American journal of physiology. Gastrointestinal and liver physiology最新文献

{"title":"Hypobaric Hypoxia Exposure Impairs Colonic Goblet Cell Subpopulation via the HIF-1α Signaling Pathway.","authors":"Shaojie Zhang, Xiufang Jiang, Wangjingyi Zhang, Fansen Meng, Jiayue Gao, Xiang Cheng, Yazhuo Hu, Jing Liu, Tong Zhao, Lingling Zhu, Gangshi Wang","doi":"10.1152/ajpgi.00372.2024","DOIUrl":"https://doi.org/10.1152/ajpgi.00372.2024","url":null,"abstract":"<p><p>Exposure to hypobaric hypoxia during rapid ascent to high altitudes significantly impacts intestinal barrier function. Goblet cells, as one of the primary cell types in the intestinal mucosa, play a crucial role in maintaining this barrier. However, the effects of hypobaric hypoxia on goblet cell function and the underlying molecular mechanisms remain unclear. In this study, we established a mouse model of hypobaric hypoxia exposure (simulating an altitude of 6,000 meters) and studied its effects on colonic goblet cells by transcriptomic analysis. Additionally, the hypoxia-treated (1% O₂) goblet cell line Ls174t was used to investigate potential mechanisms underlying hypoxia-induced changes in goblet cells. In the present study, we discovered that hypobaric hypoxia exposure not only reduced the number of colonic goblet cells in mice by 27.6% but also impaired their mucus secretion. Transcriptome sequencing analysis of sorted goblet cells from the mice colon revealed significant changes in gene expression profiles, particularly in the expression of canonical goblet cell markers such as calcium-activated chloride channel regulator 1 (Clca1) and Fcγ-binding protein (Fcgbp). We confirmed the effects of hypobaric hypoxia/hypoxia exposure on CLCA1 and FCGBP expression at both mRNA and protein levels in mouse colonic tissues and in Ls174t cells. The expression of these canonical goblet cell marker genes was dependent on HIF-1α activity; their expression decreased upon hypoxia-induced activation of HIF-1α and increased when HIF-1α was knocked down using siRNA. Thus, hypobaric hypoxia exposure regulates the distribution and function of colonic goblet cell subsets through the HIF-1α signaling pathway.</p>","PeriodicalId":7725,"journal":{"name":"American journal of physiology. Gastrointestinal and liver physiology","volume":" ","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143707861","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"<i>Mycobacterium avium</i> subspecies <i>paratuberculosis</i> targets M cells in enteroid-derived monolayers through interactions with β1 integrins.","authors":"Grace Baruta, Kyle L Flannigan, Laurie Alston, Andrew Thorne, Hong Zhang, Jeroen De Buck, Pina Colarusso, Simon A Hirota","doi":"10.1152/ajpgi.00250.2024","DOIUrl":"https://doi.org/10.1152/ajpgi.00250.2024","url":null,"abstract":"<p><p>Paratuberculosis is an infectious disease caused by the bacterium, <i>Mycobacterium avium</i> subspecies <i>paratuberculosis</i> (MAP). MAP infection of ruminants triggers progressive wasting disease characterized by granulomatous lymphadenitis, enteritis, and severe intestinal pathology that often requires early culling of the animal. The resulting economic burden is significant and MAP exposure in the workplace constitutes a significant zoonotic risk. While it has been established the MAP propagates within resident immune cells, less is known about how it traverses the epithelium. It's currently thought that MAP infects the small intestinal epithelium by targeting both enterocytes and M cells, with a potential tropism for the latter. In the current study, we developed and validated an enteroid-based in vitro assay containing functional M cells to identify the target cells for MAP's entry. Upon exposure to MAP, the bacteria were detected within both enterocytes and M cells, however quantitative image analysis revealed significant tropism for the latter. Complementary studies using the Caco-2/Raji-B co-culture system provided similar results. Since other mycobacteria have been shown to initiate cell attachment and entry by using a fibronectin-bridging process, we tested whether these interactions were involved in MAP's targeting of M cells. We found that MAP's M cell tropism was enhanced by fibronectin and that this effect was abolished when monolayers were pretreated with an integrin blocking peptide. Our data demonstrate that MAP preferentially targets M cells and that this involves a fibronectin-bridging process. Furthermore, our study supports the utility of M cell containing enteroids to study host-pathogen interaction at the intestinal epithelium.