochondrial fission protein) in the pathogenesis of myocardial insulin resistance. Methods and Results: DRP1-expressing H9c2 myocytes, which had fragmented mitochondria with mitochondrial membrane potential (ΔΨ m ) depolarization, exhibited attenuated insulin signaling and 2-deoxy-D-glucose (2-DG) uptake, indicating insulin resistance. Treatment of the DRP1-expressing myocytes with Mn(III)tetrakis(1-methyl-4-pyridyl)porphyrin pentachloride (TMPyP) significantly improved insulin resistance and mitochondrial dysfunction. When myocytes were exposed to hydrogen peroxide (H 2 O 2 ), they increased DRP1 expression and mitochondrial fragmentation, resulting in ΔΨ m depolarization and insulin resistance. When DRP1 was suppressed by siRNA, H 2 O 2 -induced mitochondrial dysfunction and insulin resistance were restored. Our results suggest that a mutual enhancement between DRP1 and reactive oxygen species could induce mitochondrial dysfunction and myocardial insulin resistance. In palmitate-induced insulin-resistant myocytes, neither DRP1-suppression nor TMPyP restored the ΔΨ m depolarization and impaired 2-DG uptake, however they improved insulin signaling. Conclusions: A mutual enhancement between DRP1 and ROS could promote mitochondrial dysfunction and inhibition of insulin signal transduction. However, other mechanisms, including lipid metabolite-induced mitochondrial dysfunction, may be involved in palmitate-induced insulin resistance. - Highlights: • DRP1 promotes mitochondrial fragmentation and insulin-resistance. • A mutual enhancement between DRP1 and ROS ipromotes insulin-resistance. • Palmitate increases DRP1 expression and induces insulin-resistance. • Inhibition of DRP or ROS

Roles of mitochondrial fragmentation and reactive oxygen species in mitochondrial dysfunction and myocardial insulin resistance

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Watanabe, Tomoyuki [Internal Medicine III, Hamamatsu University School of Medicine, 1-20-1 Handayama, Higashi-ku, Hamamatsu 431-3192 (Japan); Saotome, Masao, E-mail: msaotome@hama-med.ac.jp [Internal Medicine III, Hamamatsu University School of Medicine, 1-20-1 Handayama, Higashi-ku, Hamamatsu 431-3192 (Japan); Nobuhara, Mamoru; Sakamoto, Atsushi; Urushida, Tsuyoshi; Katoh, Hideki; Satoh, Hiroshi [Internal Medicine III, Hamamatsu University School of Medicine, 1-20-1 Handayama, Higashi-ku, Hamamatsu 431-3192 (Japan); Funaki, Makoto [Clinical Research Center for Diabetes, Tokushima University Hospital, 2-50-1 Kuramoto-cho, Tokushima 770-8503 (Japan); Hayashi, Hideharu [Internal Medicine III, Hamamatsu University School of Medicine, 1-20-1 Handayama, Higashi-ku, Hamamatsu 431-3192 (Japan)

2014-05-01

Purpose: Evidence suggests an association between aberrant mitochondrial dynamics and cardiac diseases. Because myocardial metabolic deficiency caused by insulin resistance plays a crucial role in heart disease, we investigated the role of dynamin-related protein-1 (DRP1; a mitochondrial fission protein) in the pathogenesis of myocardial insulin resistance. Methods and Results: DRP1-expressing H9c2 myocytes, which had fragmented mitochondria with mitochondrial membrane potential (ΔΨ{sub m}) depolarization, exhibited attenuated insulin signaling and 2-deoxy-D-glucose (2-DG) uptake, indicating insulin resistance. Treatment of the DRP1-expressing myocytes with Mn(III)tetrakis(1-methyl-4-pyridyl)porphyrin pentachloride (TMPyP) significantly improved insulin resistance and mitochondrial dysfunction. When myocytes were exposed to hydrogen peroxide (H{sub 2}O{sub 2}), they increased DRP1 expression and mitochondrial fragmentation, resulting in ΔΨ{sub m} depolarization and insulin resistance. When DRP1 was suppressed by siRNA, H{sub 2}O{sub 2}-induced mitochondrial dysfunction and insulin resistance were restored. Our results suggest that a mutual enhancement between DRP1 and reactive oxygen species could induce mitochondrial dysfunction and myocardial insulin resistance. In palmitate-induced insulin-resistant myocytes, neither DRP1-suppression nor TMPyP restored the ΔΨ{sub m} depolarization and impaired 2-DG uptake, however they improved insulin signaling. Conclusions: A mutual enhancement between DRP1 and ROS could promote mitochondrial dysfunction and inhibition of insulin signal transduction. However, other mechanisms, including lipid metabolite-induced mitochondrial dysfunction, may be involved in palmitate-induced insulin resistance. - Highlights: • DRP1 promotes mitochondrial fragmentation and insulin-resistance. • A mutual enhancement between DRP1 and ROS ipromotes insulin-resistance. • Palmitate increases DRP1 expression and induces insulin

9 CFR 93.517 - Swine from Canada.

Science.gov (United States)

2010-01-01

... 9 Animals and Animal Products 1 2010-01-01 2010-01-01 false Swine from Canada. 93.517 Section 93... CONVEYANCE AND SHIPPING CONTAINERS Swine Canada 7 § 93.517 Swine from Canada. (a) For purposes other than immediate slaughter. Swine offered for importation from Canada for purposes other than immediate slaughter...

Mitochondrial Damage-Associated Molecular Patterns: From Inflammatory Signaling to Human Diseases

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Serge Grazioli

2018-05-01

Full Text Available Over the recent years, much has been unraveled about the pro-inflammatory properties of various mitochondrial molecules once they are leaving the mitochondrial compartment. On entering the cytoplasm or the extracellular space, mitochondrial DAMPs (also known as mitochondrial alarmins can become pro-inflammatory and initiate innate and adaptive immune responses by activating cell surface and intracellular receptors. Current evidence indicates that uncontrolled and excessive release of mitochondrial DAMPs is associated with severity, has prognosis value in human diseases, and contributes to the dysregulated process observed in numerous inflammatory and autoimmune conditions, as well as in ischemic heart disease and cancer. Herein, we review that the expanding research field of mitochondrial DAMPs in innate immune responses and the current knowledge on the association between mitochondrial DAMPs and human diseases.

Splenectomy Versus Sham Splenectomy in a Swine Model of Controlled Hemorrhagic Shock.

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Boysen, Søren R; Caulkett, Nigel A; Brookfield, Caroline E; Warren, Amy; Pang, Jessica M

2016-10-01

Splenectomy is controversial in acute hemorrhagic shock models. To compare splenectomized (SP) versus sham-splenectomized (SSP) swine during acute controlled hemorrhage. Twenty-six male Landrace White swine (mean body weight ± standard deviation, 33.8 ± 2.9 kg) were used. Ethics approval was obtained. Landrace swine underwent splenectomy (n = 13) or sham-splenectomy (n = 13), were bled to mean arterial blood pressure (MAP) of 40 mm Hg, which was held for 60 min, given 125 mL IV RescueFlow, held for a further 60 min, given whole blood, and held for a final 60 min. Tissue oxygen saturation, thromboelastography, oncotic pressure, urine volume and specific gravity, complete blood count, serum chemistry, body temperature, hematocrit, total solids, arterial and mixed venous blood gas, bispectral index, SAP, MAP, DAP, cardiac index, total blood volume (TBV) removed and returned, rate of hemorrhage and transfusion, spleen weight, heart rate (HR), arterial pH, lactate, PaO2, PaCO2, respiratory rate, cranial mesenteric and renal artery blood flow were recorded. Groups were compared using two-way ANOVA with post hoc Bonferroni (P splenectomy for the duration of the experiment (P splenectomy (P Splenectomy likely accounts for the transient increase in hematocrit and the higher HR in SP swine prior to hemorrhage, and the differences in TBV removed between the two groups during hemorrhage. With a fixed end point model using a moderate rate of acute hemorrhage and an MAP of 40 mm Hg, splenectomy is not necessary and may confound results.

Faster and stronger manifestation of mitochondrial diseases in skeletal muscle than in heart related to cytosolic inorganic phosphate (Pi) accumulation.

Science.gov (United States)

Korzeniewski, Bernard

2016-08-01

A model of the cell bioenergetic system was used to compare the effect of oxidative phosphorylation (OXPHOS) deficiencies in a broad range of moderate ATP demand in skeletal muscle and heart. Computer simulations revealed that kinetic properties of the system are similar in both cases despite the much higher mitochondria content and "basic" OXPHOS activity in heart than in skeletal muscle, because of a much higher each-step activation (ESA) of OXPHOS in skeletal muscle than in heart. Large OXPHOS deficiencies lead in both tissues to a significant decrease in oxygen consumption (V̇o2) and phosphocreatine (PCr) and increase in cytosolic ADP, Pi, and H(+) The main difference between skeletal muscle and heart is a much higher cytosolic Pi concentration in healthy tissue and much higher cytosolic Pi accumulation (level) at low OXPHOS activities in the former, caused by a higher PCr level in healthy tissue (and higher total phosphate pool) and smaller Pi redistribution between cytosol and mitochondria at OXPHOS deficiency. This difference does not depend on ATP demand in a broad range. A much greater Pi increase and PCr decrease during rest-to-moderate work transition in skeletal muscle at OXPHOS deficiencies than at normal OXPHOS activity significantly slows down the V̇o2 on-kinetics. Because high cytosolic Pi concentrations cause fatigue in skeletal muscle and can compromise force generation in skeletal muscle and heart, this system property can contribute to the faster and stronger manifestation of mitochondrial diseases in skeletal muscle than in heart. Shortly, skeletal muscle with large OXPHOS deficiencies becomes fatigued already during low/moderate exercise. Copyright © 2016 the American Physiological Society.

First description of a novel mitochondrial mutation in the MT-TI gene associated with multiple mitochondrial DNA deletion and depletion in family with severe dilated mitochondrial cardiomyopathy.

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Alila-Fersi, Olfa; Tabebi, Mouna; Maalej, Marwa; Belguith, Neila; Keskes, Leila; Mkaouar-Rebai, Emna; Fakhfakh, Faiza

2018-03-18

Mitochondria are essential for early cardiac development and impaired mitochondrial function was described associated with heart diseases such as hypertrophic or dilated mitochondrial cardiomyopathy. In this study, we report a family including two individuals with severe dilated mitochondrial cardiomyopathy. The whole mitochondrial genome screening showed the presence of several variations and a novel homoplasmic mutation m.4318-4322delC in the MT-TI gene shared by the two patients and their mother and leading to a disruption of the tRNA Ile secondary structure. In addition, a mitochondrial depletion was present in blood leucocyte of the two affected brother whereas a de novo heteroplasmic multiple deletion in the major arc of mtDNA was present in blood leucocyte and mucosa of only one of them. These deletions in the major arc of the mtDNA resulted to the loss of several protein-encoding genes and also some tRNA genes. The mtDNA deletion and depletion could result to an impairment of the oxidative phosphorylation and energy metabolism in the respiratory chain in the studied patients. Our report is the first description of a family with severe lethal dilated mitochondrial cardiomyopathy and presenting several mtDNA abnormalities including punctual mutation, deletion and depletion. Copyright © 2018 Elsevier Inc. All rights reserved.

Seroprevalence of hepatitis E in swine abattoir workers.

African Journals Online (AJOL)

The disease poses economic ... III and IV infect both swine and humans; and are re- ... associated with transmission in swine abattoir workers in ..... tal evidence for cross-species infection by swine hepatitis ... A novel virus in swine is closely.

Hippo pathway deficiency reverses systolic heart failure after infarction.

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Leach, John P; Heallen, Todd; Zhang, Min; Rahmani, Mahdis; Morikawa, Yuka; Hill, Matthew C; Segura, Ana; Willerson, James T; Martin, James F

2017-10-12

Mammalian organs vary widely in regenerative capacity. Poorly regenerative organs, such as the heart are particularly vulnerable to organ failure. Once established, heart failure commonly results in mortality. The Hippo pathway, a kinase cascade that prevents adult cardiomyocyte proliferation and regeneration, is upregulated in human heart failure. Here we show that deletion of the Hippo pathway component Salvador (Salv) in mouse hearts with established ischaemic heart failure after myocardial infarction induces a reparative genetic program with increased scar border vascularity, reduced fibrosis, and recovery of pumping function compared with controls. Using translating ribosomal affinity purification, we isolate cardiomyocyte-specific translating messenger RNA. Hippo-deficient cardiomyocytes have increased expression of proliferative genes and stress response genes, such as the mitochondrial quality control gene, Park2. Genetic studies indicate that Park2 is essential for heart repair, suggesting a requirement for mitochondrial quality control in regenerating myocardium. Gene therapy with a virus encoding Salv short hairpin RNA improves heart function when delivered at the time of infarct or after ischaemic heart failure following myocardial infarction was established. Our findings indicate that the failing heart has a previously unrecognized reparative capacity involving more than cardiomyocyte renewal.

Swine Influenza/Variant Influenza Viruses

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... Address What's this? Submit What's this? Submit Button Influenza Types Seasonal Avian Swine Variant Pandemic Other Information on Swine Influenza/Variant Influenza Virus Language: English (US) Español Recommend ...

Epidemiology of swine trichinellosis in China

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Wang Z.Q.

2001-06-01

Full Text Available Swine trichinellosis has been reported in 26 provinces, autonomous regions or municipalities (P/A/M of China. The prevalence rate in swine varied from 0.12 % to 34.2 % in five P/A/M, from 0.01 % to 0.0001 % in other P/A/M. The seroepidemiological survey of swine trichinellosis was carried out by ELISA in seven P/A/M, the seroprevalence varied from 0.09 % to 29.63 %. The prevalence of Thchinella infection in pork sold at the market was from 0.29 % to 5.6 % in four provinces. The transmission of trichinellosis by garbage is the main features of epidemiology of swine trichinellosis in China. Rat is an important reservoir in the domestic cycle of trichinellosis. The prevalence rates of T. spiralis infection in rats were from 1.98 % to 15.06 % in six provinces or autonomous regions. The treatment-prophylaxis with forage contained albendazole has been applied to the control of swine trichinellosis in Nanyang area of Henan province, the prevalence of swine trichinellosis had decreased from 32.2 % before prophylaxis to 0.12 % after prophylaxis.

eNOS se correlaciona com a biogênese mitocondrial em corações com cardiopatia congênita e cianose eNOS correlates with mitochondrial biogenesis in hearts of congenital heart disease with cyanosis

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Juan Xiao

2012-09-01

cardiopatia congênita com cianose, que poderia ser a resposta adaptativa à hipóxia crônica e possivelmente envolve suprarregulação da eNOS. (Arq Bras Cardiol. 2012; [online].ahead print, PP.0-0BACKGROUND: Mitochondrial biogenesis program in heart appears to exhibit adaptive remodeling following biomechanical and oxidative stress. The adaptive mechanisms that protect myocardium metabolism during hypoxia are coordinated in part by nitric oxide (NO. OBJECTIVE: To observe mitochondrial biogenesis and nitric oxide synthase (NOS expression in hearts of congenital heart disease with cyanosis, discuss mitochondrial response to chronic hypoxia in myocardium. METHODS: 20 patients with cyanotic (n=10 or acyanotic cardiac defects (n=10 were investigated. Samples from the right ventricular outflow tract myocardium taken during operation were studied. Morphometric analysis of mitochondria was performed with transmission electron microscope. Relative mtDNA/nDNA ratio was determined with real-time PCR. Cytochrome c oxidase subunit I (COXI, peroxisome-proliferator-activated receptor γ coactivator-1α (PGC-1α, nuclear respiratory factor 1 (NRF1, and mitochondrial transcription factor A (Tfam transcript levels were detected by real-time fluorescent RT-PCR. COXI and nNOS, iNOS and eNOS protein levels were measured with western blot. RESULTS: Mitochondrial volume density (Vv and numerical density (Nv were significantly elevated in patients with cyanotic compared to acyanotic congenital heart disease. Elevated mtDNA and up-regulated COXI, PGC-1α, NRF1 and Tfam mRNA levels were observed in cyanotic patients. Protein levels of COXI and eNOS were significantly higher in the myocardium of cyanotic than of acyanotic patients. PGC-1α transcript levels correlated with the levels of eNOS. Conclusion: Mitochondrial biogenesis is activated in right ventricular outflow tract myocardium in congenital heart disease with cyanosis, which could be the adaptive response to chronic hypoxia and possibly

Induction of anaesthesia with remifentanil after bolus midazolam administration in Landrace/Large White swine

DEFF Research Database (Denmark)

Zacharioudaki, Argyro; Lelovas, Pavlos; Sergentanis, Theodoros N.

2017-01-01

relaxation, resistance to the laryngoscope, vocal cord position, vocal cord movement and response to intubation. The time required to intubate and necessity for an additional midazolam dose were recorded. Baseline and post-intubation variables were compared with paired t tests, whereas for differences......Objective To investigate an alternative combination for anaesthesia induction in swine. Study design Randomized, ‘blinded’ experimental study. Animals Forty-five Landrace/Large White swine weighing 20.0 ± 1.5 kg. Methods Pulse oximetry, heart rate (HR) and blood pressure were measured after...... = 0.008 and p = 0.032, respectively) between baseline and post-intubation phase; in groups R3 and R4, there were decreases in systolic blood pressure (p = 0.040 and p = 0.019, respectively). In the multivariate analysis, remifentanil dose was not associated with the observed changes in haemodynamic...

Swine Flu -A Comprehensive View

Science.gov (United States)

Singh, Vandana; Sood, Meenakshi

2012-07-01

The present article is aimed on comprehensive view of Swine flu. It was first isolated from pigs in 1930 in USA. Pandemic caused by H1N1 in 2009 brought it in limelight. Itís a viral respiratory disease caused by viruses that infects pigs, resulting in nasal secretions, barking cough, decreased appetite, and listless behavior. Swine virus consist of eight RNA strands, one strand derived from human flu strains, two from avian (bird) strains, and five from swine strains. Swine flu spreads from infected person to healthy person by inhalation or ingestion of droplets contaminated with virus while sneezing or coughing. Two antiviral agents have been reported to help prevent or reduce the effects of swine flu, flu shot and nasal spray. WHO recommended for pandemic period to prevent its future outbreaks through vaccines or non-vaccines means. Antiviral drugs effective against this virus are Tamiflu and Relenza. Rapid antigen testing (RIDT), DFA testing, viral culture, and molecular testing (RT-PCR) are used for its diagnosis in laboratory

Feed quality in swine diet

Directory of Open Access Journals (Sweden)

Živković Branislav

2002-01-01

Full Text Available The paper will demonstrate the quality of some feed used in swine diet. The emphasis will be on feed whose incorporation into mixes could result in unfavorable effects on production, health and economic production of swine. Data will be presented on maize and its possible negative effects, having in mind toxins. Soybean meal, or genetically modified soybean meal, will also be observed. The next feed which will be discussed will be soybean whey obtained by different procedures and the potential dangers of its use in swine diet rations. Sunflower meal, feed of animal origin, with emphasis on fish flour and meat-bone flour will also be covered in the work. A feed which has been attracting particular attention lately is yeast imported from Italy. Its quality characteristics will be discussed, the so-called non-protein nitrogen. Analyses of mineral feed will include sources of phosphorus, phosphates (monocalciumphosphate, dicalcium phosphate phytases and resolving the problem of phosphorus in swine rations. Finally, an inevitable segment are synthetic amino acids, especially lysine and its role in swine diet.

Mitochondrial events responsible for morphine's cardioprotection against ischemia/reperfusion injury

Energy Technology Data Exchange (ETDEWEB)

He, Haiyan [Department of Physiology & Pathophysiology, Tianjin Medical University, Tianjin 300070 (China); Department of Pharmacology, Tianjin Medical University, Tianjin 300070 (China); Huh, Jin [Department of Anesthesia and Pain Medicine, Medical College, Kangwon National University, Chuncheon City (Korea, Republic of); Wang, Huihua [Department of Anesthesiology, The Second Affiliated Hospital of Zhejiang University, Hangzhou, Zhejiang Province (China); Kang, Yi; Lou, Jianshi [Department of Pharmacology, Tianjin Medical University, Tianjin 300070 (China); Xu, Zhelong, E-mail: zxu@tmu.edu.cn [Department of Physiology & Pathophysiology, Tianjin Medical University, Tianjin 300070 (China)

2016-01-01

Morphine may induce cardioprotection by targeting mitochondria, but little is known about the exact mitochondrial events that mediate morphine's protection. We aimed to address the role of the mitochondrial Src tyrosine kinase in morphine's protection. Isolated rat hearts were subjected to 30 min ischemia and 2 h of reperfusion. Morphine was given before the onset of ischemia. Infarct size and troponin I release were measured to evaluate cardiac injury. Oxidative stress was evaluated by measuring mitochondrial protein carbonylation and mitochondrial ROS generation. HL-1 cells were subjected to simulated ischemia/reperfusion and LDH release and mitochondrial membrane potential (ΔΨm) were measured. Morphine reduced infarct size as well as cardiac troponin I release which were aborted by the selective Src tyrosine kinase inhibitors PP2 and Src-I1. Morphine also attenuated LDH release and prevented a loss of ΔΨm at reperfusion in a Src tyrosine kinase dependent manner in HL-1 cells. However, morphine failed to reduce LDH release in HL-1 cells transfected with Src siRNA. Morphine increased mitochondrial Src phosphorylation at reperfusion and this was abrogated by PP2. Morphine attenuated mitochondrial protein carbonylation and mitochondrial superoxide generation at reperfusion through Src tyrosine kinase. The inhibitory effect of morphine on the mitochondrial complex I activity was reversed by PP2. These data suggest that morphine induces cardioprotection by preventing mitochondrial oxidative stress through mitochondrial Src tyrosine kinase. Inhibition of mitochondrial complex I at reperfusion by Src tyrosine kinase may account for the prevention of mitochondrial oxidative stress by morphine. - Highlights: • Morphine induced mito-Src phosphorylation and reduced infarct size in rat hearts. • Morphine failed to reduce I/R-induced LDH release in Src-silencing HL-1 cells. • Morphine prevented mitochondria damage caused by I/R through Src. • Morphine

Mitochondrial DNA as an inflammatory mediator in cardiovascular diseases.

Science.gov (United States)

Nakayama, Hiroyuki; Otsu, Kinya

2018-03-06

Mitochondria play a central role in multiple cellular functions, including energy production, calcium homeostasis, and cell death. Currently, growing evidence indicates the vital roles of mitochondria in triggering and maintaining inflammation. Chronic inflammation without microbial infection - termed sterile inflammation - is strongly involved in the development of heart failure. Sterile inflammation is triggered by the activation of pattern recognition receptors (PRRs) that sense endogenous ligands called damage-associated molecular patterns (DAMPs). Mitochondria release multiple DAMPs including mitochondrial DNA, peptides, and lipids, which induce inflammation via the stimulation of multiple PRRs. Among the mitochondrial DAMPs, mitochondrial DNA (mtDNA) is currently highlighted as the DAMP that mediates the activation of multiple PRRs, including Toll-like receptor 9, Nod-like receptors, and cyclic GMP-AMP synthetase/stimulator of interferon gene pathways. These PRR signalling pathways, in turn, lead to the activation of nuclear factor-κB and interferon regulatory factor, which enhances the transcriptional activity of inflammatory cytokines and interferons, and induces the recruitment of inflammatory cells. As the heart is an organ comprising abundant mitochondria for its ATP consumption (needed to maintain constant cyclic contraction and relaxation), the generation of massive amounts of mitochondrial radical oxygen species and mitochondrial DAMPs are predicted to occur and promote cardiac inflammation. Here, we will focus on the role of mtDNA in cardiac inflammation and review the mechanism and pathological significance of mtDNA-induced inflammatory responses in cardiac diseases. © 2018 The Author(s).

Mitochondrial respiration and ROS emission during β-oxidation in the heart: An experimental-computational study.

Science.gov (United States)

Cortassa, Sonia; Sollott, Steven J; Aon, Miguel A

2017-06-01

Lipids are main fuels for cellular energy and mitochondria their major oxidation site. Yet unknown is to what extent the fuel role of lipids is influenced by their uncoupling effects, and how this affects mitochondrial energetics, redox balance and the emission of reactive oxygen species (ROS). Employing a combined experimental-computational approach, we comparatively analyze β-oxidation of palmitoyl CoA (PCoA) in isolated heart mitochondria from Sham and streptozotocin (STZ)-induced type 1 diabetic (T1DM) guinea pigs (GPs). Parallel high throughput measurements of the rates of oxygen consumption (VO2) and hydrogen peroxide (H2O2) emission as a function of PCoA concentration, in the presence of L-carnitine and malate, were performed. We found that PCoA concentration PCoA > 600 nmol/mg mito prot, in both control and diabetic animals. Also, for the first time, we show that an integrated two compartment mitochondrial model of β-oxidation of long-chain fatty acids and main energy-redox processes is able to simulate the relationship between VO2 and H2O2 emission as a function of lipid concentration. Model and experimental results indicate that PCoA oxidation and its concentration-dependent uncoupling effect, together with a partial lipid-dependent decrease in the rate of superoxide generation, modulate H2O2 emission as a function of VO2. Results indicate that keeping low levels of intracellular lipid is crucial for mitochondria and cells to maintain ROS within physiological levels compatible with signaling and reliable energy supply.

Microbiota in fermented feed and swine gut.

Science.gov (United States)

Wang, Cheng; Shi, Changyou; Zhang, Yu; Song, Deguang; Lu, Zeqing; Wang, Yizhen

2018-04-01

Development of alternatives to antibiotic growth promoters (AGP) used in swine production requires a better understanding of their impacts on the gut microbiota. Supplementing fermented feed (FF) in swine diets as a novel nutritional strategy to reduce the use of AGP and feed price, can positively affect the porcine gut microbiota, thereby improving pig productivities. Previous studies have noted the potential effects of FF on the shift in benefit of the swine microbiota in different regions of the gastrointestinal tract (GIT). The positive influences of FF on swine gut microbiota may be due to the beneficial effects of both pre- and probiotics. Necessarily, some methods should be adopted to properly ferment and evaluate the feed and avoid undesired problems. In this mini-review, we mainly discuss the microbiota in both fermented feed and swine gut and how FF influences swine gut microbiota.

9 CFR 71.19 - Identification of swine in interstate commerce.

Science.gov (United States)

2010-01-01

... production system representative. In the event of oral notification, written confirmation shall be given as... within a swine production system. Swine moving within a swine production system to other than slaughter... identified in a valid swine production health plan for that swine production system. (2) The swine production...

Comparative Prevalence of Immune Evasion Complex Genes Associated with β-Hemolysin Converting Bacteriophages in MRSA ST5 Isolates from Swine, Swine Facilities, Humans with Swine Contact, and Humans with No Swine Contact.

Directory of Open Access Journals (Sweden)

Samantha J Hau

Full Text Available Livestock associated methicillin-resistant Staphylococcus aureus (LA-MRSA draws concern from the public health community because in some countries these organisms may represent the largest reservoir of MRSA outside hospital settings. Recent studies indicate LA-MRSA strains from swine are more genetically diverse than the first reported sequence type ST398. In the US, a diverse population of LA-MRSA is found including organisms of the ST398, ST9, and ST5 lineages. Occurrence of ST5 MRSA in swine is of particular concern since ST5 is among the most prevalent lineages causing clinical infections in humans. The prominence of ST5 in clinical disease is believed to result from acquisition of bacteriophages containing virulence or host-adapted genes including the immune-evasion cluster (IEC genes carried by β-hemolysin converting bacteriophages, whose absence in LA-MRSA ST398 is thought to contribute to reduced rates of human infection and transmission associated with this lineage. The goal of this study was to investigate the prevalence of IEC genes associated with β-hemolysin converting bacteriophages in MRSA ST5 isolates obtained from agricultural sources, including swine, swine facilities, and humans with short- or long-term swine exposure. To gain a broader perspective, the prevalence of these genes in LA-MRSA ST5 strains was compared to the prevalence in clinical MRSA ST5 strains from humans with no known exposure to swine. IEC genes were not present in any of the tested MRSA ST5 strains from agricultural sources and the β-hemolysin gene was intact in these strains, indicating the bacteriophage's absence. In contrast, the prevalence of the β-hemolysin converting bacteriophage in MRSA ST5 strains from humans with no exposure to swine was 90.4%. The absence of β-hemolysin converting bacteriophage in LA-MRSA ST5 isolates is consistent with previous reports evaluating ST398 strains and provides genetic evidence indicating LA-MRSA ST5 isolates

Comparative Prevalence of Immune Evasion Complex Genes Associated with β-Hemolysin Converting Bacteriophages in MRSA ST5 Isolates from Swine, Swine Facilities, Humans with Swine Contact, and Humans with No Swine Contact

Science.gov (United States)

Hau, Samantha J.; Sun, Jisun; Davies, Peter R.; Frana, Timothy S.; Nicholson, Tracy L.

2015-01-01

Livestock associated methicillin-resistant Staphylococcus aureus (LA-MRSA) draws concern from the public health community because in some countries these organisms may represent the largest reservoir of MRSA outside hospital settings. Recent studies indicate LA-MRSA strains from swine are more genetically diverse than the first reported sequence type ST398. In the US, a diverse population of LA-MRSA is found including organisms of the ST398, ST9, and ST5 lineages. Occurrence of ST5 MRSA in swine is of particular concern since ST5 is among the most prevalent lineages causing clinical infections in humans. The prominence of ST5 in clinical disease is believed to result from acquisition of bacteriophages containing virulence or host-adapted genes including the immune-evasion cluster (IEC) genes carried by β-hemolysin converting bacteriophages, whose absence in LA-MRSA ST398 is thought to contribute to reduced rates of human infection and transmission associated with this lineage. The goal of this study was to investigate the prevalence of IEC genes associated with β-hemolysin converting bacteriophages in MRSA ST5 isolates obtained from agricultural sources, including swine, swine facilities, and humans with short- or long-term swine exposure. To gain a broader perspective, the prevalence of these genes in LA-MRSA ST5 strains was compared to the prevalence in clinical MRSA ST5 strains from humans with no known exposure to swine. IEC genes were not present in any of the tested MRSA ST5 strains from agricultural sources and the β-hemolysin gene was intact in these strains, indicating the bacteriophage’s absence. In contrast, the prevalence of the β-hemolysin converting bacteriophage in MRSA ST5 strains from humans with no exposure to swine was 90.4%. The absence of β-hemolysin converting bacteriophage in LA-MRSA ST5 isolates is consistent with previous reports evaluating ST398 strains and provides genetic evidence indicating LA-MRSA ST5 isolates may harbor a

Glutaredoxin-2 controls cardiac mitochondrial dynamics and energetics in mice, and protects against human cardiac pathologies

Directory of Open Access Journals (Sweden)

Georges N. Kanaan

2018-04-01

Full Text Available Glutaredoxin 2 (GRX2, a mitochondrial glutathione-dependent oxidoreductase, is central to glutathione homeostasis and mitochondrial redox, which is crucial in highly metabolic tissues like the heart. Previous research showed that absence of Grx2, leads to impaired mitochondrial complex I function, hypertension and cardiac hypertrophy in mice but the impact on mitochondrial structure and function in intact cardiomyocytes and in humans has not been explored. We hypothesized that Grx2 controls cardiac mitochondrial dynamics and function in cellular and mouse models, and that low expression is associated with human cardiac dysfunction. Here we show that Grx2 absence impairs mitochondrial fusion, ultrastructure and energetics in primary cardiomyocytes and cardiac tissue. Moreover, provision of the glutathione precursor, N-acetylcysteine (NAC to Grx2-/- mice did not restore glutathione redox or prevent impairments. Using genetic and histopathological data from the human Genotype-Tissue Expression consortium we demonstrate that low GRX2 is associated with fibrosis, hypertrophy, and infarct in the left ventricle. Altogether, GRX2 is important in the control of cardiac mitochondrial structure and function, and protects against human cardiac pathologies. Keywords: Human heart, Mitochondria, Oxidative stress, Redox, Cardiac metabolism, Cardiac hypertrophy

African Swine Fever Virus, Siberia, Russia, 2017.

Science.gov (United States)

Kolbasov, Denis; Titov, Ilya; Tsybanov, Sodnom; Gogin, Andrey; Malogolovkin, Alexander

2018-04-01

African swine fever (ASF) is arguably the most dangerous and emerging swine disease worldwide. ASF is a serious problem for the swine industry. The first case of ASF in Russia was reported in 2007. We report an outbreak of ASF in Siberia, Russia, in 2017.

9 CFR 78.31 - Brucellosis reactor swine.

Science.gov (United States)

2010-01-01

... 9 Animals and Animal Products 1 2010-01-01 2010-01-01 false Brucellosis reactor swine. 78.31... AGRICULTURE INTERSTATE TRANSPORTATION OF ANIMALS (INCLUDING POULTRY) AND ANIMAL PRODUCTS BRUCELLOSIS Restrictions on Interstate Movement of Swine Because of Brucellosis § 78.31 Brucellosis reactor swine. (a...

9 CFR 78.32 - Brucellosis exposed swine.

Science.gov (United States)

2010-01-01

... 9 Animals and Animal Products 1 2010-01-01 2010-01-01 false Brucellosis exposed swine. 78.32... AGRICULTURE INTERSTATE TRANSPORTATION OF ANIMALS (INCLUDING POULTRY) AND ANIMAL PRODUCTS BRUCELLOSIS Restrictions on Interstate Movement of Swine Because of Brucellosis § 78.32 Brucellosis exposed swine. (a...

Antihypertrophic Effects of Small Molecules that Maintain Mitochondrial ATP Levels Under Hypoxia

Directory of Open Access Journals (Sweden)

Hiroaki Nagai

2017-10-01

Full Text Available Since impaired mitochondrial ATP production in cardiomyocytes is thought to lead to heart failure, a drug that protects mitochondria and improves ATP production under disease conditions would be an attractive treatment option. In this study, we identified small-molecule drugs, including the anti-parasitic agent, ivermectin, that maintain mitochondrial ATP levels under hypoxia in cardiomyocytes. Mechanistically, transcriptomic analysis and gene silencing experiments revealed that ivermectin increased mitochondrial ATP production by inducing Cox6a2, a subunit of the mitochondrial respiratory chain. Furthermore, ivermectin inhibited the hypertrophic response of human induced pluripotent stem cell-derived cardiomyocytes. Pharmacological inhibition of importin β, one of the targets of ivermectin, exhibited protection against mitochondrial ATP decline and cardiomyocyte hypertrophy. These findings indicate that maintaining mitochondrial ATP under hypoxia may prevent hypertrophy and improve cardiac function, providing therapeutic options for mitochondrial dysfunction.

Isolation and characterization of a Ca/sup 2 +/ carrier candidate from calf heart inner mitochondrial membrane

Energy Technology Data Exchange (ETDEWEB)

Jeng, A.Y.

1979-01-01

A protein was isolated from calf heart inner mitochondrial membrane with the aid of an electron paramagnetic resonance assay based on the relative binding properties of Ca/sup 2 +/, Mn/sup 2 +/, and Mg/sup 2 +/ to the protein. Partial delipidation of the protein was performed by using either the organic solvent extraction procedure or the silicic acid column chromatography. Control experiments indicated that the Ca/sup 2 +/ transport properties of the isolated protein were not due to the contaminating phospholipids. A complete delipidation procedure was developd by using Sephadex LH-20 column chromatography. Further characterization of the physical and chemical properties of the delipidated protein showed that delipidated protein becomes more hydrophobic in the presence of Ca/sup 2 +/ and alkaline pH in the organic solvent extraction experiments. Two possible models of calciphorin-mediated Ca/sup 2 +/ transport in mitochondria are proposed. (PCS)

9 CFR 93.508 - Articles accompanying swine.

Science.gov (United States)

2010-01-01

... 9 Animals and Animal Products 1 2010-01-01 2010-01-01 false Articles accompanying swine. 93.508 Section 93.508 Animals and Animal Products ANIMAL AND PLANT HEALTH INSPECTION SERVICE, DEPARTMENT OF... FOR MEANS OF CONVEYANCE AND SHIPPING CONTAINERS Swine § 93.508 Articles accompanying swine. No litter...

Radiation-induced damage of the Wistar Rat heart

International Nuclear Information System (INIS)

Cilliers, G.D.; Lochner, A.

1993-01-01

A time sequence study was performed on Wistar rats to investigate the early effects of radiation on the mechanical function and energy metabolism of the heart. Two series of rats were exposed to 20 Gy electron irradiation to a field including the heart and approximately a third of the lungs. The hearts were excised at varying time intervals (8-180 days) post irradiation. In one series of hearts the mechanical function was measured using the isolated perfused working rat heart model. At the end of the perfusion the hearts were freeze-clamped for analysis of the high energy phosphate contents (ATP, ADP, AMP and creatine phosphate). In the second series, mitochondria were isolated and the oxidative phosphorylation function measured polarographically (substrate: glutamate). Maximal depression of mechanical function was observed at 60 days post irradiation. Thereafter the work performance of these hearts improved significantly, almost reaching control levels after 180 days. The mitochondrial oxidative phosphorylation function (as measured on the total mitochondrial population) was significantly depressed 30-120 days post irradiation. As in the case of the mechanical changes, the depression was transient and after 180 days post irradiation, values similar to those of controls were obtained. Myocardial high energy phosphates remained unaltered throughout the experiment. (author)

9 CFR 93.521 - Declaration for swine.

Science.gov (United States)

2010-01-01

... CERTAIN ANIMALS, BIRDS, FISH, AND POULTRY, AND CERTAIN ANIMAL, BIRD, AND POULTRY PRODUCTS; REQUIREMENTS FOR MEANS OF CONVEYANCE AND SHIPPING CONTAINERS Swine Mexico 9 § 93.521 Declaration for swine. For all swine offered for importation from Mexico, the importer or his or her agent shall present two copies of...

Estimation of the transmission dynamics of African swine fever virus within a swine house

DEFF Research Database (Denmark)

Nielsen, J. P.; Larsen, T. S.; Hisham Beshara Halasa, Tariq

2017-01-01

The spread of African swine fever virus (ASFV) threatens to reach further parts of Europe. In countries with a large swine production, an outbreak of ASF may result in devastating economic consequences for the swine industry. Simulation models can assist decision makers setting up contingency plans......·00 (95% CI 0-1). Furthermore, we simulated the spread of ASFV within a pig house using a modified SEIR-model to establish the time from infection of one animal until ASFV is detected in the herd. Based on a chosen detection limit of 2·55% equivalent to 10 dead pigs out of 360, the disease would...

The Responses of Tissues from the Brain, Heart, Kidney, and Liver to Resuscitation following Prolonged Cardiac Arrest by Examining Mitochondrial Respiration in Rats.

Science.gov (United States)

Kim, Junhwan; Villarroel, José Paul Perales; Zhang, Wei; Yin, Tai; Shinozaki, Koichiro; Hong, Angela; Lampe, Joshua W; Becker, Lance B

2016-01-01

Cardiac arrest induces whole-body ischemia, which causes damage to multiple organs. Understanding how each organ responds to ischemia/reperfusion is important to develop better resuscitation strategies. Because direct measurement of organ function is not practicable in most animal models, we attempt to use mitochondrial respiration to test efficacy of resuscitation on the brain, heart, kidney, and liver following prolonged cardiac arrest. Male Sprague-Dawley rats are subjected to asphyxia-induced cardiac arrest for 30 min or 45 min, or 30 min cardiac arrest followed by 60 min cardiopulmonary bypass resuscitation. Mitochondria are isolated from brain, heart, kidney, and liver tissues and examined for respiration activity. Following cardiac arrest, a time-dependent decrease in state-3 respiration is observed in mitochondria from all four tissues. Following 60 min resuscitation, the respiration activity of brain mitochondria varies greatly in different animals. The activity after resuscitation remains the same in heart mitochondria and significantly increases in kidney and liver mitochondria. The result shows that inhibition of state-3 respiration is a good marker to evaluate the efficacy of resuscitation for each organ. The resulting state-3 respiration of brain and heart mitochondria following resuscitation reenforces the need for developing better strategies to resuscitate these critical organs following prolonged cardiac arrest.

Cadmium affects the mitochondrial viability and the acid soluble thiols concentration in liver, kidney, heart and gills of Ancistrus brevifilis (Eigenmann, 1920

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P. Velasquez-Vottelerd

2015-11-01

Full Text Available The freshwater fish Ancistrus brevifilis, which is found in Venezuelan rivers, is considered a potential sentinel fish in ecotoxicological studies. The cadmium (Cd effect on the mitochondrial viability (MV and acid soluble thiols levels (AST in A. brevifilis tissues (liver, kidney, heart, and gill was evaluated. Forty-two fish with similar sizes and weights were randomly selected, of which 7 fish (with their respective replicate were exposed for 7 and 30 days to a Cd sublethal concentration (0.1 mg.l-1. We determined the MV through a Janus Green B colorimetric assay and we obtained the concentration of AST by Ellman’s method. Mitochondrial viability decreased in fish exposed to Cd for 30 days with the liver being the most affected tissue. We also detected a significant decrease in AST levels was in fishes exposed to Cd for 7 days in liver and kidney tissues; these results suggests that AST levels are elevated in some tissues may act as cytoprotective and adaptive alternative mechanism related to the ROS detoxification, maintenance redox status and mitochondrial viability. Organ-specifics variations were observed in both assays. We conclude that the Cd exposure effect on AST levels and MV, vary across fish tissues and is related to the exposure duration, the molecule dynamics in different tissues, the organism and environmental conditions.

Mitochondrial DNA Unwinding Enzyme Required for Liver Regeneration | Center for Cancer Research

Science.gov (United States)

The liver has an exceptional capacity to proliferate. This ability allows the liver to regenerate its mass after partial surgical removal or injury and is the key to successful partial liver transplants. Liver cells, called hepatocytes, are packed with mitochondria, and regulating mitochondrial DNA (mtDNA) copy number is crucial to mitochondrial function, including energy production, during proliferation. Yves Pommier, M.D., Ph.D., of CCR’s Developmental Therapeutics Branch, and his colleagues recently showed that the vertebrate mitochondrial topoisomerase, Top1mt, was critical in maintaining mitochondrial function in the heart after doxorubicin-induced damage. The group wondered whether Top1mt might play a similar role in liver regeneration.

Quantitative approach for the risk assessment of African swine fever and Classical swine fever introduction into the United States through legal imports of pigs and swine products.

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Diana María Herrera-Ibatá

Full Text Available The US livestock safety strongly depends on its capacity to prevent the introduction of Transboundary Animal Diseases (TADs. Therefore, accurate and updated information on the location and origin of those potential TADs risks is essential, so preventive measures as market restrictions can be put on place. The objective of the present study was to evaluate the current risk of African swine fever (ASF and Classical swine fever (CSF introduction into the US through the legal importations of live pigs and swine products using a quantitative approach that could be later applied to other risks. Four quantitative stochastic risk assessment models were developed to estimate the monthly probabilities of ASF and CSF release into the US, and the exposure of susceptible populations (domestic and feral swine to these introductions at state level. The results suggest a low annual probability of either ASF or CSF introduction into the US, by any of the analyzed pathways (5.5*10-3. Being the probability of introduction through legal imports of live pigs (1.8*10-3 for ASF, and 2.5*10-3 for CSF higher than the risk of legally imported swine products (8.90*10-4 for ASF, and 1.56*10-3 for CSF. This could be caused due to the low probability of exposure associated with this type of commodity (products. The risk of feral pigs accessing to swine products discarded in landfills was slightly higher than the potential exposure of domestic pigs through swill feeding. The identification of the months at highest risk, the origin of the higher risk imports, and the location of the US states most vulnerable to those introductions (Iowa, Minnesota and Wisconsin for live swine and California, Florida and Texas for swine products, is valuable information that would help to design prevention, risk-mitigation and early-detection strategies that would help to minimize the catastrophic consequences of potential ASF/CSF introductions into the US.

Isolation of a Reassortant H1N2 Swine Flu Strain of Type “Swine-Human-Avian” and Its Genetic Variability Analysis

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Long-Bai Wang

2018-01-01

Full Text Available We isolated an influenza strain named A/Swine/Fujian/F1/2010 (H1N2 from a pig suspected to be infected with swine flu. The results of electron microscopy, hemagglutination (HA assay, hemagglutination inhibition (HI assay, and whole genome sequencing analysis suggest that it was a reassortant virus of swine (H1N1 subtype, human (H3N2 subtype, and avian influenza viruses. To further study the genetic evolution of A/Swine/Fujian/F1/2010 (H1N2, we cloned its whole genome fragments using RT-PCR and performed phylogenetic analysis on the eight genes. As a result, the nucleotide sequences of HA, NA, PB1, PA, PB2, NP, M, and NS gene are similar to those of A/Swine/Shanghai/1/2007(H1N2 with identity of 98.9%, 98.9%, 99.0%, 98.6%, 99.0%, 98.9%, 99.3%, and 99.3%, respectively. Similar to A/Swine/Shanghai/1/2007(H1N2, we inferred that the HA, NP, M, and NS gene fragments of A/Swine/Fujian/F1/2010 (H1N2 strain were derived from classical swine influenza H3N2 subtype, NA and PB1 were derived from human swine influenza H3N2 subtype, and PB2 and PA genes were derived from avian influenza virus. This further validates the role of swine as a “mixer” for influenza viruses.

The role of mitochondrial superoxide anion (O2-) on physiological aging in C57BL/6J mice

International Nuclear Information System (INIS)

Miyazawa, Masaki; Ishii, Takamasa; Yasuda, Kayo; Onouchi, Hiromi; Ishii, Naoaki; Noda, Setsuko; Hartman, Philip S.

2009-01-01

Much attention has been focused on the mitochondrial superoxide anion (O 2 - ), which is also a critical free radical produced by ionizing radiation. The specific role of the mitochondrial O 2 - on physiological aging in mammals is still nuclear despite wide-spread evidence that oxidative stress is involved in aging and age-related diseases. The major endogenous source of O 2 - is generated as a byproduct of energy metabolism from mitochondria. In order to better understand how O 2 - relates to metazoan aging, we have comprehensively examined age-related changes in the levels of oxidative damage, mitochondrial O 2 - production, mitochondrial antioxidant enzyme activity and apoptosis induction in key organs of an inbred mouse strain (C57BL/6J). Oxidative damage accumulated and excess apoptosis occurred in the brain, oculus and kidney with aging, but comparatively little occurred in the heart and muscle. These rates are correlated with O 2 - levels. Mitochondrial O 2 - production levels increased with aging in the brain, oculus and kidney, and did not significantly increased in the heart and muscle. In contrast to O 2 - production, mitochondrial SOD activities increased in heart and muscle, and remained unchanged in the brain, oculus and kidney with aging. These results suggest that O 2 - production has high organ specificity, and oxidative damage by O 2 - from mitochondria mediated apoptosis can lead to organ atrophy and physiological dysfunction. In addition, O 2 - from mitochondria plays a core role in physiological aging. (author)

The role of mitochondrial superoxide anion (O2(-)) on physiological aging in C57BL/6J mice.

Science.gov (United States)

Miyazawa, Masaki; Ishii, Takamasa; Yasuda, Kayo; Noda, Setsuko; Onouchi, Hiromi; Hartman, Philip S; Ishii, Naoaki

2009-01-01

Much attention has been focused on the mitochondrial superoxide anion (O2(-)), which is also a critical free radial produced by ionizing radiation. The specific role of the mitochondrial O2(-) on physiological aging in mammals is still unclear despite wide-spread evidence that oxidative stress is involved in aging and age-related diseases. The major endogenous source of O2(-) is generated as a byproduct of energy metabolism from mitochondria. In order to better understand how O2(-)relates to metazoan aging, we have comprehensively examined age-related changes in the levels of oxidative damage, mitochondrial O2(-) production, mitochondrial antioxidant enzyme activity and apoptosis induction in key organs of an inbred mouse strain (C57BL/6J). Oxidative damage accumulated and excess apoptosis occurred in the brain, oculus and kidney with aging, but comparatively little occurred in the heart and muscle. These rates are correlated with O2(-) levels. Mitochondrial O2(-) production levels increased with aging in the brain, oculus and kidney, and did not significantly increased in the heart and muscle. In contrast to O2(-) production, mitochondrial SOD activities increased in heart and muscle, and remained unchanged in the brain, oculus and kidney with aging. These results suggest that O2(-) production has high organ specificity, and oxidative damage by O2(-) from mitochondria mediated apoptosis can lead to organ atrophy and physiological dysfunction. In addition, O2(-) from mitochondria plays a core role in physiological aging.

Influenza D Virus Infection in Feral Swine Populations, United States.

Science.gov (United States)

Ferguson, Lucas; Luo, Kaijian; Olivier, Alicia K; Cunningham, Fred L; Blackmon, Sherry; Hanson-Dorr, Katie; Sun, Hailiang; Baroch, John; Lutman, Mark W; Quade, Bianca; Epperson, William; Webby, Richard; DeLiberto, Thomas J; Wan, Xiu-Feng

2018-06-01

Influenza D virus (IDV) has been identified in domestic cattle, swine, camelid, and small ruminant populations across North America, Europe, Asia, South America, and Africa. Our study investigated seroprevalence and transmissibility of IDV in feral swine. During 2012-2013, we evaluated feral swine populations in 4 US states; of 256 swine tested, 57 (19.1%) were IDV seropositive. Among 96 archived influenza A virus-seropositive feral swine samples collected from 16 US states during 2010-2013, 41 (42.7%) were IDV seropositive. Infection studies demonstrated that IDV-inoculated feral swine shed virus 3-5 days postinoculation and seroconverted at 21 days postinoculation; 50% of in-contact naive feral swine shed virus, seroconverted, or both. Immunohistochemical staining showed viral antigen within epithelial cells of the respiratory tract, including trachea, soft palate, and lungs. Our findings suggest that feral swine might serve an important role in the ecology of IDV.

Modification of the mitochondrial sulfonylurea receptor by thiol reagents.

Science.gov (United States)

Szewczyk, A; Wójcik, G; Lobanov, N A; Nalecz, M J

1999-08-19

The purpose of this study was to investigate the effects exerted by thiol-modifying reagents on themitochondrial sulfonylurea receptor. The thiol-oxidizing agents (timerosal and 5, 5'-dithio-bis(2-nitrobenzoic acid)) were found to produce a large inhibition (70% to 80%) of specific binding of [(3)H]glibenclamide to the beef heart mitochondrial membrane. Similar effects were observed with membrane permeable (N-ethylmaleimide) and non-permeable (mersalyl) thiol modifying agents. Glibenclamide binding was also decreased by oxidizing agents (hydrogen peroxide) but not by reducing agents (reduced gluthatione, dithiothreitol and the 2,3-dihydroxy-1,4-dithiolbutane). The results suggest that intact thiol groups, facing the mitochondrial matrix, are essential for glibenclamide binding to the mitochondrial sulfonylurea receptor. Copyright 1999 Academic Press.

