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

{"title":"Probiotic-mediated regulation of arginine metabolism to improve intestinal barrier function: a metabolic makeover for IBD?","authors":"Yevheniya Shevchenko, Michael A Schumacher","doi":"10.1152/ajpgi.00277.2025","DOIUrl":"10.1152/ajpgi.00277.2025","url":null,"abstract":"","PeriodicalId":7725,"journal":{"name":"American journal of physiology. Gastrointestinal and liver physiology","volume":" ","pages":"G557-G558"},"PeriodicalIF":3.3,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12482146/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145068889","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Serotonin, a downstream effector of GLP-2, enhances lacteal contractility and lymph flow.","authors":"Lili Tian, Majid Mufaqam Syed-Abdul, Gary F Lewis","doi":"10.1152/ajpgi.00205.2025","DOIUrl":"10.1152/ajpgi.00205.2025","url":null,"abstract":"<p><p>Glucagon-like peptide-2 (GLP-2) is known to exert some of its biological effects through the release of neurotransmitters, and in view of the absolute requirement for the enteric nervous system (ENS) demonstrated in our recent GLP-2-induced lipid mobilization studies, we aimed to identify the neurotransmitter that mediates GLP-2's effect on intestinal lipid mobilization. We also examined the role of vascular endothelial growth factor receptor 3 (VEGFR3) as an intermediate in the signaling cascade. Using a rat lymph fistula model, 5 h after an intraduodenal (id) lipid bolus, the following intraperitoneal (ip) administrations were applied in two different sets of experiments: <i>Experiment 1: 1</i>) placebo, <i>2</i>) GLP-2, and <i>3</i>) GLP-2 + ketanserin (serotonin receptor antagonist). <i>Experiment 2: 1</i>) placebo, <i>2</i>) serotonin, <i>3</i>) serotonin + MAZ-51 (a VEGFR3 inhibitor), <i>4</i>) serotonin + SAR131675 (a second VEGFR3 inhibitor). Lymph flow and triglyceride (TG) output were assessed for 60 min (<i>experiment 1</i>) or 90 min (<i>experiment 2</i>) after administration. In another set of animals, GLP-2 or serotonin was administered intraperitoneally, and blood samples were collected to quantify plasma serotonin concentration. Intravital imaging of a prospero-related homeobox 1-enhanced green fluorescent protein rat model was used to assess lacteal contractility after placebo or serotonin administration. We demonstrated that single-dose GLP-2 administration acutely increased serotonin concentration in plasma, serotonin enhanced lymph flow, lymph TG output, and lacteal contractility. Antagonism of the serotonin receptor decreases GLP-2-enhanced mesenteric lymph flow and TG output, and inhibition of VEGFR3 abolishes serotonin-induced lymph flow and TG output<b>NEW & NOTEWORTHY</b> Our data suggests that the neurotransmitter serotonin mediates glucagon-like peptide-2 (GLP-2)'s effect on intestinal lipid mobilization by enhancing lymph flow and lacteal contractility, and vascular endothelial growth factor receptor 3 (VEGFR3) is one of the downstream targets of serotonin involved in this cascade.</p>","PeriodicalId":7725,"journal":{"name":"American journal of physiology. Gastrointestinal and liver physiology","volume":" ","pages":"G562-G570"},"PeriodicalIF":3.3,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145068860","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":"Pioglitazone Reduces Hepatic Alpha-1 Antitrypsin Accumulation Through Autophagy and AMPK Activation in Alpha-1 Antitrypsin Deficient Mice.","authors":"Yuanqing Lu, Regina Oshins, Nesmine R Maptue, Qingyang Shen, Chalermchai Khemtong, Kenneth Cusi, Mark Brantly, Nazli Khodayari","doi":"10.1152/ajpgi.00272.2025","DOIUrl":"https://doi.org/10.1152/ajpgi.00272.2025","url":null,"abstract":"<p><p><b>Background:</b> Alpha-1 antitrypsin deficiency (AATD) is a genetic disorder characterized by accumulation of misfolded Z α-1 antitrypsin (ZAAT) in hepatocytes, leading to liver injury and metabolic dysfunction. There is no therapy to reduce ZAAT accumulation and restore proteostasis. Pioglitazone activates AMP-activated protein kinase (AMPK), enhance autophagy, and modulate ER