Objective This study compared the protective effects of curcumin （CUR） and Tetrahydrocurcumin （THC） against T2DM-related myocardial injury and delved into the differences in their mechanisms. Methods A mouse model of Type 2 diabetes mellitus （T2DM） was established by using a high-fat diet in combination with low-dose streptozotocin. The mice were randomly divided into four groups： the normal control group， the model group， the CUR dietary intervention group （800 mg/kg diet）， and the THC dietary intervention group （800 mg/kg diet）. Dietary supplements were administered concurrently with model induction. Myocardial morphology， fibrosis， and glycogen deposition were evaluated through hematoxylin and eosin （HE）， Masson， and periodic acid-Schiff （PAS） staining. Oxidative stress indicators and plasma cardiac injury markers， such as lactate dehydrogenase （LDH） and cardiac troponin I （cTnI）， were measured via colorimetric assays. Differentially expressed proteins were screened by proteomics， and the expression levels of pathway-related proteins were verified by Western blotting. Results Compared with the model group， both THC and CUR significantly alleviated myocardial disarray， diminished interstitial fibrosis （P 0.01） and glycogen deposition （P 0.05）， and decreased plasma levels of LDH and cTnI （P 0.05）. Moreover， they reduced myocardial malondialdehyde （MDA） levels （P 0.001） and enhanced total antioxidant capacity （T-AOC） （P 0.01）， superoxide dismutase （SOD） （P 0.05）， and glutathione （GSH） activities （T2DM+THC vs. T2DM， P 0.01）. Notably， THC exhibited more pronounced improvement than CUR across all these parameters. Correlation analysis indicated a significant positive correlation between fasting blood glucose levels and the cardiac injury markers LDH and cTnI， implying that the improvement of glycemic control is closely related to myocardial protection （P 0.001）. Mechanistically， proteomics combined with Western blot validation showed that THC more effectively inhibited the over-activation of the STK3-LATS1 axis in the Hippo pathway compared with CUR， as manifested by a remarkable down-regulation of the phosphorylation levels of STK3 and LATS1 induced by T2DM （P 0.001）. Conclusion THC may alleviate myocardial injury in T2DM mice by inhibiting the Hippo signaling pathway. It exhibits more potent cardioprotective effects than CUR， and therefore has the potential to serve as a natural dietary supplement for the prevention and treatment of T2DM-related myocardial injury.

Objective To investigate whether the circadian timing of symptom onset influences the severity of myocardial ischemia-reperfusion injury （MIRI） following primary percutaneous coronary intervention （PCI） in patients with acute ST-segment elevation myocardial infarction （STEMI）. Methods This retrospective study included 362 consecutive STEMI patients who underwent primary PCI within 12 hours of symptom onset at the Affiliated Hospital of Yangzhou University between January 2021 and December 2024. Patients were stratified into four circadian groups based on symptom onset time： nighttime， morning， afternoon， and evening. Primary outcomes included peak creatine kinase-MB （CK-MB） and cardiac troponin I （cTnI） levels. Secondary outcomes encompassed post-PCI TIMI flow grade， incidence of no-reflow phenomenon， left ventricular ejection fraction （LVEF） at 7 days， and major adverse cardiovascular events （MACE） at 7 and 30 days. Group comparisons used Kruskal-Wallis or one-way ANOVA tests as appropriate. Multivariable linear and logistic regression models identified independent associations between circadian timing and myocardial injury markers or no-reflow risk. Results Peak CK-MB and cTnI levels were significantly higher in the nighttime and morning groups compared with the afternoon and evening groups （all P 0.05）. The nighttime group exhibited the highest incidence of no-reflow phenomenon （24.3% vs. 9.7% in the afternoon group， P = 0.018）. LVEF at 7 days was lowest in the nighttime group （51.3 ± 7.8） % and highest in the afternoon group ［（57.2 ± 6.4）%， P = 0.003］. After adjustment for total ischemic time， infarct location， and Killip class， nighttime and morning onset remained independent predictors of elevated peak cTnI. Nighttime onset was independently associated with no-reflow risk. Conclusions The circadian timing of symptom onset is independently associated with MIRI severity following primary PCI for STEMI. Patients with nighttime onset experience greater myocardial necrosis， higher rates of microvascular obstruction， and impaired early ventricular recovery. These findings suggest that circadian biology may modulate ischemia-reperfusion pathophysiology， supporting the integration of symptom onset timing into risk stratification protocols for STEMI management.

Objective To evaluate the clinical utility of myocardial contrast echocardiography （MCE） combined with two-dimensional speckle tracking echocardiography （2D-STE） for the early quantitative assessment of myocardial microcirculation and left heart function in patients with heart failure with preserved ejection fraction （HFpEF）. Methods This study enrolled 80 patients hospitalized for HFpEF and 60 age- and sex-matched healthy controls. All participants underwent MCE to quantify myocardial perfusion parameters， including plateau peak intensity （A）， refilling rate constant （β）， and myocardial blood flow index （A×β）. 2D-STE was used to measure left ventricular global longitudinal strain （GLS） and left atrial peak longitudinal strains during ventricular systole （LAS-s） and atrial systole （LAS-a）. Conventional echocardiography and plasma BNP levels were also obtained. Group differences， inter-parameter correlations， and independent predictors of HFpEF were analyzed. Diagnostic performance was evaluated using receiver operating characteristic （ROC） curve analysis. Results Compared with controls， the HFpEF group exhibited significantly higher BNP， IVST， LAD， LAVI， LVMI， and E/e′ ratios， alongside significantly lower A， β， A×β， LAS-s， and LAS-a values （all P 0.05）. BNP correlated negatively with LAS-s （r = -0.646） and LAS-a （r = -0.575）， and positively with LAVI， LVMI， and E/e′ （all P 0.05）. A×β correlated inversely with IVST （r = -0.522， P 0.05）. Multivariate logistic regression identified LAS-s， LAS-a， LAVI， BNP， A×β， A， and β as independent predictors of HFpEF. ROC analysis determined optimal cutoff values for HFpEF prediction： LAS-s 28%， LAS-a 12%， A×β 7.2 dB²/s， A 8.2 dB， and β 1.04 dB/s. Conclusions HFpEF is characterized by impaired myocardial microvascular perfusion and reduced left atrial strain， with microvascular dysfunction inversely associated with ventricular wall thickening. The integration of MCE and 2D-STE provides a sensitive， quantitative approach for detecting subclinical myocardial and hemodynamic alterations in HFpEF， offering complementary diagnostic value for early clinical intervention.

