Nanobiotechnology has driven transformative advancements in healthcare, particularly in the development of innovative solutions for wound treatment, a persistent and costly global health concern. Among these advancements, the combination of biopolymers and metallic nanoparticles has attracted considerable interest due to their excellent biocompatibility and potent antimicrobial activity. This scoping review explores recent technological progress in wound care, with a focus on alginate-based dressings functionalized with metallic nanoparticles. Alginate, a highly versatile biopolymer, was frequently employed in diverse formats, including hydrogels, sponges, beads, films/membranes, and fibers, across the analyzed studies. Silver nanoparticles were the most extensively investigated agents, owing to their well-established efficacy and the development of strategies to mitigate associated risks. Other metallic nanoparticles were also reported, contributing to a growing body of evidence supporting their therapeutic relevance. The synergistic integration of alginate and metallic nanoparticles has shown promising potential to enhance the performance of wound dressings, representing a significant step forward in the design of next-generation materials for effective and targeted wound management.

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.

Skin cancer, the most common global malignancy, is linked to ultraviolet (UV)-driven serum 25-hydroxyvitamin D (25(OH)D)synthesis, with its controversial role possibly reflecting cumulative UV exposure. This study aimed to assess the association and causality between 25(OH)D levels and skin cancer risk using the National Health and Nutrition Examination Survey (1999–2018) data and Mendelian randomization (MR) analyses, evaluating 25(OH)D as a screening biomarker.

We integrated data from the National Health and Nutrition Examination Survey (1999–2018; n = 21,357 U.S. adults, including 631 skin cancer cases) with MR analyses using genome-wide association study-derived genetic variants to assess the causal relationship between serum 25(OH)D levels and skin cancer risk.

Higher 25(OH)D levels were associated with increased risks of nonmelanoma skin cancer [odds ratio (OR) (95% confidence interval (CI)) = 2.94 (2.10, 4.20)], melanoma [OR (95% CI) = 2.94 (1.73, 5.28)], and other skin cancers [OR (95% CI) = 2.10 (1.36, 3.36)]. MR analyses supported a causal relationship for nonmelanoma skin cancer [OR (95% CI) = 1.01 (1.00, 1.02)] and melanoma [OR (95% CI) = 1.00 (1.00, 1.01)]. Risks were highest in males, older adults, and individuals with obesity.

Higher serum 25(OH)D levels are associated with increased skin cancer risk, likely reflecting cumulative UV exposure. Routine monitoring of 25(OH)D, combined with UV exposure management, is recommended for risk stratification in skin cancer screening, particularly among high-risk groups. Validation in multiethnic cohorts is needed to confirm these findings.

Delirium, commonly observed in critically ill patients following intracerebral hemorrhage (ICH), is an acute neuropsychiatric disorder characterized by disturbances in attention, consciousness, and cognition. The underlying brain network mechanisms remain poorly understood. This study aimed to explore the functional connectivity (FC) of the ascending reticular activating system (ARAS) in delirium patients with basal ganglia ICH and to identify potential biomarkers for predicting delirium onset.

In this cross-sectional study, brain networkomics techniques were used to examine the FC within the ARAS in ICH patients with and without delirium. A two-sample t-test compared differences in ARAS connectivity between delirium and non-delirium groups, identifying abnormal brain regions and their corresponding FC values. Receiver operating characteristic curve analysis was then performed to evaluate the predictive value of FC for delirium onset.

A significant disruption in FC between the brainstem ARAS nuclei and the left parahippocampal gyrus was observed in ICH patients with delirium. The FC strength between these regions was a reliable predictor of delirium occurrence, with an area under the curve of 0.893, indicating high predictive accuracy.

The disruption of FC between the brainstem ARAS nuclei and the left parahippocampal gyrus may represent a key mechanism underlying delirium pathogenesis. The strength of this connectivity could serve as a potential biomarker for predicting delirium onset. Future research should focus on strategies to restore this connectivity as a potential treatment for early reversal of delirium.

Liver failure syndromes are characterised by a dysregulated immune response leading to immune paralysis. Adrenomedullin (ADM) is a potent vasodilator and immunoregulator. This study aimed to explore the role of ADM in liver failure, hypothesising that there is a detrimental imbalance between ADM and adrenomedullin binding protein (AMBP)1 that promotes a switch of monocytes/macrophages towards a pro-restorative phenotype and function.

Consecutive patients with acute liver failure (ALF), acute-on-chronic liver failure (ACLF), and decompensated cirrhosis, as well as healthy controls (HC) were included between April 2020 and June 2024. Peripheral blood mononuclear cells/monocytes were isolated and used for RNA sequencing and cell culture. ADM and AMBP1 were measured by enzyme-linked immunosorbent assay.