stress responses, suggesting a potential effect on ZAAT clearance. Our objective is to examine whether pioglitazone can protect against AATD-mediated liver disease. <b>Methods:</b> Huh7.5 cells expressing ZAAT (HuhZ) and Pi*Z transgenic mice were used to investigate pioglitazone treatment on hepatic ZAAT accumulation, autophagy activation, and AMPK signaling. Histological, molecular, and metabolic analyses were conducted to assess changes in ZAAT content, autophagy markers, AMPK phosphorylation, and proteostasis. <b>Results:</b> Pioglitazone significantly reduced intracellular ZAAT and decreased lipid droplet accumulation in HuhZ cells. Pioglitazone markedly lowered hepatic ZAAT content in Pi*Z mice, suggesting enhanced degradation. This reduction was mediated through the AMPK pathway, indicated by increased phosphorylation of AMPK and ULK1. Pioglitazone induced autophagy, shown by decreased p62 and increased ATG5 and LC3B-II. This is indicative of enhanced autophagy. Although total hepatic AAT levels were reduced, PASD-positive ZAAT aggregates exhibited only a downward trend, suggesting these may be more resistant to clearance. <b>Conclusion:</b> These findings demonstrate pioglitazone reduces hepatic ZAAT accumulation by activating AMPK and inducing autophagy in AATD-associated liver disease, supporting its potential for therapeutic repurposing. As pioglitazone is FDA-approved with benefits for metabolic liver health, further studies are warranted to evaluate efficacy in restoring proteostasis and reducing hepatic ZAAT.</p>","PeriodicalId":7725,"journal":{"name":"American journal of physiology. Gastrointestinal and liver physiology","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145190615","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":"Dynamic Cholangiocyte Responses in a Murine Model of Reversible Cholestasis: Macrophage Remodeling and NF-Y Mediated TGFβ1 Expression.","authors":"Kirsta E Olson, Anuradha Krishnan, Patrick Splinter, Alexander Q Wixom, Maria Eugenia Guicciardi, Nidhi Jalan-Sakrikar, Adiba Azad, Nicholas F LaRusso, Gregory J Gores","doi":"10.1152/ajpgi.00243.2025","DOIUrl":"https://doi.org/10.1152/ajpgi.00243.2025","url":null,"abstract":"<p><p>During cholestasis, cholangiocytes become activated, promoting macrophage-associated periductal infiltration and fibrosis. The cholangiocyte specific mechanisms responsible for these processes are unclear. To gain insight into the cholangiocyte signaling mechanisms contributing to these pathophysiologic processes, mice were fed a DDC diet for 10 days to induce liver injury and then switched to a chow diet to permit recovery, designated as R days. Profiling of isolated intrahepatic leukocytes by mass spectrometry revealed an abundant CX3CR1⁺ macrophage population on the DDC diet which declined during the recovery period. This observation was confirmed using <i>Cx3cr1</i>^GFP mice. Next, cholangiocytes were isolated from control, DDC, and R15 mice, and RNA-seq performed. Cholangiocyte CX3CL1 expression, the cognate ligand for CX3CR1, increased in DDC fed mice and returned to basal values by R15, implicating cholangiocytes in CX3CR1⁺ macrophage recruitment. Ingenuity pathway analysis (IPA) of the RNAseq data revealed upregulation of the pathogen induced cytokine storm pathway in cholangiocytes activated from DDC fed mice, and resolution of this pathway in R15 isolated cholangiocytes. SCENIC regulon analysis identified that NF-Y, a transcription factor complex, was activated only on the DDC diet, but not in control or R15 mice. Finally, siRNA targeted suppression of NF-YA in normal human cholangiocytes (NHC) reduced cholangiocyte expression of the profibrogenic ligand <i>TGFβ1</i>. Consistent with this observation, <i>Tgfβ1</i> was increased in cholangiocytes from DDC fed animals which returned to control values at day R15. Collectively, these observations provide mechanistic insights into cholangiocyte pathobiology during cholestasis.