Objective To apply an artificial intelligence (AI) -based pelvic floor optimization training system using human motion analysis technique in patients undergoing pelvic floor rehabilitation, so as to assist clinicians in providing guidance, improving clinical efficiency, and enhancing the efficacy of patients' independent training. Methods A total of 60 patients with overactive bladder (OAB) complicated with urgent urinary incontinence (UUI) treated in our hospital during Sep. 2024 and Dec. 2025 were enrolled and randomly divided into the routine guidance group (n=30) and AI guidance group (n=30). The routine guidance group received conventional pelvic floor optimization training under clinicians' instruction, while the AI guidance group underwent training with the AI-based pelvic floor optimization system using human motion analysis. After 6 weeks of intervention, outcomes were compared between the two groups, including the international consultation on incontinence questionnaire-short form (ICI-Q-SF), incontinence quality of life scale (I-QoL), overactive bladder symptom score (OABSS), patient's perception of bladder condition (PPBC) score, pelvic floor muscle function (myoelectric values in the preresting, post-resting, type Ⅰ muscle, type Ⅱ muscle, and endurance test phases), urine output, average flow rate (Qavg), and maximum flow rate (Qmax). Results After 6 weeks of treatment, the ICI-Q-SF, I-QoL, OABSS, PPBC score, type I muscle myoelectric value, Qavg and Qmax were significantly improved in both groups compared with baseline (P＜0.05). After 6 weeks of intervention, the I-QoL score was significantly higher in the AI guidance group than in the routine guidance group[81.82 (79.55, 84.38) vs.77.84 (75.00, 79.55) ], with significant difference (P＜0.05). Compared with the routine guidance group, the AI guidance group showed significant improvements in myoelectric values in the pre-resting, post-resting, type I muscle and endurance testing phases (P＜0.05). Conclusion The AI-based pelvic floor optimization training system can effectively assist clinicians in guiding patients to complete pelvic floor optimization training, improve rehabilitation efficiency and efficacy of independent exercise, and reduce dependence on specialized clinicians, which exhibits favorable safety.

Objective To analyze the emergency testing results of a mixed poisoning incident involving methyl acetate and dimethyl carbonate in a composite fabric processing enterprise. Methods A mixed poisoning incident involving methyl acetate and dimethyl carbonate occurred at a composite fabric processing enterprise in a city of Guangdong Province. On-site occupational health investigation data and laboratory testing results related to this incident were collected, and an integrated analysis was conducted. Results The on-site occupational health investigation revealed inadequate ventilation and non-standard use of personal protective equipment. Volatile organic component analysis of raw and auxiliary materials showed that methyl acetate and dimethyl carbonate had relatively high percentages of peak area among all used volatile organic chemical agents in post-incident emergency testing, accounting for 65.10% and 38.25%, respectively. The exposure concentration of short term (C_STE) of methyl acetate in the production line air was 15.13 mg/m³. In the chemical storage area, C_STE of methyl acetate and methanol were 451.04 and <0.21 mg/m³, respectively, all below their respective occupational exposure limits (500.00 and 50.00 mg/m³). In the poisoned workers, blood methanol, blood formic acid, and urinary formic acid levels were 147, 414, and 4 389 mg/L, respectively. Conclusion Occupational exposure to methyl acetate and dimethyl carbonate may lead to acute occupational poisoning and cause health damage. Employers should fulfill their responsibilities for occupational disease prevention by ensuring proper operation of protective facilities, while workers should enhance awareness of occupational disease prevention and correctly use personal protective equipment.

