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    Original Article Open Access
    Unmasking Inflammatory Bowel Disease in Nigeria: A Multicenter Cross-sectional Analysis of Clinico-pathological and Endoscopic Findings
    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
    Journal of Translational Gastroenterology, Published online July 9, 2025. 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.

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    Original Article Open Access
    ATOX1 Promotes Hepatocellular Carcinoma Carcinogenesis via Activation of the c-Myb/PI3K/AKT Signaling Pathway
    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
    Journal of Clinical and Translational Hepatology, Published online July 7, 2025. 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.

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    Research Letter Open Access
    Development and Validation of a Novel Noninvasive Model to Predict Liver Fibrosis Staging in Untreated Patients with Chronic Hepatitis B
    Jianhua Hu, Xiaoli Zhang, Zhibo Zhou, Fangfang Geng, Hongyu Jia, Linfeng Jin, Weixiang Zhong, Guodong Yu, Xue Wen, Hainv Gao, Yida Yang
    Journal of Clinical and Translational Hepatology, Published online July 7, 2025. doi:10.14218/JCTH.2025.00175
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    Review Article Open Access
    Environmental Triggers’ Involvement in the Development of Type 1 Diabetes Mellitus
    Tajudeen Olanrewaju Yahaya, Umar Usman Liman, Caleb Dikko Obadiah, Zafira Illo Zakari, Daniel Anyebe, Boniface Gomo Clement, Balkisu Marafa Muhammad
    Exploratory Research and Hypothesis in Medicine, Published online July 27, 2022. doi:10.14218/ERHM.2022.00051
    Abstract
    The huge burden of type 1 diabetes mellitus (T1DM) has been a source of concern globally since the Industrial Revolution in the 18th–19th centuries. To this end, studies have shown [...] Read more.

    The huge burden of type 1 diabetes mellitus (T1DM) has been a source of concern globally since the Industrial Revolution in the 18th–19th centuries. To this end, studies have shown that certain environmental changes that accompanied the Revolution may have increased the risk and burden of the disease in genetically predisposed individuals. However, documented studies that synthesize these environmental triggers are scarce. As a result, the current study was conceived to synthesize the environmental triggers of T1DM to boost public awareness. Relevant information was retrieved from reputable academic databases; namely, Scopus, PubMed, SpringerLink, and Embase. The results showed that chemical exposure, viral infection, gut microbiome disruption, vitamin and mineral deficiencies, inadequate or exclusive breastfeeding, as well as early exposure to infant feeding formulas could increase the risk and burden of T1DM in genetically predisposed individuals. As a consequence, these triggers could compromise the expression of certain genes involved in insulin synthesis and immune function, such as the human leukocyte antigen (HLA), insulin (INS), cytotoxic T lymphocyte-associated antigen 4 (CTLA-4), and protein tyrosine phosphatase non-receptor type 22 (PTPN22) genes. This would result in a dysfunctional immune system in which immune cells, such as T-cells and B-cells and molecules, such as cytokines would attack self-tissues, thus causing autoimmunity of the pancreatic beta cells. Environmental triggers could also induce the T1DM pathophysiology by modifying the epigenome of the mentioned genes. Furthermore, some epigenetic changes could be reversed, which would infer that treatment procedures that would include the pathophysiology of the environmental triggers could be more effective.

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    Original Article Open Access
    Overexpression of RBM34 Promotes Tumor Progression and Correlates with Poor Prognosis of Hepatocellular Carcinoma
    Wei Wang, Rui Zhang, Ning Feng, Longzhen Zhang, Nianli Liu
    Journal of Clinical and Translational Hepatology, Published online July 13, 2022. doi:10.14218/JCTH.2022.00166
    Abstract
    Emerging evidence suggests that RNA-binding motif (RBM) proteins are involved in hepatocarcinogenesis and act either as oncogenes or tumor suppressors. The objective of this study [...] Read more.

    Emerging evidence suggests that RNA-binding motif (RBM) proteins are involved in hepatocarcinogenesis and act either as oncogenes or tumor suppressors. The objective of this study was to investigate the role of RBM34, an RBM protein, in hepatocellular carcinoma (HCC).

    We first examined the expression of RBM34 across cancers. The correlation of RBM34 with clinicopathological features and the prognostic value of RBM34 for HCC was then investigated. Functional enrichment analysis of RBM34-related differentially expressed genes (DEGs) was performed to explore its biological function. RNA sequencing (RNA-seq) was applied to identify downstream genes and pathways affected upon RBM34 knockout. The correlation of RBM34 with immune characteristics was also analyzed. The oncogenic function of RBM34 was examined in in vitro and in vivo experiments.

    RBM34 was highly expressed in hepatocellular carcinoma and correlated with poor clinicopathological features and prognosis. RBM34 was positively associated with tumor immune cell infiltration, biomarkers of immune cells, and immune checkpoint expression. A positive correlation was also observed between RBM34, T cell exhaustion, and regulatory T cell marker genes. Knockout of RBM34 significantly inhibited cell proliferation, migration, and xenograft tumor growth, and sensitized HCC cells to sorafenib treatment. RBM34 inhibition reduced FGFR2 expression and affected PI3K-AKT pathway activation in HCC cells.