</p>","PeriodicalId":7725,"journal":{"name":"American journal of physiology. Gastrointestinal and liver physiology","volume":" ","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143668903","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Spatiotemporal Development of Mesenteric Lymphatic Changes in the TNF^ΔARE/+ Mouse Model of Terminal Ileitis.","authors":"Keith Keane, Matthew Stephens, Simon Roizes, Jingna Xue, Shan Liao, Pierre-Yves von der Weid","doi":"10.1152/ajpgi.00334.2024","DOIUrl":"https://doi.org/10.1152/ajpgi.00334.2024","url":null,"abstract":"<p><p>Crohn's disease (CD) is a chronic inflammatory bowel disease which also encompasses significant alterations of the mesenteric lymphatic system. Whether these changes are a mere consequence of, or directly contribute to the inflammation is unknown. Here we characterized the spatial and temporal development of these events in the TNF^ΔARE/+ mouse, which develops CD-like ileitis and significant mesenteric lymphatic alterations. At 8-, 12-, 20-, and 28 weeks of age, specific pathogen-free (SPF), germ-free (GF) TNF^ΔARE/+ and WT mice were assessed for ileitis via myeloperoxidase activity (MPO) while mesenteric lymphatic alterations were assessed by confocal immunofluorescence imaging. Lymphatic alterations in the SPF TNF^ΔARE/+ occurred in a stepwise manner between 8 and 28 weeks of age beginning with the development of mesenteric lymphadenopathy at 8 weeks despite no significant ileitis. By 12 weeks ileal MPO significantly elevates concomitantly with lymphangiectasia of the mesenteric collecting lymphatic vessels (CLV) and clustering of CD45⁺ immune cells around them. At 20 weeks, significant lymphangiogenesis of the initials (ILV) and tertiary lymphoid organs aligned along lymphatic collectors (CA-TLOs) had developed. At 28 weeks, lymphangiectasia, lymphangiogenesis, and CA-TLOs increased. However, 28-week-old GF TNF^ΔARE/+, while displaying no ileitis, presented with mesenteric lymphadenopathy, lymphangiectasia, and lymphangiogenesis but no immune cell clustering nor CA-TLOs. The TNF^ΔARE/+ mice develop terminal ileitis and lymphatic alterations in a stepwise manner beginning with MLN lymphadenopathy and ileal inflammation, followed by CLV dilation and lymphangiogenesis. These lymphatic alterations are exacerbated by the gut microbiome, with immune cell clustering and TLO formation being entirely dependent of its presence.</p>","PeriodicalId":7725,"journal":{"name":"American journal of physiology. Gastrointestinal and liver physiology","volume":" ","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143584378","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"DIFFERENTIAL RESPONSES TO PROSTAGLANDINS IN THE CIRCULAR AND LONGITUDINAL MUSCLE LAYERS OF THE MURINE ILEUM.","authors":"Joong Goo Kwon, Sung Jin Hwang, Elizabeth A H Beckett, Kenton M Sanders, Sean Ward","doi":"10.1152/ajpgi.00400.2024","DOIUrl":"https://doi.org/10.1152/ajpgi.00400.2024","url":null,"abstract":"<p><p>Prostaglandin E₂ (PGE₂) actions on intestinal motility are complex due the differential expression of the PGE₂ receptors EP1-EP4. We sought to determine the actions of PGE₂ on electrical pacemaker and contractile activity of the circular and longitudinal muscle layers of the murine small intestine. Intracellular microelectrode and isometric force measurements were performed to examine the effects of PGE₂ receptor activation on circular and longitudinal muscle layers. In the two muscle layers PGE₂ produced differential responses. In the circular muscle layer PGE₂ caused dose-dependent membrane hyperpolarization and reduction in slow wave amplitude, accompanied by a decrease in the amplitude of phasic contractions. Membrane hyperpolarization and the reduction in slow wave amplitude and phasic contractions were insensitive to TTX and L-NNA, but inhibited by the K_ATP channel antagonist, glibenclamide. The