ObjectiveSpinal cord injury (SCI) directly impairs the regulatory function of the autonomic nervous system, induces intestinal dysfunction, and significantly reduces patients’ quality of life. Preclinical studies have shown that electroacupuncture (EA) therapy can regulate the brain-gut axis and is used to treat central nervous system diseases such as major depressive disorder, Alzheimer’s disease and Parkinson’s disease. Recent research has established that fecal microbiota transplantation (FMT) from EA-treated SCI rats restored intestinal motility and colonic morphology. However, it remains unclear whether the regulation of gut microbiota by EA therapy directly contributes to neural repair after SCI. This study aims to explore whether gut microbiota mediates the neuroprotective effect of EA in the treatment of SCI and its possible mechanism. MethodsThe study employed RNA transcriptome analysis of spinal cord tissue to characterize gene expression profiles and to identify key signaling pathways following EA treatment for SCI. Hematoxylin-Eosin (HE) staining and Nissl staining were used to observe the morphological changes in spinal cord tissue. Western blot (WB) and enzyme-linked immunosorbent assay (ELISA) were applied to detect the effects of EA on the expression of proteins related to nucleotide-binding domain leucine-rich repeat and pyrin domain-containing receptor 3 (NLRP3) -dependent pyroptosis. Using 16S rDNA sequencing, the study observed alterations in gut microbiota diversity and community composition in SCI rats. Prior to establishing SCI models, rats were pretreated with an antibiotic cocktail to induce gut dysbiosis, and the effects on intestinal function and spinal cord neural repair were evaluated. FMT was performed to investigate the regulatory effects of post-EA FMT on motor function, general status, liver and spleen indices, and NLRP3-mediated pyroptosis in SCI rats. ResultsEA improved motor function and reduced regulated neuronal cell death in SCI rats. Transcriptomic analysis demonstrated the activation of immune- and inflammation-related pathways post-SCI, including NOD-like receptors, nuclear factor-kappa B(NF-κB), and Toll-like receptor (TLR) pathways. EA primarily influenced intestinal inflammation and autoimmune functions. 16S rDNA sequencing illustrated that EA did not alter the diversity of gut microbiota. However, EA altered the gut microbiota composition in SCI rats, increasing Lactobacillus and Akkermansia genera while rebalancing the Firmicutes/Bacteroidetes ratio. Furthermore, depletion of gut microbiota by antibiotics disrupted the intestinal barrier, reduced the expression of intestinal barrier proteins Zonula Occludens-1 (ZO-1) and Occludin, elevated serum lipopolysaccharide-binding protein (LBP) levels, exacerbated spinal cord tissue damage, and hindered motor function recovery in SCI rats. FMT from donors treated with EA reduced LBP levels in the intestine, blood, and spinal cord of rats, inhibited the TLR4 myeloid differentiation primary response protein 88 (MyD88)-NF‑κB pathway and NLRP3-dependent pyroptosis, and improved motor function. On the other hand, FMT treatment resulted in decreased body weight and food intake, whereas FMT using EA-treated donors effectively alleviated these alterations. ConclusionEA effectively alleviated neuroinflammatory responses in rats with SCI, primarily through regulating the gut microbiota and suppressing the NLRP3-dependent pyroptosis signaling pathway.

ObjectiveSpinal cord injury (SCI) directly impairs the regulatory function of the autonomic nervous system, induces intestinal dysfunction, and significantly reduces patients’ quality of life. Preclinical studies have shown that electroacupuncture (EA) therapy can regulate the brain-gut axis and is used to treat central nervous system diseases such as major depressive disorder, Alzheimer’s disease and Parkinson’s disease. Recent research has established that fecal microbiota transplantation (FMT) from EA-treated SCI rats restored intestinal motility and colonic morphology. However, it remains unclear whether the regulation of gut microbiota by EA therapy directly contributes to neural repair after SCI. This study aims to explore whether gut microbiota mediates the neuroprotective effect of EA in the treatment of SCI and its possible mechanism. MethodsThe study employed RNA transcriptome analysis of spinal cord tissue to characterize gene expression profiles and to identify key signaling pathways following EA treatment for SCI. Hematoxylin-Eosin (HE) staining and Nissl staining were used to observe the morphological changes in spinal cord tissue. Western blot (WB) and enzyme-linked immunosorbent assay (ELISA) were applied to detect the effects of EA on the expression of proteins related to nucleotide-binding domain leucine-rich repeat and pyrin domain-containing receptor 3 (NLRP3) -dependent pyroptosis. Using 16S rDNA sequencing, the study observed alterations in gut microbiota diversity and community composition in SCI rats. Prior to establishing SCI models, rats were pretreated with an antibiotic cocktail to induce gut dysbiosis, and the effects on intestinal function and spinal cord neural repair were evaluated. FMT was performed to investigate the regulatory effects of post-EA FMT on motor function, general status, liver and spleen indices, and NLRP3-mediated pyroptosis in SCI rats. ResultsEA improved motor function and reduced regulated neuronal cell death in SCI rats. Transcriptomic analysis demonstrated the activation of immune- and inflammation-related pathways post-SCI, including NOD-like receptors, nuclear factor-kappa B(NF-κB), and Toll-like receptor (TLR) pathways. EA primarily influenced intestinal inflammation and autoimmune functions. 16S rDNA sequencing illustrated that EA did not alter the diversity of gut microbiota. However, EA altered the gut microbiota composition in SCI rats, increasing Lactobacillus and Akkermansia genera while rebalancing the Firmicutes/Bacteroidetes ratio. Furthermore, depletion of gut microbiota by antibiotics disrupted the intestinal barrier, reduced the expression of intestinal barrier proteins Zonula Occludens-1 (ZO-1) and Occludin, elevated serum lipopolysaccharide-binding protein (LBP) levels, exacerbated spinal cord tissue damage, and hindered motor function recovery in SCI rats. FMT from donors treated with EA reduced LBP levels in the intestine, blood, and spinal cord of rats, inhibited the TLR4 myeloid differentiation primary response protein 88 (MyD88)-NF‑κB pathway and NLRP3-dependent pyroptosis, and improved motor function. On the other hand, FMT treatment resulted in decreased body weight and food intake, whereas FMT using EA-treated donors effectively alleviated these alterations. ConclusionEA effectively alleviated neuroinflammatory responses in rats with SCI, primarily through regulating the gut microbiota and suppressing the NLRP3-dependent pyroptosis signaling pathway.

