ObjectiveTo evaluate pharmacological effects of Shengmai injection（SMI）on cerebral ischemia and study its neuroprotective mechanism. MethodsMale specific pathogen-free （SPF） Sprague-Dawley （SD） rats were randomly divided into a sham group， a model group， a low-dose SMI group（3 mL·kg^-1）， a middle-dose SMI group（6 mL·kg^-1）， a high-dose SMI group（12 mL·kg^-1）， and a Ginaton group（4 mL·kg^-1）according to the random number table method， with 12 rats in each group. The rat model of cerebral ischemia-reperfusion（MCAO/R）was prepared via the suture method. The administration groups were intraperitoneally injected with corresponding concentrations of SMI or Ginaton injection after reperfusion， which was conducted for 3 consecutive days. The sham group and model group were administered the equivalent volume of physiological saline. The pharmacological effects of SMI on brain injury in MCAO/R rats were evaluated by neurological function scores， cerebral infarction area， hematoxylin-eosin （HE） staining， Nissl staining， terminal deoxynucleotidyl transferase dUTP nick-end labeling （TUNEL） staining， and Western blot. The dominant link and key protein of SMI treating cerebral injury were explored using proteomic analysis. The related mechanisms of SMI were further validated using enzyme-linked immunosorbent assay （ELISA）， Western blot， and chloride ion fluorescence probe with oxygen-glucose deprivation/reoxygenation（OGD/R）-treated PC12 cells and MCAO/R rats. ResultsCompared with the sham group， the model group showed significantly increased neurological function scores， cerebral infarction area， neuronal apoptosis rate， and expression levels of apoptosis related proteins （P<0.05， P<0.01）and significantly decreased density of Nissl bodies and neurons（P<0.01）. Compared with the model group， the SMI groups exhibited significantly decreased neurological function scores， cerebral infarction area， neuronal apoptosis rate， and expression levels of apoptosis related proteins （P<0.05， P<0.01）and significantly increased density of Nissl bodies and neurons （P<0.05）. The proteomic analysis results showed that oxidative stress and inflammatory response were important processes of SMI intervening in MCAO/R injury， and the chloride intracellular channel protein 1 （CLIC1） was one of key proteins in its action network. The levels of representative indicators of oxidative stress and inflammatory response in the MCAO/R rats of the SMI groups were significantly reduced， compared with those in the model group（P<0.05， P<0.01）， and the expression levels of CLIC1 and downstream NOD-like receptor protein 3 （NLRP3） decreased （P<0.01）. In addition， the experimental results based on the OGD/R PC12 cells showed that SMI significantly increased the cell survival rate（P<0.01） and significantly decreased the intracellular chloride ion concentration（P<0.05）. ConclusionSMI has neuroprotective effects. Oxidative stress and inflammatory response are key processes of SMI intervening in MCAO/R injury. The potential mechanism is closely related to the regulation of CLIC1.

Type 2 diabetes mellitus is a metabol-ic disease characterized by high blood sugar levels.Traditionally,amino acids are primarily viewed as the basic building blocks for proteins and peptide synthesis.However,in recent years,amino acids have gained increased attention as signaling mole-cules that play crucial roles in the maintenance and regulation of metabolic homeostasis.It has been found that there is a close correlation between the metabolism of branched-chain and/or aromatic amino acids and the occurrence or development of type 2 diabetes mellitus.Furthermore,there have been successive reports on the regulation mecha-nism involved.This article will focus on the meta-bolic processes,mechanisms and clinical value of branched-chain and aromatic amino acids in type 2 diabetes mellitus.It will also summarize and pro-vide an outlook on the current state of amino acid metabolism in the treatment of diabetes mellitus,with the aim of offering new ideas for the treat-ment of type 2 diabetes mellitus.

Objective:To explore the relationship between general demographic characteristics,inflammatory indicators,nutritional indicators,pathological data and lymph node metastasis in endometrial cancer(EC)pa-tients,and to construct and validate a model for preoperative prediction of lymph node status in endometrial canc-er patients.Methods:The preoperative clinical data of 473 patients with EC who underwent surgical treatment in the Zhu Jiang Hospital of Southern Medical University from January 2010 to April 2024 were retrospectively ana-lyzed.The independent risk factors of lymph node metastasis of endometrial cancer were screened by univariate and multivariate Logistic regression analyses,and the nomogram prediction model was constructed by R soft-ware.The performance of the model was evaluated by the receiver operating characteristic(ROC)curve,calibra-tion curve and clinical decision curve.Results:Menopausal status,high grade biopsy pathology,CA125 ≥24.47U/ml,systemic immune inflammatory index(SII)≥710.91,and prognostic nutritional index(PNI)＜52.90 were in-dependent risk factors for lymph node metastasis in endometrial cancer(OR＞1,P＜0.05).The nomogram model constructed based on these five factors had an AUC of 0.853 in the training set and 0.871 in the test set.The cali-bration curve fitted well,and the clinical decision curve shows a positive benefit.Conclusions:The endometrial cancer lymph node metastasis prediction model constructed based on menopausal status,biopsy pathology,CA125,SII,and PNI has good accuracy and fit,with certain clinical application value.