actions of PGE₂ on the circular muscle layer were mimicked by the selective EP₂ and EP₄ agonists ONO AE1-259 and ONO AE1-329, respectively. The actions of PGE₂ were partially inhibited by the EP4 antagonist ONO AE3-208. The EP₁ agonist ONO DI-004 produced little effect while the EP3 agonist ONO AE-248 caused dose-dependent membrane depolarization. In comparison, PGE₂ produced increased tone and phasic contractions in the longitudinal muscle layer that was mimicked by ONO DI-004 and ONO AE-248, while EP₂ and EP₄ agonists had little effect on contractile activity. These data suggest that differential expression of PGE₂ receptors on intestinal muscle layers can produce antagonistic actions on intestinal motility.</p>","PeriodicalId":7725,"journal":{"name":"American journal of physiology. Gastrointestinal and liver physiology","volume":" ","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143565583","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Diet-microbiome-ENS connection: impact of the cafeteria diet.","authors":"Arun Balasubramaniam, Shanthi Srinivasan","doi":"10.1152/ajpgi.00391.2024","DOIUrl":"10.1152/ajpgi.00391.2024","url":null,"abstract":"","PeriodicalId":7725,"journal":{"name":"American journal of physiology. Gastrointestinal and liver physiology","volume":" ","pages":"G179-G181"},"PeriodicalIF":3.9,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143051370","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prenatal lipopolysaccharide stimulation modulates gastrointestinal immunity and oxidative status in weaned pigs.","authors":"Ty M Mitchell, Nicole C Burdick Sanchez, Jeff A Carroll, Paul R Broadway, Jerrad F Legako, Brooke M Bowen, Amy L Petry","doi":"10.1152/ajpgi.00268.2024","DOIUrl":"10.1152/ajpgi.00268.2024","url":null,"abstract":"<p><p>Gastrointestinal immunity and antioxidant defenses may be bolstered in young animals through prenatal immune stimulation (PIS), but this is largely uninvestigated in swine. This study tested the hypothesis that PIS could regulate offspring's gastrointestinal immune response and oxidative stress profile. To this end, a PIS model was utilized in sows, delivering low-dose lipopolysaccharide (LPS) during the final third of gestation to target the developing immune system. On day 78 ± 1.8 of gestation, 14 Camborough sows (parity = 2.6 ± 1.4) received either saline (Control, CON) or LPS from <i>Escherichia coli</i> O111:B4 (2.5 µg/kg of body wt). A subset of 34 weaned barrows (<i>n</i> = 17 CON, PIS), weaned at 21 ± 1.3 days, were anesthetized for subcutaneous temperature loggers and jugular catheter placement. Following recovery, all pigs received an intravenous injection of LPS (10 µg/kg·body wt) from <i>E. coli</i> O111:B4. Our findings demonstrate that PIS enhances the gut immune response by upregulating key inflammatory cytokines, indicative of a proinflammatory profile. Consistently across the jejunum and ileum, stem cell factor was modulated with heightened expression in PIS than CON (<i>P</i> ≤ 0.05). In the ileum alone, PIS exhibited heightened expression of proinflammatory cytokines and chemokines, including TNFα, IL-6, IL-1β, and CCL3L1, compared with CON (<i>P</i> ≤ 0.05). Exposure to PIS resulted in reduced systemic total antioxidant capacity at <i>hours 2</i> and <i>4</i> postchallenge (<i>P</i> = 0.004). Piglets exposed to PIS had decreased jejunal tissue malondialdehyde concentrations (<i>P</i> = 0.049). Together, these data indicate that exposure to PIS alters the inflammatory profile of the gastrointestinal immune response and oxidative status in weaned pigs.<b>NEW & NOTEWORTHY</b> These studies represent novel investigations into the influence of prenatal immune stimulation (PIS) in swine on the gastrointestinal immune response and oxidative status of offspring following subsequent immune challenge. Notable alterations were observed in gut protein biomarkers, particularly the upregulation of proinflammatory cytokines TNFα, IL-6, and IL-1β in PIS-exposed pigs, but has variable effects on oxidative status. Altered intestinal immune development may contribute to an increased risk for inflammatory disease associated with prenatal immune stimulation.