Journal of Clinical and Translational Hepatology最新文献

{"title":"Anti-hepatitis B Virus Treatment with Tenofovir Amibufenamide Has No Impact on Blood Lipids: A Real-world, Prospective, 48-week Follow-up Study.","authors":"Yue Chen, Wenkang Gao, Huikuan Chu, Afnan Ahmed Mohamed Al-Asbahi, Shengqi Yan, Hang Yuan, Jiake Che, Zilu Cheng, Zexuan Li, Jin Ye, Rong Lin, Xiaohua Hou, Fan Du, Ling Yang","doi":"10.14218/JCTH.2024.00237","DOIUrl":"10.14218/JCTH.2024.00237","url":null,"abstract":"<p><strong>Background and aims: </strong>The effect of tenofovir amibufenamide (TMF) on blood lipid profiles in patients with chronic hepatitis B (CHB) remains unclear. This study aimed to explore whether TMF affects blood lipids during 48 weeks in patients with CHB.</p><p><strong>Methods: </strong>A total of 91 patients with CHB undergoing TMF treatment for 48 weeks were divided into two groups: Lipid Normal (n = 42) and Lipid Abnormal (n = 49), based on baseline blood lipid levels. Lipid indices, virological responses, and biochemical indicators were compared between the two groups. Clinical observations were further verified through <i>in vitro</i> experiments.</p><p><strong>Results: </strong>After an average follow-up of 373 ± 121 days, lipid indices in all 91 patients had not significantly changed compared with baseline (total cholesterol: 4.67 vs. 4.69 mmol/L, <i>P</i> = 0.2499; triglycerides: 1.08 vs. 1.04 mmol/L, <i>P</i> = 0.4457; high-density lipoprotein cholesterol: 1.25 vs. 1.25 mmol/L, <i>P</i> = 0.3063; low-density lipoprotein cholesterol: 3.03 vs. 3.02 mmol/L, <i>P</i> = 0.5765). Subgroup comparisons showed lipid indices remained stable. Among treatment-naïve patients (n = 82), complete viral suppression rates were 23.2%, 59.8%, 70.7%, and 86.6% at four, 12, 24, and 48 weeks, respectively. Cellular experiments revealed that TMF did not promote lipid metabolism in primary hepatocytes and AML12 cells.</p><p><strong>Conclusions: </strong>Regardless of baseline blood lipid characteristics, 48 weeks of antiviral treatment with TMF in patients with CHB had no significant lipid-raising effect.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"12 12","pages":"997-1008"},"PeriodicalIF":3.1,"publicationDate":"2024-12-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11622202/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142794893","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":"Advanced Liver Fibrosis Predicts Liver Outcomes in Biopsy-proven Metabolic Dysfunction-associated Steatotic Liver Disease: A U.S.-based Single-center Retrospective Cohort Study.","authors":"Robert Lam, Dhanpat Jain, Yanhong Deng, Eesha Acharya, Joseph K Lim","doi":"10.14218/JCTH.2024.00189","DOIUrl":"10.14218/JCTH.2024.00189","url":null,"abstract":"<p><strong>Background and aims: </strong>Data regarding risk factors and long-term outcomes of U.S. patients with biopsy-proven metabolic dysfunction-associated steatotic liver disease (MASLD) are limited. This study aimed to investigate the role of clinical and histologic risk factors on long-term outcomes in patients with MASLD.</p><p><strong>Methods: </strong>A retrospective cohort study of 451 adults with biopsy-proven MASLD was conducted at a U.S. academic hospital from 2012 to 2020. An experienced pathologist evaluated the index liver biopsy. Patients with a prior liver transplant or alternative etiologies of chronic liver disease were excluded. The duration of the risk exposure was determined from the date of the index liver biopsy to an outcome event or the last follow-up examination. Outcome events of interest included incident liver-related events, liver decompensation, and all-cause mortality.</p><p><strong>Results: </strong>In the final cohort of 406 patients followed for a median of 3.7 years (interquartile range: 4.8 years), 35 patients died, 41 developed hepatic decompensation, and 70 experienced a liver-related event. Among histologic risk factors, stage 3 (adjusted Hazard ratio (aHR) 2.68, 95% confidence interval (CI) 1.18-6.11) and stage 4 (aHR 6.96, 95% CI 3.55-13.64) fibrosis were associated with incident liver-related events compared to stage 0-1 fibrosis. Stage 4 (aHR 8.46, 95% CI 3.26-21.99) fibrosis alone was associated with incident liver decompensation events compared to stage 0-1 fibrosis. Among clinical risk factors, hypertension (aHR 2.58, 95% CI 1.05-6.34) was associated with incident liver decompensation.</p><p><strong>Conclusions: </strong>In a U.S. single-center cohort of patients with biopsy-proven MASLD, advanced fibrosis was the primary risk factor for incident liver decompensation and liver-related events.