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21
Original Article Open Access
Chitta Ranjan Khatua, Prajna Anirvan, Manas Kumar Panigrahi, Shivaram Prasad Singh
Published online July 17, 2025
Journal of Translational Gastroenterology. doi:10.14218/JTG.2025.00004
Abstract
Prognostic scores are valuable tools for predicting survival in patients with chronic liver disease. Recently, the albumin-bilirubin (ALBI) score has emerged as a potential prognostic [...] Read more.

Prognostic scores are valuable tools for predicting survival in patients with chronic liver disease. Recently, the albumin-bilirubin (ALBI) score has emerged as a potential prognostic indicator in liver-related conditions. This study aimed to compare the prognostic efficacy of the ALBI score with the Model for End-stage Liver Disease (MELD), MELD-Na+, and Child-Turcotte-Pugh (CTP) scores in predicting survival among patients with alcohol-associated liver disease (ALD).

This study included consecutive ALD patients admitted to the Medicine and Gastroenterology wards of MKCG Medical College and Hospital, Berhampur, Odisha, India, between November 2019 and November 2022. Upon hospitalization, baseline characteristics, clinical and laboratory parameters, ALBI, MELD, MELD-Na+, and CTP scores were recorded. The accuracy of these scores in predicting survival up to three years was compared.

A total of 490 ALD patients were included. Higher ALBI scores were observed in patients who died during hospitalization (p < 0.001), at 28 days (p < 0.001), 90 days (p < 0.001), six months (p < 0.001), one year (p < 0.001), two years (p < 0.001), and three years (p < 0.001), compared to those who survived. However, the area under the receiver operating characteristic (AUROC) curves showed that the ALBI score was inferior to MELD, MELD-Na+, and CTP scores in predicting survival at admission [AUROC: ALBI (0.719), MELD-Na+ (0.823), MELD (0.817), CTP (0.770)] and at three years [AUROC: ALBI (0.755), MELD-Na+ (0.787), MELD (0.758), CTP (0.784)]. Furthermore, Cox regression analysis revealed that components used in the MELD, MELD-Na+, and CTP scores—such as serum creatinine, serum sodium, and hepatic encephalopathy—were independent predictors of mortality, whereas the components of the ALBI score (serum albumin and serum bilirubin) were not.

All hospitalized ALD patients had a grade 3 ALBI score, with significantly higher scores observed among non-survivors compared to survivors. However, MELD, MELD-Na+, and CTP scores were superior to the ALBI score in predicting survival both during hospitalization and over a three-year follow-up period.

Full article
22
Original Article Open Access
Gong Feng, Giovanni Targher, Christopher D. Byrne, Na He, Man Mi, Yi Liu, Hongbin Zhu, Ming-Hua Zheng, Feng Ye
Published online July 16, 2025
Journal of Clinical and Translational Hepatology. doi:10.14218/JCTH.2025.00270
Abstract
The causal biomarkers for metabolic dysfunction-associated steatotic liver disease (MASLD) and their clinical value remain unclear. In this study, we aimed to identify biomarkers [...] Read more.

The causal biomarkers for metabolic dysfunction-associated steatotic liver disease (MASLD) and their clinical value remain unclear. In this study, we aimed to identify biomarkers for MASLD and evaluate their diagnostic and prognostic significance.

We conducted a Mendelian randomization analysis to assess the causal effects of 2,925 molecular biomarkers (from proteomics data) and 35 clinical biomarkers on MASLD. Mediation analysis was performed to determine whether clinical biomarkers mediated the effects of molecular biomarkers. The association between key clinical biomarkers and MASLD was externally validated in a hospital-based cohort (n = 415). A machine learning–based diagnostic model for MASLD was developed and validated using the identified molecular biomarkers. Prognostic significance was evaluated for both molecular and clinical biomarkers.