The Responses of Tissues from the Brain, Heart, Kidney, and Liver to Resuscitation following Prolonged Cardiac Arrest by Examining Mitochondrial Respiration in Rats

Directory of Open Access Journals (Sweden)

Junhwan Kim

2016-01-01

Full Text Available Cardiac arrest induces whole-body ischemia, which causes damage to multiple organs. Understanding how each organ responds to ischemia/reperfusion is important to develop better resuscitation strategies. Because direct measurement of organ function is not practicable in most animal models, we attempt to use mitochondrial respiration to test efficacy of resuscitation on the brain, heart, kidney, and liver following prolonged cardiac arrest. Male Sprague-Dawley rats are subjected to asphyxia-induced cardiac arrest for 30 min or 45 min, or 30 min cardiac arrest followed by 60 min cardiopulmonary bypass resuscitation. Mitochondria are isolated from brain, heart, kidney, and liver tissues and examined for respiration activity. Following cardiac arrest, a time-dependent decrease in state-3 respiration is observed in mitochondria from all four tissues. Following 60 min resuscitation, the respiration activity of brain mitochondria varies greatly in different animals. The activity after resuscitation remains the same in heart mitochondria and significantly increases in kidney and liver mitochondria. The result shows that inhibition of state-3 respiration is a good marker to evaluate the efficacy of resuscitation for each organ. The resulting state-3 respiration of brain and heart mitochondria following resuscitation reenforces the need for developing better strategies to resuscitate these critical organs following prolonged cardiac arrest.

Relations of mitochondrial genetic variants to measures of vascular function.

Science.gov (United States)

Fetterman, Jessica L; Liu, Chunyu; Mitchell, Gary F; Vasan, Ramachandran S; Benjamin, Emelia J; Vita, Joseph A; Hamburg, Naomi M; Levy, Daniel

2018-05-01

Mitochondrial genetic variation with resultant alterations in oxidative phosphorylation may influence vascular function and contribute to cardiovascular disease susceptibility. We assessed relations of peptide-encoding variants in the mitochondrial genome with measures of vascular function in Framingham Heart Study participants. Of 258 variants assessed, 40 were predicted to have functional consequences by bioinformatics programs. A maternal pattern of heritability was estimated to contribute to the variability of aortic stiffness. A putative association with a microvascular function measure was identified that requires replication. The methods we have developed can be applied to assess the relations of mitochondrial genetic variation to other phenotypes. Copyright © 2017 Elsevier B.V. and Mitochondria Research Society. All rights reserved.

The cholesterol system of the swine

International Nuclear Information System (INIS)

Aigueperse, Jocelyne

1979-01-01

The purpose of this work was to characterize the dynamic system of adult female Large White swine. The content of this system and its relationships with both the external environment and between the different parts of the system were explained. The analysis of these results in terms of compared physiology showed that the structure of the cholesterol system was the same in man and in the swine. Consequently, the swine constitutes a good biological tool to study human cholesterol indirectly and to foresee the changes that might be induced in various physio-pathological cases. (author) [fr

Pre-ischemic mitochondrial substrate constraint by inhibition of malate-aspartate shuttle preserves mitochondrial function after ischemia-reperfusion

DEFF Research Database (Denmark)

Jespersen, Nichlas Riise; Yokota, Takashi; Støttrup, Nicolaj Brejnholt

2017-01-01

KEY POINTS: Pre-ischaemic administration of aminooxiacetate (AOA), an inhibitor of the malate-aspartate shuttle (MAS), provides cardioprotection against ischaemia-reperfusion injury. The underlying mechanism remains unknown. We examined whether transient inhibition of the MAS during ischaemia......, but not IPC, reduced the myocardial interstitial concentration of tricarboxylic acid cycle intermediates at the onset of reperfusion. The results obtained in the present study demonstrate that metabolic regulation by inhibition of the MAS at the onset of reperfusion may be beneficial for the preservation...... of mitochondrial function during late reperfusion in an IR-injured heart. ABSTRACT: Mitochondrial dysfunction plays a central role in ischaemia-reperfusion (IR) injury. Pre-ischaemic administration of aminooxyacetate (AOA), an inhibitor of the malate-aspartate shuttle (MAS), provides cardioprotection against IR...

Safety and Efficacy of an Absorbable Filter in the Inferior Vena Cava to Prevent Pulmonary Embolism in Swine.

Science.gov (United States)

Huang, Steven Y; Eggers, Mitchell; McArthur, Mark J; Dixon, Katherine A; McWatters, Amanda; Dria, Stephen; Hill, Lori R; Melancon, Marites P; Steele, Joseph R; Wallace, Michael J

2017-12-01

Purpose To evaluate the immediate and long-term safety as well as thrombus-capturing efficacy for 5 weeks after implantation of an absorbable inferior vena cava (IVC) filter in a swine model. Materials and Methods This study was approved by the institutional animal care and use committee. Eleven absorbable IVC filters made from polydioxanone suture were deployed via a catheter in the IVC of 11 swine. Filters remained in situ for 2 weeks (n = 2), 5 weeks (n = 2), 12 weeks (n = 2), 24 weeks (n = 2), and 32 weeks (n = 3). Autologous thrombus was administered from below the filter in seven swine from 0 to 35 days after filter placement. Fluoroscopy and computed tomography follow-up was performed after filter deployment from weeks 1-6 (weekly), weeks 7-20 (biweekly), and weeks 21-32 (monthly). The infrarenal IVC, lungs, heart, liver, kidneys, and spleen were harvested at necropsy. Continuous variables were evaluated with a Student t test. Results There was no evidence of IVC thrombosis, device migration, caval penetration, or pulmonary embolism. Gross pathologic analysis showed gradual device resorption until 32 weeks after deployment. Histologic assessment demonstrated neointimal hyperplasia around the IVC filter within 2 weeks after IVC filter deployment with residual microscopic fragments of polydioxanone suture within the caval wall at 32 weeks. Each iatrogenic-administered thrombus was successfully captured by the filter until resorbed (range, 1-4 weeks). Conclusion An absorbable IVC filter can be safely deployed in swine and resorbs gradually over the 32-week testing period. The device is effective for the prevention of pulmonary embolism for at least 5 weeks after placement in swine. © RSNA, 2017.

Fatty old hearts: role of cardiac lipotoxicity in age-related cardiomyopathy

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Konstantinos Drosatos

2016-08-01

Full Text Available Age-related cardiomyopathy accounts for a significant part of heart failure cases. Imbalance of the energetic equilibrium of the heart along with mitochondrial dysfunction and impaired β-adrenergic receptor signaling contributes in the aggravation of cardiac function in the elderly. In this review article, studies that correlate cardiac aging with lipotoxicity are summarized. The involvement of inhibition of peroxisome proliferator-activated receptor-α, β-adrenergic receptor desensitization, and mitochondrial dysfunction as underlying mechanisms for the lipid-driven age-related cardiomyopathy are presented with the aim to indicate potential therapeutic targets for cardiac aging.

9 CFR 93.505 - Certificate for swine.

Science.gov (United States)

2010-01-01

... certificate shall show that the entire region of origin is free of classical swine fever. (b) Swine from..., Equatorial Guinea, French Guiana, Gabon, Gambia, Ghana, Guinea, Guinea-Bissau, Guyana, Haiti, India...

Dioxin-induced acute cardiac mitochondrial oxidative damage and increased activity of ATP-sensitive potassium channels in Wistar rats

International Nuclear Information System (INIS)

Pereira, Susana P.; Pereira, Gonçalo C.; Pereira, Cláudia V.; Carvalho, Filipa S.; Cordeiro, Marília H.; Mota, Paula C.; Ramalho-Santos, João; Moreno, António J.; Oliveira, Paulo J.

2013-01-01

The environmental dioxin 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is classified as a Group 1 human carcinogen and teratogenic agent. We hypothesize that TCDD-induced oxidative stress may also interfere with mitochondrial ATP-sensitive potassium channels (mitoKATP), which are known to regulate and to be regulated by mitochondrial redox state. We investigated the effects of an acute treatment of male Wistar rats with TCDD (50 μg/kg i.p.) and measured the regulation of cardiac mitoKATP. While the function of cardiac mitochondria was slightly depressed, mitoKATP activity was 52% higher in animals treated with TCDD. The same effects were not observed in liver mitochondria isolated from the same animals. Our data also shows that regulation of mitochondrial ROS production by mitoKATP activity is different in both groups. To our knowledge, this is the first report to show that TCDD increases mitoKATP activity in the heart, which may counteract the increased oxidative stress caused by the dioxin during acute exposure. -- Highlights: •Acute TCDD treatment of Wistar rats causes cardiac oxidative stress. •Acute TCDD treatment causes cardiac mitochondrial alterations. •Mitochondrial liver vs. heart alterations are distinct. •TCDD treatment resulted in altered activity of cardiac mitochondrial K-ATP channels. -- Dioxin alters the regulation of cardiac mitochondrial ATP-sensitive potassium channels and disturbs mitochondrial physiology

Mitochondrial and cellular mechanisms for managing lipid excess

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Miguel A Aon

2014-07-01

Full Text Available Current scientific debates center on the impact of lipids and mitochondrial function on diverse aspects of human health, nutrition and disease, among them the association of lipotoxicity with the onset of insulin resistance in skeletal muscle, and with heart dysfunction in obesity and diabetes. Mitochondria play a fundamental role in aging and in prevalent acute or chronic diseases. Lipids are main mitochondrial fuels however these molecules can also behave as uncouplers and inhibitors of oxidative phosphorylation. Knowledge about the functional composition of these contradictory effects and their impact on mitochondrial-cellular energetics/redox status is incomplete.Cells store fatty acids (FAs as triacylglycerol and package them into cytoplasmic lipid droplets (LDs. New emerging data shows the LD as a highly dynamic storage pool of FAs that can be used for energy reserve. Lipid excess packaging into LDs can be seen as an adaptive response to fulfilling energy supply without hindering mitochondrial or cellular redox status and keeping low concentration of lipotoxic intermediates.Herein we review the mechanisms of action and utilization of lipids by mitochondria reported in liver, heart and skeletal muscle under relevant physiological situations, e.g. exercise. We report on perilipins, a family of proteins that associate with LDs in response to loading of cells with lipids. Evidence showing that in addition to physical contact, mitochondria and LDs exhibit metabolic interactions is presented and discussed. A hypothetical model of channeled lipid utilization by mitochondria is proposed. Direct delivery and channeled processing of lipids in mitochondria could represent a reliable and efficient way to maintain ROS within levels compatible with signaling while ensuring robust and reliable energy supply.

Effects of heme oxygenase-1 gene modulated mesenchymal stem cells on vasculogenesis in ischemic swine hearts.

Science.gov (United States)

Jiang, Yi-Bo; Zhang, Xiao-Li; Tang, Yao-Liang; Ma, Gen-Shan; Shen, Cheng-Xing; Wei, Qin; Zhu, Qi; Yao, Yu-Yu; Liu, Nai-Feng

2011-02-01

Mesenchymal stem cells (MSCs) transplantation may partially restore heart function in the treatment of acute myocardial infarction (AMI). The aim of this study was to explore the beneficial effects of MSCs modified with heme xygenase-1 (HO-1) on post-infarct swine hearts to determine whether the induction of therapeutic angiogenesis is modified by the angiogenic cytokines released from the implanted cells. In vitro, MSCs were divided into four groups: (1) non-transfected MSCs (MSCs group), (2) MSCs transfected with the pcDNA3.1-Lacz plasmid (Lacz-MSCs group), (3) MSCs transfected with pcDNA3.1-hHO-1 (HO-1-MSCs group), and (4) MSCs transfected with pcDNA3.1-hHO-1 and pretreatment with an HO inhibitor, tin protoporphyrin (SnPP) (HO-1-MSCs + SnPP group). Cells were cultured in an airtight incubation bottle for 24 hours, in which the oxygen concentration was maintained at < 1%, followed by 12 hours of reoxygenation. After hypoxia/reoxygen treatment, ELISA was used to measure transforming growth factor (TGF-β) and fibroblast growth factor (FGF-2) in the supernatant. In vivo, 28 Chinese mini-pigs were randomly allocated to the following treatment groups: (1) control group (saline), (2) Lacz-MSCs group, (3) HO-1-MSCs group, and (4) HO-1-MSCs + SnPP group. About 1 × 10(7) of autologous stem cells or an identical volume of saline was injected intracoronary into porcine hearts 1 hour after MI. Magnetic resonance imaging (MRI) assay and postmortem analysis were assessed four weeks after stem cell transplantation. Post hypoxia/reoxygenation in vitro, TGF-β in the supernatant was significantly increased in the HO-1-MSCs ((874.88 ± 68.23) pg/ml) compared with Lacz-MSCs ((687.81 ± 57.64) pg/ml, P < 0.001). FGF-2 was also significantly increased in the HO-1-MSCs ((1106.48 ± 107.06) pg/ml) compared with the Lacz-MSCs ((853.85 ± 74.44) pg/ml, P < 0.001). In vivo, at four weeks after transplantation, HO-1 gene transfer increased the capillary density in the peri-infarct area

MitoMiner: a data warehouse for mitochondrial proteomics data.

Science.gov (United States)

Smith, Anthony C; Blackshaw, James A; Robinson, Alan J

2012-01-01

MitoMiner (http://mitominer.mrc-mbu.cam.ac.uk/) is a data warehouse for the storage and analysis of mitochondrial proteomics data gathered from publications of mass spectrometry and green fluorescent protein tagging studies. In MitoMiner, these data are integrated with data from UniProt, Gene Ontology, Online Mendelian Inheritance in Man, HomoloGene, Kyoto Encyclopaedia of Genes and Genomes and PubMed. The latest release of MitoMiner stores proteomics data sets from 46 studies covering 11 different species from eumetazoa, viridiplantae, fungi and protista. MitoMiner is implemented by using the open source InterMine data warehouse system, which provides a user interface allowing users to upload data for analysis, personal accounts to store queries and results and enables queries of any data in the data model. MitoMiner also provides lists of proteins for use in analyses, including the new MitoMiner mitochondrial proteome reference sets that specify proteins with substantial experimental evidence for mitochondrial localization. As further mitochondrial proteomics data sets from normal and diseased tissue are published, MitoMiner can be used to characterize the variability of the mitochondrial proteome between tissues and investigate how changes in the proteome may contribute to mitochondrial dysfunction and mitochondrial-associated diseases such as cancer, neurodegenerative diseases, obesity, diabetes, heart failure and the ageing process.

Regenerative abilities of mesenchymal stem cells through mitochondrial transfer.

Science.gov (United States)

Paliwal, Swati; Chaudhuri, Rituparna; Agrawal, Anurag; Mohanty, Sujata

2018-03-30

The past decade has witnessed an upsurge in studies demonstrating mitochondrial transfer as one of the emerging mechanisms through which mesenchymal stem cells (MSCs) can regenerate and repair damaged cells or tissues. It has been found to play a critical role in healing several diseases related to brain injury, cardiac myopathies, muscle sepsis, lung disorders and acute respiratory disorders. Several studies have shown that various mechanisms are involved in mitochondrial transfer that includes tunnel tube formation, micro vesicle formation, gap junctions, cell fusion and others modes of transfer. Few studies have investigated the mechanisms that contribute to mitochondrial transfer, primarily comprising of signaling pathways involved in tunnel tube formation that facilitates tunnel tube formation for movement of mitochondria from one cell to another. Various stress signals such as release of damaged mitochondria, mtDNA and mitochondrial products along with elevated reactive oxygen species levels trigger the transfer of mitochondria from MSCs to recipient cells. However, extensive cell signaling pathways that lead to mitochondrial transfer from healthy cells are still under investigation and the changes that contribute to restoration of mitochondrial bioenergetics in recipient cells remain largely elusive. In this review, we have discussed the phenomenon of mitochondrial transfer from MSCs to neighboring stressed cells, and how this aids in cellular repair and regeneration of different organs such as lung, heart, eye, brain and kidney. The potential scope of mitochondrial transfer in providing novel therapeutic strategies for treatment of various pathophysiological conditions has also been discussed.

Cardioprotective properties of citicoline against hyperthyroidism-induced reperfusion damage in rat hearts.

Science.gov (United States)

Hernández-Esquivel, Luz; Pavón, Natalia; Buelna-Chontal, Mabel; González-Pacheco, Héctor; Belmont, Javier; Chávez, Edmundo

2015-06-01

Hyperthyroidism represents an increased risk factor for cardiovascular morbidity, especially when the heart is subjected to an ischemia/reperfusion process. The aim of this study was to explore the possible protective effect of the nucleotide citicoline on the susceptibility of hyperthyroid rat hearts to undergo reperfusion-induced damage, which is associated with mitochondrial dysfunction. Hence, we analyzed the protective effect of citicoline on the electrical behavior and on the mitochondrial function in rat hearts. Hyperthyroidism was established after a daily i.p. injection of triiodothyronine (at 2 mg/kg of body weight) during 5 days. Thereafter, citicoline was administered i.p. (at 125 mg/kg of body weight) for 5 days. In hyperthyroid rat hearts, citicoline protected against reperfusion-induced ventricular arrhythmias. Moreover, citicoline maintained the accumulation of mitochondrial Ca(2+), allowing mitochondria to reach a high transmembrane electric gradient that protected against the release of cytochrome c. It also preserved the activity of the enzyme aconitase that inhibited the release of cytokines. The protection also included the inhibition of oxidative stress-induced mDNA disruption. We conclude that citicoline protects against the reperfusion damage that is found in the hyperthyroid myocardium. This effect might be due to its inhibitory action on the permeability transition in mitochondria.

Remodeling pathway control of mitochondrial respiratory capacity by temperature in mouse heart: electron flow through the Q-junction in permeabilized fibers.

Science.gov (United States)

Lemieux, Hélène; Blier, Pierre U; Gnaiger, Erich

2017-06-06

Fuel substrate supply and oxidative phosphorylation are key determinants of muscle performance. Numerous studies of mammalian mitochondria are carried out (i) with substrate supply that limits electron flow, and (ii) far below physiological temperature. To analyze potentially implicated biases, we studied mitochondrial respiratory control in permeabilized mouse myocardial fibers using high-resolution respirometry. The capacity of oxidative phosphorylation at 37 °C was nearly two-fold higher when fueled by physiological substrate combinations reconstituting tricarboxylic acid cycle function, compared with electron flow measured separately through NADH to Complex I or succinate to Complex II. The relative contribution of the NADH pathway to physiological respiratory capacity increased with a decrease in temperature from 37 to 25 °C. The apparent excess capacity of cytochrome c oxidase above physiological pathway capacity increased sharply under hypothermia due to limitation by NADH-linked dehydrogenases. This mechanism of mitochondrial respiratory control in the hypothermic mammalian heart is comparable to the pattern in ectotherm species, pointing towards NADH-linked mt-matrix dehydrogenases and the phosphorylation system rather than electron transfer complexes as the primary drivers of thermal sensitivity at low temperature. Delineating the link between stress and remodeling of oxidative phosphorylation is important for understanding metabolic perturbations in disease evolution and cardiac protection.

Physical examination of swine.

Science.gov (United States)

Masters, B J; Hamilton, M; Masters, P G

1992-07-01

Swine may be examined to evaluate a disease state or a lowered economic performance or as a herd health consultation. As much of the examination as possible should be performed without handling the animal. A thorough history, evaluation of herd records, environmental examination, and herd examination should be performed prior to the evaluation of an individual animal. All necessary equipment should be available when starting the individual examination. The animals is then restrained and examined, and necessary samples are taken. Post-mortem examinations or slaughter house evaluations are a very frequent part of a health examination on swine. All samples taken should be in accordance with the standards of the laboratory that you use. You should work closely with the laboratory to obtain the best results. Physical examination of swine can be rewarding for the veterinarian as well as the producer. The most important aspect to remember is to have enough information and the proper equipment available to handle the animals for the minimal amount of time to gain the maximum benefits. Vietnamese pot-bellied pigs are similar to domestic swine in terms of their diseases and health but are dissimilar in management; pot-bellied pigs are frequently brought to the veterinarian for individual examinations. History is the most valuable part of the examination, followed by observation. Pot-bellied pigs prefer to be held securely with a hand under the chin and rump. The examination is conducted similarly to the examination of any companion animal. Chemical restraint often is necessary for sampling or minor surgical procedures. Owners should be consulted prior to the use of any restraint. This will help win their approval and confidence when working on their pets. While performing the physical examination, look at the pig's overall health as well as specific breed characteristics. Try to stay abreast of swine vaccination recommendations; you may be consulted in this regard. Most

Microbiome overview in swine lungs.

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Franciele Maboni Siqueira

Full Text Available Mycoplasma hyopneumoniae is the etiologic agent of swine enzootic pneumonia. However other mycoplasma species and secondary bacteria are found as inhabitants of the swine respiratory tract, which can be also related to disease. In the present study we have performed a total DNA metagenomic analysis from the lungs of pigs kept in a field condition, with suggestive signals of enzootic pneumonia and without any infection signals to evaluate the bacteria variability of the lungs microbiota. Libraries from metagenomic DNA were prepared and sequenced using total DNA shotgun metagenomic pyrosequencing. The metagenomic distribution showed a great abundance of bacteria. The most common microbial families identified from pneumonic swine's lungs were Mycoplasmataceae, Flavobacteriaceae and Pasteurellaceae, whereas in the carrier swine's lungs the most common families were Mycoplasmataceae, Bradyrhizobiaceae and Flavobacteriaceae. Analysis of community composition in both samples confirmed the high prevalence of M. hyopneumoniae. Moreover, the carrier lungs had more diverse family population, which should be related to the lungs normal flora. In summary, we provide a wide view of the bacterial population from lungs with signals of enzootic pneumonia and lungs without signals of enzootic pneumonia in a field situation. These bacteria patterns provide information that may be important for the establishment of disease control measures and to give insights for further studies.

MITOCHONDRIAL BKCa CHANNEL

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Enrique eBalderas

2015-03-01

Full Text Available Since its discovery in a glioma cell line 15 years ago, mitochondrial BKCa channel (mitoBKCa has been studied in brain cells and cardiomyocytes sharing general biophysical properties such as high K+ conductance (~300 pS, voltage-dependency and Ca2+-sensitivity. Main advances in deciphering the molecular composition of mitoBKCa have included establishing that it is encoded by the Kcnma1 gene, that a C-terminal splice insert confers mitoBKCa ability to be targeted to cardiac mitochondria, and evidence for its potential coassembly with β subunits. Notoriously, β1 subunit directly interacts with cytochrome c oxidase and mitoBKCa can be modulated by substrates of the respiratory chain. mitoBKCa channel has a central role in protecting the heart from ischemia, where pharmacological activation of the channel impacts the generation of reactive oxygen species and mitochondrial Ca2+ preventing cell death likely by impeding uncontrolled opening of the mitochondrial transition pore. Supporting this view, inhibition of mitoBKCa with Iberiotoxin, enhances cytochrome c release from glioma mitochondria. Many tantalizing questions remain. Some of them are: how is mitoBKCa coupled to the respiratory chain? Does mitoBKCa play non-conduction roles in mitochondria physiology? Which are the functional partners of mitoBKCa? What are the roles of mitoBKCa in other cell types? Answers to these questions are essential to define the impact of mitoBKCa channel in mitochondria biology and disease.

The global antigenic diversity of swine influenza A viruses

DEFF Research Database (Denmark)

Lewis, Nicola S; Russell, Colin A; Langat, Pinky

2016-01-01

Swine influenza presents a substantial disease burden for pig populations worldwide and poses a potential pandemic threat to humans. There is considerable diversity in both H1 and H3 influenza viruses circulating in swine due to the frequent introductions of viruses from humans and birds coupled...... with geographic segregation of global swine populations. Much of this diversity is characterized genetically but the antigenic diversity of these viruses is poorly understood. Critically, the antigenic diversity shapes the risk profile of swine influenza viruses in terms of their epizootic and pandemic potential...

Evaluation of swine fertilisation medium (SFM) efficiency in preserving spermatozoa quality during long-term storage in comparison to four commercial swine extenders.

Science.gov (United States)

Fantinati, P; Zannoni, A; Bernardini, C; Forni, M; Tattini, A; Seren, E; Bacci, M L

2009-02-01

In pig production, artificial insemination is widely carried out and the use of fresh diluted semen is predominant. For this reason, there are increasing interests in developing new extenders and in establishing the optimal storage conditions for diluted spermatozoa. In the last few decades, we utilised a homemade diluent (swine fertilisation medium (SFM)) for spermatozoa manipulation and biotechnological application as the production of transgenic pigs utilising the sperm-mediated gene transfer technique. The purpose of the present study is therefore to analyse the ability of SFM, in comparison to four commercial extenders, in preserving the quality of diluted boar semen stored at 16.5°C till 15 days. We utilised some of the main predictive tests as objectively measured motility, acrosome and sperm membrane integrity, high mitochondrial membrane potential and pH. Based on our in vitro study, SFM could be declared as a good long-term extender, able to preserve spermatozoa quality as well as Androhep Enduraguard for up to 6 to 9 days and more.

Production system dynamism and parasitic interac- tion of swine in ...

African Journals Online (AJOL)

pasture and on swine with poor body condition compared to zero grazing, and on swine with ... Many countries practice different kinds of production approaches. ... farms with an average herd size of 29 swine were sampled by random sam-.

MELAS syndrome associated with a new mitochondrial tRNA-Val gene mutation (m.1616A>G).

Science.gov (United States)

Toyoshima, Yuka; Tanaka, Yuji; Satomi, Kazuo

2017-09-11

We describe the case of a 40-year-old-man with mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS) syndrome, with cardiomyopathy and severe heart failure. He had a mitochondrial transfer RNA (tRNA) mutation (m.1616A>G) of the (tRNA-Val) gene, and it was not found in MELAS syndrome ever before. The presence of this newly observed tRNA-Val mutation (m.1616A>G) may induce multiple respiratory chain enzyme deficiencies and contribute to MELAS syndrome symptoms that are associated with mitochondrial DNA (mtDNA) mutations. We report that the pathognomonic symptom in MELAS syndrome caused by this newly observed mtDNA mutation may be rapid progression of cardiomyopathy and severe heart failure. © BMJ Publishing Group Ltd (unless otherwise stated in the text of the article) 2017. All rights reserved. No commercial use is permitted unless otherwise expressly granted.

Exercise training restores cardiac protein quality control in heart failure.

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Juliane C Campos

Full Text Available Exercise training is a well-known coadjuvant in heart failure treatment; however, the molecular mechanisms underlying its beneficial effects remain elusive. Despite the primary cause, heart failure is often preceded by two distinct phenomena: mitochondria dysfunction and cytosolic protein quality control disruption. The objective of the study was to determine the contribution of exercise training in regulating cardiac mitochondria metabolism and cytosolic protein quality control in a post-myocardial infarction-induced heart failure (MI-HF animal model. Our data demonstrated that isolated cardiac mitochondria from MI-HF rats displayed decreased oxygen consumption, reduced maximum calcium uptake and elevated H₂O₂ release. These changes were accompanied by exacerbated cardiac oxidative stress and proteasomal insufficiency. Declined proteasomal activity contributes to cardiac protein quality control disruption in our MI-HF model. Using cultured neonatal cardiomyocytes, we showed that either antimycin A or H₂O₂ resulted in inactivation of proteasomal peptidase activity, accumulation of oxidized proteins and cell death, recapitulating our in vivo model. Of interest, eight weeks of exercise training improved cardiac function, peak oxygen uptake and exercise tolerance in MI-HF rats. Moreover, exercise training restored mitochondrial oxygen consumption, increased Ca²⁺-induced permeability transition and reduced H₂O₂ release in MI-HF rats. These changes were followed by reduced oxidative stress and better cardiac protein quality control. Taken together, our findings uncover the potential contribution of mitochondrial dysfunction and cytosolic protein quality control disruption to heart failure and highlight the positive effects of exercise training in re-establishing cardiac mitochondrial physiology and protein quality control, reinforcing the importance of this intervention as a non-pharmacological tool for heart failure therapy.

Nutrient removal from swine lagoon effluent by duckweed

Energy Technology Data Exchange (ETDEWEB)

Bergmann, B.A.; Cheng, J.; Classen, J.; Stomp, A.M.

2000-04-01

Three duckweed geographic isolates were grown on varying concentrations of swine lagoon effluent in a greenhouse to determine their ability to remove nutrients from the effluent. Duckweed biomass was harvested every other day over a 12-day period. Duckweed biomass production, nutrient loss from the swine lagoon effluent, and nutrient content of duckweed biomass were used to identify effluent concentrations/geographic isolate combinations that are effective in terms of nutrient utilization from swine lagoon effluent and production of healthy duckweed biomass. When Lemna minor geographic isolate 8627 was grown on 50% swine lagoon effluent, respective losses of TKN, NH{sub 3}-N, TP, OPO{sub 4}-P, TOC, K, Cu, and Zn were 83, 100, 49, 31, 68, 21, 28 and 67%.

Mitochondrial Approaches to Protect Against Cardiac Ischemia and Reperfusion Injury

Science.gov (United States)

Camara, Amadou K. S.; Bienengraeber, Martin; Stowe, David F.

2011-01-01

The mitochondrion is a vital component in cellular energy metabolism and intracellular signaling processes. Mitochondria are involved in a myriad of complex signaling cascades regulating cell death vs. survival. Importantly, mitochondrial dysfunction and the resulting oxidative and nitrosative stress are central in the pathogenesis of numerous human maladies including cardiovascular diseases, neurodegenerative diseases, diabetes, and retinal diseases, many of which are related. This review will examine the emerging understanding of the role of mitochondria in the etiology and progression of cardiovascular diseases and will explore potential therapeutic benefits of targeting the organelle in attenuating the disease process. Indeed, recent advances in mitochondrial biology have led to selective targeting of drugs designed to modulate or manipulate mitochondrial function, to the use of light therapy directed to the mitochondrial function, and to modification of the mitochondrial genome for potential therapeutic benefit. The approach to rationally treat mitochondrial dysfunction could lead to more effective interventions in cardiovascular diseases that to date have remained elusive. The central premise of this review is that if mitochondrial abnormalities contribute to the etiology of cardiovascular diseases (e.g., ischemic heart disease), alleviating the mitochondrial dysfunction will contribute to mitigating the severity or progression of the disease. To this end, this review will provide an overview of our current understanding of mitochondria function in cardiovascular diseases as well as the potential role for targeting mitochondria with potential drugs or other interventions that lead to protection against cell injury. PMID:21559063

Mitochondrial approaches to protect against cardiac ischemia and reperfusion injury

Directory of Open Access Journals (Sweden)

Amadou K.S. Camara

2011-04-01

Full Text Available The mitochondrion is a vital component in cellular energy metabolism and intracellular signaling processes. Mitochondria are involved in a myriad of complex signaling cascades regulating cell death vs. survival. Importantly, mitochondrial dysfunction and the resulting oxidative and nitrosative stress are central in the pathogenesis of numerous human maladies including cardiovascular diseases, neurodegenerative diseases, diabetes, and retinal diseases, many of which are related. This review will examine the emerging understanding of the role of mitochondria in the etiology and progression of cardiovascular diseases and will explore potential therapeutic benefits of targeting the organelle in attenuating the disease process. Indeed, recent advances in mitochondrial biology have led to selective targeting of drugs designed to modulate or manipulate mitochondrial function, to the use of light therapy directed to the mitochondrial function, and to modification of the mitochondrial genome for potential therapeutic benefit. The approach to rationally treat mitochondrial dysfunction could lead to more effective interventions in cardiovascular diseases that to date have remained elusive. The central premise of this review is that if mitochondrial abnormalities contribute to the etiology of cardiovascular diseases (e.g. ischemic heart disease, alleviating the mitochondrial dysfunction will contribute to mitigating the severity or progression of the disease. To this end, this review will provide an overview of our current understanding of mitochondria function in cardiovascular diseases as well as the potential role for targeting mitochondria with potential drugs or other interventions that lead to protection against cell injury.

Vacuum pyrolysis of swine manure : biochar production and characteristics

Energy Technology Data Exchange (ETDEWEB)

Verma, M. [Inst. de recherche et de developpement en agroenvironnement Inc., Quebec City, PQ (Canada); Centre de recherche industrielle du Quebec, Quebec City, PQ (Canada); Godbout, S.; Larouche, J.P.; Lemay, S.P.; Pelletier, F. [Inst. de recherche et de developpement en agroenvironnement Inc., Quebec City, PQ (Canada); Solomatnikova, O. [Centre de recherche industrielle du Quebec, Quebec City, PQ (Canada); Brar, S.K. [Inst. national de la recherche scientifique, eau, terre et environnement, Quebec City, PQ (Canada)

2010-07-01

Quebec accounts for nearly 25 per cent of swine production in Canada. The issue of swine manure is addressed through land spreading and conversion into fertilizer. However, current regulations restrict the use of swine manure as fertilizer on most farmlands due to the problem of surplus phosphorus and nitrogen. Although many technologies exist to separate phosphorus and nitrogen from the organic-rich dry matter in swine manure, about 40 per cent of the treated waste matter must still be disposed in an environmentally sound manner. This study investigated the technical feasibility of pretreating the swine manure solids into biofuels on a farm-scale basis using vacuum pyrolysis process. A custom built stainless steel pressure vessel was used to carry out pyrolysis reaction of swine manure biomass at a temperature range between 200 to 600 degrees C under vacuum. The pyrolytic vapour was condensed in 2 glass condensers in series. The biochar was collected directly from the pyrolysis vessel following completion of the pyrolysis batch. The non condensable vapour and gases were considered as losses. Biochar, bio-oil, an aqueous phase and a gas mixture were the 4 products of the pyrolysis process. A thermogravimetric analysis of the swine manure samples was conducted before the pyrolysis tests. The study showed that 238 degrees C is the optimal pyrolysis temperature for biochar production.

Polymerase Discordance in Novel Swine Influenza H3N2v Constellations Is Tolerated in Swine but Not Human Respiratory Epithelial Cells

Science.gov (United States)

Powell, Joshua D.; Dlugolenski, Daniel; Nagy, Tamas; Gabbard, Jon; Lee, Christopher; Tompkins, Stephen M.; Tripp, Ralph A.

2014-01-01

Swine-origin H3N2v, a variant of H3N2 influenza virus, is a concern for novel reassortment with circulating pandemic H1N1 influenza virus (H1N1pdm09) in swine because this can lead to the emergence of a novel pandemic virus. In this study, the reassortment prevalence of H3N2v with H1N1pdm09 was determined in swine cells. Reassortants evaluated showed that the H1N1pdm09 polymerase (PA) segment occurred within swine H3N2 with ∼80% frequency. The swine H3N2-human H1N1pdm09 PA reassortant (swH3N2-huPA) showed enhanced replication in swine cells, and was the dominant gene constellation. Ferrets infected with swH3N2-huPA had increased lung pathogenicity compared to parent viruses; however, swH3N2-huPA replication in normal human bronchoepithelial cells was attenuated - a feature linked to expression of IFN-β and IFN-λ genes in human but not swine cells. These findings indicate that emergence of novel H3N2v influenza constellations require more than changes in the viral polymerase complex to overcome barriers to cross-species transmission. Additionally, these findings reveal that while the ferret model is highly informative for influenza studies, slight differences in pathogenicity may not necessarily be indicative of human outcomes after infection. PMID:25330303

AKIP1 expression modulates mitochondrial function in rat neonatal cardiomyocytes.

Directory of Open Access Journals (Sweden)

Hongjuan Yu

Full Text Available A kinase interacting protein 1 (AKIP1 is a molecular regulator of protein kinase A and nuclear factor kappa B signalling. Recent evidence suggests AKIP1 is increased in response to cardiac stress, modulates acute ischemic stress response, and is localized to mitochondria in cardiomyocytes. The mitochondrial function of AKIP1 is, however, still elusive. Here, we investigated the mitochondrial function of AKIP1 in a neonatal cardiomyocyte model of phenylephrine (PE-induced hypertrophy. Using a seahorse flux analyzer we show that PE stimulated the mitochondrial oxygen consumption rate (OCR in cardiomyocytes. This was partially dependent on PE mediated AKIP1 induction, since silencing of AKIP1 attenuated the increase in OCR. Interestingly, AKIP1 overexpression alone was sufficient to stimulate mitochondrial OCR and in particular ATP-linked OCR. This was also true when pyruvate was used as a substrate, indicating that it was independent of glycolytic flux. The increase in OCR was independent of mitochondrial biogenesis, changes in ETC density or altered mitochondrial membrane potential. In fact, the respiratory flux was elevated per amount of ETC, possibly through enhanced ETC coupling. Furthermore, overexpression of AKIP1 reduced and silencing of AKIP1 increased mitochondrial superoxide production, suggesting that AKIP1 modulates the efficiency of electron flux through the ETC. Together, this suggests that AKIP1 overexpression improves mitochondrial function to enhance respiration without excess superoxide generation, thereby implicating a role for AKIP1 in mitochondrial stress adaptation. Upregulation of AKIP1 during different forms of cardiac stress may therefore be an adaptive mechanism to protect the heart.

Insulin Signaling and Heart Failure

Science.gov (United States)

Riehle, Christian; Abel, E. Dale

2016-01-01

Heart failure is associated with generalized insulin resistance. Moreover, insulin resistant states such as type 2 diabetes and obesity increases the risk of heart failure even after adjusting for traditional risk factors. Insulin resistance or type 2 diabetes alters the systemic and neurohumoral milieu leading to changes in metabolism and signaling pathways in the heart that may contribute to myocardial dysfunction. In addition, changes in insulin signaling within cardiomyocytes develop in the failing heart. The changes range from activation of proximal insulin signaling pathways that may contribute to adverse left ventricular remodeling and mitochondrial dysfunction to repression of distal elements of insulin signaling pathways such as forkhead (FOXO) transcriptional signaling or glucose transport which may also impair cardiac metabolism, structure and function. This article will review the complexities of insulin signaling within the myocardium and ways in which these pathways are altered in heart failure or in conditions associated with generalized insulin resistance. The implications of these changes for therapeutic approaches to treating or preventing heart failure will be discussed. PMID:27034277

Metabonomic study of the biochemical profiles of heterozygous myostatin knockout swine

Directory of Open Access Journals (Sweden)

Jianxiang XU,Dengke PAN,Jie ZHAO,Jianwu WANG,Xiaohong HE,Yuehui MA,Ning LI

2015-03-01

Full Text Available Myostatin is a transforming growth factor-β family member that normally acts to limit skeletal muscle growth. Myostatin gene (MSTN knockout (KO mice show possible effects for the prevention or treatment of metabolic disorders such as obesity and type 2 diabetes. We applied chromatography and mass spectrometry based metabonomics to assess system-wide metabolic response of heterozygous MSTN KO (MSTN+/- swine. Most of the metabolic data for MSTN+/- swine were similar to the data for wild type (WT control swine. There were, however, metabolic changes related to fatty acid metabolism, glucose utilization, lipid metabolism, as well as BCAA catabolism caused by monoallelic MSTN depletion.The statistical analyses suggested that: (1 most metabolic changes were not significant in MSTN+/- swine compared to WT swine; (2 only a few metabolic properties were significantly different between KO and WT swine, especially for lipid metabolism. Significantly, these minor changes were most evident in female KO swine and suggested differences in gender sensitivity to myostatin.

A novel fission-independent role of dynamin-related protein 1 in cardiac mitochondrial respiration.

Science.gov (United States)

Zhang, Huiliang; Wang, Pei; Bisetto, Sara; Yoon, Yisang; Chen, Quan; Sheu, Shey-Shing; Wang, Wang

2017-02-01

Mitochondria in adult cardiomyocytes exhibit static morphology and infrequent dynamic changes, despite the high abundance of fission and fusion regulatory proteins in the heart. Previous reports have indicated that fusion proteins may bear functions beyond morphology regulation. Here, we investigated the role of fission protein, dynamin-related protein 1 (DRP1), on mitochondrial respiration regulation in adult cardiomyocytes. By using genetic or pharmacological approaches, we manipulated the activity or protein level of fission and fusion proteins and found they mildly influenced mitochondrial morphology in adult rodent cardiomyocytes, which is in contrast to their significant effect in H9C2 cardiac myoblasts. Intriguingly, inhibiting endogenous DRP1 by dominant-negative DRP1 mutation (K38A), shRNA, or Mdivi-1 suppressed maximal respiration and respiratory control ratio in isolated mitochondria from adult mouse heart or in adult cardiomyocytes from rat. Meanwhile, basal respiration was increased due to increased proton leak. Facilitating mitofusin-mediated fusion by S3 compound, however, failed to inhibit mitochondrial respiration in adult cardiomyocytes. Mechanistically, DRP1 inhibition did not affect the maximal activity of individual respiratory chain complexes or the assembly of supercomplexes. Knocking out cyclophilin D, a regulator of mitochondrial permeability transition pore (mPTP), abolished the effect of DRP1 inhibition on respiration. Finally, DRP1 inhibition decreased transient mPTP-mediated mitochondrial flashes, delayed laser-induced mPTP opening and suppressed mitochondrial reactive oxygen species (ROS). These results uncover a novel non-canonical function of the fission protein, DRP1 in maintaining or positively stimulating mitochondrial respiration, bioenergetics and ROS signalling in adult cardiomyocyte, which is likely independent of morphological changes. Published on behalf of the European Society of Cardiology. All rights reserved. © The

Cell Death and Heart Failure in Obesity: Role of Uncoupling Proteins

Directory of Open Access Journals (Sweden)

Angélica Ruiz-Ramírez

2016-01-01

Full Text Available Metabolic diseases such as obesity, metabolic syndrome, and type II diabetes are often characterized by increased reactive oxygen species (ROS generation in mitochondrial respiratory complexes, associated with fat accumulation in cardiomyocytes, skeletal muscle, and hepatocytes. Several rodents studies showed that lipid accumulation in cardiac myocytes produces lipotoxicity that causes apoptosis and leads to heart failure, a dynamic pathological process. Meanwhile, several tissues including cardiac tissue develop an adaptive mechanism against oxidative stress and lipotoxicity by overexpressing uncoupling proteins (UCPs, specific mitochondrial membrane proteins. In heart from rodent and human with obesity, UCP2 and UCP3 may protect cardiomyocytes from death and from a state progressing to heart failure by downregulating programmed cell death. UCP activation may affect cytochrome c and proapoptotic protein release from mitochondria by reducing ROS generation and apoptotic cell death. Therefore the aim of this review is to discuss recent findings regarding the role that UCPs play in cardiomyocyte survival by protecting against ROS generation and maintaining bioenergetic metabolism homeostasis to promote heart protection.

Influence of mycotoxin zearalenone on the swine reproductive failure

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Prodanov-Radulović Jasna Z.

2013-01-01

Full Text Available Reproductive failure in swine is often a difficult diagnostic problem. If diagnoses of infectious disease or management related problems are not obtained, feed quality and safety may be questioned. Mycotoxins are often present in swine feed in the amount that can have detrimental impact on production and reproduction. Problems are expressed only as alterations of the reproductive cycle, reduced feed intake, slow growth or impaired feed efficiency. In Serbia, generally speaking, high concentrations of mycotoxins were noticed, especially mycotoxin zearalenone. High presence of zearalenone in swine feed is probably due to climatic influence and should be monitored constantly. This paper includes field observations regarding the influence of moldy feed containing mycotoxin zearalenone on the occurrence of the reproductive failure in swine breeding categories (sows, gilts and boars. The material for this research was obtained from four swine farms where certain reproductive disorders and health problems in breeding animals were detected. Depending on the specificity of each evaluated case and available material, the applied research methods included: anamnestic and clinical evaluation, pathomorphological examination, standard laboratory testing for detection of aerobic and anaerobic bacteria, and microbiological feed testing, in order to examine the presence of fungi and mycotoxins by applying the method of thin layer chromatography. On the basis of the obtained results, it could be concluded that mycotoxin zearalenone was detected in all examined feed samples. The presence of mycotoxin in feed was directly related to the reproductive failures in the examined swine categories (vulvovaginitis, endometritis, rebreeding, infertility. Swine reproduction represents the base for intensive swine production. The presence of mycotoxins in swine feed have influence on the reproduction and health status of pigs and under certain conditions may significantly

Polymerase discordance in novel swine influenza H3N2v constellations is tolerated in swine but not human respiratory epithelial cells.

Directory of Open Access Journals (Sweden)

Joshua D Powell

Full Text Available Swine-origin H3N2v, a variant of H3N2 influenza virus, is a concern for novel reassortment with circulating pandemic H1N1 influenza virus (H1N1pdm09 in swine because this can lead to the emergence of a novel pandemic virus. In this study, the reassortment prevalence of H3N2v with H1N1pdm09 was determined in swine cells. Reassortants evaluated showed that the H1N1pdm09 polymerase (PA segment occurred within swine H3N2 with ∼ 80% frequency. The swine H3N2-human H1N1pdm09 PA reassortant (swH3N2-huPA showed enhanced replication in swine cells, and was the dominant gene constellation. Ferrets infected with swH3N2-huPA had increased lung pathogenicity compared to parent viruses; however, swH3N2-huPA replication in normal human bronchoepithelial cells was attenuated - a feature linked to expression of IFN-β and IFN-λ genes in human but not swine cells. These findings indicate that emergence of novel H3N2v influenza constellations require more than changes in the viral polymerase complex to overcome barriers to cross-species transmission. Additionally, these findings reveal that while the ferret model is highly informative for influenza studies, slight differences in pathogenicity may not necessarily be indicative of human outcomes after infection.

9 CFR 93.511 - Swine quarantine facilities.

Science.gov (United States)

2010-01-01

...) Privately operated quarantine facilities. The importer, or his or her agent, of swine subject to quarantine... of any import permit. The facilities occupied by swine should be kept clean and sanitary to the... described in paragraph (b) of this section. The importer, or his or her agent, shall request in writing such...

Swine flu (H1N1 influenza): awareness profile of visitors of swine flu screening booths in Belgaum city, Karnataka.

Science.gov (United States)

Viveki, R G; Halappanavar, A B; Patil, M S; Joshi, A V; Gunagi, Praveena; Halki, Sunanda B

2012-06-01

The 2009 flu pandemic was a global outbreak of a new strain of H1N1 influenza virus often referred colloquially as "swine flu". The objectives of the study were: (1) To know the sociodemographic and awareness profile of visitors attending swine flu screening booths. (2) To reveal sources of information. The present cross-sectional study was undertaken among the visitors (18 years and above) attending swine flu screening booths organised within the Belgaum city during Ganesh festival from 28-08-2009 to 03-09-2009 by interviewing them using predesigned, pretested structured questionnaire on swine flu. The data was collected and analysed using SPSS software programme for windows (version 16). Chi-square test was applied. Out of 206 visitors, 132 (64.1%) were males and 107 (51.9%) were in the age group of 30-49 years; 183 (88.8%) had heard about swine flu. More than a third of the visitors (38.3%) disclosed that there was a vaccine to prevent swine flu. Majority responded that it could be transmitted by being in close proximity to pigs (49.0%) and by eating pork (51.5%). Newspaper/magazine (64.6%), television (61.7%), and public posters/pamphlets (44.2%) were common sources of information. The present study revealed that doctors/public health workers have played little role in creating awareness in the community. The improved communication between doctors and the community would help to spread correct information about the disease and the role that the community can play in controlling the spread of the disease.

The Romanian Swine Market in the EU Context

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Silvius STANCIU

2014-12-01

Full Text Available Pork is a traditional food product for Romania, representing more than half of the annual meat consumption per capita. Swine farming is an activity mainly at full time households, ensuring subsistence, representing a source for commercial exchanges, ensuring workforce stability in the rural areas. The Romanian pork production has presented a slightly fluctuating evolution in recent years. The paper proposes a review of the domestic production, consumption, origin and price of swine sold in the Romanian market. The comunity competitive conditions, the export limitation and food crisis (horse meat scandal, spoiled meat scandal, swine fever or swine flu affected domestic production and exports. Data used in this paper represent statistical information provided by specialized national, European or global institutions, information presented in the media, journals, food industry treatises/dissertations or official information submitted by the Ministry of Agriculture.

Comparative fecal metagenomics unveils unique functional capacity of the swine gut

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Martinson John

2011-05-01

Full Text Available Abstract Background Uncovering the taxonomic composition and functional capacity within the swine gut microbial consortia is of great importance to animal physiology and health as well as to food and water safety due to the presence of human pathogens in pig feces. Nonetheless, limited information on the functional diversity of the swine gut microbiome is available. Results Analysis of 637, 722 pyrosequencing reads (130 megabases generated from Yorkshire pig fecal DNA extracts was performed to help better understand the microbial diversity and largely unknown functional capacity of the swine gut microbiome. Swine fecal metagenomic sequences were annotated using both MG-RAST and JGI IMG/M-ER pipelines. Taxonomic analysis of metagenomic reads indicated that swine fecal microbiomes were dominated by Firmicutes and Bacteroidetes phyla. At a finer phylogenetic resolution, Prevotella spp. dominated the swine fecal metagenome, while some genes associated with Treponema and Anareovibrio species were found to be exclusively within the pig fecal metagenomic sequences analyzed. Functional analysis revealed that carbohydrate metabolism was the most abundant SEED subsystem, representing 13% of the swine metagenome. Genes associated with stress, virulence, cell wall and cell capsule were also abundant. Virulence factors associated with antibiotic resistance genes with highest sequence homology to genes in Bacteroidetes, Clostridia, and Methanosarcina were numerous within the gene families unique to the swine fecal metagenomes. Other abundant proteins unique to the distal swine gut shared high sequence homology to putative carbohydrate membrane transporters. Conclusions The results from this metagenomic survey demonstrated the presence of genes associated with resistance to antibiotics and carbohydrate metabolism suggesting that the swine gut microbiome may be shaped by husbandry practices.

Two genotypes of H1N2 swine influenza viruses appeared among pigs in China.

Science.gov (United States)

Xu, Chuantian; Zhu, Qiyun; Yang, Huanliang; Zhang, Xiumei; Qiao, Chuanling; Chen, Yan; Xin, Xiaoguang; Chen, Hualan

2009-10-01

H1N2 is one of the main subtypes of influenza, which circulates in swine all over the world. To investigate the prevalence and genetic of H1N2 in swine of China. Two H1N2 swine influenza viruses were isolated from Tianjin and Guangdong province of China in 2004 and 2006, respectively. The molecular evolution of eight gene segments was analyzed. A/Swine/Tianjin/1/2004 has low identity with A/Swine/Guangdong/2006; in the phylogenetic tree of PA gene, A/Swine/Guangdong/1/2006 and A/Swine/Guangxi/1/2006 along with the H1N2 swine isolates of North America formed a cluster; and A/Swine/Tianjin/2004 and A/Swine/Zhejiang/2004, along with the classical H1N1 swine isolates formed another cluster; except that NA gene of A/Swine/Tianjin/1/2004 fell into the cluster of the H3N2 human influenza virus, indicating the reassortment between H3N2 human and H1N1 swine influenza viruses. Two different genotypes of H1N2 appeared among pigs in China. A/swine/Guangdong/1/06 was probably from H1N2 swine influenza viruses of North America; while A/swine/Tianjin/1/04 maybe come from reassortments of classical H1N1 swine and H3N2 human viruses prevalent in North America.

mtDNA depletion myopathy: elucidation of the tissue specificity in the mitochondrial thymidine kinase (TK2) deficiency.

