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Article ; Online: Sex-specific effects of acute chlordane exposure in the context of steatotic liver disease, energy metabolism and endocrine disruption.

Luo, Jianzhu / Watson, Walter H / Gripshover, Tyler C / Qaissi, Zayna / Wahlang, Banrida

Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association

2023 Volume 180, Page(s) 114024

Abstract: Chlordane is an organochlorine pesticide (OCP) that is environmentally persistent. Although exposures to OCPs including chlordane have been associated with elevated liver enzymes, current knowledge on OCPs' contribution to toxicant-associated steatotic ... ...

Abstract	Chlordane is an organochlorine pesticide (OCP) that is environmentally persistent. Although exposures to OCPs including chlordane have been associated with elevated liver enzymes, current knowledge on OCPs' contribution to toxicant-associated steatotic liver disease (TASLD) and underlying sex-specific metabolic/endocrine disruption are still widely limited. Therefore, the objective of this study was to investigate the sex-dependent effects of chlordane in the context of TASLD. Age-matched male and female C57BL/6 mice were exposed to chlordane (20 mg/kg, one-time oral gavage) for two weeks. Female mice generally exhibited lower bodyfat content but more steatosis and hepatic lipid levels, consistent with increased hepatic mRNA levels of genes involved in lipid synthesis and uptake. Surprisingly, chlordane-exposed females demonstrated lower hepatic cholesterol levels. With regards to metabolic disruption, chlordane exposure decreased expression of genes involved in glycogen and glucose metabolism (Pklr, Gck), while chlordane-exposed females also exhibited decreased gene expression of HNF4A, an important regulator of liver identity and function. In terms of endocrine endpoints, chlordane augmented plasma testosterone levels in males. Furthermore, chlordane activated hepatic xenobiotic receptors, including the constitutive androstane receptor, in a sex-dependent manner. Overall, chlordane exposure led to altered hepatic energy metabolism, and potential chlordane-sex interactions regulated metabolic/endocrine disruption and receptor activation outcomes.
MeSH term(s)	Male ; Female ; Mice ; Animals ; Chlordan/toxicity ; Chlordan/metabolism ; Mice, Inbred C57BL ; Hydrocarbons, Chlorinated ; Fatty Liver/chemically induced ; Fatty Liver/metabolism ; Liver ; Hazardous Substances ; Lipids ; Energy Metabolism
Chemical Substances	Chlordan (12789-03-6) ; Hydrocarbons, Chlorinated ; Hazardous Substances ; Lipids
Language	English
Publishing date	2023-09-04
Publishing country	England
Document type	Journal Article
ZDB-ID	782617-5
ISSN	1873-6351 ; 0278-6915
ISSN (online)	1873-6351
ISSN	0278-6915
DOI	10.1016/j.fct.2023.114024
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Zs.A 529: Show issues

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Article: Investigating the Acute Metabolic Effects of the N-Methyl Carbamate Insecticide, Methomyl, on Mouse Liver.

Groswald, Amy M / Gripshover, Tyler C / Watson, Walter H / Wahlang, Banrida / Luo, Jianzhu / Jophlin, Loretta L / Cave, Matthew C

Metabolites

2023 Volume 13, Issue 8

Abstract: Many pesticides have been identified as endocrine and metabolism-disrupting chemicals with hepatotoxic effects. However, data are limited for insecticides in the n-methyl carbamate class, including methomyl. Here, we investigate the liver and systemic ... ...

Abstract	Many pesticides have been identified as endocrine and metabolism-disrupting chemicals with hepatotoxic effects. However, data are limited for insecticides in the n-methyl carbamate class, including methomyl. Here, we investigate the liver and systemic metabolic effects of methomyl in a mouse model. We hypothesize that methomyl exposure will disrupt xenobiotic and intermediary metabolism and promote hepatic steatosis in mice. Male C57BL/6 mice were exposed daily to 0-5 mg/kg methomyl for 18 days. Mice were fed water and regular chow diet ad libitum. Metabolic phenotyping was performed, and tissue samples were collected. Effects were generally greatest at the highest methomyl dose, which induced
Language	English
Publishing date	2023-08-01
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2662251-8
ISSN	2218-1989
ISSN	2218-1989
DOI	10.3390/metabo13080901
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Article ; Online: Mice lacking α4 nicotinic acetylcholine receptors are protected against alcohol-associated liver injury.