Objective To investigate whether the extent of preoperative left ventricular （LV） remodeling， indexed by LV end-systolic dimension （LVESD）， influences the recovery trajectory of LV ejection fraction （LVEF） and long-term prognosis following mitral valve surgery in patients with moderate-to-severe mitral regurgitation （MR）. Methods A total of 157 patients undergoing mitral valve surgery for moderate-to-severe MR between January 2020 and December 2024 were prospectively enrolled. Participants were stratified into quartiles （Q1 - Q4） based on preoperative LVESD. The primary outcome was the longitudinal trajectory of LVEF assessed at pre-discharge， 3 months， and 6 months postoperatively， analyzed using linear mixed-effects models. The secondary outcome was a composite endpoint of heart failure rehospitalization or all-cause mortality， evaluated by Cox proportional hazards regression. Results CCompared with the Q1 group， patients in the Q4 group exhibited significantly lower preoperative LVEF and higher NT-proBNP levels （P 0.05）. LVEF improved significantly over time across the cohort （time effect， P 0.001）； however， the Q4 group demonstrated consistently lower LVEF than Q1 at all postoperative timepoints （group effect， P 0.001）， with a modest attenuation of between-group differences over time （time × group interaction， P = 0.008）. After multivariable adjustment， LVEF in the Q4 group remained 13.10， 12.28， and 12.03 percentage points lower than in Q1 at pre-discharge， 3 months， and 6 months， respectively （all P 0.001）. The cumulative incidence of the composite endpoint was significantly higher in Q4 （30.0%） versus Q1 （5.1%， log-rank P = 0.016）. Multivariable Cox analysis identified Q4 membership as an independent predictor of adverse outcomes （adjusted HR = 2.39， 95% CI： 1.11 ? 5.13， P = 0.026）， with a significant dose?response relationship across LVESD quartiles （P for trend = 0.018）. Sensitivity analyses using LVESD ≥ 40 mm as a binary cutoff or modeling LVESD as a continuous variable yielded consistent results. Conclusions Preoperative LVESD， as a marker of LV remodeling severity， independently predicts both the trajectory of early- to mid-term LVEF recovery and adverse clinical outcomes after mitral valve surgery for MR. Although patients with advanced remodeling （higher LVESD） exhibit postoperative LVEF improvement， their absolute recovery remains suboptimal， and they face substantially elevated risks of heart failure rehospitalization or mortality. These findings support earlier surgical intervention before irreversible LV dilation occurs.

Objective To evaluate the diagnostic accuracy and clinical utility of SonoVCADheart， a volume ultrasound-based computer-aided diagnosis system for the fetal heart， in assessing fetal coronary artery morphology compared with conventional fetal echocardiography. Methods A total of 322 high-risk pregnant women in the second and third trimesters were prospectively enrolled between July 2024 and September 2025. All participants underwent both conventional fetal echocardiography and SonoVCADheart imaging. Postnatal echocardiography served as the reference standard. Diagnostic performance for coronary artery origin， course， and luminal diameter was compared between the two modalities. Twenty-two cases were excluded due to inadequate image quality （four-chamber view score ≤ 2）， leaving 300 for final analysis. Results Among the 300 analyzed fetuses， postnatal follow-up confirmed normal coronary anatomy in 278 and abnormalities in 22 （7.33%）， comprising 2 anomalous origins and 20 diffuse dilations （all associated with fetal growth restriction）. SonoVCADheart demonstrated significantly higher overall diagnostic accuracy than conventional echocardiography （P 0.05）. Specifically， SonoVCADheart identified 20 true positives， 2 false positives， 276 true negatives， and 2 false negatives （sensitivity 90.9%， specificity 99.3%）， whereas conventional echocardiography detected 16 true positives， 7 false positives， 271 true negatives， and 6 false negatives （sensitivity 72.7%， specificity 97.5%）. Although sensitivity， specificity， positive predictive value， and negative predictive value were numerically higher for SonoVCADheart， these differences did not reach statistical significance （all P 0.05）. For coronary artery diameter measurements， Pearson correlation coefficients between the two methods were 0.865 for the left main and 0.859 for the right coronary artery （both P 0.05）. Intraclass correlation coefficients （ICCs） were 0.848 and 0.853， respectively， indicating strong inter-method agreement. Conclusions SonoVCADheart provides superior diagnostic accuracy and more reliable quantitative measurements of fetal coronary artery morphology compared with conventional echocardiography. It effectively reduces missed diagnoses and misclassifications， particularly for coronary origin anomalies and secondary dilations， offering valuable support for precise prenatal detection， classification， and clinical management.

Objective To investigate the differences in clinical manifestations and computed tomography pulmonary angiography （CTPA） features between primary pulmonary artery sarcoma （PPAS） and chronic pulmonary thromboembolism （CPTE）， aiming to improve the differential diagnosis of these two conditions. Methods Clinical data and CTPA signs of 28 patients with pathologically confirmed PPAS and 28 patients with CPTE were retrospectively analyzed. The differences in clinical symptoms， laboratory findings， and CTPA features were compared between the two groups. Results In the PPAS group， there were 12 males and 16 females， with a mean age of （50.7 ± 13.6） years. In the CPTE group， there were 18 males and 10 females， with a mean age of （48.7 ± 15.0） years. There were no statistically significant differences in gender and age between the two groups （P = 0.108 for gender， P = 0.602 for age）. The incidences of chest pain and cough with expectoration， along with the positive rate of neuron-specific enolase， were significantly higher in PPAS patients compared to those in the CPTE group （all P 0.05）. The incidences of chest tightness， shortness of breath， lower extremity deep venous thrombosis （DVT）， and the positive rate of N-terminal brain natriuretic peptide precursor （NT-proBNP） in the CPTE group were significantly higher than those in the PPAS group （all P 0.05）. The disease course in the PPAS group was shorter than that in the CPTE group ［5.5 （3.5， 9.6） months vs. 24.0 （9.0， 66.0） months， P 0.001］. The proportions of lesions involving the main pulmonary artery， bilateral pulmonary trunks， pulmonary valve， and right ventricular outflow tract in the PPAS group were significantly higher than those in the CPTE group. PPAS patients more frequently presented with complete filling defects， convex proximal margins， and distal pulmonary artery aneurysmal dilatation. In contrast， the CPTE group predominantly showed mural partial filling defects and flat proximal margins. The ratios of right ventricular diameter to left ventricular diameter and main pulmonary artery diameter to ascending aorta diameter in the CPTE group were significantly higher than those in the PPAS group ［（1.06 ± 0.19） vs. （0.93 ± 0.18） for the right-to-left ventricular diameter ratio， （1.20 ± 0.22） vs. （0.85 ± 0.12） for the main pulmonary artery to ascending aorta diameter ratio； all P 0.05）］. Conclusions The presence of a short disease course， prominent chest pain and cough， and filling defects that occupy the entire lumen of the central pulmonary arteries and exhibit a proximal bulging shape is highly suggestive of PPAS. In contrast， the presence of a long disease course， predominant chest tightness and shortness of breath， complicated DVT， elevated NT-proBNP， mural partial filling defect， and right heart enlargement along with main pulmonary artery dilation may strongly indicate CPTE. Fully recognizing these differences is beneficial for improving the early diagnosis of PPAS， avoiding misdiagnosis and mistreatment， and providing preliminary clues for clinical differential diagnosis.