Science.gov (United States)

Saada, Ann; Shaag, Avraham; Elpeleg, Orly

2003-05-01

Decreased mitochondrial thymidine kinase (TK2) activity is associated with mitochondrial DNA (mtDNA) depletion and respiratory chain dysfunction and is manifested by isolated, fatal skeletal myopathy. Other tissues such as liver, brain, heart, and skin remain unaffected throughout the patients' life. In order to elucidate the mechanism of tissue specificity in the disease we have investigated the expression of the mitochondrial deoxynucleotide carrier, the mtDNA content and the activity of TK2 in mitochondria of various tissues. Our results suggest that low basal TK2 activity combined with a high requirement for mitochondrial encoded proteins in muscle predispose this tissue to the devastating effect of TK2 deficiency.

9 CFR 309.5 - Swine; disposal because of hog cholera.

Science.gov (United States)

2010-01-01

... 9 Animals and Animal Products 2 2010-01-01 2010-01-01 false Swine; disposal because of hog cholera... INSPECTION AND CERTIFICATION ANTE-MORTEM INSPECTION § 309.5 Swine; disposal because of hog cholera. (a) All swine found by an inspector to be affected with hog cholera shall be identified as U.S. Condemned and...

Simulating the epidemiological and economic effects of an African swine fever epidemic in industrialized swine populations

DEFF Research Database (Denmark)

Hisham Beshara Halasa, Tariq; Bøtner, Anette; Mortensen, Sten

2016-01-01

to simulate the spread of ASF virus between domestic swine herds exemplified by the Danish swine population. ASF was simulated to spread via animal movement, low- or medium-risk contacts and local spread. Each epidemic was initiated in a randomly selected herd – either in a nucleus herd, a sow herd......African swine fever (ASF) is a notifiable infectious disease with a considerable impact on animal health and is currently one of the most important emerging diseases of domestic pigs. ASF was introduced into Georgia in 2007 and subsequently spread to the Russian Federation and several Eastern...... European countries. Consequently, there is a non-negligible risk of ASF spread towards Western Europe. Therefore it is important to develop tools to improve our understanding of the spread and control of ASF for contingency planning. A stochastic and dynamic spatial spread model (DTU-DADS) was adjusted...

Prospective surveillance for influenza. virus in Chinese swine farms.

Science.gov (United States)

Anderson, Benjamin D; Ma, Mai-Juan; Wang, Guo-Lin; Bi, Zhen-Qiang; Lu, Bing; Wang, Xian-Jun; Wang, Chuang-Xin; Chen, Shan-Hui; Qian, Yan-Hua; Song, Shao-Xia; Li, Min; Zhao, Teng; Wu, Meng-Na; Borkenhagen, Laura K; Cao, Wu-Chun; Gray, Gregory C

2018-05-16

Pork production in China is rapidly increasing and swine production operations are expanding in size and number. However, the biosecurity measures necessary to prevent swine disease transmission, particularly influenza. viruses (IAV) that can be zoonotic, are often inadequate. Despite this risk, few studies have attempted to comprehensively study IAV ecology in swine production settings. Here, we present environmental and animal sampling data collected in the first year of an ongoing five-year prospective epidemiological study to assess IAV ecology as it relates to swine workers, their pigs, and the farm environment. From March 2015 to February 2016, we collected 396 each of environmental swab, water, bioaerosol, and fecal/slurry samples, as well as 3300 pig oral secretion samples from six farms in China. The specimens were tested with molecular assays for IAV. Of these, 46 (11.6%) environmental swab, 235 (7.1%) pig oral secretion, 23 (5.8%) water, 20 (5.1%) bioaerosol, and 19 (4.8%) fecal/slurry specimens were positive for influenza. by qRT-PCR. Risk factors for IAV detection among collected samples were identified using bivariate logistic regression. Overall, these first year data suggest that IAV is quite ubiquitous in the swine production environment and demonstrate an association between the different types of environmental sampling used. Given the mounting evidence that some of these viruses freely move between pigs and swine workers, and that mixing of these viruses can yield progeny viruses with pandemic potential, it seems imperative that routine surveillance for novel IAVs be conducted in commercial swine farms.

Serological and molecular evidence of hepadnavirus infection in swine

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Yasmine R Vieira

2015-02-01

Full Text Available [b]Introduction and objective[/b]. Recently, investigations in a swine herd identified evidence of the existence of a novel member of the Hepadnavirus family endemic in swine. The aim of this study was to investigate the serological and molecular markers of Hepadnavirus circulation in Brazilian domestic swine and wild boar herds, and to evaluate the identity with HBV and other Hepadnaviruses reported previously. [b]Materials and methods[/b]. For the study, 376 swine were screened for hepatitis B virus serological markers. Analyses were performed in serum samples using commercial enzyme-linked immunosorbent assay (ELISA kits (DiaSorin® for anti-HBc, HBsAg and anti-HBs. Reactive and undetermined swine serum samples were selected to perform DNA viral extraction (QIAamp DNA Mini Kit, Qiagen®, partial genome amplification and genome sequencing. [b]Results[/b]. From 376 swine samples analysed, 28 (7.45% were reactive to anti-HBc, 3 (0.80% to HBsAg and 6 (1.6% to anti-HBs. Besides, more 17 (4.52% swine samples analyzed were classified in the grey zone of the EIA test to anti-HBc and 2 (0.53% to HBsAg. From 49 samples molecularly analyzed after serological trial, 4 samples showed a positive result for the qualitative PCR for Hepadnavirus. Phylogenetic reconstruction using partial genome sequencing (360 bp of 3 samples showed similarity with HBV with 90.8–96.3% of identity. [b]Conclusions.[/b] Serological and molecular data showed evidence of the circulation of a virus similar to hepatitis B virus in swine.

Swine production.

Science.gov (United States)

Plain, Ronald L; Lawrence, John D

2003-07-01

The US swine industry is large and growing. The quantity of pork desired by consumers of US pork is growing at the rate of 1.5%/y. New production systems and new technology have enabled production per sow to grow at a rate of 4% annually in recent years. Consequently, the number of sows in the United States is declining. Because productivity growth is outpacing demand growth, the deflated price of hogs and pork is declining. Hog production and prices continue to exhibit strong seasonal and cyclic patterns. Pork production is usually lowest in the summer and highest in the fall. Production and prices tend to follow 4-year patterns. The US swine industry continues to evolve toward fewer and larger producers who rely on contracts for both hog production and marketing. In 2000, over half of the hogs marketed were from approximately 156 firms marketing more than 50,000 head annually. These producers finished 60% of their production in contract facilities. Over 90% of their marketings were under contract or were owned by a packer. These producers expressed a high level of satisfaction with hog production. Both they and their contract growers were satisfied with production contracts. These large producers were satisfied with their marketing contracts and planned to continue them in the future. The hog industry has changed a great deal in the last decade. There is little reason to believe this rapid rate of change will not continue. This swine industry is highly competitive and profit driven. Profit margins are too small to allow producers the luxury of ignoring new technology and innovative production systems. Consequently, hog production will continue its rapid evolution from traditional agriculture to typical industry.

Mitochondrial membrane studies using impedance spectroscopy with parallel pH monitoring.

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Divya Padmaraj

Full Text Available A biological microelectromechanical system (BioMEMS device was designed to study complementary mitochondrial parameters important in mitochondrial dysfunction studies. Mitochondrial dysfunction has been linked to many diseases, including diabetes, obesity, heart failure and aging, as these organelles play a critical role in energy generation, cell signaling and apoptosis. The synthesis of ATP is driven by the electrical potential across the inner mitochondrial membrane and by the pH difference due to proton flux across it. We have developed a tool to study the ionic activity of the mitochondria in parallel with dielectric measurements (impedance spectroscopy to gain a better understanding of the properties of the mitochondrial membrane. This BioMEMS chip includes: 1 electrodes for impedance studies of mitochondria designed as two- and four-probe structures for optimized operation over a wide frequency range and 2 ion-sensitive field effect transistors for proton studies of the electron transport chain and for possible monitoring other ions such as sodium, potassium and calcium. We have used uncouplers to depolarize the mitochondrial membrane and disrupt the ionic balance. Dielectric spectroscopy responded with a corresponding increase in impedance values pointing at changes in mitochondrial membrane potential. An electrical model was used to describe mitochondrial sample's complex impedance frequency dependencies and the contribution of the membrane to overall impedance changes. The results prove that dielectric spectroscopy can be used as a tool for membrane potential studies. It can be concluded that studies of the electrochemical parameters associated with mitochondrial bioenergetics may render significant information on various abnormalities attributable to these organelles.

Fisetin Confers Cardioprotection against Myocardial Ischemia Reperfusion Injury by Suppressing Mitochondrial Oxidative Stress and Mitochondrial Dysfunction and Inhibiting Glycogen Synthase Kinase 3β Activity

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Karthi Shanmugam

2018-01-01

Full Text Available Acute myocardial infarction (AMI is the leading cause of morbidity and mortality worldwide. Timely reperfusion is considered an optimal treatment for AMI. Paradoxically, the procedure of reperfusion can itself cause myocardial tissue injury. Therefore, a strategy to minimize the reperfusion-induced myocardial tissue injury is vital for salvaging the healthy myocardium. Herein, we investigated the cardioprotective effects of fisetin, a natural flavonoid, against ischemia/reperfusion (I/R injury (IRI using a Langendorff isolated heart perfusion system. I/R produced significant myocardial tissue injury, which was characterized by elevated levels of lactate dehydrogenase and creatine kinase in the perfusate and decreased indices of hemodynamic parameters. Furthermore, I/R resulted in elevated oxidative stress, uncoupling of the mitochondrial electron transport chain, increased mitochondrial swelling, a decrease of the mitochondrial membrane potential, and induction of apoptosis. Moreover, IRI was associated with a loss of the mitochondrial structure and decreased mitochondrial biogenesis. However, when the animals were pretreated with fisetin, it significantly attenuated the I/R-induced myocardial tissue injury, blunted the oxidative stress, and restored the structure and function of mitochondria. Mechanistically, the fisetin effects were found to be mediated via inhibition of glycogen synthase kinase 3β (GSK3β, which was confirmed by a biochemical assay and molecular docking studies.

Fisetin Confers Cardioprotection against Myocardial Ischemia Reperfusion Injury by Suppressing Mitochondrial Oxidative Stress and Mitochondrial Dysfunction and Inhibiting Glycogen Synthase Kinase 3β Activity.

Science.gov (United States)

Shanmugam, Karthi; Ravindran, Sriram; Kurian, Gino A; Rajesh, Mohanraj

2018-01-01

Acute myocardial infarction (AMI) is the leading cause of morbidity and mortality worldwide. Timely reperfusion is considered an optimal treatment for AMI. Paradoxically, the procedure of reperfusion can itself cause myocardial tissue injury. Therefore, a strategy to minimize the reperfusion-induced myocardial tissue injury is vital for salvaging the healthy myocardium. Herein, we investigated the cardioprotective effects of fisetin, a natural flavonoid, against ischemia/reperfusion (I/R) injury (IRI) using a Langendorff isolated heart perfusion system. I/R produced significant myocardial tissue injury, which was characterized by elevated levels of lactate dehydrogenase and creatine kinase in the perfusate and decreased indices of hemodynamic parameters. Furthermore, I/R resulted in elevated oxidative stress, uncoupling of the mitochondrial electron transport chain, increased mitochondrial swelling, a decrease of the mitochondrial membrane potential, and induction of apoptosis. Moreover, IRI was associated with a loss of the mitochondrial structure and decreased mitochondrial biogenesis. However, when the animals were pretreated with fisetin, it significantly attenuated the I/R-induced myocardial tissue injury, blunted the oxidative stress, and restored the structure and function of mitochondria. Mechanistically, the fisetin effects were found to be mediated via inhibition of glycogen synthase kinase 3 β (GSK3 β ), which was confirmed by a biochemical assay and molecular docking studies.

Removal of nitrogen from anaerobically digested swine wastewater ...

African Journals Online (AJOL)

This result indicates that the sulfur-packed biofilter would be used as an efficient option for denitrification by autotrophic denitrifiers during swine wastewater treatment. Key words: Biological nitrogen removal, nitrification, denitrification, chemical oxygen demand (COD), intermittent aeration, sulfur-packed bed reactor, swine ...

Modeling livestock population structure: a geospatial database for Ontario swine farms.

Science.gov (United States)

Khan, Salah Uddin; O'Sullivan, Terri L; Poljak, Zvonimir; Alsop, Janet; Greer, Amy L

2018-01-30

Infectious diseases in farmed animals have economic, social, and health consequences. Foreign animal diseases (FAD) of swine are of significant concern. Mathematical and simulation models are often used to simulate FAD outbreaks and best practices for control. However, simulation outcomes are sensitive to the population structure used. Within Canada, access to individual swine farm population data with which to parameterize models is a challenge because of privacy concerns. Our objective was to develop a methodology to model the farmed swine population in Ontario, Canada that could represent the existing population structure and improve the efficacy of simulation models. We developed a swine population model based on the factors such as facilities supporting farm infrastructure, land availability, zoning and local regulations, and natural geographic barriers that could affect swine farming in Ontario. Assigned farm locations were equal to the swine farm density described in the 2011 Canadian Census of Agriculture. Farms were then randomly assigned to farm types proportional to the existing swine herd types. We compared the swine population models with a known database of swine farm locations in Ontario and found that the modeled population was representative of farm locations with a high accuracy (AUC: 0.91, Standard deviation: 0.02) suggesting that our algorithm generated a reasonable approximation of farm locations in Ontario. In the absence of a readily accessible dataset providing details of the relative locations of swine farms in Ontario, development of a model livestock population that captures key characteristics of the true population structure while protecting privacy concerns is an important methodological advancement. This methodology will be useful for individuals interested in modeling the spread of pathogens between farms across a landscape and using these models to evaluate disease control strategies.

Basal Ganglia Calcification with Tetanic Seizure Suggest Mitochondrial Disorder.

Science.gov (United States)

Finsterer, Josef; Enzelsberger, Barbara; Bastowansky, Adam

2017-04-09

BACKGROUND Basal ganglia calcification (BGC) is a rare sporadic or hereditary central nervous system (CNS) abnormality, characterized by symmetric or asymmetric calcification of the basal ganglia. CASE REPORT We report the case of a 65-year-old Gypsy female who was admitted for a tetanic seizure, and who had a history of polyneuropathy, restless-leg syndrome, retinopathy, diabetes, hyperlipidemia, osteoporosis with consecutive hyperkyphosis, cervicalgia, lumbalgia, struma nodosa requiring thyroidectomy and consecutive hypothyroidism, adipositas, resection of a vocal chord polyp, arterial hypertension, coronary heart disease, atheromatosis of the aorta, peripheral artery disease, chronic obstructive pulmonary disease, steatosis hepatis, mild renal insufficiency, long-term hypocalcemia, hyperphosphatemia, impingement syndrome, spondylarthrosis of the lumbar spine, and hysterectomy. History and clinical presentation suggested a mitochondrial defect which also manifested as hypoparathyroidism or Fanconi syndrome resulting in BGC. After substitution of calcium, no further tetanic seizures occurred. CONCLUSIONS Patients with BGC should be investigated for a mitochondrial disorder. A mitochondrial disorder may also manifest as tetanic seizure.

Evaluation of Cardiac Mitochondrial Function by a Nuclear Imaging Technique using Technetium-99m-MIBI Uptake Kinetics

International Nuclear Information System (INIS)

Matsuo, Shinro; Nakajima, Kenichi; Kinuya, Seigo

2013-01-01

Mitochondria play an important role in energy production for the cell. The proper function of a myocardial cell largely depends on the functional capacity of the mitochondria. Therefore it is necessary to establish a novel and reliable method for a non-invasive assessment of mitochondrial function and metabolism in humans. Although originally designed for evaluating myocardial perfusion, 99m Tc-MIBI can be also used to evaluate cardiac mitochondrial function. In a clinical study on ischemic heart disease, reverse redistribution of 99m Tc-MIBI was evident after direct percutaneous transluminal coronary angioplasty. The presence of increased washout of 99m Tc-MIBI was associated with the infarct-related artery and preserved left ventricular function. In non-ischemic cardiomyopathy, an increased washout rate of 99m Tc-MIBI, which correlated inversely with left ventricular ejection fraction, was observed in patients with congestive heart failure. Increased 99m Tc-MIBI washout was also observed in mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS) and in doxorubicin-induced cardiomyopathy. Noninvasive assessment of cardiac mitochondrial function could be greatly beneficial in monitoring possible cardiotoxic drug use and in the evaluation of cardiac damage in clinical medicine

Occurrence of Staphylococcus aureus in swine and swine workplace environments on industrial and antibiotic-free hog operations in North Carolina, USA: A One Health pilot study.

Science.gov (United States)

Davis, Meghan F; Pisanic, Nora; Rhodes, Sarah M; Brown, Alexis; Keller, Haley; Nadimpalli, Maya; Christ, Andrea; Ludwig, Shanna; Ordak, Carly; Spicer, Kristoffer; Love, David C; Larsen, Jesper; Wright, Asher; Blacklin, Sarah; Flowers, Billy; Stewart, Jill; Sexton, Kenneth G; Rule, Ana M; Heaney, Christopher D

2018-05-01

Occupational exposure to swine has been associated with increased Staphylococcus aureus carriage, including antimicrobial-resistant strains, and increased risk of infections. To characterize animal and environmental routes of worker exposure, we optimized methods to identify S. aureus on operations that raise swine in confinement with antibiotics (industrial hog operation: IHO) versus on pasture without antibiotics (antibiotic-free hog operation: AFHO). We associated findings from tested swine and environmental samples with those from personal inhalable air samplers on worker surrogates at one IHO and three AFHOs in North Carolina using a new One Health approach. We determined swine S. aureus carriage status by collecting swab samples from multiple anatomical sites, and we determined environmental positivity for airborne bioaerosols with inhalable and impinger samplers and a single-stage impactor (ambient air) cross-sectionally. All samples were analyzed for S. aureus, and isolates were tested for antimicrobial susceptibility, absence of scn (livestock marker), and spa type. Seventeen of twenty (85%) swine sampled at the one IHO carried S. aureus at >1 anatomical sites compared to none of 30 (0%) swine sampled at the three AFHOs. All S. aureus isolates recovered from IHO swine and air samples were scn negative and spa type t337; almost all isolates (62/63) were multidrug resistant. S. aureus was recovered from eight of 14 (67%) ambient air and two (100%) worker surrogate personal air samples at the one IHO, whereas no S. aureus isolates were recovered from 19 ambient and six personal air samples at the three AFHOs. Personal worker surrogate inhalable sample findings were consistent with both swine and ambient air data, indicating the potential for workplace exposure. IHO swine and the one IHO environment could be a source of potential pathogen exposure to workers, as supported by the detection of multidrug-resistant S. aureus (MDRSA) with livestock-associated spa

Influenza A Viruses of Human Origin in Swine, Brazil.

Science.gov (United States)

Nelson, Martha I; Schaefer, Rejane; Gava, Danielle; Cantão, Maurício Egídio; Ciacci-Zanella, Janice Reis

2015-08-01

The evolutionary origins of the influenza A(H1N1)pdm09 virus that caused the first outbreak of the 2009 pandemic in Mexico remain unclear, highlighting the lack of swine surveillance in Latin American countries. Although Brazil has one of the largest swine populations in the world, influenza was not thought to be endemic in Brazil's swine until the major outbreaks of influenza A(H1N1)pdm09 in 2009. Through phylogenetic analysis of whole-genome sequences of influenza viruses of the H1N1, H1N2, and H3N2 subtypes collected in swine in Brazil during 2009-2012, we identified multiple previously uncharacterized influenza viruses of human seasonal H1N2 and H3N2 virus origin that have circulated undetected in swine for more than a decade. Viral diversity has further increased in Brazil through reassortment between co-circulating viruses, including A(H1N1)pdm09. The circulation of multiple divergent hemagglutinin lineages challenges the design of effective cross-protective vaccines and highlights the need for additional surveillance.

Molecular diagnostics of swine infection caused by Mycoplasma suis

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Potkonjak Aleksandar

2009-01-01

Full Text Available The presence of two types of haemoplasm can be established in the swine population. Pathogenic haemoplasm, named Mycoplasma suis (previously called Eperythrozoon suis is the cause of swine eperythrozoonosis or swine ichtheroanaemia. The cause of this disease can also infect humans. The disease has spread all over the world. The most frequent form is latent infection of swine caused by M. suis. The disease is clinically manifest following action by the stress factor. The acute course of the disease is characterized by the occurrence of a febrile condition and ichtheroanaemia. The disease is usually diagnosed based on an epizootiological poll, a clinical examination, and a microscopic examination of a blood smear stained most often according to Giemsa. Contemporary methods of molecular biology have been developed, such as PCR, which are more sensitive and specific in making a diagnosis of swine infection caused by M. suis. In these investigations, the presence of M. suis on pig farms in the Republic of Serbia has been determined using the PCR test. .

Anaerobic digestion of swine manure: Inhibition by ammonia

DEFF Research Database (Denmark)

Hansen, Kaare Hvid; Angelidaki, Irini; Ahring, Birgitte Kiær

1998-01-01

A stable anaerobic degradation of swine manure with ammonia concentration of 6 g-N/litre was obtained in continuously stirred tank reactors with a hydraulic retention time of 15 days, at Four different temperatures. Methane yields of 188, 141, 67 and 22 ml-CH4/g-VS were obtained at 37, 45, 55...... and 60 degrees C, respectively. The yields were significantly lower than the potential biogas yield of the swine manure used (300 ml-CH4/g-VS). A free ammonia concentration of 1.1 g-N/litre or more was found to cause inhibition in batch cultures at pH 8.0 (reactor pH), and higher free ammonia...... concentrations resulted in a decreased apparent specific growth rate. Batch experiments with various mixtures of swine and cattle manure showed that the biogas process was inhibited when the swine-to-cattle manure ratio was higher than 25:75, corresponding to a free ammonia concentration of approximately 1.1 g...

Overview of Classical Swine Fever (Hog Cholera, Classical Swine fever)

Science.gov (United States)

Classical swine fever is a contagious often fatal disease of pigs clinically characterized by high body temperature, lethargy, yellowish diarrhea, vomits and purple skin discoloration of ears, lower abdomen and legs. It was first described in the early 19th century in the USA. Later, a condition i...

A mutation in the mitochondrial fission gene Dnm1l leads to cardiomyopathy.

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Houman Ashrafian

2010-06-01

Full Text Available Mutations in a number of genes have been linked to inherited dilated cardiomyopathy (DCM. However, such mutations account for only a small proportion of the clinical cases emphasising the need for alternative discovery approaches to uncovering novel pathogenic mutations in hitherto unidentified pathways. Accordingly, as part of a large-scale N-ethyl-N-nitrosourea mutagenesis screen, we identified a mouse mutant, Python, which develops DCM. We demonstrate that the Python phenotype is attributable to a dominant fully penetrant mutation in the dynamin-1-like (Dnm1l gene, which has been shown to be critical for mitochondrial fission. The C452F mutation is in a highly conserved region of the M domain of Dnm1l that alters protein interactions in a yeast two-hybrid system, suggesting that the mutation might alter intramolecular interactions within the Dnm1l monomer. Heterozygous Python fibroblasts exhibit abnormal mitochondria and peroxisomes. Homozygosity for the mutation results in the death of embryos midway though gestation. Heterozygous Python hearts show reduced levels of mitochondria enzyme complexes and suffer from cardiac ATP depletion. The resulting energy deficiency may contribute to cardiomyopathy. This is the first demonstration that a defect in a gene involved in mitochondrial remodelling can result in cardiomyopathy, showing that the function of this gene is needed for the maintenance of normal cellular function in a relatively tissue-specific manner. This disease model attests to the importance of mitochondrial remodelling in the heart; similar defects might underlie human heart muscle disease.

Mitochondrial miRNA (MitomiR): a new player in cardiovascular health.

Science.gov (United States)

Srinivasan, Hemalatha; Das, Samarjit

2015-10-01

Cardiovascular disease is one of the major causes of human morbidity and mortality in the world. MicroRNAs (miRNAs) are small RNAs that regulate gene expression and are known to be involved in the pathogenesis of heart diseases, but the translocation phenomenon and the mode of action in mitochondria are largely unknown. Recent mitochondrial proteome analysis unveiled at least 2000 proteins, of which only 13 are made by the mitochondrial genome. There are numerous studies demonstrating the translocation of proteins into the mitochondria and also translocation of ribosomal RNA (viz., 5S rRNA) into mitochondria. Recent studies have suggested that miRNAs contain sequence elements that affect their subcellular localization, particularly nuclear localization. If there are sequence elements that direct miRNAs to the nucleus, it is also possible that similar sequence elements exist to direct miRNAs to the mitochondria. In this review we have summarized most of the miRNAs that have been shown to play an important role in mitochondrial function, either by regulating mitochondrial genes or by regulating nuclear genes that are known to influence mitochondrial function. While the focus of this review is cardiovascular diseases, we also illustrate the role of mitochondrial miRNA (MitomiR) in the initiation and progression of various diseases, including cardiovascular diseases, metabolic diseases, and cancer. Our goal here is to summarize the miRNAs that are localized to the mitochondrial fraction of cells, and how these miRNAs modulate cardiovascular health.

Increased intrinsic mitochondrial function in humans with mitochondrial haplogroup H

DEFF Research Database (Denmark)

Larsen, Steen; Díez-Sánchez, Carmen; Rabøl, Rasmus

2014-01-01

and determined their mitochondrial haplogroup, mitochondrial oxidative phosphorylation capacity (OXPHOS), mitochondrial content (citrate synthase (CS)) and VO2max. Intrinsic mitochondrial function is calculated as mitochondrial OXPHOS capacity divided by mitochondrial content (CS). Haplogroup H showed a 30......% higher intrinsic mitochondrial function compared with the other haplo group U. There was no relationship between haplogroups and VO2max. In skeletal muscle from men with mitochondrial haplogroup H, an increased intrinsic mitochondrial function is present....

Influenza A Viruses of Human Origin in Swine, Brazil

Science.gov (United States)

Schaefer, Rejane; Gava, Danielle; Cantão, Maurício Egídio; Ciacci-Zanella, Janice Reis

2015-01-01

The evolutionary origins of the influenza A(H1N1)pdm09 virus that caused the first outbreak of the 2009 pandemic in Mexico remain unclear, highlighting the lack of swine surveillance in Latin American countries. Although Brazil has one of the largest swine populations in the world, influenza was not thought to be endemic in Brazil’s swine until the major outbreaks of influenza A(H1N1)pdm09 in 2009. Through phylogenetic analysis of whole-genome sequences of influenza viruses of the H1N1, H1N2, and H3N2 subtypes collected in swine in Brazil during 2009–2012, we identified multiple previously uncharacterized influenza viruses of human seasonal H1N2 and H3N2 virus origin that have circulated undetected in swine for more than a decade. Viral diversity has further increased in Brazil through reassortment between co-circulating viruses, including A(H1N1)pdm09. The circulation of multiple divergent hemagglutinin lineages challenges the design of effective cross-protective vaccines and highlights the need for additional surveillance. PMID:26196759

Swine farm wastewater and mineral fertilization in corn cultivation

Directory of Open Access Journals (Sweden)

Pâmela A. M. Pereira

2016-01-01

Full Text Available ABSTRACT In the long run, swine wastewater can provide benefits to the soil-plant relationship, when its use is planned and the potential environmental impacts are monitored. The objective of this study was to investigate the effects of continuous application of swine wastewater, associated with mineral fertilization, after six years of management in no-tillage and crop rotation (14 production cycles, on the chemical conditions of the soil and the corn crop. The doses of wastewater were 0, 100, 200, 300 m3 ha-1 during the cycle. The effects of the association between mineral fertilization at sowing and swine wastewater were evaluated simultaneously. Swine wastewater at the dose of 100 m3 ha-1 promoted availability and absorption of P, K+, Mg2+ and Zn2+ without causing toxicity to plants or damage to the soil, constituting a viable, low-cost alternative of water reuse and fertilization for farmers. The nutrients N, P, K+ and B must be complemented with mineral fertilization. Special attention should be directed to the accumulation of Zn2+ in the soil along the time of swine wastewater application.

Heart tissue of harlequin (hq)/Big Blue mice has elevated reactive oxygen species without significant impact on the frequency and nature of point mutations in nuclear DNA

Energy Technology Data Exchange (ETDEWEB)

Crabbe, Rory A. [Department of Biology, University of Western Ontario, London, Ontario, N6A 5B7 (Canada); Hill, Kathleen A., E-mail: khill22@uwo.ca [Department of Biology, University of Western Ontario, London, Ontario, N6A 5B7 (Canada)

2010-09-10

Age is a major risk factor for heart disease, and cardiac aging is characterized by elevated mitochondrial reactive oxygen species (ROS) with compromised mitochondrial and nuclear DNA integrity. To assess links between increased ROS levels and mutations, we examined in situ levels of ROS and cII mutation frequency, pattern and spectrum in the heart of harlequin (hq)/Big Blue mice. The hq mouse is a model of premature aging with mitochondrial dysfunction and increased risk of oxidative stress-induced heart disease with the means for in vivo mutation detection. The hq mutation produces a significant downregulation in the X-linked apoptosis-inducing factor gene (Aif) impairing both the antioxidant and oxidative phosphorylation functions of AIF. Brain and skin of hq disease mice have elevated frequencies of point mutations in nuclear DNA and histopathology characterized by cell loss. Reports of associated elevations in ROS in brain and skin have mixed results. Herein, heart in situ ROS levels were elevated in hq disease compared to AIF-proficient mice (p < 0.0001) yet, mutation frequency and pattern were similar in hq disease, hq carrier and AIF-proficient mice. Heart cII mutations were also assessed 15 days following an acute exposure to an exogenous ROS inducer (10 mg paraquat/kg). Acute paraquat exposure with a short mutant manifestation period was insufficient to elevate mutation frequency or alter mutation pattern in the post-mitotic heart tissue of AIF-proficient mice. Paraquat induction of ROS requires mitochondrial complex I and thus is likely compromised in hq mice. Results of this preliminary survey and the context of recent literature suggest that determining causal links between AIF deficiency and the premature aging phenotypes of specific tissues is better addressed with assay of mitochondrial ROS and large-scale changes in mitochondrial DNA in specific cell types.

Heart tissue of harlequin (hq)/Big Blue mice has elevated reactive oxygen species without significant impact on the frequency and nature of point mutations in nuclear DNA

International Nuclear Information System (INIS)

Crabbe, Rory A.; Hill, Kathleen A.

2010-01-01

Age is a major risk factor for heart disease, and cardiac aging is characterized by elevated mitochondrial reactive oxygen species (ROS) with compromised mitochondrial and nuclear DNA integrity. To assess links between increased ROS levels and mutations, we examined in situ levels of ROS and cII mutation frequency, pattern and spectrum in the heart of harlequin (hq)/Big Blue mice. The hq mouse is a model of premature aging with mitochondrial dysfunction and increased risk of oxidative stress-induced heart disease with the means for in vivo mutation detection. The hq mutation produces a significant downregulation in the X-linked apoptosis-inducing factor gene (Aif) impairing both the antioxidant and oxidative phosphorylation functions of AIF. Brain and skin of hq disease mice have elevated frequencies of point mutations in nuclear DNA and histopathology characterized by cell loss. Reports of associated elevations in ROS in brain and skin have mixed results. Herein, heart in situ ROS levels were elevated in hq disease compared to AIF-proficient mice (p < 0.0001) yet, mutation frequency and pattern were similar in hq disease, hq carrier and AIF-proficient mice. Heart cII mutations were also assessed 15 days following an acute exposure to an exogenous ROS inducer (10 mg paraquat/kg). Acute paraquat exposure with a short mutant manifestation period was insufficient to elevate mutation frequency or alter mutation pattern in the post-mitotic heart tissue of AIF-proficient mice. Paraquat induction of ROS requires mitochondrial complex I and thus is likely compromised in hq mice. Results of this preliminary survey and the context of recent literature suggest that determining causal links between AIF deficiency and the premature aging phenotypes of specific tissues is better addressed with assay of mitochondrial ROS and large-scale changes in mitochondrial DNA in specific cell types.

Accurate quantification of mouse mitochondrial DNA without co-amplification of nuclear mitochondrial insertion sequences.

Science.gov (United States)

Malik, Afshan N; Czajka, Anna; Cunningham, Phil

2016-07-01

Mitochondria contain an extra-nuclear genome in the form of mitochondrial DNA (MtDNA), damage to which can lead to inflammation and bioenergetic deficit. Changes in MtDNA levels are increasingly used as a biomarker of mitochondrial dysfunction. We previously reported that in humans, fragments in the nuclear genome known as nuclear mitochondrial insertion sequences (NumtS) affect accurate quantification of MtDNA. In the current paper our aim was to determine whether mouse NumtS affect the quantification of MtDNA and to establish a method designed to avoid this. The existence of NumtS in the mouse genome was confirmed using blast N, unique MtDNA regions were identified using FASTA, and MtDNA primers which do not co-amplify NumtS were designed and tested. MtDNA copy numbers were determined in a range of mouse tissues as the ratio of the mitochondrial and nuclear genome using real time qPCR and absolute quantification. Approximately 95% of mouse MtDNA was duplicated in the nuclear genome as NumtS which were located in 15 out of 21 chromosomes. A unique region was identified and primers flanking this region were used. MtDNA levels differed significantly in mouse tissues being the highest in the heart, with levels in descending order (highest to lowest) in kidney, liver, blood, brain, islets and lung. The presence of NumtS in the nuclear genome of mouse could lead to erroneous data when studying MtDNA content or mutation. The unique primers described here will allow accurate quantification of MtDNA content in mouse models without co-amplification of NumtS. Copyright © 2016 Elsevier B.V. and Mitochondria Research Society. All rights reserved.

Modeling the mitochondrial cardiomyopathy of Barth syndrome with induced pluripotent stem cell and heart-on-chip technologies

NARCIS (Netherlands)

Wang, Gang; McCain, Megan L.; Yang, Luhan; He, Aibin; Pasqualini, Francesco Silvio; Agarwal, Ashutosh; Yuan, Hongyan; Jiang, Dawei; Zhang, Donghui; Zangi, Lior; Geva, Judith; Roberts, Amy E.; Ma, Qing; Ding, Jian; Chen, Jinghai; Wang, Da-Zhi; Li, Kai; Wang, Jiwu; Wanders, Ronald J. A.; Kulik, Wim; Vaz, Frédéric M.; Laflamme, Michael A.; Murry, Charles E.; Chien, Kenneth R.; Kelley, Richard I.; Church, George M.; Parker, Kevin Kit; Pu, William T.

2014-01-01

Study of monogenic mitochondrial cardiomyopathies may yield insights into mitochondrial roles in cardiac development and disease. Here, we combined patient-derived and genetically engineered induced pluripotent stem cells (iPSCs) with tissue engineering to elucidate the pathophysiology underlying

Radiation inactivation method provides evidence that membrane-bound mitochondrial creatine kinase is an oligomer

International Nuclear Information System (INIS)

Quemeneur, E.; Eichenberger, D.; Goldschmidt, D.; Vial, C.; Beauregard, G.; Potier, M.

1988-01-01

Lyophilized suspensions of rabbit heart mitochondria have been irradiated with varying doses of gamma rays. Mitochondrial creatine kinase activity was inactivated exponentially with a radiation inactivation size of 352 or 377 kDa depending upon the initial medium. These values are in good agreement with the molecular mass previously deduced from by permeation experiments: 357 kDa. This is the first direct evidence showing that the native form of mitochondrial creatine kinase is associated to the inner membrane as an oligomer, very likely an octamer

A heart that beats for 500 years: age-related changes in cardiac proteasome activity, oxidative protein damage and expression of heat shock proteins, inflammatory factors, and mitochondrial complexes in Arctica islandica, the longest-living noncolonial animal.

Science.gov (United States)

Sosnowska, Danuta; Richardson, Chris; Sonntag, William E; Csiszar, Anna; Ungvari, Zoltan; Ridgway, Iain

2014-12-01

Study of negligibly senescent animals may provide clues that lead to better understanding of the cardiac aging process. To elucidate mechanisms of successful cardiac aging, we investigated age-related changes in proteasome activity, oxidative protein damage and expression of heat shock proteins, inflammatory factors, and mitochondrial complexes in the heart of the ocean quahog Arctica islandica, the longest-lived noncolonial animal (maximum life span potential: 508 years). We found that in the heart of A. islandica the level of oxidatively damaged proteins did not change significantly up to 120 years of age. No significant aging-induced changes were observed in caspase-like and trypsin-like proteasome activity. Chymotrypsin-like proteasome activity showed a significant early-life decline, then it remained stable for up to 182 years. No significant relationship was observed between the extent of protein ubiquitination and age. In the heart of A. islandica, an early-life decline in expression of HSP90 and five mitochondrial electron transport chain complexes was observed. We found significant age-related increases in the expression of three cytokine-like mediators (interleukin-6, interleukin-1β, and tumor necrosis factor-α) in the heart of A. islandica. Collectively, in extremely long-lived molluscs, maintenance of protein homeostasis likely contributes to the preservation of cardiac function. Our data also support the concept that low-grade chronic inflammation in the cardiovascular system is a universal feature of the aging process, which is also manifest in invertebrates. © The Author 2013. Published by Oxford University Press on behalf of The Gerontological Society of America. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.

Mitochondrial Disease

OpenAIRE

Bulent Kurt; Turgut Topal

2013-01-01

Mitochondria are the major energy source of cells. Mitochondrial disease occurs due to a defect in mitochondrial energy production. A valuable energy production in mitochondria depend a healthy interconnection between nuclear and mitochondrial DNA. A mutation in nuclear or mitochondrial DNA may cause abnormalities in ATP production and single or multiple organ dysfunctions, secondarily. In this review, we summarize mitochondrial physiology, mitochondrial genetics, and clinical expression and ...

A case of mitochondrial cardiomyopathy with restrictive transmitral filling pattern

Directory of Open Access Journals (Sweden)

Otsui K

2012-04-01

Full Text Available Kazunori Otsui, Nobutaka Inoue, Anna Tamagawa, Kazuo OnishiDepartment of Cardiovascular Medicine, Kobe Rosai Hospital, Kobe, JapanAbstract: A 61-year-old diabetic woman with a mitochondrial A3243G mutation was hospitalized for evaluation of breathlessness, general fatigue, and leg edema. Chest radiography revealed cardiomegaly with massive pleural effusion. Serum lactate, pyruvate, and brain natriuretic peptide concentrations were elevated. Transthoracic echocardiography revealed a restrictive pattern of transmitral flow, although systolic function of the left ventricle was only mildly impaired. Based on these findings and her clinical course, the patient was diagnosed with right-sided heart failure caused by mitochondrial cardiomyopathy associated with a restrictive transmitral filling pattern. Treatment with furosemide, enalapril, and eplerenone was effective, and improvement in her symptoms was associated with amelioration of transthoracic echocardiographic findings and a reduction in serum brain natriuretic peptide levels. Previous reports have indicated heterogeneity in the clinical features of mitochondrial cardiomyopathy in patients carrying the A3243G mutation; the present case highlights the substantial variability in the clinical features of this disease.Keywords: mitochondrial disease, A3243G mutation, diastolic dysfunction, transmitral flow

Reverse zoonosis of influenza to swine: new perspectives on the human-animal interface.

Science.gov (United States)

Nelson, Martha I; Vincent, Amy L

2015-03-01

The origins of the 2009 influenza A (H1N1) pandemic in swine are unknown, highlighting gaps in our understanding of influenza A virus (IAV) ecology and evolution. We review how recently strengthened influenza virus surveillance in pigs has revealed that influenza virus transmission from humans to swine is far more frequent than swine-to-human zoonosis, and is central in seeding swine globally with new viral diversity. The scale of global human-to-swine transmission represents the largest 'reverse zoonosis' of a pathogen documented to date. Overcoming the bias towards perceiving swine as sources of human viruses, rather than recipients, is key to understanding how the bidirectional nature of the human-animal interface produces influenza threats to both hosts. Published by Elsevier Ltd.

African Swine Fever Virus Biology and Vaccine Approaches.

Science.gov (United States)

Revilla, Yolanda; Pérez-Núñez, Daniel; Richt, Juergen A

2018-01-01

African swine fever (ASF) is an acute and often fatal disease affecting domestic pigs and wild boar, with severe economic consequences for affected countries. ASF is endemic in sub-Saharan Africa and the island of Sardinia, Italy. Since 2007, the virus emerged in the republic of Georgia, and since then spread throughout the Caucasus region and Russia. Outbreaks have also been reported in Belarus, Ukraine, Lithuania, Latvia, Estonia, Romania, Moldova, Czech Republic, and Poland, threatening neighboring West European countries. The causative agent, the African swine fever virus (ASFV), is a large, enveloped, double-stranded DNA virus that enters the cell by macropinocytosis and a clathrin-dependent mechanism. African Swine Fever Virus is able to interfere with various cellular signaling pathways resulting in immunomodulation, thus making the development of an efficacious vaccine very challenging. Inactivated preparations of African Swine Fever Virus do not confer protection, and the role of antibodies in protection remains unclear. The use of live-attenuated vaccines, although rendering suitable levels of protection, presents difficulties due to safety and side effects in the vaccinated animals. Several African Swine Fever Virus proteins have been reported to induce neutralizing antibodies in immunized pigs, and vaccination strategies based on DNA vaccines and recombinant proteins have also been explored, however, without being very successful. The complexity of the virus particle and the ability of the virus to modulate host immune responses are most likely the reason for this failure. Furthermore, no permanent cell lines able to sustain productive virus infection by both virulent and naturally attenuated African Swine Fever Virus strains exist so far, thus impairing basic research and the commercial production of attenuated vaccine candidates. © 2018 Elsevier Inc. All rights reserved.

Effect of Irradiated Yeast Fermented Cassava on Performance of Starter and Growing Swine

International Nuclear Information System (INIS)

Khammeng, Terdsak; Sanchisuriya, Pitcharat; Nontaso, Ngarmnit; Piadang, Nattayana

2006-09-01

The objective of this study was to evaluate the effect of a supplementation of fermented cassava with Saccharomyces sp. KKU.1 on the swine diet. The fermented products were added in the rat in at 0, 3, 6, and 9%, respectively. Thirty-two (4 week-old) crossbreed swine (Large white x Land race x Duroc) were randomly allotted according to Completely Randomize Design in two periods. Four dietary treatments and four replications (1 male and 1 female) were tested in the starting swine. Four dietary treatments and two replications (2 male and 2 female) were tested in the growing swine. The swine were tested for 6 week (August 2006-September 2006) at the swine unit, Deparment of Animal Science, Khon Kaen University. The results revealed that the fermented cassava in the diet had no affect (P>0.05) on productive performance (growth rate and feed conversion ratio) of swine in both periods.

Effect of desferrioxamine on reperfusion damage of rat heart ...

African Journals Online (AJOL)

1990-09-01

Sep 1, 1990 ... ... deferrioxamine on rat heart mitochondrial oxidative phosphorylation after normothermic ischemic cardiac arrest and of reperfusion. Res Commun Chem Pathol Pharmacol 1988;. 62: 419-434. IL Sordahl LA, Johnson C, Blailock ZR. Schwartz A. The mitochondrion. Mechods Phannacol1971; 1: 247-286.

Effect of exercise training intensity on mitochondrial dynamics and mitophagy in post myocardial infarction rats

Directory of Open Access Journals (Sweden)

Babak Ebadi

2018-06-01

Full Text Available Myocardial infarction (MI is the most common type of heart disease. According to recent studies, mitochondrial dysfunction has been suggested as a central player in cardiac disease and evidences point out the association of mitochondrial morphology with development of heart diseases. Exercise training plays a protective role against cardiovascular disease. However, the role of exercise training on proteins involved in mitochondrial dynamics and mitophagy system are not well understood. Therefore, the aim of the present study was to investigate these on cardiac mitochondrial dynamic and mitophagy proteins in rats with myocardial infarction. The present study was post-test design experiment with the control group. after MI with ligation of the left anterior descending coronary artery (LAD and ensuring the creation of MI by echocardiography, male rats were subjected to high intensity interval training (HIIT, moderate (MIIT, low (LIIT, sedentary myocardial infarction (SED-MI and healthy control groups. After six weeks exercise, the levels of MFN2, DRP1, Parkin, P62 and PGC-1α proteins were measured by ELISA method. Data analysis showed that proteins levels of MFN2, PGC-1α, Parkin and P62 decreased significantly in SED-MI group compared to healthy control while DRP1 protein levels increased significantly (P≤0.05. Also, MFN2 and PGC-1α proteins increased in MIIT group compared with SED-MI group and DRP1 protein levels were significantly decreased (P≤0.05. Moderate-intensity interval training (MIIT resulted to improve mitochondrial fusion and fusion proteins in rats with myocardial infarction. While high and low intensity interval training (HIIT, LIIT, despite increasing MFN2 and PGC-1α and reducing DRP1, failed to improve fusion and mitochondrial fission

Mitochondrial Dynamics: Coupling Mitochondrial Fitness with Healthy Aging.

Science.gov (United States)

Sebastián, David; Palacín, Manuel; Zorzano, Antonio

2017-03-01

Aging is associated with a decline in mitochondrial function and the accumulation of abnormal mitochondria. However, the precise mechanisms by which aging promotes these mitochondrial alterations and the role of the latter in aging are still not fully understood. Mitochondrial dynamics is a key process regulating mitochondrial function and quality. Altered expression of some mitochondrial dynamics proteins has been recently associated with aging and with age-related alterations in yeast, Caenorhabditis elegans, mice, and humans. Here, we review the link between alterations in mitochondrial dynamics, aging, and age-related impairment. We propose that the dysregulation of mitochondrial dynamics leads to age-induced accumulation of unhealthy mitochondria and contributes to alterations linked to aging, such as diabetes and neurodegeneration. Copyright © 2017 Elsevier Ltd. All rights reserved.

A reaction-diffusion model of ROS-induced ROS release in a mitochondrial network.

Directory of Open Access Journals (Sweden)

Lufang Zhou

2010-01-01

Full Text Available Loss of mitochondrial function is a fundamental determinant of cell injury and death. In heart cells under metabolic stress, we have previously described how the abrupt collapse or oscillation of the mitochondrial energy state is synchronized across the mitochondrial network by local interactions dependent upon reactive oxygen species (ROS. Here, we develop a mathematical model of ROS-induced ROS release (RIRR based on reaction-diffusion (RD-RIRR in one- and two-dimensional mitochondrial networks. The nodes of the RD-RIRR network are comprised of models of individual mitochondria that include a mechanism of ROS-dependent oscillation based on the interplay between ROS production, transport, and scavenging; and incorporating the tricarboxylic acid (TCA cycle, oxidative phosphorylation, and Ca(2+ handling. Local mitochondrial interaction is mediated by superoxide (O2.- diffusion and the O2.(--dependent activation of an inner membrane anion channel (IMAC. In a 2D network composed of 500 mitochondria, model simulations reveal DeltaPsi(m depolarization waves similar to those observed when isolated guinea pig cardiomyocytes are subjected to a localized laser-flash or antioxidant depletion. The sensitivity of the propagation rate of the depolarization wave to O(2.- diffusion, production, and scavenging in the reaction-diffusion model is similar to that observed experimentally. In addition, we present novel experimental evidence, obtained in permeabilized cardiomyocytes, confirming that DeltaPsi(m depolarization is mediated specifically by O2.-. The present work demonstrates that the observed emergent macroscopic properties of the mitochondrial network can be reproduced in a reaction-diffusion model of RIRR. Moreover, the findings have uncovered a novel aspect of the synchronization mechanism, which is that clusters of mitochondria that are oscillating can entrain mitochondria that would otherwise display stable dynamics. The work identifies the

Mitochondrial Cyclophilin D in Vascular Oxidative Stress and Hypertension.

Science.gov (United States)

Itani, Hana A; Dikalova, Anna E; McMaster, William G; Nazarewicz, Rafal R; Bikineyeva, Alfiya T; Harrison, David G; Dikalov, Sergey I

2016-06-01

Vascular superoxide (O˙2 (-)) and inflammation contribute to hypertension. The mitochondria are an important source of O˙2 (-); however, the regulation of mitochondrial O˙2 (-) and the antihypertensive potential of targeting the mitochondria remain poorly defined. Angiotensin II and inflammatory cytokines, such as interleukin 17A and tumor necrosis factor-α (TNFα) significantly contribute to hypertension. We hypothesized that angiotensin II and cytokines co-operatively induce cyclophilin D (CypD)-dependent mitochondrial O˙2 (-) production in hypertension. We tested whether CypD inhibition attenuates endothelial oxidative stress and reduces hypertension. CypD depletion in CypD(-/-) mice prevents overproduction of mitochondrial O˙2 (-) in angiotensin II-infused mice, attenuates hypertension by 20 mm Hg, and improves vascular relaxation compared with wild-type C57Bl/6J mice. Treatment of hypertensive mice with the specific CypD inhibitor Sanglifehrin A reduces blood pressure by 28 mm Hg, inhibits production of mitochondrial O˙2 (-) by 40%, and improves vascular relaxation. Angiotensin II-induced hypertension was associated with CypD redox activation by S-glutathionylation, and expression of the mitochondria-targeted H2O2 scavenger, catalase, abolished CypD S-glutathionylation, prevented stimulation mitochondrial O˙2 (-), and attenuated hypertension. The functional role of cytokine-angiotensin II interplay was confirmed by co-operative stimulation of mitochondrial O˙2 (-) by 3-fold in cultured endothelial cells and impairment of aortic relaxation incubated with combination of angiotensin II, interleukin 17A, and tumor necrosis factor-α which was prevented by CypD depletion or expression of mitochondria-targeted SOD2 and catalase. These data support a novel role of CypD in hypertension and demonstrate that targeting CypD decreases mitochondrial O˙2 (-), improves vascular relaxation, and reduces hypertension. © 2016 American Heart Association, Inc.

Volatile organic compounds at swine facilities: a critical review.