Six molecular biomarkers—including canopy FGF signaling regulator 4 (CNPY4), ectonucleoside triphosphate diphosphohydrolase 6 (ENTPD6), and major histocompatibility complex, class I, A (HLA-A)—and eight clinical biomarkers (e.g., serum total protein (STP)) were identified as causally related to MASLD. STP partially mediated the effect of HLA-A on MASLD (23.61%) and was associated with MASLD in the external cohort (odds ratio = 1.080, 95% confidence interval: 1.011–1.155). A random forest model demonstrated high diagnostic performance (AUC = 0.941 in training; 0.875 in validation). High expression levels of CNPY4 and ENTPD6 were associated with the development of and poorer survival from hepatocellular carcinoma. Low STP (<60 g/L) predicted all-cause mortality (HR = 2.50, 95% confidence interval: 1.22–5.09).

This study identifies six causal molecular biomarkers (e.g., CNPY4, ENTPD6, HLA-A) and eight clinical biomarkers for MASLD. Notably, STP mediates the effect of HLA-A on MASLD and is associated with all-cause mortality.

Full article
23
Corrigendum Open Access
Sunny Rathee, Umesh K. Patil, Sanjay K. Jain
Published online July 15, 2025
Journal of Exploratory Research in Pharmacology. doi:10.14218/JERP.2023.00050C
24
Corrigendum Open Access
Nilanga Aki Bandara, Dhruv Lalkiya, Ryan Vethanayagam, Quaila-Lee Trang, Srinjoy Ray, Monica Anand, Parsa Khatami, Lea Lough, Anahita Nikmanesh, Malisha Ratnayake, Xuan Randy Zhou, David Harriman, Miles Mannas, Vahid Mehrnoush, Jay Herath
Published online July 15, 2025
Journal of Exploratory Research in Pharmacology. doi:10.14218/JERP.2023.00057C
25
Review Article Open Access
Wanchun Zhu, Yu Cui, Jiahao Qiu, Xin Zhang, Yueqiu Gao, Zhi Shang, Lingying Huang
Published online July 15, 2025
Journal of Clinical and Translational Hepatology. doi:10.14218/JCTH.2025.00029
Abstract
Liver fibrosis is a pathological process resulting from various chronic liver injuries that lead to the formation of liver fibrous scars. It can further progress to cirrhosis and [...] Read more.

Liver fibrosis is a pathological process resulting from various chronic liver injuries that lead to the formation of liver fibrous scars. It can further progress to cirrhosis and even liver cancer. Currently, there are no effective drugs specifically approved for the treatment of liver fibrosis; etiological therapy remains the main treatment strategy. Therefore, it is necessary to develop anti-fibrotic drugs targeting different pathways involved in liver fibrosis. Transforming growth factor-beta (TGF-β) is a key driver of fibrosis, and targeting TGF-β can effectively reduce liver fibrosis. In this review, we discussed the anti-liver fibrosis effects of TGF-β inhibitors through different signaling pathways, including the application of certain active ingredients from Traditional Chinese Medicine.

Full article
26
Corrigendum Open Access
Benjamin O. Ezema, Chijioke Nwoye Eze, Thecla Okeahunwa Ayoka, Charles Okeke Nnadi
Published online July 15, 2025
Journal of Exploratory Research in Pharmacology. doi:10.14218/JERP.2024.00020C
27
Corrigendum Open Access
Anil K. Philip, Betty Annie Samuel, Bassim A. Mohammed, Hayder A. Al-Aubaidy
Published online July 15, 2025
Journal of Exploratory Research in Pharmacology. doi:10.14218/JERP.2024.00027C
28
Mini Review Open Access
Yanjun Hou, Deyin Xing, Zaibo Li
Published online July 14, 2025
Journal of Clinical and Translational Pathology. doi:10.14218/JCTP.2025.00020
Abstract
Mesonephric carcinoma (MC) is a rare type of cervical carcinoma that arises from mesonephric remnants. It is characterized by a mixture of a wide variety of growth patterns and [...] Read more.