</p>","PeriodicalId":7725,"journal":{"name":"American journal of physiology. Gastrointestinal and liver physiology","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145190640","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":"Temporal Transcriptional and Functional Dynamics of Jejunal Mucosal Response to Early Weaning in Piglets.","authors":"Ty M Mitchell, Heather Ann Moeser, Adam J Moeser","doi":"10.1152/ajpgi.00022.2025","DOIUrl":"https://doi.org/10.1152/ajpgi.00022.2025","url":null,"abstract":"<p><p>Early-life adversity, including abrupt weaning, imposes significant psychosocial and environmental stress during a critical window of gastrointestinal (GI) development, leading to long-term consequences for gut function and disease susceptibility. In piglets, early weaning profoundly disrupts GI development, altering the intestinal epithelial barrier, reshaping immune function, and inducing lasting changes in the enteric nervous system. Despite these adverse outcomes, the early molecular mechanisms that initiate these alterations and set the gut on a divergent developmental trajectory remain poorly understood. Here, we utilized RNA sequencing and bioinformatic analyses to delineate early transcriptional changes in the jejunal mucosa of early-weaned male castrates compared to unweaned littermates. Ex vivo Ussing chamber experiments validated functional changes associated with these transcriptional alterations. Weaning triggered rapid transcriptional shifts observable within 3 hours, including suppressed mitochondrial energy production and increased glucose transporter expression. Pathway analysis revealed upregulation of ion channel transport genes (KCN, SCN, TRP, SLC) and neurotransmitter receptors (cholinergic, dopaminergic, GABAergic, glutamatergic), indicating early neuronal adaptations. Functional assays confirmed enhanced SGLT-mediated glucose transport and neural-evoked secretory responses 24 hours post-weaning, supporting transcriptomic findings. These findings reveal previously unexamined early transcriptional and functional changes that may serve as inciting mechanisms altering gut trajectory during this critical developmental window, providing new insight into how psychosocial stress and early weaning contribute to long-term gut dysfunction, with broader implications for preterm birth, neonatal GI injury, and other early-life stressors that impact lifelong GI health.</p>","PeriodicalId":7725,"journal":{"name":"American journal of physiology. Gastrointestinal and liver physiology","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145111730","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 synergistic interplay between vitamin A, dietary fiber, and the microbiota-gut-brain axis: a potential mechanism for preventing Alzheimer's disease.","authors":"Shadt Skawratananond, Grace E McCrea, Paul Lie, Matthew B Buxton, Sean P Daly, Nicholas A Vojtkofsky, Shane C Smith, Charlie Zhang, Matthew Hernandez, Ashly Hindle, Aric F Logsdon, J Josh Lawrence","doi":"10.1152/ajpgi.00097.2025","DOIUrl":"10.1152/ajpgi.00097.2025","url":null,"abstract":"<p><p>The human gastrointestinal tract harbors a vast and diverse microbial community, with the gut microbiome playing a fundamental role in numerous biological processes that influence overall health and disease progression. Emerging evidence has identified bacterial lipopolysaccharides in the hippocampus of patients with Alzheimer's disease (AD), highlighting the intricate relationship between the gastrointestinal tract, gut microbiome, and the central and enteric nervous systems-commonly referred to as the \"microbiota-gut-brain axis.\" In this review, we explore the mechanisms by which the microbiota-gut-brain axis contributes to AD pathogenesis. We propose that sufficient levels of all-trans retinoic acid (ATRA), the bioactive form of vitamin A, enhance intestinal barrier integrity by upregulating tight junction proteins and modulating immune function through the induction of regulatory T-cell differentiation, thereby mitigating inflammation. Furthermore, dietary fiber complements this process by promoting the production of short-chain fatty acids, such as butyrate, via bacterial fermentation. Butyrate, in turn, acts as a histone deacetylase inhibitor, upregulating ATRA