Wuhan No.1 Hospital

Background Postoperative pain management following thoracoscopic lobectomy remains challenging, potentially impairing pulmonary function and recovery. This study evaluated the effects of ultrasound-guided erector spinae plane block (ESPB) on pain control and pulmonary function in these patients. Methods This retrospective cohort study included 120 patients who underwent thoracoscopic lobectomy between January 2022 and December 2024 at a tertiary care center. Patients received either ultrasound-guided ESPB with 0.375% ropivacaine ( n = 60) or conventional analgesia alone ( n = 60). All patients received standardized general anesthesia and patient-controlled analgesia with morphine postoperatively. Primary outcomes included 0–10 visual analog scale (VAS) pain scores at 1, 6, 12, and 24 h and pulmonary function parameters (FEV 1 , FVC) on postoperative days 1 and 3. Secondary outcomes included morphine consumption, time to first analgesic request, complications, hospital stay, and patient satisfaction. Results The ESPB group demonstrated significantly lower VAS scores at all-time points compared to controls (24-h VAS: 3.2 vs. 5.6; p < 0.001; Cohen’s d = 1.91). Total 24-h morphine consumption was reduced by 42.6% in the ESPB group (20.5 mg vs. 35.7 mg; p < 0.001). Pulmonary function was significantly better preserved in the ESPB group, with higher FEV 1 and FVC values on postoperative days 1 and 3 (all p < 0.01). Pain scores negatively correlated with pulmonary function parameters across the entire cohort, independent of group ( r = –0.45 to –0.50; p < 0.001). Hospital stay was shorter (5.2 vs. 6.5 days; p = 0.001) and patient satisfaction higher (4.5 vs. 3.8; p < 0.001) in the ESPB group. Complication rates were comparable between groups. Conclusion Ultrasound-guided ESPB enhances postoperative pain control and pulmonary function recovery without added risks, supporting its integration into multimodal analgesia protocols for thoracoscopic lobectomy.

BackgroundUlcerative colitis (UC) is a chronic and relapsing inflammatory bowel disease (IBD), that lacks specific therapeutic drugs. Prim-O-glucosylcimifugin (POG), a furanochromone glycoside derived from Saposhnikovia divaricata, exhibits anti-inflammatory, antioxidant, and anti-inflammasome activities. It has also been shown to inhibit the activation of the NLR family pyrin domain containing 3 (NLRP3) inflammasome. Given that ulcerative colitis (UC) is a chronic inflammatory bowel disease characterized by intestinal barrier dysfunction and NLRP3 activation, this study aims to investigate the therapeutic effects and underlying mechanisms of POG in a murine model of UC induced by dextran sulfate sodium (DSS), and to evaluate its potential translational significance for UC intervention.MethodsA DSS-induced UC mouse model was employed to evaluate POG’s therapeutic efficacy. Disease activity index, colon length, spleen index, and histopathological alterations of the colonic mucosa were assessed by H&E and AB-PAS staining, transmission electron microscopy, and immunofluorescence. Proinflammatory cytokines (TNF-α, IL-6, IL-18, IL-1β) were measured by ELISA, and NLRP3 inflammasome–related proteins were analyzed by Western blot.ResultsPOG treatment alleviated weight loss, colon shortening, splenomegaly, and inflammatory infiltration. It also restored goblet cell mucin droplets and tight junction proteins (Occludin, ZO-1, Claudin-1, MUC2), and reduced villi exfoliation. Serum levels of TNF-α, IL-6, IL-1β, and IL-18 were decreased. Western blot and ELISA revealed that POG suppressed NLRP3 inflammasome formation, inhibited GSDMD activation, and reduced cleavage and release of IL-1β and IL-18. Collectively, these findings indicate that POG not only attenuates inflammatory injury but also protects epithelial barrier structure and function, supporting its potential value in mechanism-based UC therapy development.ConclusionPOG ameliorates experimental UC by inhibiting NLRP3 inflammasome activation, thereby mitigating colonic inflammation, preserving mucosal barrier integrity, and blocking downstream inflammatory responses. POG shows promise as a therapeutic agent for UC and provides a rationale for further preclinical optimization and future clinical translation.