Mesonephric carcinoma (MC) is a rare type of cervical carcinoma that arises from mesonephric remnants. It is characterized by a mixture of a wide variety of growth patterns and typically exhibits positive immunoreactivity for GATA binding protein 3, thyroid transcription factor 1, and apical common acute lymphoblastic leukemia antigen. A subset of adenocarcinomas in the uterine corpus and ovary with similar morphology and immunophenotype is classified as mesonephric-like adenocarcinoma (MLA) in the current World Health Organization classification. This review aimed to summarize the clinicopathological features of mesonephric remnants, mesonephric hyperplasia, and MC, provide an update on the current understanding of MLA, and highlight the molecular differences between MC and MLA.

A literature review was conducted on mesonephric remnants, mesonephric hyperplasia, MC, and MLA. The clinicopathological and molecular features were summarized from previously published studies and compared across these entities.

Both MC and MLA exhibit a mixture of growth patterns and show immunoreactivity for GATA binding protein 3, thyroid transcription factor 1, and common acute lymphoblastic leukemia antigen. They commonly harbor genetic alterations in KRAS and NRAS. However, key differences exist between these two entities. MC is associated with mesonephric remnants, whereas no such association has been identified for MLA. Additionally, although KRAS and NRAS mutations are common in both, a subset of MLA cases also harbors PIK3CA and/or PTEN mutations, genetic alterations commonly seen in endometrioid adenocarcinoma.

Although the exact pathogenesis of MLA remains unclear, it is favored to originate from Müllerian-derived epithelium undergoing differentiation along the mesonephric pathway, rather than from true mesonephric remnants. Both MC and MLA tend to follow a relatively aggressive clinical course, underscoring the importance of accurate diagnosis.

Full article
29
Corrigendum Open Access
30
Corrigendum Open Access
Tomas Koltai, Larry Fliegel
Published online July 14, 2025
Gene Expression. doi:10.14218/GE.2023.00014C
31
Corrigendum Open Access
Seyed Mohammad Hadi Safaei, Mohammadreza Mohammadabadi, Borhan Moradi, Oleksandr Kalashnyk, Nataliia Klopenko, Olena Babenko, Oleksandr Oleksandrovich Borshch, Volodymyr Afanasenko
Published online July 14, 2025
Gene Expression. doi:10.14218/GE.2023.00020C
32
Corrigendum Open Access
Victor M. Color-Aparicio, Angeles C. Tecalco-Cruz, Blanca Delgado-Coello, Marcela Sosa-Garrocho, Jaime Mas-Oliva, Genaro Vázquez-Victorio, Marina Macías-Silva
Published online July 11, 2025
Gene Expression. doi:10.14218/GE.2023.00192C
33
Corrigendum Open Access
34
Original Article Open Access
Yusuf Musa, Habib Tijjani Saleh, Chinwe Philomena Onyia, Abubakar Sadiq Aminu, Kenechukwu Chukwuemeka Okonkwo, Oluwafunmilayo Funke Adeniyi, Abdulkareem Lukman Olaitan, Hafizu Abdullahi Zubairu, Nasiru Altine Dankiri, Muhammad Manko, Matthew Olumuyiwa Bojuwoye, Owoseni Opeyemi Olubukola, Emuobor Odeghe, Yusuf Shehu Umar, Ganiyat Kikelomo Oyeleke, Isa Mustapha, Chinenye Unoma Nwoko, Evaristus Sunday Chukwudike
Published online July 9, 2025
Journal of Translational Gastroenterology. doi:10.14218/JTG.2025.00011
Abstract
Inflammatory bowel disease (IBD) is a chronic condition with significant health implications worldwide. In Nigeria, data on its prevalence and characteristics are limited, highlighting [...] Read more.

Inflammatory bowel disease (IBD) is a chronic condition with significant health implications worldwide. In Nigeria, data on its prevalence and characteristics are limited, highlighting the need for comprehensive studies to better understand its epidemiology and clinical features in the region. This study aimed to assess the clinical presentation, endoscopic findings, and management challenges of IBD among patients undergoing colonoscopy in Nigeria.

