Hepatology Communications最新文献

{"title":"CD63-high macrophage-derived exosomal miR-6876-5p promotes hepatocellular carcinoma stemness via PTEN/Akt-mediated EMT pathway.","authors":"Shuairan Zhang, Shiqi Liu, Hang Dong, Xiuli Jin, Jing Sun, Ji Sun, Gang Wu, Yiling Li","doi":"10.1097/HC9.0000000000000616","DOIUrl":"10.1097/HC9.0000000000000616","url":null,"abstract":"<p><strong>Objective: </strong>Accumulating evidence suggests that microRNAs derived from macrophage exosomes can regulate the stemness and progression of cancer. However, the interaction mechanisms between HCC cells and tumor-associated macrophages remain unclear.</p><p><strong>Methods: </strong>Exosomes were extracted from control or CD63 overexpression macrophages and co-cultured with HCC cells. The stemness, proliferation, epithelial-mesenchymal transition, and in vivo tumorigenicity of HCC cells were assessed to determine the role of CD63-high macrophage-derived exosomal miR-6876-5p in HCC. The binding relationship between miR-6876-5p and the PTEN/Akt axis was also investigated.</p><p><strong>Results: </strong>Elevated CD63 expression was associated with increased tumor-associated macrophage infiltration and poorer prognosis in HCC. CD63-high macrophage-derived exosomes enhanced HCC cell proliferation, stemness, and epithelial-mesenchymal transition. miR-6876-5p within these exosomes was identified as a key mediator, promoting HCC progression by targeting PTEN and activating the Akt signaling pathway. In vivo studies confirmed that CD63-high macrophage-derived exosomal miR-6876-5p accelerated tumor growth and enhanced stemness in HCC cells.</p><p><strong>Conclusions: </strong>CD63-high macrophage-derived exosomes, particularly those enriched with miR-6876-5p, play a pivotal role in HCC progression by enhancing stemness and promoting epithelial-mesenchymal transition through the PTEN/Akt pathway. Targeting these exosomes and their microRNAs offers a promising therapeutic strategy forHCC.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"9 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11717501/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142946864","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hsa_circ_0109623 regulates the progression of autoimmune liver disease through Hsa_miR_146b-3p/Sortilin 1-mediated activation of CD4+ T cells.","authors":"Xinliang Lv, Li Zhu, Shijie Feng, Siyu Yang, Guohua Li, Jinqin Zhan, Yuchun Tan, Yuquan Liu, Jinliang Zhang, Yujin Wang, Yucheng Cheng, Ping Fu, Yushan Xu, Chenhong Zheng","doi":"10.1097/HC9.0000000000000607","DOIUrl":"10.1097/HC9.0000000000000607","url":null,"abstract":"<p><strong>Background: </strong>Autoimmune hepatitis (AIH) is a chronic liver disease characterized by immune-mediated liver inflammation. Despite its global prevalence, the pathogenesis of AIH remains poorly understood, and there is a lack of specific biomarkers and targeted treatments. This study aimed to investigate the role of hsa_circ_0109623, hsa-miR-146b-3p, and Sortilin 1 (SORT1) in AIH and their potential as therapeutic targets.</p><p><strong>Methods: </strong>We collected liver tissue samples and peripheral blood mononuclear cells from patients with AIH and healthy controls and performed RT-PCR, western blotting, flow cytometry, and other molecular biology techniques to analyze the expression of hsa_circ_0109623, hsa-miR-146b-3p, and SORT1. We also used bioinformatics tools to predict the interaction between these molecules and conducted luciferase reporter assays to confirm their binding.</p><p><strong>Results: </strong>hsa_circ_0109623 was significantly upregulated in patients with AIH and positively correlated with inflammatory activity. We also found that hsa_circ_0109623 could enhance CD4+ T-cell activation and promote the expression of proinflammatory cytokines. Conversely, hsa-miR-146b-3p was downregulated in patients with AIH and negatively correlated with the expression of hsa_circ_0109623 and SORT1. In addition, hsa-miR-146b-3p acted as a sponge for hsa_circ_0109623, inhibiting CD4+ Th1 cell polarization and cytokine production. SORT1 was also upregulated in patients with AIH and acted as a sponge for hsa-miR-146b-3p, promoting CD4+ Th1 cell polarization and cytokine expression. Furthermore, hsa_miR_146b-3p/SORT1 can regulate the STAT1/STAT4 signaling pathway mediating the progression of AIH.</p><p><strong>Conclusions: </strong>The hsa_circ_0109623/hsa-miR-146b-3p/SORT1 axis plays a crucial role in the pathogenesis of AIH by regulating CD4+ T-cell activation and cytokine production. These molecules may serve as potential biomarkers and therapeutic targets for AIH. Further research is needed to validate these findings and explore their clinical applications.