OBJECTIVE: To investigate the therapeutic potential of pseudolaric acid B (PAB) on non-alcoholic fatty liver disease (NAFLD) and its underlying molecular mechanism in vitro and in vivo. METHODS: Eight-week-old male C57BL/6J mice (n=32) were fed either a normal chow diet (NCD) or a high-fat diet (HFD) for 8 weeks. The HFD mice were divided into 3 groups according to a simple random method, including HFD, PAB low-dose [10 mg/(kg·d), PAB-L], and PAB high-dose [20 mg/(kg·d), PAB-H] groups. After 8 weeks of treatment, glucose metabolism and insulin resistance were assessed by oral glucose tolerance test (OGTT) and insulin tolerance test (ITT). Biochemical assays were used to measure the serum and cellular levels of total cholesterol (TC), triglycerides (TG), aspartate aminotransferase (AST), alanine aminotransferase (ALT), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C). White adipose tissue (WAT), brown adipose tissue (BAT) and liver tissue were subjected to hematoxylin and eosin (H&E) staining or Oil Red O staining to observe the alterations in adipose tissue and liver injury. PharmMapper and DisGeNet were used to predict the NAFLD-related PAB targets. Peroxisome proliferator-activated receptor alpha (PPARα) pathway involvement was suggested by Kyoto Encyclopedia of Genes and Genomes (KEGG) and search tool Retrieval of Interacting Genes (STRING) analyses. Luciferase reporter assay, cellular thermal shift assay (CETSA), and drug affinity responsive target stability assay (DARTS) were conducted to confirm direct binding of PAB with PPARα. Molecular dynamics simulations were applied to further validate target engagement. RT-qPCR and Western blot were performed to assess the downstream genes and proteins expression, and validated by PPARα inhibitor MK886. RESULTS: PAB significantly reduced serum TC, TG, LDL-C, AST, and ALT levels, and increased HDL-C level in HFD mice (P<0.01). Target prediction analysis indicated a significant correlation between PAB and PPARα pathway. PAB direct target binding with PPARα was confirmed through luciferase reporter assay, CETSA, and DARTS (P<0.05 or P<0.01). The target engagement between PAB and PPARα protein was further confirmed by molecular dynamics simulations and the top 3 amino acid residues, LEU321, MET355, and PHE273 showed the most significant changes in mutational energy. Subsequently, PAB upregulated the genes expressions involved in lipid metabolism and mitochondrial biogenesis downstream of PPARα (P<0.05 or P<0.01). Significantly, the PPARα inhibitor MK886 effectively reversed the lipid-lowering and PPARα activation properties of PAB (P<0.05 or P<0.01). CONCLUSION PAB mitigates lipid accumulation, ameliorates liver damage, and improves mitochondrial biogenesis by binding with PPARα, thus presenting a potential candidate for pharmaceutical development in the treatment of NAFLD.
Animals ; PPAR alpha/metabolism* ; Non-alcoholic Fatty Liver Disease/pathology* ; Male ; Mice, Inbred C57BL ; Lipid Metabolism/drug effects* ; Diterpenes/therapeutic use* ; Organelle Biogenesis ; Diet, High-Fat ; Humans ; Mice ; Liver/metabolism* ; Insulin Resistance ; Mitochondria/metabolism* ; Molecular Docking Simulation

Cancer is still the main cause of death in the world. With the promotion of early cancer screening and the development of diagnosis and treatment technology, the 5-year survival rate of cancer patients has gradually increased, and more attention has been paid to the whole-process management of cancer patients. However, the incidence of tumor-related emergencies remains high, including a wide range of emergencies caused by initial tumor presentation, surgical complications, progression of known diseases, recurrence of previous cancers, and adverse reactions to treatment, some of which are life-threatening. In this review, we reviewed the current situation and management experience of gastrointestinal tumor-related emergencies.

Objective : To investigate the antagonistic activity of Lactococcus garvieae SHAMU-LG6 against Staphy- lococcus . Methods : VITEK 2 GP identification card , Microflex LT MALDI-TOF mass spectrometer and 16S rDNA amplification sequencing were used to identify the strain species . The antagonistic activity of L. garvieae SHAMU- LG6 against different Staphylococcus was detected by Oxford cup method for bacterial inhibition ; the antimicrobial active components were preliminarily isolated and purified by adsorption on XAD16 nonionic macroporous resin , gradient ethanol elution and rotary evaporation drying. Results : L. garvieae SHAMU-LG6 exhibited potent antago- nistic effect against methicillin-resistant Staphylococcus aureus , methicillin-susceptible S. aureus , S. epidermidis , S. saprophyticus , S. lugdunensis , S. hominis , S. capitis and S. warneri , with inhibitory indices of 3 . 3 , 3 . 0 , 4. 3 , 2. 0 , 4. 0 , 3 . 5 , 3 . 8 , and 3 . 5 , respectively. The antimicrobial active components produced by L. garvieae SHAMU-LG6 were mainly present in 70% and 80% ethanol eluates . Conclusion L. garvieae SHAMU-LG6 ex- hibits a potent antagonistic effect on Staphylococcus , and the antimicrobial active components produced by it are ex- pected to be a lead compound for the development of novel antimicrobial agents .

