Objective To investigate the depressive state of patients with Parkinson's disease (PD), and to analyze the correlation of depressive state with autonomic dysfunction. Methods A total of 327 patients with PD in the hospital were selected from March 2022 to March 2024. The depressive state was evaluated by Hamilton Depression Scale (HAMD). The autonomic nerve function was assessed using the Scale for Outcomes in PD for Autonomic Symptoms (SCOPA-AUT) and heart rate variability [standard deviation of sinus RR interval (SDNN), standard deviation of average sinus RR interval (SDANN), and percentage of successive NN interval differences above 50 ms (pNN50)]. According to the positive depression (HAMD>20 points), the patients were divided into a depression group and a non-depression group. The clinical data and autonomic nerve function indicators were compared between the two groups. Pearson correlation coefficient analysis was performed to analyze the correlation between depressive state and autonomic dysfunction in PD patients. Results The positive rate of depression in patients with PD was 31.19%. There were 102 patients in the depression group and 225 patients in the non-depression group. The years of education and the proportion of mild Hoehn-Yahr stage (H-Y stage) in the depression group were lower than those in the non-depression group, while the disease course was longer, and the Unified Parkinson's Disease Rating Scale (UPDRS) II score and UPDRS III score were higher than those in the non-depression group (P<0.05). The SCOPA-AUT score in the depression group was higher while the SDNN, SDANN and pNN50 were lower compared to the non-depression group (P<0.05). HAMD score was positively correlated with SCOPA-AUT score (r=0.685), and was negatively correlated with SDNN, SDANN and pNN50 (r=-0.578, -0.685, and -0.439) (P<0.05). Conclusion Depression is a common state among patients with PD, and its level is positively correlated with the severity of autonomic dysfunction in patients.

Objective To investigate the role and potential mechanism of glutathione peroxidase 3 (GPX3) in ischemia-reperfusion injury (IRI) during kidney transplantation. Methods C57BL/6 mice were divided into four groups according to different interventions: sham operation group (Sham group), kidney transplantation group (KT group), kidney transplantation + GPX3 overexpression group (KT+GPX3 group) and kidney transplantation + GPX3 overexpression + reactive oxygen species (ROS) agonist group (KT+GPX3+CADD522 group). Twenty-four hours after model establishment, inferior vena cava blood was collected to detect blood urea nitrogen (BUN) and serum creatinine (Scr). Left renal tissues were harvested for immunofluorescence staining to detect ROS and NADPH oxidase 2 (NOX2). Enzyme-linked immunosorbent assay (ELISA) was performed to measure neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), tumor necrosis factor (TNF) -α and interleukin (IL)-1β. Western blotting was used to detect myeloperoxidase (MPO) and citrullinated histone H3 (CitH3). Results Compared with the Sham group, the expression level of GPX3 was decreased in the KT group; compared with the KT group, GPX3 expression was increased in the KT+GPX3 group; compared with the KT+GPX3 group, GPX3 expression was reduced in the KT+GPX3+CADD522 group (all P<0.05). Compared with the Sham group, the levels of Scr, BUN, NGAL and KIM-1 were elevated in the KT group; compared with the KT group, the above indicators were decreased in the KT+GPX3 group; compared with the KT+GPX3 group, the levels of Scr, BUN, NGAL and KIM-1 were increased in the KT+GPX3+CADD522 group (all P<0.05). Compared with the Sham group, the expression levels of NOX2 and ROS were increased in the KT group; compared with the KT group, NOX2 and ROS levels were decreased in the KT+GPX3 group; compared with the KT+GPX3 group, NOX2 and ROS levels were upregulated in the KT+GPX3+CADD522 group (all P<0.05). Compared with the Sham group, the expression levels of MPO and CitH3 were increased in the KT group; compared with the KT group, MPO and CitH3 levels were decreased in the KT+GPX3 group; compared with the KT+GPX3 group, MPO and CitH3 levels were increased in the KT+GPX3+CADD522 group (all P<0.05). Compared with the Sham group, the expression levels of TNF-α and IL-1β were increased in the KT group; compared with the KT group, TNF-α and IL-1β levels were decreased in the KT+GPX3 group; compared with the KT+GPX3 group, TNF-α and IL-1β levels were increased in the KT+GPX3+CADD522 group (all P<0.05). Conclusions GPX3 may alleviate renal tissue inflammation by inhibiting ROS-mediated neutrophil extracellular trap (NET) formation, thereby attenuating IRI in renal transplantation.

