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Article: Assessment of enzyme linked immunosorbent assay based diagnostic kits (Toxokit-G and Toxokit-M) for the detection of IgG and IgM antibodies to Toxoplasma gondii in human serum.

Bhopale, G M / Naik, S R / Bhave, G G / Naik, S S / Gogate, A

Comparative immunology, microbiology and infectious diseases

1997 Volume 20, Issue 4, Page(s) 309–314

Abstract: ... of diagnostic kits (Toxokit-G and Toxokit-M) for the detection of IgG and IgM antibodies to Toxoplasma gondii ... Toxoplasmosis/IgG (Behring Co., Germany), TOXOTEK-G (Flow Lab., U.K.) and Toxoplasma IgM Microassay (Diamedix ... reliability between these diagnostic kits. Toxokit-G has 86.66 and 96.05% sensitivity and specificity ...

Abstract	An enzyme linked immunosorbent assay (ELISA) using penicillinase was developed in the form of diagnostic kits (Toxokit-G and Toxokit-M) for the detection of IgG and IgM antibodies to Toxoplasma gondii. The performance of both the kits was compared with commercially available diagnostic kits, i.e. Enzygnost-Toxoplasmosis/IgG (Behring Co., Germany), TOXOTEK-G (Flow Lab., U.K.) and Toxoplasma IgM Microassay (Diamedix Corp., U.S.A.) by testing toxoplasma-suspected human serum samples. The results indicate a good reliability between these diagnostic kits. Toxokit-G has 86.66 and 96.05% sensitivity and specificity respectively. The main advantage of Toxokit-G is that the end result can be assessed visually without using sophisticated instruments. Toxokit-M has 100% sensitivity and specificity and test results were not affected by the presence of antitoxoplasma IgG antibodies, rheumatoid factor or antinuclear antibodies.
MeSH term(s)	Animals ; Antibodies, Protozoan/blood ; Double-Blind Method ; Enzyme-Linked Immunosorbent Assay ; Humans ; Immunoglobulin G/blood ; Immunoglobulin M/blood ; Penicillinase/chemistry ; Reagent Kits, Diagnostic/standards ; Toxoplasma/immunology ; Toxoplasmosis/diagnosis ; Toxoplasmosis/immunology
Chemical Substances	Antibodies, Protozoan ; Immunoglobulin G ; Immunoglobulin M ; Reagent Kits, Diagnostic ; Penicillinase (EC 3.5.2.-)
Language	English
Publishing date	1997-09
Publishing country	England
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	436522-7
ISSN	1878-1667 ; 0147-9571
ISSN (online)	1878-1667
ISSN	0147-9571
DOI	10.1016/s0147-9571(97)00011-8
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Article ; Online: Neuroinflammation with increased glymphatic flow in a murine model of decompression sickness.

Thom, Stephen R / Bhopale, Veena M / Bhat, Abid R / Arya, Awadhesh K / Ruhela, Deepa / Qiao, Guanda / Li, Xin / Tang, Shiyu / Xu, Su

Journal of neurophysiology

2023 Volume 129, Issue 3, Page(s) 662–671

Abstract: This project investigated glial-based lymphatic (glymphatic) function and its role in a murine model of decompression sickness (DCS). DCS pathophysiology is traditionally viewed as being related to gas bubble formation from insoluble gas on decompression. ...

