Hepatic metastasis (HM) and lymph node metastasis in pancreatic ductal adenocarcinoma (PDAC) are associated with worse overall survival, largely due to the immunosuppressive microenvironment. However, the key immunosuppressive cells within this microenvironment remain inadequately defined. This study aimed to identify the cells contributing to HM and lymph node metastasis in PDAC and to investigate their regulatory mechanisms.

Single-cell RNA sequencing was used to profile the tumor microenvironment in HM, lymph node-negative, and lymph node-positive (LNP) PDAC tissues. Bioinformatic analyses revealed subtypes of immunosuppressive myeloid-derived suppressor cells (MDSCs). Immunofluorescence and flow cytometry were performed to detect the distribution and proportion of interleukin-1 receptor antagonist (IL1RA+) MDSCs. The immunosuppressive and pro-tumorigenic functions of IL1RA+ MDSCs were analyzed using enzyme-linked immunosorbent assay, quantitative reverse transcription polymerase chain reaction, Western blotting, and Transwell assays. Patient-derived xenograft mouse models were employed to validate the role of IL1RA+ MDSCs in vivo.

Polymorphonuclear-MDSCs were found to be recruited to metastatic PDAC tissues. Among these, IL1RA+ MDSCs were enriched in HM/LNP tissues and correlated with poorer prognosis. IL1RA+ MDSCs promoted M2 macrophage polarization and suppressed the activity of natural killer cells and cytotoxic T cells. Furthermore, IL1RA+ MDSCs accelerated PDAC migration and progression by upregulating epithelial–mesenchymal transition-related proteins in both in vitro and in vivo models.

IL1RA+ MDSCs represent a key immunosuppressive and pro-tumorigenic subtype in HM/LNP PDAC, providing a solid theoretical basis for prognostic prediction and the development of immunotherapeutic strategies targeting these cells in HM/LNP PDAC.

Artificial intelligence (AI) translation in genitourinary (GU) pathology has progressed unevenly across organs and tasks. This review addresses a central clinical question: which GU pathology AI applications are deployment-ready, which require further validation, and what frameworks can guide safe implementation? We synthesize evidence across GU organs and introduce pragmatic translation frameworks to guide deployment and prioritize translational research.

Narrative review integrating foundational literature with targeted 2023–2025 publications, emphasizing regulatory milestones, external validation, and prospective studies. Literature was identified through PubMed, Embase, and conference proceedings using structured search terms for AI, digital pathology, and GU organ-specific queries. For each organ/task, we mapped evidence strength, regulatory maturity, generalizability, workflow integration, safety, and feasibility to a Translational Readiness Index (TRI) rubric (0–30 scale).

Prostate biopsy AI demonstrates the strongest maturity (TRI 26/30), supported by U.S. Food and Drug Administration-cleared systems, multi-site validation, and prospective implementations showing efficiency gains and reduced ancillary testing. Bladder cytology shows moderate readiness (TRI 19/30), with commercial offerings supporting pilotable prescreening workflows aligned with the Paris System when paired with uncertainty-aware deferral. Bladder histology, renal neoplasia, and low-prevalence domains (testis, penis) remain emerging (TRI 6–15/30), constrained by label variability, rare subtype underrepresentation, and limited external validation.

The TRI rubric, SURE-Path safety bundle, and VALIDATED/ORCHESTRATE implementation pathway provide a practical template for evidence-based deployment in GU pathology. Clinically defensible translation requires matching intended use to validation evidence, with explicit safeguards for emerging applications.

Pediatric low-grade gliomas (pLGGs) exhibit distinct biological and clinical characteristics compared to adult gliomas, and their treatment strategies differ substantially from those used in adults. Since the release of the 2016 World Health Organization Classification of Tumors of the Central Nervous System and its subsequent updates, significant advances have been made in understanding the diagnosis and management of pLGGs. Therefore, updated guidelines tailored to current clinical practice are needed. In this document, we present the consensus guidelines for the diagnosis and management of pLGGs in China. The recommendations were developed through a comprehensive review of relevant domestic and international guidelines and literature, combined with expert consensus meetings and external peer review to ensure rigorous validation. The guideline integrates the levels of evidence from published studies, expert consensus, and practical clinical considerations. All recommendations were reviewed and approved by a multidisciplinary panel of experts from the Pediatric Neurosurgery Group. This guideline is intended to serve as guidance for healthcare professionals involved in pediatric neuro-oncology, as well as for patients, caregivers, and other healthcare providers participating in the management of pLGGs.

