Liver Research最新文献

{"title":"Genetic variants in the 6p21.3 region influence hepatitis B virus clearance and chronic hepatitis B risk in the Han Chinese population","authors":"Jiancheng Huang ,&nbsp;Mingkuan Su ,&nbsp;Fanhui Kong ,&nbsp;Hongbin Chen ,&nbsp;Shuiqing Wu ,&nbsp;Jianfeng Guo ,&nbsp;Haiying Wu","doi":"10.1016/j.livres.2024.02.001","DOIUrl":"https://doi.org/10.1016/j.livres.2024.02.001","url":null,"abstract":"<div><h3>Background and aim</h3><p>A genome-wide association study has indicated the association of numerous genes in the 6p21.3 region with chronic hepatitis B virus (HBV) infection. In this study, we screened 12 representative single-nucleotide polymorphisms (SNPs) from the 6p21.3 region and investigated their association with the risk of chronic hepatitis B (CHB) to better understand the molecular etiology underlying CHB risk in the Han Chinese population.</p></div><div><h3>Methods</h3><p>Between March 2021 and November 2022, we included 183 patients with CHB (case group) and 196 with natural HBV clearance (control group). Allele typing of the selected SNPs was performed using snapshot technology. The correlation between the 12 chosen SNPs and the risk of chronic HBV infection was examined using binary logistic regression analysis. Interacting genes of the variants were identified, and expression quantitative trait loci (eQTL) were analyzed using the 3DSNP database.</p></div><div><h3>Results</h3><p>We validated 12 previously reported CHB susceptibility sites, including rs1419881 of transcription factor 19 (<em>TCF19</em>), rs3130542 and rs2853953 of human leukocyte antigen (<em>HLA</em>)<em>-C</em>, rs652888 of euchromatic histone-lysine-methyltransferase 2 (<em>EHMT2</em>), rs2856718, rs9276370, rs7756516, and rs7453920 of <em>HLA-DQ</em>, rs378352 of <em>HLA-DOA</em>, and rs3077, rs9277535, and rs9366816 of <em>HLA-DP</em>. Logistic regression analyses revealed that polymorphisms such as rs9276370, rs7756516, rs7453920, rs3077, rs9277535, and rs9366816 were positively correlated with natural HBV clearance in the dominant model. Conversely, rs3130542 and rs378352 were identified as risk factors for CHB. Haplotype analysis revealed that rs9276370, rs7756516, and rs7453920 in <em>HLA-DQ</em> were TTG and GCA haplotypes. Although the TTG haplotype was positively correlated with a higher risk of CHB, the GCA haplotype significantly influenced the natural clearance of HBV. Bioinformatics analysis demonstrated that rs378352, rs3077, and rs9366816 were located within enhancer states; rs3077 and rs9366816 overlapped with nine transcription factor-binding sites, whereas rs378352 altered five sequence motifs. Furthermore, eQTL analysis demonstrated the functional tendencies of eight statistically significant SNPs (rs3130542, rs9276370, rs7756516, rs7453920, rs378352, rs3077, rs9277535, and rs9366816).</p></div><div><h3>Conclusions</h3><p>Genetic variations within the 6p21.3 region were associated with chronic HBV infection in the Han Chinese population in southern China. Furthermore, the GCA haplotype including rs9276370, rs7756516, and rs7453920 of <em>HLA-DQ</em> contributed significantly to natural HBV clearance, implying that multiple SNPs exert a cumulative allelic effect on HBV infection.</p></div>","PeriodicalId":36741,"journal":{"name":"Liver Research","volume":"8 1","pages":"Pages 54-60"},"PeriodicalIF":0.0,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2542568424000035/pdfft?md5=c552965074bc3e0d17f6b385b80c27c0&pid=1-s2.0-S2542568424000035-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140296803","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of the portal system in liver regeneration: From molecular mechanisms to clinical management","authors":"Hanzhi Xu ,&nbsp;Xun Qiu ,&nbsp;Zhoucheng Wang ,&nbsp;Kai Wang ,&nbsp;Yawen Tan ,&nbsp;Fengqiang Gao ,&nbsp;Marcos Vinicius Perini ,&nbsp;Xiao Xu","doi":"10.1016/j.livres.2024.01.002","DOIUrl":"10.1016/j.livres.2024.01.002","url":null,"abstract":"<div><p>The liver has a strong regenerative capacity that ensures patient recovery after hepatectomy and liver transplantation. The portal system plays a crucial role