Objective To investigate the functional role and underlying mechanism of long non-coding RNA GASAL1 and its interaction with eukaryotic translation initiation factor 2 alpha kinase 2 （EIF2AK2） in esophageal squamous cell carcinoma （ESCC）. Methods LncRNA GASAL1 expression in ESCC tissues and cell lines was quantified using quantitative real-time PCR （qRT-PCR） and validated by fluorescence in situ hybridization （FISH）. Clinical correlations were assessed using patient clinicopathological data. Subcellular localization was determined via RNA-FISH and nucleocytoplasmic fractionation. Cell viability， proliferation， migration， and invasion were evaluated using CCK-8， colony formation， wound healing， and Transwell assays， respectively. RNA immunoprecipitation （RIP） followed by western blotting was used to verify the direct interaction between GASAL1 and EIF2AK2. RNA-protein colocalization was visualized by combined FISH and immunofluorescence staining. Rescue experiments were performed to determine whether EIF2AK2 mediates the oncogenic effects of GASAL1. Results GASAL1 was significantly upregulated in ESCC tissues and cell lines compared to controls. Elevated GASAL1 expression positively correlated with lymph node metastasis and advanced clinical stage. Both GASAL1 and EIF2AK2 were predominantly localized in the cytoplasm. Functionally， GASAL1 knockdown significantly impaired ESCC cell viability， proliferation， migration， and invasion. RNA pull-down coupled with mass spectrometry identified EIF2AK2 as a direct binding partner， which was subsequently validated by RIP assays. Rescue experiments revealed that EIF2AK2 knockdown recapitulated the tumor-suppressive effects of GASAL1 silencing， whereas GASAL1 overexpression rescued the malignant phenotypes inhibited by EIF2AK2 depletion. Conclusions GASAL1 is upregulated in ESCC and correlates with aggressive clinicopathological features， suggesting its potential as a prognostic biomarker. Mechanistically， cytoplasmic GASAL1 promotes ESCC progression by interacting with EIF2AK2 to enhance tumor cell proliferation， migration， and invasion. The GASAL1/EIF2AK2 axis represents a promising therapeutic target for ESCC management.

Objective To investigate the clinical significance of the proportion of S100A9-high-expressing cells in the malignant cell population of acute myeloid leukemia （AML）， and to analyze its association with chemotherapeutic response and patient prognosis， so as to provide evidence for the identification and prognostic evaluation of high-risk AML patients. Methods Survival curves were initially generated using the BeatAML and TCGA datasets based on S100A9 transcript expression levels. Subsequently， a total of 80 patients with AML， consisting of 44 chemotherapy-sensitive cases and 36 chemotherapy-resistant cases， along with 10 healthy donors， were recruited. Multiparameter flow cytometry was carried out to assess the proportion of S100A9-high-expressing cells within the pre-defined AML malignant cell population. The relationships between this proportion and post-chemotherapy response as well as survival outcomes were analyzed. Immunocytochemistry and immunohistochemistry were further employed for validation. Results Survival analysis based on the overall expression of S100A9 mRNA revealed no statistically significant difference in either the TCGA or BeatAML dataset. Nevertheless， the proportion of malignant cells with high S100A9 expression was significantly higher in non-remission AML patients compared to those who achieved remission. The area under the receiver operating characteristic （ROC） curve was 0.765， and the optimal cutoff value was determined to be 12.65%. Patients characterized by a high proportion of malignant cells with high S100A9 expression， as defined by this cutoff， exhibited poorer survival outcomes and an unfavorable prognosis. Conclusions The proportion of S100A9-high-expressing malignant cells in AML could serve as a potential prognostic indicator. In comparison to the overall S100A9 expression， this parameter might be more effective in identifying high-risk AML patients.

Objective To evaluate the association between local anesthesia and procedural pain in patients undergoing fine-needle aspiration （FNA） of thyroid nodules. Methods A total of 207 patients with thyroid nodules who were referred for FNA were prospectively enrolled. Among them， 99 patients received local anesthesia before the procedure， whereas the remaining 108 patients underwent FNA without anesthesia. Pain levels were evaluated using the Numeric Rating Scale （NRS） at two specific time points： immediately after the procedure （within 5 minutes） and during a delayed period （5 - 30 minutes after the procedure）. Linear regression models with robust standard errors and Bonferroni correction were employed for statistical analysis. Results Local anesthesia was associated with a reduction in delayed post-procedural pain NRS at 5 - 30 minutes （β = -0.937， 95%CI： -1.293 - -0.580， adjusted P 0.001）. Older age was associated with less delayed pain （β = -0.01， P = 0.043）， and a longer puncture duration was associated with higher pain scores during this time frame （β = 0.07， P = 0.007）. The association between local anesthesia and immediate post-procedural pain （within 5 minutes） did not reach statistical significance after Bonferroni correction （adjusted P = 0.046； Bonferroni-corrected α = 0.025）. Conclusion Local anesthesia was associated with a reduction in delayed pain （5 - 30 minutes） after thyroid FNA， but not with immediate pain （ 5 minutes）.

Rheumatoid arthritis （RA） is a multifactorial chronic autoimmune disease characterized pathologically by synovial inflammation， pannus formation， cartilage destruction， and bone erosion. Although standardized mortality rates for RA have declined， its escalating global prevalence and trend toward earlier onset continue to substantially exacerbate the disease burden. In traditional Chinese medicine （TCM）， RA is primarily categorized under “Bi syndrome.” Within this framework， blood stasis functions not only as a pathological consequence but also as a core pathogenic mechanism that persists throughout the disease course， contributing significantly to its refractory nature. Consequently， therapeutic strategies that activate blood circulation and resolve stasis play a pivotal role in clinical management. Ferroptosis is an iron-dependent form of regulated cell death characterized primarily by intracellular iron accumulation， lipid peroxidation， and redox imbalance. Emerging evidence indicates that ferroptosis exacerbates RA pathology by driving synovial inflammation and joint destruction， highlighting targeted ferroptosis inhibition as a promising therapeutic strategy. Notably， blood stasis and ferroptosis appear to share pathophysiological overlaps in RA progression. Iron accumulation aligns with the clinical manifestations of blood stasis and may critically contribute to its development， while subsequent lipid peroxidation further aggravates stasis formation. Furthermore， pharmacological studies demonstrate that active compounds from blood-activating and stasis-resolving herbs can suppress ferroptosis in RA models by enhancing endogenous antioxidant defenses. Therefore， elucidating RA-related ferroptosis through the lens of “blood stasis” theory may provide novel scientific insights into targeting this cell death pathway， offering a mechanistic rationale for applying blood-activating and stasis-resolving therapies to mitigate RA progression.