ObjectiveTo systematically summarize the relevant pathophysiology underlying muscle fatigue in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). MethodsDatabases including PubMed, Web of Science Core Collection, Embase, Cochrane Library, EBSCO (CINAHL), CNKI, Wanfang Data and VIP Database were searched from their inception to July, 2025 for basic and clinical studies related to ME/CFS. Multidimensional evidence involving mitochondrial, neuromuscular junction dysfunction, autonomic dysregulation and immune-inflammatory responses was integrated. The role of muscles in the central-immune-metabolic-neural regulatory network and its association with clinical phenotypes were evaluated. ResultsPatients with ME/CFS commonly presented with impaired mitochondrial energy supply, oxidative stress, ion homeostasis disorders, reduced stability of neuromuscular junction transmission, insufficient central drive and postural intolerance. These abnormalities resulted in a predisposition to cross the anaerobic threshold and trigger post-exertional malaise. ConclusionMuscle pathophysiology plays a critical role in the pathogenesis and symptom persistence of ME/CFS. Rehabilitation practice should prioritize safety boundaries to avoid post-exertional malaise.

Objective To explore the potential functional targets of ischemia-reperfusion injury (IRI) in renal allografts derived from different donor sources. Methods Based on the transcriptome sequencing dataset GSE43974 of kidney transplantation IRI from different donor sources, weighted gene co-expression network analysis (WGCNA) and protein-protein interaction (PPI) network analysis were performed to screen Hub genes and characterize their expression profiles. A nomogram model was established to evaluate the diagnostic efficacy of these Hub genes, which was further validated using the dataset GSE30718. Immune infiltration analysis was conducted to clarify the correlations between Hub genes and immune cell infiltration. A mouse kidney transplantation IRI model was adopted to verify the expression levels of Hub genes in vivo. Results A total of five Hub genes were finally identified, namely PPP1CC, GART, BIRC6, PMSD11 and TMEM192. Nomogram analysis confirmed that these Hub genes possessed favorable diagnostic performance for kidney transplantation IRI in kidneys from different donors. Immune infiltration analysis revealed distinct infiltration patterns of various immune cells in IRI kidneys from different donors, and Hub genes were closely correlated with the regulation of multiple immune cell infiltration. A total of 390 differentially expressed genes were screened between renal tissues of mice in the kidney transplantation group and sham operation group. Gene Ontology (GO) enrichment analysis indicated that these differentially expressed genes were mainly enriched in biological processes including oxidative stress, inflammation and pyroptosis. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis showed significant enrichment in glutathione metabolism, neutrophil extracellular trap formation and other signaling pathways. Transcriptome sequencing verified that the expression levels of the five Hub genes were significantly different between the two groups (all P < 0.05). Conclusions Five Hub genes are identified in kidney transplantation IRI using donor kidneys from different sources. Glutathione metabolism and neutrophil extracellular trap formation may participate in the pathogenesis of kidney transplantation IRI.

Oral squamous cell carcinoma(OSCC)is a malignant lesion originating from the oral mucosal squamous epithelium,account-ing for over 80％of oral and maxillofacial malignancies.Key etiological factors include tobacco,alcohol abuse,and betel quid chewing.In China,its incidence has shown an overall upward trend,posing a significant threat to public health.OSCC exhibits high local invasive-ness,making early diagnosis critical for improving prognosis.Its clinical management requires close multidisciplinary collaboration among oral and maxillofacial surgery,head and neck surgery,radiation oncology,medical oncology,reconstructive surgery,radiology,patholo-gy,and nutritional support teams.Given the increasing disease burden of OSCC and rapid development of multidisciplinary collaborative models,an expert panel has formulated this integrated management consensus based on evidence-based medicine and extensive deliber-ation.Centered on the'Prevention-Screening-Diagnosis-Treatment-Rehabilitation'framework,the consensus provides comprehensive guidance for the entire disease course of OSCC patients,aiming to standardize clinical practice.