bioavailability by elevating aldehyde dehydrogenase gene expression. Our mechanistic framework is supported by the endotoxin hypothesis of AD, which maintains that the movement of infectious pathogens across the blood-brain barrier causes a vicious cycle of inflammation, a key factor of AD pathogenesis, leading to amyloid-β deposition, microglial activation, and CYP26A1-mediated ATRA degradation. Finally, we discuss microbiome-based therapeutic strategies and dietary interventions, including prebiotic compounds, probiotic bacteria, fecal microbiota transplantation, the Mediterranean-DASH Intervention for Neurodegenerative Delay (MIND) diet, and a combined approach featuring vitamins A/D and dietary fiber, as potential approaches to prevent progression to AD via the microbiota-gut-brain axis.</p>","PeriodicalId":7725,"journal":{"name":"American journal of physiology. Gastrointestinal and liver physiology","volume":" ","pages":"G484-G499"},"PeriodicalIF":3.3,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144833715","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":"Liquid nutrient drink testing induces gastric myoelectrical abnormalities that correlate with gastroduodenal symptoms.","authors":"Hassan Shaaban, Chris Varghese, Gabriel Schamberg, India Wallace, Mikaela Law, Nooriyah Poonawala, William Xu, Christopher N Andrews, Armen Gharibans, Jan Tack, Gregory O'Grady, Stefan Calder","doi":"10.1152/ajpgi.00070.2025","DOIUrl":"https://doi.org/10.1152/ajpgi.00070.2025","url":null,"abstract":"<p><p>Chronic gastroduodenal symptoms experienced in functional dyspepsia, chronic nausea and vomiting syndromes, and gastroparesis affect over 10% of the global population and impose a significant healthcare burden. The relationship between aberrant gastric myoelectrical activity and symptom genesis remains incompletely defined. In this study, we evaluated the effects of gastric distension induced by a liquid nutrient drink test (LNDT) on gastric myoelectrical activity in healthy volunteers using noninvasive body surface gastric mapping (BSGM) with the Gastric Alimetry system (Auckland, New Zealand). Twenty healthy participants (10 females) underwent BSGM with 30-min fasting baseline, LNDT with Ensure administered at 30 mL/min until maximal toleration, and 4-h postprandial recording. Gastric Alimetry Rhythm Index (GA-RI), principal gastric frequency (PGF), and BMI-adjusted amplitude were analyzed across time and in relation to symptoms using mixed models. During LNDT, PGF decreased significantly (2.7 ± 0.2 vs. an overall average 3.0 ± 0.2 cycles/min, <i>P</i> < 0.001) and GA-RI declined (β = -0.11, 95% CI -0.21 to -0.002, <i>P</i> = 0.047) with a concurrent increase in nausea ratings. In the first postprandial hour, bloating, nausea, and overall symptom burden were elevated, with sustained reductions in GA-RI and PGF correlating with higher symptom scores. Spectral analyses revealed transient abnormalities temporally aligned with symptom genesis. These findings indicate that excessive gastric distension provokes aberrant gastric myoelectrical activity that is closely associated with foregut symptoms, supporting the role of these abnormalities in the pathophysiology of neurogastroduodenal disorders.<b>NEW & NOTEWORTHY</b> Body surface gastric mapping with liquid nutrient drink test found that excessive gastric distension provokes dysrhythmias that are closely associated with foregut symptoms, supporting the role of disrupted gastric myoelectrical function in the pathophysiology of neurogastroduodenal disorders.