Objective To investigate the effect of extracorporeal shock wave therapy （ESWT） on high glucose-induced endothelial?mesenchymal transition （EndMT） in human aortic endothelial cells （HAECs） and explore its potential mechanism. Methods HAECs were cultured in a high?glucose medium to establish an EndMT model. The cells were divided into five distinct groups： the normal control group （CON）， the control+shockwave group （CE）， the high?glucose group （HG）， the high?glucose + ESWT group （ESWT）， and the Snail inhibitor group （CYD19）. In the CON and CE groups， the glucose concentration was set at 5 mmol/L， while in the HG， ESWT， and CYD19 groups， it was 25 mmol/L. After culturing the cells for 7 days， the cells in the intervention groups were resuspended and subjected to shockwave treatment （8 Hz， 0.1 mJ/mm2， 1 000 pulses） once every 2 days， with a total of 3 treatments. Calcium deposition was detected using Alizarin Red S staining. The expression levels of endothelial markers （CD31， VEGF） and mesenchymal markers （α?SMA， FSP?1， OPG） were determined through Western blot and immunofluorescence analyses. Additionally， the expression of Snail， along with the total and phosphorylated levels of ERK1/2 and p38， were also measured. Results Alizarin Red S staining demonstrated that calcium deposition was significantly elevated in the HG group when compared with the CON group， and ESWT intervention notably reduced calcium deposition. In comparison with the CON group， the HG group showed a significant decrease in the expression of CD31 and VEGF， but an increase in the expression of α?SMA， FSP?1， and OPG. Meanwhile， the total and phosphorylated levels of ERK1/2 and p38， along with Snail expression， were significantly upregulated. When compared with the HG group， ESWT intervention significantly upregulated the expression of CD31 and VEGF， downregulated the expression of α?SMA， FSP?1， and OPG， inhibited the expression and phosphorylation of ERK1/2 and p38， and reduced the levels of Snail protein. Moreover， Snail expression was significantly decreased in both the ESWT and CYD19 groups as compared with the HG group. Conclusions The biological effects mediated by ESWT can effectively ameliorate the calcification of HAECs in a high?glucose environment. The underlying mechanism is likely that ESWT downregulates the expression and phosphorylation of p38 and ERK1/2 in the MAPK signaling pathway， thus inhibiting the expression of the downstream transcription factor Snail and reversing EndMT.

Objective To compare the effects of subcutaneous injection and intravenous injection of human Umbilical Cord Mesenchymal Stem Cells （hUC-MSCs） on skin lesions， splenic immune indexes， pathological changes， and key inflammatory factors in imiquimod-induced psoriasis mice， aiming to provide experimental evidence for clinical administration selection. Methods 35 specific-pathogen-free （SPF） C57BL/6J male mice were randomly divided into 7 groups （n = 5）： a blank control group， an intravenous phosphate-buffered saline （PBS） group， a subcutaneous PBS group， a subcutaneous hUC-MSCs group， an intravenous hUC-MSCs group， a subcutaneous hUC-MSCs combined with topical rhubarb group， and a topical rhubarb alone group. A psoriasis mouse model was established by applying 5% imiquimod cream on the back for 6 consecutive days. Corresponding interventions were administered on the 2nd and 4th days of modeling. Skin lesion changes were observed and scored using the Psoriasis Area and Severity Index （PASI）. Spleen weight was measured to calculate the spleen index. Skin histopathological changes were observed through hematoxylin and eosin （HE） staining. The levels of interleukin-17A （IL-17A）， interleukin-23 （IL-23）， and tumor necrosis factor-α （TNF-α） in serum and skin tissue were detected by enzyme-linked immunosorbent assay （ELISA）. Results There were highly significant differences in PASI scores， skin lesion thickness， spleen weight， and spleen index among all groups （P 0.01）. Both subcutaneous and intravenous administration of hUC-MSCs downregulated the levels of IL-17A， IL-23， and TNF-α in serum and skin tissue （P 0.05）. Intravenous injection of hUC-MSCs was more effective than subcutaneous injection in improving skin lesions， regulating the systemic immune system， and inhibiting inflammation. The overall efficacy of subcutaneous hUC-MSCs combined with topical rhubarb was superior to that of subcutaneous hUC-MSCs alone （P 0.05）. Conclusions hUC-MSCs can effectively alleviate psoriasis-like skin lesions， as well as local and systemic inflammatory responses in mice induced by imiquimod. Intravenous injection exhibits better overall efficacy compared to subcutaneous injection. Moreover， subcutaneous hUC-MSCs combined with topical rhubarb have a synergistic effect.

Objective To investigate the mechanism by which Moshen Formula treats idiopathic membranous nephropathy （IMN） through the regulation of autophagy via the TRPC6 signaling pathway. Methods Forty male SD rats were randomly divided into a control group （n = 8） and a model group （n = 32）. The model group was induced by cationic bovine serum albumin and then further divided into four subgroups： the model subgroup， the Moshen Formula subgroup， the TRPC6 inhibitor subgroup， and the Moshen Formula + TRPC6 agonist subgroup， with 8 rats in each subgroup. The control group and the model subgroup were administered normal saline by gavage， whereas the other three subgroups were given corresponding drugs for 4 weeks. The general condition of the rats was observed. The levels of serum creatinine， serum albumin， and 24-hour urinary protein were measured. Hematoxylin-eosin （HE） staining was carried out to observe the thickening of the glomerular basement membrane and the infiltration of inflammatory cells. Immunofluorescence was employed to detect the deposition of IgG in the glomeruli. Transmission electron microscopy was utilized to observe the glomerular basement membrane， foot processes， and autophagosomes. Western blot was conducted to detect the expression levels of transient receptor potential cation channel 6 （TRPC6）， microtubule-associated protein 1 light chain 3-Ⅱ （LC3-Ⅱ）， phosphorylated extracellular signal-regulated kinase 1/2 （p-ERK1/2）， phosphorylated mammalian target of rapamycin （p-mTOR）， ubiquitin-binding protein p62， podocin， and phospholipase A2 receptor （PLA2R） in renal tissues. Results Compared with the control group， the rats in the model group exhibited lethargy， a reduction in food intake， loose stools， and dull hair. Additionally， there were significant increases in serum creatinine， a decrease in serum albumin， and an elevation in 24-hour urinary protein （P 0.01）. The expression levels of TRPC6， p-ERK1/2， p-mTOR， p62， and PLA2R were significantly elevated （P 0.01）， whereas the expression levels of LC3-Ⅱ and podocin were decreased （P 0.01）. Renal pathological examination indicated marked thickening of the glomerular basement membrane， interstitial inflammatory infiltration， an increase in IgG deposition， extensive foot-process fusion， disrupted mitochondrial cristae， and impaired autophagy. Compared with the model group， the rats in the Moshen Formula group showed improvements in their general condition， biochemical indicators， and pathological injury. There was a restoration of autophagic flux， a decrease in the expression levels of TRPC6， p-ERK1/2， p-mTOR， and p62 （P 0.01）， and an increase in the expression levels of LC3-II and podocin （P 0.01）. Compared with the Moshen Formula group， the TRPC6 inhibitor group demonstrated more significant decreases in the expression of TRPC6， p-mTOR， and p62 （P 0.05）. However， there were no significant differences in biochemical parameters， podocin， and LC3-Ⅱ expression （P 0.05）. After the combination of the Moshen Formula with a TRPC6 agonist， the pathway-regulating and autophagy-improving effects were attenuated （P 0.05）. Conclusions The Moshen Formula effectively enhances the general condition， biochemical parameters， and alleviates renal pathological damage in rats with IMN. Its mechanism might involve the inhibition of the TRPC6 signaling pathway， the down-regulation of ERK/mTOR， the restoration of autophagic flux， and the up-regulation of podocin. Based on comprehensive phenotypes， the Moshen Formula demonstrated comparable efficacy to a TRPC6 inhibitor. In contrast， the activation of TRPC6 diminished the protective effects of the Moshen Formula， indicating that TRPC6 is a crucial target for the renoprotective action of the Moshen Formula.

