ObjectiveZheng’s San Qi San (ZSQS) power, a classic traditional Chinese medicine (TCM) formula, is used for treating soft tissue injuries involving muscles, tendons, and ligaments. However, its underlying therapeutic mechanisms remain unclear. This study aimed to screen and identify pharmaceutically active ingredients and their candidate biomolecule targets, and further elucidate the molecular mechanism of ZSQS in the treatment of skeletal muscle injury. MethodsNetwork pharmacology was employed to construct “ZSQS-component-target”, “protein-protein interaction (PPI)” and “active ingredient-core protein-pathway” networks to predict the key active ingredients and potential core targets of ZSQS for skeletal muscle injury. The predicted results were then validated via microarray data from the GEO database. Molecular docking was then performed to assess the binding ability between the screened active ingredients of ZSQS and the candidate core targets. Moreover, liquid chromatography-mass spectrometry (LC-MS) was used for qualitative and quantitative analysis to verify the active components of the drug and ZSQS serum. Finally, an animal model of eccentric exercise-induced skeletal muscle injury and a myotube cell model of oxidative stress-induced injury were established to validate the effects of ZSQS and its interventional effects on the biological functions of critical targets, thereby demonstrating the potential therapeutic mechanism of ZSQS. ResultsAmong the 111 active components identified in ZSQS and their corresponding 204 targets related to the skeletal muscle injury repair process, 14 core targets (including AKT1) and 4 core active components (quercetin, luteolin, kaempferol, and β‑sitosterol) were screened out, while the corresponding metabolites of quercetin, luteolin and kaempferol were detected in the ZSQS serum. Among these targets, 5 candidate genes (IL-6, CASP3, HIF1A, STAT3, and JUN) overlapped with the differential expression screening results with GEO data, and IL-6 was confirmed to be enriched in the PI3K/AKT pathway. Combined with the prediction results of the AKT expression levels, these findings suggest that the phosphorylation level of AKT1 plays a core role in the therapeutic mechanism of ZSQS. Molecular docking analysis further revealed that the PH domain of AKT1 had high binding energy with all 4 core active components, as verified by LC-MS. Finally, animal model studies have shown the promoting effect of ZSQS administration on skeletal muscle injury repair and its possible antioxidant damage mechanism. Cell model studies further demonstrated that ZSQS-containing serum, core active ingredient combination therapy, and quercetin monomer could increase the phosphorylation level of AKT, promote the nuclear translocation of Nrf2, upregulate the expression of downstream antioxidant enzymes (SOD, GPx, and GR), and inhibit the expression of inflammatory factors (IL-6 and TNF-α), thereby alleviating oxidative stress and the inflammatory response. ConclusionZSQS alleviates skeletal muscle injury mainly by activating the AKT/Nrf2 signaling pathway, enhancing cellular antioxidant and anti-inflammatory capabilities. The results of this study provide a scientific basis for the clinical application and modernized development of ZSQS.

Obesity, as a chronic recurrent disease, has become a major public health challenge in China. To implement the requirements of the Healthy China Initiative (2019—2030), under domestic guidelines or consensus statements on overweight and obesity, and in alignment with the latest scientific advances globally, the Quality control protocol for adult overweight and obesity screening in health management (examination) institutions (2025 edition) was developed. This protocol was drafted by the Health Management Center of Shanghai Changzheng Hospital and formulated through multiple rounds of deliberation by experts in China’s health examination quality control field. The protocol establishes unified standards for screening facilities, personnel qualifications, and measurement or testing procedures. It defines specific screening items, outlines a standardized screening pathway, and sets requirements for the final medical review, ensuring the scientific validity, effectiveness, and safety of the screening process. The implementation of this protocol will enhance the consistency of weight management practices for adults across health examination institutions and strengthen the quality control of overweight and obesity screening programs.

Recently, there has been an increasing risk of importation of tropical diseases into China and the resultant re-transmission in the country with the in-depth implementation of the “Belt and Road” Initiative, which poses a serious threat to the national public health security. To effectively respond to the cross-border transmission risk of tropical diseases and facilitate the process towards tropical disease control and elimination in China and the countries along the “Belt and Road” Initiative, this article analyzes the current status and governance risks of major imported tropical diseases, cross-border joint prevention and control polices implemented for tropical diseases and challenges in the establishment of the joint prevention and control system for tropical diseases in China, and discusses the establishment and implementation path of the joint prevention and control system for tropical diseases in countries along the “Belt and Road” Initiative. This path covers the establishment of cross-border cooperation mechanisms, research and development and pilot production of Chinese public health products, and implementation of key cross-border tropical disease prevention and control projects. The establishment of this system will further improve Chinese prevention and control capabilities for key cross-border tropical diseases, build a demonstrative prevention and control model for tropical diseases, and promote international technical exchanges and cooperation of tropical diseases.