in the dual blood supply to the liver, making it a significant factor in hepatic function. Several surgical strategies, such as portal vein ligation, associating liver partition and portal vein ligation for staged hepatectomy, and dual vein embolization, have highlighted the portal system's importance in liver regeneration. Following hepatectomy or liver transplantation, the hemodynamic properties of the portal system change dramatically, triggering regeneration via shear stress and the induction of hypoxia. However, excessive portal hyperperfusion can harm the liver and negatively affect patient outcomes. Furthermore, as the importance of the gut–liver axis has gradually been revealed, the effect of metabolites and cytokines from gut microbes carried by portal blood on liver regeneration has been acknowledged. From these perspectives, this review outlines the molecular mechanisms of the portal system's role in liver regeneration and summarizes therapeutic strategies based on the portal system intervention to promote liver regeneration.</p></div>","PeriodicalId":36741,"journal":{"name":"Liver Research","volume":"8 1","pages":"Pages 1-10"},"PeriodicalIF":0.0,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2542568424000023/pdfft?md5=622f9be0188cb2c7281e914cd7c00c48&pid=1-s2.0-S2542568424000023-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139633506","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Viral hepatitis E: Clinical manifestations, treatment, and prevention","authors":"Qiumin Luo ,&nbsp;Jia Chen ,&nbsp;Yeqiong Zhang ,&nbsp;Wenxiong Xu ,&nbsp;Ying Liu ,&nbsp;Chan Xie ,&nbsp;Liang Peng","doi":"10.1016/j.livres.2024.01.001","DOIUrl":"10.1016/j.livres.2024.01.001","url":null,"abstract":"<div><p>Hepatitis E is a globally distributed infection that varies in seroprevalence between developed and developing regions. In the less developed regions of Asia and Africa, a high seropositivity rate has been reported for hepatitis E virus (HEV) antibodies. Although acute hepatitis E is often self-limited and has a favorable prognosis, some populations experience severe manifestations, which may progress to liver failure. Moreover, some immunocompromised patients are at risk of developing chronic HEV infection and cirrhosis. Proactive screening, reducing misdiagnosis, improving patient management, timely antiviral therapy for severe and chronic cases, and vaccination of high-risk groups are important measures to reduce the morbidity of hepatitis E. This review focused on the clinical presentation, management, and prevention of hepatitis E.</p></div>","PeriodicalId":36741,"journal":{"name":"Liver Research","volume":"8 1","pages":"Pages 11-21"},"PeriodicalIF":0.0,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2542568424000011/pdfft?md5=a81de35d4a3a39aa3f885f8dcf39374d&pid=1-s2.0-S2542568424000011-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139391573","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting nuclear receptors for NASH/MASH: From bench to bedside","authors":"Rohit A. Sinha","doi":"10.1016/j.livres.2024.03.002","DOIUrl":"10.1016/j.livres.2024.03.002","url":null,"abstract":"<div><p>The onset of metabolic dysfunction-associated steatohepatitis (MASH) or non-alcoholic steatohepatitis (NASH) represents a tipping point leading to liver injury and subsequent hepatic complications in the natural progression of what is now termed metabolic dysfunction-associated steatotic liver diseases (MASLD), formerly known as non-alcoholic fatty liver disease (NAFLD). With no pharmacological treatment currently available for MASH/NASH, the race is on to develop drugs targeting multiple facets of hepatic metabolism, inflammation, and pro-fibrotic events, which are major drivers of MASH. Nuclear receptors (NRs) regulate genomic transcription upon binding to lipophilic ligands and govern multiple aspects of liver metabolism and inflammation. Ligands of NRs may include hormones, lipids, bile acids, and synthetic ligands, which upon binding to NRs regulate the transcriptional activities of target genes. NR ligands are presently the most promising drug candidates expected to receive approval from the United States Food and Drug Administration as a pharmacological treatment for MASH. This review aims to cover the current understanding of NRs, including nuclear hormone receptors, non-steroid hormone receptors, circadian NRs, and orphan NRs, which are currently undergoing clinical trials for MASH treatment, along with NRs that have shown promising results in preclinical studies.