Objective To investigate the effects of Jiawei Yanghe Decoction on the levels of serum secretory glycoprotein-3α （Wnt-3α）， osteoclast-related receptor （OSCAR）， receptor activator of NF-κB ligand （RANKL）， and the knee joint function in patients with type 2 diabetes mellitus complicated by knee osteoarthritis. Methods A total of 98 patients with type 2 diabetes mellitus complicated by knee osteoarthritis were randomly divided into a control group （celecoxib + conventional hypoglycemic therapy） and an observation group （celecoxib + conventional hypoglycemic therapy + Jiawei Yanghe Decoction） using the random number table method， with 49 cases in each group. Both groups received treatment for 4 weeks. The clinical efficacy， score of traditional Chinese medicine syndrome， levels of serum Wnt-3α， OSCAR， RNKL， glucose and lipid metabolism indexes， insulin-like growth factor （IGF）， transforming growth factor-β （TGF-β）， 25-hydroxyvitamin D₃ ［25（OH）D₃］， inflammatory factors， pain， and knee joint function were compared between the two groups. Results After 4 weeks of treatment， the total effective rate of the observation group was significantly higher than that of the control group （P 0.05）. Moreover， after 4 weeks of treatment， the scores of joint pain， pain fixation， swelling， limited joint activity， aversion to wind and cold， preference for joint warmth and stimulation， as well as the levels of serum Wnt-3α， RNKL， fasting blood glucose （FPG）， glycosylated hemoglobin （HbA_1c）， triglyceride （TG）， total cholesterol （TC）， IGF， interleukin-1 （IL-1）， interleukin-6 （IL-6）， scores of visual analogue scale （VAS）， and Western Ontario and McMaster University Osteoarthritis Index （WOMAC） in both groups were lower compared to those before treatment. Notably， the values in the observation group were significantly lower than those in the control group （P 0.05）. In addition， the levels of serum OSCAR， TGF-β， and 25（OH）D₃ were higher than those before treatment， and the levels in the observation group were significantly higher than those in the control group （P 0.05）. Conclusions Jiawei Yanghe decoction， in combination with celecoxib and routine hypoglycemic therapy， can effectively enhance the traditional Chinese medicine syndrome score of patients with type 2 diabetes mellitus complicated by knee osteoarthritis. It can also regulate the serum levels of Wnt-3α， OSCAR， RNKL， IGF， TGF-β， and 25（OH）D₃， reduce the inflammatory response， alleviate pain， and improve the body's glucose and lipid metabolism as well as knee joint function， demonstrating good clinical efficacy.

Objective To explore the relationship between serum 3-oxoacid CoA-transferase 1 （OXCT1）， Xin actin-binding repeat-containing protein 2 （XIRP2）， and the severity and prognosis of atopic dermatitis （AD） in children. Methods Thirty children with moderate-to-severe AD who were treated at the Dermatology Outpatient Department of Guangdong Provincial Hospital of Chinese Medicine were enrolled in the observation group. According to the severity of their conditions， they were divided into a moderate group （n = 15） and a severe group （n = 15）. After 12 weeks of treatment， they were further classified into a good prognosis group （n = 20） and a poor prognosis group （n = 10）. Meanwhile， 30 healthy children with no previous history of allergic diseases were selected as the control group. Serum proteomic levels were measured by data-independent acquisition mass spectrometry （DIA-MS） to determine the expression levels of OXCT1 and XIRP2. Clinical data， immunoglobulin E （IgE） levels， and eosinophil counts of the AD children were collected. Logistic regression analysis was used to identify the factors influencing the poor prognosis in children with AD. Receiver operating characteristic （ROC） curve analysis was carried out to evaluate the value of serum OXCT1 and XIRP2， either individually or in combination. Results When compared with the control group， the serum OXCT1 level in the observation group showed a significant increase， and the XIRP2 level presented a significant decrease （P 0.05）. Serum OXCT1 levels gradually rose as the disease severity worsened， while serum XIRP2 levels gradually declined （P 0.05）. In comparison with the good prognosis group， there were no statistically significant differences in clinical data， IgE levels， or eosinophil counts in the poor prognosis groups （P 0.05）. Serum XIRP2 was identified as an independent risk factor for poor prognosis in children with AD， whereas serum OXCT1 was identified as an independent protective factor （P 0.05）. The area under the ROC curve （AUC） for poor prognosis was 0.940 for OXCT1， 0.885 for XIRP2， and 0.945 for the combination of both markers. The combined prediction AUC remained higher than that of either marker alone. Conclusions Serum OXCT1 levels were significantly elevated， and XIRP2 levels were significantly decreased in children with atopic dermatitis. These two factors may play biological roles at different stages of disease development and prognosis. OXCT1 functions as a protective factor， whereas XIRP2 serves as a risk factor for poor prognosis. The combined assessment of serum OXCT1 and XIRP2 shows good predictive efficacy for the prognosis of children with atopic dermatitis.

Objective To investigate the clinical factors associated with bone erosion in patients with tophi detected by ultrasound and to construct and internally validate a nomogram-based risk assessment model. Methods Clinical data of 226 gout patients who underwent musculoskeletal ultrasonography and were diagnosed with tophi at Zhengzhou Central Hospital Affiliated to Zhengzhou University from January 2022 to October 2025 were retrospectively collected. The presence of bone erosion was set as the outcome variable. General characteristics， medical history， and laboratory indicators of these patients were collected. Subsequently， the patients were randomly divided into a training set and an internal validation set at a ratio of 7∶3. Univariate analysis was carried out to screen candidate variables， and multivariate logistic regression analysis was employed to identify independent factors associated with bone erosion in patients with ultrasound-detected tophi. Based on these factors， a nomogram model was constructed. The discriminatory ability of the model was evaluated through receiver operating characteristic （ROC） curve analysis. Calibration and goodness of fit were respectively assessed by using calibration curves and the Hosmer-Lemeshow test. Decision curve analysis （DCA） was utilized to evaluate the clinical utility of the model. Results The bone erosion group was characterized by an older age， a longer disease duration， higher serum uric acid levels， a higher proportion of polyarticular involvement， and lower estimated glomerular filtration rate and albumin levels compared to the non-bone erosion group； all these differences were statistically significant （all P 0.05）. Multivariate logistic regression analysis revealed that an older age， a longer disease duration， polyarticular involvement， higher serum uric acid levels， and a lower estimated glomerular filtration rate were independently associated with bone erosion in patients with ultrasound-detected tophi. A nomogram model was constructed based on these factors. Receiver operating characteristic curve analysis demonstrated that the areas under the curve of the model were 0.950 （95%CI： 0.903 - 0.997） in the training set and 0.915 （95%CI： 0.874 - 0.957） in the internal validation set， indicating that the model had a certain discriminative ability within this cohort. The calibration curve showed an acceptable agreement between the predicted and observed probabilities. The Hosmer-Lemeshow goodness-of-fit test indicated an acceptable model fit in both the training and internal validation sets （χ2 = 5.164 and 3.353， respectively； P = 0.740 and 0.910， respectively）. Decision curve analysis showed that the model had a certain clinical net benefit within a range of threshold probabilities. Conclusions Advanced age， extended disease duration， polyarticular involvement， elevated serum uric acid levels， and reduced estimated glomerular filtration rate were independently associated with bone erosion in patients with ultrasound-detected tophi. The nomogram model constructed based on these factors exhibited a certain degree of predictive value and could offer a reference for clinical risk assessment and stratified management.