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"12 12","pages":"988-996"},"PeriodicalIF":3.1,"publicationDate":"2024-12-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11622200/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142794892","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":"Prolonged Direct Hyperbilirubinemia Following Acute Hepatitis: When Not to Worry?","authors":"Danzhu Zhao, George Y Wu","doi":"10.14218/JCTH.2024.00265","DOIUrl":"10.14218/JCTH.2024.00265","url":null,"abstract":"","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"12 12","pages":"985-987"},"PeriodicalIF":3.1,"publicationDate":"2024-12-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11622201/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142794488","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":"Guideline for the Prevention and Treatment of Metabolic Dysfunction-associated Fatty Liver Disease (Version 2024).","authors":"Jian-Gao Fan, Xiao-Yuan Xu, Rui-Xu Yang, Yue-Min Nan, Lai Wei, Ji-Dong Jia, Hui Zhuang, Jun-Ping Shi, Xiao-Ying Li, Chao Sun, Jie Li, Vincent Wai-Sun Wong, Zhong-Ping Duan","doi":"10.14218/JCTH.2024.00311","DOIUrl":"10.14218/JCTH.2024.00311","url":null,"abstract":"<p><p>With the rising epidemic of obesity, metabolic syndrome, and type 2 diabetes mellitus in China, metabolic dysfunction-associated non-alcoholic fatty liver disease has become the most prevalent chronic liver disease. This condition frequently occurs in Chinese patients with alcoholic liver disease and chronic hepatitis B. To address the impending public health crisis of non-alcoholic fatty liver disease and its underlying metabolic issues, the Chinese Society of Hepatology and the Chinese Medical Association convened a panel of clinical experts to revise and update the \"Guideline of prevention and treatment of non-alcoholic fatty liver disease (2018, China)\". The new edition, titled \"Guideline for the prevention and treatment of metabolic dysfunction-associated fatty liver disease (Version 2024)\", offers comprehensive recommendations on key clinical issues, including screening and monitoring, diagnosis and evaluation, treatment, and follow-up for metabolic dysfunction-associated fatty liver disease and metabolic dysfunction-associated steatotic liver disease. Metabolic dysfunction-associated fatty liver disease is now the preferred English term and is used interchangeably with metabolic dysfunction-associated steatotic liver disease. Additionally, the guideline emphasizes the importance of multidisciplinary collaboration among hepatologists and other specialists to manage cardiometabolic disorders and liver disease effectively.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"12 11","pages":"955-974"},"PeriodicalIF":3.1,"publicationDate":"2024-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11557364/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142621258","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":"The Multifaceted Role of Bilirubin in Liver Disease: A Literature Review.","authors":"Mariana M Ramírez-Mejía, Stephany M Castillo-Castañeda, Shreya C Pal, Xingshun Qi, Nahum Méndez-Sánchez","doi":"10.14218/JCTH.2024.00156","DOIUrl":"10.14218/JCTH.2024.00156","url":null,"abstract":"<p><p>Bilirubin, the primary breakdown product of hemoproteins, particularly hemoglobin, plays a key role in the diagnosis, prognosis, and monitoring of liver diseases. In acute liver diseases, such as acute liver failure, drug-induced liver injury, and viral hepatitis, bilirubin serves as a biomarker reflecting the extent of hepatocyte loss and liver damage. Chronic liver diseases, including alcohol-related liver disease, chronic hepatitis C virus infection, metabolic dysfunction-associated fatty liver disease, and autoimmune liver diseases, are marked by persistent liver injury and inflammation. Bilirubin levels in chronic liver diseases provide insight into liver function, disease severity, and prognosis. As a versatile biomarker, bilirubin offers valuable information on the pathophysiology of liver diseases and aids in guiding clinical decision-making regarding the treatment of liver diseases and their complications. This review aimed to explore the multifunctional role of bilirubin in liver diseases by analyzing its biological functions beyond its role as a biomarker of liver damage.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"12 11","pages":"939-948"},"PeriodicalIF":3.1,"publicationDate":"2024-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11557368/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142621276","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":"Mouse Models for the Study of Liver Fibrosis Regression <i>In Vivo</i> and <i>Ex Vivo</i>.","authors":"Milena Schönke, Patrick C N Rensen","doi":"10.14218/JCTH.2024.00212","DOIUrl":"10.14218/JCTH.2024.00212","url":null,"abstract":"<p><p>This review discussed experimental mouse models used in the pre-clinical study of liver fibrosis regression, a pivotal process in preventing the progression of metabolic dysfunction-associated steatohepatitis to irreversible liver cirrhosis. These models provide a valuable resource for understanding the cellular and molecular processes underlying fibrosis regression in different contexts. The