Over five years (2019–2024), a multicenter, cross-sectional survey was conducted involving clinicians across Nigeria’s six geopolitical zones. It included a retrospective review of records from 18 centers. Data collection was conducted in two phases via Google Forms, focusing on care practices and detailed case information, including demographics, clinical features, histology, and treatment. Data analysis used descriptive statistics and tests for associations, with significance set at p < 0.05.

A total of 459 suspected IBD cases (9.7%) were identified among over 4,700 colonoscopies, with histological confirmation in 208 cases (4.4%), indicating the prevalence of IBD in the Nigerian patient population. The most common subtype was ulcerative colitis (53.9%), followed by Crohn’s disease (21.0%) and indeterminate colitis (25.0%). Regional variations were observed, with higher diagnosis rates in some zones (North-West: 14.9%; South-East: 1.4%). The predominant clinical feature was rectal bleeding. Endoscopic findings frequently showed pan-colitis (62%), with significant regional differences (p < 0.001), and management mainly involved medications such as acetylsalicylic acid derivatives (60.0%), with surgical options rarely employed (0.6%). Challenges included high medication costs and limited availability, which affected nearly half of the patients (49.4%; 46.2%).

IBD, though under-recognized, is present in the Nigerian population, with notable regional variation in prevalence and presentation. The primary clinical features align with global patterns, and significant barriers, such as medication costs and availability, hinder effective management. Increasing awareness, improving diagnostic infrastructure, and addressing treatment challenges are essential to enhance care and outcomes for patients with IBD in Nigeria.

Full article
35
Original Article Open Access
Qin Ouyang, Siyu Jia, Qianyu Zhu, Yanmeng Li, Huaduan Zi, Sisi Chen, Pingping He, Hengcheng Tang, Yanling Li, Anjian Xu, Bei Zhang, Xiaomin Wang, Xiaojuan Ou, Donghu Zhou, Jian Huang
Published online July 7, 2025
Journal of Clinical and Translational Hepatology. doi:10.14218/JCTH.2024.00422
Abstract
Despite advancements in diagnostic and therapeutic strategies, hepatocellular carcinoma (HCC) remains a leading cause of cancer-related mortality. Antioxidant-1 (ATOX1) has been [...] Read more.

Despite advancements in diagnostic and therapeutic strategies, hepatocellular carcinoma (HCC) remains a leading cause of cancer-related mortality. Antioxidant-1 (ATOX1) has been implicated in oncogenic processes across various cancer types; however, its specific role in HCC remains unclear. This study aimed to investigate the function of ATOX1 and its underlying molecular mechanisms in HCC.

Immunohistochemical analysis was conducted to assess ATOX1 expression in HCC tissues. Cell Counting Kit-8, colony formation, Transwell migration, flow cytometry, and reactive oxygen species (ROS) assays were employed to evaluate the malignant behaviors of tumor cells. A xenograft mouse model was employed to assess the effects of ATOX1 knockdown on tumor growth in vivo. DCAC50 treatment was performed to inhibit the copper transport function of ATOX1. RNA sequencing was conducted to explore the potential molecular mechanisms of ATOX1 in HCC.

ATOX1 expression was significantly elevated in HCC tumor tissues. ATOX1 promoted cell proliferation, colony formation, and migration. Knockdown of ATOX1 suppressed tumor growth in vivo. Mechanistically, ATOX1 activated c-Myb, and thus enhanced the malignant phenotype of HCC cells via activation of the PI3K/AKT signaling pathway. Additionally, ATOX1 reduced intracellular copper accumulation and inhibited ROS production and apoptosis. Inhibition of ATOX1 by DCAC50 decreased cell proliferation while increasing ROS levels and apoptosis in HCC cells. Notably, acetylcysteine reversed the reduction in c-Myb expression induced by ATOX1 knockdown.

ATOX1 may promote HCC carcinogenesis through the activation of the c-Myb/PI3K/AKT pathway and the inhibition of copper accumulation and oxidative stress.