Abstract	This project investigated glial-based lymphatic (glymphatic) function and its role in a murine model of decompression sickness (DCS). DCS pathophysiology is traditionally viewed as being related to gas bubble formation from insoluble gas on decompression. However, a body of work implicates a role for a subset of inflammatory extracellular vesicles, 0.1 to 1 µm microparticles (MPs) that are elevated in human and rodent models in response to high gas pressure and rise further after decompression. Herein, we describe immunohistochemical and Western blot evidence showing that following high air pressure exposure, there are elevations of astrocyte NF-κB and microglial-ionized calcium-binding adaptor protein-1 (IBA-1) along with fluorescence contrast and MRI findings of an increase in glymphatic flow. Concomitant elevations of central nervous system-derived MPs coexpressing thrombospondin-1 (TSP) drain to deep cervical nodes and then to blood where they cause neutrophil activation. A new set of blood-borne MPs are generated that express filamentous actin at the surface that exacerbate neutrophil activation. Blood-brain barrier integrity is disrupted due to activated neutrophil sequestration that causes further astrocyte and microglial perturbation. When postdecompression node or blood MPs are injected into naïve mice, the same spectrum of abnormalities occur and they are blocked with coadministration of antibody to TSP. We conclude that high pressure/decompression causes neuroinflammation with an increased glymphatic flow. The resulting systemic liberation of TSP-expressing MPs sustains the neuroinflammatory cycle lasting for days.
MeSH term(s)	Animals ; Humans ; Mice ; Decompression Sickness/metabolism ; Disease Models, Animal ; Neuroinflammatory Diseases ; Neutrophil Activation/physiology ; Neutrophils/metabolism ; Glymphatic System/physiology
Language	English
Publishing date	2023-02-08
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, Non-U.S. Gov't
ZDB-ID	80161-6
ISSN	1522-1598 ; 0022-3077
ISSN (online)	1522-1598
ISSN	0022-3077
DOI	10.1152/jn.00005.2023
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Article: Pathogenesis of toxoplasmosis.

Bhopale, G M

Comparative immunology, microbiology and infectious diseases

2003 Volume 26, Issue 4, Page(s) 213–222

Abstract: The present review article deals with the pathogenesis of toxoplasmosis. The article briefly highlights some important aspects such as different strains, mode of infection and clinical characteristics, entry into host cell, immune response, host parasite ...

Abstract	The present review article deals with the pathogenesis of toxoplasmosis. The article briefly highlights some important aspects such as different strains, mode of infection and clinical characteristics, entry into host cell, immune response, host parasite interaction, tissue cyst formation and disease recurrence.
MeSH term(s)	Animals ; Cysts/parasitology ; Host-Parasite Interactions ; Humans ; Recurrence ; Toxoplasma/physiology ; Toxoplasmosis/etiology ; Toxoplasmosis/immunology ; Toxoplasmosis/parasitology
Language	English
Publishing date	2003-07
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	436522-7
ISSN	1878-1667 ; 0147-9571
ISSN (online)	1878-1667
ISSN	0147-9571
DOI	10.1016/S0147-9571(02)00058-9
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Article ; Online: Factors Associated with Nitric Oxide-mediated β2 Integrin Inhibition of Neutrophils.

Bhopale, Veena M / Yang, Ming / Yu, Kevin / Thom, Stephen R

The Journal of biological chemistry

2015 Volume 290, Issue 28, Page(s) 17474–17484

Abstract: ... arrested by protein kinase G activated with 8-bromo-cyclic GMP and by a high (•)NO flux (∼ 112 nmol/min ...