BackgroundA newer and novel index, the Cholesterol, High-Density Lipoprotein, and Glucose (CHG) index, has been proposed as a potential index for metabolic disorders. However, research on the relationship between CHG changes and cardiovascular disease (CVD) is limited. Our research aims to investigate the association between cumulative exposure and dynamic trajectories of CHG and cardiovascular disease risk.MethodsParticipants aged 45 and older were recruited from the China Health and Retirement Longitudinal Study (CHARLS). CVD was defined as self-reported description. K-means clustering analysis was used to classify dynamic CHG changes, and cumulative CHG (cuCHG) was calculated as follows: cuCHG=(CHG2012 + CHG2015)/time interval (2012–2015). Cox proportional hazards regression and restricted cubic spline (RCS) regression models were conducted to evaluate the association between cumulative exposure and dynamic trajectories of CHG and CVD risk.ResultsA total of 6,171 participants were included in the study, among whom 1,136 (18.4%) experienced incident of CVD. The risk of CVD increased with higher levels of cuCHG. K-means clustering indicated three distinct trajectories CHG variation. Compared to the stable reference group (Cluster 3), participants in the high-risk slowly increasing trajectory (Cluster 2) had a significantly higher risk of CVD (HR = 1.28, 95%CI: 1.10–1.49, P = 0.002). However, the moderate-decreasing trajectory (Cluster 1) was not significantly associated with CVD risk (HR = 1.09, 95%CI: 0.98–1.21, P = 0.126). In the Cox regression analysis, compared with the lowest quartile (Q1), participants in the highest quartile (Q4) had a significantly increased risk of CVD by 22% (HR = 1.22, 95% CI: 1.06–1.40, P = 0.005, adjusted P = 0.007). Furthermore, CVD risk increased progressively across ascending cuCHG quartiles (P for trend < 0.05). RCS analysis demonstrated a linear association between cuCHG and CVD risk (for overall, P < 0.001).ConclusionOur research indicates that both cuCHG and CHG changes are associated with CVD risk in middle-aged and older adults, particularly for those with consistently high-risk CHG levels, which are linked to a significantly increased CVD risk. In clinical practice, monitoring long-term CHG changes and maintaining relatively stable levels may help prevent CVD in this population.Graphical Supplementary InformationThe online version contains supplementary material available at 10.1186/s12933-026-03137-9.

Mental health problems among university students are increasingly severe, with symptoms such as depression, anxiety, loneliness, and suicidal ideation frequently co-occurring to form complex symptom networks. This study systematically analyzed association patterns of mental health symptoms among UK university students through multilayer network analysis. A cross-sectional survey was conducted with 1,285 students from five UK universities, who are assessed using eight validated psychometric instruments evaluating depression, anxiety, mania, sleep quality, stress, suicidal ideation, psychotic experiences, and loneliness. A dual-level network analysis approach was employed, constructing both a scale-level network with 8 nodes to identify macro-association patterns and an item-level network with 33 nodes for in-depth analysis of depression, loneliness, and suicidal ideation connections. The EBICglasso algorithm estimated network structure, and key symptoms were identified through centrality indices. The scale-level network revealed depressive symptoms as most prominent across all centrality indices, establishing their core position. The strongest connections existed between anxiety-depression (edge weight = 0.37) and anxiety-stress (edge weight = 0.35), while loneliness connected with psychotic experiences (edge weight = 0.23) and suicidal ideation (edge weight = 0.144). In item-level analysis, thoughts of death (PHQ_9), lack of companionship (UCLA3_4), and frequency of suicidal thoughts (SBQ2) demonstrated strongest bridge centrality. Network stability analysis showed CS coefficients reached the good standard of 0.5. These findings demonstrate that depressive symptoms occupy a core network position, loneliness plays a unique bridging role, and suicidal ideation closely associates with depression and loneliness, providing evidence for network-based precision intervention strategies.