The incidence and mortality of stroke are gradually increasing. In this context, post-stroke neuronal loss and the related long-term complications, along with costly treatment strategies, are significant concerns for healthcare professionals, and effective, convenient, and inexpensive therapeutic modalities are required. Natural and easily accessible herbal remedies may be the optimal option in post-stroke recovery. This narrative review aims to summarize the neuroprotective properties of Withania somnifera (Ashwagandha) and its therapeutic efficacy in neuronal plasticity and recovery after stroke. Original research articles, reviews, and case studies were sourced from databases such as PubMed, Web of Science, Scopus, Google Scholar, Medline, and Embase. Only full articles published in English up to July 2025 were considered. Keywords including W. somnifera, Ashwagandha, stroke, cerebral ischemia, neurodegeneration, neuronal loss, and post-stroke recovery were utilized for the literature search. It has been found that various plant parts of W. somnifera are abundant in bioactive compounds. The neuroprotective effects of W. somnifera are documented in numerous diseases. Nevertheless, W. somnifera is reported to be involved in modulating various biological pathways to mitigate neuroinflammation, apoptosis, and oxidative stress in stroke. W. somnifera promotes cell proliferation and enhances neurogenesis. Preclinical experiments on murine models show the effectiveness of W. somnifera in post-stroke recovery by enhancing neural plasticity and reducing neuronal loss in the infarct area. Furthermore, W. somnifera boosts neurotransmitter levels, improves motor functions, and enhances memory. It also decreases neutrophil infiltration in the infarct region and lessens neuronal loss. Therefore, the application of W. somnifera may prove advantageous in facilitating post-stroke recovery by enhancing neural function. However, well-designed clinical trials are needed to confirm the efficacy of W. somnifera in post-stroke recovery in humans.

Early and accurate prognostic assessment is crucial to avoid serious disease progression in patients with liver failure. Thyroid hormone is an important metabolic regulator involved in hepatic function. This review examines the pathophysiological regulation in detail of the hypothalamic-pituitary-thyroid axis in patients with liver failure and emphasizes the importance of thyroid profiling (thyroid-stimulating hormone, T3, and T4) in prognostic assessment and risk stratification. T3 can enhance liver regeneration. The clinical application of thyroid hormone replacement therapy in patients with acute-on-chronic liver failure complicated by non-thyroidal illness syndrome is controversial. This review aims to inform clinical practice regarding the relevance of thyroid hormone level assessment in liver failure and to provide novel insights into the prognostic evaluation and comprehensive care of liver failure complicated by thyroid dysfunction.

Febrile neutropenia (FN) is one of the acute and serious complications of chemotherapy-induced myelosuppression in tumor patients. Antibiotics and granulocyte colony-stimulating factor are the mainstays of its treatment. However, this therapy still faces many challenges and may trigger drug resistance, as well as adverse effects such as bone pain and vasculitis. How to minimize treatment-related toxicity while ensuring therapeutic efficacy has become a key issue to be addressed in current clinical practice. In recent years, traditional Chinese medicine (TCM) has demonstrated unique advantages in the prevention and treatment of FN. We conducted a comprehensive search of the PubMed, Web of Science, and CNKI databases using keywords such as TCM and FN, covering the period from their establishment to May 2025. Clinical studies have shown that the combination of TCM and modern medicine can significantly reduce the incidence of FN, while also enhancing the number of granulocytes, shortening the duration of fever, improving the quality of life of patients, and reducing other toxic effects of chemotherapy. These results suggest that TCM is a promising and safe complementary therapy. However, more high-quality trials are needed to verify its benefits. This review summarizes the latest progress in the treatment of FN with TCM and discusses future development directions.

Metabolic dysfunction-associated steatotic liver disease (MASLD) and sarcopenia frequently coexist, yet their causal relationship and underlying mechanisms remain poorly defined. This study aimed to investigate whether a bidirectional causal link exists between MASLD and sarcopenia and to identify the molecular mediators involved in liver-muscle crosstalk.

We applied Mendelian randomization to test the causal effect of sarcopenia-related traits on MASLD risk. To capture distinct clinical features, we established complementary mouse models, including diet-induced and genetic (ob/ob) MASLD models, a stelic animal model, and a drug-induced muscle atrophy model. Multi-tissue transcriptomic profiling was performed on liver and muscle to uncover altered pathways.