Objective To explore the osteogenic efficacy and molecular mechanism of the EPO/pDA/BCP composite scaffold， this study focuses on verifying whether it promotes the osteogenic differentiation of bone marrow mesenchymal stem cells （BMSCs） and the repair of critical bone defects in vivo by activating the PI3K/AKT pathway and up-regulating MTSS1 and CYTL1. Methods The EPO/pDA/BCP composite material was fabricated by grafting dopamine and erythropoietin onto a biphasic calcium phosphate scaffold. In in-vitro experiments， four groups were established： the control group， the BCP group， the EPO/pDA/BCP group， and the EPO/pDA/BCP + LY294002 group with the addition of a PI3K/AKT pathway inhibitor. The cell proliferation and osteogenic differentiation capacity were assessed using the CCK-8 method， alkaline phosphatase activity assay， RT-qPCR， and Western blotting. The expression levels of the PI3K/AKT pathway and its downstream genes MTSS1 and CYTL1 were determined by RT-qPCR and Western blotting. In in-vivo experiments， a critical bone defect model of the femoral condyle in SD rats was created and randomly assigned to the blank group， the BCP group， and the EPO/pDA/BCP group for intervention. At 4 and 12 weeks after surgery， Micro-CT， hematoxylin-eosin staining， Masson staining， and immunohistochemical analysis were carried out to evaluate bone regeneration. Results The CCK-8 experiment verified that the EPO/pDA/BCP composite material exhibited excellent biocompatibility. The outcomes of the alkaline phosphatase activity assay， RT-qPCR， and Western blot demonstrated that， in comparison with the BCP group and the control group， the EPO/pDA/BCP group could notably promote the osteogenic differentiation of BMSCs （P 0.05）. Following the addition of the inhibitor LY294002， the osteogenic effect was markedly weakened， and the expression of molecules associated with the PI3K/AKT signaling pathway （p-PI3K， p-AKT， CYTL1， and MTSS1） was down-regulated （P 0.05）. Micro-CT scanning revealed that the new bone volume fraction and bone density in the bone defect area of the EPO/pDA/BCP group were significantly higher than those of the blank group and the BCP group （P 0.05）. Histological staining results suggested that the bone tissue regeneration in the EPO/pDA/BCP group was more comprehensive and mature than that in the other two groups. Immunohistochemical staining further indicated that the positive staining intensities of the osteogenic markers bone morphogenetic protein-2 and osteocalcin in the bone defect area of the EPO/pDA/BCP group were significantly higher than those of the BCP group and the blank control group. Conclusion The EPO/pDA/BCP bioceramic exhibits excellent osteogenic properties both in vitro and in vivo， and this effect might be associated with the activation of the expression of PI3K/AKT signaling pathway proteins.

Objective To explore the predictive value of the combination of ankle brachial index （ABI）， vascular endothelial growth factor （VEGF）， neutrophil and lymphocyte ratio （NLR）， serum amyloid A （SAA）， and soluble triggering receptor expressed on human myeloid cells-1 （sTREM-1） in predicting the prognosis of endovascular interventional therapy （EVT） in patients with lower extremity arteriosclerosis obliterans （ASO） complicated with ischemic gangrene infection. Methods A total of 304 patients with ASO complicated by ischemic gangrene infection， who underwent EVT in the hospital from March 2019 to March 2024， were selected for the study. The long-term patency rate of the surgical site was analyzed. The patients were divided into a restenosis group （n = 102） and a patency group （n = 202） based on whether restenosis occurred within 2 years after the surgery. The clinical data， preoperative ABI， VEGF， NLR， SAA， and sTREM-1 levels were compared between the two groups. Spearman correlation analysis was employed to analyze the correlation between preoperative ABI， VEGF， NLR， SAA， and sTREM-1 levels and restenosis after interventional therapy in patients with ASO. Binary logistic regression analysis was utilized to analyze the influencing factors affecting the prognosis of EVT in patients with ASO complicated by ischemic gangrene infection. The receiver operating characteristic （ROC） curve was used to analyze the predictive value of preoperative ABI， VEGF， NLR， SAA， and sTREM-1 for the prognosis of EVT. Results The proportions of complete occlusion， TASC grade B， vascular lesion length， neutrophil count （NEUT）， serum C-reactive protein （CRP）， procalcitonin （PCT）， VEGF， NLR， SAA， and （sTREM-1） in the restenosis group were significantly higher than those in the patency group （P 0.05）， whereas the lymphocyte count （LYM） and ABI value were significantly lower （P 0.05）. Spearman correlation analysis indicated that the levels of VEGF， NLR， SAA， and sTREM-1 were significantly positively correlated with restenosis after interventional therapy （P 0.05）， and ABI was significantly negatively correlated with restenosis after interventional therapy （P 0.05）. Binary logistic regression analysis demonstrated that an increase in the length of vascular lesions， elevated preoperative levels of PCT， VEGF， NLR， SAA， and sTREM-1 were risk factors for restenosis after EVT in patients with ASO complicated with ischemic gangrene infection， and an increase in ABI was a protective factor （P 0.05）. ROC curve analysis showed that the sensitivities of preoperative ABI， VEGF， NLR， SAA， and sTREM-1， either alone or in combination， for predicting the prognosis of EVT were 79.41%， 81.37%， 82.35%， 80.39%， 83.33%， and 92.15%， respectively； the specificities were 75.25%， 71.78%， 70.79%， 71.29%， 69.31%， and 68.31%， respectively； and the areas under the curve （AUCs） were 0.815， 0.794， 0.785， 0.773， 0.784， and 0.984， respectively. The combined diagnosis showed a higher value. Conclusions ABI， VEGF， NLR， SAA， and sTREM-1 are influencing factors for restenosis after EVT in patients with ASO complicated by ischemic gangrene infection. These factors can effectively predict the risk of postoperative restenosis.