Parkinson's disease(PD)is a common progressive neurodegenerative disease mainly affecting the motor system.Various genetic factors and cellular mechanisms underlying PD have recently been discovered.Emerging evidence suggests that epigenetic modifications play a very important role in the pathogenesis,prevention,and treatment of PD.Epigenetic modification mediates genetic and environmental interactions mainly through complex interactions of DNA methylation,histone modification,and non-coding RNA,thereby affecting expression in the absence of changes in DNA sequence.In this review,we summarize the epigenetic modification mechanisms involved in the pathogenesis of Parkinson's disease.In this review,we summarize the epigenetic modification mechanisms involved in the pathogenesis of Parkinson's disease.Recent studies have found that traditional Chinese medicine can participate in the regulation of abnormal epigenetic modifications in the treatment of PD.Traditional Chinese medicine benefits from its multi-level and multi-target regulatory effects,and various traditional Chinese medicine monomers,compound prescriptions,and techniques have been evaluated,confirming that this is a promising approach for improving symptoms in PD.This review summarizes the mechanisms by which epigenetic modifications contribute to P D,explores the role of traditional Chinese medicine,and provides new ideas for clinical treatment and drug development in PD through epigenetic intervention.

In recent decades,the incidence of human papillomavirus(HPV)-associated oropharyngeal squamous cell carcinoma(OPSCC)has shown a marked increase.Significant changes have also occurred in the OPSCC diagnosis and treatment paradigm.Deter-mining HPV status prior to treatment is now essential,and radiotherapy/chemotherapy,immunotherapy,and minimally invasive surgical techniques have progressively emerged as key modalities for managing OPSCC.However,alongside these paradigm shifts,a comprehen-sive technical consensus guiding the entire diagnostic and therapeutic process for OPSCC patients is currently lacking.Given China's large population base and the rising incidence of OPSCC,an expert panel convened to develop a clinical technical consensus on OPSCC diagno-sis and management tailored to China's specific context.This consensus aims to further enhance and standardize understanding of OPSCC management techniques among relevant healthcare professionals.

Objective:To investigate the effect of local food-source enteral nutrition(EN) to improve the nutritional status of stroke patients.Methods:The clinical data of 180 patients with ischemic stroke admitted to the First People′s Hospital of Chengdu and the Second People′s Hospital of Chengdu during the period from June 2021 to June 2023 were selected retrospectively, patients in both groups received EN at 24 to 48 h after admission, and total energy intake was evaluated 7 d later, which was divided into the standard calorie group (90 cases) and the low- calorie group (90 cases) according to total energy intake. The total energy intake of patients in the standard calorie group increased to 125 -146 kJ/ (kg·d) after 7 d. Patients in the low-calorie group gradually increased to 105 kJ/ (kg·d) after 7 d. The changes in inflammatory factors and nutritional indexes before and after treatment were compared between the two groups, and the incidence of malnutrition and neurological function deficit before and after treatment were compared between the two groups.Results:After treatment, the levels of serum interleukin 1β, tumor necrosis factor-α, ultrasensitive C-reactive protein in the low-calorie group were lower than those in the standard calorie group: (16.74 ± 4.33) ng/L vs. (20.15 ± 5.68) ng/L, (25.58 ± 5.09)ng/L vs. (30.04 ± 6.46) ng/L, (12.41 ± 3.29) mg/L vs.(15.24 ± 4.18) mg/L, there were statistical differences ( P<0.05); the levels of serum total protein, albumin, transferrin were higher than those in the standard calorie group: (66.42 ± 8.32) g/L vs. (60.58 ± 8.32) g/L, (46.32 ± 6.39) g/L vs. (41.42 ± 5.34) g/L, (3.44 ± 0.65) g/L vs. (3.12 ± 0.31) g/L, there were statistical differences ( P<0.05). The incidence of malnutrition in the low-calorie group was lower than that in the standard calorie group: 3.33%(3/90) vs. 12.22%(11/90), there was statistical difference ( χ2 = 9.05, P<0.05). After 1 month and 3 months of treatment, the scores of National Institute of Health stroke scale (NIHSS) scores in the low-calorie group were lower than that in the standard calorie group: (15.76 ± 3.54) scores vs. (22.34 ± 6.24) scores, (8.65 ± 2.74) scores vs. (11.76 ± 4.83) scores, there were statistical differences ( P<0.05). Conclusions:Early local food-borne EN can improve the nutritional status of stroke patients, reduce the expression of inflammatory factors, and facilitate the improvement of neurological damage.

