Terminal ileum intubation is considered the completion step of colonoscopy and is usually performed to assess the ileum. The histological examination of the ileal mucosa, which is acquired during terminal ileum intubation, may allow an accurate diagnosis. However, there is no absolute consensus on when ileoscopy and biopsy should be attempted. As a result, we aimed to evaluate whether terminal ileum intubation and biopsy should be performed routinely.

Systematic searches were performed in the PubMed, EMBASE, and Cochrane Library databases, as well as the Science Citation Index via the Web of Science platform. Reference lists from the identified papers were manually searched. Systematic searches were performed from January 1, 1971, to October 1, 2025. Studies reporting on terminal ileum intubation and biopsy during colonoscopy were included. Case reports, letters, reviews, and animal studies were excluded. The primary outcomes were the diagnostic yield of terminal ileum intubation and the rate of necessitating a change in management. Data were extracted independently by three reviewers.

Thirty-six studies were included. The subtotal diagnostic yield and the rate of necessary change among the selected patients were much greater than those among the unselected patients (5.1% versus 2.5% and 1.5% versus 0.4%, respectively). In addition, the diagnostic yield was found more frequently for inflammatory bowel disease, anemia, abdominal pain, and chronic diarrhea than for the other indications (26.7%, 16.1%, 14.9%, 12.4%, and 3.2%, respectively). The yield of ileal histopathology with a normal endoscopic appearance was low in both unselected and selected patients (3.5% and 2.4%, respectively).

Terminal ileum intubation is recommended as gold standard for completing colonoscopy. Biopsy should be considered in patients with abnormal endoscopic findings or specific high-risk symptoms.

Unlike the traditional staging treatment of tumors, the core of “Green Tumor Treatment” is to divide the treatment of tumors into three stages: Hegemony (directly targeting the cancer focus), Kingship (supporting the body’s vital energy and eliminating pathogenic factors), and Imperialism (improving the internal environment), based on the urgency of the tumor and the patient’s physical condition. This approach guides the clinical treatment of tumors. Its treatment system incorporates all minimally invasive and low-damage treatment methods, combining internal and external treatments, traditional Chinese medicine and Western medicine, as well as local and systemic treatments. It aims to maximize treatment outcomes while ensuring the patient’s quality of life, which is highly consistent with the treatment goals for primary liver cancer. This review aims to explore the integrated Traditional Chinese and Western medicine treatment model for primary liver cancer under the guidance of the Green Tumor Treatment concept.

Dysphagia, a severe comorbidity of many neurological diseases, often lacks targeted therapies. Electrical stimulation of cranial nerves represents a novel therapeutic class. This critical review assessed the clinical effectiveness and safety of various approaches for electrical stimulation of the cranial nerves for treating dysphagia, categorized as implantable (directly targeting the nerve), minimally invasive (pharyngeal electrical stimulation), and non-invasive (transcutaneous). A critical literature review was conducted following the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines. The PubMed database was comprehensively searched, and studies were rigorously assessed for inclusion and exclusion criteria. The Newcastle–Ottawa Scale was used to assess the risk of bias. The analysis included 15 clinical studies: four assessing vagus nerve stimulation (including implantable and transcutaneous approaches) and eleven assessing pharyngeal electrical stimulation. Most evaluated studies, particularly for pharyngeal electrical stimulation and transcutaneous vagus nerve stimulation, demonstrated significant beneficial effects on validated dysphagia outcome measures. Importantly, no long-term severe adverse effects were reported across the evaluated stimulation approaches. Cumulative evidence indicates that vagus nerve stimulation and pharyngeal electrical stimulation approaches can effectively alleviate dysphagia symptoms. The different stimulation approaches appear to be complementary, with distinct profiles rendering them suitable for different therapeutic contexts (e.g., short-term hospital-based vs. long-term at-home treatment). Consequently, they represent distinct and valuable options for individualized dysphagia therapy.

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.

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.

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.