Clinical and Experimental Hepatology最新文献

{"title":"1,400 genetically predicted plasma metabolites in relation to risk of primary biliary cholangitis: a bi-directional, two-sample Mendelian randomization analysis.","authors":"Wenqian Geng, Xiajie Wen, Ronghua Jin, Xiaoxue Yuan","doi":"10.5114/ceh.2025.148221","DOIUrl":"https://doi.org/10.5114/ceh.2025.148221","url":null,"abstract":"<p><strong>Aim of the study: </strong>Primary biliary cholangitis (PBC) is a complex, chronic, cholestatic liver disease with an autoimmune etiology. While plasma metabolites are crucial indicators of physiological and pathological states, their involvement in PBC pathogenesis remains unclear. To address this knowledge gap, we performed a rigorous two-sample Mendelian randomization (MR) analysis to assess the causal associations of 1,400 plasma metabolites with PBC.</p><p><strong>Material and methods: </strong>Genome-wide association data for 1,400 plasma metabolites and PBC were obtained from established public databases. The inverse-variance weighted (IVW) method was the primary method used for MR analysis. Sensitivity analyses and heterogeneity tests were conducted to assess the stability of the MR results. A reverse MR analysis was performed to investigate the possibility of reverse causality.</p><p><strong>Results: </strong>Four plasma metabolites were identified as potential predictors for the occurrence of PBC. Specifically, sphingosine 1-phosphate (OR = 0.65, 95% CI: 0.42-0.98, <i>p</i> = 0.04) and docosadienoate (22:2n6) (OR = 0.57, 95% CI: 0.36-0.90, <i>p</i> = 0.01) were implicated in conferring a protective effect against PBC. Conversely, homoarginine (OR = 1.34, 95% CI: 1.04-1.72, <i>p</i> = 0.02) and campesterol (OR = 1.19, 95% CI: 1.01-1.40, <i>p</i> = 0.03) were associated with an increased risk of PBC. There was no evidence of reverse causality between PBC and the identified plasma metabolites.</p><p><strong>Conclusions: </strong>This study utilized a two-sample Mendelian randomization approach to explore the causal relationship between 1,400 plasma metabolites and PBC. We identified four plasma metabolites that may have a causal relationship with the development of PBC. The metabolites identified hold promise as prognostic indicators and could illuminate novel pathways for therapeutic intervention in PBC.</p>","PeriodicalId":10281,"journal":{"name":"Clinical and Experimental Hepatology","volume":"11 1","pages":"61-70"},"PeriodicalIF":1.5,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12035705/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143954999","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":"Identifying the genetic link between type 1 diabetes and autoimmune liver diseases.","authors":"Guo Yu, Tao Dong, Haoyuan Gu, Depeng Liang, Liming Song, Jijing Shi, Xibin Duan, Chao Ma","doi":"10.5114/ceh.2025.149078","DOIUrl":"https://doi.org/10.5114/ceh.2025.149078","url":null,"abstract":"<p><strong>Introduction: </strong>It appears that type 1 diabetes mellitus (T1DM) and autoimmune liver diseases (AILDs) are associated, but there is no evidence linking them causally or in a specific direction. This study aims to evaluate the causal relationship between T1DM and AILDs.</p><p><strong>Material and methods: </strong>We performed a two-sample Mendelian randomization (MR) analysis. Following thorough evaluation, the dataset from the genome-wide association study was utilized to identify potential candidate single nucleotide polymorphisms. Inverse variance weighting (IVW) served as the primary analytical method, complemented by four sensitivity analysis approaches to evaluate result robustness.