Abstract	This investigation explored the mechanism for inhibition of β2 integrin adhesion molecules when neutrophils are exposed to nitric oxide ((•)NO). Roles for specific proteins were elucidated using chemical inhibitors, depletion with small inhibitory RNA, and cells from knock-out mice. Optimal inhibition occurs with exposures to a (•)NO flux of ∼ 28 nmol/min for 2 min or more, which sets up an autocatalytic cascade triggered by activating type 2 nitric-oxide synthase (NOS-2) and NADPH oxidase (NOX). Integrin inhibition does not occur with neutrophils exposed to a NOX inhibitor (Nox2ds), a NOS-2 inhibitor (1400 W), or with cells from mice lacking NOS-2 or the gp91(phox) component of NOX. Reactive species cause S-nitrosylation of cytosolic actin that enhances actin polymerization. Protein cross-linking and actin filament formation assays indicate that increased polymerization occurs because of associations involving vasodilator-stimulated phosphoprotein, focal adhesion kinase, and protein-disulfide isomerase in proximity to actin filaments. These effects were inhibited in cells exposed to ultraviolet light which photo-reverses S-nitrosylated cysteine residues and by co-incubations with cytochalasin D. The autocatalytic cycle can be arrested by protein kinase G activated with 8-bromo-cyclic GMP and by a high (•)NO flux (∼ 112 nmol/min) that inactivates NOX.
MeSH term(s)	Actins/metabolism ; Animals ; CD18 Antigens/metabolism ; Cell Adhesion ; Cyclic GMP/analogs & derivatives ; Cyclic GMP/pharmacology ; Guanylate Cyclase/antagonists & inhibitors ; Guanylate Cyclase/genetics ; Guanylate Cyclase/metabolism ; Humans ; Hydrazines/pharmacology ; Membrane Glycoproteins/deficiency ; Membrane Glycoproteins/genetics ; Membrane Glycoproteins/metabolism ; Mice ; Mice, Knockout ; NADPH Oxidase 2 ; NADPH Oxidases/deficiency ; NADPH Oxidases/genetics ; NADPH Oxidases/metabolism ; Neutrophils/drug effects ; Neutrophils/metabolism ; Nitric Oxide/metabolism ; Nitric Oxide Synthase Type II/deficiency ; Nitric Oxide Synthase Type II/genetics ; Nitric Oxide Synthase Type II/metabolism ; RNA, Small Interfering/genetics
Chemical Substances	Actins ; CD18 Antigens ; Hydrazines ; Membrane Glycoproteins ; RNA, Small Interfering ; 8-bromocyclic GMP (31356-94-2) ; Nitric Oxide (31C4KY9ESH) ; 1,1-diethyl-2-hydroxy-2-nitrosohydrazine (86831-65-4) ; Nitric Oxide Synthase Type II (EC 1.14.13.39) ; Nos2 protein, mouse (EC 1.14.13.39) ; Cybb protein, mouse (EC 1.6.3.-) ; NADPH Oxidase 2 (EC 1.6.3.-) ; NADPH Oxidases (EC 1.6.3.-) ; Guanylate Cyclase (EC 4.6.1.2) ; Cyclic GMP (H2D2X058MU)
Language	English
Publishing date	2015-06-01
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1074/jbc.M115.651620
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Article ; Online: Activation of AMP-activated protein kinase attenuates ethanol-induced ER/oxidative stress and lipid phenotype in human pancreatic acinar cells.

Srinivasan, Mukund P / Bhopale, Kamlesh K / Caracheo, Anna A / Amer, Samir M / Khan, Shamis / Kaphalia, Lata / Loganathan, Gopalakrishnan / Balamurugan, Appakalai N / Kaphalia, Bhupendra S

Biochemical pharmacology

2020 Volume 180, Page(s) 114174

