{"title":"Rifaximin and sarcopenia in cirrhosis: Commentary on a promising but complex relationship.","authors":"Mohamed El-Kassas, Khalid AlNaamani","doi":"10.4254/wjh.v17.i9.108951","DOIUrl":"10.4254/wjh.v17.i9.108951","url":null,"abstract":"<p><p>We commend Worland <i>et al</i> for their work associating rifaximin-α use with improved muscle mass in individuals with liver cirrhosis. This observation adds momentum to the evolving gut-liver-muscle axis hypothesis. However, the retrospective design and lack of functional outcomes invite caution in interpretation. Mechanistically, rifaximin may exert benefit beyond ammonia reduction through modulation of systemic inflammation, tumor necrosis factor alpha suppression, and restoration of myocyte integrity. Additionally, concerns about long-term antimicrobial resistance must be acknowledged. Overall, this study represents a valuable first step, but its implications require validation in future, prospective, mechanistically informed clinical trials.</p>","PeriodicalId":23687,"journal":{"name":"World Journal of Hepatology","volume":"17 9","pages":"108951"},"PeriodicalIF":2.5,"publicationDate":"2025-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12476699/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145192909","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":"Extracellular vesicles in metabolic dysfunction-associated steatotic liver disease: From intercellular signaling to clinical translation.","authors":"Bootsakorn Boonkaew, Denita Charoenthanakitkul, Nuchanart Suntornnont, Chaiyaboot Ariyachet, Pisit Tangkijvanich","doi":"10.4254/wjh.v17.i9.108259","DOIUrl":"10.4254/wjh.v17.i9.108259","url":null,"abstract":"<p><p>Metabolic dysfunction-associated steatotic liver disease (MASLD) poses a substantial global health burden, progressing from simple steatosis to metabolic dysfunction-associated steatohepatitis and cirrhosis. A deeper understanding of the underlying mechanisms and associated complications is crucial for developing effective therapies. Extracellular vesicles (EVs), nanoscale membrane-enclosed particles carrying bioactive cargoes such as proteins and noncoding RNAs, including microRNAs and long noncoding RNAs, play crucial roles in intercellular communication and have emerged as critical mediators of MASLD pathogenesis. This article details the current understanding of the function of EVs in MASLD progression, emphasizing specific cell-derived EVs implicated in disease development. We elucidate how EVs facilitate intercellular communication and influence key pathological processes, including lipotoxicity, inflammation, and fibrosis. Furthermore, we examine the involvement of EVs in MASLD-associated complications and evaluate their potential as minimally invasive tools for disease diagnosis, staging, and prognosis. We also explore EV-based therapeutic strategies, encompassing preclinical studies, while acknowledging current challenges and future opportunities. Finally, we discuss emerging research trends, the potential for personalized medicine, and areas necessitating further investigation, particularly the utilization of EVs as therapeutic targets or delivery vehicles. This review underscores the pivotal role of EVs in MASLD, providing insights into their translational potential for improved patient outcomes.</p>","PeriodicalId":23687,"journal":{"name":"World Journal of Hepatology","volume":"17 9","pages":"108259"},"PeriodicalIF":2.5,"publicationDate":"2025-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12476723/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145193158","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":"Rapamycin nanoparticles suppress autoreactive lymphocytes and reduce anti-mitochondrial antibodies in primary biliary cholangitis: Mechanisms and implications.","authors":"Payal Bhatnagar, Nabil Eid","doi":"10.4254/wjh.v17.i9.110674","DOIUrl":"10.4254/wjh.v17.i9.110674","url":null,"abstract":"<p><p>Primary biliary cholangitis (PBC) is an autoimmune disease characterized by the selective destruction of intrahepatic small bile ducts, primarily by infiltrating lymphocytes, and has limited therapeutic options. A growing body of evidence suggests that nanoparticles encapsulating rapamycin (ImmTOR) can suppress autoreactive lymphocytes and reduce inflammatory cytokine levels in various autoimmune diseases. In