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"9 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11717529/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142947946","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CD36 in liver diseases.","authors":"Yi Liu, Wenwei Yin","doi":"10.1097/HC9.0000000000000623","DOIUrl":"10.1097/HC9.0000000000000623","url":null,"abstract":"<p><p>Cluster of differentiation 36 (CD36) is a transmembrane glycoprotein with the ability to bind to multiple ligands and perform diverse functions. Through the recognition of long-chain fatty acids, proteins containing thrombospondin structural homology repeat domains such as thrombospondin-1, and molecules with molecular structures consistent with danger- or pathogen-associated molecular patterns, CD36 participates in various physiological and pathological processes of the body. CD36 is widely expressed in various cell types, including hepatocytes and KCs in the liver, where it plays a pivotal role in lipid metabolism, inflammation, and oxidative stress. Accumulating evidence suggests that CD36 plays a complex role in the development of nonalcoholic simple fatty liver disease and NASH and contributes to the pathogenesis of inflammatory liver injury, hepatitis B/hepatitis C, liver fibrosis, and liver cancer. This review summarizes the current understanding of the structural properties, expression patterns, and functional mechanisms of CD36 in the context of liver pathophysiology. Furthermore, the potential of CD36 as a therapeutic target for the prevention and treatment of liver diseases is highlighted.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"9 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11717518/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142946669","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neurogastroenterology and motility disorders in patients with cirrhosis.","authors":"Francisco Idalsoaga, Gustavo Ayares, Hanna Blaney, Daniel Cabrera, Javier Chahuan, Hugo Monrroy, Ayah Matar, Houssam Halawi, Marco Arrese, Juan Pablo Arab, Luis Antonio Díaz","doi":"10.1097/HC9.0000000000000622","DOIUrl":"10.1097/HC9.0000000000000622","url":null,"abstract":"<p><p>Neurogastroenterology and motility disorders are complex gastrointestinal conditions that are prevalent worldwide, particularly affecting women and younger individuals. These conditions significantly impact the quality of life of people suffering from them. There is increasing evidence linking these disorders to cirrhosis, with a higher prevalence compared to the general population. However, the link between neurogastroenterology and motility disorders and cirrhosis remains unclear due to undefined mechanisms. In addition, managing these conditions in cirrhosis is often limited by the adverse effects of drugs commonly used for these disorders, presenting a significant clinical challenge in the routine management of patients with cirrhosis. This review delves into this connection, exploring potential pathophysiological links and clinical interventions between neurogastroenterology disorders and cirrhosis.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"9 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11717532/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142948012","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hepcidin inhibits hepatocyte apoptosis through the PERK pathway in acute liver injury and fibrosis.","authors":"Changying Li, Guojin Pang, Weihua Zhao, Yingying Liu, Xiaoli Huang, Wei Chen, Xinyan Zhao, Tianhui Liu, Ping Wang, Xu Fan, Ming Gao, Min Cong","doi":"10.1097/HC9.0000000000000604","DOIUrl":"10.1097/HC9.0000000000000604","url":null,"abstract":"<p><strong>Background: </strong>Hepcidin, a peptide hormone primarily produced by the liver, regulates iron metabolism by interacting with its receptor, ferroportin. Studies have demonstrated that hepcidin participates in the progression of liver fibrosis by regulating HSC activation, but its regulatory effect on hepatocytes remains largely unknown.</p><p><strong>Methods: </strong>A carbon tetrachloride (CCl4)-induced liver fibrosis model was established in C57BL/6 wild-type (WT) and hepcidin knockout (Hamp-/-) mice. Liver injury and inflammation were assessed in WT and Hamp-/- mice at 24 and 48 hours following acute CCl4 exposure. In addition, transcriptomic sequencing of primary hepatocytes was performed to compare gene expression profiles between WT and Hamp-/- mice 24 hours after liver injury. The function of the identified molecule Eif2ak3/PERK (protein kinase R(PKR)-like endoplasmic reticulum kinase), was evaluated both in vitro and in vivo.</p><p><strong>Results: </strong>We found that serum hepcidin significantly increased during the progression of liver fibrosis induced by CCl4 and bile duct ligation. In addition, CCl4-treated Hamp-/- mice developed more severe liver injury, liver fibrosis, and hepatocyte apoptosis, with elevated Bax and decreased Bcl-2 expression, compared to the WT mice. Transcriptomic analysis of primary hepatocytes revealed that PERK was upregulated in Hamp-/- mice after CCl4 treatment, promoting apoptosis by regulating Bax and Bcl-2 expression. Subsequently, we demonstrated that hepcidin prevents hepatocyte apoptosis by inhibiting PERK both in vitro and in vivo.