Science.gov (United States)

Ni, Ji-Qin; Robarge, Wayne P; Xiao, Changhe; Heber, Albert J

2012-10-01

Volatile organic compounds (VOCs) are regulated aerial pollutants that have environmental and health concerns. Swine operations produce and emit a complex mixture of VOCs with a wide range of molecular weights and a variety of physicochemical properties. Significant progress has been made in this area since the first experiment on VOCs at a swine facility in the early 1960s. A total of 47 research institutions in 15 North American, European, and Asian countries contributed to an increasing number of scientific publications. Nearly half of the research papers were published by U.S. institutions. Investigated major VOC sources included air inside swine barns, in headspaces of manure storages and composts, in open atmosphere above swine wastewater, and surrounding swine farms. They also included liquid swine manure and wastewater, and dusts inside and outside swine barns. Most of the sample analyses have been focusing on identification of VOC compounds and their relationship with odors. More than 500 VOCs have been identified. About 60% and 10% of the studies contributed to the quantification of VOC concentrations and emissions, respectively. The largest numbers of VOC compounds with reported concentrations in a single experimental study were 82 in air, 36 in manure, and 34 in dust samples. The relatively abundant VOC compounds that were quantified in at least two independent studies included acetic acid, butanoic acid (butyric acid), dimethyl disulfide, dimethyl sulfide, iso-valeric, p-cresol, propionic acid, skatole, trimethyl amine, and valeric acid in air. They included acetic acid, p-cresol, iso-butyric acid, butyric acid, indole, phenol, propionic acid, iso-valeric acid, and skatole in manure. In dust samples, they were acetic acid, propionic acid, butyric acid, valeric acid, p-cresol, hexanal, and decanal. Swine facility VOCs were preferentially bound to smaller-size dusts. Identification and quantification of VOCs were restricted by using instruments based on

Selective replacement of mitochondrial DNA increases the cardioprotective effect of chronic continuous hypoxia in spontaneously hypertensive rats

Czech Academy of Sciences Publication Activity Database

Neckář, Jan; Svatoňová, Anna; Weissová, Romana; Drahota, Zdeněk; Zajíčková, Pavlína; Brabcová, I.; Kolář, D.; Alánová, Petra; Vašinová, Jana; Šilhavý, Jan; Hlaváčková, Markéta; Tauchmannová, Kateřina; Milerová, Marie; Ošťádal, Bohuslav; Červenka, L.; Žurmanová, J.; Kalous, M.; Nováková, Olga; Novotný, J.; Pravenec, Michal; Kolář, František

2017-01-01

Roč. 131, č. 9 (2017), s. 865-881 ISSN 0143-5221 R&D Projects: GA ČR(CZ) GA13-10267S; GA ČR(CZ) GB14-36804G; GA MŠk(CZ) LL1204 Institutional support: RVO:67985823 Keywords : chronic hypoxia * heart * hypertension * ischaemia–reperfusion injury * mitochondrial genome * mitochondrial permeability transition pore Subject RIV: FA - Cardiovascular Diseases incl. Cardiotharic Surgery OBOR OECD: Physiology (including cytology) Impact factor: 4.936, year: 2016

Mitochondria and ageing: role in heart, skeletal muscle and adipose tissue

Science.gov (United States)

Boengler, Kerstin; Kosiol, Maik; Mayr, Manuel; Schulz, Rainer

2017-01-01

Abstract Age is the most important risk factor for most diseases. Mitochondria play a central role in bioenergetics and metabolism. In addition, several lines of evidence indicate the impact of mitochondria in lifespan determination and ageing. The best‐known hypothesis to explain ageing is the free radical theory, which proposes that cells, organs, and organisms age because they accumulate reactive oxygen species (ROS) damage over time. Mitochondria play a central role as the principle source of intracellular ROS, which are mainly formed at the level of complex I and III of the respiratory chain. Dysfunctional mitochondria generating less ATP have been observed in various aged organs. Mitochondrial dysfunction comprises different features including reduced mitochondrial content, altered mitochondrial morphology, reduced activity of the complexes of the electron transport chain, opening of the mitochondrial permeability transition pore, and increased ROS formation. Furthermore, abnormalities in mitochondrial quality control or defects in mitochondrial dynamics have also been linked to senescence. Among the tissues affected by mitochondrial dysfunction are those with a high‐energy demand and thus high mitochondrial content. Therefore, the present review focuses on the impact of mitochondria in the ageing process of heart and skeletal muscle. In this article, we review different aspects of mitochondrial dysfunction and discuss potential therapeutic strategies to improve mitochondrial function. Finally, novel aspects of adipose tissue biology and their involvement in the ageing process are discussed. PMID:28432755

Increased Heme Levels in the Heart Lead to Exacerbated Ischemic Injury.

Science.gov (United States)

Sawicki, Konrad Teodor; Shang, Meng; Wu, Rongxue; Chang, Hsiang-Chun; Khechaduri, Arineh; Sato, Tatsuya; Kamide, Christine; Liu, Ting; Naga Prasad, Sathyamangla V; Ardehali, Hossein

2015-07-31

Heme is an essential iron-containing molecule for cardiovascular physiology, but in excess it may increase oxidative stress. Failing human hearts have increased heme levels, with upregulation of the rate-limiting enzyme in heme synthesis, δ-aminolevulinic acid synthase 2 (ALAS2), which is normally not expressed in cardiomyocytes. We hypothesized that increased heme accumulation (through cardiac overexpression of ALAS2) leads to increased oxidative stress and cell death in the heart. We first showed that ALAS2 and heme levels are increased in the hearts of mice subjected to coronary ligation. To determine the causative role of increased heme in the development of heart failure, we generated transgenic mice with cardiac-specific overexpression of ALAS2. While ALAS2 transgenic mice have normal cardiac function at baseline, their hearts display increased heme content, higher oxidative stress, exacerbated cell death, and worsened cardiac function after coronary ligation compared to nontransgenic littermates. We confirmed in cultured cardiomyoblasts that the increased oxidative stress and cell death observed with ALAS2 overexpression is mediated by increased heme accumulation. Furthermore, knockdown of ALAS2 in cultured cardiomyoblasts exposed to hypoxia reversed the increases in heme content and cell death. Administration of the mitochondrial antioxidant MitoTempo to ALAS2-overexpressing cardiomyoblasts normalized the elevated oxidative stress and cell death levels to baseline, indicating that the effects of increased ALAS2 and heme are through elevated mitochondrial oxidative stress. The clinical relevance of these findings was supported by the finding of increased ALAS2 induction and heme accumulation in failing human hearts from patients with ischemic cardiomyopathy compared to nonischemic cardiomyopathy. Heme accumulation is detrimental to cardiac function under ischemic conditions, and reducing heme in the heart may be a novel approach for protection against the

H1N1 influenza viruses varying widely in hemagglutinin stability transmit efficiently from swine to swine and to ferrets.

Directory of Open Access Journals (Sweden)

Marion Russier

2017-03-01

Full Text Available A pandemic-capable influenza virus requires a hemagglutinin (HA surface glycoprotein that is immunologically unseen by most people and is capable of supporting replication and transmission in humans. HA stabilization has been linked to 2009 pH1N1 pandemic potential in humans and H5N1 airborne transmissibility in the ferret model. Swine have served as an intermediate host for zoonotic influenza viruses, yet the evolutionary pressure exerted by this host on HA stability was unknown. For over 70 contemporary swine H1 and H3 isolates, we measured HA activation pH to range from pH 5.1 to 5.9 for H1 viruses and pH 5.3 to 5.8 for H3 viruses. Thus, contemporary swine isolates vary widely in HA stability, having values favored by both avian (pH >5.5 and human and ferret (pH ≤5.5 species. Using an early 2009 pandemic H1N1 (pH1N1 virus backbone, we generated three viruses differing by one HA residue that only altered HA stability: WT (pH 5.5, HA1-Y17H (pH 6.0, and HA2-R106K (pH 5.3. All three replicated in pigs and transmitted from pig-to-pig and pig-to-ferret. WT and R106 viruses maintained HA genotype and phenotype after transmission. Y17H (pH 6.0 acquired HA mutations that stabilized the HA protein to pH 5.8 after transmission to pigs and 5.5 after transmission to ferrets. Overall, we found swine support a broad range of HA activation pH for contact transmission and many recent swine H1N1 and H3N2 isolates have stabilized (human-like HA proteins. This constitutes a heightened pandemic risk and underscores the importance of ongoing surveillance and control efforts for swine viruses.

Cardiac abnormalities in diabetic patients with mutation in the mitochondrial tRNA {sup Leu(UUR)}Gene

Energy Technology Data Exchange (ETDEWEB)

Ueno, Hiroshi [Hyogo Medical Center for Adults, Akashi (Japan); Shiotani, Hideyuki

1999-11-01

An A-to-G transition at position 3243 of the mitochondrial DNA is known to be a pathogenic factor for mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS), diabetes and cardiomyopathy. This mutation causes dysfunction of the central nervous system in MELAS. Because the heart, as well as the brain and nervous system, is highly dependent on the energy produced by mitochondrial oxidation, these tissues are more vulnerable to mitochondrial defects. Cardiac abnormalities were assessed in 10 diabetic patients associated with this mutation using echocardiography and {sup 123}I-metaiodobenzylguanidine (MIBG) scintigraphy, and compared with 19 diabetic patients without the mutation. Duration of diabetes, therapy, control of blood glucose and diabetic complications, such as diabetic retinopathy and nephropathy, were not different between the 2 groups. Diabetic patients with the mutation had a significantly thicker interventricular septum (16.8{+-}3.7 vs 11.0{+-}1.6 mm, p<0.001) than those without the mutation. Fractional shortening was lower in diabetic patients with the mutation than those without it (30.7{+-}7.0 vs 42.5{+-}6.6, p<0.001). MIBG uptake on the delayed MIBG image was significantly lower in diabetic patients with the mutation than in those without the mutation (mean value of the heart to mediastinum ratio: 1.6{+-}0.2 vs 2.0{+-}0.4, p>0.05). In conclusion, left ventricular hypertrophy with or without abnormal wall motion and severely reduced MIBG uptake may be characteristic in diabetic patients with a mutation in the mitochondrial tRNA {sup Leu(UUR)} gene. (author)

Kinetics of Methane Production from Swine Manure and Buffalo Manure.

Science.gov (United States)

Sun, Chen; Cao, Weixing; Liu, Ronghou

2015-10-01

The degradation kinetics of swine and buffalo manure for methane production was investigated. Six kinetic models were employed to describe the corresponding experimental data. These models were evaluated by two statistical measurements, which were root mean square prediction error (RMSPE) and Akaike's information criterion (AIC). The results showed that the logistic and Fitzhugh models could predict the experimental data very well for the digestion of swine and buffalo manure, respectively. The predicted methane yield potential for swine and buffalo manure was 487.9 and 340.4 mL CH4/g volatile solid (VS), respectively, which was close to experimental values, when the digestion temperature was 36 ± 1 °C in the biochemical methane potential assays. Besides, the rate constant revealed that swine manure had a much faster methane production rate than buffalo manure.

Genotoxicity of swine effluents.

Science.gov (United States)

Techio, V H; Stolberg, J; Kunz, A; Zanin, E; Perdomo, C C

2011-01-01

This study aimed at the investigation of genotoxic effects of swine effluents from different stages of a treatment system for swine wastes through bioassay of stamen hairs and micronuclei in Tradescantia (clone BNL 4430). No significant differences (p≥0.05) regarding the genic mutations were found in the bioassay of stamen hairs, independently of the effluent analysed. For the genotoxicity test with micronuclei, the plants exposed to raw wastes, to sludge, and to effluent of the biodigester have presented higher rates of chromosomal damages (micronuclei), with significant differences in relation to the control group and other effluent of the waste treatment system (p≤0.05). The association between the chemical parameters and the genotoxicity data have shown that the variables COD and TKN have presented significant correlation (p≤0.05) with the number of mutagenic events in the tetrads.

Market Concentration Rate and Market Performance of China’s Swine Industry

Institute of Scientific and Technical Information of China (English)

Jia ZHANG; Yucheng HE

2016-01-01

Empirical study on market concentration rate and market performance of China’s Swine Industry indicates that higher market concentration rate brings higher overall performance of swine industry. There exists no obvious causal relation between market concentration rate and market performance,but market performance is highly correlated with market concentration rate. The improvement in performance of swine industry is dependent on further optimization of market concentration rate and other factors.

Molecular characterization of African swine fever virus in apparently ...

African Journals Online (AJOL)

African swine fever (ASF) is a highly lethal and economically significant disease of domestic pigs in Uganda where outbreaks regularly occur. There is neither a vaccine nor treatment available for ASF control. Twenty two African swine fever virus (ASFV) genotypes (I - XXII) have been identified based on partial sequencing ...

Zoonotic pathogens from feral swine that pose a significant threat to public health.

Science.gov (United States)

Brown, V R; Bowen, R A; Bosco-Lauth, A M

2018-06-01

The natural fecundity of suids, great ability to adapt to new habitats and desire for local hunting opportunities leading to translocation of feral pigs to regions where they are not yet established have all been instrumental in the home range expansion of feral swine. Feral swine populations in the United States continue to expand, wreaking havoc on agricultural lands, further compromising threatened and endangered species, and posing a microbiological threat to humans, domestic livestock and companion animals. This manuscript thoroughly reviews zoonotic diseases of concern including brucellosis, bovine tuberculosis, leptospirosis, enteric pathogens, both Salmonella spp. and shiga toxin-producing Escherichia coli, and hepatitis E. These pathogens are not a comprehensive list of microbes that are capable of infecting both humans and feral swine, but rather have been selected as they are known to infect US feral swine, direct transmission between wild suids and humans has previously been documented, or they have been shown to be readily transmitted during processing or consumption of feral swine pork. Humans that interact directly or indirectly with feral swine are at much higher risk for the development of a number of zoonotic pathogens. Numerous case reports document transmission events from feral swine and wild boar to humans, and the resulting diseases may be mild and self-limiting, chronic or fatal. Individuals that interact with feral swine should take preventative measures to minimize the risk of disease transmission and all meat should be thoroughly cooked. Additionally, public health campaigns to increase knowledge of the risks associated with feral swine are imperative. © 2018 Blackwell Verlag GmbH.

Swine influenza viruses isolated in 1983, 2002 and 2009 in Sweden exemplify different lineages

Directory of Open Access Journals (Sweden)

Metreveli Giorgi

2010-12-01

Full Text Available Abstract Swine influenza virus isolates originating from outbreaks in Sweden from 1983, 2002 and 2009 were subjected to nucleotide sequencing and phylogenetic analysis. The aim of the studies was to obtain an overview on their potential relatedness as well as to provide data for broader scale studies on swine influenza epidemiology. Nonetheless, analyzing archive isolates is justified by the efforts directed to the comprehension of the appearance of pandemic H1N1 influenza virus. Interestingly, this study illustrates the evolution of swine influenza viruses in Europe, because the earliest isolate belonged to 'classical' swine H1N1, the subsequent ones to Eurasian 'avian-like' swine H1N1 and reassortant 'avian-like' swine H1N2 lineages, respectively. The latter two showed close genetic relatedness regarding their PB2, HA, NP, and NS genes, suggesting common ancestry. The study substantiates the importance of molecular surveillance for swine influenza viruses.

Effects of repeated simulated removal activities on feral swine movements and space use

Science.gov (United States)

Fischer, Justin W.; McMurtry , Dan; Blass, Chad R.; Walter, W. David; Beringer, Jeff; VerCauterren, Kurt C.

2016-01-01

Abundance and distribution of feral swine (Sus scrofa) in the USA have increased dramatically during the last 30 years. Effective measures are needed to control and eradicate feral swine populations without displacing animals over wider areas. Our objective was to investigate effects of repeated simulated removal activities on feral swine movements and space use. We analyzed location data from 21 feral swine that we fitted with Global Positioning System harnesses in southern MO, USA. Various removal activities were applied over time to eight feral swine before lethal removal, including trapped-and-released, chased with dogs, chased with hunter, and chased with helicopter. We found that core space-use areas were reduced following the first removal activity, whereas overall space-use areas and diurnal movement distances increased following the second removal activity. Mean geographic centroid shifts did not differ between pre- and post-periods for either the first or second removal activities. Our information on feral swine movements and space use precipitated by human removal activities, such as hunting, trapping, and chasing with dogs, helps fill a knowledge void and will aid wildlife managers. Strategies to optimize management are needed to reduce feral swine populations while preventing enlarged home ranges and displacing individuals, which could lead to increased disease transmission risk and human-feral swine conflict in adjacent areas.

[Antibodies against Toxoplasma gondii in swine in Costa Rica: epidemiologic importance].

Science.gov (United States)

Torres, A L; Chinchilla, M; Reyes, L

1991-01-01

On a three hundred swine sera sample collected from a Municipal Slaughter house and a Research Laboratory at the Ministerio de Agricultura y Ganadería a 26% of positivity against T. gondii was found using the carbon immunoassay. A relationship between the age and swine race are made. The epidemiological significance of this findings are discussed focused mainly on the role of swine meat as a source of human infection in Costa Rica.

Detection of African swine fever, classical swine fever, and foot-and-mouth disease viruses in swine oral fluids by multiplex reverse transcription real-time polymerase chain reaction.

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Grau, Frederic R; Schroeder, Megan E; Mulhern, Erin L; McIntosh, Michael T; Bounpheng, Mangkey A

2015-03-01

African swine fever (ASF), classical swine fever (CSF), and foot-and-mouth disease (FMD) are highly contagious animal diseases of significant economic importance. Pigs infected with ASF and CSF viruses (ASFV and CSFV) develop clinical signs that may be indistinguishable from other diseases. Likewise, various causes of vesicular disease can mimic clinical signs caused by the FMD virus (FMDV). Early detection is critical to limiting the impact and spread of these disease outbreaks, and the ability to perform herd-level surveillance for all 3 diseases rapidly and cost effectively using a single diagnostic sample and test is highly desirable. This study assessed the feasibility of simultaneous ASFV, CSFV, and FMDV detection by multiplex reverse transcription real-time polymerase chain reaction (mRT-qPCR) in swine oral fluids collected through the use of chewing ropes. Animal groups were experimentally infected independently with each virus, observed for clinical signs, and oral fluids collected and tested throughout the course of infection. All animal groups chewed on the ropes readily before and after onset of clinical signs and before onset of lameness or serious clinical signs. ASFV was detected as early as 3 days postinoculation (dpi), 2-3 days before onset of clinical disease; CSFV was detected at 5 dpi, coincident with onset of clinical disease; and FMDV was detected as early as 1 dpi, 1 day before the onset of clinical disease. Equivalent results were observed in 4 independent studies and demonstrate the feasibility of oral fluids and mRT-qPCR for surveillance of ASF, CSF, and FMD in swine populations. © 2015 The Author(s).

Mitochondrial myopathies.

Science.gov (United States)

DiMauro, Salvatore

2006-11-01

Our understanding of mitochondrial diseases (defined restrictively as defects of the mitochondrial respiratory chain) is expanding rapidly. In this review, I will give the latest information on disorders affecting predominantly or exclusively skeletal muscle. The most recently described mitochondrial myopathies are due to defects in nuclear DNA, including coenzyme Q10 deficiency and mutations in genes controlling mitochondrial DNA abundance and structure, such as POLG, TK2, and MPV17. Barth syndrome, an X-linked recessive mitochondrial myopathy/cardiopathy, is associated with decreased amount and altered structure of cardiolipin, the main phospholipid of the inner mitochondrial membrane, but a secondary impairment of respiratory chain function is plausible. The role of mutations in protein-coding genes of mitochondrial DNA in causing isolated myopathies has been confirmed. Mutations in tRNA genes of mitochondrial DNA can also cause predominantly myopathic syndromes and--contrary to conventional wisdom--these mutations can be homoplasmic. Defects in the mitochondrial respiratory chain impair energy production and almost invariably involve skeletal muscle, causing exercise intolerance, cramps, recurrent myoglobinuria, or fixed weakness, which often affects extraocular muscles and results in droopy eyelids (ptosis) and progressive external ophthalmoplegia.

Mitochondrial nucleoid interacting proteins support mitochondrial protein synthesis.

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He, J; Cooper, H M; Reyes, A; Di Re, M; Sembongi, H; Litwin, T R; Gao, J; Neuman, K C; Fearnley, I M; Spinazzola, A; Walker, J E; Holt, I J

2012-07-01

Mitochondrial ribosomes and translation factors co-purify with mitochondrial nucleoids of human cells, based on affinity protein purification of tagged mitochondrial DNA binding proteins. Among the most frequently identified proteins were ATAD3 and prohibitin, which have been identified previously as nucleoid components, using a variety of methods. Both proteins are demonstrated to be required for mitochondrial protein synthesis in human cultured cells, and the major binding partner of ATAD3 is the mitochondrial ribosome. Altered ATAD3 expression also perturbs mtDNA maintenance and replication. These findings suggest an intimate association between nucleoids and the machinery of protein synthesis in mitochondria. ATAD3 and prohibitin are tightly associated with the mitochondrial membranes and so we propose that they support nucleic acid complexes at the inner membrane of the mitochondrion.

Swine Influenza Virus Antibodies in Humans, Western Europe, 2009

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Gerloff, Nancy A.; Kremer, Jacques R.; Charpentier, Emilie; Sausy, Aurélie; Olinger, Christophe M.; Weicherding, Pierre; Schuh, John; Van Reeth, Kristien

2011-01-01

Serologic studies for swine influenza viruses (SIVs) in humans with occupational exposure to swine have been reported from the Americas but not from Europe. We compared levels of neutralizing antibodies against 3 influenza viruses—pandemic (H1N1) 2009, an avian-like enzootic subtype H1N1 SIV, and a 2007–08 seasonal subtype H1N1—in 211 persons with swine contact and 224 matched controls in Luxembourg. Persons whose profession involved contact with swine had more neutralizing antibodies against SIV and pandemic (H1N1) 2009 virus than did the controls. Controls also had antibodies against these viruses although exposure to them was unlikely. Antibodies against SIV and pandemic (H1N1) 2009 virus correlated with each other but not with seasonal subtype H1N1 virus. Sequential exposure to variants of seasonal influenza (H1N1) viruses may have increased chances for serologic cross-reactivity with antigenically distinct viruses. Further studies are needed to determine the extent to which serologic responses correlate with infection. PMID:21392430

Deciphering the Swine-Flu Pandemics of 1918 and 2009

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Goldstein, Richard; Dos Reis, Mario; Tamuri, Asif; Hay, Alan

The devastating "Spanish flu" of 1918 killed an estimated 50 million people worldwide, ranking it as the deadliest pandemic in recorded human history. It is generally believed that the virus transferred from birds directly to humans shortly before the start of the pandemic, subsequently jumping from humans to swine. By developing 'non-homogeneous' substitution models that consider that substitution patterns may be different in human, avian, and swine hosts, we can determine the timing of the host shift to mammals. We find it likely that the Spanish flu of 1918, like the current 2009 pandemic, was a 'swine-origin' influenza virus. Now that we are faced with a new pandemic, can we understand how influenza is able to change hosts? Again by modelling the evolutionary process, considering the different selective constraints for viruses in the different hosts, we can identify locations that seem to be under different selective constraints in humans and avian hosts. This allows us to identify changes that may have facilitated the establishment of the 2009 swine-origin flu in humans.

Swine Brucellosis: Current Perspectives

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Brucella suis is a significant zoonosis that is present in domestic livestock and wildlife in many countries worldwide. Transmission from animal reservoirs is the source of human infection as human to human transmission is very rare. Although swine brucellosis causes economic losses in domestic liv...

EVIDENCE OF PSEUDORABIES VIRUS SHEDDING IN FERAL SWINE ( SUS SCROFA) POPULATIONS OF FLORIDA, USA.

Science.gov (United States)

Hernández, Felipe A; Sayler, Katherine A; Bounds, Courtney; Milleson, Michael P; Carr, Amanda N; Wisely, Samantha M

2018-01-01

:  Feral swine ( Sus scrofa) are a pathogen reservoir for pseudorabies virus (PrV). The virus can be fatal to wildlife and contributes to economic losses in the swine industry worldwide. National surveillance efforts in the US use serology to detect PrV-specific antibodies in feral swine populations, but PrV exposure is not a direct indicator of pathogen transmission among conspecifics or to non-suid wildlife species. We measured antibody production and the presence of PrV DNA in four tissue types from feral swine populations of Florida, US. We sampled blood, nasal, oral, and genital swabs from 551 individuals at 39 sites during 2014-16. Of the animals tested for antibody production, 224 of 436 (51%) feral swine were antibody positive while 38 of 549 feral swine (7%) tested for viral shedding were quantitative polymerase chain reaction (qPCR)-positive for PrV. The detection of PrV DNA across all the collected sample types (blood, nasal, oral, and genital [vaginal] swabs) suggested viral shedding via direct (oronasal or venereal), and potentially indirect (through carcass consumption), routes of transmission among infected and susceptible animals. Fourteen of 212 seronegative feral swine were qPCR-positive, indicating 7% false negatives in the serologic assay. Our findings suggest that serology may underestimate the actual infection risk posed by feral swine to other species and that feral swine populations in Florida are capable of shedding the virus through multiple routes.

Effect of soy protein on swine intestinal lipoproteins

International Nuclear Information System (INIS)

Ho, H.T.

1987-01-01

Hypocholesterolemic effect of soy protein appears to be the result of reduced cholesterol absorption and enhanced cholesterol excretion. The objective of this study is to delineate the underlying mechanism of soy protein effect on cholesterol absorption. At the end of a 5-week soy-protein or casein diet, swine were subjected to cannulation of mesenteric lymph duct under halothane anesthesia. A single dose of 250 μCi [ 14 C]-cholesterol and 10 mCi [ 3 H]-leucine was infused into the upper jejunum two hours after one-fifth of daily food was given. Then lymph was collected hourly for three hours and the lipoprotein fractions were separated by ultracentrifugation. SDS-PAGE (5%) was used to measure the concentrations of individual apoproteins by densitometric scanning. The three-hour lymphatic transport of cholesterol in casein-fed swine was significantly higher than in those fed soy protein. Triglyceride transports were similar in two groups. The [ 3 H]-leucine incorporation study revealed that transport of apo B-48 bore a significant positive relationship to transport of cholesterol in both chylomicron and VLDL fractions of mesenteric lymph. A greater apo B-48 secretion with higher specific activity was probably responsible for the greater transport of cholesterol in chylomicrons in casein-fed swine. On the other hand, the lesser cholesterol transport in chylomicrons in soy protein-fed swine was probably caused by lower apo B-48 secretion. Similarly, the transport of lymph VLDL cholesterol in swine fed casein or soy protein paralleled the amount of accompanying apo B-48. Dietary proteins probably influence the intestinal synthesis of apo B-48 which in turn affects cholesterol transport into the lymphatics

Characterization of Conserved and Non-conserved Imprinted Genes in Swine

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In order to increase our understanding of the role of imprinted genes in swine reproduction we used two complementary approaches, analysis of imprinting by pyrosequencing, and expression profiling of parthenogenetic fetuses, to carry out a comprehensive analysis of this gene family in swine. Using A...

Respiratory control in the glucose perfused heart. A /sup 31/P NMR and NADH fluorescence study

Energy Technology Data Exchange (ETDEWEB)

Katz, L A; Koretsky, A P; Balaban, R S

1987-09-14

The phosphate metabolites, adenosine diphosphate (ADP), inorganic phosphate (P/sub i/), and adenosine triphosphate (ATP), are potentially important regulators of mitochondrial respiration in vivo. However, previous studies on the heart in vivo and in vitro have not consistently demonstrated an appropriate correlation between the concentration of these phosphate metabolites and moderate changes in work and respiration. Recently, mitochondrial NAD(P)H levels have been proposed as a potential regulator of cardiac respiration during alterations in work output. In order to understand better the mechanism of respiratory control under these conditions, we investigated the relationship between the phosphate metabolites, the NAD(P)H levels, and oxygen consumption (Q/sub O(sub 2)/) in the isovolumic perfused rat heart during alterations in work output with pacing. ATP, creatine phosphate (CrP), P/sub i/ and intracellular pH were measured using /sup 31/P NMR. Mitochondrial NAD(P)H levels were monitored using spectrofluorometric techniques. 33 refs.; 3 figs.; 2 tabs.

The role of mitochondria in protection of the heart by preconditioning

Science.gov (United States)

Halestrap, Andrew P.; Clarke, Samantha J.; Khaliulin, Igor

2007-01-01

A prolonged period of ischaemia followed by reperfusion irreversibly damages the heart. Such reperfusion injury (RI) involves opening of the mitochondrial permeability transition pore (MPTP) under the conditions of calcium overload and oxidative stress that accompany reperfusion. Protection from MPTP opening and hence RI can be mediated by ischaemic preconditioning (IP) where the prolonged ischaemic period is preceded by one or more brief (2–5 min) cycles of ischaemia and reperfusion. Following a brief overview of the molecular characterisation and regulation of the MPTP, the proposed mechanisms by which IP reduces pore opening are reviewed including the potential roles for reactive oxygen species (ROS), protein kinase cascades, and mitochondrial potassium channels. It is proposed that IP-mediated inhibition of MPTP opening at reperfusion does not involve direct phosphorylation of mitochondrial proteins, but rather reflects diminished oxidative stress during prolonged ischaemia and reperfusion. This causes less oxidation of critical thiol groups on the MPTP that are known to sensitise pore opening to calcium. The mechanisms by which ROS levels are decreased in the IP hearts during prolonged ischaemia and reperfusion are not known, but appear to require activation of protein kinase Cε, either by receptor-mediated events or through transient increases in ROS during the IP protocol. Other signalling pathways may show cross-talk with this primary mechanism, but we suggest that a role for mitochondrial potassium channels is unlikely. The evidence for their activity in isolated mitochondria and cardiac myocytes is reviewed and the lack of specificity of the pharmacological agents used to implicate them in IP is noted. Some K+ channel openers uncouple mitochondria and others inhibit respiratory chain complexes, and their ability to produce ROS and precondition hearts is mimicked by bona fide uncouplers and respiratory chain inhibitors. IP may also provide continuing

ω-3 Polyunsaturated fatty acids prevent pressure overload-induced ventricular dilation and decrease in mitochondrial enzymes despite no change in adiponectin

Directory of Open Access Journals (Sweden)

O'Shea Karen M

2010-09-01

Full Text Available Abstract Background Pathological left ventricular (LV hypertrophy frequently progresses to dilated heart failure with suppressed mitochondrial oxidative capacity. Dietary marine ω-3 polyunsaturated fatty acids (ω-3 PUFA up-regulate adiponectin and prevent LV dilation in rats subjected to pressure overload. This study 1 assessed the effects of ω-3 PUFA on LV dilation and down-regulation of mitochondrial enzymes in response to pressure overload; and 2 evaluated the role of adiponectin in mediating the effects of ω-3 PUFA in heart. Methods Wild type (WT and adiponectin-/- mice underwent transverse aortic constriction (TAC and were fed standard chow ± ω-3 PUFA for 6 weeks. At 6 weeks, echocardiography was performed to assess LV function, mice were terminated, and mitochondrial enzyme activities were evaluated. Results TAC induced similar pathological LV hypertrophy compared to sham mice in both strains on both diets. In WT mice TAC increased LV systolic and diastolic volumes and reduced mitochondrial enzyme activities, which were attenuated by ω-3 PUFA without increasing adiponectin. In contrast, adiponectin-/- mice displayed no increase in LV end diastolic and systolic volumes or decrease in mitochondrial enzymes with TAC, and did not respond to ω-3 PUFA. Conclusion These findings suggest ω-3 PUFA attenuates cardiac pathology in response to pressure overload independent of an elevation in adiponectin.

Farming styles and cooperatives disputes of swine farmers under economic pressure in southern France

NARCIS (Netherlands)

Commandeur, M.A.M.

2010-01-01

In Southern France, the regression of swine farms and swine is ongoing. It involves reorientation of socio-professional networks, especially the farmers’ cooperatives. For understanding the various ways of maintaining swine production under the regressive circumstances, we focus on the farmers’

Population dynamics of swine influenza virus in finishing pigs

NARCIS (Netherlands)

Loeffen, W.L.A.

2008-01-01

Influenza virus infections in swine were first noticed in the US in 1918, during the human pandemic of the Spanish flu. In Europe, seroprevalences for the three most common swine influenza strains at the moment, H1N1, H3N2 and H1N2, range from 20-80% in finishing pigs at the end of the finishing

Economic losses to Iberian swine production from forest fires

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Juan Ramon Molina Martinez; Miguel Herrera Machuca; Ricardo Zamora Diaz; Fancisco Rodriguez y Silva; Armando Gonzalez-Caban

2011-01-01

Most forestry property in Andalusia is privately held. One of the most important possibilities for economic development of rural areas is the use of pasture lands (dehesa in Spanish). During the spring–summer season, swine grazing takes advantage of grasses between the trees, and during winter (harsher times), they use Quercus tree fruit. Swine production has a direct...

Comparative prevalence of immune evasion complex genes associated with beta-hemolysin converting bacteriophages in MRSA ST5 isolates from swine, swine facilities, humans with swine contact, and humans with no swine contact

Science.gov (United States)

Livestock associated methicillin-resistant Staphylococcus aureus (LA-MRSA) draws concern from the public health community because in some countries these organisms may represent the largest reservoir of MRSA outside hospital settings. Recent studies indicate LA-MRSA strains from swine are more genet...

Alloxan-induced diabetes exacerbates coronary atherosclerosis and calcification in Ossabaw miniature swine with metabolic syndrome.

Science.gov (United States)

Badin, Jill K; Kole, Ayeeshik; Stivers, Benjamin; Progar, Victor; Pareddy, Anisha; Alloosh, Mouhamad; Sturek, Michael

2018-03-09

There is a preponderance of evidence implicating diabetes with increased coronary artery disease (CAD) and calcification (CAC) in human patients with metabolic syndrome (MetS), but the effect of diabetes on CAD severity in animal models remains controversial. We investigated whether diabetes exacerbates CAD/CAC and intracellular free calcium ([Ca 2+ ] i ) dysregulation in the clinically relevant Ossabaw miniature swine model of MetS. Sixteen swine, eight with alloxan-induced diabetes, were fed a hypercaloric, atherogenic diet for 6 months. Alloxan-induced pancreatic beta cell damage was examined by immunohistochemical staining of insulin. The metabolic profile was confirmed by body weight, complete blood panel, intravenous glucose tolerance test (IVGTT), and meal tolerance test. CAD severity was assessed with intravascular ultrasound and histology. [Ca 2+ ] i handling in coronary smooth muscle (CSM) cells was assessed with fura-2 ratiometric imaging. Fasting and post-prandial blood glucose, total cholesterol, and serum triglycerides were elevated in MetS-diabetic swine. This group also exhibited hypoinsulinemia during IVGTT and less pancreatic beta cell mass when compared to lean and MetS-nondiabetic swine. IVUS analysis revealed that MetS-diabetic swine had greater percent wall coverage, percent plaque burden, and calcium index when compared to lean and MetS-nondiabetic swine. Fura-2 imaging of CSM [Ca 2+ ] i revealed that MetS-nondiabetic swine exhibited increased sarcoplasmic reticulum Ca 2+ store release and Ca 2+ influx through voltage-gated Ca 2+ channels compared to lean swine. MetS-diabetic swine exhibited impaired Ca 2+ efflux. Diabetes exacerbates coronary atherosclerosis and calcification in Ossabaw miniature swine with MetS, accompanied by progression of [Ca 2+ ] i dysregulation in advanced CAD/CAC. These results recapitulate increased CAD in humans with diabetes and establish Ossabaw miniature swine as an animal model for future Met

Carbon dioxide hepatic arterial DSA and CT angiography in swine model

International Nuclear Information System (INIS)

Tan Huaqiao; Hu Hongjie; Huang Wenxin; Zhang Shizheng; Dong Yonghua; Zhou Dachun

2005-01-01

Objective: To evaluate the imaging findings of carbon dioxide hepatic arterial DSA and CT angiography in normal swine. Methods: In general anaesthesia, hepatic arterial DSA was performed with 10 ml iodinated contrast medium (5 ml/s, 10 ml) in 5 normal swine, and then repeated hepatic arterial CO 2 -DSA was performed with a total of 30-50 ml CO 2 injected by manually operated syringe at the velocity of 5-8 ml/s, followed by CO 2 -CT angiography. All the swine were sacrificed after the procedure, the selective hepatic segments were removed, and pathological examination was carried out. The radiological features of hepatic arterial DSA with iodinated contrast medium and CO 2 and CT angiography with CO 2 were analyzed. The ability of showing the arterio-venous shunt was compared. Results: Hepatic arterio-portal shunt was found in the advanced arterial phase of CO 2 -DSA in three of five swine, which was furthermore demonstrated by CO 2 -CT angiography, but iodinated contrast medium DSA showed no arterio-portal shunt in all swine. The gaseous CO 2 in portal vein was absorbed within 1-3 minutes. No CO 2 shunted into the hepatic vein during CO 2 -DSA and CO 2 -CTA. Histology didn't reveal any abnormal changes caused by CO 2 shunt in the swine liver. Conclusion: (1) Hepatic arterial CO 2 -DSA and CO 2 -CTA can reveal arterio-portal shunt that isn't seen with iodinated contrast medium, the gaseous CO 2 in portal vein was absorbed within 1-3 minutes. (2) The gaseous CO 2 can't shunt into hepatic vein when the hepatic artery is perfused with CO 2 in normal swine. (authors)

Swine slurry application and soil management on double-cropped oat/maize

Directory of Open Access Journals (Sweden)

Marlo Adriano Bison Pinto

2014-06-01

Full Text Available The swine production in southern Brazil is concentrated in small farms that use residues as a nutrient source for crops of economic interest. This study aimed to evaluate the use of swine slurry associated with tillage systems on double-cropped oat/maize. The experiment was carried out in the 2009/2010 and 2010/2011 cropping seasons, in Taquaruçu do Sul, Rio Grande do Sul State, Brazil. The experimental design was randomized blocks in a factorial scheme, with four replications. Treatments consisted of the interaction of four swine slurry doses (no swine slurry, 20 m3 ha-1, 40 m3 ha-1 and 80 m3 ha-1 and mineral fertilization, in three tillage systems (no-tillage, chiseling and chiseling + disking. The swine slurry application on doublecropped oat/maize increased the dry matter and grain yield. The 80 m3 ha-1 dose provided a response statistically similar to the mineral fertilization recommended for maize. The interaction between the 80 m3 ha-1 dose and the immediate incorporation of slurry into the soil reduced N losses by ammonia volatilization, promoting a significant increase in maize grain yield, when grown on a clayish soil.

Effect of radiation on certain animal viruses in liquid swine manure

International Nuclear Information System (INIS)

Simon, J.; Mocsari, E.; Di Gleria, M.; Felkai, V.

1983-01-01

The virucidal effect of 60 Co γ-radiation was studied in cell culture medium and in liquid swine manure involving the most important porcine viruses that can be spread by liquid manure. The radiation doses, 20 and 30 kGy, were determined in preliminary experiments. At a radiation dose of 30 kGy, the activity of extracellular and cell-associated test viruses, except swine vesicular disease virus (SVDV), was completely destroyed both in cell culture medium and in liquid swine manure. The infectivity of SVDV decreased significantly (P 10 TCID 50 , both in cell culture medium and in liquid manure and this value corresponded to the international effectiveness demand for a disinfectant. The results showed that the safe disinfection virus in liquid swine manure by ionizing radiation requires a radiation dose of 30 kGy. (author)

Identification of atypical porcine pestivirus infection in swine herds in China.

Science.gov (United States)

Zhang, K; Wu, K; Liu, J; Ge, S; Xiao, Y; Shang, Y; Ning, Z

2017-08-01

Atypical porcine pestivirus (APPV) have been detected in swine herds from the USA, Germany, the Netherlands, Spain and most recently in Austria, suggesting a wide geographic distribution of this novel virus. Here, for the first time, we reported APPV infection in swine herds in China. Newborn piglets from two separate swine herds in Guangdong province were found showing typical congenital tremors in July and August 2016. RT-PCR, sequencing and phylogenetic analysis showed APPV infection occurred. Phylogenetic analysis showed that Chinese APPV strains, GD1 and GD2, formed independent branch from the USA, Germany and the Netherlands. Nucleotide identities between members of the APPV ranged between 83.1% and 83.5%, and this showed APPV is highly diverse. It is apparent that this provides the first molecular evidence of APPV infection in swine herds in China. © 2017 Blackwell Verlag GmbH.

Real-Time Fluorescence Measurements of ROS and [Ca2+] in Ischemic / Reperfused Rat Hearts: Detectable Increases Occur only after Mitochondrial Pore Opening and Are Attenuated by Ischemic Preconditioning.

Science.gov (United States)

Andrienko, Tatyana; Pasdois, Philippe; Rossbach, Andreas; Halestrap, Andrew P

2016-01-01

Mitochondrial permeability transition pore (mPTP) opening is critical for ischemia / reperfusion (I/R) injury and is associated with increased [Ca2+] and reactive oxygen species (ROS). Here we employ surface fluorescence to establish the temporal sequence of these events in beating perfused hearts subject to global I/R. A bespoke fluorimeter was used to synchronously monitor surface fluorescence and reflectance of Langendorff-perfused rat hearts at multiple wavelengths, with simultaneous measurements of hemodynamic function. Potential interference by motion artefacts and internal filtering was assessed and minimised. Re-oxidation of NAD(P)H and flavoproteins on reperfusion (detected using autofluorescence) was rapid (t0.5 ROS increases during early reperfusion. However, two different fluorescent cytosolic ROS probes did detect ROS increases after 2-3 min of reperfusion, which was shown to be after initiation of mPTP opening. Cyclosporin A (CsA) and IP attenuated these responses and reduced infarct size. [Ca2+]i (monitored with Indo-1) increased progressively during ischemia, but dropped rapidly within 90 s of reperfusion when total mitochondrial [Ca2+] was shown to be increased. These early changes in [Ca2+] were not attenuated by IP, but substantial [Ca2+] increases were observed after 2-3 min reperfusion and these were prevented by both IP and CsA. Our data suggest that the major increases in ROS and [Ca2+] detected later in reperfusion are secondary to mPTP opening. If earlier IP-sensitive changes occur that might trigger initial mPTP opening they are below our limit of detection. Rather, we suggest that IP may inhibit initial mPTP opening by alternative mechanisms such as prevention of hexokinase 2 dissociation from mitochondria during ischemia.

Tetracycline resistance in semi-arid agricultural soils under long-term swine effluent application.

Science.gov (United States)

Popova, Inna E; Josue, Rosemarie D R; Deng, Shiping; Hattey, Jeffory A

2017-05-04

Annually, millions pounds of antibiotics are released unmetabolized into environment along with animal wastes. Accumulation of antibiotics in soils could potentially induce the persistence of antibiotic resistant bacteria. Antibiotics such as tetracyclines and tetracycline-resistant bacteria have been previously detected in fields fertilized with animal manure. However, little is known about the accumulation of tetracyclines and the development of tetracycline resistance in semi-arid soils. Here we demonstrate that continuous land application with swine effluent, containing trace amounts of chlortetracycline, does not necessarily induce tetracycline resistance in soil bacteria. Based on the testing of more than 3,000 bacteria isolated from the amended soils, we found no significant increase in the occurrence and level of chlortetracycline resistant bacteria in soils after 15 years of continuous swine effluent fertilization. To account for a possible transfer of tetracycline-resistant bacteria originated from the swine effluent to soils, we analyzed two commonly found tetracycline resistant genes, tet(O) and tet(M), in the swine effluent and fertilized soils. Both genes were present in the swine effluent, however, they were not detectable in soils applied with swine effluent. Our data demonstrate that agronomic application of manure from antibiotic treated swine effluent does not necessarily result in the development of antibiotic bacterial resistance in soils. Apparently, concentrations of chlortetracycline present in manure are not significant enough to induce the development of antibiotic bacterial resistance.

Molecular Characterization of Swine Manure Lagoon Microbial and Antibiotic Resistant Populations

Science.gov (United States)

Background: The differences in swine manure lagoon effluent based on differing management styles or approaches such as different stages of swine rearing determines the presence of variable antibiotic resistance determinants and functional microbial populations. These concerns determine the suitabil...

Aerobic degradation of tylosin in cattle, chicken, and swine excreta

International Nuclear Information System (INIS)

Scott Teeter, Jerold; Meyerhoff, R.D.

2003-01-01

Tylosin, a fermentation-derived macrolide antibiotic, was tested to determine its aerobic degradation rate in cattle, chicken, and swine excreta. For chicken, excreta from a hen administered 14 C-tylosin as part of a metabolism study were used. For cattle and swine, 14 C-tylosin was added to control excreta. The formation of 14 C volatile breakdown products and 14 CO 2 was not observed throughout the study. Material balance for the cabon-14 label ranged between 94% and 104%. Initial, day-0, concentrations of tylosin-A averaged 119.52±4.39, 35.01±1.34, and 62.82±2.11 μg/g (dry weight basis) for cattle, chicken, and swine excreta samples, respectively. After 30 days, samples averaged 4.16±0.69 and 4.11±0.69 μg/g tylosin-A in cattle and swine excreta, respectively. No residues of tylosin-A or its factors were apparent in the chicken excreta samples after 30 days of incubation. In each case, tylosin declined to less than 6.5% of the initial level after 30 days. Calculated first-order half-lives under the test conditions were 6.2 days, <7.6 days, and 7.6 days for cattle, chicken, and swine excreta, respectively. The results indicate that tylosin residues degrade rapidly in animal excreta. Therefore, tylosin residues should not persist in the environment

An integrated model of cardiac mitochondrial energy metabolism and calcium dynamics.

Science.gov (United States)

Cortassa, Sonia; Aon, Miguel A; Marbán, Eduardo; Winslow, Raimond L; O'Rourke, Brian

2003-04-01

We present an integrated thermokinetic model describing control of cardiac mitochondrial bioenergetics. The model describes the tricarboxylic acid (TCA) cycle, oxidative phosphorylation, and mitochondrial Ca(2+) handling. The kinetic component of the model includes effectors of the TCA cycle enzymes regulating production of NADH and FADH(2), which in turn are used by the electron transport chain to establish a proton motive force (Delta mu(H)), driving the F(1)F(0)-ATPase. In addition, mitochondrial matrix Ca(2+), determined by Ca(2+) uniporter and Na(+)/Ca(2+) exchanger activities, regulates activity of the TCA cycle enzymes isocitrate dehydrogenase and alpha-ketoglutarate dehydrogenase. The model is described by twelve ordinary differential equations for the time rate of change of mitochondrial membrane potential (Delta Psi(m)), and matrix concentrations of Ca(2+), NADH, ADP, and TCA cycle intermediates. The model is used to predict the response of mitochondria to changes in substrate delivery, metabolic inhibition, the rate of adenine nucleotide exchange, and Ca(2+). The model is able to reproduce, qualitatively and semiquantitatively, experimental data concerning mitochondrial bioenergetics, Ca(2+) dynamics, and respiratory control. Significant increases in oxygen consumption (V(O(2))), proton efflux, NADH, and ATP synthesis, in response to an increase in cytoplasmic Ca(2+), are obtained when the Ca(2+)-sensitive dehydrogenases are the main rate-controlling steps of respiratory flux. These responses diminished when control is shifted downstream (e.g., the respiratory chain or adenine nucleotide translocator). The time-dependent behavior of the model, under conditions simulating an increase in workload, closely reproduces experimentally observed mitochondrial NADH dynamics in heart trabeculae subjected to changes in pacing frequency. The steady-state and time-dependent behavior of the model support the hypothesis that mitochondrial matrix Ca(2+) plays an

SK2 channels regulate mitochondrial respiration and mitochondrial Ca2+ uptake.

Science.gov (United States)

Honrath, Birgit; Matschke, Lina; Meyer, Tammo; Magerhans, Lena; Perocchi, Fabiana; Ganjam, Goutham K; Zischka, Hans; Krasel, Cornelius; Gerding, Albert; Bakker, Barbara M; Bünemann, Moritz; Strack, Stefan; Decher, Niels; Culmsee, Carsten; Dolga, Amalia M

2017-05-01

Mitochondrial calcium ([Ca 2+ ] m ) overload and changes in mitochondrial metabolism are key players in neuronal death. Small conductance calcium-activated potassium (SK) channels provide protection in different paradigms of neuronal cell death. Recently, SK channels were identified at the inner mitochondrial membrane, however, their particular role in the observed neuroprotection remains unclear. Here, we show a potential neuroprotective mechanism that involves attenuation of [Ca 2+ ] m uptake upon SK channel activation as detected by time lapse mitochondrial Ca 2+ measurements with the Ca 2+ -binding mitochondria-targeted aequorin and FRET-based [Ca 2+ ] m probes. High-resolution respirometry revealed a reduction in mitochondrial respiration and complex I activity upon pharmacological activation and overexpression of mitochondrial SK2 channels resulting in reduced mitochondrial ROS formation. Overexpression of mitochondria-targeted SK2 channels enhanced mitochondrial resilience against neuronal death, and this effect was inhibited by overexpression of a mitochondria-targeted dominant-negative SK2 channel. These findings suggest that SK channels provide neuroprotection by reducing [Ca 2+ ] m uptake and mitochondrial respiration in conditions, where sustained mitochondrial damage determines progressive neuronal death.

Fuzzy comprehensive evaluation of multiple environmental factors for swine building assessment and control.

Science.gov (United States)

Xie, Qiuju; Ni, Ji-Qin; Su, Zhongbin

2017-10-15

In confined swine buildings, temperature, humidity, and air quality are all important for animal health and productivity. However, the current swine building environmental control is only based on temperature; and evaluation and control methods based on multiple environmental factors are needed. In this paper, fuzzy comprehensive evaluation (FCE) theory was adopted for multi-factor assessment of environmental quality in two commercial swine buildings using real measurement data. An assessment index system and membership functions were established; and predetermined weights were given using analytic hierarchy process (AHP) combined with knowledge of experts. The results show that multi-factors such as temperature, humidity, and concentrations of ammonia (NH 3 ), carbon dioxide (CO 2 ), and hydrogen sulfide (H 2 S) can be successfully integrated in FCE for swine building environment assessment. The FCE method has a high correlation coefficient of 0.737 compared with the method of single-factor evaluation (SFE). The FCE method can significantly increase the sensitivity and perform an effective and integrative assessment. It can be used as part of environmental controlling and warning systems for swine building environment management to improve swine production and welfare. Copyright © 2017 Elsevier B.V. All rights reserved.

75 FR 56912 - Live Goats and Swine for Export; Removal of Certain Testing Requirements

Science.gov (United States)

2010-09-17

.... APHIS-2009-0067] RIN 0579-AD18 Live Goats and Swine for Export; Removal of Certain Testing Requirements... tuberculosis and brucellosis testing of goats and breeding swine intended for export to countries that do not require such tests. This action would facilitate the exportation of goats and breeding swine by...

Cardiac abnormalities in diabetic patients with mutation in the mitochondrial tRNA Leu(UUR)Gene

International Nuclear Information System (INIS)

Ueno, Hiroshi; Shiotani, Hideyuki

1999-01-01

An A-to-G transition at position 3243 of the mitochondrial DNA is known to be a pathogenic factor for mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS), diabetes and cardiomyopathy. This mutation causes dysfunction of the central nervous system in MELAS. Because the heart, as well as the brain and nervous system, is highly dependent on the energy produced by mitochondrial oxidation, these tissues are more vulnerable to mitochondrial defects. Cardiac abnormalities were assessed in 10 diabetic patients associated with this mutation using echocardiography and 123 I-metaiodobenzylguanidine (MIBG) scintigraphy, and compared with 19 diabetic patients without the mutation. Duration of diabetes, therapy, control of blood glucose and diabetic complications, such as diabetic retinopathy and nephropathy, were not different between the 2 groups. Diabetic patients with the mutation had a significantly thicker interventricular septum (16.8±3.7 vs 11.0±1.6 mm, p 0.05). In conclusion, left ventricular hypertrophy with or without abnormal wall motion and severely reduced MIBG uptake may be characteristic in diabetic patients with a mutation in the mitochondrial tRNA Leu(UUR) gene. (author)

Educating youth swine exhibitors on influenza A virus transmission at agricultural fairs.