Objective:To explore the relationship between general demographic characteristics,inflammatory indicators,nutritional indicators,pathological data and lymph node metastasis in endometrial cancer(EC)pa-tients,and to construct and validate a model for preoperative prediction of lymph node status in endometrial canc-er patients.Methods:The preoperative clinical data of 473 patients with EC who underwent surgical treatment in the Zhu Jiang Hospital of Southern Medical University from January 2010 to April 2024 were retrospectively ana-lyzed.The independent risk factors of lymph node metastasis of endometrial cancer were screened by univariate and multivariate Logistic regression analyses,and the nomogram prediction model was constructed by R soft-ware.The performance of the model was evaluated by the receiver operating characteristic(ROC)curve,calibra-tion curve and clinical decision curve.Results:Menopausal status,high grade biopsy pathology,CA125 ≥24.47U/ml,systemic immune inflammatory index(SII)≥710.91,and prognostic nutritional index(PNI)＜52.90 were in-dependent risk factors for lymph node metastasis in endometrial cancer(OR＞1,P＜0.05).The nomogram model constructed based on these five factors had an AUC of 0.853 in the training set and 0.871 in the test set.The cali-bration curve fitted well,and the clinical decision curve shows a positive benefit.Conclusions:The endometrial cancer lymph node metastasis prediction model constructed based on menopausal status,biopsy pathology,CA125,SII,and PNI has good accuracy and fit,with certain clinical application value.

Type 2 diabetes mellitus is a metabol-ic disease characterized by high blood sugar levels.Traditionally,amino acids are primarily viewed as the basic building blocks for proteins and peptide synthesis.However,in recent years,amino acids have gained increased attention as signaling mole-cules that play crucial roles in the maintenance and regulation of metabolic homeostasis.It has been found that there is a close correlation between the metabolism of branched-chain and/or aromatic amino acids and the occurrence or development of type 2 diabetes mellitus.Furthermore,there have been successive reports on the regulation mecha-nism involved.This article will focus on the meta-bolic processes,mechanisms and clinical value of branched-chain and aromatic amino acids in type 2 diabetes mellitus.It will also summarize and pro-vide an outlook on the current state of amino acid metabolism in the treatment of diabetes mellitus,with the aim of offering new ideas for the treat-ment of type 2 diabetes mellitus.

Background: Heart failure (HF) is the leading cause of death worldwide. Myocardial infarction (MI) is a major contributor to HF. Shengmai injection (SMI) has exhibited protective efficacy in preventing HF. However, the advantages of SMI in the progression of MI-induced HF remain unclear. Objective: To reveal the advantages of SMI in the progression of MI-induced HF. Methods: The differently expressed proteins in rat models with ischemia at the 7th, 14th, 21st, and 28th days were obtained from PubMed. The “compound-target” network of SMI was constructed via the Bioinformatics Analysis Tool for Molecular mechANism of Traditional Chinese Medicine database. The protein-protein interaction relationship was constructed, and biological function was applied to evaluate the advantage effect of SMI in the progression of MI-induced HF. In addition, the prediction results were validated in rats with left anterior descending coronary artery ligation. The cardiac function and heart performance were observed via echocardiography, hematoxylin-eosin staining, and Masson staining, and the levels of procollagen type I carboxy-terminal propeptide, recombinant versican (VCAN), and collagen 1A1 (COL1A1) weremeasured via enzyme-linked immunosorbent assay in rat plasma. In vitro, H9c2 cells were treated with Angiotensin II (Ang II), and the cell viability, the level of reactive oxygen species (ROS) and Ca , and the expression of ANP and connective tissue growth factor were evaluated. Furthermore, the schizandrin A was identified as one of the possible key compounds. After schizandrin A treatment, the level of ROS and Ca and the expression of COL1A1 and VCAN were evaluated. Results: There were 189 compounds and 1612 targets involved in the “compound-target” network, and an interaction relationship was constructed. According to the top subnetwork, the Gene Ontology annotation revealed that SMI may have an antifibrotic and cardiac protective effect against MI-induced HF. In rats, SMI increased ejection fraction, left ventricular fractional shortening, and cardiac output and decreased fibrosis injury; moreover, SMI decreased the levels of procollagen type I carboxy-terminal propeptide, VCAN, and COL1A1 within 35 days. When compared with the Ang II treatment group, SMI increased cell viability and decreased cellular calcium concentration, ROS generation, and the expression of ANP and connective tissue growth factor in vitro. Furthermore, schizandrin A was discovered to be a possible compound in myocardial protection. Schizandrin A increased cell viability after Ang II treatment while decreasing COL1A1 and VCAN levels. Conclusions: This method demonstrates that SMI has an antifibrotic effect. This study provides a promising perspective on translating omics data to clinical applications, as well as an appealing approach to investigating the precise intervention of a multicomponent drug.