</p><p><strong>Conclusions: </strong>Hepcidin inhibits hepatocyte apoptosis through suppression of the PERK pathway, highlighting its protective role in liver fibrosis and identifying a potential therapeutic target for the treatment of liver fibrosis.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"9 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11661744/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142854020","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Thyroid hormone and the Liver.","authors":"Lorraine Soares De Oliveira, Megan J Ritter","doi":"10.1097/HC9.0000000000000596","DOIUrl":"10.1097/HC9.0000000000000596","url":null,"abstract":"<p><p>It is known that thyroid hormone can regulate hepatic metabolic pathways including cholesterol, de novo lipogenesis, fatty acid oxidation, lipophagy, and carbohydrate metabolism. Thyroid hormone action is mediated by the thyroid hormone receptor (THR) isoforms and their coregulators, and THRβ is the main isoform expressed in the liver. Dysregulation of thyroid hormone levels, as seen in hypothyroidism, has been associated with dyslipidemia and metabolic dysfunction-associated fatty liver disease. Given the beneficial effects of thyroid hormone in liver metabolism and the advances illuminating the use of thyroid hormone analogs such as resmetirom as therapeutic agents in the treatment of metabolic dysfunction-associated fatty liver disease, this review aims to further explore the relationship between TH, the liver, and metabolic dysfunction-associated fatty liver disease. Herein, we summarize the current clinical therapies and highlight future areas of research.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"9 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11661762/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142854046","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Erratum: Missense variants in the TRPM7 α-kinase domain are associated with recurrent pediatric acute liver failure.","authors":"","doi":"10.1097/HC9.0000000000000631","DOIUrl":"10.1097/HC9.0000000000000631","url":null,"abstract":"","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"9 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11661727/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142854010","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PPAR agonists for the treatment of cholestatic liver diseases: Over a decade of clinical progress.","authors":"Colleen M Hayes, Gina M Gallucci, James L Boyer, David N Assis, Nisanne S Ghonem","doi":"10.1097/HC9.0000000000000612","DOIUrl":"10.1097/HC9.0000000000000612","url":null,"abstract":"<p><p>Primary biliary cholangitis (PBC) and primary sclerosing cholangitis (PSC) are characterized by the destruction of the small bile ducts and the formation of multifocal biliary strictures, respectively, impairing bile flow. This leads to the hepatic accumulation of bile acids, causing liver injury and the risk of progression to cirrhosis and liver failure. First-line therapy for PBC is ursodeoxycholic acid, although up to 40% of treated individuals are incomplete responders, and there is no effective therapy for PSC, highlighting the need for better therapeutic options in these diseases. In addition, pruritus is a common symptom of cholestasis that has severe consequences for quality of life and is often undertreated or untreated. Nuclear receptors are pharmacological targets to treat cholestasis due to their multifactorial regulation of hepatic enzymatic pathways, particularly in bile acid metabolism. The peroxisome proliferator-activated receptor (PPAR) is of significant clinical interest due to its role in regulating bile acid synthesis and detoxification pathways. PPAR agonism by fibrates has traditionally been explored due to PPARα's expression in the liver; however, recent interest has expanded to focus on newer PPAR agonists that activate other PPAR isoforms, for example, δ, γ, alone or in combination. Several PPAR agonists have been investigated as second-line therapy for people living with PBC, including the recent accelerated United States Food and Drug Administration approval of elafibranor and seladelpar. This review evaluates available data on the efficacy and safety of the five PPAR agonists investigated for the treatment of cholestasis and associated pruritus in PBC and PSC, namely fenofibrate, bezafibrate, saroglitazar, elafibranor, and seladelpar.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"9 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11661771/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142854025","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Spatial analyses revealed CXCL5 and SLC6A14 as the markers of microvascular invasion in intrahepatic cholangiocarcinoma.","authors":"Guangyu Fan, Liyuan Dai, Tongji Xie, Lin Li, Le Tang, Xiaohong Han, Yuankai Shi","doi":"10.1097/HC9.0000000000000597","DOIUrl":"10.1097/HC9.0000000000000597","url":null,"abstract":"<p><strong>Background: </strong>Microvascular invasion (MVI) is a critical prognostic factor in intrahepatic cholangiocarcinoma (ICC), strongly associated with postoperative recurrence. However, the phenotypic features and spatial organization of MVI remain inadequately understood.