primary focus of this review is on the most commonly used models with diet- or hepatotoxin-induced fibrosis, but it also touches upon genetic models and mouse models with biliary atresia or parasite-induced fibrosis. In addition to emphasizing <i>in vivo</i> models, we briefly summarized current <i>in vitro</i> approaches designed for studying fibrosis regression and provided an outlook on evolving methodologies that aim to refine and reduce the number of experimental animals needed for these studies. Together, these models contribute significantly to unraveling the underlying mechanisms of liver fibrosis regression and offer insights into potential therapeutic interventions. By presenting a comprehensive overview of these models and highlighting their respective advantages and limitations, this review serves as a roadmap for future research.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"12 11","pages":"930-938"},"PeriodicalIF":3.1,"publicationDate":"2024-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11557367/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142621271","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":"Surveillance Imaging and GAAD/GALAD Scores for Detection of Hepatocellular Carcinoma in Patients with Chronic Hepatitis.","authors":"Chung-Feng Huang, Konstantin Kroeniger, Chih-Wen Wang, Tyng-Yuan Jang, Ming-Lun Yeh, Po-Cheng Liang, Yu-Ju Wei, Po-Yao Hsu, Ching-I Huang, Ming-Yen Hsieh, Yi-Hung Lin, Jee-Fu Huang, Chia-Yen Dai, Wan-Long Chuang, Ashish Sharma, Ming-Lung Yu","doi":"10.14218/JCTH.2024.00172","DOIUrl":"10.14218/JCTH.2024.00172","url":null,"abstract":"<p><strong>Background and aims: </strong>Early detection of hepatocellular carcinoma (HCC) is crucial for improving survival in patients with chronic hepatitis. The GALAD algorithm combines gender (biological sex), age, α-fetoprotein (AFP), <i>Lens culinaris</i> agglutinin-reactive fraction of AFP (AFP-L3), and protein induced by vitamin K absence or antagonist-II (PIVKA-II) for HCC detection. Similarly, the GAAD algorithm incorporates gender (biological sex), age, AFP, and PIVKA-II. This study aimed to assess the clinical utility of AFP-L3 in the GALAD algorithm and its potential synergies with ultrasound. We compared the clinical performance of GALAD with GAAD; AFP; AFP-L3; and PIVKA-II, with or without ultrasound, in Taiwanese adults.</p><p><strong>Methods: </strong>A total of 439 serum samples were analyzed using a Cobas^® e 601 analyzer (healthy controls, n = 200; chronic liver disease controls, n = 177; HCC cases, n = 62). Performance was assessed through receiver operating characteristic curve analyses to calculate the area under the curve.</p><p><strong>Results: </strong>The area under the curve for differentiating early-stage HCC from patients with chronic liver disease was optimal for PIVKA-II (84.9%), GAAD (79.8%), and GALAD (79.4%), with slightly improved performance for detecting all-stage HCC. Clinical performance was unaffected by disease stage or etiology. Sensitivity for early-stage HCC was highest for GAAD (57.6%) and GALAD (57.6%). Sensitivity for each strategy was further enhanced when combined with ultrasound, regardless of disease stage or etiology (<i>P</i> < 0.01).</p><p><strong>Conclusions: </strong>These findings indicate that the role of AFP-L3 in the GALAD algorithm is minimal, supporting the use of GAAD for HCC detection. A combination of GAAD, GALAD, or PIVKA-II with ultrasound may improve diagnostic efficiency compared with recommended strategies.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"12 11","pages":"907-916"},"PeriodicalIF":3.1,"publicationDate":"2024-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11557369/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142621273","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":"Chinese Clinical Practice Guidelines for the Prevention and Treatment of Mother-to-child Transmission of Hepatitis B Virus (Version 2024).","authors":"Jinfeng Liu, Qinglei Zeng, Fanpu Ji, Hong Ren, Wenhong Zhang, Lanjuan Li, Yingren Zhao","doi":"10.14218/JCTH.2024.00258","DOIUrl":"10.14218/JCTH.2024.00258","url":null,"abstract":"<p><p>The <i>Chinese Clinical Practice Guidelines for the Prevention and Treatment of Mother-to-child Transmission of Hepatitis B Virus</i>, developed by the Chinese Society of Infectious Diseases of the Chinese Medical Association in 2019, serves as a valuable reference for standardizing the prevention of mother-to-child transmission in China. As new evidence continues to emerge, it is essential to update these guidelines regularly to optimize clinical practice and research. To this end, the Infectious Disease Physician Branch of the Chinese Medical Doctor Association and the Chinese Society of Infectious Diseases of the Chinese Medical Association, in collaboration with multidisciplinary experts, have updated the guidelines based on the latest domestic and international research advancements and clinical practices, providing up-to-date guidance for clinicians and maternal and child healthcare workers.