Complementing prior genetic evidence establishing MASLD as a causal factor for sarcopenia, our Mendelian randomization analysis revealed that diminished muscle mass and muscle function contribute to an elevated risk of MASLD. In mice with MASLD, we observed loss of muscle mass, reduced strength, and ectopic lipid deposition in skeletal muscle. Conversely, muscle atrophy exacerbated hepatic steatosis, inflammation, and fibrosis in MASLD mice. Transcriptional profiling revealed that sarcopenia impairs hepatic metabolic homeostasis by enhancing fatty acid uptake and impairing oxidative phosphorylation, while MASLD, in turn, promotes muscle dysfunction by exacerbating inflammatory responses and metabolic dysfunction. We further identified C-C motif chemokine ligand 2 as a key myokine that drives MASLD, and adrenomedullin as a key hepatokine that triggers sarcopenia.

Our findings suggest a potential bidirectional causal relationship between MASLD and sarcopenia, which may be partially mediated by C-C motif chemokine ligand 2 and adrenomedullin.

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.

A long-term high-fat diet (HFD) exerts lipotoxic effects on multiple organs, particularly the liver, leading to metabolic diseases. This study aimed to delineate the dynamic effects of HFD on lipid metabolism, elucidate the mechanisms underlying hepatic lipotoxicity, and investigate the protective effects of Ganoderma lucidum against lipotoxicity both in vitro and in vivo.

C57BL/6 mice were fed either a 45% or 60% HFD, followed by measurements of body composition, serum lipid profile, and liver pathology at four, eight, twelve, and sixteen weeks. Inflammatory responses, the unfolded protein response (UPR), and endoplasmic reticulum (ER)-phagy were examined in the livers of mice at 16 weeks. Male C57BL/6 mice were randomly assigned to four groups (n = 12 per group): normal diet, 45% HFD, and two HFD + Ganoderma lucidum water extract (GLE) groups (1 g/kg/d and 2 g/kg/d of crude drug, orally administered by gavage for eight weeks following a four-week HFD induction).

Body weight, body fat, serum lipids, and hepatic steatosis increased progressively, accompanied by impaired glucose tolerance and liver injury, as indicated by elevated serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels. HFD also induced activation of the STING and NF-κB signaling pathways, as well as the PERK and IRE1 branches of the UPR. Similarly, ER-phagy selective receptors, particularly FAM134B, which is primarily expressed in hepatocytes as shown by single-cell sequencing, were upregulated after 16 weeks of HFD feeding. Furthermore, GLE mitigated palmitic acid-induced lipotoxicity in primary hepatocytes, as evidenced by improved cell viability, reduced ALT, AST, and lactate dehydrogenase levels in the culture supernatant, and decreased transferase dUTP nick-end labeling-positive cell counts. In 45% HFD-fed mice, GLE reduced serum total cholesterol, low-density lipoprotein, and hepatic triglyceride levels.

HFD-induced lipotoxicity causes hepatic tissue injury and inflammatory responses, which may be alleviated by coordinated regulation of compensatory UPR and ER-phagy. Ganoderma lucidum shows promise as a dietary supplement for managing metabolic disorders.

Terahertz (THz) radiation is increasingly explored for biomedical applications, however, its non-thermal effects on cellular metabolism and regulatory networks remain insufficiently characterized. This study aimed to investigate how 2.3 THz radiation affects metabolic pathways and membrane-associated signaling in human melanoma cells.

SK-MEL-28 melanoma cells were exposed to 2.3 THz radiation for 45 min using the 1st Novosibirsk free-electron laser. Cell viability was assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and trypan blue assays. Metabolic alterations were detected by targeted metabolomics using liquid chromatography–tandem mass spectrometry. Gene network analysis was performed using the ANDSystem platform to reconstruct gene and protein interaction networks linking altered metabolites to membrane receptors, lipid raft proteins, and signaling pathways. Overrepresentation analysis of biological processes was applied to identify enriched functional categories.

THz exposure did not affect cell viability but induced significant alterations in purine metabolism, pantothenate/CoA biosynthesis, and the pentose phosphate pathway. Network analysis revealed that these metabolic changes were associated with membrane raft reorganization and receptor-mediated signaling involving epidermal growth factor receptor and G-protein subunits. Additional effects were observed in pathways related to chromatin organization and post-translational regulation.

THz radiation induces coordinated remodeling of metabolic and regulatory networks in melanoma cells without cytotoxicity. These findings highlight the role of membrane-associated signaling in mediating THz-induced cellular responses and provide insight into potential biomedical applications of THz technologies.