Objective To explore the relationship between levels of vascular endothelial growth factor(VEGF),insulin-like growth factor 1(IGF-1),and transforming growth factor-β1(TGF-β1)in the synovial fluid of children with avascular necrosis of the femoral head(also known as Perthes disease)and the efficacy of postoperative revascularization,aiming to provide a basis for subsequent diagnosis and treatment.Methods A retrospective study was conducted on 262 children with Perthes disease admitted to the Affiliated Hospital of Gansu University of Chinese Medicine from January 2023 to June 2024.Based on postoperative revascularization efficacy,patients were divided into good revascularization group(n=228)and poor revascularization group(n=34).For poor revascularization group,a 1:2 matched case-control design was used to select 68 age-matched children with hip synovitis who underwent hip joint fluid puncture as control group.Additionally,82 children with Perthes disease treated at the hospital from June 2024 to January 2025 were enrolled as a validation cohort for nomogram model verification.The expression levels of VEGF,IGF-1 and TGF-β1 in the synovial fluid of three groups were compared.Confounding biases were controlled through univariate and stratified analyses.Binary logistic regression analysis was used to identify independent factors affecting the revascularization effect.R software was utilized to draw and verify the nomogram model for predicting the postoperative revascularization effect.Results The levels of VEGF,IGF-1 and TGF-β1 in the synovial fluid of children in poor revascularization group were all higher than those in control group and good revascularization group(P<0.05).After three types of reconstructive surgeries,the levels of VEGF,IGF-1 and TGF-β1 in the synovial fluid of children with poor revascularization were all higher than those in children with good revascularization(P<0.05);however,there was no statistically significant difference in the above indicators among different surgical types(P>0.05).Binary logistic regression analysis showed that the levels of VEGF,IGF-1,and TGF-β1 in the synovial fluid were independent risk factors for poor postoperative revascularization in children with Perthes disease.The area under the ROC curve of the nomogram model established accordingly for predicting poor postoperative revascularization in children with Perthes disease was 0.875(95%CI 0.805-0.945),with a sensitivity of 0.874 and a specificity of 0.851.Moreover,the calibration curve and decision curve analysis(DCA)indicated that the model had good clinical applicability.Conclusions The increased levels of VEGF,IGF-1 and TGF-β1 in synovial fluid are associated with poor postoperative revascularization in children with Perthes disease.These three factors are expected to become prognostic indicators for children with Perthes disease.

Objective:To investigate the impact of early invasive arterial blood pressure (IBP) monitoring on survival and neurological outcomes in out-of-hospital cardiac arrest (OHCA) patients undergoing extracorporeal cardiopulmonary resuscitation (ECPR).Methods:This retrospective cohort study analyzed 44 OHCA patients receiving ECPR between January 2021 and January 2023. Patients were divided into: Early intervention group : IBP established within 3 min of ECMO initiation; Late intervention group : IBP established after ICU admission. Baseline characteristics, ECMO parameters, and clinical outcomes were compared. Multivariable logistic regression (adjusted for age, initial rhythm, etc.) and Spearman's correlation were used.Results:This study included a total of 44 patients treated with OHCA and ECPR, divided into an early intervention group of 23 cases and a late intervention group of 21 cases. The early intervention group showed significantly higher: Survival to discharge (43.5% vs. 9.5%, P<0.05), Good neurological recovery (CPC 1-2: 34.8% vs. 9.5%, P<0.05).Early intervention independently predicted survival (adjusted OR=18.84, 95% CI:1.97-179.98, P=0.01). Stratified analysis by pH (cutoff 7.0) demonstrated consistent benefits in both pH>7.0 ( aOR=0.392, 95% CI:0.106-0.678) and pH≤7.0 subgroups ( aOR=0.385, 95% CI: 0.075-0.695; interaction P=0.183). Early IBP positively correlated with CPC scores ( ρ=0.40, P=0.007). Conclusions:Early IBP monitoring significantly improves survival and neurological outcomes in OHCA-ECPR patients, supporting its integration into standardized protocols.