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"12 11","pages":"975-983"},"PeriodicalIF":3.1,"publicationDate":"2024-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11557363/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142621185","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":"A Case of Severe Cholestatic Hepatitis Induced by a Novel Dual Agonist of Glucagon-like Peptide-1 and Glucose-dependent Insulinotropic Polypeptide Receptors.","authors":"Junmin Jiang, Meifeng Shi, Shuduo Wu, Minling Cao","doi":"10.14218/JCTH.2024.00287","DOIUrl":"10.14218/JCTH.2024.00287","url":null,"abstract":"<p><p>Glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) receptor agonists are increasingly used in the management of type 2 diabetes mellitus and obesity due to their ability to stimulate insulin secretion, delay gastric emptying, and suppress appetite. The combination of GLP-1 and GIP agonists improves glycemic control and promotes weight loss. However, the introduction of these novel therapies has raised safety concerns, including the risk of cholestatic hepatitis. We report a case of a patient with obesity who was prescribed a GLP-1/GIP dual-receptor agonist as part of his treatment regimen. Importantly, both before the initiation of this therapy and during the course of treatment, the patient was not taking any other medications. Shortly after receiving four doses of the therapy, the patient developed symptoms of severe cholestatic hepatitis, including jaundice and elevated liver enzyme levels. During hospitalization, no alternative causes for the condition were identified, and a liver biopsy confirmed the diagnosis of drug-induced cholestatic hepatitis. This is the first recorded case of cholestatic hepatitis induced by a GLP-1/GIP dual agonist, and it aimed to raise global awareness of this potential side effect.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"12 11","pages":"949-954"},"PeriodicalIF":3.1,"publicationDate":"2024-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11557366/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142621240","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":"GPX4 Promoter Hypermethylation Induced by Ischemia/Reperfusion Injury Regulates Hepatocytic Ferroptosis.","authors":"Chen Bai, Peilun Xiao, Yuting Chen, Fangfang Chu, Yue Jiao, Jiaqi Fan, Yuexia Zhang, Jiao Liu, Jiying Jiang, Shuna Yu","doi":"10.14218/JCTH.2024.00135","DOIUrl":"10.14218/JCTH.2024.00135","url":null,"abstract":"<p><strong>Background and aims: </strong>Glutathione peroxidase 4 (GPX4) is a key factor in ferroptosis, which is involved in ischemia-reperfusion injury. However, little is known about its role in hepatic ischemia-reperfusion injury (HIRI). This study aimed to investigate the role of GPX4 methylation in ferroptosis during HIRI.</p><p><strong>Methods: </strong>For the <i>in vitro</i> experiments, an oxygen and glucose deprivation cell model was established. For the <i>in vivo</i> experiments, an ischemia-reperfusion model was created by subjecting mice to simulated HIRI. Ferroptosis occurrence, <i>GPX4</i> promoter methylation, and global methylation levels were then assessed.</p><p><strong>Results: </strong>Ferroptosis was observed in oxygen and glucose deprivation, characterized by a significant decrease in cellular viability (<i>P</i> < 0.05), an increase in lipid peroxidation (<i>P</i> < 0.01), iron overload (<i>P</i> < 0.05), and down-regulation of GPX4 (<i>P</i> < 0.05). This ferroptosis was exacerbated by GPX4 knockdown (<i>P</i> < 0.01) and mitigated by exogenous glutathione (<i>P</i> < 0.01). Similarly, ferroptosis was evident in mice subjected to HIRI, with a down-regulation of GPX4 mRNA and protein expression (all <i>P</i> < 0.01), and an upregulation of acyl-CoA synthetase long-chain family member 4 mRNA and protein (all <i>P</i> < 0.01), as well as prostaglandin-endoperoxide synthase 2 mRNA and protein expression (all <i>P</i> < 0.05). Methylation levels increased, evidenced by upregulation of DNA methylation transferase expression (<i>P</i> < 0.05) and down-regulation of Ten-eleven translocation family demethylases (<i>P</i> < 0.01), along with an upregulation of <i>GPX4</i> promoter methylation.</p><p><strong>Conclusions: </strong>Ferroptosis may be the primary mode of cell death in hepatocytes following ischemia-reperfusion injury. The methylation of the <i>GPX4</i> promoter and elevated levels of global hepatic methylation are involved in the regulation of ferroptosis.</p>","PeriodicalId":15484,"journal":{"name":"Journal of Clinical and Translational Hepatology","volume":"12 11","pages":"917-929"},"PeriodicalIF":3.1,"publicationDate":"2024-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11557362/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142621257","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}