</p><p><strong>Results: </strong>Mendelian randomization analysis demonstrated a significant positive causal association between genetically elevated risk of T1DM and autoimmune hepatitis (AIH) (OR = 1.168, 95% CI: 1.060-1.287, <i>p</i> = 0.001), primary biliary cholangitis (PBC) (OR = 1.186, 95% CI: 1.050-1.341, <i>p</i> = 0.006), as well as primary sclerosing cholangitis (PSC) (OR = 1.291, 95% CI: 1.016-1.642, <i>p</i> = 0.037). MR-Egger regression analysis suggested a potential influence of horizontal pleiotropy on the causal association for these conditions (AIH: intercept = -0.026, <i>p</i> = 0.451; PBC: intercept = 0.014, <i>p</i> = 0.745; PSC: intercept = -0.013, <i>p</i> = 0.862). Sensitivity analysis utilizing the leave-one-out method supported the robustness of the Mendelian randomization findings. Conversely, reverse Mendelian randomization analysis revealed that genetically predisposed PBC also raises the likelihood of developing T1DM (OR = 1.236, 95% CI: 1.085-1.407, <i>p</i> = 0.001). Conversely, no causal association was found between AIH and T1DM (OR = 1.032, 95% CI: 0.983-1.084, <i>p</i> = 0.207) or between PSC and T1DM (OR = 0.989, 95% CI: 0.849-1.152, <i>p</i> = 0.888).</p><p><strong>Conclusions: </strong>Employing two-sample MR analysis, we explored the association between T1DM and AILDs, finding that T1DM elevates the risk of AIH, PBC, and PSC. Further elucidation of the genomic landscape of T1DM and AILDs necessitates large-scale cross-disease genome-wide association studies (GWAS).</p>","PeriodicalId":10281,"journal":{"name":"Clinical and Experimental Hepatology","volume":"11 1","pages":"52-60"},"PeriodicalIF":1.5,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12035703/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143978969","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":"Changes in liver stiffness and steatosis in children after successful treatment with sofosbuvir/velpatasvir: Results of the PANDAA-PED study.","authors":"Maria Pokorska-Śpiewak, Ewa Talarek, Małgorzata Aniszewska, Magdalena Pluta, Anna Dobrzeniecka, Magdalena Marczyńska, Giuseppe Indolfi","doi":"10.5114/ceh.2024.146131","DOIUrl":"https://doi.org/10.5114/ceh.2024.146131","url":null,"abstract":"<p><strong>Aim of the study: </strong>The aim of this study was to analyze changes in liver stiffness and steatosis using noninvasive methods in children aged 6 to 18 years up to one year after successful treatment with sofosbuvir/velpatasvir (SOF/VEL).</p><p><strong>Material and methods: </strong>Evaluation of liver stiffness and steatosis was performed in 49 patients at 12 weeks and one year after treatment using noninvasive methods. Liver stiffness measurement (LSM) and the controlled attenuation parameter (CAP) were obtained by transient elastography (FibroScan 530, Echosens).</p><p><strong>Results: </strong>At baseline, LSM corresponded to a METAVIR F score of 0/1 in 48/49 (98%) participants. There was a decrease in mean LSM values from baseline to posttreatment visits (from 4.63 kPa to 4.26 kPa at 12 weeks, and 4.15 kPa at one year after treatment). In one girl who presented with significant fibrosis (LSM 11.3 kPa, F3) before the treatment, regression of stiffness was observed to 7.6 kPa (F2) at 12 weeks after treatment and 5.4 kPa (F0/1) at one year after treatment. There was an increase in the mean CAP value of +12.44 dB/m at 12 weeks after treatment compared to baseline, but the difference at one year after treatment was insignificant. A correlation between higher CAP values and older participants' age was observed at all the visits. Children with body mass index (BMI) z-score values > 1.0 presented with higher CAP values both before and after treatment.</p><p><strong>Conclusions: </strong>Most children with chronic hepatitis C present with normal liver stiffness. However, its regression may occur to some extent after successful treatment with SOF/VEL. A transient increase in hepatic steatosis was observed after eradication of HCV, which requires further investigation.