Watson, Walter H / Ritzenthaler, Jeffrey D / Torres-Gonzalez, Edilson / Arteel, Gavin E / Roman, Jesse

Alcoholism, clinical and experimental research

2022 Volume 46, Issue 8, Page(s) 1371–1383

Abstract: Background: Chronic heavy alcohol consumption is a major risk factor for the development of liver steatosis, fibrosis, and cirrhosis, but the mechanisms by which alcohol causes liver damage remain incompletely elucidated. This group has reported that α4 ...

Abstract	Background: Chronic heavy alcohol consumption is a major risk factor for the development of liver steatosis, fibrosis, and cirrhosis, but the mechanisms by which alcohol causes liver damage remain incompletely elucidated. This group has reported that α4 nicotinic acetylcholine receptors (α4 nAChRs) act as sensors for alcohol in lung cells. This study tested the hypothesis that α4 nAChRs mediate the effects of alcohol in the liver. Methods: Expression of acetylcholine receptor subunits in mouse liver was determined by RNA sequencing (RNA-seq). α4 nAChR knockout (α4 KO) mice were generated in C57BL/6J mice by introducing a mutation encoding an early stop codon in exon 4 of Chrna4, the gene encoding the α4 subunit of the nAChR. The presence of the inactivating mutation was established by polymerase chain reaction and genomic sequencing, and the lack of α4 nAChR function was confirmed in primary fibroblasts isolated from the α4 KO mice. Wild-type (WT) and α4 KO mice were fed the Lieber-DeCarli diet (with 36% of calories from alcohol) or pair fed an isocaloric maltose-dextrin control diet for a 6-week period that included a ramping up phase of increasing dietary alcohol. Results: Chrna4 was the most abundantly expressed nAChR subunit gene in mouse livers. After 6 weeks of alcohol exposure, WT mice had elevated serum transaminases and their livers showed increased fat accumulation, decreased Sirt1 protein levels, and accumulation of markers of oxidative stress and inflammation including Cyp2E1, Nos2, Sod1, Slc7a11, TNFα, and PAI1. All these responses to alcohol were either absent or significantly attenuated in α4 KO animals. Conclusion: Together, these observations support the conclusion that activation of α4 nAChRs by alcohol or one of its metabolites is one of the initial events promoting the accumulation of excess fat and expression of inflammatory mediators. Thus, α4 nAChRs may represent viable targets for intervention in chronic alcohol-related liver disease.
MeSH term(s)	Animals ; Chemical and Drug Induced Liver Injury/genetics ; Ethanol/toxicity ; Liver/drug effects ; Liver/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Receptors, Nicotinic/genetics ; Receptors, Nicotinic/metabolism
Chemical Substances	Receptors, Nicotinic ; nicotinic acetylcholine receptor alpha4 subunit ; Ethanol (3K9958V90M)
Language	English
Publishing date	2022-07-03
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	428999-7
ISSN	1530-0277 ; 0145-6008
ISSN (online)	1530-0277
ISSN	0145-6008
DOI	10.1111/acer.14893
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Article ; Online: Novel self-stratifying bioelectrochemical system for municipal wastewater treatment halves nitrous oxide emissions.

Walter, Xavier Alexis / Kostrytsia, Anastasiia / Watson, Helen / Winfield, Jonathan / Baran, Anna / Gillman, Sarah

Bioresource technology

2023 Volume 392, Page(s) 129969

Abstract: Reducing carbon footprint and greenhouse gas emissions are prime global goals. Wastewater treatment contributes significantly, and this study developed a technology with a focus on utilisation in small-decentralised plants. Bioelectrochemical systems ( ... ...