Science.gov (United States)

Nolting, J M; Midla, J; Whittington, M S; Scheer, S D; Bowman, A S

2018-02-01

Influenza A virus (IAV) is a major zoonotic pathogen that threatens global public health. Novel strains of influenza A viruses pose a significant risk to public health due to their pandemic potential, and transmission of influenza A viruses from animals to humans is an important mechanism in the generation and introduction of IAVs that threaten human health. The purpose of this descriptive correlational study was to develop real-life training scenarios to better inform swine exhibitors of the risks they may encounter when influenza A viruses are present in swine. Educational activities were implemented in five Ohio counties where exhibition swine had historically been shedding influenza A viruses during the county fair. A total of 146 youth swine exhibitors participated in the educational programme, and an increase in the knowledge base of these youth was documented. It is expected that educating youth exhibitors about exposure to influenza A virus infections in the swine they are exhibiting will result in altered behaviours and animal husbandry practices that will improve both human and animal health. © 2017 Blackwell Verlag GmbH.

Characterization of Leptospira interrogans serovar Pomona isolated from swine in Brazil

NARCIS (Netherlands)

Miraglia, Fabiana; Moreno, Luisa Z.; Morais, Zenaide M.; Langoni, Helio; Shimabukuro, Fabio H.; Dellagostin, Odir A.; Hartskeerl, Rudy; Vasconcellos, Silvio A.; Moreno, Andrea Micke

2015-01-01

Leptospira interrogans swine infection is a cause of serious economic loss and a potential human health hazard. In Brazil, the most common serovars associated with swine infections are Pomona, Icterohaemorrhagie and Tarassovi. Cross-reactions among serovars and the failure of infected animals to

Mitochondrial tRNA cleavage by tRNA-targeting ribonuclease causes mitochondrial dysfunction observed in mitochondrial disease

Energy Technology Data Exchange (ETDEWEB)

Ogawa, Tetsuhiro, E-mail: atetsu@mail.ecc.u-tokyo.ac.jp; Shimizu, Ayano; Takahashi, Kazutoshi; Hidaka, Makoto; Masaki, Haruhiko, E-mail: amasaki@mail.ecc.u-tokyo.ac.jp

2014-08-15

Highlights: • MTS-tagged ribonuclease was translocated successfully to the mitochondrial matrix. • MTS-tagged ribonuclease cleaved mt tRNA and reduced COX activity. • Easy and reproducible method of inducing mt tRNA dysfunction. - Abstract: Mitochondrial DNA (mtDNA) is a genome possessed by mitochondria. Since reactive oxygen species (ROS) are generated during aerobic respiration in mitochondria, mtDNA is commonly exposed to the risk of DNA damage. Mitochondrial disease is caused by mitochondrial dysfunction, and mutations or deletions on mitochondrial tRNA (mt tRNA) genes are often observed in mtDNA of patients with the disease. Hence, the correlation between mt tRNA activity and mitochondrial dysfunction has been assessed. Then, cybrid cells, which are constructed by the fusion of an enucleated cell harboring altered mtDNA with a ρ{sup 0} cell, have long been used for the analysis due to difficulty in mtDNA manipulation. Here, we propose a new method that involves mt tRNA cleavage by a bacterial tRNA-specific ribonuclease. The ribonuclease tagged with a mitochondrial-targeting sequence (MTS) was successfully translocated to the mitochondrial matrix. Additionally, mt tRNA cleavage, which resulted in the decrease of cytochrome c oxidase (COX) activity, was observed.

Anaerobic digestion of chicken feather with swine manure or slaughterhouse sludge for biogas production.

Science.gov (United States)

Xia, Yun; Massé, Daniel I; McAllister, Tim A; Beaulieu, Carole; Ungerfeld, Emilio

2012-03-01

Biogas production from anaerobic digestion of chicken feathers with swine manure or slaughterhouse sludge was assessed in two separate experiments. Ground feathers without any pre-treatment were added to 42-L digesters inoculated with swine manure or slaughterhouse sludge, representing 37% and 23% of total solids, respectively and incubated at 25°C in batch mode. Compared to the control without feather addition, total CH(4) production increased by 130% (Pswine manure and the slaughterhouse sludge digesters, respectively. Mixed liquor NH(4)N concentration increased (Pdigestion to 6.9 and 3.5 g/L at the end of digestion in the swine manure and the slaughterhouse sludge digesters, respectively. The fraction of proteolytic microorganisms increased (Pdigestion from 12.5% to 14.5% and 11.3% to 13.0% in the swine manure and the slaughterhouse sludge digesters with feather addition, respectively, but decreased in the controls. These results are reflective of feather digestion. Feather addition did not affect CH(4) yields of the swine manure digesters (P=0.082) and the slaughterhouse sludge digesters (P=0.21), indicating that feathers can be digested together with swine manure or slaughterhouse sludge without negatively affecting the digestion of swine manure and slaughterhouse sludge. Crown Copyright © 2011. Published by Elsevier Ltd. All rights reserved.

76 FR 29991 - Live Goats and Swine for Export; Removal of Certain Testing Requirements

Science.gov (United States)

2011-05-24

...-0067] RIN 0579-AD18 Live Goats and Swine for Export; Removal of Certain Testing Requirements AGENCY... testing of goats and breeding swine intended for export to countries that do not require such tests. This action will facilitate the exportation of goats and breeding swine by eliminating the need to conduct pre...

[11C]-Acetoacetate PET imaging: a potential early marker for cardiac heart failure

International Nuclear Information System (INIS)

Croteau, Etienne; Tremblay, Sébastien; Gascon, Suzanne; Dumulon-Perreault, Véronique; Labbé, Sébastien M.; Rousseau, Jacques A.; Cunnane, Stephen C.; Carpentier, André C.; Bénard, François; Lecomte, Roger

2014-01-01

The ketone body acetoacetate could be used as an alternate nutrient for the heart, and it also has the potential to improve cardiac function in an ischemic–reperfusion model or reduce the mitochondrial production of oxidative stress involved in cardiotoxicity. In this study, [ 11 C]-acetoacetate was investigated as an early marker of intracellular damage in heart failure. Methods: A rat cardiotoxicity heart failure model was induced by doxorubicin, Dox(+). [ 14 C]-Acetoacetate, a non-positron (β −) emitting radiotracer, was used to characterize the arterial blood input function and myocardial mitochondrial uptake. Afterward, [ 11 C]-acetoacetate (β +) myocardial PET images were obtained for kinetic analysis and heart function assessment in control Dox(−) (n = 15) and treated Dox(+) (n = 6) rats. The uptake rate (K 1 ) and myocardial clearance rate (k 2 or k mono ) were extracted. Results: [ 14 C]-Acetoacetate in the blood was increased in Dox(+), from 2 min post-injection until the last withdrawal point when the heart was harvested, as well as the uptake in the heart and myocardial mitochondria (unpaired t-test, p < 0.05). PET kinetic analysis of [ 11 C]-acetoacetate showed that rate constants K 1 , k 2 and k mono were decreased in Dox(+) (p < 0.05) combined with a reduction of 24% of the left ventricular ejection fraction (p < 0.001). Conclusion: Radioactive acetoacetate ex vivo analysis [ 14 C], and in vivo kinetic [ 11 C] studies provided evidence that [ 11 C]-acetoacetate can assess heart failure Dox(+). Contrary to myocardial flow reserve (rest–stress protocol), [ 11 C]-acetoacetate can be used to assess reduced kinetic rate constants without requirement of hyperemic stress response. The proposed [ 11 C]-acetoacetate cardiac radiotracer in the investigation of heart disease is novel and paves the way to a potential role for [ 11 C]-acetoacetate in cardiac pathophysiology

Nation-wide Salmonella enterica surveillance and control in Danish slaughter swine herds

DEFF Research Database (Denmark)

Mousing, Jan; Jensen, P.T.; Halgaard, C.

1997-01-01

ranging from four to more than 60 swine are obtained quarterly at the abattoir. A meat sample from each pig is frozen, and meat juice (harvested after thawing) is examined for specific antibodies against S. enterica using an indirect enzyme-linked immunosorbent assay (ELISA). The ELISA combines several S...... during 1995 ranged from a mean of 2.9% in smaller herds (101-200 swine slaughtered per year) to 6.1% in relatively large herds (more than 5000 swine slaughtered per year)....

Mitochondrial defects associated with β-alanine toxicity: relevance to hyper-beta-alaninemia

Science.gov (United States)

Shetewy, Aza; Shimada-Takaura, Kayoko; Warner, Danielle; Jong, Chian Ju; Mehdi, Abu-Bakr Al; Alexeyev, Mikhail; Takahashi, Kyoko; Schaffer, Stephen W.

2016-01-01

Hyper-beta-alaninemia is a rare metabolic condition that results in elevated plasma and urinary β-alanine levels and is characterized by neurotoxicity, hypotonia, and respiratory distress. It has been proposed that at least some of the symptoms are caused by oxidative stress; however, only limited information is available on the mechanism of reactive oxygen species generation. The present study examines the hypothesis that β-alanine reduces cellular levels of taurine, which are required for normal respiratory chain function; cellular taurine depletion is known to reduce respiratory function and elevate mitochondrial superoxide generation. To test the taurine hypothesis, isolated neonatal rat cardiomyocytes and mouse embryonic fibroblasts were incubated with medium lacking or containing β-alanine. β-alanine treatment led to mitochondrial superoxide accumulation in conjunction with a decrease in oxygen consumption. The defect in β-alanine-mediated respiratory function was detected in permeabilized cells exposed to glutamate/malate but not in cells utilizing succinate, suggesting that β-alanine leads to impaired complex I activity. Taurine treatment limited mitochondrial superoxide generation, supporting a role for taurine in maintaining complex I activity. Also affected by taurine is mitochondrial morphology, as β-alanine-treated fibroblasts undergo fragmentation, a sign of unhealthy mitochondria that is reversed by taurine treatment. If left unaltered, β-alanine-treated fibroblasts also undergo mitochondrial apoptosis, as evidenced by activation of caspases 3 and 9 and the initiation of the mitochondrial permeability transition. Together, these data show that β-alanine mediates changes that reduce ATP generation and enhance oxidative stress, factors that contribute to heart failure. PMID:27023909

Close Relationship of Ruminant Pestiviruses and Classical Swine Fever Virus

Science.gov (United States)

Postel, Alexander; Schmeiser, Stefanie; Oguzoglu, Tuba Cigdem; Indenbirken, Daniela; Alawi, Malik; Fischer, Nicole; Grundhoff, Adam

2015-01-01

To determine why serum from small ruminants infected with ruminant pestiviruses reacted positively to classical swine fever virus (CSFV)–specific diagnostic tests, we analyzed 2 pestiviruses from Turkey. They differed genetically and antigenically from known Pestivirus species and were closely related to CSFV. Cross-reactions would interfere with classical swine fever diagnosis in pigs. PMID:25811683

A mitochondrially targeted compound delays aging in yeast through a mechanism linking mitochondrial membrane lipid metabolism to mitochondrial redox biology

Directory of Open Access Journals (Sweden)

Michelle T. Burstein

2014-01-01

Full Text Available A recent study revealed a mechanism of delaying aging in yeast by a natural compound which specifically impacts mitochondrial redox processes. In this mechanism, exogenously added lithocholic bile acid enters yeast cells, accumulates mainly in the inner mitochondrial membrane, and elicits an age-related remodeling of phospholipid synthesis and movement within both mitochondrial membranes. Such remodeling of mitochondrial phospholipid dynamics progresses with the chronological age of a yeast cell and ultimately causes significant changes in mitochondrial membrane lipidome. These changes in the composition of membrane phospholipids alter mitochondrial abundance and morphology, thereby triggering changes in the age-related chronology of such longevity-defining redox processes as mitochondrial respiration, the maintenance of mitochondrial membrane potential, the preservation of cellular homeostasis of mitochondrially produced reactive oxygen species, and the coupling of electron transport to ATP synthesis.

Angiotensin receptor blockade improves cardiac mitochondrial activity in response to an acute glucose load in obese insulin resistant rats

Directory of Open Access Journals (Sweden)

Max Thorwald

2018-04-01

Full Text Available Hyperglycemia increases the risk of oxidant overproduction in the heart through activation of a multitude of pathways. Oxidation of mitochondrial enzymes may impair their function resulting in accumulation of intermediates and reverse electron transfer, contributing to mitochondrial dysfunction. Furthermore, the renin-angiotensin system (RAS becomes inappropriately activated during metabolic syndrome, increasing oxidant production. To combat excess oxidant production, the transcription factor, nuclear factor erythriod-2- related factor 2 (Nrf2, induces expression of many antioxidant genes. We hypothesized that angiotensin II receptor type 1 (AT1 blockade improves mitochondrial function in response to an acute glucose load via upregulation of Nrf2. To address this hypothesis, an oral glucose challenge was performed in three groups prior to dissection (n = 5–8 animals/group/time point of adult male rats: 1 Long Evans Tokushima Otsuka (LETO; lean strain-control, 2 insulin resistant, obese Otsuka Long Evans Tokushima Fatty (OLETF, and 3 OLETF + angiotensin receptor blocker (ARB; 10 mg olmesartan/kg/d × 6 weeks. Hearts were collected at T0, T60, and T120 minutes post-glucose infusion. ARB increased Nrf2 binding 32% compared to OLETF at T60. Total superoxide dismutase (SOD and catalase (CAT activities were increased 45% and 66% respectively in ARB treated animals compared to OLETF. Mitochondrial enzyme activities of aconitase, complex I, and complex II increased by 135%, 33% and 66%, respectively in ARB compared to OLETF. These data demonstrate the protective effects of AT1 blockade on mitochondrial function during the manifestation of insulin resistance suggesting that the inappropriate activation of AT1 during insulin resistance may impair Nrf2 translocation and subsequent antioxidant activities and mitochondrial function. Keywords: Angiotensin II, Mitochondria, Cardiac, Antioxidant enzymes, TCA cycle

Development and Resuscitation of a Sedated, Mature Male Miniature Swine Severe Hemorrhage Model

Science.gov (United States)

2011-07-01

control. Results: Hemorrhage resulted in a characteristic hypotension and metabolic acidosis . Survival time for the control swine was 64 minutes...domestic swine4 and was characteristic of a hemorrhage- induced metabolic acidosis , with a decrease in blood HCO3, and BE and an increase in blood...Hammett M, Asher L, et al. Effects of bovine polymerized hemoglobin on coagulation in controlled hemorrhagic shock in swine. Shock. 2005;24:145–152

Common Deletion (CD) in mitochondrial DNA of irradiated rat heart

Energy Technology Data Exchange (ETDEWEB)

Siqueira, Raquel Gomes; Ferreira-Machado, Samara C.; Almeida, Carlos E.V. de, E-mail: raquelgsiqueira@gmail.com [Universidade do Estado do Rio de Janeiro (UERJ), RJ (Brazil). Instituto de Biologia Roberto Alcanatara Gomes. Lab. de Ciencias Radiologicas; Silva, Dayse A. da; Carvalho, Elizeu F. de [Universidade do Estado do Rio de Janeiro (UERJ), RJ (Brazil). Instituto de Biologia Roberto Alcanatara Gomes. Lab. de Diagnosticos por DNA; Melo, Luiz D.B. de [Universidade do Estado do Rio de Janeiro (UERJ), RJ (Brazil). Instituto de Biofisica Carlos Chagas Filho. Lab. de Parasitologia Molecular

2014-05-15

The purpose of this study was to map the common deletion (CD) area in mtDNA and investigate the levels of this deletion in irradiated heart. The assays were developed in male Wistar rats that were irradiated with three different single doses (5, 10 or 15 Gy) delivered directly to the heart and the analyses were performed at various times post-irradiation (3, 15 or 120 days). The CDs area were sequenced and the CD quantified by real-time PCR. Our study demonstrated that the CD levels progressively decreased from the 3rd until the 15th day after irradiation, and then increased thereafter. Additionally, it was observed that the levels of CD are modulated differently according to the different categories of doses (moderate and high). This study demonstrated an immediate response to ionizing radiation, measured by the presence of mutations in the CD area and a decrease in the CD levels. (author)

A Novel Swine Model for Evaluation of Potential Intravascular Hemostatic Agents

Science.gov (United States)

2007-06-01

bovine polymerized hemoglobin on coagulation in controlled hemorrhagic shock in swine. Shock 24:145–152. 2. Bellamy RF. 1984. The causes of death in...WZ, Pusateri AE, Uscilowicz JM, Delgado AV, Holcomb JB. 2005. Independent contributions of hypothermia and acidosis to coagulopathy in swine. J

Melatonin: A Mitochondrial Targeting Molecule Involving Mitochondrial Protection and Dynamics

Science.gov (United States)

Tan, Dun-Xian; Manchester, Lucien C.; Qin, Lilan; Reiter, Russel J.

2016-01-01

Melatonin has been speculated to be mainly synthesized by mitochondria. This speculation is supported by the recent discovery that aralkylamine N-acetyltransferase/serotonin N-acetyltransferase (AANAT/SNAT) is localized in mitochondria of oocytes and the isolated mitochondria generate melatonin. We have also speculated that melatonin is a mitochondria-targeted antioxidant. It accumulates in mitochondria with high concentration against a concentration gradient. This is probably achieved by an active transportation via mitochondrial melatonin transporter(s). Melatonin protects mitochondria by scavenging reactive oxygen species (ROS), inhibiting the mitochondrial permeability transition pore (MPTP), and activating uncoupling proteins (UCPs). Thus, melatonin maintains the optimal mitochondrial membrane potential and preserves mitochondrial functions. In addition, mitochondrial biogenesis and dynamics is also regulated by melatonin. In most cases, melatonin reduces mitochondrial fission and elevates their fusion. Mitochondrial dynamics exhibit an oscillatory pattern which matches the melatonin circadian secretory rhythm in pinealeocytes and probably in other cells. Recently, melatonin has been found to promote mitophagy and improve homeostasis of mitochondria. PMID:27999288

No evidence of African swine fever virus replication in hard ticks

NARCIS (Netherlands)

Carvalho Ferreira, de H.C.; Zúquete, S.T.; Wijnveld, M.; Weesendorp, E.; Jongejan, F.; Stegeman, J.A.; Loeffen, W.L.A.

2014-01-01

African swine fever (ASF) is caused by African swine fever virus (ASFV), a tick-borne DNA virus. Soft ticks of the genus Ornithodoros are the only biological vectors of ASFV recognized so far. Although other hard ticks have been tested for vector competence, two commonly found tick species in

No evidence of African swine fever virus replication in hard ticks

NARCIS (Netherlands)

de Carvalho Ferreira, Helena C; Tudela Zúquete, Sara; Wijnveld, Michiel; Weesendorp, Eefke; Jongejan, Frans; Stegeman, Arjan; Loeffen, Willie L A

African swine fever (ASF) is caused by African swine fever virus (ASFV), a tick-borne DNA virus. Soft ticks of the genus Ornithodoros are the only biological vectors of ASFV recognized so far. Although other hard ticks have been tested for vector competence, two commonly found tick species in

Temperature modulation with an esophageal heat transfer device - a pediatric swine model study.

Science.gov (United States)

Kulstad, Erik B; Naiman, Melissa; Shanley, Patrick; Garrett, Frank; Haryu, Todd; Waller, Donald; Azarafrooz, Farshid; Courtney, Daniel Mark

2015-01-01

An increasing number of conditions appear to benefit from control and modulation of temperature, but available techniques to control temperature often have limitations, particularly in smaller patients with high surface to mass ratios. We aimed to evaluate a new method of temperature modulation with an esophageal heat transfer device in a pediatric swine model, hypothesizing that clinically significant modulation in temperature (both increases and decreases of more than 1°C) would be possible. Three female Yorkshire swine averaging 23 kg were anesthetized with inhalational isoflurane prior to placement of the esophageal device, which was powered by a commercially available heat exchanger. Swine temperature was measured rectally and cooling and warming were performed by selecting the appropriate external heat exchanger mode. Temperature was recorded over time in order to calculate rates of temperature change. Histopathology of esophageal tissue was performed after study completion. Average swine baseline temperature was 38.3°C. Swine #1 exhibited a cooling rate of 3.5°C/hr; however, passive cooling may have contributed to this rate. External warming blankets maintained thermal equilibrium in swine #2 and #3, demonstrating maximum temperature decrease of 1.7°C/hr. Warming rates averaged 0.29°C/hr. Histopathologic analysis of esophageal tissue showed no adverse effects. An esophageal heat transfer device successfully modulated the temperature in a pediatric swine model. This approach to temperature modulation may offer a useful new modality to control temperature in conditions warranting temperature management (such as maintenance of normothermia, induction of hypothermia, fever control, or malignant hyperthermia).

Subunits Rip1 and Cox9p of the respiratory chain contribute to diclofenac-induced mitochondrial dysfunction

NARCIS (Netherlands)

van Leeuwen, J.S.; Orij, R.; Luttik, M.A.; Smits, G.J.; Vermeulen, N.P.E.; Vos, J.C.

2010-01-01

The widely used drug diclofenac can cause serious heart, liver and kidney injury, which may be related to its ability to cause mitochondrial dysfunction. Using Saccharomyces cerevisiae as a model system, we studied the mechanisms of diclofenac toxicity and the role of mitochondria therein. We found

MLN64 induces mitochondrial dysfunction associated with increased mitochondrial cholesterol content

Directory of Open Access Journals (Sweden)

Elisa Balboa

2017-08-01

Full Text Available MLN64 is a late endosomal cholesterol-binding membrane protein that has been implicated in cholesterol transport from endosomal membranes to the plasma membrane and/or mitochondria, in toxin-induced resistance, and in mitochondrial dysfunction. Down-regulation of MLN64 in Niemann-Pick C1 deficient cells decreased mitochondrial cholesterol content, suggesting that MLN64 functions independently of NPC1. However, the role of MLN64 in the maintenance of endosomal cholesterol flow and intracellular cholesterol homeostasis remains unclear. We have previously described that hepatic MLN64 overexpression increases liver cholesterol content and induces liver damage. Here, we studied the function of MLN64 in normal and NPC1-deficient cells and we evaluated whether MLN64 overexpressing cells exhibit alterations in mitochondrial function. We used recombinant-adenovirus-mediated MLN64 gene transfer to overexpress MLN64 in mouse liver and hepatic cells; and RNA interference to down-regulate MLN64 in NPC1-deficient cells. In MLN64-overexpressing cells, we found increased mitochondrial cholesterol content and decreased glutathione (GSH levels and ATPase activity. Furthermore, we found decreased mitochondrial membrane potential and mitochondrial fragmentation and increased mitochondrial superoxide levels in MLN64-overexpressing cells and in NPC1-deficient cells. Consequently, MLN64 expression was increased in NPC1-deficient cells and reduction of its expression restore mitochondrial membrane potential and mitochondrial superoxide levels. Our findings suggest that MLN64 overexpression induces an increase in mitochondrial cholesterol content and consequently a decrease in mitochondrial GSH content leading to mitochondrial dysfunction. In addition, we demonstrate that MLN64 expression is increased in NPC cells and plays a key role in cholesterol transport into the mitochondria.

Mutation of Mitochondrial DNA G13513A Presenting with Leigh Syndrome, Wolff-Parkinson-White Syndrome and Cardiomyopathy

Directory of Open Access Journals (Sweden)

Shi-Bing Wang

2008-08-01

Full Text Available Mutation of mitochondrial DNA (mtDNA G13513A, encoding the ND5 subunit of respiratory chain complex I, can cause mitochondrial encephalopathy with lactic acidosis and stroke-like episodes (MELAS and Leigh syndrome. Wolff-Parkinson-White (WPW syndrome and optic atrophy were reported in a high proportion of patients with this mutation. We report an 18-month-old girl, with an 11-month history of psychomotor regression who was diagnosed with WPW syndrome and hypertrophic cardiomyopathy, in association with Leigh syndrome. Supplementation with coenzyme Q10, thiamine and carnitine prevented further regression in gross motor function but the patient's heart function deteriorated and dilated cardiomyopathy developed 11 months later. She was found to have a mutation of mtDNA G13513A. We suggest that mtDNA G13513A mutation is an important factor in patients with Leigh syndrome associated with WPW syndrome and/or optic atrophy, and serial heart function monitoring by echocardiography is recommended in this group of patients.

Meta-analysis to define a core microbiota in the swine gut

Science.gov (United States)

Background The swine gut microbiota encompasses a large and diverse population of bacteria that play a significant role in pig health. As such, a number of recent studies have utilized high-throughput sequencing of the 16S rRNA gene to characterize the composition and structure of the swine gut micr...

Post-hatching development of mitochondrial function, organ mass and metabolic rate in two ectotherms, the American alligator (Alligator mississippiensis and the common snapping turtle (Chelydra serpentina

Directory of Open Access Journals (Sweden)

Sarah K. G. Sirsat

2016-04-01

Full Text Available The ontogeny of endothermy in birds is associated with disproportionate growth of thermogenic organs and increased mitochondrial oxidative capacity. However, no similar study has been made of the development of these traits in ectotherms. For comparison, we therefore investigated the metabolism, growth and muscle mitochondrial function in hatchlings of a turtle and a crocodilian, two ectotherms that never develop endothermy. Metabolic rate did not increase substantially in either species by 30 days post-hatching. Yolk-free body mass and heart mass did not change through 30 days in alligators and heart mass was a constant proportion of body mass, even after 1 year. Yolk-free body mass and liver mass grew 36% and 27%, respectively, in turtles during the first 30 days post-hatch. The mass-specific oxidative phosphorylation capacity of mitochondria, assessed using permeabilized muscle fibers, increased by a non-significant 47% in alligator thigh and a non-significant 50% in turtle thigh over 30 days, but did not increase in the heart. This developmental trajectory of mitochondrial function is slower and shallower than that previously observed in ducks, which demonstrate a 90% increase in mass-specific oxidative phosphorylation capacity in thigh muscles over just a few days, a 60% increase in mass-specific oxidative phosphorylation capacity of the heart over a few days, and disproportionate growth of the heart and other organs. Our data thus support the hypothesis that these developmental changes in ducks represent mechanistic drivers for attaining endothermy.

Post-hatching development of mitochondrial function, organ mass and metabolic rate in two ectotherms, the American alligator (Alligator mississippiensis) and the common snapping turtle (Chelydra serpentina).

Science.gov (United States)

Sirsat, Sarah K G; Sirsat, Tushar S; Price, Edwin R; Dzialowski, Edward M

2016-04-15

The ontogeny of endothermy in birds is associated with disproportionate growth of thermogenic organs and increased mitochondrial oxidative capacity. However, no similar study has been made of the development of these traits in ectotherms. For comparison, we therefore investigated the metabolism, growth and muscle mitochondrial function in hatchlings of a turtle and a crocodilian, two ectotherms that never develop endothermy. Metabolic rate did not increase substantially in either species by 30 days post-hatching. Yolk-free body mass and heart mass did not change through 30 days in alligators and heart mass was a constant proportion of body mass, even after 1 year. Yolk-free body mass and liver mass grew 36% and 27%, respectively, in turtles during the first 30 days post-hatch. The mass-specific oxidative phosphorylation capacity of mitochondria, assessed using permeabilized muscle fibers, increased by a non-significant 47% in alligator thigh and a non-significant 50% in turtle thigh over 30 days, but did not increase in the heart. This developmental trajectory of mitochondrial function is slower and shallower than that previously observed in ducks, which demonstrate a 90% increase in mass-specific oxidative phosphorylation capacity in thigh muscles over just a few days, a 60% increase in mass-specific oxidative phosphorylation capacity of the heart over a few days, and disproportionate growth of the heart and other organs. Our data thus support the hypothesis that these developmental changes in ducks represent mechanistic drivers for attaining endothermy. © 2016. Published by The Company of Biologists Ltd.

The Brain Renin-Angiotensin System and Mitochondrial Function: Influence on Blood Pressure and Baroreflex in Transgenic Rat Strains

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Manisha Nautiyal

2013-01-01

Full Text Available Mitochondrial dysfunction is implicated in many cardiovascular diseases, including hypertension, and may be associated with an overactive renin-angiotensin system (RAS. Angiotensin (Ang II, a potent vasoconstrictor hormone of the RAS, also impairs baroreflex and mitochondrial function. Most deleterious cardiovascular actions of Ang II are thought to be mediated by NADPH-oxidase- (NOX- derived reactive oxygen species (ROS that may also stimulate mitochondrial oxidant release and alter redox-sensitive signaling pathways in the brain. Within the RAS, the actions of Ang II are counterbalanced by Ang-(1–7, a vasodilatory peptide known to mitigate against increased oxidant stress. A balance between Ang II and Ang-(1–7 within the brain dorsal medulla contributes to maintenance of normal blood pressure and proper functioning of the arterial baroreceptor reflex for control of heart rate. We propose that Ang-(1–7 may negatively regulate the redox signaling pathways activated by Ang II to maintain normal blood pressure, baroreflex, and mitochondrial function through attenuating ROS (NOX-generated and/or mitochondrial.

The neuropsychiatric aspects of influenza/swine flu: A selective review

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Narayana Manjunatha

2011-01-01

Full Text Available The world witnessed the influenza virus during the seasonal epidemics and pandemics. The current strain of H1N1 (swine flu pandemic is believed to be the legacy of the influenza pandemic (1918-19. The influenza virus has been implicated in many neuropsychiatric disorders. In view of the recent pandemic, it would be interesting to review the neuropsychiatric aspects of influenza, specifically swine flu. Author used popular search engine ′PUBMED′ to search for published articles with different MeSH terms using Boolean operator (AND. Among these, a selective review of the published literature was done. Acute manifestations of swine flu varied from behavioral changes, fear of misdiagnosis during outbreak, neurological features like seizures, encephalopathy, encephalitis, transverse myelitis, aseptic meningitis, multiple sclerosis, and Guillian-Barre Syndrome. Among the chronic manifestations, schizophrenia, Parkinson′s disease, mood disorder, dementia, and mental retardation have been hypothesized. Further research is required to understand the etiological hypothesis of the chronic manifestations of influenza. The author urges neuroscientists around the world to make use of the current swine flu pandemic as an opportunity for further research.

Codigestion of Taihu blue algae with swine manure for biogas production

International Nuclear Information System (INIS)

Miao, Hengfeng; Wang, Shouquan; Zhao, Mingxing; Huang, Zhenxing; Ren, Hongyan; Yan, Qun; Ruan, Wenquan

2014-01-01

Highlights: • Codigestion of blue algae with swine manure has the highest CH 4 yield at ISR 2.0. • pH, TAN, N-NH 3 and VFAs confirmed the appropriate stability of the codigestion. • 35.44% VS reduction was achieved by codigestion of blue algae with swine manure. • Three key enzyme characteristics demonstrated the higher efficiencies of codigestion. - Abstract: Anaerobic digestion (AD) of Taihu blue algae and its codigestion with swine manure was evaluated at different inoculum substrate ratios (ISRs) from 0.5 to 3.0. Results showed that codigestion of blue algae with swine manure led to the highest methane (CH 4 ) production of 212.7 mL g −1 VS at ISR 2.0, while digestion of blue algae inoculated with granular sludge brought out the optimized CH 4 production of 73.5 mL g −1 VS at ISR 3.0. The values of pH, total ammonia nitrogen (TAN), free ammonia nitrogen (N-NH 3 ) and volatile fatty acids (VFAs) showed no significant difference between the digestion and codigestion, confirming the appropriate stability of the two batch anaerobic processes. Closer examination of VS removal rates and key enzymes variation proved codigestion had higher efficiencies in biodegradation and methanation, which demonstrated that AD of blue algae with swine manure was a promising technology for both solid wastes treatment and renewable-energy production

Targeted Transgenic Overexpression of Mitochondrial Thymidine Kinase (TK2) Alters Mitochondrial DNA (mtDNA) and Mitochondrial Polypeptide Abundance

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Hosseini, Seyed H.; Kohler, James J.; Haase, Chad P.; Tioleco, Nina; Stuart, Tami; Keebaugh, Erin; Ludaway, Tomika; Russ, Rodney; Green, Elgin; Long, Robert; Wang, Liya; Eriksson, Staffan; Lewis, William

2007-01-01

Mitochondrial toxicity limits nucleoside reverse transcriptase inhibitors (NRTIs) for acquired immune deficiency syndrome. NRTI triphosphates, the active moieties, inhibit human immunodeficiency virus reverse transcriptase and eukaryotic mitochondrial DNA polymerase pol-γ. NRTI phosphorylation seems to correlate with mitochondrial toxicity, but experimental evidence is lacking. Transgenic mice (TGs) with cardiac overexpression of thymidine kinase isoforms (mitochondrial TK2 and cytoplasmic TK1) were used to study NRTI mitochondrial toxicity. Echocardiography and nuclear magnetic resonance imaging defined cardiac performance and structure. TK gene copy and enzyme activity, mitochondrial (mt) DNA and polypeptide abundance, succinate dehydrogenase and cytochrome oxidase histochemistry, and electron microscopy correlated with transgenesis, mitochondrial structure, and biogenesis. Antiretroviral combinations simulated therapy. Untreated hTK1 or TK2 TGs exhibited normal left ventricle mass. In TK2 TGs, cardiac TK2 gene copy doubled, activity increased 300-fold, and mtDNA abundance doubled. Abundance of the 17-kd subunit of complex I, succinate dehydrogenase histochemical activity, and cristae density increased. NRTIs increased left ventricle mass 20% in TK2 TGs. TK activity increased 3 logs in hTK1 TGs, but no cardiac phenotype resulted. NRTIs abrogated functional effects of transgenically increased TK2 activity but had no effect on TK2 mtDNA abundance. Thus, NRTI mitochondrial phosphorylation by TK2 is integral to clinical NRTI mitochondrial toxicity. PMID:17322372

[An overview on swine influenza viruses].

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Yang, Shuai; Zhu, Wen-Fei; Shu, Yue-Long

2013-05-01

Swine influenza viruses (SIVs) are respiratory pathogens of pigs. They cause both economic bur den in livestock-dependent industries and serious global public health concerns in humans. Because of their dual susceptibility to human and avian influenza viruses, pigs are recognized as intermediate hosts for genetic reassortment and interspecies transmission. Subtypes H1N1, H1N2, and H3N2 circulate in swine populations around the world, with varied origin and genetic characteristics among different continents and regions. In this review, the role of pigs in evolution of influenza A viruses, the genetic evolution of SIVs and interspecies transmission of SIVs are described. Considering the possibility that pigs might produce novel influenza viruses causing more outbreaks and pandemics, routine epidemiological surveillance of influenza viruses in pig populations is highly recommended.

Passive surveillance of Leptospira infection in swine in Germany.

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Strutzberg-Minder, Katrin; Tschentscher, Astrid; Beyerbach, Martin; Homuth, Matthias; Kreienbrock, Lothar

2018-01-01

As no current data are available on the prevalence of leptospiral infection in swine in Germany, we analysed laboratory data from diagnostic examinations carried out on samples from swine all over Germany from January 2011 to September 2016. A total of 29,829 swine sera were tested by microscopic agglutination test (MAT) for antibodies against strains of eleven Leptospira serovars. Overall, 20.2% (6025) of the total sample collection tested positive for leptospiral infection. Seropositivity ranged between 16.3% (964) in 2011 and 30.9% (941) in 2016 (January to September only). Of all samples, 11.6% (57.3% of the positives) reacted with only one Leptospira serovar, and only 8.6% (42.7% of the positives) reacted simultaneously with two or more serovars. The most frequently detected serovar was Bratislava, which was found in 11.6% (3448) of all samples, followed by the serovars Australis in 7.3% (2185), Icterohaemorrhagiae in 4.0% (1191), Copenhageni in 4.0% (1182), Autumnalis in 3.7% (1054), Canicola in 2.0% (585), and Pomona in 1.2% (368). Modelling shows that both the year and the reason for testing at the laboratory had statistically strong effects on the test results; however, no interactions were determined between those factors. The results support the suggestion that the seropositivities found may be considered to indicate the state of leptospiral infections in the German swine population. Although data from passive surveillance are prone to selection bias, stratified analysis by initial reason for examination and analyses by model approaches may correct for biases. A prevalence of about 20% for a leptospiral infection is most probable for sows with reproductive problems in Germany, with an increasing trend. Swine in Germany are probably a reservoir host for serovar Bratislava, but in contrast to other studies not for Pomona and Tarassovi.

Prevalence and Characterization of Shiga Toxin-Producing Escherichia coli in Swine Feces Recovered in the National Animal Health Monitoring System's Swine 2000 Study

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Fratamico, Pina M.; Bagi, Lori K.; Bush, Eric J.; Solow, Barbara T.

2004-01-01

A study was conducted to determine the prevalence of Shiga toxin-producing Escherichia coli (STEC) in swine feces in the United States as part of the National Animal Health Monitoring System's Swine 2000 study. Fecal samples collected from swine operations from 13 of the top 17 swine-producing states were tested for the presence of STEC. After enrichment of swine fecal samples in tryptic soy broth, the samples were tested for the presence of stx1 and stx2 by use of the TaqMan E. coli STX1 and STX2 PCR assays. Enrichments of samples positive for stx1 and/or stx2 were plated, and colony hybridization was performed using digoxigenin-labeled probes complementary to the stx1 and stx2 genes. Positive colonies were picked and confirmed by PCR for the presence of the stx1, stx2, or stx2e genes, and the isolates were serotyped. Out of 687 fecal samples tested using the TaqMan assays, 70% (484 of 687) were positive for Shiga toxin genes, and 54% (370 of 687), 64% (436 of 687), and 38% (261 of 687) were positive for stx1, stx2, and both toxin genes, respectively. Out of 219 isolates that were characterized, 29 (13%) produced stx1, 14 (6%) produced stx2, and 176 (80%) produced stx2e. Twenty-three fecal samples contained at least two STEC strains that had different serotypes but that had the same toxin genes or included a strain that possessed stx1 in addition to a strain that possessed stx2 or stx2e. The STEC isolates belonged to various serogroups, including O2, O5, O7, O8, O9, OX10, O11, O15, OX18, O20, O57, O65, O68, O69, O78, O91, O96, O100, O101, O120, O121, O152, O159, O160, O163, and O untypeable. It is noteworthy that no isolates of serogroup O157 were recovered. Results of this study indicate that swine in the United States harbor STEC that can potentially cause human illness. PMID:15574914

Expression Dynamics of Innate Immunity in Influenza Virus-Infected Swine

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Massimo Amadori

2017-04-01

Full Text Available The current circulating swine influenza virus (IV subtypes in Europe (H1N1, H1N2, and H3N2 are associated with clinical outbreaks of disease. However, we showed that pigs could be susceptible to other IV strains that are able to cross the species barrier. In this work, we extended our investigations into whether different IV strains able to cross the species barrier might give rise to different innate immune responses that could be associated with pathological lesions. For this purpose, we used the same samples collected in a previous study of ours, in which healthy pigs had been infected with a H3N2 Swine IV and four different H3N8 IV strains circulating in different animal species. Pigs had been clinically inspected and four subjects/group were sacrificed at 3, 6, and 21 days post infection. In the present study, all groups but mock exhibited antibody responses to IV nucleoprotein protein. Pulmonary lesions and high-titered viral replication were observed in pigs infected with the swine-adapted virus. Interestingly, pigs infected with avian and seal H3N8 strains also showed moderate lesions and viral replication, whereas equine and canine IVs did not cause overt pathological signs, and replication was barely detectable. Swine IV infection induced interferon (IFN-alpha and interleukin-6 responses in bronchoalveolar fluids (BALF at day 3 post infection, as opposed to the other non-swine-adapted virus strains. However, IFN-alpha responses to the swine-adapted virus were not associated with an increase of the local, constitutive expression of IFN-alpha genes. Remarkably, the Equine strain gave rise to a Serum Amyloid A response in BALF despite little if any replication. Each virus strain could be associated with expression of cytokine genes and/or proteins after infection. These responses were observed well beyond the period of virus replication, suggesting a prolonged homeostatic imbalance of the innate immune system.

A wind tunnel study of air flow near model swine confinement buildings

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One of the most significant and persistent environmental concerns regarding swine production is the transport of odor constituents, trace gases, and particulates from animal production and manure storage facilities. The objectives of this study were to determine how swine housing unit orientation af...

Are Swine Workers in the United States at Increased Risk of Infection with Zoonotic Influenza Virus?

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Myers, Kendall P.; Olsen, Christopher W.; Setterquist, Sharon F.; Capuano, Ana W.; Donham, Kelley J.; Thacker, Eileen L.; Merchant, James A.; Gray, Gregory C.

2006-01-01

Background Pandemic influenza strains originate in nonhuman species. Pigs have an important role in interspecies transmission of the virus. We examined multiple swine-exposed human populations in the nation's number 1 swine-producing state for evidence of previous swine influenza virus infection. Methods We performed controlled, cross-sectional seroprevalence studies among 111 farmers, 97 meat processing workers, 65 veterinarians, and 79 control subjects using serum samples collected during the period of 2002–2004. Serum samples were tested using a hemagglutination inhibition assay against the following 6 influenza A virus isolates collected recently from pigs and humans: A/Swine/WI/238/97 (H1N1), A/Swine/WI/R33F/01 (H1N2), A/Swine/Minnesota/593/99 (H3N2), A/New Caledonia/20/99 (H1N1), A/Panama/2007/99 (H3N2), and A/Nanchang/933/95 (H3N2). Results Using multivariable proportional odds modeling, all 3 exposed study groups demonstrated markedly elevated titers against the H1N1 and H1N2 swine influenza virus isolates, compared with control subjects. Farmers had the strongest indication of exposure to swine H1N1 virus infection (odds ratio [OR], 35.3; 95% confidence interval [CI], 7.7–161.8), followed by veterinarians (OR, 17.8; 95% CI, 3.8–82.7), and meat processing workers (OR, 6.5; 95% CI, 1.4–29.5). Similarly, farmers had the highest odds for exposure to swine H1N2 virus (OR, 13.8; 95% CI, 5.4–35.4), followed by veterinarians (OR, 9.5; 95% CI, 3.6–24.6) and meat processing workers (OR, 2.7; 95% CI, 1.1–6.7). Conclusions Occupational exposure to pigs greatly increases workers' risk of swine influenza virus infection. Swine workers should be included in pandemic surveillance and in antiviral and immunization strategies. PMID:16323086

Lethal Cardiomyopathy in Mice Lacking Transferrin Receptor in the Heart

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Wenjing Xu

2015-10-01

Full Text Available Both iron overload and iron deficiency have been associated with cardiomyopathy and heart failure, but cardiac iron utilization is incompletely understood. We hypothesized that the transferrin receptor (Tfr1 might play a role in cardiac iron uptake and used gene targeting to examine the role of Tfr1 in vivo. Surprisingly, we found that decreased iron, due to inactivation of Tfr1, was associated with severe cardiac consequences. Mice lacking Tfr1 in the heart died in the second week of life and had cardiomegaly, poor cardiac function, failure of mitochondrial respiration, and ineffective mitophagy. The phenotype could only be rescued by aggressive iron therapy, but it was ameliorated by administration of nicotinamide riboside, an NAD precursor. Our findings underscore the importance of both Tfr1 and iron in the heart, and may inform therapy for patients with heart failure.

miR-26a suppresses autophagy in swine Sertoli cells by targeting ULK2.

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Ran, M; Li, Z; Cao, R; Weng, B; Peng, F; He, C; Chen, B

2018-05-14

A large number of microRNAs (miRNAs) have been detected from porcine testicular tissues thanks to the development of high-throughput sequencing technology. However, the regulatory roles of most identified miRNAs in swine testicular development or spermatogenesis are poorly understood. In our previous study, ULK2 (uncoordinated-51-like kinase 2) was predicted as a target gene of miR-26a. In this study, we aimed to investigate the role of miR-26a in swine Sertoli cell autophagy. The relative expression of miR-26a and ULK2 levels has a significant negative correlation (R 2  = .5964, p ≤ .01) in nine developmental stages of swine testicular tissue. Dual-luciferase reporter assay results show that miR-26a directly targets the 3'UTR of the ULK2 gene (position 618-624). In addition, both the mRNA and protein expression of ULK2 were downregulated by miR-26a in swine Sertoli cells. These results indicate that miR-26a targets the ULK2 gene and downregulates its expression in swine Sertoli cells. Based on the expression of marker genes (LC3, p62 and Beclin-1), overexpression of miR-26a or knock-down of ULK2 inhibits swine Sertoli cell autophagy. Taken together, these findings demonstrate that miR-26a suppresses autophagy in swine Sertoli cells by targeting ULK2. © 2018 Blackwell Verlag GmbH.

Potential of Duckweed for Swine Wastewater Nutrient removal and Biomass Valorisation through Anaerobic Co-digestion

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Luis Pena

2017-06-01

Full Text Available Over the last decades, phytodepuration has been considered an efficient technology to treat wastewaters. The present study reports a bench scale depuration assay of swine wastewater using Lemna minor. The highest observed growth rate obtained in swine wastewater was 3.1 ± 0.3 gDW m−2 day−1 and the highest nitrogen and phosphorus uptake were 140 mg N m−2 day−1 and 3.47 mg P m−2 day−1, respectively. The chemical oxygen demand removal efficiency in the swine wastewater assay was 58.9 ± 2.0%. Furthermore, the biomass valorisation by anaerobic co-digestion with swine wastewater was assessed. Results showed a clear improvement in specific methane production rate (around 40% when compared to mono-substrate anaerobic digestion. The highest methane specific production, 131.0 ± 0.8 mL CH4 g−1 chemical oxygen demand, was obtained with a mixture containing 100 g of duckweed per liter of pre-treated swine wastewater. The water-nutrients-energy nexus approach showed to be promising for swine waste management.

Reassortant swine influenza viruses isolated in Japan contain genes from pandemic A(H1N1) 2009.

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Kanehira, Katsushi; Takemae, Nobuhiro; Uchida, Yuko; Hikono, Hirokazu; Saito, Takehiko

2014-06-01

In 2013, three reassortant swine influenza viruses (SIVs)-two H1N2 and one H3N2-were isolated from symptomatic pigs in Japan; each contained genes from the pandemic A(H1N1) 2009 virus and endemic SIVs. Phylogenetic analysis revealed that the two H1N2 viruses, A/swine/Gunma/1/2013 and A/swine/Ibaraki/1/2013, were reassortants that contain genes from the following three distinct lineages: (i) H1 and nucleoprotein (NP) genes derived from a classical swine H1 HA lineage uniquely circulating among Japanese SIVs; (ii) neuraminidase (NA) genes from human-like H1N2 swine viruses; and (iii) other genes from pandemic A(H1N1) 2009 viruses. The H3N2 virus, A/swine/Miyazaki/2/2013, comprised genes from two sources: (i) hemagglutinin (HA) and NA genes derived from human and human-like H3N2 swine viruses and (ii) other genes from pandemic A(H1N1) 2009 viruses. Phylogenetic analysis also indicated that each of the reassortants may have arisen independently in Japanese pigs. A/swine/Miyazaki/2/2013 were found to have strong antigenic reactivities with antisera generated for some seasonal human-lineage viruses isolated during or before 2003, whereas A/swine/Miyazaki/2/2013 reactivities with antisera against viruses isolated after 2004 were clearly weaker. In addition, antisera against some strains of seasonal human-lineage H1 viruses did not react with either A/swine/Gunma/1/2013 or A/swine/Ibaraki/1/2013. These findings indicate that emergence and spread of these reassortant SIVs is a potential public health risk. © 2014 The Societies and Wiley Publishing Asia Pty Ltd.

The Inability to Screen Exhibition Swine for Influenza A Virus Using Body Temperature.

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Bowman, A S; Nolting, J M; Workman, J D; Cooper, M; Fisher, A E; Marsh, B; Forshey, T

2016-02-01

Agricultural fairs create an unconventional animal-human interface that has been associated with swine-to-human transmission of influenza A virus (IAV) in recent years. Early detection of IAV-infected pigs at agricultural fairs would allow veterinarians to better protect swine and human health during these swine exhibitions. This study assessed the use of swine body temperature measurement, recorded by infrared and rectal thermometers, as a practical method to detect IAV-infected swine at agricultural fairs. In our first objective, infrared thermometers were used to record the body surface temperature of 1,092 pigs at the time of IAV nasal swab collection at the end of the exhibition period of 55 agricultural fairs. IAV was recovered from 212 (19.4%) pigs, and the difference in mean infrared body temperature measurement of IAV-positive and IAV-negative pigs was 0.83°C. In a second objective, snout wipes were collected from 1,948 pigs immediately prior to the unloading of the animals at a single large swine exhibition. Concurrent to the snout wipe collection, owners took the rectal temperatures of his/her pigs. In this case, 47 (2.4%) pigs tested positive for IAV before they entered the swine barn. The mean rectal temperatures differed by only 0.19°C between IAV-positive and IAV-negative pigs. The low prevalence of IAV among the pigs upon entry to the fair in the second objective provides evidence that limiting intraspecies spread of IAV during the fairs will likely have significant impacts on the zoonotic transmission. However, in both objectives, the high degree of similarity in the body temperature measurements between the IAV-positive and IAV-negative pigs made it impossible to set a diagnostically meaningful cut point to differentiate IAV status of the individual animals. Unfortunately, body temperature measurement cannot be used to accurately screen exhibition swine for IAV. © 2015 Blackwell Verlag GmbH.

9 CFR 91.9 - Swine.

Science.gov (United States)

2010-01-01

... 9 Animals and Animal Products 1 2010-01-01 2010-01-01 false Swine. 91.9 Section 91.9 Animals and Animal Products ANIMAL AND PLANT HEALTH INSPECTION SERVICE, DEPARTMENT OF AGRICULTURE EXPORTATION AND IMPORTATION OF ANIMALS (INCLUDING POULTRY) AND ANIMAL PRODUCTS INSPECTION AND HANDLING OF LIVESTOCK FOR...

CRISPR-Cas9, a tool to efficiently increase the development of recombinant African swine fever viruses

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African swine fever is a contagious and often lethal disease for domestic pigs with a significant economic impact on the swine industry. The etiological agent, African swine fever virus (ASFV), is a highly structurally complex double stranded DNA virus. No effective vaccines or antiviral treatment ...

Genes indicative of zoonotic and swine pathogens are persistent in stream water and sediment following a swine manure spill

Science.gov (United States)

Haack, Sheridan K.; Duris, Joseph W.; Kolpin, Dana W.; Fogarty, Lisa R.; Johnson, Heather E.; Gibson, Kristen E.; Focazio, Michael J.; Schwab, Kellogg J.; Hubbard, Laura E.; Foreman, William T.