Objective This study aims to explore the mechanism through which resveratrol （Res） mitigates homocysteine （Hcy）-induced oxidative damage in mouse pancreatic β-cells by regulating the expression and methylation level of the Toll-like receptor 4 （TLR4） gene. Methods The effects of different concentrations of homocysteine and resveratrol on the viability of mouse pancreatic β-cells were evaluated using the CCK-8 assay. In each group， the levels of malondialdehyde （MDA）， the activity of glutathione peroxidase （GSH-Px）， and the levels of insulin were measured using an MDA kit， a GSH-Px activity kit， and enzyme-linked immunosorbent assay （ELISA）， respectively. The oxidative stress status was assessed through fluorescence staining. The protein and mRNA expression levels of TLR4 in the control group， the Hcy group， and the homocysteine + resveratrol （Hcy + Res） co-treatment group were detected via Western blot and qRT-PCR. The DNA methylation level of TLR4 was determined using nested methylation-specific PCR， and the protein expression of DNMT1 （DNA methyltransferase 1） was measured by Western blot. Small interfering RNA fragments targeting DNMT1 were constructed and transfected into pancreatic β-cells. Subsequently， the TLR4 protein expression was detected by Western blot. The MDA levels， GSH-Px activity， and insulin levels in the DNMT1 knockdown groups were measured using the aforementioned kits. Likewise， small interfering RNA fragments targeting TLR4 were constructed and transfected into pancreatic β-cells， and then the MDA levels， GSH-Px activity， and insulin levels were measured. Results Cell viability decreased after treatment with 100 μmol/L Hcy. In contrast， intervention with 10 μmol/L Res effectively mitigated the Hcy-induced damage to pancreatic β-cells. Results from the MDA assay and fluorescence staining indicated that， when compared with the Control group， the Hcy group had elevated MDA and reactive oxygen species （ROS） levels （P 0.05）， while these levels declined in the Hcy+Res group （P 0.05）. Findings from the GSH-Px activity assay and ELISA demonstrated that， relative to the Control group， the Hcy group had reduced GSH-Px activity and insulin levels （P 0.05）， whereas the Hcy + Res group showed increased levels （P 0.05）. Western blot and qRT-PCR results showed that the expression levels of TLR4 protein and mRNA were significantly higher in the Hcy group than in the Control group （P 0.05）， while they were significantly lower in the Hcy + Res group （P 0.05）. Conversely， results from nested methylation-specific PCR showed that the TLR4 DNA methylation levels displayed an opposite trend. The expression of DNMT1 protein was lower in the Hcy group （P 0.05） and higher in the Hcy + Res group （P 0.05） compared with the Control group. The expression of TLR4 protein was significantly higher in the Hcy + si-DNMT1 group than in the Hcy + si-NC group （P 0.05）， and it was further increased in the Hcy + Res + si-DNMT1 group compared with the Hcy + Res group （P 0.05）. Compared with the Hcy + si-NC group， the MDA levels were significantly elevated in the Hcy + si-DNMT1 group （P 0.05）. Moreover， when compared with the Hcy + Res group， the MDA levels were further increased in the Hcy + Res + si-DNMT1 group （P 0.05）. The changes in GSH-Px activity and insulin levels were opposite to those of MDA. Further knockdown of TLR4 led to a decrease in MDA levels （P 0.05）， and there was an even greater reduction after Res intervention （P 0.05）. Conversely， GSH-Px activity and insulin levels increased （P 0.05）， and there was a further elevation after Res intervention （P 0.05）. Conclusion Resveratrol alleviates the oxidative damage in pancreatic β-cells induced by homocysteine， a process that is associated with alterations in TLR4 expression and its methylation level.

Objective To evaluate the efficacy and electroencephalographic （EEG） spectral changes of perampanel combined with levetiracetam in children with Self-Limited Epilepsy with Centrotemporal Spikes （SeLECTS） complicated by Electrical Status Epilepticus during Sleep （ESES）. Methods A total of 86 children with SeLECTS complicated by ESES， admitted to our hospital between June 2023 and June 2025， were enrolled. Participants were randomly assigned to a control group （n = 43） or an observation group （n = 43） using a random number table. The control group received oral levetiracetam monotherapy， while the observation group received perampanel added to the levetiracetam regimen. Both groups underwent a 6-month treatment course. Seizure frequency， seizure duration， and EEG spike-wave discharge index were recorded before and after treatment. Serum neuron-specific enolase （NSE） levels and EEG spectral parameters （relative power of delta， theta， alpha， and beta bands） were compared. Cognitive function was assessed using the Wechsler Intelligence Scale for Children （WISC）， evaluating performance IQ， verbal IQ， and full-scale IQ. Adverse events were systematically documented. Results Following treatment， the observation group demonstrated significantly lower seizure frequency， shorter seizure duration， and a reduced spike-wave discharge index compared with the control group （all P 0.05）. EEG spectral analysis revealed higher relative power of theta and delta waves， alongside lower beta and alpha wave power， in the observation group than in the control group （P 0.05）. The observation group also exhibited significantly lower NSE levels and higher WISC scores than the control group （P 0.05）. No significant difference was observed in the incidence of adverse events between the two groups （χ2 = 1.042， P = 0.307）. Conclusion The combination of perampanel and levetiracetam effectively reduces seizure burden， ameliorates EEG abnormalities， mitigates neuronal injury， and improves cognitive function in children with SeLECTS complicated by ESES， while maintaining a favorable safety profile comparable to levetiracetam monotherapy.

Objective To investigate the therapeutic effect and the underlying mechanism of ferulic acid （FA） on the delayed wound healing induced by arsenic poisoning in a mouse skin wound model. Methods （1） Male C57BL/6 mice were administered drinking water containing NaAsO₂ for 3 months to establish an arsenic poisoning model. （2） Full-thickness skin defects were created on the backs of normal and arsenic-poisoned mice. Subsequently， normal saline or FA solution was topically applied. The mice were divided into four groups： the control group， the FA group， the NaAsO₂ group， and the NaAsO₂+FA group. Wound healing was evaluated through photographic monitoring. Wound tissues were collected for HE staining and Masson staining to assess the degree of healing. Inflammatory factors were detected by Real-time PCR， and the expression levels of tight junction proteins （Claudin-1 and Occludin） as well as key proteins of the nuclear factor κB （NF-κB） pathway （p65 and P-p65） were measured by Western blot. （3） Human umbilical vein endothelial cells （HUVECs） were divided into four groups： the control group， the NaAsO₂ group， the NaAsO₂+FA group， and the FA group. The study aimed to verify the effects of NaAsO? on the proliferation and migration capabilities of HUVECs， as well as on the expression of inflammatory factors， tight junction proteins， and the NF-κB pathway. Results （1） When compared to the control group， the NaAsO? group in mice demonstrated significantly slower wound healing （P 0.05）. Additionally， there was a decrease in the expression of collagen fibers and tight-junction proteins in the wound tissues （P 0.05）， an increase in the expression of inflammatory factors （P 0.05）， and activation of the NF-κB pathway （P 0.05）. In contrast to the NaAsO? group， the NaAsO?+FA group showed accelerated wound healing （P 0.05）， an elevation in the expression of collagen fibers and tight-junction proteins （P 0.05）， a reduction in the expression of inflammatory factors （P 0.05）， and inhibition of the NF-κB pathway （P 0.05）. （2） In HUVEC cells， stimulation with NaAsO? significantly inhibited cell proliferation and migration （P 0.05）， down-regulated the expression of tight-junction proteins （P 0.05）， promoted the expression of inflammatory factors， and activated the NF-κB signaling pathway （P 0.05）. The combined intervention with FA could significantly reverse the adverse effects induced by NaAsO? （P 0.05）. Conclusion FA can inhibit the inflammatory response by suppressing the NF-κB signaling pathway and upregulate the expression of tight junction proteins， which in turn improves the delayed wound healing caused by arsenic poisoning.