    Our study suggests that RBM34 may serve as a new prognostic marker and therapeutic target of HCC.

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    Original Article Open Access
    Naringenin is a Potential Immunomodulator for Inhibiting Liver Fibrosis by Inhibiting the cGAS-STING Pathway
    Li Chen, Siwei Xia, Shuqi Wang, Yuanyuan Zhou, Feixia Wang, Zhanghao Li, Yang Li, Desong Kong, Zili Zhang, Jiangjuan Shao, Xuefen Xu, Feng Zhang, Shizhong Zheng
    Journal of Clinical and Translational Hepatology, Published online April 28, 2022. doi:10.14218/JCTH.2022.00120
    Abstract
    Naringenin is an anti-inflammatory flavonoid that has been studied in chronic liver disease. The mechanism specific to its antifibrosis activity needs further investigation This [...] Read more.

    Naringenin is an anti-inflammatory flavonoid that has been studied in chronic liver disease. The mechanism specific to its antifibrosis activity needs further investigation This study was to focused on the cyclic guanosine monophosphate-adenosine monophosphate synthase (cGAS) pathway in hepatic stellate cells and clarified the antifibrosis mechanism of naringenin.

    The relationship between the cGAS-stimulator of interferon genes (STING) pathway and liver fibrosis was analyzed using the Gene Expression Omnibus database. Histopathology, immunohistochemistry, fluorescence staining, Western blotting and polymerase chain reaction were performed to assess gene and protein expression levels associated with the cGAS pathway in clinical liver tissue samples and mouse livers. Molecular docking was performed to evaluate the relationship between naringenin and cGAS, and western blotting was performed to study the expression of inflammatory factors downstream of cGAS in vitro.

    Clinical database analyses showed that the cGAS-STING pathway is involved in the occurrence of chronic liver disease. Naringenin ameliorated liver injury and liver fibrosis, decreased collagen deposition and cGAS expression, and inhibited inflammation in carbon tetrachloride (CCl4)-treated mice. Molecular docking found that cGAS may be a direct target of naringenin. Consistent with the in vivo results, we verified the inhibitory effect of naringenin on activated hepatic stellate cells (HSCs). By using the cGAS-specific agonist double-stranded (ds)DNA, we showed that naringenin attenuated the activation of cGAS and its inflammatory factors affected by dsDNA. We verified that naringenin inhibited the cGAS-STING pathway, thereby reducing the secretion of inflammatory factors by HSCs to ameliorate liver fibrosis.

    Interrupting the cGAS-STING pathway helped reverse the fibrosis process. Naringenin has potential as an antihepatic fibrosis drug.

    Full article
Special Features

Call for Papers for Special Issue 'Updates of Cytopathology Reporting Systems'

Journal: Journal of Clinical and Translational Pathology
Special Issue: Updates of Cytopathology Reporting Systems
Submission deadline: November 30, 2023
Publication date: An article will be published online as soon as it is accepted

Call for Papers for Special Issue 'Frontier research on the toxicity and efficacy of Chinese medicine'

Journal: Future Integrative Medicine
Special Issue: Frontier research on the toxicity and efficacy of Chinese medicine
Submission deadline: June 30, 2023
Publication date: An article will be published online as soon as it is accepted

Call for Papers for Special Issue ‘New Translational Challenges in Primary Biliary Cholangitis’

Journal: Journal Clinical and Translational Hepatology
Special Issue: New Translational Challenges in Primary Biliary Cholangitis
Submission deadline: June 30, 2023
Publication date: An article will be published online as soon as it is accepted

Call for Papers for Special Issue ‘A Spotlight on Progress and Pitfalls in NAFLD/MAFLD Studies, 2022’

Journal: Journal of Clinical and Translational Hepatology
Special Issue: A Spotlight on Progress and Pitfalls in NAFLD/MAFLD Studies, 2022
Submission deadline: March 30, 2023
Publication date: An article will be published online as soon as it is accepted

Call for Papers for Special Issue 'Comparative study of traditional medicine in the world'

Journal: Future Integrative Medicine
Special Issue: Comparative study of traditional medicine in the world
Submission deadline: June 30, 2023
Publication date: An article will be published online as soon as it is accepted

Call for Papers for Special Issue 'Therapeutic effects of herbal medicines on neurological impairment and related mental disorders based on the evidence of clinical and basic studies'

Journal: Future Integrative Medicine
Special Issue: Therapeutic effects of herbal medicines on neurological impairment and related mental disorders based on the evidence of clinical and basic studies
Submission deadline: June 30, 2023
Publication date: An article will be published online as soon as it is accepted

Call for Papers for Special Issue ‘Immunoregulatory Mechanisms of Herbal Medicines in Cancer and Infectious Diseases’

Journal: Future Integrative Medicine
Special Issue: Immunoregulatory Mechanisms of Herbal Medicines in Cancer and Infectious Diseases
Submission deadline: June 30, 2023
Publication date: An article will be published online as soon as it is accepted
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