Objective Exploring the therapeutic mechanism of Yishen Jiangzhuo Granules(YSJZG)on chronic kidney disease(CKD)based on mitochondrial dynamics and apoptosis of renal tubular epithelial cells.Methods The CKD model of rats with 5/6 nephrectomy was adopted and divided into 6 groups according to random number table:sham operation control group,model group,emodin group(500 mg/kg/d),Yishen Jiangzhuo granule low,middle and high dose groups.After 8 weeks of treatment with YSJZG,serum creatinine(SCR)and urea nitrogen(BUN),pathological changes of renal cortex,mitochondrial morphology and ultrastructure were detected,and mitochondrial kinetic protein in renal tubular epithelial cells was detected by immunohistochemistry(Drp1,Fis1)and fusion proteins(Opa1,Mfn1)were detected by Western blot,and apoptotic proteins(CytC,Bax)in cytoplasm and mitochondria were detected by real-time PCR.Results Renal injury:Compared with the model group,YSJZG groups significantly reduced the levels of SCR and BUN,renal tubular degeneration and necrosis,and mitochondrial structural damage in rats.Renal tubule mitochondrial dynamic protein:Compared with the model group,the expression of division proteins Drp1 and Fis1 was downregulated,the expression of fusion proteins Opa1 and Mfn1 was upregulated,and transmission electron microscopy observed that the mitochondrial fragmentation changes were relatively mild.Apoptosis related indicators and mtDNA copy number of renal tubular cells:Compared with the model group,the content of Bax protein in renal tubular epithelial cells of YSJZG groups increased significantly in cytoplasm(P<0.05)and decreased significantly in mitochondria(P<0.05).The content of CytC protein decreased significantly in cytoplasm(P<0.05)and increased significantly in mitochondria(P<0.05).The copy number of mtDNA increased significantly(P<0.05),and the total levels of SMAC,CytC and Bax mRNA decreased significantly(P<0.05).Correlation between mitochondrial dynamic protein and apoptosis in renal tubular cells:Pearson correlation analysis showed that the expression of Drp1 and Fis1 was negatively correlated with the expression of CytC in mitochondria,and positively correlated with the expression of CytC in cytoplasm.The expression levels of fusion proteins Opa1 and Mfn1 showed a significant positive correlation with CytC expression in mitochondria,and a significant negative correlation with CytC expression in cytoplasm.Conclusion YSJZG can significantly delay the progression of CKD,and its mechanism may be achieved by regulating mitochondrial dynamics of renal tubular epithelial cells,thereby inhibiting endogenous cell apoptosis pathway.