Abstract: Primary toxicity targets of alcohol and its metabolites in the pancreas are cellular energetics and endoplasmic reticulum (ER). Therefore, the role of AMP-Activated Protein Kinase (AMPKα) in amelioration of ethanol (EtOH)-induced pancreatic acinar cell ... ...

Abstract	Primary toxicity targets of alcohol and its metabolites in the pancreas are cellular energetics and endoplasmic reticulum (ER). Therefore, the role of AMP-Activated Protein Kinase (AMPKα) in amelioration of ethanol (EtOH)-induced pancreatic acinar cell injury including ER/oxidative stress, inflammatory responses, the formation of fatty acid ethyl esters (FAEEs) and mitochondrial bioenergetics were determined in human pancreatic acinar cells (hPACs) and AR42J cells incubated with/without AMPKα activator [5-aminoimidazole-4-carboxamide ribonucleotide (AICAR)]. EtOH treated hPACs showed concentration and time-dependent increases for FAEEs and inactivation of AMPKα, along with the upregulation of ACC1 and FAS (key lipogenic proteins) and downregulation of CPT1A (involved β-oxidation of fatty acids). These cells also showed significant ER stress as evidenced by the increased expression for GRP78, IRE1α, and PERK/CHOP arm of unfolded protein response promoting apoptosis and activating p-JNK1/2 and p-ERK1/2 with increased secretion of cytokines. AR42J cells treated with EtOH showed increased oxidative stress, impaired mitochondrial biogenesis, and decreased ATP production rate. However, AMPKα activation by AICAR attenuated EtOH-induced ER/oxidative stress, lipogenesis, and inflammatory responses as well as the formation of FAEEs and restored mitochondrial function in hPACs as well as AR42J cells. Therefore, it is likely that EtOH-induced inactivation of AMPKα plays a crucial role in acinar cell injury leading to pancreatitis. Findings from this study also suggest that EtOH-induced inactivation of AMPKα is closely related to ER/oxidative stress and synthesis of FAEEs, as activation of AMPKα by AICAR attenuates formation of FAEEs, ER/oxidative stress and lipogenesis, and improves inflammatory responses and mitochondrial bioenergetics.
MeSH term(s)	AMP-Activated Protein Kinases/metabolism ; Acinar Cells/drug effects ; Acinar Cells/enzymology ; Acyltransferases/metabolism ; Adult ; Cells, Cultured ; Dose-Response Relationship, Drug ; Endoplasmic Reticulum/drug effects ; Endoplasmic Reticulum/enzymology ; Ethanol/pharmacology ; Fatty Acids, Nonesterified/metabolism ; Female ; Humans ; Lipids ; Male ; Middle Aged ; Oxidative Stress/drug effects ; Oxidative Stress/physiology ; Pancreas/cytology ; Pancreas/drug effects ; Pancreas/enzymology ; Phenotype
Chemical Substances	Fatty Acids, Nonesterified ; Lipids ; Ethanol (3K9958V90M) ; Acyltransferases (EC 2.3.-) ; AMP-Activated Protein Kinases (EC 2.7.11.31) ; fatty acyl ethyl ester synthase (EC 3.1.1.67)
Language	English
Publishing date	2020-07-25
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	208787-x
ISSN	1873-2968 ; 0006-2952
ISSN (online)	1873-2968
ISSN	0006-2952
DOI	10.1016/j.bcp.2020.114174
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Article: Effect of nutrients on production of Hamycin antibiotic by Streptomyces pimprina Thirum.