</p>","PeriodicalId":7725,"journal":{"name":"American journal of physiology. Gastrointestinal and liver physiology","volume":"329 3","pages":"G363-G370"},"PeriodicalIF":3.3,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144939482","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 novel gene therapy for ARPKD based on CFTR.","authors":"Cristian Ciobanu, Patricia Outeda, William B Guggino, Liudmila Cebotaru","doi":"10.1152/ajpgi.00109.2025","DOIUrl":"10.1152/ajpgi.00109.2025","url":null,"abstract":"<p><p>Autosomal recessive polycystic kidney disease (ARPKD) is associated with cysts derived from abnormal bile ducts. We focused on targeting the cysts and show that a gene therapy for ARPKD that targets the abnormal bile ducts is feasible. We injected 1-mo-old, <i>Pkhd1</i>^{del3-4/del3-4} mice intraperitoneally with 2 × 10¹² particles/kg of adeno-associated virus (AAV1) containing either a GFP vector or a truncated cystic fibrosis transmembrane conductance regulator (CFTR) vector, Δ27-264-CFTR, or left them untreated. Two months after treatment, the cyst area and size in the liver were lower in the CFTR vector-treated mice than in mice receiving the GFP vector. We detected vector genomes and mRNA expression only in mice receiving the corresponding CFTR or GFP vector. We observed abundant GFP immunofluorescence in the cholangiocytes of the cysts and also saw expression of GFP and CFTR proteins above background levels in the corresponding treated mice. CFTR immunofluorescence was predominantly apically located in the ARPKD cholangiocytes, but after CFTR vector installation, it increased in the basolateral membrane. We stained mouse livers with <i>Maackia amurensis</i> lectin (MAL) or <i>Sambucus nigra</i> lectin (SNA), specific for α2,3- and α2,6-N-linked sialic acid, respectively, to detect the presence of sialic acid moieties contributing to AAV1 binding. Although immunofluorescent SNA was detected in the wild-type bile ducts, MAL 1 was not. MAL immunofluorescence was present in remarkably high levels on the apical surfaces of the cysts in cholangiocytes, offering a good target for AAV gene therapy. A gene therapy using an AAV1-based vector containing a truncated CFTR could be therapeutic in ARPKD.<b>NEW & NOTEWORTHY</b> Autosomal recessive polycystic kidney disease (ARPKD) causes severe disease in babies in the womb. Those who survive the neonatal period face chronic kidney and liver disease throughout their life. The overall goal of our study here is to develop a gene therapy to treat ARPKD.</p>","PeriodicalId":7725,"journal":{"name":"American journal of physiology. Gastrointestinal and liver physiology","volume":" ","pages":"G434-G442"},"PeriodicalIF":3.3,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144788060","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":"Budding baboon blues: the prenatal diet lands a lasting gut punch.","authors":"Anna Grigorian, Mengyun Wu, Jerrold R Turner","doi":"10.1152/ajpgi.00252.2025","DOIUrl":"10.1152/ajpgi.00252.2025","url":null,"abstract":"","PeriodicalId":7725,"journal":{"name":"American journal of physiology. Gastrointestinal and liver physiology","volume":" ","pages":"G510-G512"},"PeriodicalIF":3.3,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144939552","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":"Emerging advances in intestinal models for in vitro preclinical research.","authors":"Precious Adedayo Adesina, Masato Ooka, Charlotte TeKrony, Menghang Xia","doi":"10.1152/ajpgi.00087.2025","DOIUrl":"10.1152/ajpgi.00087.2025","url":null,"abstract":"<p><p>Traditional in vitro intestinal model systems frequently fail to accurately replicate human intestinal physiology for absorption, distribution, metabolism, excretion, and toxicity (ADMET) assessments. These limitations, coupled with the growing demand for faster drug discovery and high-throughput screening capabilities, have refined more physiologically relevant models. Recent advancements have led to the development of cell-based intestinal systems that better reflect in vivo conditions, ranging from monolayer and coculture models to complex three-dimensional (3-D) cell culture systems, microfluidic devices, and bioengineered models. This review provides a comprehensive overview of current progress, ongoing challenges, and future directions in developing and applying human in vitro intestinal models for chemical testing.</p>","PeriodicalId":7725,"journal":{"name":"American journal of physiology. Gastrointestinal and liver physiology","volume":" ","pages":"G403-G416"},"PeriodicalIF":3.3,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144717322","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}