Full article
36
Research Letter Open Access
Jianhua Hu, Xiaoli Zhang, Zhibo Zhou, Fangfang Geng, Hongyu Jia, Linfeng Jin, Weixiang Zhong, Guodong Yu, Xue Wen, Hainv Gao, Yida Yang
Published online July 7, 2025
Journal of Clinical and Translational Hepatology. doi:10.14218/JCTH.2025.00175
37
Original Article Open Access
Dawu Zeng, Yanfang Huang, Sheng Lin, Naling Kang, Yanxue Lin, Jiaji Jiang, Yueyong Zhu, Qi Zheng, Jiming Zhang
Published online July 4, 2025
Journal of Clinical and Translational Hepatology. doi:10.14218/JCTH.2025.00205
Abstract
Patients with chronic hepatitis B virus (HBV) infection in the immune-tolerant phase may still experience hepatic inflammation and disease progression, and could benefit from early [...] Read more.

Patients with chronic hepatitis B virus (HBV) infection in the immune-tolerant phase may still experience hepatic inflammation and disease progression, and could benefit from early antiviral treatment. This study aimed to investigate changes in the cumulative hepatitis B surface antigen (HBsAg)/HBV DNA ratio in immune-tolerant patients during the transition to the immune-active phase, and to evaluate its potential in predicting the risk of disease progression.

This longitudinal study included 127 untreated immune-tolerant patients, who were followed for up to 10 years. An independent cohort of 109 subjects was retrospectively enrolled for external validation. The relationship between the cumulative HBsAg/HBV DNA ratio and the duration of immune tolerance or transition to the immune-active phase was examined. The predictive value of the ratio was assessed and validated.

The relationship between the cumulative HBsAg/HBV DNA ratio and disease progression risk showed a non-linear pattern: below a ratio of 1.791, the risk of disease progression decreased rapidly as the ratio increased; above 1.791, the risk plateaued. The area under the curve for predicting disease progression was 0.67, 0.64, and 0.85 for cumulative HBsAg, HBV DNA, and the HBsAg/HBV DNA ratio, respectively. Multivariable Cox regression analysis revealed the cumulative HBsAg/HBV DNA ratio as an independent predictor of disease progression, with higher ratios associated with a lower risk. Prediction models incorporating this ratio were developed and externally validated, demonstrating strong performance and clinical utility.

The cumulative HBsAg/HBV DNA ratio is an independent factor influencing the duration of immune tolerance and shows superior predictive performance. It may serve as a valuable marker for assessing the risk of disease progression in patients with chronic HBV infection.

Full article
38
Review Article Open Access
Mark D. Lucock, Robert J. Leeming
Published online July 4, 2025
Exploratory Research and Hypothesis in Medicine. doi:10.14218/ERHM.2025.00020
Abstract
The importance of putative folate-biopterin metabolic interactions lies in the role they may play in the expression of several clinically relevant phenotypes. However, to date, [...] Read more.

The importance of putative folate-biopterin metabolic interactions lies in the role they may play in the expression of several clinically relevant phenotypes. However, to date, clinical studies on folate-biopterin interactions have been limited. The purpose of this article was to highlight the close relationship between these two cofactors, which share structural similarities and exhibit overlapping metabolic pathways. This folate-biopterin crosstalk has generated several ideas and hypotheses that are critical to advancing the biochemical understanding of several important and seemingly disparate clinical and/or biologically important phenotypes. These phenotypes include melanization/pigmentation, phenylketonuria, autism, neural tube defects, affective disorders, and vascular disease. This review provides a timely, integrated overview of this important area of biochemistry, which is under-represented in the literature and would benefit from further scientific and clinical investigation using improved metabolite-specific analytical methodologies applied to clinically relevant questions.