Oral squamous cell carcinoma (OSCC) is a malignant tumor characterized by both clinical and molecular heterogeneity. Its rising global incidence and mortality rates pose considerable clinical challenges. Accumulating evidence suggests that dysregulation of mitochondria-associated pan-cell death, a process integrating multiple mitochondrial-related cell death modalities, is closely linked to tumor initiation and progression. Nevertheless, the identification of key therapeutic targets among mitochondria-associated pan-cell death-related genes (MAPGs) in OSCC remains an unresolved issue, underscoring the need for further investigation. We systematically investigated the expression patterns, prognostic relevance, and immune microenvironmental features of mitochondria-associated pan-cell death-related genes (MAPGs) in OSCC by integrating data from The Cancer Genome Atlas (TCGA), Gene Expression Omnibus (GEO) datasets (GSE42743, GSE41613, GSE75538, GSE164241, GSE172577, and GSM6339633), and the MitoCarta3.0 database. Using nine machine learning algorithms, we compared the importance and prognostic value of MAPGs and identified INHBA as the most pivotal MAPG. Its predictive power and functional relevance were further explored through enrichment analysis. We validated INHBA mRNA expression levels in clinical OSCC samples using quantitative real-time PCR (qRT‑PCR). Pan-cancer analysis was performed to assess the potential of INHBA as a therapeutic target across multiple cancer types. Single-cell RNA sequencing, spatial transcriptomics, and cell-cell communication analyses were integrated to elucidate the spatial distribution of INHBA in OSCC and its crosstalk with the immune microenvironment. Finally, drug sensitivity profiling was conducted using the GDSC and PRISM databases. A total of 19 MAPGs with the greatest prognostic value were screened out. Among them, INHBA emerged as the most critical MAPG, which was overexpressed in HNSCC and strongly correlated with poor prognosis in OSCC patients (p < 0.05). Meanwhile, INHBA expression was elevated in cancer-associated fibroblasts (CAFs). Spatial transcriptomic analysis further revealed strong spatial colocalization between INHBA and CAF-localized regions. These results indicated that INHBA primarily functioned within CAFs, especially myCAFs, and may promote OSCC progression through modulation of the immune microenvironment. Elevated INHBA expression served as a prognostic indicator in OSCC, a finding consistent with its prognostic relevance in broader HNSCC analyses. Selumetinib and naltrexone showed high sensitivity in INHBA-high contexts. INHBA is a crucial MAPG that is upregulated in OSCC and mainly functions in CAFs. It likely affects the poor prognosis of OSCC by regulating the immune microenvironment. Selumetinib and naltrexone hold promise as innovative therapeutic agents, potentially opening up new treatment avenues for OSCC patients.

Pediatric hemorrhagic moyamoya disease (MMD) is a critical subtype associated with high morbidity; however, hemorrhage-specific prognostic factors remain poorly defined. The aim of this study was to define the clinical course, identify factors associated with hemorrhagic presentation and recurrence, and evaluate long-term outcomes in a large pediatric cohort. This retrospective cohort study included children diagnosed with MMD between 2003 and 2023. Hemorrhagic MMD was defined as acute intracranial hemorrhage on CT/MRI within 72 hours of symptom onset, excluding traumatic or aneurysmal causes. Standardized data collection encompassed Suzuki staging, posterior communicating artery (PcomA) and anterior choroidal artery (AChA) dilatation, modified Rankin Scale (mRS) scores at admission and follow-up, and recurrence events. Multivariable logistic regression and Cox proportional hazards models were used to identify factors associated with hemorrhagic MMD and stroke recurrence. Among 1,446 pediatric patients with MMD, 117 had hemorrhagic presentation. The hemorrhagic cohort was significantly older (mean age 10.9 ± 4.1 years vs 7.6 ± 4.5 years, p < 0.001) and had a higher proportion of female patients (68.4% vs 50.0%, p < 0.001). Factors independently associated with hemorrhagic MMD included AChA dilatation (adjusted odds ratio [aOR] 5.95, 95% CI 3.56-9.92, p < 0.001), PcomA dilatation (aOR 4.23, 95% CI 2.48-7.20, p < 0.001), and admission mRS score ≥2 (aOR 2.38, 95% CI 1.44-3.96, p < 0.001). The hemorrhagic group showed higher rates of hematoma recurrence (7.7% vs 0.8%, p < 0.001). AChA dilatation was strongly associated with recurrent hematoma (hazard ratio [HR] 8.85, 95% CI 3.06-25.58, p < 0.001). Admission mRS score ≥2 was significantly associated with all recurrence subtypes: stroke (HR 13.32), hematoma (HR 5.58), and infarction (HR 52.16; all p ≤ 0.002). The Kaplan-Meier analysis confirmed markedly reduced 8-year hematoma recurrence-free survival in hemorrhagic MMD (50% vs >80% in ischemic, p < 0.0001). Hemorrhagic MMD is an aggressive subtype characterized by posterior collateral vulnerability, female predominance, and older age. Admission mRS score ≥2 and AChA dilatation are key factors strongly associated with adverse outcomes. Conventional angiographic classification does not demonstrate a significant association with hemorrhage outcome; assessment of the posterior circulation is critical for stratifying patient outcomes and guiding early intervention.