Dongare, Ramesh G / Bhalange, Smita P / Bhopale, Girish M

Hindustan antibiotics bulletin

2009 Volume 51, Issue 1-4, Page(s) 39–41

MeSH term(s)	Antifungal Agents/metabolism ; Culture Media ; Polyenes/metabolism ; Streptomyces/growth & development ; Streptomyces/metabolism
Chemical Substances	Antifungal Agents ; Culture Media ; Polyenes ; hamycin (1403-71-0)
Language	English
Publishing date	2009
Publishing country	India
Document type	Journal Article
ZDB-ID	820210-2
ISSN	0018-1935
ISSN	0018-1935
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Article ; Online: Alcohol oxidizing enzymes and ethanol-induced cytotoxicity in rat pancreatic acinar AR42J cells.

Bhopale, Kamlesh K / Falzon, Miriam / Ansari, G A S / Kaphalia, Bhupendra S

In vitro cellular & developmental biology. Animal

2013 Volume 50, Issue 4, Page(s) 373–380

Abstract: Alcoholic chronic pancreatitis (ACP) is a serious inflammatory disease causing significant morbidity and mortality. Due to lack of a suitable animal model, the underlying mechanism of ACP is poorly understood. Chronic alcohol abuse inhibits alcohol ... ...

Abstract	Alcoholic chronic pancreatitis (ACP) is a serious inflammatory disease causing significant morbidity and mortality. Due to lack of a suitable animal model, the underlying mechanism of ACP is poorly understood. Chronic alcohol abuse inhibits alcohol dehydrogenase (ADH) and facilitates nonoxidative metabolism of ethanol to fatty acid ethyl esters (FAEEs) in the pancreas frequently damaged during chronic ethanol abuse. Earlier, we reported a concentration-dependent formation of FAEEs and cytotoxicity in ethanol-treated rat pancreatic tumor (AR42J) cells, which express high FAEE synthase activity as compared to ADH and cytochrome P450 2E1. Therefore, the present study was undertaken to investigate the role of various ethanol oxidizing enzymes in ethanol-induced pancreatic acinar cell injury. Confluent AR42J cells were pre-treated with inhibitors of ADH class I and II [4-methylpyrazole (MP)] or class I, II, and III [1,10-phenanthroline (PT)], cytochrome P450 2E1 (trans-1,2-dichloroethylene) or catalase (sodium azide) followed by incubation with 800 mg% ethanol at 37°C for 6 h. Ethanol metabolism, cell viability, cytotoxicity (apoptosis and necrosis), cell proliferation status, and formation of FAEEs in AR42J cells were measured. The cell viability and cell proliferation rate were significantly reduced in cells pretreated with 1,10-PT + ethanol followed by those with 4-MP + ethanol. In situ formation of FAEEs was twofold greater in cells incubated with 1,10-PT + ethanol and ∼1.5-fold in those treated with 4-MP + ethanol vs. respective controls. However, cells treated with inhibitors of cytochrome P450 2E1 or catalase in combination of ethanol showed no significant changes either for FAEE formation, cell death or proliferation rate. Therefore, an impaired ADH class I-III catalyzed oxidation of ethanol appears to be a key contributing factor in ethanol-induced pancreatic injury via formation of nonoxidative metabolites of ethanol.
MeSH term(s)	Acinar Cells/drug effects ; Acinar Cells/enzymology ; Alcohol Dehydrogenase/antagonists & inhibitors ; Alcohol Dehydrogenase/metabolism ; Alcoholism/enzymology ; Alcoholism/metabolism ; Alcoholism/pathology ; Animals ; Apoptosis/drug effects ; Ethanol/toxicity ; Fatty Acids/metabolism ; Fomepizole ; Oxidation-Reduction ; Pancreas/cytology ; Pancreas/enzymology ; Pancreatitis, Chronic/chemically induced ; Pancreatitis, Chronic/enzymology ; Pancreatitis, Chronic/metabolism ; Pyrazoles/pharmacology ; Rats
Chemical Substances	Fatty Acids ; Pyrazoles ; Ethanol (3K9958V90M) ; Fomepizole (83LCM6L2BY) ; Alcohol Dehydrogenase (EC 1.1.1.1)
Language	English
Publishing date	2013-11-27
Publishing country	Germany
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1077810-x
ISSN	1543-706X ; 0883-8364 ; 1071-2690
ISSN (online)	1543-706X
ISSN	0883-8364 ; 1071-2690
DOI	10.1007/s11626-013-9700-7
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Article: Prospects for hepatitis C vaccine.

Bhopale, G M / Nanda, R K

Acta virologica

2004 Volume 48, Issue 4, Page(s) 215–221

Abstract: Hepatitis C virus (HCV) is a major cause of chronic liver disease, cirrhosis and hepatocellular carcinoma worldwide. Unfortunately, neither a vaccine nor any effective therapy is available. Efforts are now directed towards the development of an effective ...

Abstract	Hepatitis C virus (HCV) is a major cause of chronic liver disease, cirrhosis and hepatocellular carcinoma worldwide. Unfortunately, neither a vaccine nor any effective therapy is available. Efforts are now directed towards the development of an effective vaccine besides chemotherapy. This review briefly summarizes the properties of an effective vaccine for the control of HCV infection. The mechanisms of protective immune response induced by HCV are not well understood. It is presumed that humoral and cellular immune responses play an important role. Even though there are various obstacles in the development of HCV vaccine, we describe a few promising approaches such as DNA vaccine, recombinant virus vaccine, HCV-like particles (HCV-LPs), peptide-based vaccine and plant-derived recombinant subunit vaccine.
MeSH term(s)	Hepacivirus/immunology ; Humans ; Vaccines, DNA/immunology ; Vaccines, Synthetic/immunology ; Viral Hepatitis Vaccines/immunology ; Virion/immunology
Chemical Substances	Vaccines, DNA ; Vaccines, Synthetic ; Viral Hepatitis Vaccines
Language	English
Publishing date	2004
Publishing country	Slovakia
Document type	Journal Article ; Review
ZDB-ID	210452-0
ISSN	1336-2305 ; 0001-723X
ISSN (online)	1336-2305
ISSN	0001-723X
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Article: Blood coagulation factor VIII: An overview.

Bhopale, G M / Nanda, R K

Journal of biosciences

2003 Volume 28, Issue 6, Page(s) 783–789

Abstract: Factor VIII (FVIII) functions as a co-factor in the blood coagulation cascade for the proteolytic activation of factor X by factor IXa. Deficiency of FVIII causes hemophilia A, the most commonly inherited bleeding disorder. This review highlights current ...