Full article
39
Original Article Open Access
Xiuding Zhang, Haoda Weng, Qinzhi Deng, Min Deng, Xuwei Wu, Zuxiong Huang, Shourong Liu, Rui Wu, Chunlian Ma, Yao Xu, Jianfeng Zhong, Jie Yang, Yinxia Wu, Huajiang Shen, Feng Ding, Fang Wang, Xuezhen Zhai, Chunxian Peng, Haotang Ren, Jie Jin, Xiangfei Xu, Xiaofei Li, Xiaoting Ye, Guoqing Qian, Shuilin Sun, Xuebing Yao, Haifeng Miao, Qianggu Xiao, Shaoheng Ye, Qing Zhang, Xinyi Xu, Xia Yu, Yue Yu, Yan Lan, Huilan Tu, Xianbin Xu, Xinrong Zhang, Rui Huang, Xiaohan Qian, Qiao Yang, Jifang Sheng, Yu Shi
Published online July 3, 2025
Journal of Clinical and Translational Hepatology. doi:10.14218/JCTH.2025.00211
Abstract
Epidemiological data on bacterial infections in cirrhosis in China remain limited. Therefore, we aimed to conduct a multicenter study to investigate the characteristics and outcomes [...] Read more.

Epidemiological data on bacterial infections in cirrhosis in China remain limited. Therefore, we aimed to conduct a multicenter study to investigate the characteristics and outcomes of patients with cirrhosis and bacterial infections in China.

We retrospectively enrolled 1,438 hospitalized adult patients with cirrhosis and bacterial or fungal infections from 24 hospitals across China between January 2018 and September 2024. Data on demographics, clinical features, microbiology, treatment, and outcomes were collected.

A total of 1,783 infection episodes were recorded, including 1,668 first infections and 115 second infections. Most infections were community-acquired (86.6%). Pneumonia was the most common infection type (26.7%), followed by spontaneous bacterial peritonitis (19.5%) and spontaneous bacteremia (14.1%). Among 754 pathogens isolated from 620 patients, Klebsiella pneumoniae (20.1%) was nearly as common as Escherichia coli (21.7%). Multidrug-resistant (MDR) organisms accounted for 41.0% of all isolates, with extended-spectrum β-lactamase-producing Escherichia coli being the most prevalent MDR strain (8.9% of patients). Adherence to empirical antibiotic treatment guidelines from the European Association for the Study of the Liver was significantly lower in this cohort compared to the global study (21.5% vs. 61.2%, P < 0.001), accompanied by a lower clinical resolution rate (63.5% vs. 79.8%, P < 0.001).

The clinical and microbiological characteristics of bacterial infections in patients with cirrhosis in China differ substantially from those reported in other regions. These findings highlight the need for region-specific management and prevention strategies, particularly in light of the changing microbiological landscape, high MDR prevalence, and suboptimal antibiotic practices.

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40
Review Article Open Access
Luiz Alexandre Chisini, Luana Carla Salvi, Rodrigo Varella de Carvalho, Francine dos Santos Costa, Flávio Fernando Demarco, Marcos Britto Correa
Published online July 1, 2025
Gene Expression. doi:10.14218/GE.2025.00018
Abstract
This review presents the latest evidence on the link between genetic single nucleotide polymorphisms and dental caries, highlighting key genes and pathways involved, introducing [...] Read more.

This review presents the latest evidence on the link between genetic single nucleotide polymorphisms and dental caries, highlighting key genes and pathways involved, introducing foundational concepts, and discussing essential methodological considerations for future research. Several genes have been identified as significantly associated with caries experience, including those related to tooth mineral tissues, taste perception, salivary composition and flow, and immune response. Epistatic interactions appear to be crucial in explaining genetic influence. Inconsistencies in the literature are attributed to variations in caries classification, age groups, ethnic backgrounds, limited statistical power, and linkage disequilibrium. Population stratification often confounds results, and few studies adequately control for genetic ancestry. Ensuring Hardy-Weinberg equilibrium and accounting for linkage disequilibrium are essential to avoid bias. Bonferroni corrections for multiple comparisons are fundamental but rarely applied, contributing to inconsistent findings. In conclusion, genetic epidemiology studies suggest that dental caries has a genetic component, accounting for significant individual differences in disease risk.

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