End-stage liver disease (ESLD) is characterized by a dramatic deterioration of liver function, frequently accompanied by systemic inflammatory storms and multiple organ failures. Central to the onset and progression of ESLD, systemic inflammation arises from complex interactions among various inflammatory signaling molecules and immune cells within and beyond the liver. As key inflammatory modulatory molecules, bioactive oxylipins have been increasingly recognized for their complex molecular mechanisms implicated in various diseases. This review aims to summarize recent findings regarding the molecular and immunological mechanisms through which oxylipins contribute to the development of liver injury and failure, with emphasis on both substantial intrahepatic and extrahepatic immune and inflammatory dysregulation associated with ESLD. Furthermore, this review discusses the translational potential of targeting oxylipins for clinical diagnosis, prognosis, and therapeutic intervention in ESLD.

Identifying patients at high risk for poor bowel preparation preceding a colonoscopy is critical to successful colorectal cancer screening. High-risk patients, such as those who are obese, diabetic, opioid users, or former smokers, often have comorbidity, medication, and sociodemographic factors that lead to suboptimal bowel preparation even when following protocol. Suboptimal preparation results in missed lesions, longer procedure times, and increased healthcare costs. Optimal visualization of the colon mucosa is achieved through effective bowel preparation. Polyethylene glycol (PEG) solutions are preferred for their safety, especially in patients with kidney or cardiac disease. Split-dose PEG regimens with a low-residue diet are recommended by the American Gastroenterological Association to promote cleansing and patient tolerance. Tailored regimens can be employed in high-risk patients, including those with chronic constipation, opioid dependence, or diabetes. Educational interventions, such as written and verbal instructions, patient navigators, and mobile device reminders, improve compliance. Medical strategies include split-dose PEG-electrolyte lavage solution with bisacodyl, additional purgatives for select patients, and avoidance of sodium phosphate in elderly or renally impaired individuals. Open-access colonoscopy services have expanded following the COVID-19 pandemic to manage backlogs and improve access. Improving education, simplifying regimens, and targeting interventions can reduce repeat procedures and enhance colorectal cancer detection. This narrative review summarizes patient-, medication-, and system-level risk factors for inadequate bowel preparation in high-risk populations and synthesizes practical, evidence-based strategies to optimize colonoscopy quality, including in open-access settings.

This Consensus aims to establish a physician–pharmacist co-management model to standardize the rational clinical application of anti-immunoglobulin E monoclonal antibodies in the treatment of allergic asthma. Focusing on the critical components of physician–pharmacist co-management, key issues related to anti-immunoglobulin E monoclonal antibody therapy were identified through a systematic literature review and clinical practice experience. Evidence quality was evaluated using an evidence grading system, and the Delphi method was applied to reach expert consensus. Centered on omalizumab, the Consensus presents 12 recommendations covering the work model of physician–pharmacist co-management, clinical management pathways, hierarchical diagnosis and treatment systems, as well as training and competency assessment. The Delphi process achieved a high degree of consensus (agreement >80%) on 12 key recommendations, emphasizing a 60-min observation period post-injection and quarterly follow-up evaluations. It establishes a standardized framework for the co-management of omalizumab therapy in allergic asthma. Results highlighted that co-management effectively monitors omalizumab dosage (75–600 mg) and maintains a consensus threshold of >80% for patient safety protocols. The Consensus provides a standardized framework for physician–pharmacist co-management, which is expected to facilitate rational drug use and improve patient care pathways in omalizumab 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.