Objective:To explore the changes in the synergy mode of human lower limb muscles during the fatigue run-ning,in order to reveal the mechanism by which the central system regulates lower limb movement to adapt to fatigue accumulation. Method:Eleven male runners received constant speed running fatigue intervention,and the electromyograph-ic data of the lower limb muscles was collected during the whole intervention process.The non-negative ma-trix factorization algorithm was used to extract analysis indicators such as the number of lower limb muscle synergists,the peak activation time of muscle synergists,and the muscle relative weight at different interven-tion times. Result:A total of six types of muscle synergists were analyzed throughout the entire process of running fa-tigue intervention to dominate human lower limb joint activities,but each subject would only randomly mobi-lize four to five of them at different fatigue moments,and the number of muscle synergists participating in each fatigue moment had no significant change(P＞0.05).The peak activation time of synergy 1 decreased sig-nificantly at 33％、100％time(P＜0.05).The relative weight of semitendinosus of synergy 1 was significantly reduced at 33％、67％and 100％time(P＜0.05).The relative weight of rectus femoris of synergy 2 decreased significantly at 33％time(P＜0.05).The relative weight of biceps femoris of synergy 4 decreased significantly at 67％time(P＜0.05),but increased significantly at 100％time(P＜0.05). Conclusion:In the process of running fatigue,the human central system will regulate the muscle synergy mode of lower limbs to adapt to fatigue accumulation and reduce the risk of lower limb injury.The specific performance of this regulation process includes:stabilizing the number of lower limb muscle synergists in-volved,reducing the peak activation time of muscle synergists in the early stance stage,dynamically adjusting the relative weight of rectus femoris and semitendinosus in the early stance stage and biceps femoris in the middle swing stage.

The purpose of this study was to investigate the damage mechanism of pathogenic E.coli on mouse brain microvascular endothelial cells(BMEC cells)and mouse alveolar macrophages(MH-S cells),as well as the lung and brain of healthy mice.In this study,BMEC cells and MH-S cells were infected with pathogenic E.coli strains,and cell morphological changes were observed.Plate counting method was used to detect the adhesion and invasion ability of the strains to cells and the number of bacteria in the lungs and brains of mice.RT-qPCR was used to detect the ex-pression of TNF-α,IL-1β and IL-6 genes in cells and mouse organs at different time periods.West-ern blot was used to detect the expression of p-NF-κB,p-JAK2 and p-STAT3 proteins related to inflammation in cells and mouse organs after infection.The results showed that the cell culture medium of the infection group was turbid,the cell vision became dark and blurred,some cells shrank and died,and more fragments were produced.The adhesion rate and invasion rate of BMEC cells at 3 h were significantly lower than those at 6 h(P＜0.050),and the adhesion rate and inva-sion rate of MH-S cells at 3 h were significantly higher than those at 6 h(P＜0.010).Infected mice had a large area of swelling and bleeding in the brain,and the lungs had different degrees of swell-ing and bleeding.The bacterial load in the brain and lung was the highest at 12 h.Compared with the control group,the mRNA expression levels of IL-1β,IL-6 and TNF-α in the infection group were significantly increased at 3 h and 6 h(P＜0.050),and the mRNA expression levels of inflam-matory factors in BMEC cells and MH-S cells were the highest at 6 and 3 h,respectively.The mR-NA expression of inflammatory factors in the brain and lung of infected mice showed a trend of in-creasing first and then decreasing with time,with the highest expression at 12 h after infection.The expression levels of p-NF-κB protein in BMEC cells,MH-S cells,lung and brain tissues of mice in the infection group were significantly higher than those in the control group(P＜0.001),and the expression levels of p-JAK2 protein and p-STAT3 protein were significantly lower than those in the control group(P＜0.050).The above results showed that pathogenic E.coli could adhere and invade BMEC cells and MH-S cells,colonize in lung and brain tissues of mice,promote the expres-sion of NF-κB protein in cells and tissues,inhibit the expression of JAK2 protein and STAT3 pro-tein,and then stimulate cells and tissues to produce inflammatory response.