2015-01-01

Manure spills to streams are relatively frequent, but no studies have characterized stream contamination with zoonotic and veterinary pathogens, or fecal chemicals, following a spill. We tested stream water and sediment over 25 days and downstream for 7.6 km for: fecal indicator bacteria (FIB); the fecal indicator chemicals cholesterol and coprostanol; 20 genes for zoonotic and swine-specific bacterial pathogens by presence/absence polymerase chain reaction (PCR) for viable cells; one swine-specific Escherichia coli toxin gene (STII) by quantitative PCR (qPCR); and nine human and animal viruses by qPCR, or reverse-transcriptase qPCR. Twelve days post-spill, and 4.2 km downstream, water concentrations of FIB, cholesterol, and coprostanol were 1-2 orders of magnitude greater than those detected before, or above, the spill, and genes indicating viable zoonotic or swine-infectious Escherichia coli, were detected in water or sediment. STII increased from undetectable before, or above the spill, to 105 copies/100 mL water 12 days post-spill. Thirteen of 14 water (8/9 sediment) samples had viable STII-carrying cells post-spill. Eighteen days post-spill porcine adenovirus and teschovirus were detected 5.6 km downstream. Sediment FIB concentrations (per gram wet weight) were greater than in water, and sediment was a continuous reservoir of genes and chemicals post-spill. Constituent concentrations were much lower, and detections less frequent, in a runoff event (200 days post-spill) following manure application, although the swine-associated STII and stx2e genes were detected. Manure spills are an underappreciated pathway for livestock-derived contaminants to enter streams, with persistent environmental outcomes, and the potential for human and veterinary health consequences.

Induction of Robust Immune Responses in Swine by Using a Cocktail of Adenovirus-Vectored African Swine Fever Virus Antigens.

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Lokhandwala, Shehnaz; Waghela, Suryakant D; Bray, Jocelyn; Martin, Cameron L; Sangewar, Neha; Charendoff, Chloe; Shetti, Rashmi; Ashley, Clay; Chen, Chang-Hsin; Berghman, Luc R; Mwangi, Duncan; Dominowski, Paul J; Foss, Dennis L; Rai, Sharath; Vora, Shaunak; Gabbert, Lindsay; Burrage, Thomas G; Brake, David; Neilan, John; Mwangi, Waithaka

2016-11-01

The African swine fever virus (ASFV) causes a fatal hemorrhagic disease in domestic swine, and at present no treatment or vaccine is available. Natural and gene-deleted, live attenuated strains protect against closely related virulent strains; however, they are yet to be deployed and evaluated in the field to rule out chronic persistence and a potential for reversion to virulence. Previous studies suggest that antibodies play a role in protection, but induction of cytotoxic T lymphocytes (CTLs) could be the key to complete protection. Hence, generation of an efficacious subunit vaccine depends on identification of CTL targets along with a suitable delivery method that will elicit effector CTLs capable of eliminating ASFV-infected host cells and confer long-term protection. To this end, we evaluated the safety and immunogenicity of an adenovirus-vectored ASFV (Ad-ASFV) multiantigen cocktail formulated in two different adjuvants and at two immunizing doses in swine. Immunization with the cocktail rapidly induced unprecedented ASFV antigen-specific antibody and cellular immune responses against all of the antigens. The robust antibody responses underwent rapid isotype switching within 1 week postpriming, steadily increased over a 2-month period, and underwent rapid recall upon boost. Importantly, the primed antibodies strongly recognized the parental ASFV (Georgia 2007/1) by indirect fluorescence antibody (IFA) assay and Western blotting. Significant antigen-specific gamma interferon-positive (IFN-γ + ) responses were detected postpriming and postboosting. Furthermore, this study is the first to demonstrate induction of ASFV antigen-specific CTL responses in commercial swine using Ad-ASFV multiantigens. The relevance of the induced immune responses in regard to protection needs to be evaluated in a challenge study. Copyright © 2016, American Society for Microbiology. All Rights Reserved.

Mitochondrial electron transport chain functions in long-lived Ames dwarf mice

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Choksi, Kashyap B.; Nuss, Jonathan E.; DeFord, James H.; Papaconstantinou, John

2011-01-01

The age-associated decline in tissue function has been attributed to ROS-mediated oxidative damage due to mitochondrial dysfunction. The long-lived Ames dwarf mouse exhibits resistance to oxidative stress, a physiological characteristic of longevity. It is not known, however, whether there are differences in the electron transport chain (ETC) functions in Ames tissues that are associated with their longevity. In these studies we analyzed enzyme activities of ETC complexes, CI-CV and the coupled CI-CII and CII-CIII activities of mitochondria from several tissues of young, middle aged and old Ames dwarf mice and their corresponding wild type controls to identify potential mitochondrial prolongevity functions. Our studies indicate that post-mitotic heart and skeletal muscle from Ames and wild-type mice show similar changes in ETC complex activities with aging, with the exception of complex IV. Furthermore, the kidney, a slowly proliferating tissue, shows dramatic differences in ETC functions unique to the Ames mice. Our data show that there are tissue specific mitochondrial functions that are characteristic of certain tissues of the long-lived Ames mouse. We propose that this may be a factor in the determination of extended lifespan of dwarf mice. PMID:21934186

Antimicrobial Susceptibility Patterns of Brachyspira Species Isolated from Swine Herds in the United States

OpenAIRE

Mirajkar, Nandita S.; Davies, Peter R.; Gebhart, Connie J.

2016-01-01

Outbreaks of swine dysentery, caused by Brachyspira hyodysenteriae and the recently discovered “Brachyspira hampsonii,” have reoccurred in North American swine herds since the late 2000s. Additionally, multiple Brachyspira species have been increasingly isolated by North American diagnostic laboratories. In Europe, the reliance on antimicrobial therapy for control of swine dysentery has been followed by reports of antimicrobial resistance over time. The objectives of our study were to determi...

History of Swine influenza viruses in Asia.

Science.gov (United States)

Zhu, Huachen; Webby, Richard; Lam, Tommy T Y; Smith, David K; Peiris, Joseph S M; Guan, Yi

2013-01-01

The pig is one of the main hosts of influenza A viruses and plays important roles in shaping the current influenza ecology. The occurrence of the 2009 H1N1 pandemic influenza virus demonstrated that pigs could independently facilitate the genesis of a pandemic influenza strain. Genetic analyses revealed that this virus was derived by reassortment between at least two parent swine influenza viruses (SIV), from the northern American triple reassortant H1N2 (TR) and European avian-like H1N1 (EA) lineages. The movement of live pigs between different continents and subsequent virus establishment are preconditions for such a reassortment event to occur. Asia, especially China, has the largest human and pig populations in the world, and seems to be the only region frequently importing pigs from other continents. Virological surveillance revealed that not only classical swine H1N1 (CS), and human-origin H3N2 viruses circulated, but all of the EA, TR and their reassortant variants were introduced into and co-circulated in pigs in this region. Understanding the long-term evolution and history of SIV in Asia would provide insights into the emergence of influenza viruses with epidemic potential in swine and humans.

Laboratory and in-situ reductions of soluble phosphorus in swine waste slurries.

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Burns, R T; Moody, L B; Walker, F R; Raman

2001-11-01

Laboratory and field experiments were conducted using magnesium chloride (MgCl2) to force the precipitation of struvite (MgNH4PO4 x 6H2O) and reduce the concentration of soluble phosphorus (SP) in swine waste. In laboratory experiments, reductions of SP of 76% (572 to 135 mg P l(-1)) were observed in raw swine manure after addition of magnesium chloride (MgCl2) at a rate calculated to provide a 1.6:1 molar ratio of magnesium (Mg) to total phosphorus. Adjusting the pH of the treated manure to pH 9.0 with sodium hydroxide (NaOH) increased SP reduction to 91% (572 to 50 mg P l(-1)). X-ray diffraction of the precipitate recovered from swine waste slurry treated only with MgCl2 confirmed the presence ofstruvite. The molar N:P:Mg ratio of the recovered precipitate was 1:1.95:0.24, suggesting that compounds in addition to struvite were formed. In a field experiment conducted in a swine manure holding pond, a 90% reduction in SP concentration was observed in approximately 140,000 l of swine manure slurry treated before land application with 2,000 l MgCl2 (64% solution) at ambient slurry temperatures ranging from 5 to 10 degrees C.

Adaptive evolution during the establishment of European avian-like H1N1 influenza A virus in swine.

Science.gov (United States)

Joseph, Udayan; Vijaykrishna, Dhanasekaran; Smith, Gavin J D; Su, Yvonne C F

2018-04-01

An H1N1 subtype influenza A virus with all eight gene segments derived from wild birds (including mallards), ducks and chickens, caused severe disease outbreaks in swine populations in Europe beginning in 1979 and successfully adapted to form the European avian-like swine (EA-swine) influenza lineage. Genes of the EA-swine lineage that are clearly segregated from its closest avian relatives continue to circulate in swine populations globally and represent a unique opportunity to study the adaptive process of an avian-to-mammalian cross-species transmission. Here, we used a relaxed molecular clock model to test whether the EA-swine virus originated through the introduction of a single avian ancestor as an entire genome, followed by an analysis of host-specific selection pressures among different gene segments. Our data indicated independent introduction of gene segments via transmission of avian viruses into swine followed by reassortment events that occurred at least 1-4 years prior to the EA-swine outbreak. All EA-swine gene segments exhibit greater selection pressure than avian viruses, reflecting both adaptive pressures and relaxed selective constraints that are associated with host switching. Notably, we identified key amino acid mutations in the viral surface proteins (H1 and N1) that play a role in adaptation to new hosts. Following the establishment of EA-swine lineage, we observed an increased frequency of intrasubtype reassortment of segments compared to the earlier strains that has been associated with adaptive amino acid replacements, disease severity and vaccine escape. Taken together, our study provides key insights into the adaptive changes in viral genomes following the transmission of avian influenza viruses to swine and the early establishment of the EA-swine lineage.

Subunits Rip1p and Cox9p of the respiratory chain contribute to diclofenac-induced mitochondrial dysfunction

NARCIS (Netherlands)

van Leeuwen, J.S.; Orij, R.; Luttik, M.A.H.; Smits, G.J.; Vermeulen, N.P.E.; Vos, J. C.

2011-01-01

The widely used drug diclofenac can cause serious heart, liver and kidney injury, which may be related to its ability to cause mitochondrial dysfunction. Using Saccharomyces cerevisiae as a model system, we studied the mechanisms of diclofenac toxicity and the role of mitochondria therein. We found

Mitochondrial H2O2 signaling is controlled by the concerted action of peroxiredoxin III and sulfiredoxin: Linking mitochondrial function to circadian rhythm.

Science.gov (United States)

Rhee, Sue Goo; Kil, In Sup

2016-11-01

Mitochondria produce hydrogen peroxide (H 2 O 2 ) during energy metabolism in most mammalian cells as well as during the oxidation of cholesterol associated with the synthesis of steroid hormones in steroidogenic cells. Some of the H 2 O 2 produced in mitochondria is released into the cytosol, where it serves as a key regulator of various signaling pathways. Given that mitochondria are equipped with several H 2 O 2 -eliminating enzymes, however, it had not been clear how mitochondrial H 2 O 2 can escape destruction by these enzymes for such release. Peroxiredoxin III (PrxIII) is the most abundant and efficient H 2 O 2 -eliminating enzyme in mitochondria of most cell types. We found that PrxIII undergoes reversible inactivation through hyperoxidation of its catalytic cysteine residue to cysteine sulfinic acid, and that release of mitochondrial H 2 O 2 likely occurs as a result of such PrxIII inactivation. The hyperoxidized form of PrxIII (PrxIII-SO 2 H) is reduced and reactivated by sulfiredoxin (Srx). We also found that the amounts of PrxIII-SO 2 H and Srx undergo antiphasic circadian oscillation in mitochondria of the adrenal gland, heart, and brown adipose tissue of mice maintained under normal conditions. Cytosolic Srx was found to be imported into mitochondria via a mechanism that requires formation of a disulfide-linked complex with heat shock protein 90, which is likely promoted by H 2 O 2 released from mitochondria. The imported Srx was found to be degraded by Lon protease in a manner dependent on PrxIII hyperoxidation state. The coordinated import and degradation of Srx underlie Srx oscillation and consequent PrxIII-SO 2 H oscillation in mitochondria. The rhythmic change in the amount of PrxIII-SO 2 H suggests that mitochondrial release of H 2 O 2 is also likely a circadian event that conveys temporal information on steroidogenesis in the adrenal gland and on energy metabolism in heart and brown adipose tissue to cytosolic signaling pathways. Copyright �

Continuous anaerobic digestion of swine manure: ADM1-based modelling and effect of addition of swine manure fibers pretreated with aqueous ammonia soaking

OpenAIRE

Jurado, E.; Antonopoulou, G.; Lyberatos, G.; Gavala, Hariklia N.; Skiadas, Ioannis V.

2016-01-01

Anaerobic digestion of manure fibers presents challenges due to their low biodegradability. Aqueous ammonia soaking (AAS) has been tested as a simple method to disrupt the lignocellulose and increase the methane yield of manure fibers. In the present study, mesophilic anaerobic digestion of AAS pretreated manure fibers was performed in CSTR-type digesters, fed with swine manure and/or a mixtureof swine manure and AAS pretreated manure fibers (at a total solids based ratio of 0.52 manure per0....

DETECTION OF CLASSICAL SWINE FEVER VIRUS BY RT-PCR IN WEST BENGAL, INDIA

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Sumit Chowdhury

2016-12-01

Full Text Available Classical swine fever is a deadly disease of swine, caused by a RNA virus. The present study has identified presence of the classical swine fever virus (CSFV in pigs of West Bengal by one step reverse transcriptase PCR (RT-PCR performed using 5’ NTR specific primers. Internal organs from clinically affected pigs were examined from three districts of West Bengal. RT-PCT has identified presence of CSFV in all the tissues examined confirming presence of CSFV in different parts of the state.

The tissue residues of sodium dehydroacetate used as feed preservative in swine.

Science.gov (United States)

Liu, Hao; Han, Lingling; Xie, Jiayu; Wu, Yingchao; Xie, Yang; Zhang, Yumei

2018-01-01

Sodium dehydroacetate (Na-DHA) is a food and feed additive with antimicrobial effects. There is little information on Na-DHA residue levels in foods derived from animals. In this study, Na-DHA residue levels in swine tissues were determined by HLPC, and the pharmacokinetics of Na-DHA in tissues were determined. The Na-DHA residue levels in swine tissues were liver > muscle > fat. The pharmacokinetics of Na-DHA followed a binomial regression model, and the half-time of Na-DHA in swine tissues was 9.07 days for kidney, 7.19 days for liver, 6.66 days for muscle, and 5.39 days for fat tissue. The accuracy of the HPLC method for Na-DHA determination ranged from 80.18% to 91.33% recovery, with coefficients of variation swine diet is a safe feed additive based on residue elimination and ADI values reported. © 2017 Society of Chemical Industry. © 2017 Society of Chemical Industry.

Mitochondrial NUDIX hydrolases: A metabolic link between NAD catabolism, GTP and mitochondrial dynamics.

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Long, Aaron; Klimova, Nina; Kristian, Tibor

2017-10-01

NAD + catabolism and mitochondrial dynamics are important parts of normal mitochondrial function and are both reported to be disrupted in aging, neurodegenerative diseases, and acute brain injury. While both processes have been extensively studied there has been little reported on how the mechanisms of these two processes are linked. This review focuses on how downstream NAD + catabolism via NUDIX hydrolases affects mitochondrial dynamics under pathologic conditions. Additionally, several potential targets in mitochondrial dysfunction and fragmentation are discussed, including the roles of mitochondrial poly(ADP-ribose) polymerase 1(mtPARP1), AMPK, AMP, and intra-mitochondrial GTP metabolism. Mitochondrial and cytosolic NUDIX hydrolases (NUDT9α and NUDT9β) can affect mitochondrial and cellular AMP levels by hydrolyzing ADP- ribose (ADPr) and subsequently altering the levels of GTP and ATP. Poly (ADP-ribose) polymerase 1 (PARP1) is activated after DNA damage, which depletes NAD + pools and results in the PARylation of nuclear and mitochondrial proteins. In the mitochondria, ADP-ribosyl hydrolase-3 (ARH3) hydrolyzes PAR to ADPr, while NUDT9α metabolizes ADPr to AMP. Elevated AMP levels have been reported to reduce mitochondrial ATP production by inhibiting the adenine nucleotide translocase (ANT), allosterically activating AMPK by altering the cellular AMP: ATP ratio, and by depleting mitochondrial GTP pools by being phosphorylated by adenylate kinase 3 (AK3), which uses GTP as a phosphate donor. Recently, activated AMPK was reported to phosphorylate mitochondria fission factor (MFF), which increases Drp1 localization to the mitochondria and promotes mitochondrial fission. Moreover, the increased AK3 activity could deplete mitochondrial GTP pools and possibly inhibit normal activity of GTP-dependent fusion enzymes, thus altering mitochondrial dynamics. Published by Elsevier Ltd.

Mass and Energy Balances of Dry Thermophilic Anaerobic Digestion Treating Swine Manure Mixed with Rice Straw

OpenAIRE

Zhou, Sheng; Zhang, Jining; Zou, Guoyan; Riya, Shohei; Hosomi, Masaaki

2015-01-01

To evaluate the feasibility of swine manure treatment by a proposed Dry Thermophilic Anaerobic Digestion (DT-AD) system, we evaluated the methane yield of swine manure treated using a DT-AD method with rice straw under different C/N ratios and solid retention time (SRT) and calculated the mass and energy balances when the DT-AD system is used for swine manure treatment from a model farm with 1000 pigs and the digested residue is used for forage rice production. A traditional swine manure trea...

Knowledge, Attitude and Practices regarding Swine Flu among adult population

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Harjot Kaur

2015-09-01

Full Text Available Introduction: Prevention is the most appropriate measure to control H1N1 flu pandemic and awareness of H1N1 flu is ranked very high in preventive measures. Keeping this in view, study was designed to assess the awareness level and to compare it among urban and rural participants. Aims and objectives: To assess the knowledge, attitude and practices regarding swine flu among adult population, to assess whether there is any difference among rural and urban population and to assess the response generated by the media coverage and the Government efforts.Methods: This cross-sectional study was done from April to July 2015 on 300 houses from the urban area and 150 houses from rural area, chosen from study population by random sampling. Mean and standard deviation for continuous variables and percentages for categorical were calculated. Results: 94% of urban and 91.3% of the rural participants had previously heard about swine flu, main source being TV. 46% of urban and 74% of rural participants had myth about spread of swine flu by eating pork. 41.3% of urban and 8.7% of rural population thought that government measures are sufficient for controlling swine flu. Conclusion: Knowledge regarding swine flu pandemic is good among study participants but role of health care providers is minimal and requires more dedicated effort. Lack of awareness among study population regarding some key focus areas like health promoting habits, vaccination and myths regarding the spread is of serious concern and needs to be addressed by the media, health workers and the Government efforts

Metabolic Modulators in Heart Disease: Past, Present, and Future.

Science.gov (United States)

Lopaschuk, Gary D

2017-07-01

Ischemic heart disease and heart failure are leading causes of mortality and morbidity worldwide. They continue to be major burden on health care systems throughout the world, despite major advances made over the past 40 years in developing new therapeutic approaches to treat these debilitating diseases. A potential therapeutic approach that has been underutilized in treating ischemic heart disease and heart failure is "metabolic modulation." Major alterations in myocardial energy substrate metabolism occur in ischemic heart disease and heart failure, and are associated with an energy deficit in the heart. A metabolic shift from mitochondrial oxidative metabolism to glycolysis, as well as an uncoupling between glycolysis and glucose oxidation, plays a crucial role in the development of cardiac inefficiency (oxygen consumed per work performed) and functional impairment in ischemic heart disease as well as in heart failure. This has led to the concept that optimizing energy substrate use with metabolic modulators can be a potentially promising approach to decrease the severity of ischemic heart disease and heart failure, primarily by improving cardiac efficiency. Two approaches for metabolic modulator therapy are to stimulate myocardial glucose oxidation and/or inhibit fatty acid oxidation. In this review, the past, present, and future of metabolic modulators as an approach to optimizing myocardial energy substrate metabolism and treating ischemic heart disease and heart failure are discussed. This includes a discussion of pharmacological interventions that target enzymes involved in fatty acid uptake, fatty acid oxidation, and glucose oxidation in the heart, as well as enzymes involved in ketone and branched chain amino acid catabolism in the heart. Copyright © 2017 Canadian Cardiovascular Society. Published by Elsevier Inc. All rights reserved.

[The eradication of African swine fever in Brazil, 1978-1984].

Science.gov (United States)

Lyra, T M P

2006-04-01

The African swine fever episode in Brazil was due to trade and tourism between Spain, Portugal and Brazil, at a time when outbreaks were on the rise in Europe. The eradication of the disease, the slaughter of pigs, the elimination of the carcasses and the isolation of affected farms were given wide media coverage, and had a major socio-economic impact. It was forbidden to raise pigs in garbage dumps or to give them feed considered hazardous. Analyses performed in Brazil as well as national and international investigations by researchers from reference laboratories concluded that the disease had spread from Rio de Janeiro to other states, as is stated in official reports. Following emergency measures, a control programme was implemented, leading to enhanced quality in the pig farming sector. The authors describe epidemiological surveillance of African swine fever, classical swine fever and related diseases, biosafety in swine farming, and the emergency action plan comprising animal health training for veterinarians and social workers. The results of the eradication programme were excellent, despite the controversy over compulsory sacrifice in a country with serious social problems. In 2004, Brazil was the fourth largest pork producer and exporter, with an output of 2.679 million tons and exports of 508,000 tons to international markets with very high standards.

Reversible infantile mitochondrial diseases.

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Boczonadi, Veronika; Bansagi, Boglarka; Horvath, Rita

2015-05-01

Mitochondrial diseases are usually severe and progressive conditions; however, there are rare forms that show remarkable spontaneous recoveries. Two homoplasmic mitochondrial tRNA mutations (m.14674T>C/G in mt-tRNA(Glu)) have been reported to cause severe infantile mitochondrial myopathy in the first months of life. If these patients survive the first year of life by extensive life-sustaining measures they usually recover and develop normally. Another mitochondrial disease due to deficiency of the 5-methylaminomethyl-2-thiouridylate methyltransferase (TRMU) causes severe liver failure in infancy, but similar to the reversible mitochondrial myopathy, within the first year of life these infants may also recover completely. Partial recovery has been noted in some other rare forms of mitochondrial disease due to deficiency of mitochondrial tRNA synthetases and mitochondrial tRNA modifying enzymes. Here we summarize the clinical presentation of these unique reversible mitochondrial diseases and discuss potential molecular mechanisms behind the reversibility. Understanding these mechanisms may provide the key to treatments of potential broader relevance in mitochondrial disease, where for the majority of the patients no effective treatment is currently available.

miR-27 regulates mitochondrial networks by directly targeting the mitochondrial fission factor.

Science.gov (United States)

Tak, Hyosun; Kim, Jihye; Jayabalan, Aravinth Kumar; Lee, Heejin; Kang, Hoin; Cho, Dong-Hyung; Ohn, Takbum; Nam, Suk Woo; Kim, Wook; Lee, Eun Kyung

2014-11-28

Mitochondrial morphology is dynamically regulated by forming small, fragmented units or interconnected networks, and this is a pivotal process that is used to maintain mitochondrial homeostasis. Although dysregulation of mitochondrial dynamics is related to the pathogenesis of several human diseases, its molecular mechanism is not fully elucidated. In this study, we demonstrate the potential role of miR-27 in the regulation of mitochondrial dynamics. Mitochondrial fission factor (MFF) mRNA is a direct target of miR-27, whose ectopic expression decreases MFF expression through binding to its 3'-untranslated region. Expression of miR-27 results in the elongation of mitochondria as well as an increased mitochondrial membrane potential and mitochondrial ATP level. Our results suggest that miR-27 is a novel regulator affecting morphological mitochondrial changes by targeting MFF.

Novel reassortant swine influenza viruses are circulating in Danish pigs

DEFF Research Database (Denmark)

Breum, Solvej Østergaard; Hjulsager, Charlotte Kristiane; Trebbien, Ramona

of the reassortant viruses comprised a HA gene similar to H1 of H1N1 avian-like swine influenza virus (SIV) and a NA gene most closely related to N2 gene of human H3N2 influenza virus that circulated in humans in the mid 1990s. The internal genes of this reassortant virus with the subtype H1avN2hu all belonged...... to the H1N1 avian-like SIV lineages. Until now this novel virus H1avN2hu has only been detected in Danish swine. The other novel reassortant virus contained the HA gene from H1N1pdm09 virus and a NA gene similar to the N2 gene of H3N2 SIV that have been circulating in European swine since the mid 1980s...

9 CFR 96.2 - Prohibition of casings due to African swine fever and bovine spongiform encephalopathy.

Science.gov (United States)

2010-01-01

... 9 Animals and Animal Products 1 2010-01-01 2010-01-01 false Prohibition of casings due to African swine fever and bovine spongiform encephalopathy. 96.2 Section 96.2 Animals and Animal Products ANIMAL... spongiform encephalopathy. (a) Swine casings. The importation of swine casings that originated in or were...

Real-Time Fluorescence Measurements of ROS and [Ca2+] in Ischemic / Reperfused Rat Hearts: Detectable Increases Occur only after Mitochondrial Pore Opening and Are Attenuated by Ischemic Preconditioning.

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Tatyana Andrienko

Full Text Available Mitochondrial permeability transition pore (mPTP opening is critical for ischemia / reperfusion (I/R injury and is associated with increased [Ca2+] and reactive oxygen species (ROS. Here we employ surface fluorescence to establish the temporal sequence of these events in beating perfused hearts subject to global I/R. A bespoke fluorimeter was used to synchronously monitor surface fluorescence and reflectance of Langendorff-perfused rat hearts at multiple wavelengths, with simultaneous measurements of hemodynamic function. Potential interference by motion artefacts and internal filtering was assessed and minimised. Re-oxidation of NAD(PH and flavoproteins on reperfusion (detected using autofluorescence was rapid (t0.5 < 15 s and significantly slower following ischemic preconditioning (IP. This argues against superoxide production from reduced Complex 1 being a critical mediator of initial mPTP opening during early reperfusion. Furthermore, MitoPY1 (a mitochondria-targeted H2O2-sensitive fluorescent probe and aconitase activity measurements failed to detect matrix ROS increases during early reperfusion. However, two different fluorescent cytosolic ROS probes did detect ROS increases after 2-3 min of reperfusion, which was shown to be after initiation of mPTP opening. Cyclosporin A (CsA and IP attenuated these responses and reduced infarct size. [Ca2+]i (monitored with Indo-1 increased progressively during ischemia, but dropped rapidly within 90 s of reperfusion when total mitochondrial [Ca2+] was shown to be increased. These early changes in [Ca2+] were not attenuated by IP, but substantial [Ca2+] increases were observed after 2-3 min reperfusion and these were prevented by both IP and CsA. Our data suggest that the major increases in ROS and [Ca2+] detected later in reperfusion are secondary to mPTP opening. If earlier IP-sensitive changes occur that might trigger initial mPTP opening they are below our limit of detection. Rather, we suggest that

Antiarrhythmic effect of tamoxifen on the vulnerability induced by hyperthyroidism to heart ischemia/reperfusion damage.

Science.gov (United States)

Pavón, Natalia; Hernández-Esquivel, Luz; Buelna-Chontal, Mabel; Chávez, Edmundo

2014-09-01

Hyperthyroidism, known to have deleterious effects on heart function, and is associated with an enhanced metabolic state, implying an increased production of reactive oxygen species. Tamoxifen is a selective antagonist of estrogen receptors. These receptors make the hyperthyroid heart more susceptible to ischemia/reperfusion. Tamoxifen is also well-known as an antioxidant. The aim of the present study was to explore the possible protective effect of tamoxifen on heart function in hyperthyroid rats. Rats were injected daily with 3,5,3'-triiodothyronine at 2mg/kg body weight during 5 days to induce hyperthyroidism. One group was treated with 10mg/kg tamoxifen and another was not. The protective effect of the drug on heart rhythm was analyzed after 5 min of coronary occlusion followed by 5 min reperfusion. In hyperthyroid rats not treated with tamoxifen, ECG tracings showed post-reperfusion arrhythmias, and heart mitochondria isolated from the ventricular free wall lost the ability to accumulate and retain matrix Ca(2+) and to form a high electric gradient. Both of these adverse effects were avoided with tamoxifen treatment. Hyperthyroidism-induced oxidative stress caused inhibition of cis-aconitase and disruption of mitochondrial DNA, effects which were also avoided by tamoxifen treatment. The current results support the idea that tamoxifen inhibits the hypersensitivity of hyperthyroid rat myocardium to reperfusion damage, probably because its antioxidant activity inhibits the mitochondrial permeability transition. Copyright © 2014 Elsevier Ltd. All rights reserved.

Co-pyrolysis of swine manure with agricultural plastic waste: laboratory-scale study.

Science.gov (United States)

Ro, Kyoung S; Hunt, Patrick G; Jackson, Michael A; Compton, David L; Yates, Scott R; Cantrell, Keri; Chang, SeChin

2014-08-01

Manure-derived biochar is the solid product resulting from pyrolysis of animal manures. It has considerable potential both to improve soil quality with high levels of nutrients and to reduce contaminants in water and soil. However, the combustible gas produced from manure pyrolysis generally does not provide enough energy to sustain the pyrolysis process. Supplementing this process may be achieved with spent agricultural plastic films; these feedstocks have large amounts of available energy. Plastic films are often used in soil fumigation. They are usually disposed in landfills, which is wasteful, expensive, and environmentally unsustainable. The objective of this work was to investigate both the energetics of co-pyrolyzing swine solids with spent plastic mulch films (SPM) and the characteristics of its gas, liquid, and solid byproducts. The heating value of the product gas from co-pyrolysis was found to be much higher than that of natural gas; furthermore, the gas had no detectable toxic fumigants. Energetically, sustaining pyrolysis of the swine solids through the energy of the product gas could be achieved by co-pyrolyzing dewatered swine solids (25%m/m) with just 10% SPM. If more than 10% SPM is used, the co-pyrolysis would generate surplus energy which could be used for power generation. Biochars produced from co-pyrolyzing SPM and swine solid were similar to swine solid alone based on the surface area and the (1)H NMR spectra. The results of this study demonstrated the potential of using pyrolysis technology to manage two prominent agricultural waste streams (SPM and swine solids) while producing value-added biochar and a power source that could be used for local farm operations. Published by Elsevier Ltd.

Analysis of DNA methylation in various swine tissues.

Directory of Open Access Journals (Sweden)

Chun Yang

Full Text Available DNA methylation is known to play an important role in regulating gene expression during biological development and tissue differentiation in eukaryotes. In this study, we used the fluorescence-labeled methylation-sensitive amplified polymorphism (F-MSAP method to assess the extent and pattern of cytosine methylation in muscle, heart, liver, spleen, lung, kidney and stomach from the swine strain Laiwu, and we also examined specific methylation patterns in the seven tissues. In total, 96,371 fragments, each representing a recognition site cleaved by either or both EcoRI + HpaII and EcoRI + MspI, the HpaII and MspI are isoschizomeric enzymes, were amplified using 16 pairs of selective primers. A total of 50,094 sites were found to be methylated at cytosines in seven tissues. The incidence of DNA methylation was approximately 53.99% in muscle, 51.24% in the heart, 50.18% in the liver, 53.31% in the spleen, 51.97% in the lung, 51.15% in the kidney and 53.39% in the stomach, as revealed by the incidence of differential digestion. Additionally, differences in DNA methylation levels imply that such variations may be related to specific gene expression during tissue differentiation, growth and development. Three types of bands were generated in the F-MSAP profile, the total numbers of these three types of bands in the seven tissues were 46,277, 24,801 and 25,293, respectively.In addition, different methylation patterns were observed in seven tissues from pig, and almost all of the methylation patterns detected by F-MSAP could be confirmed by Southern analysis using the isolated amplified fragments as probes. The results clearly demonstrated that the F-MSAP technique can be adapted for use in large-scale DNA methylation detection in the pig genome.

Thyroid hormone-induced oxidative damage on lipids, glutathione and DNA in the mouse heart.

Science.gov (United States)

Gredilla, R; Barja, G; López-Torres, M

2001-10-01

Oxygen radicals of mitochondrial origin are involved in oxidative damage. In order to analyze the possible relationship between metabolic rate, oxidative stress and oxidative damage, OF1 female mice were rendered hyper- and hypothyroid by chronic administration of 0.0012% L-thyroxine (T4) and 0.05% 6-n-propyl-2-thiouracil (PTU), respectively, in their drinking water for 5 weeks. Hyperthyroidism significantly increased the sensitivity to lipid peroxidation in the heart, although the endogenous levels of lipid peroxidation were not altered. Thyroid hormone-induced oxidative stress also resulted in higher levels of GSSG and GSSG/GSH ratio. Oxidative damage to mitochondrial DNA was greater than that to genomic DNA. Hyperthyroidism decreased oxidative damage to genomic DNA. Hypothyroidism did not modify oxidative damage in the lipid fraction but significantly decreased GSSG and GSSG/GSH ratio and oxidative damage to mitochondrial DNA. These results indicate that thyroid hormones modulate oxidative damage to lipids and DNA, and cellular redox potential in the mouse heart. A higher oxidative stress in the hyperthyroid group is presumably neutralized in the case of nuclear DNA by an increase in repair activity, thus protecting this key molecule. Treatment with PTU, a thyroid hormone inhibitor, reduced oxidative damage in the different cell compartments.

Sevoflurane postconditioning improves myocardial mitochondrial respiratory function and reduces myocardial ischemia-reperfusion injury by up-regulating HIF-1.

Science.gov (United States)

Yang, Long; Xie, Peng; Wu, Jianjiang; Yu, Jin; Yu, Tian; Wang, Haiying; Wang, Jiang; Xia, Zhengyuan; Zheng, Hong

2016-01-01

Sevoflurane postconditioning (SPostC) can exert myocardial protective effects similar to ischemic preconditioning. However, the exact myocardial protection mechanism by SPostC is unclear. Studies indicate that hypoxia-inducible factor-1 (HIF-1) maintains cellular respiration homeostasis by regulating mitochondrial respiratory chain enzyme activity under hypoxic conditions. This study investigated whether SPostC could regulate the expression of myocardial HIF-1α and to improve mitochondrial respiratory function, thereby relieving myocardial ischemia-reperfusion injury in rats. The myocardial ischemia-reperfusion rat model was established using the Langendorff isolated heart perfusion apparatus. Additionally, postconditioning was performed using sevoflurane alone or in combination with the HIF-1α inhibitor 2-methoxyestradiol (2ME2). The changes in hemodynamic parameters, HIF-1α protein expression levels, mitochondrial respiratory function and enzyme activity, mitochondrial reactive oxygen species (ROS) production rates, and mitochondrial ultrastructure were measured or observed. Compared to the ischemia-reperfusion (I/R) group, HIF-1α expression in the SPostC group was significantly up-regulated. Additionally, cardiac function indicators, mitochondrial state 3 respiratory rate, respiratory control ratio (RCR), cytochrome C oxidase (C c O), NADH oxidase (NADHO), and succinate oxidase (SUCO) activities, mitochondrial ROS production rate, and mitochondrial ultrastructure were significantly better than those in the I/R group. However, these advantages were completely reversed by the HIF-1α specific inhibitor 2ME2 ( P <0.05). The myocardial protective function of SPostC might be associated with the improvement of mitochondrial respiratory function after up-regulation of HIF-1α expression.

Financial benefit from the eradication of swine dysentery.

Science.gov (United States)

Wood, E N; Lysons, R J

1988-03-19

Swine dysentery was eradicated from a 270 sow herd by using medication in conjunction with cleaning and disinfection, without reducing the herd size. The feed conversion efficiency, cost per kg liveweight gain and veterinary costs in the herd were compared with similar Meat and Livestock Commission recorded herds before swine dysentery entered the farm, while it was present and after its eradication. During the four years when the disease was endemic in the herd the feed conversion efficiency deteriorated by 0.58, equivalent to 7.31 pounds per pig, the cost per kg liveweight gain was 15 per cent higher and the costs of veterinary care and medicines were 1.38 pounds per pig greater. Although there were pigs with clinical swine dysentery in the herd during the four year period, the poor production figures were attributed mainly to subclinical disease. The cost of eradicating the disease was more than 20,000 pounds but this sum was recouped within 12 months by the improved production and reduced drug usage. The chances of success of such a programme have been estimated to be between 54 and 90 per cent.

Toxins in botanical dietary supplements: blue cohosh components disrupt cellular respiration and mitochondrial membrane potential.

Science.gov (United States)

Datta, Sandipan; Mahdi, Fakhri; Ali, Zulfiqar; Jekabsons, Mika B; Khan, Ikhlas A; Nagle, Dale G; Zhou, Yu-Dong

2014-01-24

Certain botanical dietary supplements have been associated with idiosyncratic organ-specific toxicity. Similar toxicological events, caused by drug-induced mitochondrial dysfunction, have forced the withdrawal or U.S. FDA "black box" warnings of major pharmaceuticals. To assess the potential mitochondrial liability of botanical dietary supplements, extracts from 352 authenticated plant samples used in traditional Chinese, Ayurvedic, and Western herbal medicine were evaluated for the ability to disrupt cellular respiration. Blue cohosh (Caulophyllum thalictroides) methanol extract exhibited mitochondriotoxic activity. Used by some U.S. midwives to help induce labor, blue cohosh has been associated with perinatal stroke, acute myocardial infarction, congestive heart failure, multiple organ injury, and neonatal shock. The potential link between mitochondrial disruption and idiosyncratic herbal intoxication prompted further examination. The C. thalictroides methanol extract and three saponins, cauloside A (1), saponin PE (2), and cauloside C (3), exhibited concentration- and time-dependent mitochondriotoxic activities. Upon treatment, cell respiration rate rapidly increased and then dramatically decreased within minutes. Mechanistic studies revealed that C. thalictroides constituents impair mitochondrial function by disrupting membrane integrity. These studies provide a potential etiological link between this mitochondria-sensitive form of cytotoxicity and idiosyncratic organ damage.

Toxins in Botanical Dietary Supplements: Blue Cohosh Components Disrupt Cellular Respiration and Mitochondrial Membrane Potential

Science.gov (United States)

Datta, Sandipan; Mahdi, Fakhri; Ali, Zulfiqar; Jekabsons, Mika B.; Khan, Ikhlas A.; Nagle, Dale G.; Zhou, Yu-Dong

2014-01-01

Certain botanical dietary supplements have been associated with idiosyncratic organ-specific toxicity. Similar toxicological events, caused by drug-induced mitochondrial dysfunction, have forced the withdrawal or U.S. FDA “Black Box” warnings of major pharmaceuticals. To assess the potential mitochondrial liability of botanical dietary supplements, extracts from 352 authenticated plant samples used in traditional Chinese, Ayurvedic, and Western herbal medicine were evaluated for the ability to disrupt cellular respiration. Blue cohosh (Caulophyllum thalictroides) methanol extract exhibited mitochondriotoxic activity. Used by some U.S. midwives to help induce labor, blue cohosh has been associated with perinatal stroke, acute myocardial infarction, congestive heart failure, multiple organ injury, and neonatal shock. The potential link between mitochondrial disruption and idiosyncratic herbal intoxication prompted further examination. The C. thalictroides methanol extract and three saponins, cauloside A (1), saponin PE (2), and cauloside C (3) exhibited concentration- and time-dependent mitochondriotoxic activities. Upon treatment, cell respiration rate rapidly increased and then dramatically decreased within minutes. Mechanistic studies revealed that C. thalictroides constituents impair mitochondrial function by disrupting membrane integrity. These studies provide a potential etiological link between this mitochondria-sensitive form of cytotoxicity and idiosyncratic organ damage. PMID:24328138

The progressive adaptation of a georgian isolate of African swine fever virus to vero cells leads to a gradual attenuation of virulence in swine corresponding to major modifications of the viral genome.

Science.gov (United States)

Krug, Peter W; Holinka, Lauren G; O'Donnell, Vivian; Reese, Bo; Sanford, Brenton; Fernandez-Sainz, Ignacio; Gladue, Douglas P; Arzt, Jonathan; Rodriguez, Luis; Risatti, Guillermo R; Borca, Manuel V

2015-02-01

African swine fever virus (ASFV) causes a contagious and often lethal disease of feral and domestic swine. Experimental vaccines derived from naturally occurring, genetically modified, or cell culture-adapted ASFV have been evaluated, but no commercial vaccine is available to control African swine fever (ASF). We report here the genotypic and phenotypic analysis of viruses obtained at different passages during the process of adaptation of a virulent ASFV field isolate from the Republic of Georgia (ASFV-G) to grow in cultured cell lines. ASFV-G was successively passaged 110 times in Vero cells. Viruses obtained at passages 30, 60, 80, and 110 were evaluated in vitro for the ability to replicate in Vero cells and primary swine macrophages cultures and in vivo for assessing virulence in swine. Replication of ASFV-G in Vero cells increased with successive passages, corresponding to a decreased replication in primary swine macrophages cultures. In vivo, progressive loss of virus virulence was observed with increased passages in Vero cells, and complete attenuation of ASFV-G was observed at passage 110. Infection of swine with the fully attenuated virus did not confer protection against challenge with virulent parental ASFV-G. Full-length sequence analysis of each of these viruses revealed significant deletions that gradually accumulated in specific areas at the right and left variable ends of the genome. Mutations that result in amino acid substitutions and frameshift mutations were also observed, though in a rather limited number of genes. The potential importance of these genetic changes in virus adaptation/attenuation is discussed. The main problem in controlling ASF is the lack of vaccines. Attempts to produce vaccines by adaptation of ASFV to cultured cell lines have been made. These attempts led to the production of attenuated viruses that conferred only homologous protection. Specifics regarding adaptation of these isolates to cell cultures have been

[Swine influenza virus: evolution mechanism and epidemic characterization--a review].

Science.gov (United States)

Qi, Xian; Lu, Chengping

2009-09-01

Pigs may play an important role in the evolution and ecology of influenza A virus. The tracheal epithelium of pigs contain both SA alpha 2,6 Gal and SA alpha 2,3 Gal receptors and can be infected with swine, human and avian viruses, therefore, pigs have been considered as an intermediate host for the adaptation of avian influenza viruses to humans or as mixing vessels for the generation of genetically reassortant viruses. Evolution patterns among swine influenza viruses including evolution of host adaptation, antigenic drift and genetic reassortment, and the latter is the main one. Unlike human influenza viruses, swine viruses have different epizootiological patterns in different areas of world, which is enzootic and geographic dependence. Currently, three predominant subtypes of influenza virus are prevalent in pig populations worldwide: H1N1, H3N2, and H1N2, and these include classical swine H1N1, avian-like H1N1, human-like H3N2, reassortant H3N2 and various genotype H1N2 viruses. In Europe, North America and China, influenza A viruses circulating in pigs are distinct in the genetic characteristics and genetic sources. Since 1979, three subtypes, avian-like H1N1, reassortant H1N2 and H3N2 viruses, have been co-circulating in European swine. Before 1998, classical H1N1 viruses were the exclusive cause of swine influenza in North America. However, after that, three triple-reassortant H1N2, H3N2 and H1N1 viruses with genes of human, swine and avian virus began to emerge in pigs. Genetically, the pandemic viruses emerging in human, so called influenza A (H1N1) viruses, contain genes from both Europe and North American SIV lineages. SIV is not the same as Europe and the United States in the prevalence and genetic background in China, mainly classical swine H1N1 and human-like H3N2 type virus. However, in recent years, SIV from Europe and North America have been introduced into Chinese pig herds, so more attention should be given on the evolutionary of SIV in China

Development of a Swine-Specific Fecal Pollution Marker Based on Host Differences in Methanogen mcrA Genes▿

OpenAIRE

Ufnar, Jennifer A.; Ufnar, David F.; Wang, Shiao Y.; Ellender, R. D.

2007-01-01

The goal of this study was to evaluate methanogen diversity in animal hosts to develop a swine-specific archaeal molecular marker for fecal source tracking in surface waters. Phylogenetic analysis of swine mcrA sequences compared to mcrA sequences from the feces of five animals (cow, deer, sheep, horse, and chicken) and sewage showed four distinct swine clusters, with three swine-specific clades. From this analysis, six sequences were chosen for molecular marker development and initial testin...

Functional analysis of replication determinantsin classical swine fever virus

DEFF Research Database (Denmark)

Hadsbjerg, Johanne

and animal pathogens should facilitate finding new approaches for efficient disease control. The principal aim of this thesis is to characterise determinants involved in the replication of classical swine fever virus (CSFV). Classical swine fever is a highly contagious virus disease of domestic pigs and wild...... in cell culture. Knowledge of these sequence variations and putative long-range interactions will provide valuable insights into mechanisms underlying virustranslation and replication. In manuscript 3, a selection marker has been inserted into a CSFV-based replicon making it suitable for screening...

Evaluation of Faecalibacterium 16S rDNA genetic markers for accurate identification of swine faecal waste by quantitative PCR.

Science.gov (United States)

Duan, Chuanren; Cui, Yamin; Zhao, Yi; Zhai, Jun; Zhang, Baoyun; Zhang, Kun; Sun, Da; Chen, Hang

2016-10-01

A genetic marker within the 16S rRNA gene of Faecalibacterium was identified for use in a quantitative PCR (qPCR) assay to detect swine faecal contamination in water. A total of 146,038 bacterial sequences were obtained using 454 pyrosequencing. By comparative bioinformatics analysis of Faecalibacterium sequences with those of numerous swine and other animal species, swine-specific Faecalibacterium 16S rRNA gene sequences were identified and Polymerase Chain Okabe (PCR) primer sets designed and tested against faecal DNA samples from swine and non-swine sources. Two PCR primer sets, PFB-1 and PFB-2, showed the highest specificity to swine faecal waste and had no cross-reaction with other animal samples. PFB-1 and PFB-2 amplified 16S rRNA gene sequences from 50 samples of swine with positive ratios of 86 and 90%, respectively. We compared swine-specific Faecalibacterium qPCR assays for the purpose of quantifying the newly identified markers. The quantification limits (LOQs) of PFB-1 and PFB-2 markers in environmental water were 6.5 and 2.9 copies per 100 ml, respectively. Of the swine-associated assays tested, PFB-2 was more sensitive in detecting the swine faecal waste and quantifying the microbial load. Furthermore, the microbial abundance and diversity of the microbiomes of swine and other animal faeces were estimated using operational taxonomic units (OTUs). The species specificity was demonstrated for the microbial populations present in various animal faeces. Copyright © 2016 Elsevier Ltd. All rights reserved.

Myocardial Energetics and Heart Failure: a Review of Recent Therapeutic Trials.

Science.gov (United States)

Bhatt, Kunal N; Butler, Javed

2018-06-01

Several novel therapeutics being tested in patients with heart failure are based on myocardial energetics. This review will provide a summary of the recent trials in this area, including therapeutic options targeting various aspects of cellular and mitochondrial metabolism. Agents that improve the energetic balance in myocardial cells have the potential to improve clinical heart failure status. The most promising therapies currently under investigation in this arena include (1) elamipretide, a cardiolipin stabilizer; (2) repletion of iron deficiency with intravenous ferrous carboxymaltose; (3) coenzyme Q10; and (4) the partial adenosine receptor antagonists capadenoson and neladenosone. Myocardial energetics-based therapeutics are groundbreaking in that they utilize novel mechanisms of action to improve heart failure symptoms, without causing the adverse neurohormonal side effects associated with current guideline-based therapies. The drugs appear likely to be added to the heart failure therapy armamentarium as adjuncts to current regimens in the near future.

The mitochondrial transcription factor A functions in mitochondrial base excision repair

DEFF Research Database (Denmark)

Canugovi, Chandrika; Maynard, Scott; Bayne, Anne-Cécile V

2010-01-01

Mitochondrial transcription factor A (TFAM) is an essential component of mitochondrial nucleoids. TFAM plays an important role in mitochondrial transcription and replication. TFAM has been previously reported to inhibit nucleotide excision repair (NER) in vitro but NER has not yet been detected i...

Continuous dry fermentation of swine manure for biogas production

Energy Technology Data Exchange (ETDEWEB)

Chen, Chuang; Zheng, Dan [Biogas Institute of Ministry of Agriculture, Chengdu 610041 (China); Liu, Gang–Jin [Biogas Institute of Ministry of Agriculture, Chengdu 610041 (China); Bioprocess Control AB, Scheelevägen 22, 223 63 Lund (Sweden); Deng, Liang–Wei, E-mail: dengliangwei@caas.cn [Biogas Institute of Ministry of Agriculture, Chengdu 610041 (China); Laboratory of Development and Application of Rural Renewable Energy, Ministry of Agriculture, Chengdu 610041 (China); Southwest Collaborative Innovation Center of Swine for Quality & Safety, Chengdu 611130 (China); Long, Yan; Fan, Zhan–Hui [Biogas Institute of Ministry of Agriculture, Chengdu 610041 (China)

2015-04-15

Highlights: • Continuous dry fermentation of swine manure for biogas production is feasible. • The feedstock TS concentration exerted a significant impact on biogas production. • Influences of ammonia and digestate liquidity were investigated in this study. • The results showed that the feedstock TS of swine manure should not exceed 30%. - Abstract: A down plug-flow anaerobic reactor (DPAR) was designed for the feasibility study on continuous dry fermentation of swine manure without any additional stirring. Using fresh swine manure as the feedstock with TS concentration (w/w) of 20%, 25%, 30%, and 35%, stable volumetric biogas production rates of 2.40, 1.92, 0.911, and 0.644 L·(L d){sup −1} and biogas yields of 0.665, 0.532, 0.252, and 0.178 L g{sup −1}VS were obtained respectively, and the TS degradation rates were 46.5%, 45.4%, 53.2%, and 55.6%, respectively. With the increase of feedstock TS concentration, the concentration of ammonia nitrogen grew up to the maximum value of 3500 mg L{sup −1}. Biogas production was obviously inhibited when the concentration of ammonia nitrogen was above 3000 mg L{sup −1}. The maximal volumetric biogas production rate of 2.34 L·(L d){sup −1} and biogas yield of 0.649 L g{sup −1}VS were obtained with TS concentration of 25% at 25 °C without inhibition. Liquidity experiments showed that TS concentration of digestate could be less than 15.8%, and the flow rate of digestate more than 0.98 m s{sup −1} when the feedstock TS concentration was less than 35%, which indicated the digestate could be easily discharged from a DPAR. Therefore, it is feasible to conduct a continuous dry fermentation in a DPAR using fresh swine manure as the feedstock with TS concentration less than 35%, whereas the feedstock TS concentration should not exceed 30% to achieve the maximal biogas production rate and biogas yield.