Objective : To investigate the causes of false negative results in the detection of Streptococcus agalactiae using fluorescent quantitative PCR(qPCR) targeting the CAMP factor gene(cfb),and to perform a comprehensive analysis of the associated molecular mechanisms. Methods: A total of 76 vaginal secretion samples were evaluated using both qPCR based on cfb gene and bacterial culture methods. Four suspicious strains exhibiting negative qPCR results but positive culture findings were identified using matrix-assisted laser desorption ionization time-of-flight mass spectrometry(MALDI-TOF MS),latex agglutination antigen detection,and the CAMP test. Whole genome analysis was conducted utilizing the MGI DNBSEQ-T7 and Nanopore-PromethION 48 sequencing platforms. Phylogenetic and circular evolutionary trees were constructed using the 16S rRNA gene for strain verification. Multilocus sequence typing(MLST) was conducted,and cfb sequences were aligned and analyzed based on spliced sequences and original data. Specific primers targeting the cfb gene were designed for full-length amplification,followed by verification through agarose gel electrophoresis. Results: The four strains identified as suspicious were classified as S. agalactiae through MALDI-TOF MS,antigen detection,and 16S rRNA gene analysis,with MLST typing indicating ST-862. Phenotypic analysis revealed a negative CAMP test. Whole genome sequence alignment failed to detect the cfb gene or any homologous sequences,and molecular testing confirmed the absence of cfb gene PCR amplification products,thereby confirming its complete deletion. Conclusion This deletion is identified as the molecular mechanism responsible for the false negative qPCR detection of S. agalactiae when targeting this specific gene.It is recommended that the qPCR detection targeting a single cfb gene has limitation,and this may impact clinical diagnosis and treatment decisions. This limitation warrants carefulconsideration.

Objective: To investigate the hemolytic phenotypes of Staphylococcus aureus clinical isolates． Methods: The hemolytic phenotypes of 105 Staphylococcus aureus isolates were analyzed and summarized using the three-point inoculation method．Real-time fluorescence quantitative PCR was used to measure the mRNA expression levels of four hemolysin genes (hla，hlb，hlc，and hld) ; The VITEK 2 GP639 antimicrobial susceptibility card was used to detect resistance to commonly used antibiotics ; DNA gel electrophoresis was performed to determine the prevalence of the mecA，sea，tst，and pvl genes ; The microtiter plate crystal violet staining method was used to assess biofilm formation ability ; The CCK-8 assay was used to evaluate cytotoxicity against macrophages． Results: Seven hemo- lytic phenotypes were identified among the Staphylococcus aureus clinical isolates． Differences were found among Staphylococcus aureus clinical isolates with different hemolytic phenotypes in terms of mRNA expression levels of he- molysin genes，antibiotic resistance，virulence gene prevalence，biofilm formation ability，and cytotoxicity to mouse macrophages (P ＜0. 05 ) ． Conclusion Staphylococcus aureus clinical isolates exhibit diverse hemolytic pheno- types，which should be a focus across multiple dimensions，including microbiological testing，clinical treatment， and nosocomial infection prevention and control．

Hepatocellular carcinoma(HCC)expresses abundant glycolytic enzymes and displays comprehensive glucose metabolism reprogramming.Aldolase A(ALDOA)plays a prominent role in glycolysis;however,little is known about its role in HCC development.In the present study,we aim to explore how ALDOA is involved in HCC proliferation.HCC proliferation was markedly suppressed both in vitro and in vivo following ALDOA knockout,which is consistent with ALDOA overexpression encouraging HCC prolifera-tion.Mechanistically,ALDOA knockout partially limits the glycolytic flux in HCC cells.Meanwhile,ALDOA translocated to nuclei and directly interacted with c-Jun to facilitate its Thr93 phosphorylation by P21-activated protein kinase;ALDOA knockout markedly diminished c-Jun Thr93 phosphorylation and then dampened c-Jun transcription function.A crucial site Y364 mutation in ALDOA disrupted its interaction with c-Jun,and Y364S ALDOA expression failed to rescue cell proliferation in ALDOA deletion cells.In HCC patients,the expression level of ALDOA was correlated with the phosphorylation level of c-Jun(Thr93)and poor prognosis.Remarkably,hepatic ALDOA was significantly upregulated in the promotion and progression stages of diethylnitrosamine-induced HCC models,and the knockdown of Aldoa strikingly decreased HCC development in vivo.Our study demonstrated that ALDOA is a vital driver for HCC development by activating c-Jun-mediated oncogene transcription,opening additional avenues for anti-cancer therapies.