Oral squamous cell carcinoma(OSCC)is a malignant lesion originating from the oral mucosal squamous epithelium,account-ing for over 80％of oral and maxillofacial malignancies.Key etiological factors include tobacco,alcohol abuse,and betel quid chewing.In China,its incidence has shown an overall upward trend,posing a significant threat to public health.OSCC exhibits high local invasive-ness,making early diagnosis critical for improving prognosis.Its clinical management requires close multidisciplinary collaboration among oral and maxillofacial surgery,head and neck surgery,radiation oncology,medical oncology,reconstructive surgery,radiology,patholo-gy,and nutritional support teams.Given the increasing disease burden of OSCC and rapid development of multidisciplinary collaborative models,an expert panel has formulated this integrated management consensus based on evidence-based medicine and extensive deliber-ation.Centered on the'Prevention-Screening-Diagnosis-Treatment-Rehabilitation'framework,the consensus provides comprehensive guidance for the entire disease course of OSCC patients,aiming to standardize clinical practice.

Objective·To explore the metabolic profiling and metabolic reprogramming patterns of lung cancer cells with acquired resistance to sotorasib,a specific inhibitor to KRAS.Methods·The H2122 and H358 lung cancer cell models with acquired resistance to sotorasib(H2122-SR and H358-SR cells)were established and validated by CCK-8 assay.Ultra-performance liquid chromatography tandem quadrupole time-of-flight mass spectrometry(UPLC-QTOF/MS)was employed to acquire the metabolic profiling of the resistant lung cancer cells and their homologous parental cells.Untargeted metabolomics studies and metabolic characterizations were conducted with multi-dimensional methods,including principal component analysis(PCA)and partial least squares-discriminant analysis(PLS-DA),to identify differential metabolites associated with acquired resistance to sotorasib.Then these differential metabolites were subjected to pathway enrichment analysis.Heatmap analysis was used to compare the changes in metabolites in major differential metabolic pathways between the resistant and parental cells.Results·The cell models of H2122 and H358 with acquired resistance were successfully constructed,with half-maximal inhibitory concentrations(IC50)of sotorasib being 50 times higher than those of the parental cells.Besides,the metabolic profiling was significantly different between the resistant and parental cells.A total of 48 differential metabolites were identified between H2122-SR and H2122 cells.The top 10 differential metabolites,ranked by VIP values,were uridine,xanthylic acid,indole-3-carboxylic acid,nicotinic acid,xanthosine,xanthine,N-methylnicotinamide,hypoxanthine,trigonelline,and galactonic acid.Between H358-SR and H358 cells,a total of 79 differential metabolites were identified.The top 10 differential metabolites,ranked by VIP values,were glutathione,xanthosine,2-ketoglutaric acid,carboxyethyl lysine,thymidine,purine,riboflavin,3-indoleacrylic acid,indole-3-pyruvic acid,and dihydrouracil.The differential metabolites in the two lung cancer cell lines mainly participated in purine metabolism and glycolysis/gluconeogenesis,and purine metabolism was the most significantly altered metabolic pathway.Heatmap analysis showed that many metabolites in the purine metabolism were elevated in the sotorasib-resistant cells.Conclusion·The lung cancer cells with acquired resistance to sotorasib show enhanced purine metabolism.