Objective To explore the role of the protein kinase R-like endoplasmic reticulum kinase(PERK)-mediated endoplasmic reticulum stress pathway in a model of lipopolysaccharide(LPS)-induced microglia inflammation.Methods To investigate its effects on endoplasmic reticulum(ER)stress,an inflammation model of microglia was established by stimulating with LPS at gradient concentrations for 24 hours and with 1 mg/L LPS for different durations.Cell viability was assessed by the CCK-8 assay;The mRNA and protein expression levels of related inflammatory factors were measured by Real-time PCR and ELISA kits.Cellular oxidative stress was evaluated by detecting reactive oxygen species(ROS),and Real-time PCR and Western blotting were used to examine the mRNA and protein expression levels of ER stress pathway markers associated with inflammation.Results 1.The effects of different concentrations of LPS on cell viability and morphology were not statistically significant after acting on BV-2 cells for 24 hours(P＞0.05);2.1 mg/L LPS incubated with BV-2 cells for different times and the cell viability decreased with the increase of time;3.Compared with the 0 hour group,the levels of pro-inflammatory cytokine interleukin(IL)-1β,tumor necrosis factor-α(TNF-α)mRNA and protein expression increased significantly(P＜0.05)in the LPS-stimulated 9 hours,12 hours,and 24 hours groups,and the inflammation model was successfully established;4.Compared with the 0 hour group,the protein and mRNA expression levels of the endoplasmic reticulum stress pathway-related indexes in the LPS-stimulated 9 hours,12 hours,and 24 hours groups increased significantly(P＜0.01),which showed the time-dependence;5.After adding the PERK inhibitor GSK2606414,the mRNA and protein expression levels of endoplasmic reticulum stress-related indicators in the PERK inhibitor group were significantly reduced compared with those in the LPS group(P＜0.05);6.The mRNA and protein expression levels of pro-inflammatory cytokines and the fluorescence intensity of ROS in the PERK inhibitor group were significantly reduced compared with those in the LPS group(P＜0.01).Conclusion Targeting PERK-mediated endoplasmic reticulum stress inhibits LPS-induced inflammatory responses in microglia.

Chronic non-specific lower back pain(CNLBP)is one of the most common symptoms in clinical lower back pain,which is prone to recurrence and shows a trend towards younger age.Patients with CNLBP typically experience local pain,reduced joint mobility and balance dysfunction.In depth analysis of the relevant factors that cause balance dysfunction in CNLBP patients and intervention methods can reveal the biological(mechanical)mechanisms of balance dysfunction in patients with CNLBP and provide references and basis for the subsequent improvement of CNLBP intervention methods.This review summarizes the research status of the impact of CNLBP on patients' balance function and disease intervention methods from several aspects,including balance dysfunction in patients with CNLBP,damage to the motor and nervous system,and intervention methods for the disease.The aim is to provide references for the subsequent research on the pathogenesis and intervention methods of CNLBP.

Chronic non-specific lower back pain(CNLBP)is one of the most common symptoms in clinical lower back pain,which is prone to recurrence and shows a trend towards younger age.Patients with CNLBP typically experience local pain,reduced joint mobility and balance dysfunction.In depth analysis of the relevant factors that cause balance dysfunction in CNLBP patients and intervention methods can reveal the biological(mechanical)mechanisms of balance dysfunction in patients with CNLBP and provide references and basis for the subsequent improvement of CNLBP intervention methods.This review summarizes the research status of the impact of CNLBP on patients' balance function and disease intervention methods from several aspects,including balance dysfunction in patients with CNLBP,damage to the motor and nervous system,and intervention methods for the disease.The aim is to provide references for the subsequent research on the pathogenesis and intervention methods of CNLBP.

The BTB (broad-complex, tramtrack, and bric-à-brac) domain is a highly conserved protein interaction motif in eukaryotes. They are widely involved in transcriptional regulation, protein degradation and other processes. Recently, an increasing number of studies have shown that these genes play important roles in plant growth and development, biotic and abiotic stress processes. Here, we summarize the advances of these proteins ubiquitination-mediated development and abiotic stress responses in plants based on the protein structure, which may facilitate the study of this type of gene in plants.
Eukaryota ; Plant Development/genetics* ; Proteolysis ; Ubiquitination