Hepatitis A virus (HAV) remains a significant global public health concern, particularly as a foodborne pathogen. Despite advances in vaccination and sanitation, HAV continues to cause outbreaks, especially in regions with uneven immunization coverage or inadequate hygiene infrastructure. This review comprehensively examines HAV from virological, clinical, and epidemiological perspectives, highlighting its pathogenesis, transmission routes, genomic diversity, and foodborne risks. We discuss the evolving global epidemiology of HAV, emphasizing the shift from high to low endemicity in vaccinated populations and the emergence of susceptible cohorts in moderately developed regions. The review underscores the challenges in foodborne HAV detection, including the limitations of current methods and the promise of emerging technologies like reverse transcription digital polymerase chain reaction (RT-dPCR) for enhanced sensitivity. Additionally, we summarize emerging antiviral approaches infood safety control, including plant-derived bioactive compounds and edible coatings, for controlling HAV transmission through the food chain. Finally, we present an overview of WHO-recommended vaccination strategies based on endemicity levels-targeted immunization for high-risk groups in low-endemic areas, universal childhood vaccination in moderate-endemic regions, and reliance on naturally acquired immunity in high-endemic zones. Our synthesis aims to bridge gaps between virology, clinical medicine, and food safety, offering insights for interdisciplinary collaboration in HAV prevention and control.

ObjectiveTo investigate the effects of combined Levocarnitine and Alprostadil therapy on renal function, oxidant-antioxidant balance, and systemic inflammation in patients with end-stage diabetic nephropathy (ESDN).MethodsThis retrospective study included 104 ESDN patients admitted to our hospital between April 2021 and April 2023 who met all inclusion criteria. All patients were on maintenance hemodialysis for chronic kidney failure due to ESDN. Based on the treatment regimen received, patients were divided into two groups: the control (n=51) received intravenous Alprostadil (20 μg/day) for 30 days in addition to standard care, and the observation group (n=53) received additional intravenous Levocarnitine (1.0 g/day) for 30 days. Clinical efficacy, renal function parameters [blood urea nitrogen (BUN), cystatin C (Cys-C), 24-hour urinary protein (24 h Upro)], oxidative stress markers [malondialdehyde (MDA), superoxide dismutase (SOD), reactive oxygen species (ROS)], inflammatory factors [C-reactive protein (CRP), interleukin-1β (IL-1β), interleukin-6 (IL-6)], and adverse reactions were compared between groups.ResultsThe cumulative treatment effectiveness (defined as the sum of patients with “markedly effective” and “effective” outcomes) was significantly higher in the observation group (92.45%) compared to the control group (78.43%, P<0.05). Post-treatment, the observation group demonstrated significantly greater improvements in all parameters: lower BUN (4.35±1.06 vs 5.29±1.12 mmol/L), Cys-C (1.21±0.34 vs 1.75±0.46 mg/L), 24 h Upro (66.79±18.37 vs 75.17±19.54 mg/24h), MDA (3.54±0.89 vs 4.63±1.08 nmol/mL), ROS (371.34±46.32 vs 417.53±48.16 U/mL), CRP (5.02±0.83 vs 6.63±0.94 mg/L), IL-1β (11.04±2.38 vs 13.61±2.67 pg/mL), and IL-6 (12.78±3.51 vs 16.84±4.53 pg/mL), alongside higher SOD (88.17±9.34 vs 72.49±8.71 U/mL) (P<0.05). Adverse reaction incidence showed no significant difference (16.98% vs 13.73%, P>0.05).ConclusionIn ESDN patients, the combination of Levocarnitine and Alprostadil demonstrates superior cumulative treatment effectiveness over Alprostadil monotherapy in improving renal function, reducing oxidative stress, and attenuating inflammation, without increasing the incidence of adverse reactions.