Abstract	Reducing carbon footprint and greenhouse gas emissions are prime global goals. Wastewater treatment contributes significantly, and this study developed a technology with a focus on utilisation in small-decentralised plants. Bioelectrochemical systems (BES) utilise bacteria to remove pollutants while generating power and a range of experiments were performed to investigate their suitability compared to conventional trickling filters. A lab-based trickling filter was inferior to one adapted with electrodes both in terms of organic matter (COD) and phosphate reduction, but the BES did not generate electrical output due to inferior cathode configuration. An enhanced, novel, dual-BES system was developed with improved cathode positioning and operated as a cascade. This demonstrated improved COD (79 %) and total nitrogen (102 %) removal over the trickling filter. Concomitantly it emitted 47 % less N
MeSH term(s)	Wastewater ; Nitrous Oxide/analysis ; Nitrogen/analysis ; Water Purification/methods
Chemical Substances	Wastewater ; Nitrous Oxide (K50XQU1029) ; BES (10191-18-1) ; Nitrogen (N762921K75)
Language	English
Publishing date	2023-11-16
Publishing country	England
Document type	Journal Article
ZDB-ID	1065195-0
ISSN	1873-2976 ; 0960-8524
ISSN (online)	1873-2976
ISSN	0960-8524
DOI	10.1016/j.biortech.2023.129969
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Article ; Online: Obesogenic polystyrene microplastic exposures disrupt the gut-liver-adipose axis.

Zhao, Jingjing / Adiele, Ngozi / Gomes, Daniel / Malovichko, Marina / Conklin, Daniel J / Ekuban, Abigail / Luo, Jianzhu / Gripshover, Tyler / Watson, Walter H / Banerjee, Mayukh / Smith, Melissa L / Rouchka, Eric C / Xu, Raobo / Zhang, Xiang / Gondim, Dibson D / Cave, Matthew C / O'Toole, Timothy E

Toxicological sciences : an official journal of the Society of Toxicology

2024 Volume 198, Issue 2, Page(s) 210–220

Abstract: Microplastics (MP) derived from the weathering of polymers, or synthesized in this size range, have become widespread environmental contaminants and have found their way into water supplies and the food chain. Despite this awareness, little is known ... ...

Abstract	Microplastics (MP) derived from the weathering of polymers, or synthesized in this size range, have become widespread environmental contaminants and have found their way into water supplies and the food chain. Despite this awareness, little is known about the health consequences of MP ingestion. We have previously shown that the consumption of polystyrene (PS) beads was associated with intestinal dysbiosis and diabetes and obesity in mice. To further evaluate the systemic metabolic effects of PS on the gut-liver-adipose tissue axis, we supplied C57BL/6J mice with normal water or that containing 2 sizes of PS beads (0.5 and 5 µm) at a concentration of 1 µg/ml. After 13 weeks, we evaluated indices of metabolism and liver function. As observed previously, mice drinking the PS-containing water had a potentiated weight gain and adipose expansion. Here we found that this was associated with an increased abundance of adipose F4/80+ macrophages. These exposures did not cause nonalcoholic fatty liver disease but were associated with decreased liver:body weight ratios and an enrichment in hepatic farnesoid X receptor and liver X receptor signaling. PS also increased hepatic cholesterol and altered both hepatic and cecal bile acids. Mice consuming PS beads and treated with the berry anthocyanin, delphinidin, demonstrated an attenuated weight gain compared with those mice receiving a control intervention and also exhibited a downregulation of cyclic adenosine monophosphate (cAMP) and peroxisome proliferator-activated receptor (PPAR) signaling pathways. This study highlights the obesogenic role of PS in perturbing the gut-liver-adipose axis and altering nuclear receptor signaling and intermediary metabolism. Dietary interventions may limit the adverse metabolic effects of PS consumption.
MeSH term(s)	Animals ; Mice ; Plastics/metabolism ; Plastics/pharmacology ; Polystyrenes/toxicity ; Polystyrenes/metabolism ; Microplastics/metabolism ; Microplastics/pharmacology ; Mice, Inbred C57BL ; Liver ; Non-alcoholic Fatty Liver Disease/metabolism ; Obesity/chemically induced ; Obesity/metabolism ; Weight Gain
Chemical Substances	Plastics ; Polystyrenes ; Microplastics
Language	English
Publishing date	2024-01-16
Publishing country	United States
Document type	Journal Article
ZDB-ID	1420885-4
ISSN	1096-0929 ; 1096-6080
ISSN (online)	1096-0929
ISSN	1096-6080
DOI	10.1093/toxsci/kfae013
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Zs.A 1709: Show issues

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Article ; Online: Can Zinc Supplementation Attenuate High Fat Diet-Induced Non-Alcoholic Fatty Liver Disease?