Objective To investigate the effects of low-concentration epidural analgesia combined with early postpartum bladder low-frequency pulsed electrical stimulation on maternal satisfaction and lower urinary tract function in advanced maternal age parturients undergoing vaginal delivery under an enhanced recovery after delivery pathway. Methods A prospective randomized controlled study was carried out on 120 parturients aged 35 years or older who received vaginal delivery with epidural analgesia at Wuxi Maternal and Child Health Hospital from June 2023 to June 2025. These parturients were randomly divided into four groups： Group A （conventional-concentration epidural analgesia）， Group B （low-concentration epidural analgesia）， Group C （conventional-concentration epidural analgesia plus early bladder low-frequency pulsed electrical stimulation）， and Group D （low-concentration epidural analgesia plus early bladder low-frequency pulsed electrical stimulation）， with 30 cases in each group. Comparisons were made among the four groups regarding maternal satisfaction， postpartum urinary retention （PUR）， catheterization rate， time to first voiding， post-void residual volume （PVR）， time to complete spontaneous voiding， urinary tract infection （UTI）， and visual analogue scale （VAS） scores at 6， 24， 48， and 72 h postpartum. Results There were no significant differences in the rescue analgesia rate or the total sufentanil dose among the four groups. However， the total ropivacaine dose was lower in the low-concentration groups. Maternal satisfaction scores and the length of stay differed significantly among the four groups （both P 0.01）， and group D exhibited the highest satisfaction and the shortest length of stay. Significant differences were also noted in the incidence of PUR， the catheterization rate， the time to first voiding， PVR， the time to complete spontaneous voiding， and UTI among the four groups （all P 0.05）， with group D demonstrating the best recovery of lower urinary tract function. The incidence of composite adverse urinary outcomes differed significantly among the four groups （P 0.01）， and the lowest incidence was observed in group D. No significant differences in VAS scores were detected at 6 h or 24 h postpartum （both P 0.05）， while significant differences were identified at 48 h and 72 h postpartum （both P 0.01）， and the scores in groups C and D were lower than those in groups A and B. Conclusions Under the same basic enhanced recovery after delivery management， the combination of low-concentration epidural analgesia and early postpartum bladder low-frequency pulsed electrical stimulation may enhance maternal satisfaction， reduce urinary complications， and facilitate the recovery of lower urinary tract function in advanced maternal age parturients undergoing vaginal delivery.

Objective To explore the influence of infertility-related stigma on social anxiety in the context of social media based on the SOR framework， and to verify the separate and chain mediating effects of electronic health literacy and online health information-seeking behavior， thereby providing evidence for clinical psychological intervention. Methods A total of 458 female infertile patients who were treated in a hospital from January 2023 to August 2025 were enrolled in the study. All participants completed questionnaires， which included the Infertility Stigma Scale， Online Health Information-Seeking Behavior Scale， Social Media User Social Anxiety Scale， and Electronic Health Literacy Scale. Spearman correlation analysis， linear regression， the Bootstrap method （with 5 000 iterations）， and structural equation modeling were employed to test the mediating effects. Results （1） Correlation analysis demonstrated that infertility-related stigma was negatively correlated with online health information-seeking behavior （rs = -0.472， P 0.001） and electronic health literacy （rs = -0.591， P 0.001）， and positively correlated with social media social anxiety （rs = 0.590， P 0.001）. Electronic health literacy was strongly negatively correlated with social media social anxiety （rs = -0.972， P 0.001）. （2） Linear regression indicated that infertility-related stigma significantly and positively predicted social media social anxiety （β = 0.465， P 0.001）， with a model R2 of 0.343， an adjusted R2 of 0.341， and F = 237.913 （P 0.001）. （3） Separate mediation analysis revealed significant mediation effects of electronic health literacy （a*b = 0.445， 95%CI： 0.391 - 0.497， P 0.001） and online health information-seeking behavior （a*b = -0.170， 95%CI： -0.210 - -0.132， P 0.001）. （4） Chain mediation analysis confirmed a significant chain path： "stigma→information-seeking behavior→electronic health literacy→social anxiety" （effect value = -0.154， 95%CI： -0.193 - -0.119， P 0.001）. The total indirect effect was 0.418 （95%CI： 0.365 - 0.472）， and the total effect was 0.465 （P 0.001）. Conclusions Under the SOR framework， infertility-related stigma influences social anxiety on social media via two pathways： separate mediation （electronic health literacy and online health information-seeking behavior） and chain mediation. Electronic health literacy serves as the core mediator， and the chain-mediating path is stably verified. Clinical interventions should concurrently enhance electronic health literacy and standardize information-seeking behavior to relieve social anxiety.

Objective To evaluate the efficacy and safety of ciprofol dosing calculated using different body weight scalars—total body weight （TBW）， adjusted body weight （ABW）， and ideal body weight （IBW）—combined with fentanyl for procedural sedation during gastroscopy in overweight and obese patients. Methods A total of 294 overweight and obese patients （BMI 25 - 40 kg/m2） undergoing sedated gastroscopy at The Seventh Affiliated Hospital， Sun Yat-sen University， between March and September 2024 were enrolled. Participants were randomly assigned in a 1∶1∶1 ratio to one of three groups （n = 98 per group） using a random number table： TBW group， ABW group， or IBW group. Anesthesia was induced with fentanyl 50 μg plus ciprofol 0.4 mg/kg （calculated according to the assigned body weight scalar）， followed by maintenance infusion of ciprofol at 1 mg/（kg·h） based on the same scalar. Primary outcomes included ciprofol rescue dose requirements and recovery time. Secondary outcomes encompassed sedation success rate， hemodynamic parameters （MAP， HR， SpO?） at predefined timepoints （T?： pre-induction； T?： scope insertion； T?： passage through piriform fossa； T?： pyloric examination； T?： procedure completion； T?： awakening in recovery room； T?： discharge from recovery）， and incidence of adverse events. Results Compared with the TBW group， the IBW group required a significantly higher cumulative rescue dose of ciprofol （P 0.05） and achieved shorter recovery time （P 0.05）. The ABW group also demonstrated shorter recovery time versus TBW （P 0.05）， with no significant difference in rescue dose requirements （P 0.05）. No significant differences were observed between the ABW and IBW groups regarding rescue dose or recovery time （both P 0.05）. The incidence of adverse events—including respiratory depression， hypoxemia， hypotension， bradycardia， involuntary movement， cough， singultus， dizziness， nausea， and vomiting—and the sedation success rate did not differ significantly among the three groups （all P 0.05）. Perioperative hemodynamic profiles remained stable and comparable across groups （all P 0.05）. Conclusion For overweight and obese patients undergoing sedated gastroscopy， a ciprofol-fentanyl anesthesia regimen with ciprofol dosing calculated by adjusted body weight （ABW） provides optimal balance between anesthetic efficacy and recovery efficiency， while maintaining a favorable safety profile comparable to TBW- or IBW-based dosing. ABW-based dosing is therefore recommended as the preferred weight scalar in this population.