Fifty-four patients with ALF, 25 with ACLF, 9 with decompensated cirrhosis, and 16 with HC were included. ADM expression in isolated monocytes was increased in ALF (log fold change = 5.88, p = 0.000216413) and ACLF (log fold change = 4.62, p = 0.00057122) compared to HC. Plasma ADM concentration was higher in ALF (1,684 ± 1,156 pg/mL) vs. ACLF (836.1 ± 765.2 pg/mL) and HC (164.8 ± 62.73 pg/mL). AMBP1 was significantly reduced in ALF (59.27 ± 44 µg/mL) vs. ACLF (126.3 ± 72.23 µg/mL) and HC (252.8 ± 159.7 µg/mL) (p < 0.0001, ALF vs. HC). Treatment with LPS increased ADM concentration in peripheral blood mononuclear cell supernatant (ALF n = 6; 561.4 ± 1,038 pg/mL vs. 259.2 ± 213.7 pg/mL, ACLF n = 4; 3,202 ± 491.2 vs. 1,757 ± 1,689 pg/mL). The percentage of CD14+ cells expressing Mer tyrosine kinase was reduced after culture with LPS (2.077 ± 0.87%); however, co-culture with ADM 100 nM restored the phenotype (3.852 ± 1.063%).

ADM is increased in liver failure, whereas AMBP1 is reduced. ADM affects monocyte function, increasing Mer Tyrosine Kinase and promoting a pro-restorative, anti-inflammatory phenotype.

Autoimmune hepatitis (AIH) is a severe immune-mediated liver disease with limited treatment options beyond immunosuppressants, which carry significant side effects. Existing evidence suggests that mesaconate (MSA) possesses immunomodulatory properties and may offer advantages over itaconate derivatives by avoiding succinate dehydrogenase inhibition. However, its specific role in AIH remains unclear. This study aimed to investigate the therapeutic effects of MSA on AIH and to elucidate its underlying mechanisms of action.

A murine AIH model was established via tail vein injection of concanavalin A (ConA, 20 mg/kg). MSA (250 mg/kg) was administered intraperitoneally 6 h before ConA exposure. Liver histology, serum transaminase levels, apoptosis markers, oxidative stress markers, and inflammatory cytokines were analyzed to assess the therapeutic efficacy of MSA. Additionally, RNA sequencing and Western blotting were performed to explore the mechanisms of MSA action. In vitro validation was conducted using RAW264.7 macrophages pretreated with MSA (1 mM) followed by interferon-gamma (IFN-γ, 50 ng/mL) stimulation.

MSA pretreatment effectively mitigated ConA-induced AIH by reducing inflammatory responses, oxidative stress, and apoptosis both in vivo and in vitro. The underlying protective mechanism involved MSA-mediated downregulation of IFN-γ expression and subsequent inhibition of the Janus tyrosine kinase 1/2–signal transducer and activator of transcription 1 signaling pathway. The involvement of this pathway in human AIH was also confirmed.

This study provides the first evidence that MSA ameliorates AIH by suppressing the IFN-γ–Janus tyrosine kinase 1/2–signal transducer and activator of transcription 1 signaling pathway, offering novel mechanistic insights and a promising therapeutic candidate for the future treatment of autoimmune disorders.

Radiotherapy remains one of the essential treatment modalities for brain gliomas, brain metastases, pediatric neuroblastomas, and primary central nervous system lymphomas. With continuous advancements in modern radiotherapy techniques, patients have achieved significantly improved local control rates and prolonged survival. However, the long-term complications associated with radiotherapy have become increasingly evident. Radiation-induced brain injury (RIBI) is a clinical syndrome characterized primarily by neurological dysfunction following focal or whole-brain radiotherapy. It negatively impacts patients’ quality of life and imposes a considerable burden on families and society. With the rapid development of medical imaging and artificial intelligence technologies, multimodal imaging techniques, including structural magnetic resonance imaging, diffusion-weighted imaging, functional magnetic resonance imaging, perfusion imaging, positron emission tomography-computed tomography metabolic imaging, and radiomics, have demonstrated significant potential for early detection, dynamic monitoring, and quantitative evaluation of RIBI. Meanwhile, treatment strategies for RIBI are shifting from traditional symptomatic and supportive care toward multidimensional interventions aimed at protecting the blood-brain barrier, modulating neuroinflammation, and implementing precise targeted therapies. Additionally, emerging studies have explored neuromodulation techniques and gut-brain axis regulation, offering new directions for the prevention and treatment of RIBI. Although conventional imaging methods remain valuable for diagnosing RIBI, they exhibit notable limitations in the early stages of the disease and in differentiating RIBI from tumor recurrence. This review focuses on the current state of technological development, key findings, and existing limitations, with the aim of providing a theoretical foundation and technical support for the early identification and precise intervention of RIBI.

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.

Khat (Catha edulis) is a plant native to East Africa and the Arabian Peninsula, chewed for its stimulant effects by millions worldwide. Its sympathomimetic properties, primarily due to cathinone and other pyrrolizidine alkaloids, resemble those of amphetamine. Emerging reports have linked khat use to the development of autoimmune hepatitis, supported by elevated autoimmune markers, characteristic liver biopsy findings, and clinical resolution following khat cessation or a prompt response to corticosteroid therapy without recurrence. In this review, we aimed to update knowledge on both acute and chronic forms of khat-associated AIH. We discuss cathinone metabolism, pharmacokinetics, and proposed mechanisms of khat hepatotoxicity. We also provide an updated synthesis of published cases of khat-associated autoimmune hepatitis, including our calculated Roussel-Uclaf Causality Assessment Method analysis and the simplified Hennes AIH score where data were available. Case presentations, diagnostic criteria, histopathological findings, and treatment approaches are summarized to help guide management.