BACKGROUND:Transcranial direct current stimulation(tDCS),as a non-invasive brain stimulation technique,can enhance human muscle strength or improve single-leg landing stability instantly,but no relevant research has demonstrated this yet. OBJECTIVE:To investigate the effect of tDCS on the stability of single-leg landings in human subjects. METHODS:Male undergraduate students from Wuhan Sports University were recruited as study participants.They were divided into two groups,A(n=6)and B(n=5),using a random number table.Group A underwent a sham stimulation session followed by a 3-day washout period,after which they received tDCS.Conversely,Group B received tDCS initially,followed by a 3-day washout period,and subsequently underwent the sham stimulation session.Following the respective stimulation sessions,an immediate single-leg landing test was administered to assess and collect biomechanical parameters.Data resulting from the tDCS intervention were aggregated and analyzed as the experimental group dataset,whereas data stemming from the sham stimulation were consolidated as the control group dataset. RESULTS AND CONCLUSION:Regarding core stability,the tDCS intervention showed a significant interaction with landing height on the maximal trunk flexion angle(P＜0.05).A paired comparison of the data showed a significant decrease in the maximum trunk flexion angle following true stimulation compared to sham stimulation at a 30-cm landing height.Additionally,the tDCS intervention had a significant main effect on the maximum trunk lateral bending angle and the mean trunk lateral bending angular velocity(P＜0.05).Following true stimulation,there was a significant decrease in the maximum trunk lateral bending angle and the mean trunk lateral bending angular velocity compared to sham stimulation.In terms of lower limb joint stability,the tDCS intervention had a significant main effect on the maximum dynamic ankle valgus angle(P＜0.05).This resulted in a significant decrease in the angle following true stimulation compared to sham stimulation.In addition,the tDCS intervention had a significant main effect on the peak muscle activation of the lateral head of the gastrocnemius lateralis(P＜0.05).This showed a significant increase after true stimulation compared to sham stimulation.An interaction between the tDCS intervention and landing height was observed for the peak muscle activation of the tibialis anterior(P＜0.05).Paired comparison analyses revealed a significant increase in muscle activation after true stimulation specifically at a 60-cm landing height.Regarding center of pressure stability,there were no significant interactions or main effects of the tDCS intervention on the mean lateral displacement,mean lateral displacement velocity,mean anterior-posterior displacement,or mean anterior-posterior displacement velocity at the center of pressure(P＞0.05).Furthermore,the tDCS intervention had no significant main effects on any of the center of pressure indicators(P＞0.05).In conclusion,tDCS can immediately improve core stability and lower limb joint stability during single-leg landing,making it an effective warm-up technique for improving single-leg landing stability and reducing the risk of lower limb injuries.

Objective To investigate changes of muscle activation in the lower limbs during landing impact as running fatigue pro-gresses. Methods From November to December,2022,eleven male runners were recruited from Wuhan Sports University.They performed a steady-state run at 75%of their maximum heart rate and continued until Borg rating score≥17 or 90%of their maximum heart rate.Muscle activity data were collected using a Delsys wireless surface electromy-ography system,continuously recording the EMG of the quadriceps(vastus medialis,rectus femoris,vastus later-alis),hamstrings(biceps femoris,semitendinosus),gluteus maximus,lateral head of the gastrocnemius and tibia-lis anterior.The pre-activation,post-activation and co-activation characteristics of these lower limb muscles were analyzed. Results With fatigue accumulation during running,significant differences were observed in the pre-activation level of the tibialis anterior among different fatigue points(F=2.955,P=0.048),with the 100%fatigue point showing significantly higher pre-activation levels than the start(P=0.010);as well as post-activation levels of quadriceps(F=6.609,P=0.001),with higher levels at the 100%point compared to the start(P=0.011),33%(P=0.009)and 67%(P=0.043)fatigue points;co-activation ratios of ankle joint during the pre-activation phase(F=3.287,P=0.034),with a significantly higher co-activation ratio at the 100%fatigue point compared to the start(P=0.023). Conclusion As running fatigue accumulates,the central nervous system adjusts the activation levels of various lower limb muscles to modify impact posture,reducing the risk of injury from accumulated lower limb loads.