a recent study, Yang <i>et al</i> investigated the therapeutic effects of ImmTOR in a mouse model of PBC. ImmTOR treatment reduced the expression and number of CD4+ T cells, CD8+ T cells, and B cells isolated from the liver and spleen, improved liver inflammation and enzyme levels, and was associated with a concomitant decrease in anti-mitochondrial antibody levels. In this editorial, we highlight the significance of these findings, focusing on the potential mechanisms by which ImmTOR suppresses hepatic autoreactive T cells and reduces anti-mitochondrial antibody levels, ultimately improving liver pathology, through pathways such as mammalian target of rapamycin inhibition and autophagy restoration. We also offer a perspective on future research directions for PBC in both animal models and <i>in vitro</i> studies.</p>","PeriodicalId":23687,"journal":{"name":"World Journal of Hepatology","volume":"17 9","pages":"110674"},"PeriodicalIF":2.5,"publicationDate":"2025-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12476714/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145192964","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}
Lin Wang, Han Liang, Chen Wang, Meng-Yu Liang, Qing-Lei Zeng, Peng-Fei Zhu, Jun Lv
{"title":"Functional cure in an occult hepatitis B virus infection patient on sequential therapy: A case report.","authors":"Lin Wang, Han Liang, Chen Wang, Meng-Yu Liang, Qing-Lei Zeng, Peng-Fei Zhu, Jun Lv","doi":"10.4254/wjh.v17.i9.109340","DOIUrl":"10.4254/wjh.v17.i9.109340","url":null,"abstract":"<p><strong>Background: </strong>Occult hepatitis B virus infection (OBI) is defined by the detection of replication-competent hepatitis B virus (HBV) DNA in the liver and/or blood despite the absence of detectable hepatitis B surface antigen (HBsAg) using conventional serological assays. Although OBI has been well-documented in individuals with resolved HBV infection or those receiving immunosuppressive therapy, reports of its occurrence during sequential antiviral treatment remain scarce. This report describes a case of chronic hepatitis B (CHB) transitioning through OBI during sequential combination therapy before ultimately achieving a functional cure. This case provides new insights into the emergence of OBI as a transitional phase during CHB treatment and emphasizes the importance of monitoring its clinical significance.</p><p><strong>Case summary: </strong>A 33-year-old Chinese male was diagnosed with HBV infection in 2001. The patient first presented in 2012 with abnormal liver function tests and received initial treatment with conventional interferon therapy, which failed to achieve a virological response. Antiviral therapy was subsequently switched to entecavir monotherapy. By August 2019, the patient exhibited an HBsAg level of 29.93 IU/mL with undetectable HBV DNA (< 25 IU/mL). At this point, combination therapy with entecavir and pegylated interferon α (PEG-IFN α) was initiated. Remarkably, while HBsAg declined to 0.42 IU/mL by April 2020, a paradoxical HBV DNA rebound to 173 IU/mL was observed. The regimen was consequently modified to tenofovir alafenamide and PEG-IFN α. By October 2020, the patient achieved HBsAg seroconversion (HBsAg 0.01 IU/mL, hepatitis B surface antibody 52.18 mIU/mL) for the first time, while maintaining low-level viremia (37 IU/mL), consistent with transition to OBI. The patient was then switched to PEG-IFN α monotherapy. In November 2021, he discontinued PEG-IFN α therapy, and one month later, both HBV DNA (< 10 IU/mL) and HBsAg (< 0.05 IU/mL) were negative. This response has been sustained through follow-up.</p><p><strong>Conclusion: </strong>This case study illustrates the efficacy of sequential combination therapy in achieving functional cure in CHB patients, including those with a prolonged infection history. It highlights OBI as a transitional yet underrecognized phase during sequential antiviral therapy. While the patient ultimately achieved functional cure, the transient persistence of HBV DNA despite HBsAg clearance suggests the need for continued monitoring. This case provides new insights into OBI development during treatment and underscores the importance of further research into its long-term implications.</p>","PeriodicalId":23687,"journal":{"name":"World Journal of Hepatology","volume":"17 9","pages":"109340"},"PeriodicalIF":2.5,"publicationDate":"2025-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12476752/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145193120","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}