Continuous dry fermentation of swine manure for biogas production

International Nuclear Information System (INIS)

Chen, Chuang; Zheng, Dan; Liu, Gang–Jin; Deng, Liang–Wei; Long, Yan; Fan, Zhan–Hui

2015-01-01

Highlights: • Continuous dry fermentation of swine manure for biogas production is feasible. • The feedstock TS concentration exerted a significant impact on biogas production. • Influences of ammonia and digestate liquidity were investigated in this study. • The results showed that the feedstock TS of swine manure should not exceed 30%. - Abstract: A down plug-flow anaerobic reactor (DPAR) was designed for the feasibility study on continuous dry fermentation of swine manure without any additional stirring. Using fresh swine manure as the feedstock with TS concentration (w/w) of 20%, 25%, 30%, and 35%, stable volumetric biogas production rates of 2.40, 1.92, 0.911, and 0.644 L·(L d) −1 and biogas yields of 0.665, 0.532, 0.252, and 0.178 L g −1 VS were obtained respectively, and the TS degradation rates were 46.5%, 45.4%, 53.2%, and 55.6%, respectively. With the increase of feedstock TS concentration, the concentration of ammonia nitrogen grew up to the maximum value of 3500 mg L −1 . Biogas production was obviously inhibited when the concentration of ammonia nitrogen was above 3000 mg L −1 . The maximal volumetric biogas production rate of 2.34 L·(L d) −1 and biogas yield of 0.649 L g −1 VS were obtained with TS concentration of 25% at 25 °C without inhibition. Liquidity experiments showed that TS concentration of digestate could be less than 15.8%, and the flow rate of digestate more than 0.98 m s −1 when the feedstock TS concentration was less than 35%, which indicated the digestate could be easily discharged from a DPAR. Therefore, it is feasible to conduct a continuous dry fermentation in a DPAR using fresh swine manure as the feedstock with TS concentration less than 35%, whereas the feedstock TS concentration should not exceed 30% to achieve the maximal biogas production rate and biogas yield

Antimicrobial use in Chinese swine and broiler poultry production.

Science.gov (United States)

Krishnasamy, Vikram; Otte, Joachim; Silbergeld, Ellen

2015-01-01

Antimicrobial use for growth promotion in food animal production is now widespread. A major concern is the rise of antimicrobial resistance and the subsequent impact on human health. The antimicrobials of concern are used in concentrated animal feeding operations (CAFOs) which are responsible for almost all meat production including swine and poultry in the US. With global meat consumption rising, the CAFO model has been adopted elsewhere to meet this demand. One such country where this has occurred is China, and evidence suggests 70% of poultry production now occurs outside of traditional small farms. Moreover, China is now the largest aggregate consumer of meat products in the world. With this rapid rise in consumption, the Chinese production model has changed along with the use of antimicrobials in feeds. However, the specific antibiotic use in the Chinese food animal production sector is unclear. Additionally, we are aware of high quantities of antimicrobial use because of reports of high concentrations of antimicrobials in animal waste and surface waters surrounding animal feeding operations. In this report, we estimate the volume of antibiotics used for swine and poultry production as these are the two meat sources with the highest levels of production and consumption in China. We adopt a model developed by Mellon et al. in the US for estimating drug use in feed for poultry and swine production to estimate overall antimicrobial use as well as antimicrobial use by class. We calculate that 38.5 million kg [84.9 million lbs] were used in 2012 in China's production of swine and poultry. By antibiotic class, the highest weights are tetracyclines in swine and coccidiostats in poultry. The volume of antimicrobial use is alarming. Although there are limitations to these data, we hope our report will stimulate further analysis and a sense of urgency in assessing the consequences of such high levels of utilization in terms of antibiotic resistance in the food supply

Cardiomyocyte mitochondrial respiration is reduced by receptor for advanced glycation end-product signaling in a ceramide-dependent manner.

Science.gov (United States)

Nelson, Michael B; Swensen, Adam C; Winden, Duane R; Bodine, Jared S; Bikman, Benjamin T; Reynolds, Paul R

2015-07-01

Cigarette smoke exposure is associated with an increased risk of cardiovascular complications. The role of advanced glycation end products (AGEs) is already well established in numerous comorbidities, including cardiomyopathy. Given the role of AGEs and their receptor, RAGE, in activating inflammatory pathways, we sought to determine whether ceramides could be a mediator of RAGE-induced altered heart mitochondrial function. Using an in vitro model, we treated H9C2 cardiomyocytes with the AGE carboxy-methyllysine before mitochondrial respiration assessment. We discovered that mitochondrial respiration was significantly impaired in AGE-treated cells, but not when cotreated with myriocin, an inhibitor of de novo ceramide biosynthesis. Moreover, we exposed wild-type and RAGE knockout mice to secondhand cigarette smoke and found reduced mitochondrial respiration in the left ventricular myocardium from wild-type mice, but RAGE knockout mice were protected from this effect. Finally, conditional overexpression of RAGE in the lungs of transgenic mice elicited a robust increase in left ventricular ceramides in the absence of smoke exposure. Taken together, these findings suggest a RAGE-ceramide axis as an important contributor to AGE-mediated disrupted cardiomyocyte mitochondrial function. Copyright © 2015 the American Physiological Society.

Identification of Wild Boar-Habitat Epidemiologic Cycle in African Swine Fever Epizootic.

Science.gov (United States)

Chenais, Erika; Ståhl, Karl; Guberti, Vittorio; Depner, Klaus

2018-04-01

The African swine fever epizootic in central and eastern European Union member states has a newly identified component involving virus transmission by wild boar and virus survival in the environment. Insights led to an update of the 3 accepted African swine fever transmission models to include a fourth cycle: wild boar-habitat.

Potential of low-temperature anaerobic digestion to address current environmental concerns on swine production.

Science.gov (United States)

Massé, D I; Masse, L; Xia, Y; Gilbert, Y

2010-04-01

Environmental issues associated with swine production are becoming a major concern among the general public and are thus an important challenge for the swine industry. There is now a renewed interest in environmental biotechnologies that can minimize the impact of swine production and add value to livestock by-products. An anaerobic biotechnology called psychrophilic anaerobic digestion (PAD) in sequencing batch reactors (SBR) has been developed at Agriculture and Agri-Food Canada. This very stable biotechnology recovers usable energy, stabilizes and deodorizes manure, and increases the availability of plant nutrients. Experimental results indicated that PAD of swine manure slurry at 15 to 25 degrees C in intermittently fed SBR reduces the pollution potential of manure by removing up to 90% of the soluble chemical oxygen demand. The process performs well under intermittent feeding, once to 3 times a week, and without external mixing. Bioreactor feeding activities can thus be easily integrated into the routine manure removal procedures in the barn, with minimal interference with other farm operations and use of existing manure-handling equipment. Process stability was not affected by the presence of antibiotics in manure. The PAD process was efficient in eliminating populations of zoonotic pathogens and parasites present in raw livestock manure slurries. Psychrophilic anaerobic digestion in SBR could also be used for swine mortality disposal. The addition of swine carcasses, at loading rates representing up to 8 times the normal mortality rates on commercial farms, did not affect the stability of SBR. No operational problems were related to the formation of foam and scum. The biotechnology was successfully operated at semi-industrial and full commercial scales. Biogas production rate exceeded 0.20 L of methane per gram of total chemical oxygen demand fed to the SBR. The biogas was of excellent quality, with a methane concentration ranging from 70 to 80%. The

Mitochondrial affinity for ADP is twofold lower in creatine kinase knock-out muscles - Possible role in rescuing cellular energy homeostasis

NARCIS (Netherlands)

ter Veld, F; Jeneson, JAL; Nicolay, K

Adaptations of the kinetic properties of mitochondria in striated muscle lacking cytosolic (M) and/or mitochondrial (Mi) creatine kinase (CK) isoforms in comparison to wild-type (WT) were investigated in vitro. Intact mitochondria were isolated from heart and gastrocnemius muscle of WT and single-

First reports of pseudorabies and winter ticks (Dermacentor albipictus) associated with an emerging feral swine (Sus scrofa) population in New Hampshire.

Science.gov (United States)

Musante, Anthony R; Pedersen, Kerri; Hall, Parker

2014-01-01

The expansion of feral swine (Sus scrofa) populations into new geographic regions is of concern not only due to increased range but also because they carry diseases and parasites that pose a threat to humans, livestock, and wildlife into new areas. Recently, emerging feral swine populations have been reported in the northeastern US and due to their adaptive nature will likely continue to spread. During 2009-2012, 49 feral swine were removed from three counties in New Hampshire. Of these, serum samples were submitted from 34 for disease surveillance testing. One of the feral swine was antibody-positive for pseudorabies virus (PRV) making it the first documented infection in feral swine in New Hampshire. Infestations of winter tick (Dermacentor albipictus) were also documented on two of the feral swine which had only been reported previously on feral swine in Texas. Feral swine may not only serve as an important host for an economically important commercial swine pathogen like PRV, but they could also increase host diversity for parasites such as the winter tick, a species that can regionally impact moose (Alces alces) survival. These findings warrant further investigation of expanding and established feral swine populations in New Hampshire as pathogen hosts and support continued effort to reduce numbers or regionally eradicate feral swine.

Serological and molecular epidemiology of Japanese encephalitis virus infections in swine herds in China, 2006-2012.

Science.gov (United States)

Chai, Chunxia; Wang, Qiao; Cao, Sanjie; Zhao, Qin; Wen, Yiping; Huang, Xiaobo; Wen, Xintian; Yan, Qiguai; Ma, Xiaoping; Wu, Rui

2018-01-31

Japanese encephalitis virus (JEV) is a mosquito-borne, zoonotic flavivirus causing viral encephalitis in humans and reproductive disorder in swine. JEV is prevalent throughout China in human; however, spatiotemporal analysis of JEV in Chinese swine herds has not been reported previously. Herein, we present serological and molecular epidemiological results and estimates of prevalence of JEV infections among swine herds in various regions of China. The results suggest that JEV infections are widespread and genotype I and III strains co-exist in the same regions. Therefore, there is an urgent need to monitor JEV infection status among swine herds in China.

Shotgun pyrosequencing metagenomic analyses of dusts from swine confinement and grain facilities.

Science.gov (United States)

Boissy, Robert J; Romberger, Debra J; Roughead, William A; Weissenburger-Moser, Lisa; Poole, Jill A; LeVan, Tricia D

2014-01-01

Inhalation of agricultural dusts causes inflammatory reactions and symptoms such as headache, fever, and malaise, which can progress to chronic airway inflammation and associated diseases, e.g. asthma, chronic bronchitis, chronic obstructive pulmonary disease, and hypersensitivity pneumonitis. Although in many agricultural environments feed particles are the major constituent of these dusts, the inflammatory responses that they provoke are likely attributable to particle-associated bacteria, archaebacteria, fungi, and viruses. In this study, we performed shotgun pyrosequencing metagenomic analyses of DNA from dusts from swine confinement facilities or grain elevators, with comparisons to dusts from pet-free households. DNA sequence alignment showed that 19% or 62% of shotgun pyrosequencing metagenomic DNA sequence reads from swine facility or household dusts, respectively, were of swine or human origin, respectively. In contrast only 2% of such reads from grain elevator dust were of mammalian origin. These metagenomic shotgun reads of mammalian origin were excluded from our analyses of agricultural dust microbiota. The ten most prevalent bacterial taxa identified in swine facility compared to grain elevator or household dust were comprised of 75%, 16%, and 42% gram-positive organisms, respectively. Four of the top five swine facility dust genera were assignable (Clostridium, Lactobacillus, Ruminococcus, and Eubacterium, ranging from 4% to 19% relative abundance). The relative abundances of these four genera were lower in dust from grain elevators or pet-free households. These analyses also highlighted the predominance in swine facility dust of Firmicutes (70%) at the phylum level, Clostridia (44%) at the Class level, and Clostridiales at the Order level (41%). In summary, shotgun pyrosequencing metagenomic analyses of agricultural dusts show that they differ qualitatively and quantitatively at the level of microbial taxa present, and that the bioinformatic analyses

Shotgun pyrosequencing metagenomic analyses of dusts from swine confinement and grain facilities.

Directory of Open Access Journals (Sweden)

Robert J Boissy

Full Text Available Inhalation of agricultural dusts causes inflammatory reactions and symptoms such as headache, fever, and malaise, which can progress to chronic airway inflammation and associated diseases, e.g. asthma, chronic bronchitis, chronic obstructive pulmonary disease, and hypersensitivity pneumonitis. Although in many agricultural environments feed particles are the major constituent of these dusts, the inflammatory responses that they provoke are likely attributable to particle-associated bacteria, archaebacteria, fungi, and viruses. In this study, we performed shotgun pyrosequencing metagenomic analyses of DNA from dusts from swine confinement facilities or grain elevators, with comparisons to dusts from pet-free households. DNA sequence alignment showed that 19% or 62% of shotgun pyrosequencing metagenomic DNA sequence reads from swine facility or household dusts, respectively, were of swine or human origin, respectively. In contrast only 2% of such reads from grain elevator dust were of mammalian origin. These metagenomic shotgun reads of mammalian origin were excluded from our analyses of agricultural dust microbiota. The ten most prevalent bacterial taxa identified in swine facility compared to grain elevator or household dust were comprised of 75%, 16%, and 42% gram-positive organisms, respectively. Four of the top five swine facility dust genera were assignable (Clostridium, Lactobacillus, Ruminococcus, and Eubacterium, ranging from 4% to 19% relative abundance. The relative abundances of these four genera were lower in dust from grain elevators or pet-free households. These analyses also highlighted the predominance in swine facility dust of Firmicutes (70% at the phylum level, Clostridia (44% at the Class level, and Clostridiales at the Order level (41%. In summary, shotgun pyrosequencing metagenomic analyses of agricultural dusts show that they differ qualitatively and quantitatively at the level of microbial taxa present, and that the

Common effects of lithium and valproate on mitochondrial functions: protection against methamphetamine-induced mitochondrial damage.

Science.gov (United States)

Bachmann, Rosilla F; Wang, Yun; Yuan, Peixiong; Zhou, Rulun; Li, Xiaoxia; Alesci, Salvatore; Du, Jing; Manji, Husseini K

2009-07-01

Accumulating evidence suggests that mitochondrial dysfunction plays a critical role in the progression of a variety of neurodegenerative and psychiatric disorders. Thus, enhancing mitochondrial function could potentially help ameliorate the impairments of neural plasticity and cellular resilience associated with a variety of neuropsychiatric disorders. A series of studies was undertaken to investigate the effects of mood stabilizers on mitochondrial function, and against mitochondrially mediated neurotoxicity. We found that long-term treatment with lithium and valproate (VPA) enhanced cell respiration rate. Furthermore, chronic treatment with lithium or VPA enhanced mitochondrial function as determined by mitochondrial membrane potential, and mitochondrial oxidation in SH-SY5Y cells. In-vivo studies showed that long-term treatment with lithium or VPA protected against methamphetamine (Meth)-induced toxicity at the mitochondrial level. Furthermore, these agents prevented the Meth-induced reduction of mitochondrial cytochrome c, the mitochondrial anti-apoptotic Bcl-2/Bax ratio, and mitochondrial cytochrome oxidase (COX) activity. Oligoarray analysis demonstrated that the gene expression of several proteins related to the apoptotic pathway and mitochondrial functions were altered by Meth, and these changes were attenuated by treatment with lithium or VPA. One of the genes, Bcl-2, is a common target for lithium and VPA. Knock-down of Bcl-2 with specific Bcl-2 siRNA reduced the lithium- and VPA-induced increases in mitochondrial oxidation. These findings illustrate that lithium and VPA enhance mitochondrial function and protect against mitochondrially mediated toxicity. These agents may have potential clinical utility in the treatment of other diseases associated with impaired mitochondrial function, such as neurodegenerative diseases and schizophrenia.

Antibody Repertoire Development in Swine

Czech Academy of Sciences Publication Activity Database

Butler, J. E.; Wertz, N.; Šinkora, Marek

2017-01-01

Roč. 5, FEB 17 (2017), s. 255-279 ISSN 2165-8102 R&D Projects: GA ČR GA15-02274S; GA ČR(CZ) GA16-09296S Institutional support: RVO:61388971 Keywords : swine * pre-immune antibody repertoire * ileal Peyer's patches Subject RIV: EE - Microbiology, Virology OBOR OECD: Microbiology Impact factor: 4.708, year: 2016

Identification of Wild Boar–Habitat Epidemiologic Cycle in African Swine Fever Epizootic

Science.gov (United States)

Ståhl, Karl; Guberti, Vittorio; Depner, Klaus

2018-01-01

The African swine fever epizootic in central and eastern European Union member states has a newly identified component involving virus transmission by wild boar and virus survival in the environment. Insights led to an update of the 3 accepted African swine fever transmission models to include a fourth cycle: wild boar–habitat. PMID:29553337

Mitochondrial Nucleoid: Shield and Switch of the Mitochondrial Genome

Science.gov (United States)

2017-01-01

Mitochondria preserve very complex and distinctively unique machinery to maintain and express the content of mitochondrial DNA (mtDNA). Similar to chromosomes, mtDNA is packaged into discrete mtDNA-protein complexes referred to as a nucleoid. In addition to its role as a mtDNA shield, over 50 nucleoid-associated proteins play roles in mtDNA maintenance and gene expression through either temporary or permanent association with mtDNA or other nucleoid-associated proteins. The number of mtDNA(s) contained within a single nucleoid is a fundamental question but remains a somewhat controversial issue. Disturbance in nucleoid components and mutations in mtDNA were identified as significant in various diseases, including carcinogenesis. Significant interest in the nucleoid structure and its regulation has been stimulated in relation to mitochondrial diseases, which encompass diseases in multicellular organisms and are associated with accumulation of numerous mutations in mtDNA. In this review, mitochondrial nucleoid structure, nucleoid-associated proteins, and their regulatory roles in mitochondrial metabolism are briefly addressed to provide an overview of the emerging research field involving mitochondrial biology. PMID:28680532

Mitochondrial pharmacology: electron transport chain bypass as strategies to treat mitochondrial dysfunction.

Science.gov (United States)

Atamna, Hani; Mackey, Jeanette; Dhahbi, Joseph M

2012-01-01

Mitochondrial dysfunction (primary or secondary) is detrimental to intermediary metabolism. Therapeutic strategies to treat/prevent mitochondrial dysfunction could be valuable for managing metabolic and age-related disorders. Here, we review strategies proposed to treat mitochondrial impairment. We then concentrate on redox-active agents, with mild-redox potential, who shuttle electrons among specific cytosolic or mitochondrial redox-centers. We propose that specific redox agents with mild redox potential (-0.1 V; 0.1 V) improve mitochondrial function because they can readily donate or accept electrons in biological systems, thus they enhance metabolic activity and prevent reactive oxygen species (ROS) production. These agents are likely to lack toxic effects because they lack the risk of inhibiting electron transfer in redox centers. This is different from redox agents with strong negative (-0.4 V; -0.2 V) or positive (0.2 V; 0.4 V) redox potentials who alter the redox status of redox-centers (i.e., become permanently reduced or oxidized). This view has been demonstrated by testing the effect of several redox active agents on cellular senescence. Methylene blue (MB, redox potential ≅10 mV) appears to readily cycle between the oxidized and reduced forms using specific mitochondrial and cytosolic redox centers. MB is most effective in delaying cell senescence and enhancing mitochondrial function in vivo and in vitro. Mild-redox agents can alter the biochemical activity of specific mitochondrial components, which then in response alters the expression of nuclear and mitochondrial genes. We present the concept of mitochondrial electron-carrier bypass as a potential result of mild-redox agents, a method to prevent ROS production, improve mitochondrial function, and delay cellular aging. Thus, mild-redox agents may prevent/delay mitochondria-driven disorders. Copyright © 2012 International Union of Biochemistry and Molecular Biology, Inc.

Microbial Ecology of Stored Swine Manure and Reduction of Emissions Using Condensed Tannins.

Science.gov (United States)

Management practices from large-scale swine production facilities have resulted in the increased collection and storage of manure for off-season fertilization use. Stored swine manure serves as a habitat for billions of microorganisms and is associated with the generation of odorous compounds and g...

USMARC update on swine reproduction research

Science.gov (United States)

Swine research at USMARC has continued to focus on meat quality, improvement of genomic resources and reproduction, specifically estrus traits, sow longevity and lifetime productivity. This report will focus on research in behavioral anestrus in gilts. Gilts that reach puberty at an earlier age are ...

A simplified model for assessing the impact to groundwater of swine farms at regional level

Science.gov (United States)

Massabo, Marco; Viterbo, Angelo

2013-04-01

Swine manure can be an excellent source of nutrients for crop production. Several swine farms are present in the territory of Regione Umbria and more than 200.000 of swine heads are present yearly in the whole territory while some municipalities host more than 30.000 heads over a relatively limited land. Municipality with elevated number of swine heads has registered particularly higher Nitrate concentration in groundwater that requires a management plan and intervention in order to determine the maximum allowed N loads in the specific region. Use of manure and fertilizers in agricultural field produce diffuse nitrogen (N) losses that are a major cause of excessive nitrate concentrations in ground and surface waters and have been of concern since decades. Excessive nitrate concentrations in groundwater can have toxic effects when used as drinking water and cause eutrophication in surface waters. For management and environmental planning purposes, it is necessary to assess the magnitude of diffuse N losses from agricultural fields and how they are influenced by factors such as management practices, type of fertilizers -organic or inorganic - climate and soil etc. There are several methods for assessing N leaching, they span from methods based on field test to complex models that require many input data. We use a simple index method that accounts for the type of fertilizer used - inorganic, swine or cattle manure- and hydrological and hydrogeological conditions. Hydrological conditions such as infiltration rates are estimated by a fully distributed hydrological model. Data on inorganic and organic fertilization are estimated at municipal level by using the nutrient crops needs and the statistics of swine and cattle heads within the municipality. The index method has been calibrated by using groundwater concentration as a proxy of N losses from agriculture. A time series of three years of data has been analyzed. The application of the simple index method allowed to

Mitochondrial morphology and cardiovascular disease

OpenAIRE

Ong, Sang-Bing; Hausenloy, Derek J.

2010-01-01

Mitochondria are dynamic and are able to interchange their morphology between elongated interconnected mitochondrial networks and a fragmented disconnected arrangement by the processes of mitochondrial fusion and fission, respectively. Changes in mitochondrial morphology are regulated by the mitochondrial fusion proteins (mitofusins 1 and 2, and optic atrophy 1) and the mitochondrial fission proteins (dynamin-related peptide 1 and mitochondrial fission protein 1) and have been implicated in a...

Livestock-associated methicillin-resistant Staphylococcus aureus (LA-MRSA isolates of swine origin form robust biofilms.

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Tracy L Nicholson

Full Text Available Methicillin-resistant Staphylococcus aureus (MRSA colonization of livestock animals is common and prevalence rates for pigs have been reported to be as high as 49%. Mechanisms contributing to the persistent carriage and high prevalence rates of livestock-associated methicillin-resistant Staphylococcus aureus (LA-MRSA strains in swine herds and production facilities have not been investigated. One explanation for the high prevalence of MRSA in swine herds is the ability of these organisms to exist as biofilms. In this report, the ability of swine LA-MRSA strains, including ST398, ST9, and ST5, to form biofilms was quantified and compared to several swine and human isolates. The contribution of known biofilm matrix components, polysaccharides, proteins and extracellular DNA (eDNA, was tested in all strains as well. All MRSA swine isolates formed robust biofilms similar to human clinical isolates. The addition of Dispersin B had no inhibitory effect on swine MRSA isolates when added at the initiation of biofilm growth or after pre-established mature biofilms formed. In contrast, the addition of proteinase K inhibited biofilm formation in all strains when added at the initiation of biofilm growth and was able to disperse pre-established mature biofilms. Of the LA-MRSA strains tested, we found ST398 strains to be the most sensitive to both inhibition of biofilm formation and dispersal of pre-formed biofilms by DNaseI. Collectively, these findings provide a critical first step in designing strategies to control or eliminate MRSA in swine herds.

PINK1 regulates mitochondrial trafficking in dendrites of cortical neurons through mitochondrial PKA.

Science.gov (United States)

Das Banerjee, Tania; Dagda, Raul Y; Dagda, Marisela; Chu, Charleen T; Rice, Monica; Vazquez-Mayorga, Emmanuel; Dagda, Ruben K

2017-08-01

Mitochondrial Protein Kinase A (PKA) and PTEN-induced kinase 1 (PINK1), which is linked to Parkinson's disease, are two neuroprotective serine/threonine kinases that regulate dendrite remodeling and mitochondrial function. We have previously shown that PINK1 regulates dendrite morphology by enhancing PKA activity. Here, we show the molecular mechanisms by which PINK1 and PKA in the mitochondrion interact to regulate dendrite remodeling, mitochondrial morphology, content, and trafficking in dendrites. PINK1-deficient cortical neurons exhibit impaired mitochondrial trafficking, reduced mitochondrial content, fragmented mitochondria, and a reduction in dendrite outgrowth compared to wild-type neurons. Transient expression of wild-type, but not a PKA-binding-deficient mutant of the PKA-mitochondrial scaffold dual-specificity A Kinase Anchoring Protein 1 (D-AKAP1), restores mitochondrial trafficking, morphology, and content in dendrites of PINK1-deficient cortical neurons suggesting that recruiting PKA to the mitochondrion reverses mitochondrial pathology in dendrites induced by loss of PINK1. Mechanistically, full-length and cleaved forms of PINK1 increase the binding of the regulatory subunit β of PKA (PKA/RIIβ) to D-AKAP1 to enhance the autocatalytic-mediated phosphorylation of PKA/RIIβ and PKA activity. D-AKAP1/PKA governs mitochondrial trafficking in dendrites via the Miro-2/TRAK2 complex and by increasing the phosphorylation of Miro-2. Our study identifies a new role of D-AKAP1 in regulating mitochondrial trafficking through Miro-2, and supports a model in which PINK1 and mitochondrial PKA participate in a similar neuroprotective signaling pathway to maintain dendrite connectivity. © 2017 International Society for Neurochemistry.

Overexpression of mitochondrial sirtuins alters glycolysis and mitochondrial function in HEK293 cells.

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Michelle Barbi de Moura

Full Text Available SIRT3, SIRT4, and SIRT5 are mitochondrial deacylases that impact multiple facets of energy metabolism and mitochondrial function. SIRT3 activates several mitochondrial enzymes, SIRT4 represses its targets, and SIRT5 has been shown to both activate and repress mitochondrial enzymes. To gain insight into the relative effects of the mitochondrial sirtuins in governing mitochondrial energy metabolism, SIRT3, SIRT4, and SIRT5 overexpressing HEK293 cells were directly compared. When grown under standard cell culture conditions (25 mM glucose all three sirtuins induced increases in mitochondrial respiration, glycolysis, and glucose oxidation, but with no change in growth rate or in steady-state ATP concentration. Increased proton leak, as evidenced by oxygen consumption in the presence of oligomycin, appeared to explain much of the increase in basal oxygen utilization. Growth in 5 mM glucose normalized the elevations in basal oxygen consumption, proton leak, and glycolysis in all sirtuin over-expressing cells. While the above effects were common to all three mitochondrial sirtuins, some differences between the SIRT3, SIRT4, and SIRT5 expressing cells were noted. Only SIRT3 overexpression affected fatty acid metabolism, and only SIRT4 overexpression altered superoxide levels and mitochondrial membrane potential. We conclude that all three mitochondrial sirtuins can promote increased mitochondrial respiration and cellular metabolism. SIRT3, SIRT4, and SIRT5 appear to respond to excess glucose by inducing a coordinated increase of glycolysis and respiration, with the excess energy dissipated via proton leak.

75 FR 16641 - Swine Contract Library

Science.gov (United States)

2010-04-02

...-AB06 Swine Contract Library AGENCY: Grain Inspection, Packers and Stockyards Administration, USDA... Library (SCL). The statutory authority for the library lapsed on September 30, 2005. On October 5, 2006... maintenance of a library of marketing contracts offered by certain packers to producers for the purchase of...

Mitochondrial DNA triplication and punctual mutations in patients with mitochondrial neuromuscular disorders

Energy Technology Data Exchange (ETDEWEB)

Mkaouar-Rebai, Emna, E-mail: emna.mkaouar@gmail.com [Département des Sciences de la Vie, Faculté des Sciences de Sfax, Université de Sfax (Tunisia); Felhi, Rahma; Tabebi, Mouna [Laboratoire de Génétique Moléculaire Humaine, Faculté de Médecine de Sfax, Université de Sfax (Tunisia); Alila-Fersi, Olfa; Chamkha, Imen [Département des Sciences de la Vie, Faculté des Sciences de Sfax, Université de Sfax (Tunisia); Maalej, Marwa; Ammar, Marwa [Laboratoire de Génétique Moléculaire Humaine, Faculté de Médecine de Sfax, Université de Sfax (Tunisia); Kammoun, Fatma [Service de pédiatrie, C.H.U. Hedi Chaker de Sfax (Tunisia); Keskes, Leila [Laboratoire de Génétique Moléculaire Humaine, Faculté de Médecine de Sfax, Université de Sfax (Tunisia); Hachicha, Mongia [Service de pédiatrie, C.H.U. Hedi Chaker de Sfax (Tunisia); Fakhfakh, Faiza, E-mail: faiza.fakhfakh02@gmail.com [Département des Sciences de la Vie, Faculté des Sciences de Sfax, Université de Sfax (Tunisia)

2016-04-29

Mitochondrial diseases are a heterogeneous group of disorders caused by the impairment of the mitochondrial oxidative phosphorylation system which have been associated with various mutations of the mitochondrial DNA (mtDNA) and nuclear gene mutations. The clinical phenotypes are very diverse and the spectrum is still expanding. As brain and muscle are highly dependent on OXPHOS, consequently, neurological disorders and myopathy are common features of mtDNA mutations. Mutations in mtDNA can be classified into three categories: large-scale rearrangements, point mutations in tRNA or rRNA genes and point mutations in protein coding genes. In the present report, we screened mitochondrial genes of complex I, III, IV and V in 2 patients with mitochondrial neuromuscular disorders. The results showed the presence the pathogenic heteroplasmic m.9157G>A variation (A211T) in the MT-ATP6 gene in the first patient. We also reported the first case of triplication of 9 bp in the mitochondrial NC7 region in Africa and Tunisia, in association with the novel m.14924T>C in the MT-CYB gene in the second patient with mitochondrial neuromuscular disorder. - Highlights: • We reported 2 patients with mitochondrial neuromuscular disorders. • The heteroplasmic MT-ATP6 9157G>A variation was reported. • A triplication of 9 bp in the mitochondrial NC7 region was detected. • The m.14924T>C transition (S60P) in the MT-CYB gene was found.

Enzymatic and thermodynamic profiles of a heterotetramer lactate dehydrogenase isozyme in swine

International Nuclear Information System (INIS)

Goto, Tatsufumi; Sugawara, Kotomi; Nakamura, Shigeyoshi; Kidokoro, Shun-Ichi; Wakui, Hideki; Nunomura, Wataru

2016-01-01

Lactate dehydrogenase (LDH) is a glycolytic enzyme that catalyzes the final step of glycolysis and produces NAD + . In somatic cells, LDH forms homotetramers and heterotetramers that are encoded by two different genes: LDHA (skeletal muscle type, M) and LDHB (heart type, H). Analysis of LDH isozymes is important for understanding the physiological role of homotetramers and heterotetramers and for optimizing inhibition of their enzymatic activity as it may result in distinct effects. Previously, we reported that hydroxychloroquine (HCQ) inhibited LDH activity, but we did not examine isozyme specificity. In the present study, we isolated heterotetrameric LDH (H 2 M 2 ) from swine brain, determined its kinetic and thermodynamic properties, and examined the effect of HCQ on its activity compared to homotetrameric LDH isozymes. We show that: (1) the K m values for H 2 M 2 –mediated catalysis of pyruvate or lactate were intermediate compared to those for the homotetrameric isozymes, M 4 and H 4 whereas the V max values were similar; (2) the K m and V max values for H 2 M 2 –mediated catalysis of NADH were not significantly different among LDH isozymes; (3) the values for activation energy and van't Hoff enthalpy changes for pyruvate reduction of H 2 M 2 were intermediate compared to those for the homotetrameric isozymes; (4) the temperature for half residual activity of H 2 M 2 was closer to that for M 4 than for H 4 . We also show that HCQ had different affinities for various LDH isozymes. - Highlights: • Heterotetrameric (H 2 M 2 ) LDH isozyme was isolated from swine brain. • Kinetics of H 2 M 2 were intermediate between the two homotetramers. • Thermodynamics of H 2 M 2 were also intermediate between the two homotetramers. • Hydroxychloroquine inhibited more strongly H 2 M 2 than homotetramers.

[The present epidemiological status of African swine fever].

Science.gov (United States)

Hess, G

1986-01-01

At present, African swine fever (ASF) persists as an enzootic infection both on the African continent and in Europe (Portugal, Spain, and Sardinia). The recent outbreaks of ASF in Belgium and in the Netherlands have again demonstrated the threat of this disease to the swine population in Germany. The main reasons for this threat are the great tenacity of this virus and its stability in meat and meat products together with an immense tourism into these enzootic areas. Epizootiological peculiarities, such as virus replication in ticks and inapparent infections in wild boars are the reason why eradication of the disease has failed so far, especially when pigs are allowed to roam the countryside.

Identification of swine influenza virus epitopes and analysis of multiple specificities expressed by cytotoxic T cell subsets

DEFF Research Database (Denmark)

Pedersen, Lasse Eggers; Breum, Solvej Østergaard; Riber, Ulla

2014-01-01

Background: Major histocompatibility complex (MHC) class I peptide binding and presentation are essential for antigen-specific activation of cytotoxic T lymphocytes (CTLs) and swine MHC class I molecules, also termed swine leukocyte antigens (SLA), thus play a crucial role in the process that leads...... to elimination of viruses such as swine influenza virus (SwIV). This study describes the identification of SLA-presented peptide epitopes that are targets for a swine CTL response, and further analyses multiple specificities expressed by SwIV activated CTL subsets. Findings: Four SwIV derived peptides were...

Viability analysis of EMBRAPA's swine manure treatment system

Energy Technology Data Exchange (ETDEWEB)

Miele, Marcelo; Kunz, Airton; Seganfredo, Milton Antonio; Steinmetz, Ricardo [EMBRAPA Suinos e Aves, Concordia, SC (Brazil)], E-mail: mmiele@cnpsa.embrapa.br; Bortoli, Marcelo [Universidade Federal de Santa Catarina (UFSC), Florianopolis, SC (Brazil)

2008-07-01

The swine manure treatment is based on several technologies, such as pond systems, composting, biodigesters, and compact process like the EMBRAPA's Swine Manure Treatment System. The last one can reach high quality effluent with reduced pollution, although it demands higher investment and costs. For this reason it is necessary to manage revenues with byproducts and carbon credit markets. The aim of this study was to present a viability analysis of EMBRAPA's swine manure treatment system considering its potential revenues facing higher costs. Using market prices and measured data from a prototype running in south Brazil, the study calculated costs, revenues, profit, net present value and internal rate return. It also estimated these indicators assuming scale economies. The results showed that the investment can pay its costs by its insertion in the carbon credit market and other revenues like the energy substitution. It also showed the importance to reach scale economies. (author)

Problematic effects of antibiotics on anaerobic treatment of swine wastewater.

Science.gov (United States)

Cheng, D L; Ngo, H H; Guo, W S; Chang, S W; Nguyen, D D; Kumar, S Mathava; Du, B; Wei, Q; Wei, D

2018-05-04

Swine wastewaters with high levels of organic pollutants and antibiotics have become serious environmental concerns. Anaerobic technology is a feasible option for swine wastewater treatment due to its advantage in low costs and bioenergy production. However, antibiotics in swine wastewater have problematic effects on micro-organisms, and the stability and performance of anaerobic processes. Thus, this paper critically reviews impacts of antibiotics on pH, COD removal efficiencies, biogas and methane productions as well as the accumulation of volatile fatty acids (VFAs) in the anaerobic processes. Meanwhile, impacts on the structure of bacteria and methanogens in anaerobic processes are also discussed comprehensively. Furthermore, to better understand the effect of antibiotics on anaerobic processes, detailed information about antimicrobial mechanisms of antibiotics and microbial functions in anaerobic processes is also summarized. Future research on deeper knowledge of the effect of antibiotics on anaerobic processes are suggested to reduce their adverse environmental impacts. Copyright © 2018 Elsevier Ltd. All rights reserved.

Isolation of lactic acid bacteria from swine milk and characterization of potential probiotic strains with antagonistic effects against swine-associated gastrointestinal pathogens.

Science.gov (United States)

Quilodrán-Vega, Sandra Rayén; Villena, Julio; Valdebenito, José; Salas, María José; Parra, Cristian; Ruiz, Alvaro; Kitazawa, Haruki; García, Apolinaria

2016-06-01

Probiotics are usually isolated from the gastrointestinal tract of humans and animals. The search of probiotics in human milk is a recent field of research, as the existence of the human milk microbiome was discovered only about a decade ago. To our knowledge, no reports regarding the potential probiotic effect of bacteria from swine milk have been published. In this work, we isolated several lactic acid bacteria from swine milk and evaluated them for them potential as probiotics. Among the isolated strains, Lactobacillus curvatus TUCO-5E showed antagonistic effects against swine-associated gastrointestinal pathogens. TUCO-5E was able to reduce the growth of enterotoxigenic and enterohemorrhagic Escherichia coli strains as well as pathogenic salmonella. In vitro exclusion and displacement assays in intestinal epithelial cells showed a remarkable antagonistic effect for L. curvatus TUCO-5E against Salmonella sp. strain TUCO-I7 and Salmonella enterica ATCC 13096. Moreover, by using a mouse model of Salmonella infection, we were able to demonstrate that preventative administration of L. curvatus TUCO-5E for 5 consecutive days was capable of decreasing the number of Salmonella enterica serovar Typhimurium in the liver and spleen of treated mice, compared with the controls, and prevented dissemination of the pathogen to the blood stream. Therefore, we have demonstrated here that swine milk is an interesting source of beneficial bacteria. In addition, the results of this work suggest that L. curvatus TUCO-5E is a good candidate to study in vivo the protective effect of probiotics against intestinal infection and damage induced by Salmonella infection in the porcine host.

Increased Oxidative Stress and Mitochondrial Dysfunction in Zucker Diabetic Rat Liver and Brain

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Haider Raza

2015-02-01

Full Text Available Background/Aims: The Zucker diabetic fatty (ZDF, FA/FA rat is a genetic model of type 2 diabetes, characterized by insulin resistance with progressive metabolic syndrome. We have previously demonstrated mitochondrial dysfunction and oxidative stress in the heart, kidneys and pancreas of ZDF rats. However, the precise molecular mechanism of disease progression is not clear. Our aim in the present study was to investigate oxidative stress and mitochondrial dysfunction in the liver and brain of ZDF rats. Methods: In this study, we have measured mitochondrial oxidative stress, bioenergetics and redox homeostasis in the liver and brain of ZDF rats. Results: Our results showed increased reactive oxygen species (ROS production in the ZDF rat brain compared to the liver, while nitric oxide (NO production was markedly increased both in the brain and liver. High levels of lipid and protein peroxidation were also observed in these tissues. Glutathione metabolism and mitochondrial respiratory functions were adversely affected in ZDF rats when compared to Zucker lean (ZL, +/FA control rats. Reduced ATP synthesis was also observed in the liver and brain of ZDF rats. Western blot analysis confirmed altered expression of cytochrome P450 2E1, iNOS, p-JNK, and IκB-a confirming an increase in oxidative and metabolic stress in ZDF rat tissues. Conclusions: Our data shows that, like other tissues, ZDF rat liver and brain develop complications associated with redox homeostasis and mitochondrial dysfunction. These results, thus, might have implications in understanding the etiology and pathophysiology of diabesity which in turn, would help in managing the disease associated complications.

ALDH2 restores exhaustive exercise-induced mitochondrial dysfunction in skeletal muscle

International Nuclear Information System (INIS)

Zhang, Qiuping; Zheng, Jianheng; Qiu, Jun; Wu, Xiahong; Xu, Yangshuo; Shen, Weili; Sun, Mengwei

2017-01-01

Background: Mitochondrial aldehyde dehydrogenase 2 (ALDH2) is highly expressed in heart and skeletal muscles, and is the major enzyme that metabolizes acetaldehyde and toxic aldehydes. The cardioprotective effects of ALDH2 during cardiac ischemia/reperfusion injury have been recognized. However, less is known about the function of ALDH2 in skeletal muscle. This study was designed to evaluate the effect of ALDH2 on exhaustive exercise-induced skeletal muscle injury. Methods: We created transgenic mice expressing ALDH2 in skeletal muscles. Male wild-type C57/BL6 (WT) and ALDH2 transgenic mice (ALDH2-Tg), 8-weeks old, were challenged with exhaustive exercise for 1 week to induce skeletal muscle injury. Animals were sacrificed 24 h post-exercise and muscle tissue was excised. Results: ALDH2-Tg mice displayed significantly increased treadmill exercise capacity compared to WT mice. Exhaustive exercise caused an increase in mRNA levels of the muscle atrophy markers, Atrogin-1 and MuRF1, and reduced mitochondrial biogenesis and fusion in WT skeletal muscles; these effects were attenuated in ALDH2-Tg mice. Exhaustive exercise also enhanced mitochondrial autophagy pathway activity, including increased conversion of LC3-I to LC3-II and greater expression of Beclin1 and Bnip3; the effects of which were mitigated by ALDH2 overexpression. In addition, ALDH2-Tg reversed the increase of an oxidative stress biomarker (4-hydroxynonenal) and decreased levels of mitochondrial antioxidant proteins, including manganese superoxide dismutase and NAD(P)H:quinone oxidoreductase 1, in skeletal muscle induced by exhaustive exercise. Conclusion: ALDH2 may reverse skeletal muscle mitochondrial dysfunction due to exhaustive exercise by regulating mitochondria dynamic remodeling and enhancing the quality of mitochondria. - Highlights: • Skeletal muscle ALDH2 expression and activity declines during exhaustive exercise. • ALDH2 overexpression enhances physical performance and restores muscle

Fatty Acid Oxidation and Cardiovascular Risk during Menopause: A Mitochondrial Connection?

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Paulo J. Oliveira

2012-01-01

Full Text Available Menopause is a consequence of the normal aging process in women. This fact implies that the physiological and biochemical alterations resulting from menopause often blur with those from the aging process. It is thought that menopause in women presents a higher risk for cardiovascular disease although the precise mechanism is still under discussion. The postmenopause lipid profile is clearly altered, which can present a risk factor for cardiovascular disease. Due to the role of mitochondria in fatty acid oxidation, alterations of the lipid profile in the menopausal women will also influence mitochondrial fatty acid oxidation fluxes in several organs. In this paper, we propose that alterations of mitochondrial bioenergetics in the heart, consequence from normal aging and/or from the menopausal process, result in decreased fatty acid oxidation and accumulation of fatty acid intermediates in the cardiomyocyte cytosol, resulting in lipotoxicity and increasing the cardiovascular risk in the menopausal women.

Mitochondrial shaping cuts.

Science.gov (United States)

Escobar-Henriques, Mafalda; Langer, Thomas

2006-01-01

A broad range of cellular processes are regulated by proteolytic events. Proteolysis has now also been established to control mitochondrial morphology which results from the balanced action of fusion and fission. Two out of three known core components of the mitochondrial fusion machinery are under proteolytic control. The GTPase Fzo1 in the outer membrane of mitochondria is degraded along two independent proteolytic pathways. One controls mitochondrial fusion in vegetatively growing cells, the other one acts upon mating factor-induced cell cycle arrest. Fusion also depends on proteolytic processing of the GTPase Mgm1 by the rhomboid protease Pcp1 in the inner membrane of mitochondria. Functional links of AAA proteases or other proteolytic components to mitochondrial dynamics are just emerging. This review summarises the current understanding of regulatory roles of proteolytic processes for mitochondrial plasticity.

The effect of mitochondrial calcium uniporter on mitochondrial fission in hippocampus cells ischemia/reperfusion injury

Energy Technology Data Exchange (ETDEWEB)

Zhao, Lantao; Li, Shuhong; Wang, Shilei, E-mail: wshlei@aliyun.com; Yu, Ning; Liu, Jia

2015-06-05

The mitochondrial calcium uniporter (MCU) transports free Ca{sup 2+} into the mitochondrial matrix, maintaining Ca{sup 2+} homeostasis, thus regulates the mitochondrial morphology. Previous studies have indicated that there was closely crosstalk between MCU and mitochondrial fission during the process of ischemia/reperfusion injury. This study constructed a hypoxia reoxygenation model using primary hippocampus neurons to mimic the cerebral ischemia/reperfusion injury and aims to explore the exactly effect of MCU on the mitochondrial fission during the process of ischemia/reperfusion injury and so as the mechanisms. Our results found that the inhibitor of the MCU, Ru360, decreased mitochondrial Ca{sup 2+} concentration, suppressed the expression of mitochondrial fission protein Drp1, MIEF1 and Fis1, and thus improved mitochondrial morphology significantly. Whereas spermine, the agonist of the MCU, had no significant impact compared to the I/R group. This study demonstrated that the MCU regulates the process of mitochondrial fission by controlling the Ca{sup 2+} transport, directly upregulating mitochondrial fission proteins Drp1, Fis1 and indirectly reversing the MIEF1-induced mitochondrial fusion. It also provides new targets for brain protection during ischemia/reperfusion injury. - Highlights: • We study MCU with primary neuron culture. • MCU induces mitochondrial fission. • MCU reverses MIEF1 effect.

Effect of radiation on certain animal viruses in liquid swine manure

International Nuclear Information System (INIS)

Simon, J.; Mocsari, E.; di Gleria, M.; Felkai, V.

1983-01-01

The virucidal effect of 60 Co gamma radiation was studied in cell culture medium and in liquid swine manure involving the most important porcine viruses that can be spread by liquid manure. The radiation doses (20 kGy and 30 kGy) were determined in preliminary experiments employing a porcine enterovirus from the serogroup 1 (Teschen group). In the main experiment, the following viruses were employed: swine vesicular disease (SVD) virus, type C foot-and-mouth disease (FMD) virus, a field strain of Aujeszky's disease (AD) virus, transmissible gastroenteritis (TGE) virus, as well as bovine viral diarrhoea (BVD) virus. The latter strain served as a model for hog cholera virus. The results of the experiments indicate that safe disinfection of the virus infected liquid swine manure by ionizing radiation requires a radiation dose of 30 kGy. (author)

Effect of radiation on certain animal viruses in liquid swine manure

Energy Technology Data Exchange (ETDEWEB)

Simon, J.; Mocsari, E.; di Gleria, M.; Felkai, V. (Phylaxia Oltoanyag- es Tapszertermeloe Vallalat, Budapest (Hungary); Orszagos Allategeszseguegyi Intezet, Budapest (Hungary))

1983-03-01

The virucidal effect of /sup 60/Co gamma radiation was studied in cell culture medium and in liquid swine manure involving the most important porcine viruses that can be spread by liquid manure. The radiation doses (20 kGy and 30 kGy) were determined in preliminary experiments employing a porcine enterovirus from the serogroup 1 (Teschen group). In the main experiment, the following viruses were employed: swine vesicular disease (SVD) virus, type C foot-and-mouth disease (FMD) virus, a field strain of Aujeszky's disease (AD) virus, transmissible gastroenteritis (TGE) virus, as well as bovine viral diarrhea (BVD) virus. The latter strain served as a model for hog cholera virus. The results of the experiments indicate that safe disinfection of the virus infected liquid swine manure by ionizing radiation requires a radiation dose of 30 kGy.

Effect of radiation on certain animal viruses in liquid swine manure

Energy Technology Data Exchange (ETDEWEB)

Simon, J; Mocsari, E; di Gleria, M; Felkai, V [Phylaxia Oltoanyag- es Tapszertermeloe Vallalat, Budapest (Hungary); Orszagos Allategeszseguegyi Intezet, Budapest [Hungary

1983-03-01

The virucidal effect of /sup 60/Co gamma radiation was studied in cell culture medium and in liquid swine manure involving the most important porcine viruses that can be spread by liquid manure. The radiation doses (20 kGy and 30 kGy) were determined in preliminary experiments employing a porcine enterovirus from the serogroup 1 (Teschen group). In the main experiment, the following viruses were employed: swine vesicular disease (SVD) virus, type C foot-and-mouth disease (FMD) virus, a field strain of Aujeszky's disease (AD) virus, transmissible gastroenteritis (TGE) virus, as well as bovine viral diarrhea (BVD) virus. The latter strain served as a model for hog cholera virus. The results of the experiments indicate that safe disinfection of the virus infected liquid swine manure by ionizing radiation requires a radiation dose of 30 kGy.

Development of a swine-specific fecal pollution marker based on host differences in methanogen mcrA genes.

Science.gov (United States)

Ufnar, Jennifer A; Ufnar, David F; Wang, Shiao Y; Ellender, R D

2007-08-01

The goal of this study was to evaluate methanogen diversity in animal hosts to develop a swine-specific archaeal molecular marker for fecal source tracking in surface waters. Phylogenetic analysis of swine mcrA sequences compared to mcrA sequences from the feces of five animals (cow, deer, sheep, horse, and chicken) and sewage showed four distinct swine clusters, with three swine-specific clades. From this analysis, six sequences were chosen for molecular marker development and initial testing. Only one mcrA sequence (P23-2) showed specificity for swine and therefore was used for environmental testing. PCR primers for the P23-2 clone mcrA sequence were developed and evaluated for swine specificity. The P23-2 primers amplified products in P23-2 plasmid DNA (100%), pig feces (84%), and swine waste lagoon surface water samples (100%) but did not amplify a product in 47 bacterial and archaeal stock cultures and 477 environmental bacterial isolates and sewage and water samples from a bovine waste lagoon and a polluted creek. Amplification was observed in only one sheep sample out of 260 human and nonswine animal fecal samples. Sequencing of PCR products from pig feces demonstrated 100% similarity to pig mcrA sequence from clone P23-2. The minimal amount of DNA required for the detection was 1 pg for P23-2 plasmid, 1 ng for pig feces, 50 ng for swine waste lagoon surface water, 1 ng for sow waste influent, and 10 ng for lagoon sludge samples. Lower detection limits of 10(-6) g of wet pig feces in 500 ml of phosphate-buffered saline and 10(-4) g of lagoon waste in estuarine water were established for the P23-2 marker. This study was the first to utilize methanogens for the development of a swine-specific fecal contamination marker.

Mitochondrial Morphology and Fundamental Parameters of the Mitochondrial Respiratory Chain Are Altered in Caenorhabditis elegans Strains Deficient in Mitochondrial Dynamics and Homeostasis Processes.