</p></div>","PeriodicalId":36741,"journal":{"name":"Liver Research","volume":"8 1","pages":"Pages 34-45"},"PeriodicalIF":0.0,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2542568424000060/pdfft?md5=29b254d4b61a06006290c45ed5b8e30c&pid=1-s2.0-S2542568424000060-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140279540","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Physical activity and exercise in liver cancer","authors":"Haiyan Chen ,&nbsp;Huimin Zhou ,&nbsp;Bo Wu ,&nbsp;Hanxiao Lu ,&nbsp;Jie Zhang ,&nbsp;Yan Zhang ,&nbsp;Yuanlong Gu ,&nbsp;Guangwen Zhou ,&nbsp;Jie Xiang ,&nbsp;Jun Yang","doi":"10.1016/j.livres.2024.03.001","DOIUrl":"https://doi.org/10.1016/j.livres.2024.03.001","url":null,"abstract":"<div><p>Sarcopenia and physical deconditioning are common complications in patients with liver cancer, which are frequently caused by insufficient physical activity and poor nutritional status, resulting in physical frailty and a significant impact on the patient’s physical fitness. Notably, sarcopenia, frailty, and poor cardiopulmonary endurance have all been linked to higher mortality rates among patients with liver cancer. Exercise intervention significantly improves various health parameters in liver cancer patients, including metabolic syndrome, muscle wasting, cardiorespiratory endurance, health-related quality of life, and reduction in hepatic venous pressure gradient. However, the link between physical exercise and liver cancer is commonly overlooked. In this article, we will examine the impact of exercise on liver cancer and present the most recent evidence on the best types of exercise for various stages of liver cancer. This article also summarizes and discusses the molecular mechanisms that control metabolism and systemic immune function in tumors. In brief, physical exercise should be considered an important intervention in the prevention and treatment of liver cancer and its complications.</p></div>","PeriodicalId":36741,"journal":{"name":"Liver Research","volume":"8 1","pages":"Pages 22-33"},"PeriodicalIF":0.0,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2542568424000059/pdfft?md5=78998b626ea43c8886f4937301389c06&pid=1-s2.0-S2542568424000059-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140296802","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Protective effects of cyclosporine and its analog NIM-811 in a murine model of hepatic ischemia-reperfusion injury","authors":"Joshua Hefler ,&nbsp;Rena Pawlick ,&nbsp;Braulio A. Marfil-Garza ,&nbsp;Aducio Thiesen ,&nbsp;Nerea Cuesta-Gomez ,&nbsp;Sanaz Hatami ,&nbsp;Darren H. Freed ,&nbsp;Constantine Karvellas ,&nbsp;David L. Bigam ,&nbsp;A.M. James Shapiro","doi":"10.1016/j.livres.2024.02.002","DOIUrl":"10.1016/j.livres.2024.02.002","url":null,"abstract":"<div><h3>Background and aim</h3><p>The liver is susceptible to ischemia-reperfusion injury (IRI) during hepatic surgery, when the vessels are compressed to control bleeding, or liver transplantation, when there is an obligate period of ischemia. The hallmark of IRI comprises mitochondrial dysfunction, which generates reactive oxygen species, and cell death through necrosis or apoptosis. Cyclosporine (CsA), which is a well-known immunosuppressive agent that inhibits calcineurin, has the additional effect of inhibiting the mitochondrial permeability transition pore (mPTP), thereby, preventing mitochondrial swelling and injury. NIM-811, which is the nonimmunosuppressive analog of CsA, has a similar effect on the mPTP. In this study, we tested the effect of both agents on mitigating warm hepatic IRI in a murine model.