Matheus Henrique Gonçalves de Souza, Pedro Miguel Mattos Nogueira, Cristiane Alves Villela-Nogueira
{"title":"Metabolic dysfunction-associated steatotic liver disease and diabetes: Together against the heart.","authors":"Matheus Henrique Gonçalves de Souza, Pedro Miguel Mattos Nogueira, Cristiane Alves Villela-Nogueira","doi":"10.4254/wjh.v17.i9.109737","DOIUrl":"10.4254/wjh.v17.i9.109737","url":null,"abstract":"<p><p>Cardiovascular events are the main cause of mortality in individuals with type 2 diabetes mellitus (T2DM) and also in those with metabolic dysfunction-associated steatotic liver disease (MASLD). In this editorial, we comment on the results of a meta-analysis published by Shetty <i>et al</i> that shows an addictive risk for cardiovascular events when both pathologies are together. Patients with MASLD and T2DM have the worst prognosis related to liver disease since they have a higher risk for metabolic dysfunction-associated steatohepatitis, disease progression, and hepatocarcinoma. The meta-analysis included 370013 participants and showed that, although with high heterogeneity, there is a higher prevalence of cardiovascular events in patients with T2DM when MASLD is diagnosed compared to those without MASLD. Hence, MASLD and T2DM may have a new interplay regarding cardiovascular outcomes in addition to the already known liver-related outcomes.</p>","PeriodicalId":23687,"journal":{"name":"World Journal of Hepatology","volume":"17 9","pages":"109737"},"PeriodicalIF":2.5,"publicationDate":"2025-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12476785/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145193129","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":"Toxins to treatments: Impact of environmental pollutants, gut microbiota, and natural compounds on non-alcoholic fatty liver disease progression.","authors":"Tanvi Sharma, Naveen Kaushal, Roobee Garla","doi":"10.4254/wjh.v17.i8.108772","DOIUrl":"10.4254/wjh.v17.i8.108772","url":null,"abstract":"<p><p>Non-alcoholic fatty liver disease (NAFLD) is the fastest-growing global contributor to the disease burden associated with the consequences of chronic liver disease, including cirrhosis and liver cancer. It is projected that more than fifty percent of the adult population, including women, smokers, and individuals without metabolic syndrome, will have NAFLD by 2040. Various mechanisms linking the gut microbiome to NAFLD and the consequent fibrosis have been discerned, which suggest the dysbiosis-induced impairment of gut endothelial barrier function, leading to hepatic inflammation through the translocation of bacterial components. NAFLD is progressively associated with environmental variables, especially exposure to heavy metals that impair liver metabolism, produce oxidative stress, and exacerbate inflammation, hence accelerating its progression. These toxicants also modify the composition of gut microbiota, hence intensifying liver damage. Comprehending the processes by which heavy metals contribute to NAFLD is essential for formulating tailored therapies. This review examines strategies to alleviate liver toxicity caused by heavy metals, including chelation therapy, dietary modifications (antioxidants and hepatoprotective nutrients), gut microbiome modulation <i>via</i> probiotics and postbiotics like short-chain fatty acids to restore intestinal barrier function and use of essential minerals like selenium, with potent antioxidant characteristics. Employing these measures may offer an integrated approach for addressing NAFLD in individuals subjected to heavy metal poisoning.</p>","PeriodicalId":23687,"journal":{"name":"World Journal of Hepatology","volume":"17 8","pages":"108772"},"PeriodicalIF":2.5,"publicationDate":"2025-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12400403/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144993379","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}
Xiao-Xin Gao, Xin-Xin Xu, Peng Chen, Tian-Xiao He, Cheng-Zhou Du, Qian Zhou, Guang-Fu Zhou, Xiao-Wei Guo, Jun-Rui Peng, Hong-Tao Li