Severe acute pancreatitis (SAP) is characterized by persistent organ failure and a high mortality rate, early diagnosis and disease assessment are crucial for improving patient prognosis. To investigate the expression level, diagnostic value, and mechanism of action of serum miR-331-3p in patients with SAP. One hundred eighty-five patients with AP (including 130 patients with mild-to-moderate acute pancreatitis (MAP) and 55 patients with SAP) and 100 healthy controls (HC) were enrolled. RT-qPCR was conducted to detect the expression of serum miR-331-3p, and its diagnostic efficacy was analyzed using receiver operating characteristic (ROC) curves. Correlation analysis was carried out using the Pearson correlation coefficient. The molecular mechanism was explored by combining dual-luciferase reporter gene assay and cell function experiments. The level of serum miR-331-3p expression in the SAP group was markedly lower than that in the MAP and HC groups (P < 0.05). The AUC for distinguishing MAP from SAP was 0.866 (95% CI: 0.810–0.921), with a sensitivity of 83.6% and a specificity of 73.1%. miR-331-3p was strongly negatively correlated with SAP routine indicators, severity, and inflammation (P < 0.001). Mechanistically, miR-331-3p directly targets bromodomain protein 4 (BRD4), and the overexpression of miR-331-3p alleviate the inflammatory response in the SAP cell model and promote cell proliferation, whereas BRD4 overexpression reversed the effects of miR-331-3p. Serum miR-331-3p is notably downregulated in SAP and may attenuate pancreatic inflammation through BRD4 targeting and inhibition, proposing its candidacy as a diagnostic biomarker.

Anti-neutrophil cytoplasmic antibody-associated vasculitis (AAV) is an autoimmune disease characterized by systemic small-vessel inflammation. Complement activation, particularly through the alternative pathway, has been implicated in AAV pathogenesis. However, the role and clinical significance of urinary complement C3 fragments as non-invasive biomarkers for disease activity remain unclear. This cross-sectional study enrolled 22 AAV patients and 20 healthy controls. Urinary levels of C3a, C3b, iC3b, C3c, and C3d were measured using enzyme-linked immunosorbent assay (ELISA) and normalized to urinary creatinine. Between-group comparisons were performed using independent t-tests or Mann–Whitney U tests. Correlations and independent predictors of urinary complement fragments were evaluated using Spearman correlation and multivariate linear regression, respectively. All urinary complement C3 fragment levels were significantly elevated in AAV patients compared to healthy controls (all p < 0.01). Among AAV patients, urinary C3 fragments correlated strongly with Birmingham Vasculitis Activity Score (BVAS, r = 0.793–0.900), proteinuria (r = 0.551–0.735), and hematuria (r = 0.643–0.752) (all p < 0.01), but not with serum creatinine (p > 0.05). BVAS was an independent predictor of all C3 fragments (β = 0.458–0.760, all p < 0.05), while proteinuria independently predicted all except iC3b (β = 0.302–0.455, all p < 0.05). Urinary complement C3 fragments are elevated in AAV patients and closely associated with disease activity, independent of renal function. These findings support their potential utility as non-invasive biomarkers for monitoring AAV disease activity.