</p></div><div><h3>Materials and methods</h3><p>Before ischemic insult, the mice were administered with intraperitoneal normal saline (control); CsA at 2.5, 10, or 25 mg/kg; or NIM-811 at 10 mg/kg. Thereafter, the mice were subjected to partial warm hepatic ischemia by selective pedicle clamping for 60 min, followed by 6 h of recovery after reperfusion. Serum alanine transaminase (ALT) was measured, and the liver tissue was examined histologically for the presence of apoptosis and the levels of inflammatory cytokines.</p></div><div><h3>Results</h3><p>Compared with the control mice, the mice treated with 10 and 25 mg/kg of CsA and NIM-811 had significantly lower ALT levels (<em>P</em> &lt; 0.001, 0.007, and 0.031, respectively). Moreover, the liver tissue showed reduced histological injury scores after treatment with CsA at 2.5, 10, and 25 mg/kg and NIM-811 (<em>P</em> = 0.041, &lt;0.001, 0.003, and 0.043, respectively) and significant decrease in apoptosis after treatment with CsA at all doses (<em>P</em> = 0.012, 0.007, and &lt;0.001, respectively). Levels of the pro-inflammatory cytokines, particularly interleukin (IL)-1β, IL-2, IL-4, IL-10, and keratinocyte chemoattractant/human growth-regulated oncogene significantly decreased in the mice treated with the highest dose of CsA (25 mg/kg) than those in the control mice.</p></div><div><h3>Conclusions</h3><p>Premedication with CsA or NIM-811 mitigated hepatic IRI in mice, as evidenced by the decreased ALT and reduced injury on histology. These results have potential implications on mitigating IRI during liver transplantation and resection.</p></div>","PeriodicalId":36741,"journal":{"name":"Liver Research","volume":"8 1","pages":"Pages 46-53"},"PeriodicalIF":0.0,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2542568424000047/pdfft?md5=7881619b3b18ecd5425d82119123b8f5&pid=1-s2.0-S2542568424000047-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140085444","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Should they wait? Two children under 3 years old infected by HCV 1b successfully treated by ledipasvir/sofosbuvir: A report of two cases","authors":"Mingna Li ,&nbsp;Kuerbannisa Wulayin ,&nbsp;Shutao Lin ,&nbsp;Chao Wu ,&nbsp;Lubiao Chen","doi":"10.1016/j.livres.2023.11.001","DOIUrl":"10.1016/j.livres.2023.11.001","url":null,"abstract":"<div><div>Although direct-acting antivirals (DAAs) have notably increased the sustained virological response (SVR) rates in hepatitis C virus (HCV)-infected adolescent patients, the efficacy and safety for young children under 3 years old remain unclear. Currently, no guidelines recommend DAA therapy for this situation worldwide. Furthermore, the China National Medical Products Administration has not approved any DAA for treating children below 12 years old. Here, we described the characteristics of two children approximately 2 years old, who were infected by HCV genotype 1b and had significant clinical symptoms. Both received 12 weeks of ledipasvir/sofosbuvir (Case 1: 45.00 mg/200 mg per day, weight 17 kg; Case 2: 33.75 mg/150 mg per day, weight 12 kg). They achieved SVR at 12 weeks after treatment completion without obvious treatment-related adverse effects. Therefore, the safety and benefits of ledipasvir/sofosbuvir treatment in children under 3 years old seem to be confirmed. Our findings require further evaluation.</div></div>","PeriodicalId":36741,"journal":{"name":"Liver Research","volume":"7 4","pages":"Pages 361-364"},"PeriodicalIF":0.0,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135668997","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hepatocellular carcinoma recurrence: Predictors and management","authors":"Walaa Abdelhamed ,&nbsp;Mohamed El-Kassas","doi":"10.1016/j.livres.2023.11.004","DOIUrl":"10.1016/j.livres.2023.11.004","url":null,"abstract":"<div><div>Hepatocellular carcinoma (HCC), the sixth most common cancer globally, is associated with high mortality rates and more than 830,000 annual deaths. Despite advances in the available management options including surgical resection and local ablative therapies, recurrence rates after the initial treatment exceed 50%, even among patients who have undergone curative-intent therapy. Moreover, postsurgical HCC recurrence occurs in about 70% of cases five years postoperatively. The management of recurrent HCC remains undefined. This review discusses different predictors for HCC recurrence after each treatment modality and different approaches available to stratify these patients. More specific guidelines for managing HCC recurrence and strict surveillance protocols for such recurrence after initial HCC management are needed.