{"title":"Rare complete replacement-type left hepatic artery originating from the left gastric artery: A case report.","authors":"Xiao-Xin Gao, Xin-Xin Xu, Peng Chen, Tian-Xiao He, Cheng-Zhou Du, Qian Zhou, Guang-Fu Zhou, Xiao-Wei Guo, Jun-Rui Peng, Hong-Tao Li","doi":"10.4254/wjh.v17.i8.110413","DOIUrl":"10.4254/wjh.v17.i8.110413","url":null,"abstract":"<p><strong>Background: </strong>A complete replacement left hepatic artery (LHA) solely originating from the left gastric artery (LGA), with no supply from the hepatic artery proper, is exceptionally rare. This variant places entire left lobe perfusion on the LGA. Literature review confirms no prior reports of such an isolated LHA replacement pattern in surgical/radiological publications. Unrecognized, this anatomy carries significant intraoperative injury risk during hepatobiliary/ upper gastrointestinal surgery.</p><p><strong>Case summary: </strong>A 62-year-old man underwent laparoscopic radical gastrectomy with D2 Lymphadenectomy for gastric cancer. During dissection of the hepatogastric ligament, an unexpected vascular anatomy was encountered: The LHA originated exclusively from the LGA, with no conventional branch from the hepatic artery proper. Recognizing this variant artery was essential for left liver perfusion, the LGA was ligated proximally near its celiac origin while meticulously preserving blood flow through the anomalous LHA. The gastrectomy and reconstruction were completed without complication. Postoperative recovery was smooth, with serial liver function tests remaining normal, confirming preserved hepatic arterial supply.</p><p><strong>Conclusion: </strong>Preoperative mapping detected a critical aberrant left hepatic artery; its preservation prevented liver ischemia, ensured safety.</p>","PeriodicalId":23687,"journal":{"name":"World Journal of Hepatology","volume":"17 8","pages":"110413"},"PeriodicalIF":2.5,"publicationDate":"2025-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12400383/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144993275","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}
Kent W Sabatose, Alexandra Baker, Kevin Kugler, Jude Delikat, Bethany Jowers, Ambuj Kumar, Sadaf Aslam, Jacentha Buggs, Christine Machado-Denis, Nyingi Kemmer, Kiran Dhanireddy, Rashid Syed
{"title":"Patient factors in responders and non-responders treated with steroids for acute alcohol-associated hepatitis.","authors":"Kent W Sabatose, Alexandra Baker, Kevin Kugler, Jude Delikat, Bethany Jowers, Ambuj Kumar, Sadaf Aslam, Jacentha Buggs, Christine Machado-Denis, Nyingi Kemmer, Kiran Dhanireddy, Rashid Syed","doi":"10.4254/wjh.v17.i8.108677","DOIUrl":"10.4254/wjh.v17.i8.108677","url":null,"abstract":"<p><strong>Background: </strong>Steroids remain the primary treatment for severe alcohol-associated hepatitis (AAH), though there is little available tools to predict patient response to steroids. It was hypothesized that phosphatidylethanol (PEth) value will inversely correlate with response to steroid therapy based on Lille score in AAH.</p><p><strong>Aim: </strong>To assess the relationship of patient factors, focusing on pre-steroid therapy PEth value, to steroid therapy response in AAH.</p><p><strong>Methods: </strong>A retrospective case control study was performed on patients who received ≥ 4 days of steroid therapy for AAH at our hospital between July 1, 2019 and June 30, 2022. A total of 2087 patients were screened for AAH and those treated with steroids were included for statistical analysis utilizing independent sample <i>t</i>-test and for categorical variables using the <i>χ</i> <sup>2</sup> test.</p><p><strong>Results: </strong>No correlation was found between PEth value, pre-steroids abstinence length, or number of drinks per week pre-steroids and response to steroids. Non-responder status significantly correlated with older age (<i>P</i> = 0.024), lower albumin (<i>P</i> = 0.003), and higher bilirubin (<i>P</i> = 0.010) pre-steroids. Our study suggests that age, pre-steroid albumin, and pre-steroid bilirubin levels may predict nonresponse to steroid therapy. Non-responders have increased incidence of death and higher medical costs.</p><p><strong>Conclusion: </strong>Identifying non-responders through these identified factors should prompt early referral for liver transplantation. Future prospective studies with larger population size are needed to assess the efficacy of combined pre-steroid age, albumin, bilirubin and other biochemical markers as predictors of steroid response.