Bolatimi, Oluwanifemi Esther / Head, Kimberly Z / Luo, Jianzhu / Gripshover, Tyler C / Lin, Qian / Adiele, Ngozi V / Watson, Walter H / Wilkerson, Caitlin / Cai, Lu / Cave, Matthew C / Young, Jamie L

International journal of molecular sciences

2023 Volume 24, Issue 2

Abstract: The pathogenesis of non-alcoholic fatty liver disease (NAFLD), the most prevalent chronic liver disease, is associated with zinc deficiency. Previous studies show zinc supplementation improves steatosis and glucose metabolism, but its therapeutic effects ...

Abstract	The pathogenesis of non-alcoholic fatty liver disease (NAFLD), the most prevalent chronic liver disease, is associated with zinc deficiency. Previous studies show zinc supplementation improves steatosis and glucose metabolism, but its therapeutic effects in patients with established NAFLD remain unclear. We developed an in vivo model to characterize the effects of zinc supplementation on high-fat diet (HFD) induced NAFLD and hypothesized that the established NAFLD would be attenuated by zinc supplementation. Male C57BL/6J mice were fed a control diet or HFD for 12 weeks. Mice were then further grouped into normal and zinc-supplemented diets for 8 additional weeks. Body composition and glucose tolerance were determined before and after zinc supplementation. At euthanasia, plasma and liver tissue were collected for characterization and downstream analysis. As expected, 12 weeks of HFD resulted in reduced glucose clearance and altered body composition. Eight weeks of subsequent zinc supplementation did not alter glucose handling, plasma transaminases, steatosis, or hepatic gene expression. Results from our model suggest 8-week zinc supplementation cannot reverse established NAFLD. The HFD may have caused NAFLD disease progression beyond rescue by an 8-week period of zinc supplementation. Future studies will address these limitations and provide insights into zinc as a therapeutic agent for established NAFLD.
MeSH term(s)	Male ; Mice ; Animals ; Non-alcoholic Fatty Liver Disease/drug therapy ; Non-alcoholic Fatty Liver Disease/etiology ; Non-alcoholic Fatty Liver Disease/metabolism ; Diet, High-Fat/adverse effects ; Zinc/metabolism ; Mice, Inbred C57BL ; Liver/metabolism ; Dietary Supplements ; Glucose/metabolism ; Disease Models, Animal
Chemical Substances	Zinc (J41CSQ7QDS) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2023-01-16
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms24021763
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Article ; Online: Rapid-dissolving electrospun nanofibers for intra-vaginal antibiotic or probiotic delivery.

Minooei, Farnaz / Gilbert, Nicole M / Zhang, Longyun / Sarah NeCamp, Mary / Mahmoud, Mohamed Y / Kyser, Anthony J / Tyo, Kevin M / Watson, Walter H / Patwardhan, Ruta / Lewis, Warren G / Frieboes, Hermann B / Lewis, Amanda L / Steinbach-Rankins, Jill M

European journal of pharmaceutics and biopharmaceutics : official journal of Arbeitsgemeinschaft fur Pharmazeutische Verfahrenstechnik e.V

2023 Volume 190, Page(s) 81–93

Abstract: The emergence of probiotics as an alternative and adjunct to antibiotic treatment for microbiological disturbances of the female genitourinary system requires innovative delivery platforms for vaginal applications. This study developed a new, rapid- ... ...