</p><p><strong>Methods: </strong>We performed a spatial transcriptomic analysis on 29,632 spots from six ICC samples, manually delineating MVI clusters using the cloupe software. Key biomarkers were identified and validated in an independent cohort of 135 ICC patients. Functional and survival analyses were conducted to assess clinical relevance, and cell-cell communication pathways were investigated.</p><p><strong>Results: </strong>MVI regions exhibited heightened proliferation, angiogenesis, and epithelial-mesenchymal transition, driven by increased expression of transcription factors SOX10, ZEB1, and SNAI2. CXCL5 and SLC6A14 were identified as potential MVI biomarkers and showed high expression in tumor-invasive areas. Serum CXCL5 demonstrated strong predictive power for vascular invasion (AUC = 0.92) and intrahepatic metastasis (AUC = 0.96). High expression of both CXCL5 and SLC6A14 was associated with the worst survival outcomes. MVI regions were enriched with immunosuppressive MRC1+ macrophages and exhibited elevated immune checkpoint expression, including HAVCR2 and TIGHT, indicative of immune resistance. Cell-cell communication analysis revealed CXCL5-CXCR2 and LGALS9-HAVCR2 as key ligand-receptor pairs contributing to the immunosuppressive microenvironment.</p><p><strong>Conclusions: </strong>This study identifies CXCL5 and SLC6A14 as key biomarkers of MVI, highlighting their roles in tumor proliferation, immune resistance, and poor clinical outcomes. These findings provide valuable insights into the spatial organization of MVI and its contribution to ICC progression, offering potential therapeutic targets.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"9 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2024-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11637745/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142817847","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Quantitative fibrosis identifies biliary tract involvement and is associated with outcomes in pediatric autoimmune liver disease.","authors":"Leticia Khendek, Cyd Castro-Rojas, Constance Nelson, Mosab Alquraish, Rebekah Karns, Jennifer Kasten, Xiao Teng, Alexander G Miethke, Amy E Taylor","doi":"10.1097/HC9.0000000000000594","DOIUrl":"10.1097/HC9.0000000000000594","url":null,"abstract":"<p><strong>Background: </strong>Children with autoimmune liver disease (AILD) may develop fibrosis-related complications necessitating a liver transplant. We hypothesize that tissue-based analysis of liver fibrosis by second harmonic generation (SHG) microscopy with artificial intelligence analysis can yield prognostic biomarkers in AILD.</p><p><strong>Methods: </strong>Patients from single-center studies with unstained slides from clinically obtained liver biopsies at AILD diagnosis were identified. Baseline demographics and liver biochemistries at diagnosis and 1 year were collected. Clinical endpoints studied included the presence of varices, variceal bleeding, ascites, HE, and liver transplant. In collaboration with HistoIndex, unstained slides underwent SHG/artificial intelligence analysis to map fibrosis according to 10 quantitative fibrosis parameters based on tissue location, including total, periportal, perisinusoidal, and pericentral area and length of strings.</p><p><strong>Results: </strong>Sixty-three patients with AIH (51%), primary sclerosing cholangitis (30%), or autoimmune sclerosing cholangitis (19%) at a median of 14 years old (range: 3-24) were included. An unsupervised analysis of quantitative fibrosis parameters representing total and portal fibrosis identified a patient cluster with more primary sclerosing cholangitis/autoimmune sclerosing cholangitis. This group had more fibrosis at diagnosis by METAVIR classification of histopathological review of biopsies (2.5 vs. 2; p = 0.006). This quantitative fibrosis pattern also predicted abnormal 12-month ALT with an OR of 3.6 (1.3-10, p = 0.014), liver complications with an HR of 3.2 (1.3-7.9, p = 0.01), and liver transplantation with an HR of 20.1 (3-135.7, p = 0.002).</p><p><strong>Conclusions: </strong>The application of SHG/artificial intelligence algorithms in pediatric-onset AILD provides improved insight into liver histopathology through fibrosis mapping. SHG allows objective identification of patients with biliary tract involvement, which may be associated with a higher risk for refractory disease.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"9 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2024-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11637754/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142817911","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}