Abstract	Factor VIII (FVIII) functions as a co-factor in the blood coagulation cascade for the proteolytic activation of factor X by factor IXa. Deficiency of FVIII causes hemophilia A, the most commonly inherited bleeding disorder. This review highlights current knowledge on selected aspects of FVIII in which both the scientist and the clinician should be interested.
MeSH term(s)	Factor VIII/antagonists & inhibitors ; Factor VIII/genetics ; Factor VIII/physiology ; Factor VIII/therapeutic use ; Hemophilia A/drug therapy ; Hemophilia A/genetics ; Humans ; Mutation
Chemical Substances	Factor VIII (9001-27-8)
Language	English
Publishing date	2003-08-15
Publishing country	India
Document type	Journal Article ; Review
ZDB-ID	756157-x
ISSN	0250-5991
ISSN	0250-5991
DOI	10.1007/bf02708439
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Article ; Online: Intramicroparticle nitrogen dioxide is a bubble nucleation site leading to decompression-induced neutrophil activation and vascular injury.

Thom, Stephen R / Yang, Ming / Bhopale, Veena M / Milovanova, Tatyana N / Bogush, Marina / Buerk, Donald G

Journal of applied physiology (Bethesda, Md. : 1985)

2013 Volume 114, Issue 5, Page(s) 550–558

Abstract: Inert gases diffuse into tissues in proportion to ambient pressure, and when pressure is reduced, gas efflux forms bubbles due to the presence of gas cavitation nuclei that are predicted based on theory but have never been characterized. Decompression ... ...

Abstract	Inert gases diffuse into tissues in proportion to ambient pressure, and when pressure is reduced, gas efflux forms bubbles due to the presence of gas cavitation nuclei that are predicted based on theory but have never been characterized. Decompression stress triggers elevations in number and diameter of circulating annexin V-coated microparticles (MPs) derived from vascular cells. Here we show that ∼10% MPs from wild-type (WT) but not inflammatory nitric oxide synthase-2 (iNOS) knockout (KO) mice increase in size when exposed to elevated air pressure ex vivo. This response is abrogated by a preceding exposure to hydrostatic pressure, demonstrating the presence of a preformed gas phase. These MPs have lower density than most particles, 10-fold enrichment in iNOS, and generate commensurately more reactive nitrogen species (RNS). Surprisingly, RNS only slowly diffuse from within MPs unless particles are subjected to osmotic stress or membrane cholesterol is removed. WT mice treated with iNOS inhibitor and KO mice exhibit less decompression-induced neutrophil activation and vascular leak. Contrary to injecting naïve mice with MPs from wild-type decompressed mice, injecting KO MPs triggers fewer proinflammatory events. We conclude that nitrogen dioxide is a nascent gas nucleation site synthesized in some MPs and is responsible for initiating postdecompression inflammatory injuries.
MeSH term(s)	Animals ; Annexin A5/genetics ; Annexin A5/metabolism ; Cell Membrane Permeability/genetics ; Cell Membrane Permeability/physiology ; Cell-Derived Microparticles/genetics ; Cell-Derived Microparticles/metabolism ; Cholesterol/genetics ; Cholesterol/metabolism ; Decompression Sickness/metabolism ; Inflammation/genetics ; Inflammation/metabolism ; Inflammation/physiopathology ; Mice ; Mice, Knockout ; Neutrophil Activation/genetics ; Neutrophil Activation/physiology ; Neutrophils/metabolism ; Nitric Oxide Synthase Type II/antagonists & inhibitors ; Nitric Oxide Synthase Type II/genetics ; Nitric Oxide Synthase Type II/metabolism ; Nitrogen Dioxide/metabolism ; Osmotic Pressure/physiology ; Reactive Nitrogen Species/genetics ; Reactive Nitrogen Species/metabolism ; Vascular System Injuries/genetics ; Vascular System Injuries/metabolism
Chemical Substances	Annexin A5 ; Reactive Nitrogen Species ; Cholesterol (97C5T2UQ7J) ; Nitric Oxide Synthase Type II (EC 1.14.13.39) ; Nos2 protein, mouse (EC 1.14.13.39) ; Nitrogen Dioxide (S7G510RUBH)
Language	English
Publishing date	2013-03-01
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	219139-8
ISSN	1522-1601 ; 0021-8987 ; 0161-7567 ; 8750-7587
ISSN (online)	1522-1601
ISSN	0021-8987 ; 0161-7567 ; 8750-7587
DOI	10.1152/japplphysiol.01386.2012
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