</p>","PeriodicalId":23687,"journal":{"name":"World Journal of Hepatology","volume":"17 8","pages":"108677"},"PeriodicalIF":2.5,"publicationDate":"2025-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12400396/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144993277","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":"Optimal guiding methods for transjugular intrahepatic portosystemic shunt creation: Characteristics of intravascular ultrasound <i>vs</i> other techniques.","authors":"Lei Miao, Jing-Lin Ren, He Zhao, Xiao Li","doi":"10.4254/wjh.v17.i8.109496","DOIUrl":"10.4254/wjh.v17.i8.109496","url":null,"abstract":"<p><p>A recent study in <i>World Journal of Hepatology</i> examined the use of intravascular ultrasound (IVUS) for transjugular intrahepatic portosystemic shunt (TIPS) creation. The study concluded that IVUS significantly reduces procedure time, radiation exposure, and the number of needle passes compared to conventional fluoroscopic guidance. IVUS offers real-time visualization of the portal vein, but challenges remain in terms of equipment costs and the operator learning curve. TIPS creation techniques vary widely in clinical practice, where methods, such as conventional fluoroscopy, three-dimensional image fusion, electromagnetic navigation, and IVUS, are commonly employed. In this editorial, we provide a comparative analysis of these methods based on clinical experience and the literature. By evaluating the strengths and limitations of each technique, we aim to inform clinical decision-making and enhance procedural outcomes. Future developments in TIPS creation are likely to focus on hybrid techniques that combine the strengths of IVUS, electromagnetic navigation, and real-time image fusion, potentially leading to more precise, cost-effective, and accessible methods.</p>","PeriodicalId":23687,"journal":{"name":"World Journal of Hepatology","volume":"17 8","pages":"109496"},"PeriodicalIF":2.5,"publicationDate":"2025-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12400442/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144993040","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":"Imaging insights into pediatric liver masses: A comprehensive minireview for hepatology practice.","authors":"Mina'a Shahid, Kiran Hilal, Memoona Khan, Zainab Haider Ejaz, Sadaf Altaf, Saleem Islam, Kumail Khandwala","doi":"10.4254/wjh.v17.i8.107041","DOIUrl":"10.4254/wjh.v17.i8.107041","url":null,"abstract":"<p><p>Pediatric liver masses encompass a diverse spectrum of benign and malignant lesions, with distinct patterns based on patient age. Optimal imaging is critical for timely diagnosis, management, and prognosis. This pictorial minireview categorizes pediatric liver masses by age group to guide hepatology and radiology practice, with an emphasis on imaging characteristics. In children from birth to six years of age, the most common liver masses include hepatoblastoma, the most common primary hepatic malignancy in this age group; infantile hemangioma, a benign vascular tumor with a characteristic appearance on imaging; and mesenchymal hamartoma, a rare developmental lesion. For children older than six years, liver masses are distinct, with hepatocellular carcinoma being the predominant malignant lesion. Benign masses such as focal nodular hyperplasia and hepatocellular adenoma also emerge in this age range, often linked to hormonal influences or metabolic disorders. The masses observed across all pediatric age groups include hepatic cysts, choledochal cysts, hydatid cysts, pyogenic and amebic abscesses, tuberculosis, lymphoma, and metastases, each presenting with unique imaging features essential for differential diagnosis. This minireview provides a comprehensive, age-based overview of pediatric liver masses, focusing on clinical presentation and key imaging findings to support accurate diagnosis and optimize management strategies in clinical hepatology, particularly in low resource settings.</p>","PeriodicalId":23687,"journal":{"name":"World Journal of Hepatology","volume":"17 8","pages":"107041"},"PeriodicalIF":2.5,"publicationDate":"2025-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12400384/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144993609","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}