</p>","PeriodicalId":10281,"journal":{"name":"Clinical and Experimental Hepatology","volume":"11 1","pages":"45-51"},"PeriodicalIF":1.5,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12035707/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143983797","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":"Drug-induced liver injury. Part I: Classification, diagnosis and treatment.","authors":"Dorota M Kozielewicz, Piotr Stalke, Julita Skrzypek","doi":"10.5114/ceh.2025.148329","DOIUrl":"https://doi.org/10.5114/ceh.2025.148329","url":null,"abstract":"<p><p>Drug-induced liver injury (DILI) is a growing clinical problem. Antibiotics remain the most common cause of DILI in Europe. Their clinical spectrum is very broad, from asymptomatic to acute liver failure. Currently, DILI is categorized as hepatocellular (R ≥ 5), cholestatic (R ≤ 2) or mixed (R = 2-5) injury based on the serum alanine aminotransferase (ALT)/alkaline phosphatase (ALP) ratio. DILI is a diagnosis of exclusion and requires a wide differential diagnosis. The most important step in management is discontinuation of the drug suspected of causing liver damage. The list of specific antidotes that eliminate the effects of hepatotoxins is unfortunately very short. In symptomatic treatment, glucocorticosteroids and ursodeoxycholic acid have been used in selected cases. Liver transplantation is an optional treatment in patients with acute liver failure.</p>","PeriodicalId":10281,"journal":{"name":"Clinical and Experimental Hepatology","volume":"11 1","pages":"25-33"},"PeriodicalIF":1.5,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12035709/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143989603","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":"Autoimmune hepatitis: clinicopathological characteristics and histopathological diagnosis in the light of current views.","authors":"Ewa Iżycka-Świeszewska, Natalia Walkusz, Piotr Zieliński, Katarzyna Sikorska","doi":"10.5114/ceh.2025.148233","DOIUrl":"https://doi.org/10.5114/ceh.2025.148233","url":null,"abstract":"<p><p>The diagnosis of autoimmune hepatitis (AIH) is based on clinical criteria and histopathological findings. Interpretation of lesions observed in liver biopsy specimens, in cases of suspected AIH, requires correlation with clinical data and communication between hepatologists and pathologists. The diagnostic criteria have been modified over the years, and the latest guidelines were proposed in 2022. Implementation of the current recommendations improves diagnostic accuracy for autoimmune hepatitis and related pathologies. This article presents the clinicopathological characteristics of AIH and an overview of the histopathological diagnostic approach in the light of the modern guidelines.</p>","PeriodicalId":10281,"journal":{"name":"Clinical and Experimental Hepatology","volume":"11 1","pages":"14-24"},"PeriodicalIF":1.5,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12035706/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143961291","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 GALAD score performs better than AFP in hepatocellular carcinoma screening: a single-centre, case-control study in Malaysia.","authors":"Wing Hang Woo, Khairul Najmi Muhammad Nawawi, Deborah Chia Hsin Chew, Wei Hao Kok, Zhiqin Wong, Azlanudin Azman, Nur Yazmin Yaacob, Munirah Md Mansor, Hanita Othman, Raja Affendi Raja Ali","doi":"10.5114/ceh.2025.148321","DOIUrl":"https://doi.org/10.5114/ceh.2025.148321","url":null,"abstract":"<p><strong>Aim of the study: </strong>Hepatocellular carcinoma (HCC) in Malaysia is a growing health concern, despite regular liver ultrasound and α-fetoprotein (AFP) surveillance. The GALAD model incorporates AFP, lens culinaris agglutinin- reactive α-fetoprotein (AFP-L3), protein induced by vitamin K antagonist-II (PIVKA-II), gender and age to predict the probability of HCC. Our objective was to evaluate the diagnostic ability of GALAD compared to AFP in HCC screening.</p><p><strong>Material and methods: </strong>A single-centre, case control study recruited newly diagnosed HCC and cirrhotic patients. Serum biomarkers were quantified using a microfluidic-based automated immunoanalyzer. The diagnostic ability of AFP, AFP-L3, PIVKA-II and GALAD was assessed using receiver operating characteristic curve (ROC) and corresponding area under the curve (AUC) analysis.