circPVT1 has emerged as a key regulator in disease progression and clinical outcomes. However, its prognostic relevance and association with clinicopathological parameters in solid malignancies remain to be fully elucidated. To address this, we conducted a meta-analysis to elucidate the clinical significance of circPVT1 in solid tumors.

A comprehensive literature search was conducted across multiple databases, including PubMed, Web of Science, Embase, the Cochrane Library, and CNKI, with a cutoff date of December 31, 2024. Statistical analyses were conducted using STATA 12.0 to calculate pooled hazard ratios (HRs) and odds ratios (ORs) with 95% confidence intervals (CIs), assessing the impact of circPVT1 expression on overall survival (OS) and its association with clinicopathological characteristics.

This analysis included 27 clinical studies encompassing a total of 2,219 patients. Elevated circPVT1 expression was significantly associated with poorer OS in patients with solid tumors (HR = 1.68, 95% CI: 1.39–2.02, P < 0.001). This association was particularly notable in lung cancer (HR = 2.08, 95% CI: 1.51–2.88, P < 0.001) and osteosarcoma (HR = 1.65, 95% CI: 1.38–1.97, P < 0.001), with similar trends observed in hepatocellular carcinoma, colorectal cancer, and papillary thyroid carcinoma. Furthermore, the increased circPVT1 level was correlated with larger tumor size (OR = 1.36, 95% CI: 1.11–1.67, P = 0.004), lymph node metastasis (OR = 1.56, 95% CI: 1.22–2.00, P < 0.001), distant metastasis (OR = 1.80, 95% CI: 1.10–2.92, P = 0.017), and advanced tumor-node-metastasis stage (OR = 1.84, 95% CI: 1.50–2.25, P < 0.001).

Aberrant circPVT1 expression is associated with adverse OS and unfavorable clinicopathological features in solid tumors, underscoring its potential utility as a prognostic biomarker and indicator of tumor aggressiveness.

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.

The incidence of early-onset pancreatic cancer (EOPC) is rising, yet optimal treatment strategies remain unclear. While adjuvant chemotherapy (ACT) has shown survival benefits in pancreatic ductal adenocarcinoma, its specific role in EOPC patients following neoadjuvant chemotherapy (NACT) and surgery remains underexplored. This study aimed to assess the clinical benefit of ACT in EOPC patients after NACT.

This retrospective cohort study analyzed pancreatic ductal adenocarcinoma patients from the SEER database (2006–2019) who received NACT followed by curative resection. Propensity score matching (1:1) was used to balance covariates such as tumor, lymph node, metastasis stage, chemotherapy, and radiotherapy. Overall survival (OS) and cancer-specific survival (CSS) were compared between patients with EOPC (<50 years) and average-onset pancreatic cancer (AOPC, ≥50 years). Multivariate Cox regression analysis was performed to identify prognostic factors.

After propensity score matching (124 EOPC vs. 124 AOPC), EOPC patients had significantly longer median OS (41.0 vs. 29.0 months, P = 0.042) and CSS (48.0 vs. 30.0 months, P = 0.016). ACT was an independent prognostic factor for EOPC (OS: hazard ratio = 0.495, 95% confidence interval 0.271–0.903, P = 0.022; CSS: hazard ratio = 0.419, 95% confidence interval 0.219–0.803, P = 0.009), but not for AOPC (P > 0.05). Subgroup analysis revealed that EOPC patients with tumor, lymph node, metastasis stage II disease or those receiving ACT derived the greatest survival benefit.

EOPC patients exhibit superior survival following NACT and surgical resection compared to AOPC, with ACT further enhancing outcomes in this subgroup. These findings support the use of tailored ACT for EOPC and underscore the need for prospective validation.

Coronary heart disease is an ischemic condition characterized by vascular stenosis or obstruction caused by coronary atherosclerosis, resulting in myocardial ischemia, hypoxia, or necrosis. It is one of the leading causes of death in both urban and rural populations in China. Safflower yellow pigments, the main active components of the traditional Chinese herbal medicine safflower, are primarily composed of quinochalcone compounds, including hydroxysafflor yellow A and anhydrosafflor yellow B—of which hydroxysafflor yellow A is the principal component. Studies have demonstrated that these pigments can improve myocardial ischemia, reduce ischemia-reperfusion injury, alleviate atherosclerotic damage, and address risk factors associated with coronary heart disease. This review aimed to systematically and comprehensively summarize the mechanisms of action of safflower yellow pigments and their active components in the context of coronary heart disease and its related risk factors.

Metabolic dysfunction-associated fatty liver disease, representing a spectrum of liver disorders from simple steatosis to metabolic dysfunction-associated steatohepatitis, fibrosis, and cirrhosis, has emerged as one of the most prevalent chronic liver conditions globally, affecting an estimated approximately 30% of the world's population. Its pathogenesis is highly complex, involving intricate interactions between genetic predisposition, metabolic dysregulation, inflammation, and cellular stress responses. Within this complex landscape, orphan nuclear receptors (ONRs) have gained significant attention. Defined by the lack of identified endogenous ligands, ONRs function as master transcriptional regulators controlling diverse biological processes. Crucially, they play pivotal roles in the development and progression of numerous diseases, including metabolic disorders.This review specifically focuses on elucidating the critical contributions of various ONRs to the pathogenesis of metabolic dysfunction-associated fatty liver disease. We examined how these receptors modulate key pathological drivers: lipid metabolism, inflammation,and autophagy.

Drug-induced liver injury (DILI) represents a prevalent adverse event associated with medication use. However, the exact mechanisms underlying DILI remain incompletely understood, and the lack of specific diagnostic and prognostic biomarkers poses significant challenges to the clinical diagnosis and treatment of this condition. Consequently, our study aimed to endeavor to identify serum and fecal metabolic biomarkers, enabling more accurate DILI diagnosis and improved prediction of chronic progression.

Untargeted metabolomics analysis was performed on serum and fecal samples obtained from a cohort of 32 DILI patients (causality confirmed via the updated Roussel Uclaf Causality Assessment Method) and 36 healthy controls. Utilizing techniques such as partial least squares-discriminant analysis modeling and t-tests, we identified significantly differentially expressed metabolites and metabolite sets. Causality assessment was performed using the updated Roussel Uclaf Causality Assessment Method.

The findings from the analysis of serum and fecal metabolomics association pathways suggested that perturbations in bile acid metabolism might serve as potential mechanisms underlying the progression of DILI. Our study revealed 22 overlapping differential metabolites between serum and feces, displaying significant concentration differences between the DILI and healthy control groups. Notably, we identified chenodeoxycholic acid and deoxycholic acid as promising markers that not only distinguished DILI patients from healthy individuals but also exhibited predictive potential for DILI chronicity.

The integrated analysis of serum and fecal metabolites uncovers the significant disruption of bile acid metabolites as a key contributing factor in the pathogenesis of DILI. Our study offers promising potential biomarkers for the diagnosis and prognosis of DILI, paving the way for a novel perspective in the realm of DILI diagnosis and treatment.