</div></div>","PeriodicalId":36741,"journal":{"name":"Liver Research","volume":"7 4","pages":"Pages 321-332"},"PeriodicalIF":0.0,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139304518","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The contributions of bacteria metabolites to the development of hepatic encephalopathy","authors":"Miranda Claire Gilbert,&nbsp;Tahereh Setayesh,&nbsp;Yu-Jui Yvonne Wan","doi":"10.1016/j.livres.2022.11.005","DOIUrl":"10.1016/j.livres.2022.11.005","url":null,"abstract":"<div><div>Over 20% of mortality during acute liver failure is associated with the development of hepatic encephalopathy (HE). Thus, HE is a complication of acute liver failure with a broad spectrum of neuropsychiatric abnormalities ranging from subclinical alterations to coma. HE is caused by the diversion of portal blood into systemic circulation through portosystemic collateral vessels. Thus, the brain is exposed to intestinal-derived toxic substances. Moreover, the strategies to prevent advancement and improve the prognosis of such a liver-brain disease rely on intestinal microbial modulation. This is supported by the findings that antibiotics such as rifaximin and laxative lactulose can alleviate hepatic cirrhosis and/or prevent HE. Together, the significance of the gut-liver-brain axis in human health warrants attention. This review paper focuses on the roles of bacteria metabolites, mainly ammonia and bile acids (BAs) as well as BA receptors in HE. The literature search conducted for this review included searches for phrases such as BA receptors, BAs, ammonia, farnesoid X receptor (FXR), G protein-coupled bile acid receptor 1 (GPBAR1 or TGR5), sphingosine-1-phosphate receptor 2 (S1PR2), and cirrhosis in conjunction with the phrase hepatic encephalopathy and portosystemic encephalopathy. PubMed, as well as Google Scholar, was the search engines used to find relevant publications.</div></div>","PeriodicalId":36741,"journal":{"name":"Liver Research","volume":"7 4","pages":"Pages 296-303"},"PeriodicalIF":0.0,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10786625/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47665658","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dietary pattern and hepatic lipid metabolism","authors":"Peng Zou,&nbsp;Lin Wang","doi":"10.1016/j.livres.2023.11.006","DOIUrl":"10.1016/j.livres.2023.11.006","url":null,"abstract":"<div><div>The liver is the leading site for lipid metabolism, involving not only fatty acid beta-oxidation but also <em>de novo</em> synthesis of endogenous triglycerides and ketogenesis. The liver maintains systemic lipid homeostasis by regulating lipid synthesis, catabolism, and transportation. Dysregulation of hepatic lipid metabolism precipitates disorders, such as non-alcoholic fatty liver disease (NAFLD), affecting the whole body. Thus, comprehending and studying hepatic lipid metabolism is crucial for preventing and treating metabolic liver diseases. Traditionally, researchers have investigated the impact of a single nutrient on hepatic lipid metabolism. However, real-life dietary patterns encompass diverse nutrients rather than single components. In recent years, there have been increased studies and notable progress regarding the effects of distinct dietary patterns on hepatic lipid metabolism. This review summarizes the influence of diverse dietary patterns on hepatic lipid metabolism, elucidating underlying molecular mechanisms and appraising the therapeutic potential of dietary patterns in managing hepatic steatosis.</div></div>","PeriodicalId":36741,"journal":{"name":"Liver Research","volume":"7 4","pages":"Pages 275-284"},"PeriodicalIF":0.0,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139296110","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}