Abstract	The emergence of probiotics as an alternative and adjunct to antibiotic treatment for microbiological disturbances of the female genitourinary system requires innovative delivery platforms for vaginal applications. This study developed a new, rapid-dissolving form using electrospun polyethylene oxide (PEO) fibers for delivery of antibiotic metronidazole or probiotic Lactobacillus acidophilus, and performed evaluation in vitro and in vivo. Fibers did not generate overt pathophysiology or encourage Gardnerella growth in a mouse vaginal colonization model, inducing no alterations in vaginal mucosa at 24 hr post-administration. PEO-fibers incorporating metronidazole (100 µg MET/mg polymer) effectively prevented and treated Gardnerella infections (∼3- and 2.5-log reduction, respectively, 24 hr post treatment) when administered vaginally. Incorporation of live Lactobacillus acidophilus (10
MeSH term(s)	Female ; Animals ; Mice ; Anti-Bacterial Agents/therapeutic use ; Metronidazole ; Nanofibers ; Treatment Outcome ; Lactobacillus acidophilus/physiology ; Probiotics
Chemical Substances	Anti-Bacterial Agents ; Metronidazole (140QMO216E)
Language	English
Publishing date	2023-07-19
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	1065368-5
ISSN	1873-3441 ; 0939-6411
ISSN (online)	1873-3441
ISSN	0939-6411
DOI	10.1016/j.ejpb.2023.07.009
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Article: Impact of sex, age and diet on the cysteine/cystine and glutathione/glutathione disulfide plasma redox couples in mice

Watson, Walter H / Greenwell, John C / Zheng, Yuxuan / Furmanek, Stephen / Torres-Gonzalez, Edilson / Ritzenthaler, Jeffrey D / Roman, Jesse

Journal of nutritional biochemistry. 2020 Oct., v. 84

2020

Abstract: Age, sex and diet are well-established risk factors for several diseases. In humans, each of these variables has been linked to differences in plasma redox potentials (Eₕ) of the glutathione/glutathione disulfide (GSH/GSSG) and cysteine/cystine (Cys/CySS) ...

Abstract	Age, sex and diet are well-established risk factors for several diseases. In humans, each of these variables has been linked to differences in plasma redox potentials (Eₕ) of the glutathione/glutathione disulfide (GSH/GSSG) and cysteine/cystine (Cys/CySS) redox couples. Mice have been very useful for modeling human disease processes, but it is unknown if age, sex and diet affect redox couples in mice as they do in humans. The purpose of the present study was to examine the effects of these factors on plasma redox potentials in C57BL/6J mice. We found that age had no effect on either redox couple in either sex. Plasma Eₕ Cys/CySS and Eₕ GSH/GSSG were both more oxidized (more positive) in females than in males. A 24-hour fast negated the sex differences in both redox potentials by oxidizing both redox couples in male mice, while having no effect on Eₕ Cys/CySS and a smaller effect on Eₕ GSH/GSSG in female mice. A diet with excess sulfur amino acids reduced the plasma Eₕ Cys/CySS in females to a level comparable to that seen in male mice. Thus, sex-specific differences in plasma Eₕ Cys/CySS could be normalized by two different dietary interventions. Some of these findings are consistent with reported human studies, while others are not. Most strikingly, mice do not exhibit age-dependent oxidation of plasma redox potentials. Care must be taken when designing and interpreting mouse studies to investigate redox regulation in humans.
Keywords	cysteine ; cystine ; diet ; females ; glutathione ; human diseases ; humans ; males ; mice ; oxidation ; sulfur
Language	English
Dates of publication	2020-10
Publishing place	Elsevier Inc.
Document type	Article
Note	NAL-light
ZDB-ID	1014929-6
ISSN	1873-4847 ; 0955-2863
ISSN (online)	1873-4847
ISSN	0955-2863
DOI	10.1016/j.jnutbio.2020.108431
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Lung extracellular matrix and redox regulation.

Watson, Walter H / Ritzenthaler, Jeffrey D / Roman, Jesse

Redox biology

2016 Volume 8, Page(s) 305–315

Abstract: Pulmonary fibrosis affects millions worldwide and, even though there has been a significant investment in understanding the processes involved in wound healing and maladaptive repair, a complete understanding of the mechanisms responsible for lung ... ...