Objective To explore the potential mechanism of action of paeoniflorin in diabetes mellitus,the related targets and pathways were preliminarily discussed,based on the network pharmacology and molecular docking technology.Methods Analyze the potential targets of paeoniflorin using the Swiss Target Prediction database.Genecards and OMIM databases yielded the genes of diabetes-related illnesses.After taking the intersection of the two,protein-protein interaction network(PPI)was established using STRING and Cytoscape programs to search for key genes with strong correlation and complete gene ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)enrichment analysis.Use AutoDockTools and Pymol programs to complete protein molecule docking validation.Results The pharmacologically-related study revealed 63 targets associated with paeoniflorin,4 758 genes related to diabetes,and 50 intersection targets.15 key genes including vascular endothelial growth factor A(VEGFA),epidermal growth factor receptor(EGFR),V-Ha-ras harvey(HRAS),V-src sarcoma(SRC)and heat shock protein hs 90-alpha(HSP90AA1)were screened.RAs-associated protein 1,Ras,calcium and other signaling pathways were obtained by KEGG pathway analysis.Molecular docking results showed that paeoniflorin had good binding ability with key genes.Conclusion Paeoniflorin can treat diabetes through multiple targets and pathways,and this mechanism can provide a basis for the application of paeoniflorin in anti diabetes and drug research and development.

Objective To investigate the current status of frailty in liver transplant candidates and to analyze the influencing factors.Methods The convenience sampling method was used to select 150 liver transplant candidates who were hospitalized in the Department of Liver Transplantation of a tertiary hospital in Hangzhou from July 2022 to July 2023.They were investigated by the general patient data,Fried Frailty Phenotype,Barthel Index,Nutrition Risk Screening 2002,General Health Status Scale.Statistical methods including single factor and multifactor analysis were conducted for influencing factors of frailty in liver transplant candidates.Results The pre-frailty and frailty rates in 145 liver transplant candidates were 42.07％and 45.52％,respectively,and only 12.41％were non-frailty.The results of ordered multiple Logistic regression showed that age,total bilirubin,hemoglobin,and general health status were influential factors in the frailty of liver transplant candidates(P＜0.05).Conclusion Liver transplant candidates have a high incidence of frailty.Age,total bilirubin,hemoglobin,and general health status are influential factors in frailty.Nurses should pay attention to the assessment of frailty in liver transplant candidates,and take timely and targeted nursing interventions to prevent or delay the occurrence and development of frailty.

Objective To investigate the mechanism of mitochondrial division regulating myocardi-al fatty acid oxidation in diabetic mice.Methods A total of 16 7-week-old male SPF C57BLKS/J diabetic mice were randomly divided into model group and mitochondrial division inhibitor 1(mdivi-1)intervention group(intervention group),with 8 mice in each group.Another 8 male SPF C57BLKS/J mice of the same age were fed adaptively for 1 week and served as control group.The changes in blood glucose and body mass were monitored in above groups.Echocardiography was conducted to detect LVEF and LVFS1 rate and E/A between early and late ventricular diastole.The pathological changes of myocardial tissue were observed by HE staining.The size,morpholo-gy and quantity of mitochondria were observed by TEM.Western blotting was used to detect the expression of mitochondrial dynamin-related protein 1(Drp1),peroxisome proliferator activated receptor α(PPARα),long chain acyl-CoA synthetase 4(ACSL4),carnitine palmitoyl transferase 1B(CPT1B),and fatty acid oxidation detection kit was conducted to determine the activity of fat-ty acid oxidation.Results Compared with the control group,the model group presented hyper-trophic cardiomyocytes and significantly larger cross-sectional diameter of cardiomyocytes(22.36±2.80 μm vs 12.71±1.78 μm,P＜0.01)than the control group.Mdivi-1 intervention resul-ted in greatly improved myocardial hypertrophy and obviously smaller cross-sectional diameter of cardiomyocytes(13.79±1.39 μm vs 22.36±2.8 μm,P＜0.01)when compared with the model group.The expression level of myocardial mitochondrial Drp1,number of mitochondria per unit area of myocardial tissue and the protein levels of PPARα,ACSL4 and CPT1B in myocardial cyto-plasm were significantly higher,and the average mitochondrial area of myocardial tissue,the ex-pression of PPARα,ACSL4 and CPT1B in myocardial mitochondria,and fatty acid oxidation activ-ity were significantly lower in the model group than the control group(P＜0.01).After mdivi-1 intervention,the expression level of myocardial mitochondrial Drp1,the number of mitochondria per unit area of myocardial tissue and the protein levels of PPARα,ACSL4 and CPT1B in myocar-dial mitochondria were notably lower,and the expression of PPARα,ACSL4 and CPT1B in myo-cardial mitochondria and fatty acid oxidation activity in myocardial tissue were significantly higher when compared with those in the model group(P＜0.05,P＜0.01).Conclusion In diabetic mice,increased myocardial mitochondrial division,decreased translocation of fatty acid oxidation regula-tory protein from cytoplasm to mitochondria,inhibited fatty acid oxidation,and myocardial injury are observed.Mdivi-1 intervention inhibits mitochondrial division,promotes fatty acid oxidation by increasing the translocation of fatty acid oxidation regulatory proteins to mitochondria,and thus improves cardiac function.