</p><p><strong>Results: </strong>Among the 44 HCC cases, GALAD score achieved the highest AUC value of 0.94 (95% confidence interval [CI]: 0.90-0.98, <i>p</i> < 0.0001) significantly surpassing AFP (0.89), AFP-L3 (0.84) and PIVKA-II (0.88). The GALAD score demonstrated 84.1% sensitivity and 93.8% specificity at the standard cut-off (-0.63) and 88.6%/92.2% at its best cut-off (-1.035) for detecting any stage of HCC, outperforming AFP (79.5%/92.2%), AFP-L3 (59.1%/94.9%) and PIVKA-II (79.5%/84.9%). The sensitivity of the GALAD score was 100% in earlystage HCC (BCLC0/A).</p><p><strong>Conclusions: </strong>GALAD outperformed conventional biomarkers, facilitating early detection, improved treatment options and ultimately a higher survival rate for HCC patients.</p>","PeriodicalId":10281,"journal":{"name":"Clinical and Experimental Hepatology","volume":"11 1","pages":"81-87"},"PeriodicalIF":1.5,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12035704/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143989604","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":"Identification of the shared gene signatures and biological mechanism in type 2 diabetes mellitus and hepatocellular carcinoma.","authors":"Yuxi Lin, Jiasheng Liao, Yutian Chong","doi":"10.5114/ceh.2025.148439","DOIUrl":"https://doi.org/10.5114/ceh.2025.148439","url":null,"abstract":"<p><strong>Introduction: </strong>Type 2 diabetes mellitus (T2DM) is closely related to hepatocellular carcinoma (HCC). The pathophysiological mechanism of coexistence of T2DM and HCC is unclear. The study aimed to investigate the core genes and pathways involved in the development and progression of T2DM and HCC.</p><p><strong>Material and methods: </strong>Datasets for T2DM and HCC were downloaded from the GEO to screen differentially expressed genes (DEGs). Protein-protein interaction (PPI) network analysis was performed on these DEGs to explore their functions and verify hub genes. These genes were validated by quantitative real-time polymerase chain reaction (qRT-PCR) and UALCAN analysis based on The Cancer Genome Atlas (TCGA). Finally, the transcription factor (TF)-miRNA-target gene network was constructed with hub genes, and visualized using Cytoscape software 3.6.1.</p><p><strong>Results: </strong>A total of 77 common DEGs were identified. KEGG enrichment revealed that pathways of metabolic processes are enriched in T2DM and HCC. Combining the results of MCODE and CytoHubba showed that <i>AASS</i>, <i>SDS</i>, <i>HAL</i>, <i>KYNU</i> and <i>TDO2</i> were hub genes. Then, we verified the above results by UALCAN analysis and qRT-PCR. Compared with normal liver tissues, the expression levels of 5 hub genes based on tumor grade were lower in liver hepatocellular carcinoma (LIHC) tissues. mRNA levels of these genes were significantly down-regulated in HepG2 and SNU-449 compared with LO2 cells. Furthermore, we depicted the TF-miRNA-gene interaction network.</p><p><strong>Conclusions: </strong>This study proposed a strategy for exploring pathogenic mechanisms of T2DM and HCC. Network hub genes hold promise as disease status biomarkers and treatment targets for alleviating both T2DM and HCC.</p>","PeriodicalId":10281,"journal":{"name":"Clinical and Experimental Hepatology","volume":"11 1","pages":"34-44"},"PeriodicalIF":1.5,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12035708/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143986704","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":"NADK as a molecular marker to distinguish between alcohol- and non-alcohol-associated liver cirrhosis: A pilot study.","authors":"Ki-Hoon Park, Seok-Hyung Kim, So-Woon Kim, Kiyong Na, Sunyoung Kim, Young-Il Choi, Hyung-Joo Chung, Junyang Jung, Na Young Jeong","doi":"10.5114/ceh.2025.146956","DOIUrl":"https://doi.org/10.5114/ceh.2025.146956","url":null,"abstract":"<p><strong>Aim of the study: </strong>We investigated whether nicotinamide adenine dinucleotide kinase (NADK) expression is selectively diminished in alcohol-associated liver cirrhosis (AC), and evaluated its potential as a biomarker for this condition.