</p>","PeriodicalId":7725,"journal":{"name":"American journal of physiology. Gastrointestinal and liver physiology","volume":" ","pages":"G197-G205"},"PeriodicalIF":3.9,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143031841","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A menu for microbes: unraveling appetite regulation and weight dynamics through the microbiota-brain connection across the lifespan.","authors":"Gabriela Ribeiro, Harriët Schellekens, Cristina Cuesta-Marti, Ivie Maneschy, Shámila Ismael, Amanda Cuevas-Sierra, J Alfredo Martínez, Marta P Silvestre, Cláudia Marques, André Moreira-Rosário, Ana Faria, Luis A Moreno, Conceição Calhau","doi":"10.1152/ajpgi.00227.2024","DOIUrl":"10.1152/ajpgi.00227.2024","url":null,"abstract":"<p><p>Appetite, as the internal drive for food intake, is often dysregulated in a broad spectrum of conditions associated with over- and under-nutrition across the lifespan. Appetite regulation is a complex, integrative process comprising psychological and behavioral events, peripheral and metabolic inputs, and central neurotransmitter and metabolic interactions. The microbiota-gut-brain axis has emerged as a critical mediator of multiple physiological processes, including energy metabolism, brain function, and behavior. Therefore, the role of the microbiota-gut-brain axis in appetite and obesity is receiving increased attention. Omics approaches such as genomics, epigenomics, transcriptomics, proteomics, and metabolomics in appetite and weight regulation offer new opportunities for featuring obesity phenotypes. Furthermore, gut-microbiota-targeted approaches such as pre-, pro-, post-, and synbiotic, personalized nutrition, and fecal microbiota transplantation are novel avenues for precision treatments. The aim of this narrative review is <i>1</i>) to provide an overview of the role of the microbiota-gut-brain axis in appetite regulation across the lifespan and <i>2</i>) to discuss the potential of omics and gut microbiota-targeted approaches to deepen understanding of appetite regulation and obesity.</p>","PeriodicalId":7725,"journal":{"name":"American journal of physiology. Gastrointestinal and liver physiology","volume":" ","pages":"G206-G228"},"PeriodicalIF":3.9,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142982495","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Carbon monoxide produced by HO-1 upregulation is the main factor behind the abnormal motility seen in experimental ulcerative colitis in mice.","authors":"Mengchao Zhao, Yaru Lei, Mengyuan Wang, Yixin Chen, Shaozhang Hou, Xinyuan Dai, Di Gao, Yudan Liu, Bruno Mazet, Lei Sha","doi":"10.1152/ajpgi.00179.2023","DOIUrl":"10.1152/ajpgi.00179.2023","url":null,"abstract":"<p><p>The colonic motility is altered in patients with ulcerative colitis (UC), but the mechanism is not clear. Carbon monoxide (CO) is the molecule regulating the resting membrane potential (RMP) gradient across colonic smooth muscle wall. Changes in RMP will affect the contractility of smooth muscle. In this study, we investigated the altered colonic motility in dextran sodium sulfate-induced UC mice and the role of CO. The results showed that in the UC group, the frequency of spontaneous colonic contractions was increased while the AUC was decreased compared with the control group. HO-1-, but not HO-2-, positive cells were increased in the colonic smooth muscle wall of the UC group. These HO-1-positive cells were mainly in the myenteric plexus and PGP9.5 positive, suggesting neuronal overproduction of CO. The RMP of circular smooth muscle cells (SMCs) in the colon of UC group was hyperpolarized compared with that of control group. In control group, application of CORM-3, a CO donor, altered colonic spontaneous contractions by increasing their frequency and decreasing amplitude. In the UC group, ZnPPIX, a HO-1 inhibitor, reduced the frequency and increased the amplitude. CORM-3 hyperpolarized the RMP of colonic SMCs and abolished its gradient in the control group, while ZnPPIX depolarized the RMP of colonic SMCs and restored its gradient in the UC group. CO produced by HO-1 upregulation is the main factor behind the altered colonic motility seen in UC mice. CO is a potential candidate as a therapeutic target for patients with UC who suffer from abnormal colonic motility.