Directory of Open Access Journals (Sweden)

Anthony L Luz

Full Text Available Mitochondrial dysfunction has been linked to myriad human diseases and toxicant exposures, highlighting the need for assays capable of rapidly assessing mitochondrial health in vivo. Here, using the Seahorse XFe24 Analyzer and the pharmacological inhibitors dicyclohexylcarbodiimide and oligomycin (ATP-synthase inhibitors, carbonyl cyanide 4-(trifluoromethoxy phenylhydrazone (mitochondrial uncoupler and sodium azide (cytochrome c oxidase inhibitor, we measured the fundamental parameters of mitochondrial respiratory chain function: basal oxygen consumption, ATP-linked respiration, maximal respiratory capacity, spare respiratory capacity and proton leak in the model organism Caenhorhabditis elegans. Since mutations in mitochondrial homeostasis genes cause mitochondrial dysfunction and have been linked to human disease, we measured mitochondrial respiratory function in mitochondrial fission (drp-1-, fusion (fzo-1-, mitophagy (pdr-1, pink-1-, and electron transport chain complex III (isp-1-deficient C. elegans. All showed altered function, but the nature of the alterations varied between the tested strains. We report increased basal oxygen consumption in drp-1; reduced maximal respiration in drp-1, fzo-1, and isp-1; reduced spare respiratory capacity in drp-1 and fzo-1; reduced proton leak in fzo-1 and isp-1; and increased proton leak in pink-1 nematodes. As mitochondrial morphology can play a role in mitochondrial energetics, we also quantified the mitochondrial aspect ratio for each mutant strain using a novel method, and for the first time report increased aspect ratios in pdr-1- and pink-1-deficient nematodes.

Taurine Supplementation Improves Functional Capacity, Myocardial Oxygen Consumption, and Electrical Activity in Heart Failure.

Science.gov (United States)

Ahmadian, Mehdi; Dabidi Roshan, Valiollah; Ashourpore, Eadeh

2017-07-04

Taurine is an amino acid found abundantly in the heart in very high concentrations. It is assumed that taurine contributes to several physiological functions of mammalian cells, such as osmoregulation, anti-inflammation, membrane stabilization, ion transport modulation, and regulation of oxidative stress and mitochondrial protein synthesis. The objective of the current study was to evaluate the effectiveness of taurine supplementation on functional capacity, myocardial oxygen consumption, and electrical activity in patients with heart failure. In a double-blind and randomly designed study, 16 patients with heart failure were assigned to two groups: taurine (TG, n = 8) and placebo (PG, n = 8). TG received 500-mg taurine supplementation three times per day for two weeks. Significant decrease in the values of Q-T segments (p heart failure patients. Together, these findings support the view that taurine improves cardiac function and functional capacity in patients with heart failure. This idea warrants further study.

What Is Mitochondrial DNA?

Science.gov (United States)

... DNA What is mitochondrial DNA? What is mitochondrial DNA? Although most DNA is packaged in chromosomes within ... proteins. For more information about mitochondria and mitochondrial DNA: Molecular Expressions, a web site from the Florida ...

CRISPR-Cas9, a tool to efficiently increase the development of recombinant African swine fever viruses.

Science.gov (United States)

Borca, Manuel V; Holinka, Lauren G; Berggren, Keith A; Gladue, Douglas P

2018-02-16

African swine fever virus (ASFV) causes a highly contagious disease called African swine fever. This disease is often lethal for domestic pigs, causing extensive losses for the swine industry. ASFV is a large and complex double stranded DNA virus. Currently there is no commercially available treatment or vaccine to prevent this devastating disease. Development of recombinant ASFV for producing live-attenuated vaccines or studying the involvement of specific genes in virus virulence has relied on the relatively rare event of homologous recombination in primary swine macrophages, causing difficulty to purify the recombinant virus from the wild-type parental ASFV. Here we present the use of the CRISPR-Cas9 gene editing system as a more robust and efficient system to produce recombinant ASFVs. Using CRISPR-Cas9 a recombinant virus was efficiently developed by deleting the non-essential gene 8-DR from the genome of the highly virulent field strain Georgia07 using swine macrophages as cell substrate.

Live poultry market workers are susceptible to both avian and swine influenza viruses, Guangdong Province, China.

Science.gov (United States)

Chen, Jidang; Ma, Jun; White, Sarah K; Cao, Zhenpeng; Zhen, Yun; He, Shuyi; Zhu, Wanjun; Ke, Changwen; Zhang, Yongbiao; Su, Shuo; Zhang, Guihong

2015-12-31

Guangdong Province is recognized for dense populations of humans, pigs, poultry and pets. In order to evaluate the threat of viral infection faced by those working with animals, a cross-sectional, sero-epidemiological study was conducted in Guangdong between December 2013 and January 2014. Individuals working with swine, at poultry farms, or live poultry markets (LPM), and veterinarians, and controls not exposed to animals were enrolled in this study and 11 (4 human, 3 swine, 3 avian, and 1 canine) influenza A viruses were used in hemagglutination inhibition (HI) assays (7 strains) and the cross-reactivity test (9 strains) in which 5 strains were used in both tests. Univariate analysis was performed to identify which variables were significantly associated with seropositivity. Odds ratios (OR) revealed that swine workers had a significantly higher risk of elevated antibodies against A/swine/Guangdong/L6/2009(H1N1), a classical swine virus, and A/swine/Guangdong/SS1/2012(H1N1), a Eurasian avian-like swine virus than non-exposed controls. Poultry farm workers were at a higher risk of infection with avian influenza H7N9 and H9N2. LPM workers were at a higher risk of infection with 3 subtypes of avian influenza, H5N1, H7N9, and H9N2. Interestingly, the OR also indicated that LPM workers were at risk of H1N1 swine influenza virus infection, perhaps due to the presence of pigs in the LPM. While partial confounding by cross-reactive antibodies against human viruses or vaccines cannot be ruled out, our data suggests that animal exposed people as are more likely to have antibodies against animal influenza viruses. Copyright © 2015 Elsevier B.V. All rights reserved.

Serological and molecular epidemiology of Japanese encephalitis virus infections in swine herds in China, 2006–2012

Science.gov (United States)

Chai, Chunxia; Wang, Qiao; Cao, Sanjie; Zhao, Qin; Wen, Yiping; Huang, Xiaobo; Wen, Xintian; Yan, Qiguai; Ma, Xiaoping

2018-01-01

Japanese encephalitis virus (JEV) is a mosquito-borne, zoonotic flavivirus causing viral encephalitis in humans and reproductive disorder in swine. JEV is prevalent throughout China in human; however, spatiotemporal analysis of JEV in Chinese swine herds has not been reported previously. Herein, we present serological and molecular epidemiological results and estimates of prevalence of JEV infections among swine herds in various regions of China. The results suggest that JEV infections are widespread and genotype I and III strains co-exist in the same regions. Therefore, there is an urgent need to monitor JEV infection status among swine herds in China. PMID:28693301

Genetic Reassortment Among the Influenza Viruses (Avian Influenza, Human Influenza and Swine Influenza in Pigs

Directory of Open Access Journals (Sweden)

Dyah Ayu Hewajuli

2012-12-01

Full Text Available Influenza A virus is a hazardous virus and harm to respiratory tract. The virus infect birds, pigs, horses, dogs, mammals and humans. Pigs are important hosts in ecology of the influenza virus because they have two receptors, namely NeuAc 2,3Gal and NeuAc 2,6Gal which make the pigs are sensitive to infection of influenza virus from birds and humans and genetic reassortment can be occurred. Classical swine influenza H1N1 viruses had been circulated in pigs in North America and other countries for 80 years. In 1998, triple reassortant H3N2 swine influenza viruses that contains genes of human influenza A virus (H3N2, swine influenza virus (H1N1 and avian influenza are reported as cause an outbreaks in pigs in North America. Furthermore, the circulation of triple reassortant H3N2 swine influenza virus resulting reassortant H1N1 swine influenza and reassortant H1N2 swine influenza viruses cause infection in humans. Humans who were infected by triple reassortant swine influenza A virus (H1N1 usually made direct contact with pigs. Although without any clinical symptoms, pigs that are infected by triple reassortant swine influenza A (H1N1 can transmit infection to the humans around them. In June 2009, WHO declared that pandemic influenza of reassortant H1N1 influenza A virus (novel H1N1 has reached phase 6. In Indonesia until 2009, there were 1005 people were infected by H1N1 influenza A and 5 of them died. Novel H1N1 and H5N1 viruses have been circulated in humans and pigs in Indonesia. H5N1 reassortant and H1N1 viruses or the seasonal flu may could arise because of genetic reassortment between avian influenza and humans influenza viruses that infect pigs together.

Simultaneous determination of sulfonamides, tetracyclines and tiamulin in swine wastewater by solid-phase extraction and liquid chromatography-mass spectrometry.

Science.gov (United States)

Ben, Weiwei; Qiang, Zhimin; Adams, Craig; Zhang, Heqing; Chen, Liping

2008-08-22

Little is known about the contamination level of antibiotics in swine wastewater in China. The highly complex matrix of swine wastewater, which generally has a chemical oxygen demand (COD) concentration as high as 15,000 mg/L, makes it difficult to detect antibiotics at trace levels. In this work, a highly selective and sensitive analytical method was developed for simultaneous determination of three classes of commonly used veterinary antibiotics including five sulfonamides, three tetracyclines and one macrolide in swine wastewater using solid-phase extraction (SPE) and liquid chromatography-mass spectrometry (LC-MS). The method detection limits (MDL) in the swine wastewater were determined to be between 5 and 91 ng/L, depending on specific antibiotics. Except sulfamethizole, all the other eight antibiotics were detected in the swine wastewaters collected from three concentrated swine feeding plants located in the Beijing (China) area, showing a concentration range of 0.62-32.67 microg/L. These results reveal the representative concentration levels of selected antibiotics in the swine wastewaters of Beijing area.

Swine flu - A pandemic outbreak

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Jini George

Full Text Available Hippocrates had described influenza like outbreak in 412 B.C. and since then repeated influenza like epidemics and pandemics have been recorded in recent times. One of the greatest killers of all time was the pandemic of swine flu (Spanish flu of 1918-1919, when 230 million people died. Annual influenza epidemics are estimated to affect 5–15% of the global population, resulting in severe illness in 3–5 million patients causing 250,000–500,000 deaths worldwide. Severe illness and deaths occur mainly in the high-risk populations of infants, the elderly and chronically ill patients. The 2009 outbreak of swine flu is thought to be a mutation more specifically a reassortment of four known strains of influenza A virus subtype H1N1; one endemic in humans, one endemic in birds, and two endemic in pigs. WHO officially declared the outbreak to be a pandemic on June 11, 2009, but stressed that the new designation was a result of the global "spread of the virus," not its severity. [Vet World 2009; 2(12.000: 472-474

Feed additives shift gut microbiota and enrich antibiotic resistance in swine gut.

Science.gov (United States)

Zhao, Yi; Su, Jian-Qiang; An, Xin-Li; Huang, Fu-Yi; Rensing, Christopher; Brandt, Kristian Koefoed; Zhu, Yong-Guan

2018-04-15

Antibiotic resistance genes (ARGs) are emerging environmental contaminants posing a threat to public health. Antibiotics and metals are widely used as feed additives and could consequently affect ARGs in swine gut. In this study, high-throughput quantitative polymerase chain reaction (HT-qPCR) based ARG chip and next-generation 16S rRNA gene amplicon sequencing data were analyzed using multiple statistical approaches to profile the antibiotic resistome and investigate its linkages to antibiotics and metals used as feed additives and to the microbial community composition in freshly collected swine manure samples from three large-scale Chinese pig farms. A total of 146 ARGs and up to 1.3×10 10 total ARG copies per gram of swine feces were detected. ARGs conferring resistance to aminoglycoside, macrolide-lincosamide-streptogramin B (MLSB) and tetracycline were dominant in pig gut. Total abundance of ARGs was positively correlated with in-feed antibiotics, microbial biomass and abundance of mobile genetic elements (MGEs) (Padditives and community composition (16.5%). These results suggest that increased levels of in-feed additives could aggravate the enrichment of ARGs and MGEs in swine gut. Copyright © 2017 Elsevier B.V. All rights reserved.

Mitochondrial disease and endocrine dysfunction.

Science.gov (United States)

Chow, Jasmine; Rahman, Joyeeta; Achermann, John C; Dattani, Mehul T; Rahman, Shamima

2017-02-01

Mitochondria are critical organelles for endocrine health; steroid hormone biosynthesis occurs in these organelles and they provide energy in the form of ATP for hormone production and trafficking. Mitochondrial diseases are multisystem disorders that feature defective oxidative phosphorylation, and are characterized by enormous clinical, biochemical and genetic heterogeneity. To date, mitochondrial diseases have been found to result from >250 monogenic defects encoded across two genomes: the nuclear genome and the ancient circular mitochondrial genome located within mitochondria themselves. Endocrine dysfunction is often observed in genetic mitochondrial diseases and reflects decreased intracellular production or extracellular secretion of hormones. Diabetes mellitus is the most frequently described endocrine disturbance in patients with inherited mitochondrial diseases, but other endocrine manifestations in these patients can include growth hormone deficiency, hypogonadism, adrenal dysfunction, hypoparathyroidism and thyroid disease. Although mitochondrial endocrine dysfunction frequently occurs in the context of multisystem disease, some mitochondrial disorders are characterized by isolated endocrine involvement. Furthermore, additional monogenic mitochondrial endocrine diseases are anticipated to be revealed by the application of genome-wide next-generation sequencing approaches in the future. Understanding the mitochondrial basis of endocrine disturbance is key to developing innovative therapies for patients with mitochondrial diseases.

Sex difference in the sensitivity of cardiac mitochondrial permeability transition pore to calcium load

Czech Academy of Sciences Publication Activity Database

Milerová, Marie; Drahota, Zdeněk; Chytilová, Anna; Tauchmannová, Kateřina; Houštěk, Josef; Ošťádal, Bohuslav

2016-01-01

Roč. 412, 1-2 (2016), s. 147-154 ISSN 0300-8177 R&D Projects: GA ČR(CZ) GB14-36804G; GA MZd(CZ) NT14050; GA ČR(CZ) GA13-10267S; GA ČR(CZ) GAP303/12/1162 Institutional support: RVO:67985823 Keywords : heart * mitochondrial permeability transition pore * sex difference * calcium-induced swelling Subject RIV: FA - Cardiovascular Diseases incl. Cardiotharic Surgery Impact factor: 2.669, year: 2016

Molecular evolution of H1N1 swine influenza in Guangdong, China, 2016-2017.

Science.gov (United States)

Cai, Mengkai; Huang, Junming; Bu, Dexin; Yu, Zhiqing; Fu, Xinliang; Ji, Chihai; Zhou, Pei; Zhang, Guihong

2018-06-01

Swine are the main host of the H1N1 swine influenza virus (SIV), however, H1N1 can also infect humans and occasionally cause serious respiratory disease. To trace the evolution of the SIV in Guangdong, China, we performed an epidemic investigation during the period of 2016-2017. Nine H1N1 influenza viruses were isolated from swine nasal swabs. Antigenic analysis revealed that these viruses belonged to two distinct antigenic groups, represented by A/Swine/Guangdong/101/2016 and A/Swine/Guangdong/52/2017. Additionally, three genotypes, known as GD52/17-like, GD493/17-like and GD101/16-like, were identified by phylogenetic analysis. Importantly, the genotypes including a minimum of 4 pdm/09-origin internal genes have become prevalent in China in recent years. A total of 2966 swine serum samples were used to perform hemagglutination inhibition (HI) tests, and the results showed that the seroprevalence values of SW/GD/101/16 (32.2% in 2016, 32.1% in 2017) were significantly higher than the seroprevalence values of SW/GD/52/17 (18.0% in 2016, 16.7% in 2017). Our study showed that the three reassortant genotypes of H1N1 SIV currently circulating in China are stable, but H1N1pdm09 poses challenges to human health by the introduction of internal genes into these reassortant genotypes. Strengthening SIV surveillance is therefore critical for SIV control and minimizing its potential threat to public health. Copyright © 2018 Elsevier B.V. All rights reserved.

Biogas Initiative from Swine Farm in Southern Thailand

Directory of Open Access Journals (Sweden)

Damrongsak Det

2016-01-01

Full Text Available First biogas pipeline network has been well established in southern Thailand. About 1,273 households, accountable for about 87% of the total of 1,466 households in the district, get the benefits from biogas energy in many ways. Key success to this initiative is the collaboration between all parties, i.e., swine farm owners, households, and government officials. Swine farm owners are responsible for the design and construction of the biogas plants. Households pay some contributions regarding labor work and maintenance cost on biogas system and its pipeline network. Government officials are responsible for financial and technical supports to both parties. Indeed biogas energy offers an alternative source of heat energy for cooking fuel in this region.

Loss of Intralipid®- but not sevoflurane-mediated cardioprotection in early type-2 diabetic hearts of fructose-fed rats: importance of ROS signaling.

Directory of Open Access Journals (Sweden)

Phing-How Lou

Full Text Available Insulin resistance and early type-2 diabetes are highly prevalent. However, it is unknown whether Intralipid® and sevoflurane protect the early diabetic heart against ischemia-reperfusion injury.Early type-2 diabetic hearts from Sprague-Dawley rats fed for 6 weeks with fructose were exposed to 15 min of ischemia and 30 min of reperfusion. Intralipid® (1% was administered at the onset of reperfusion. Peri-ischemic sevoflurane (2 vol.-% served as alternative protection strategy. Recovery of left ventricular function was recorded and the activation of Akt and ERK 1/2 was monitored. Mitochondrial function was assessed by high-resolution respirometry and mitochondrial ROS production was measured by Amplex Red and aconitase activity assays. Acylcarnitine tissue content was measured and concentration-response curves of complex IV inhibition by palmitoylcarnitine were obtained.Intralipid® did not exert protection in early diabetic hearts, while sevoflurane improved functional recovery. Sevoflurane protection was abolished by concomitant administration of the ROS scavenger N-2-mercaptopropionyl glycine. Sevoflurane, but not Intralipid® produced protective ROS during reperfusion, which activated Akt. Intralipid® failed to inhibit respiratory complex IV, while sevoflurane inhibited complex I. Early diabetic hearts exhibited reduced carnitine-palmitoyl-transferase-1 activity, but palmitoylcarnitine could not rescue protection and enhance postischemic functional recovery. Cardiac mitochondria from early diabetic rats exhibited an increased content of subunit IV-2 of respiratory complex IV and of uncoupling protein-3.Early type-2 diabetic hearts lose complex IV-mediated protection by Intralipid® potentially due to a switch in complex IV subunit expression and increased mitochondrial uncoupling, but are amenable to complex I-mediated sevoflurane protection.

Computerized management support for swine breeding farms

NARCIS (Netherlands)

Huirne, R.B.M.

1990-01-01

1. INTRODUCTION

The investigations described in this thesis have been directed towards computerized management support for swine breeding farms, focused on sow productivity and profitability. The study is composed of three basic parts: (1) basic description and

Hepatitis E virus infection in North Italy: high seroprevalence in swine herds and increased risk for swine workers.

NARCIS (Netherlands)

Mughini-Gras, L; Angeloni, G; Salata, C; Vonesch, N; D'Amico, W; Campagna, G; Natale, A; Zuliani, F; Ceglie, L; Monne, I; Vascellari, M; Capello, K; DI Martino, G; Inglese, N; Palù, G; Tomao, P; Bonfanti, L

2017-01-01

We determined the hepatitis E virus (HEV) seroprevalence and detection rate in commercial swine herds in Italy's utmost pig-rich area, and assessed HEV seropositivity risk in humans as a function of occupational exposure to pigs, diet, foreign travel, medical history and hunting activities. During

Hepatitis E virus infection in North Italy : high seroprevalence in swine herds and increased risk for swine workers

NARCIS (Netherlands)

Mughini-Gras, L|info:eu-repo/dai/nl/413306046; Angeloni, Giorgia; Salata, C; Vonesch, N; D'Amico, W; Campagna, G; Natale, Alda; Zuliani, Federica; Ceglie, Letizia; Monne, Isabella; Vascellari, M; Capello, Katia; DI Martino, G; Inglese, N; Palù, G; Tomao, P; Bonfanti, L.

2017-01-01

We determined the hepatitis E virus (HEV) seroprevalence and detection rate in commercial swine herds in Italy's utmost pig-rich area, and assessed HEV seropositivity risk in humans as a function of occupational exposure to pigs, diet, foreign travel, medical history and hunting activities. During

The action of certain antibiotics and ether on swine enzootic pneumonia.

Science.gov (United States)

Huhn, R G

1971-01-01

The susceptibility of Mycoplasma hyopneumoniae to the action of three antibiotics and diethyl ether was determined. Infected swine were used in an in vivo sensitivity detection system. The parameter of susceptibility was lesion prophylaxis. In vivo, Mycoplasma hyopneumoniae appeared to be resistant to diethyl ether, tylosin tartrate, and erythromycin, but was susceptible to the action of chlortetracycline. Chlortetracycline was effective in preventing the development of lesions when given at levels which would be practical in commercial swine operations.

Lumbricidae as transitory hosts in Metastrongylus infection in swine

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Pavlović Ivan

2005-01-01

Full Text Available Metastrongylidosis or lungworm disease in swine is a disease caused by several types of nematodes of the genus Metastrongylus. Metastrongylidae are biohelminths whose causes use transitory hosts for their development and maintaining their biological cycle, and in this case they are numerous species of Lumbricidae (earthworms. Depending on the geographic environment, numerous representatives of Lumbricidae persist as transitory hosts. In our environment, these are dominant earthworm species of the genus Eisenia spp, Dandreobena spp, Allopbophora spp, Lubricus spp, Octoiasium spp, Bimastus spp, and rarely those from the genus Heledrillus spp. Swine are infected perorally with Metastrongylidae when they ingest infected earthworms.

Perfluorocarbon in Delayed Recompression with a Mixed Gender Swine Model of Decompression Sickness.

Science.gov (United States)

Cronin, William A; Hall, Aaron A; Auker, Charles R; Mahon, Richard T

2018-01-01

Perfluorocarbons (PFC) are fluorinated hydrocarbons that dissolve gases to a much greater degree than plasma and hold promise in treating decompression sickness (DCS). The efficacy of PFC in a mixed gender model of DCS and safety in recompression therapy has not been previously explored. Swine (25 kg; N = 104; 51 male and 53 female) were randomized into normal saline solution (NSS) or PFC emulsion treatment groups and subjected to compression on air in a hyperbaric chamber at 200 fsw for 31 min. Then the animals were decompressed and observed for signs of DCS. Afterwards, they were treated with oxygen and either PFC (4 cc · kg-1) or NSS (4 cc · kg-1). Surviving animals were observed for 4 h, at which time they underwent recompression therapy using a standard Navy Treatment Table 6. After 24 h the animals were assessed and then euthanized. Survival rates were not significantly different between NSS (74.04%) and PFC (66.67%) treatment groups. All swine that received recompression treatment survived to the end of the study and no seizures were observed in either PFC or NSS animals. Within the saline treated swine group there were no significant differences in DCS survival between male (75.00%, N = 24) and female (73.08%, N = 26) swine. Within the PFC treated swine, survival of females (51.85%, N = 27) was significantly lower than males (81.48%, N = 27). In this large animal mixed gender efficacy study in DCS, PFC did not improve mortality or spinal cord injury, but appears safe during recompressive therapy. Gender differences in DCS treatment with PFC will need further study.Cronin WA, Hall AA, Auker CR, Mahon RT. Perfluorocarbon in delayed recompression with a mixed gender swine model of decompression sickness. Aerosp Med Hum Perform. 2018; 89(1):14-18.

Findings of bacterial microflora in piglets infected with conventional swine plague

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Prodanov Jasna

2002-01-01

Full Text Available Piglets infected with the conventional swine plague virus as a result of secondary bacterial infections sometimes show an insufficiently clear clinical and pathoanatomical picture, which is why the very procedure of diagnosis is complex and the final diagnosis unreliable. That is why these investigations were aimed at examining the presence of bacterial microflora in diseased and dead pilgets which were found to have the viral antigen for CSP using the fluorescent antibody technique, in cases where the pathomorphological finding was not characteristic for conventional swine plague. Autopsies of dead piglets most often showed changes in the digestive tract and lungs, with resulting technopathy and diseases of infective nature. Such findings on knowledge of a present bacterial microflora are especially important in cases when conventional swine plague is controlled on farms and an announcement that the disease has been contained is in the offing.

76 FR 7721 - Importation of Live Swine, Swine Semen, Pork, and Pork Products; Estonia, Hungary, Slovakia, and...

Science.gov (United States)

2011-02-11

... for the 6 BIPs in Slovenia. BVIS veterinary inspectors are present at the BIPs during working hours, but do not conduct inspections outside normal working hours without prior notice. Slovenian road... Slovenia to the region of the European Union that we recognize as a low-risk region for classical swine...

New influenza A virus reassortments have been found in Danish swine in 2011

DEFF Research Database (Denmark)

Breum, Solvej Østergaard; Hjulsager, Charlotte Kristiane; Trebbien, Ramona

2012-01-01

” viruses which have been circulating in Danish pigs since it was found for the first time in 1981. ii) H1N2 reassortant viruses which comprise HA from “avian like” H1N1 and NA from swine H3N2. The reassortant H1N2 virus was discovered in Danish pig for the first time in 2003 and is now well established......In 2011 a passive surveillance for influenza A virus was conducted in Danish swine. Tested samples were clinical samples from affected pigs submitted to the Danish National Veterinary Institute for swine influenza virus detection. In total 713 samples from 276 herds were analysed and about 24......% of the samples were positive for swine influenza virus. All influenza positive samples were tested for the H1N1pdm09 virus by a real time RT-PCR assay specific for the pandemic HA gene and 26% of the samples were positive. Subtyping of 90 samples by sequencing revealed the presence of; i) H1N1 “avian like...

Swine Influenza Virus (H1N2) Characterization and Transmission in Ferrets, Chile.

Science.gov (United States)

Bravo-Vasquez, Nicolás; Karlsson, Erik A; Jimenez-Bluhm, Pedro; Meliopoulos, Victoria; Kaplan, Bryan; Marvin, Shauna; Cortez, Valerie; Freiden, Pamela; Beck, Melinda A; Hamilton-West, Christopher; Schultz-Cherry, Stacey

2017-02-01

Phylogenetic analysis of the influenza hemagglutinin gene (HA) has suggested that commercial pigs in Chile harbor unique human seasonal H1-like influenza viruses, but further information, including characterization of these viruses, was unavailable. We isolated influenza virus (H1N2) from a swine in a backyard production farm in Central Chile and demonstrated that the HA gene was identical to that in a previous report. Its HA and neuraminidase genes were most similar to human H1 and N2 viruses from the early 1990s and internal segments were similar to influenza A(H1N1)pdm09 virus. The virus replicated efficiently in vitro and in vivo and transmitted in ferrets by respiratory droplet. Antigenically, it was distinct from other swine viruses. Hemagglutination inhibition analysis suggested that antibody titers to the swine Chilean H1N2 virus were decreased in persons born after 1990. Further studies are needed to characterize the potential risk to humans, as well as the ecology of influenza in swine in South America.

Efficacy of Influenza Vaccination and Tamiflu? Treatment ? Comparative Studies with Eurasian Swine Influenza Viruses in Pigs

OpenAIRE

Duerrwald, Ralf; Schlegel, Michael; Bauer, Katja; Vissiennon, Th?ophile; Wutzler, Peter; Schmidtke, Michaela

2013-01-01

Recent epidemiological developments demonstrated that gene segments of swine influenza A viruses can account for antigenic changes as well as reduced drug susceptibility of pandemic influenza A viruses. This raises questions about the efficacy of preventive measures against swine influenza A viruses. Here, the protective effect of vaccination was compared with that of prophylactic Tamiflu® treatment against two Eurasian swine influenza A viruses. 11-week-old pigs were infected by aerosol nebu...

Dengue virus induces mitochondrial elongation through impairment of Drp1-triggered mitochondrial fission

Energy Technology Data Exchange (ETDEWEB)

Barbier, Vincent; Lang, Diane; Valois, Sierra; Rothman, Alan L.; Medin, Carey L., E-mail: cmedin.uri@gmail.com

2017-01-15

Mitochondria are highly dynamic organelles that undergo continuous cycles of fission and fusion to maintain essential cellular functions. An imbalance between these two processes can result in many pathophysiological outcomes. Dengue virus (DENV) interacts with cellular organelles, including mitochondria, to successfully replicate in cells. This study used live-cell imaging and found an increase in mitochondrial length and respiration during DENV infection. The level of mitochondrial fission protein, Dynamin-related protein 1 (Drp1), was decreased on mitochondria during DENV infection, as well as Drp1 phosphorylated on serine 616, which is important for mitochondrial fission. DENV proteins NS4b and NS3 were also associated with subcellular fractions of mitochondria. Induction of fission through uncoupling of mitochondria or overexpression of Drp1 wild-type and Drp1 with a phosphomimetic mutation (S616D) significantly reduced viral replication. These results demonstrate that DENV infection causes an imbalance in mitochondrial dynamics by inhibiting Drp1-triggered mitochondrial fission, which promotes viral replication. - Highlights: •Mitochondrial length and respiration are increased during DENV infection. •DENV inhibits Drp1-triggered mitochondrial fission. •DENV titers are reduced by mitochondrial fragmentation, Drp1 WT and S616D expression. •Viral proteins NS4b and NS3 are associated with subcellular fractions of mitochondria.

Dengue virus induces mitochondrial elongation through impairment of Drp1-triggered mitochondrial fission

International Nuclear Information System (INIS)

Barbier, Vincent; Lang, Diane; Valois, Sierra; Rothman, Alan L.; Medin, Carey L.

2017-01-01

Mitochondria are highly dynamic organelles that undergo continuous cycles of fission and fusion to maintain essential cellular functions. An imbalance between these two processes can result in many pathophysiological outcomes. Dengue virus (DENV) interacts with cellular organelles, including mitochondria, to successfully replicate in cells. This study used live-cell imaging and found an increase in mitochondrial length and respiration during DENV infection. The level of mitochondrial fission protein, Dynamin-related protein 1 (Drp1), was decreased on mitochondria during DENV infection, as well as Drp1 phosphorylated on serine 616, which is important for mitochondrial fission. DENV proteins NS4b and NS3 were also associated with subcellular fractions of mitochondria. Induction of fission through uncoupling of mitochondria or overexpression of Drp1 wild-type and Drp1 with a phosphomimetic mutation (S616D) significantly reduced viral replication. These results demonstrate that DENV infection causes an imbalance in mitochondrial dynamics by inhibiting Drp1-triggered mitochondrial fission, which promotes viral replication. - Highlights: •Mitochondrial length and respiration are increased during DENV infection. •DENV inhibits Drp1-triggered mitochondrial fission. •DENV titers are reduced by mitochondrial fragmentation, Drp1 WT and S616D expression. •Viral proteins NS4b and NS3 are associated with subcellular fractions of mitochondria.

Inhibition of Drp-1 dependent mitochondrial fission augments alcohol-induced cardiotoxicity via dysregulated Akt signaling

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Anusha Sivakumar

2017-10-01

Full Text Available Cardiovascular disorders (CVDs still claim high mortality in spite of advancements in prognosis and treatment strategies. Alcohol is one of the most commonly consumed drugs globally and chronic/binge consumption (BAC 0.08 g/dL in 2 hours is a risk factor for CVDs. However, the aetiology and pathophysiological mechanisms of alcohol induced cardiotoxicity are still poorly understood. Mitochondria are the prime site for the ATP demands of the heart and also ethanol metabolism. These subcellular organelles depict dynamic fusion and fission events that are vital for structure and functional integrity. While fused mitochondrial improve ATP production and cell survival, increased fragmentation can be the cause or result of apoptosis. In this study, we proposed to analyze the mechanism of mitochondrial fission protein Drp-1-dependent apoptosis during alcohol toxicity. Male Wistar rats (220-250 kg body weight were given isocaloric sucrose or ethanol for 45 days, orally, via drinking water and intermittent gavage twice a week. Histopathological examination of the heart displayed hypertrophy with mild inflammation. Drp-1 immunoblotting showed over-expression of the protein during ethanol treatment. We next hypothesized that inhibiting Drp-1 could attenuate alcohol-induced cardiotoxicity. Interestingly, silencing Drp-1 with siRNA in-vitro augmented cytotoxicity. Also, crude mitochondrial fraction showed increased Bak aggregation, reduced cytochrome c release but increased SMAC/DIABLO. We analyzed the Akt cell survival signaling and found that PTEN showed over-expression at both transcriptional and translational level with no significant change in total Akt but down-regulation of p-Akt (Ser473. In conclusion, we have shown that inhibition of Drp-1 dependent mitochondrial fission is not cardioprotective against alcohol-induced apoptotic signaling and augments the cytotoxicity. To our knowledge, this study is the first to interlink cell survival AKT signaling

Evidence for Cross-species Influenza A Virus Transmission Within Swine Farms, China: A One Health, Prospective Cohort Study.

Science.gov (United States)

Ma, Mai-Juan; Wang, Guo-Lin; Anderson, Benjamin D; Bi, Zhen-Qiang; Lu, Bing; Wang, Xian-Jun; Wang, Chuang-Xin; Chen, Shan-Hui; Qian, Yan-Hua; Song, Shao-Xia; Li, Min; Lednicky, John A; Zhao, Teng; Wu, Meng-Na; Cao, Wu-Chun; Gray, Gregory C

2018-02-01

Our understanding of influenza A virus transmission between humans and pigs is limited. Beginning in 2015, we used a One Health approach and serial sampling to prospectively study 299 swine workers and 100 controls, their 9000 pigs, and 6 pig farm environments in China for influenza A viruses (IAVs) using molecular, culture, and immunological techniques. Study participants were closely monitored for influenza-like illness (ILI) events. Upon enrollment, swine workers had higher serum neutralizing antibody titers against swine H1N1 and higher nasal wash total immunoglobulin A (IgA) and specific IgA titers against swine H1N1 and H3N2 viruses. Over a period of 12 months, IAVs were detected by quantitative reverse-transcription polymerase chain reaction in 46 of 396 (11.6%) environmental swabs, 235 of 3300 (7.1%) pig oral secretion, 23 of 396 (5.8%) water, 20 of 396 (5.1%) aerosol, and 19 of 396 (4.8%) fecal-slurry specimens. Five of 32 (15.6%) participants with ILI events had nasopharyngeal swab specimens that were positive for IAV, and 17 (53.1%) demonstrated 4-fold rises in neutralization titers against a swine virus. Reassorted Eurasian avian-lineage H1N1, A(H1N1)pdm09-like, and swine-lineage H3N2 viruses were identified in pig farms. The A(H1N1)pdm09-like H1N1 viruses identified in swine were nearly genetically identical to the human H1N1 viruses isolated from the participants with ILI. There was considerable evidence of A(H1N1)pdm09-like, swine-lineage H1N1, and swine-lineage H3N2 viruses circulating, likely reassorting, and likely crossing species within the pig farms. These data suggest that stronger surveillance for novel influenza virus emergence within swine farms is imperative. © The Author(s) 2017. Published by Oxford University Press for the Infectious Diseases Society of America. All rights reserved. For permissions, e-mail: journals.permissions@oup.com.

A Review of African Swine Fever and the Potential for Introduction into the United States and the Possibility of Subsequent Establishment in Feral Swine and Native Ticks.

Science.gov (United States)

Brown, Vienna R; Bevins, Sarah N

2018-01-01

African swine fever (ASF) is caused by African swine fever virus (ASFV), which can cause substantial morbidity and mortality events in swine. The virus can be transmitted via direct and indirect contacts with infected swine, their products, or competent vector species, especially Ornithodoros ticks. Africa and much of Eastern Europe are endemic for ASF; a viral introduction to countries that are currently ASF free could have severe economic consequences due to the loss of production from infected animals and the trade restrictions that would likely be imposed as a result of an outbreak. We identified vulnerabilities that could lead to ASFV introduction or persistence in the United States or other ASF-free regions. Both legal and illegal movements of live animals, as well as the importation of animal products, byproducts, and animal feed, pose a risk of virus introduction. Each route is described, and current regulations designed to prevent ASFV and other pathogens from entering the United States are outlined. Furthermore, existing ASFV research gaps are highlighted. Laboratory experiments to evaluate multiple species of Ornithodoros ticks that have yet to be characterized would be useful to understand vector competence, host preferences, and distribution of competent soft tick vectors in relation to high pig production areas as well as regions with high feral swine (wild boar or similar) densities. Knowledge relative to antigenic viral proteins that contribute to host response and determination of immune mechanisms that lead to protection are foundational in the quest for a vaccine. Finally, sampling of illegally imported and confiscated wild suid products for ASFV could shed light on the types of products being imported and provide a more informed perspective relative to the risk of ASFV importation.

A Review of African Swine Fever and the Potential for Introduction into the United States and the Possibility of Subsequent Establishment in Feral Swine and Native Ticks

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Vienna R. Brown

2018-02-01

Full Text Available African swine fever (ASF is caused by African swine fever virus (ASFV, which can cause substantial morbidity and mortality events in swine. The virus can be transmitted via direct and indirect contacts with infected swine, their products, or competent vector species, especially Ornithodoros ticks. Africa and much of Eastern Europe are endemic for ASF; a viral introduction to countries that are currently ASF free could have severe economic consequences due to the loss of production from infected animals and the trade restrictions that would likely be imposed as a result of an outbreak. We identified vulnerabilities that could lead to ASFV introduction or persistence in the United States or other ASF-free regions. Both legal and illegal movements of live animals, as well as the importation of animal products, byproducts, and animal feed, pose a risk of virus introduction. Each route is described, and current regulations designed to prevent ASFV and other pathogens from entering the United States are outlined. Furthermore, existing ASFV research gaps are highlighted. Laboratory experiments to evaluate multiple species of Ornithodoros ticks that have yet to be characterized would be useful to understand vector competence, host preferences, and distribution of competent soft tick vectors in relation to high pig production areas as well as regions with high feral swine (wild boar or similar densities. Knowledge relative to antigenic viral proteins that contribute to host response and determination of immune mechanisms that lead to protection are foundational in the quest for a vaccine. Finally, sampling of illegally imported and confiscated wild suid products for ASFV could shed light on the types of products being imported and provide a more informed perspective relative to the risk of ASFV importation.

Disruption of mitochondrial DNA replication in Drosophila increases mitochondrial fast axonal transport in vivo.

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Rehan M Baqri

Full Text Available Mutations in mitochondrial DNA polymerase (pol gamma cause several progressive human diseases including Parkinson's disease, Alper's syndrome, and progressive external ophthalmoplegia. At the cellular level, disruption of pol gamma leads to depletion of mtDNA, disrupts the mitochondrial respiratory chain, and increases susceptibility to oxidative stress. Although recent studies have intensified focus on the role of mtDNA in neuronal diseases, the changes that take place in mitochondrial biogenesis and mitochondrial axonal transport when mtDNA replication is disrupted are unknown. Using high-speed confocal microscopy, electron microscopy and biochemical approaches, we report that mutations in pol gamma deplete mtDNA levels and lead to an increase in mitochondrial density in Drosophila proximal nerves and muscles, without a noticeable increase in mitochondrial fragmentation. Furthermore, there is a rise in flux of bidirectional mitochondrial axonal transport, albeit with slower kinesin-based anterograde transport. In contrast, flux of synaptic vesicle precursors was modestly decreased in pol gamma-alpha mutants. Our data indicate that disruption of mtDNA replication does not hinder mitochondrial biogenesis, increases mitochondrial axonal transport, and raises the question of whether high levels of circulating mtDNA-deficient mitochondria are beneficial or deleterious in mtDNA diseases.

Myocardial Po2 does not limit aerobic metabolism in the postischemic heart.

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Chung, Youngran

2016-01-15

Reperfused hypertrophic hearts are prone to develop reflow abnormalities, which are likely to impair O2 return to the myocardium. Yet, reflow deficit may not be the only factor determining postischemic oxygenation in the hypertrophic heart. Altered O2 demand may also contribute to hypoxia. In addition, the extent to which myocardial Po2 dictates energy and functional recovery in the reperfused heart remains uncertain. In the present study, moderately hypertrophied hearts from spontaneously hypertensive rats were subjected to ischemia-reperfusion, and the recovery time courses of pH and high-energy phosphates were followed by (31)P NMR. (1)H NMR measurement of intracellular myoglobin assessed tissue O2 levels. The present study found that the exacerbation of hypoxia in the postischemic spontaneously hypertensive rat heart arises mostly from impaired microvascular supply of O2. However, postischemic myocardial Po2, at least when it exceeds ∼18% of the preischemic level, does not limit mitochondrial respiration and high-energy phosphate resynthesis. It only passively reflects changes in the O2 supply-demand balance. Copyright © 2016 the American Physiological Society.

Novel mitochondrial extensions provide evidence for a link between microtubule-directed movement and mitochondrial fission

International Nuclear Information System (INIS)

Bowes, Timothy; Gupta, Radhey S.

2008-01-01

Mitochondrial dynamics play an important role in a large number of cellular processes. Previously, we reported that treatment of mammalian cells with the cysteine-alkylators, N-ethylmaleimide and ethacrynic acid, induced rapid mitochondrial fusion forming a large reticulum approximately 30 min after treatment. Here, we further investigated this phenomenon using a number of techniques including live-cell confocal microscopy. In live cells, drug-induced fusion coincided with a cessation of fast mitochondrial movement which was dependent on microtubules. During this loss of movement, thin mitochondrial tubules extending from mitochondria were also observed, which we refer to as 'mitochondrial extensions'. The formation of these mitochondrial extensions, which were not observed in untreated cells, depended on microtubules and was abolished by pretreatment with nocodazole. In this study, we provide evidence that these extensions result from of a block in mitochondrial fission combined with continued application of motile force by microtubule-dependent motor complexes. Our observations strongly suggest the existence of a link between microtubule-based mitochondrial trafficking and mitochondrial fission

Alternative risk financing instruments for swine epidemics

NARCIS (Netherlands)

Meuwissen, M.P.M.; Asseldonk, van M.A.P.M.; Huirne, R.B.M.

2003-01-01

Swine epidemics can have very large devastating financial consequences. Governments generally bear the direct losses, such as the value of destroyed animals. Consequential losses, such as the losses resulting from empty buildings and movement standstills, are completely borne by the farmers (and

Ionizing radiation induces mitochondrial reactive oxygen species production accompanied by upregulation of mitochondrial electron transport chain function and mitochondrial content under control of the cell cycle checkpoint.

Science.gov (United States)

Yamamori, Tohru; Yasui, Hironobu; Yamazumi, Masayuki; Wada, Yusuke; Nakamura, Yoshinari; Nakamura, Hideo; Inanami, Osamu

2012-07-15

Whereas ionizing radiation (Ir) instantaneously causes the formation of water radiolysis products that contain some reactive oxygen species (ROS), ROS are also suggested to be released from biological sources in irradiated cells. It is now becoming clear that these ROS generated secondarily after Ir have a variety of biological roles. Although mitochondria are assumed to be responsible for this Ir-induced ROS production, it remains to be elucidated how Ir triggers it. Therefore, we conducted this study to decipher the mechanism of Ir-induced mitochondrial ROS production. In human lung carcinoma A549 cells, Ir (10 Gy of X-rays) induced a time-dependent increase in the mitochondrial ROS level. Ir also increased mitochondrial membrane potential, mitochondrial respiration, and mitochondrial ATP production, suggesting upregulation of the mitochondrial electron transport chain (ETC) function after Ir. Although we found that Ir slightly enhanced mitochondrial ETC complex II activity, the complex II inhibitor 3-nitropropionic acid failed to reduce Ir-induced mitochondrial ROS production. Meanwhile, we observed that the mitochondrial mass and mitochondrial DNA level were upregulated after Ir, indicating that Ir increased the mitochondrial content of the cell. Because irradiated cells are known to undergo cell cycle arrest under control of the checkpoint mechanisms, we examined the relationships between cell cycle and mitochondrial content and cellular oxidative stress level. We found that the cells in the G2/M phase had a higher mitochondrial content and cellular oxidative stress level than cells in the G1 or S phase, regardless of whether the cells were irradiated. We also found that Ir-induced accumulation of the cells in the G2/M phase led to an increase in cells with a high mitochondrial content and cellular oxidative stress level. This suggested that Ir upregulated mitochondrial ETC function and mitochondrial content, resulting in mitochondrial ROS production, and that

Ventricular Effective Refraction Period and Ventricular Repolarization Analysis in Experimental Tachycardiomyopathy in Swine.

Science.gov (United States)

Noszczyk-Nowak, Agnieszka; Pasławska, Urszula; Gajek, Jacek; Janiszewski, Adrian; Pasławski, Robert; Zyśko, Dorota; Nicpoń, Józef

2016-01-01

Swine are recognized animal models of human cardiovascular diseases. However, little is known on the CHF-associated changes in the electrophysiological ventricular parameters of humans and animals. The aim of this study was to analyze changes in the durations of ventricular effective refraction period (VERP), QT and QTc intervals of pigs with chronic tachycardia-induced tachycardiomyopathy (TIC). The study was comprised of 28 adult pigs (8 females and 20 males) of the Polish Large White breed. A one-chamber pacemaker was implanted in each of the 28 pigs. Electrocardiographic, echocardiographic and electrophysiological studies were carried out prior to the pacemaker implantation and at subsequent 4-week intervals. All electrocardiographic, echocardiographic and short electrophysiological study measurements in all swine were done under general anesthesia (propofol) after premedication with midazolam, medetomidine, and ketamine. No significant changes in the duration of QT interval and corrected QT interval (QTc) were observed during consecutive weeks of the experiment. The duration of the QTc interval of female pigs was shown to be significantly longer than that of the males throughout the whole study period. Beginning from the 12th week of rapid ventricular pacing, a significant increase in duration of VERP was observed in both male and female pigs. Males and females did not differ significantly in terms of VERP duration determined throughout the whole study period. Ventricular pacing, stimulation with 2 and 3 premature impulses at progressively shorter coupling intervals and an imposed rhythm of 130 bpm or 150 bpm induced transient ventricular tachycardia in one female pig and four male pigs. One episode of permanent ventricular tachycardia was observed. The number of induced arrhythmias increased proportionally to the severity of heart failure and duration of the experiment. However, relatively aggressive protocols of stimulation were required in order to induce

Arsenic residues in livers of swine, lamb and poultry and in eggs

Energy Technology Data Exchange (ETDEWEB)

Knoeppler, H O

1975-01-01

The arsenic content of 3651 swine, 180 lamb livers, 420 egg samples and poultry livers from 175 poultry farms were determined colorimetrically. The analyses samples were all derived from bavarian farms. According to the proposed legal standards (3), 1.23% of the swine liver samples and 1.67% of the egg samples were above the tolerated values of 0.5 resp. 0.1 mg/kg. 14 references, 4 tables.

Incidence, Diversity, and Molecular Epidemiology of Sapoviruses in Swine across Europe

DEFF Research Database (Denmark)

Reuter, G.; Zimsek-Mijovski, J.; Poljsak-Prijatelj, M.

2010-01-01

report on the incidence, genetic diversity and molecular epidemiology of sapoviruses detected in domestic pigs in a comprehensive study conducted in six European countries (Denmark, Finland, Hungary, Italy, Slovenia and Spain) between 2004 and 2007. A total of 1,050 swine fecal samples from 88 pig farms......) to human sapovirus strains. Sapoviruses are commonly circulating and endemic agents in swine herds throughout Europe. Highly heterogenous and potential new genogroups of sapoviruses were found in pigs; however, no "human-like" sapoviruses were detected....

Effect of turning frequency and season on composting materials from swine high-rise facilities

Science.gov (United States)

Composting of swine manure has several advantages, liquid slurries are converted to solid, the total volume of material is reduced and the stabilized product is more easily transported off-site. Despite this, swine waste is generally stored, treated and applied in its liquid form. The high-rise fini...

Changes of mitochondrial ultrastructure and function during ageing in mice and Drosophila.

Science.gov (United States)

Brandt, Tobias; Mourier, Arnaud; Tain, Luke S; Partridge, Linda; Larsson, Nils-Göran; Kühlbrandt, Werner

2017-07-12

Ageing is a progressive decline of intrinsic physiological functions. We examined the impact of ageing on the ultrastructure and function of mitochondria in mouse and fruit flies ( Drosophila melanogaster ) by electron cryo-tomography and respirometry. We discovered distinct age-related changes in both model organisms. Mitochondrial function and ultrastructure are maintained in mouse heart, whereas subpopulations of mitochondria from mouse liver show age-related changes in membrane morphology. Subpopulations of mitochondria from young and old mouse kidney resemble those described for apoptosis. In aged flies, respiratory activity is compromised and the production of peroxide radicals is increased. In about 50% of mitochondria from old flies, the inner membrane organization breaks down. This establishes a clear link between inner membrane architecture and functional decline. Mitochondria were affected by ageing to very different extents, depending on the organism and possibly on the degree to which tissues within the same organism are protected against mitochondrial damage.

Oxidative Stress and Heart Failure in Altered Thyroid States

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Pallavi Mishra

2012-01-01

Full Text Available Increased or reduced action of thyroid hormone on certain molecular pathways in the heart and vasculature causes relevant cardiovascular derangements. It is well established that hyperthyroidism induces a hyperdynamic cardiovascular state, which is associated with a faster heart rate, enhanced left ventricular systolic and diastolic function whereas hypothyroidism is characterized by the opposite changes. Hyperthyroidism and hypothyroidism represent opposite clinical conditions, albeit not mirror images. Recent experimental and clinical studies have suggested the involvement of ROS tissue damage under altered thyroid status. Altered-thyroid state-linked changes in heart modify their susceptibility to oxidants and the extent of the oxidative damage they suffer following oxidative challenge. Chronic increase in the cellular levels of ROS can lead to a catastrophic cycle of DNA damage, mitochondrial dysfunction, further ROS generation and cellular injury. Thus, these cellular events might play an important role in the development and progression of myocardial remodeling and heart failure in altered thyroid states (hypo- and hyper-thyroidism. The present review aims at elucidating the various signaling pathways mediated via ROS and their modulation under altered thyroid state and the possibility of antioxidant therapy.

Genetic drift of HA and NA in Danish swine influenza virus from the period 2003-2012

DEFF Research Database (Denmark)

Fobian, Kristina; Breum, Solvej Østergaard; Hjulsager, Charlotte Kristiane

2012-01-01

. Currently at least three influenza A subtypes (H1N1, H1N2 and H3N2) are endemic in the Danish swine population, and since 2010 the pandemic virus (H1N1pdm09) have also frequently been detected. The focus in this study will be on H1N1 and H1N2, since the prevalence of H3N2 have declined over the past years...... will provide a more complete picture of the molecular epidemiology of the H1N1 and H1N2 swine influenza viruses in Denmark. A thorough knowledge of the antigenic drift in surface genes is very important concerning evaluation of the zoonotic potential of existing and future swine influenza virus strains......The aim of this study is to analyze; the genetic drift in hemagglutinin (HA) and neuraminidase (NA) genes from influenza viruses isolated from Danish swine over the past decade; the antigenic evolution and relatedness between swine influenza virus strains of the H1 subtype by antigenic cartography...

Surveillance programs in Denmark has revealed the circulation of novel reassortant influenza A viruses in swine

DEFF Research Database (Denmark)