</p><p><strong>Material and methods: </strong>Human liver samples were obtained during liver transplantation or resection procedures at Kosin University Gospel Hospital and classified into two groups: AC and non-AC (NAC). NAD⁺ and NADP⁺ levels were measured using liquid chromatography-mass spectrometry (LC-MS). RNA-seq data from the NCBI Gene Expression Omnibus were utilized to identify AC-specific differentially expressed genes (DEGs). Multi-level expression analyses and immunohistochemistry were performed to assess NADK expression in liver tissues.</p><p><strong>Results: </strong>LC-MS analysis indicated a significant reduction in NAD⁺ and NADP⁺ levels in AC patients compared to both normal and NAC groups, with a corresponding increase in the NAD⁺/NADP⁺ ratio (AC = 3.93, NAC = 2.75, normal = 2.64). We identified 881 AC-specific DEGs, including 27 kinase-encoding genes. Multi-level expression analyses confirmed a significant decrease in NADK gene expression in AC patients. Immunohistochemistry showed a marked reduction in NADK protein expression in AC patients, underscoring its involvement in altered metabolic processes.</p><p><strong>Conclusions: </strong>This study revealed a distinct decrease in NADK expression in AC, suggesting its utility as a molecular marker for diagnosing and understanding metabolic dysregulation in these patients. These findings provide a foundation for developing targeted therapeutic strategies for alcohol-associated liver cirrhosis.</p>","PeriodicalId":10281,"journal":{"name":"Clinical and Experimental Hepatology","volume":"11 1","pages":"71-80"},"PeriodicalIF":1.5,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12035712/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143985521","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":"Recommended vaccinations for patients with chronic liver diseases.","authors":"Justyna Janocha-Litwin, Krzysztof Simon","doi":"10.5114/ceh.2025.148265","DOIUrl":"https://doi.org/10.5114/ceh.2025.148265","url":null,"abstract":"<p><p>Patients with chronic liver diseases, particularly those with liver cirrhosis, are more vulnerable to severe superinfections compared to the general population. They face an increased risk of liver function decompensation and mortality when contracting viral or bacterial infections. Vaccination is crucial in mitigating these risks, yet its efficacy in this patient group may be limited. Despite the safety of vaccines, their effectiveness in individuals with chronic liver diseases remains constrained. A significant challenge is the inadequate implementation of vaccination protocols, often due to insufficient communication and recommendations from physicians, including hepatologists, and the high cost of vaccines.</p>","PeriodicalId":10281,"journal":{"name":"Clinical and Experimental Hepatology","volume":"11 1","pages":"1-8"},"PeriodicalIF":1.5,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12035710/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143969972","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 importance of elastography in hepatological diagnostics in children.","authors":"Eliza Łężyk-Ciemniak, Justyna Moppert, Małgorzata Pawłowska","doi":"10.5114/ceh.2025.149075","DOIUrl":"https://doi.org/10.5114/ceh.2025.149075","url":null,"abstract":"<p><p>About 30 years have passed since elastography was first used, with the greatest popularity in the last 10 years. The use of this diagnostic method is particularly important in patients with liver disease. FibroScan shows higher sensitivity in assessing the degree of organ steatosis and fibrosis compared to ultrasound. The noninvasive nature and ease of performance make it possible to perform the test in most pediatric patients. Owing to the correlation of the results with the histopathological evaluation, elastography replaces liver biopsy in many cases. Given the epidemic of childhood obesity observed in recent years, FibroScan testing appears to be increasingly necessary.</p>","PeriodicalId":10281,"journal":{"name":"Clinical and Experimental Hepatology","volume":"11 1","pages":"9-13"},"PeriodicalIF":1.5,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12035711/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143956676","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}