Abstract	Pulmonary fibrosis affects millions worldwide and, even though there has been a significant investment in understanding the processes involved in wound healing and maladaptive repair, a complete understanding of the mechanisms responsible for lung fibrogenesis eludes us, and interventions capable of reversing or halting disease progression are not available. Pulmonary fibrosis is characterized by the excessive expression and uncontrolled deposition of extracellular matrix (ECM) proteins resulting in erosion of the tissue structure. Initially considered an 'end-stage' process elicited after injury, these events are now considered pathogenic and are believed to contribute to the course of the disease. By interacting with integrins capable of signal transduction and by influencing tissue mechanics, ECM proteins modulate processes ranging from cell adhesion and migration to differentiation and growth factor expression. In doing so, ECM proteins help orchestrate complex developmental processes and maintain tissue homeostasis. However, poorly controlled deposition of ECM proteins promotes inflammation, fibroproliferation, and aberrant differentiation of cells, and has been implicated in the pathogenesis of pulmonary fibrosis, atherosclerosis and cancer. Considering their vital functions, ECM proteins are the target of investigation, and oxidation-reduction (redox) reactions have emerged as important regulators of the ECM. Oxidative stress invariably accompanies lung disease and promotes ECM expression directly or through the overproduction of pro-fibrotic growth factors, while affecting integrin binding and activation. In vitro and in vivo investigations point to redox reactions as targets for intervention in pulmonary fibrosis and related disorders, but studies in humans have been disappointing probably due to the narrow impact of the interventions tested, and our poor understanding of the factors that regulate these complex reactions. This review is not meant to provide a comprehensive review of this field, but rather to highlight what has been learned and to raise interest in this area in need of much attention.
Language	English
Publishing date	2016-08
Publishing country	Netherlands
Document type	Journal Article
ISSN	2213-2317
ISSN (online)	2213-2317
DOI	10.1016/j.redox.2016.02.005
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Article ; Online: The profibrotic and senescence phenotype of old lung fibroblasts is reversed or ameliorated by genetic and pharmacological manipulation of Slc7a11 expression.

Ritzenthaler, Jeffrey D / Torres-Gonzalez, Edilson / Zheng, Yuxuan / Zelko, Igor N / van Berkel, Victor / Nunley, David R / Kidane, Biniam / Halayko, Andrew J / Summer, Ross / Watson, Walter H / Roman, Jesse

American journal of physiology. Lung cellular and molecular physiology

2022 Volume 322, Issue 3, Page(s) L449–L461

Abstract: Increased senescence and expression of profibrotic genes in old lung fibroblasts contribute to disrepair responses. We reported that primary lung fibroblasts from old mice have lower expression and activity of the cystine transporter Slc7a11/xCT than ... ...

Abstract	Increased senescence and expression of profibrotic genes in old lung fibroblasts contribute to disrepair responses. We reported that primary lung fibroblasts from old mice have lower expression and activity of the cystine transporter Slc7a11/xCT than cells from young mice, resulting in changes in both the intracellular and extracellular redox environments. This study examines the hypothesis that low Slc7a11 expression in old lung fibroblasts promotes senescence and profibrotic gene expression. The levels of mRNA and protein of Slc7a11, senescence markers, and profibrotic genes were measured in primary fibroblasts from the lungs of old (24 mo) and young (3 mo) mice. In addition, the effects of genetic and pharmacological manipulation of Slc7a11 were investigated. We found that decreased expression of Slc7a11 in old cells was associated with elevated markers of senescence (p21, p16, p53, and β-galactosidase) and increased expression of profibrotic genes (Tgfb1, Smad3, Acta2, Fn1, Col1a1, and Col5a1). Silencing of Slc7a11 in young cells replicated the aging phenotype, whereas overexpression of Slc7a11 in old cells decreased expression of senescence and profibrotic genes. Young cells were induced to express the senescence and profibrotic phenotype by sulfasalazine, a Slc7a11 inhibitor, whereas treatment of old cells with sulforaphane, a Slc7a11 inducer, decreased senescence without affecting profibrotic genes. Like aging cells, idiopathic pulmonary fibrosis fibroblasts show decreased Slc7a11 expression and increased profibrotic markers. In short, old lung fibroblasts manifest a profibrotic and senescence phenotype that is modulated by genetic or pharmacological manipulation of Slc7a11.
MeSH term(s)	Animals ; Cellular Senescence/genetics ; Fibroblasts/metabolism ; Idiopathic Pulmonary Fibrosis/metabolism ; Lung/metabolism ; Mice ; Phenotype
Language	English
Publishing date	2022-01-05
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1013184-x
ISSN	1522-1504 ; 1040-0605
ISSN (online)	1522-1504
ISSN	1040-0605
DOI	10.1152/ajplung.00593.2020
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