<b>NEW & NOTEWORTHY</b> Carbon monoxide (CO) produced by HO-1 upregulation in myenteric plexus is the main factor that abolishes the RMP gradient across colonic muscle wall causing the altered colonic motility seen in experimental ulcerative colitis (UC) mice. CO is a potential candidate as a therapeutic target for patients with UC who suffer from abnormal colonic motility.</p>","PeriodicalId":7725,"journal":{"name":"American journal of physiology. Gastrointestinal and liver physiology","volume":" ","pages":"G311-G322"},"PeriodicalIF":3.9,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143381562","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dysregulated hepatic alcohol metabolism: a key factor involved in the pathogenesis of alcohol-associated liver disease.","authors":"Mukund Srinivasan, Sumedha Kota, Kamlesh Bhopale, Anna Caracheo, Lata Kaphalia, Jennifer Linares, Trevor Romsdahl, William Russell, Vsevolod Popov, Paul Boor, Bhupendra Kaphalia","doi":"10.1152/ajpgi.00394.2024","DOIUrl":"10.1152/ajpgi.00394.2024","url":null,"abstract":"<p><p>Alcohol use disorder is a major risk factor for alcohol-associated liver disease (ALD), characterized by reduced hepatic alcohol dehydrogenase (ADH) activity, increased body burden of alcohol, and its nonoxidative metabolism to fatty acid ethyl esters (FAEEs). However, the mechanism(s) underlying ALD remain unclear. This study investigated the metabolic basis and mechanism(s) of ALD in chronic ethanol (EtOH)-fed hepatic ADH1-deficient (ADH^-) deer mice administered with a single dose of binge EtOH with/without FAEEs. Hepatic ADH^- and ADH normal (ADH⁺) deer mice fed chronic EtOH daily for 3 mo, followed by a single dose of binge EtOH (3 g/kg·body wt) with/without FAEEs (100 mg/kg·body wt), 1 wk before euthanasia. Blood alcohol and acetaldehyde and liver injury markers in the plasma, hepatic FAEEs, lipids, and inflammatory markers were analyzed. Hepatic histology, ultrastructure, protein/mRNA expression of genes involved in alcohol metabolism and lipogenesis, cyclic adenosine monophosphate (cAMP), phosphodiesterase (PDE) activity, and AMP-activated protein kinase (AMPKα) signaling were assessed. Blood alcohol, hepatic lipids and FAEEs, inflammation, oxidative stress, and the expression of lipogenic proteins/genes were significantly increased in various chronic EtOH-fed groups of ADH^- versus ADH⁺ deer mice. In addition, hepatic cAMP levels were reduced, whereas PDE activity and plasma transaminases were elevated. Binge EtOH with/without FAEEs did not significantly exacerbate the liver injury in chronic EtOH-fed ADH^- as well as ADH⁺ deer mice. Overall, an increased body burden of EtOH and endogenously formed FAEEs due to hepatic ADH deficiency, along with dysregulated cAMP and AMPKα signaling, could be the determining factors for EtOH-induced liver injury leading to ALD.<b>NEW & NOTEWORTHY</b> Using hepatic alcohol dehydrogenase deficient (ADH^-) deer mouse, which mimics the metabolic conditions observed in chronic alcoholics, we found significant hepatic injury along with degenerative changes in endoplasmic reticulum and mitochondria. Our findings suggest that an increased nonoxidative alcohol metabolism under hepatic alcohol dehydrogenase deficiency and associated hepatic lipid dysregulation and injury appear to be the key factors involved in the pathogenesis of alcohol-associated liver disease.</p>","PeriodicalId":7725,"journal":{"name":"American journal of physiology. Gastrointestinal and liver physiology","volume":" ","pages":"G289-G308"},"PeriodicalIF":3.9,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143188204","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Modeling the kinetics of interorgan arginine metabolism during bacterial sepsis in swine.","authors":"Caitlin Vonderohe, Douglas Burrin","doi":"10.1152/ajpgi.00375.2024","DOIUrl":"10.1152/ajpgi.00375.2024","url":null,"abstract":"","PeriodicalId":7725,"journal":{"name":"American journal of physiology. Gastrointestinal and liver physiology","volume":" ","pages":"G309-G310"},"PeriodicalIF":3.9,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143063132","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}