Objective:To analyze the association of peripheral blood systemic immune-inflammation index(SII),neutrophil-to-lymphocyte ratio(NLR),platelet-to-lymphocyte ratio(PLR)with disease severity and progno-sis in elderly patients with chronic pulmonary heart disease(CPHD).Methods:A total of 180 elderly CPHD pa-tients admitted in Xuancheng Central Hospital between September 2021 and January 2023 were enrolled as case group.Healthy volunteers who simultaneously underwent physical examinations in our hospital were selected as con-trol group(n=50).According to the 28d prognosis,the case group was divided into death group(n=45)and sur-vival group(n=135).Levels of peripheral blood SII,NLR and PLR were compared among above-mentioned groups;Spearman correlation analysis was used to analyze the association of above indexes with cardiac function class and prognosis in these patients.Multivariate Logistic regression analysis was used to analyze risk factors for death in these patients.The predictive value of SII,NLR,and PLR for death in elderly CPHD patients was ana-lyzed using receiver operating characteristic(ROC)curve.Results:Compared with those in control group,those in the case group had significant higher levels of peripheral blood SII,NLR and PLR(P＜0.001 all).Compared with NYHA class Ⅱ group and class Ⅲ group,those in class Ⅳ group had significant higher levels of peripheral blood SII[(1759.87±179.43)vs.(1148.33±121.57)vs.(1392.44±146.36)],NLR[(8.65±0.89)vs.(7.14±0.75)vs.(7.76±0.81)],PLR[(152.45±16.79)vs.(125.29±13.46)vs.(138.77±13.58)];and levels of peripheral blood SII,NLR,PLR in class Ⅲ group were significantly higher than those of class Ⅱ group(P＜0.001 all).Com-pared with patients in survival group,those in death group had significant higher levels of peripheral blood SII[(1723.86±189.65)vs.(1296.81±142.33)],NLR[(8.24±0.89)vs.(7.63±0.78)],PLR[(148.75±15.26)vs.(134.41±14.58)](P＜0.001 all).Spearman correlation analysis indicated that the levels of peripheral blood SII,NLR and PLR were significant positively correlated with the severity and poor prognosis(r=0.336～0.432,P＜0.05 or＜0.01;r=0.319～0.504,P＜0.05 or＜0.01)in elderly CPHD patients.Multivariate Logistic regression analy-sis indicated that peripheral blood SII,NLR,PLR and smoking were independent risk factors for death(OR=1.024～9.514,P＜0.05 or＜0.01)in elderly CPHD patients.ROC curve indicated that area under curve(AUC)of combination of SII,NLR and PLR predicting death in elderly CPHD patients was 0.979(95％CI 0.946～0.995),significantly higher than those of each single detection[SII:0.847(95％CI 0.786～0.896),NLR:0.832(95％CI 0.769～0.883),PLR:0.881(95％CI 0.825～0.925),Z=3.988,4.386,4.217,P＜0.01 all].The nomogram calibration curve and decision curve showed good consistency and net benefit of the model.Conclusion:Peripheral blood SII,NLR and PLR are associat-ed with the severity and prognosis of elderly CPHD patients,and have certain predictive value for patient's prognosis.

To screen potential drugs for the treatment of acute Liver Injury(ALI)through network pharmacology and mitochondrial dynamics,and to investigate their actions and mechanisms.Based on the commonly utilized Liver Pure Tablets and Liver-Protecting Capsules in the market,a com-ponent library of liver disease drugs was screened and established.Pharmacological anchoring anal-ysis was carried out.Potential liver disease therapeutic drugs were screened out through molecular docking,and feedback verification was performed using animal experiments.Acute liver injury mouse models were established through excessive induction with acetaminophen(APAP),and the histopathological changes of liver tissues were examined.The protective effect of the drug on ALI was evaluated by detecting alanine aminotransferase(ALT),aspartate aminotransferase(AST),superoxide dismutase(SOD),catalase(CAT),glutathione(GSH),and malondialdehyde(MDA)using enzyme-linked immunosorbent assay(ELISA).qRT-PCR was employed to detect peroxi-some proliferator-activated receptor gamma coactivator 1-alpha(PPARG1A),mitofusin 1(MFN1),mitofusin 2(MFN2),dynamin-related protein 1(DRP1),optic atrophy 1 protein(OP A1),Steroid receptor coactivator(SRC),and advanced glycosylation end-product specific re-ceptor(AGER)to explore the protective mechanism of the drug on ALI.The result showed that Network pharmacology identified a total of 662 intersection targets of three types of prescription drugs and ALI.Eventually,72 core targets were screened out.Pathway enrichment analysis indi-cates that the potential mechanism might be associated with the lipid and atherosclerosis signaling pathways.The results of the relevant molecular docking indicate that the most likely optimal drug might be emodin(EMO).EMO ameliorated the pathological damage in mice with acute liver inju-ry,significantly decreased the contents of transferase factors ALT and AST,simultaneously in-creased the contents of antioxidant enzymes CAT,GSH and SOD,and reduced the content of oxi-dative metabolic end product MDA.It also upregulated the mRNA expression levels of MFN1、MFN2,OPA1,DRP1,SRC and PPARGC1A proteins in liver tissue,and inhibited the mRNA ex-pression level of AGER protein.The drug EMO,jointly screened out by network pharmacology through anchoring and molecular docking,might promote mitochondrial fusion metabolism,allevi-ate liver oxidative stress,and improve liver injury in ALI mice via the Lipid and atherosclerosis pathway.

Objective To design a multi-terminal collaborative medical equipment acceptance management system to enhance the informatized management of medical equipment acceptance.Methods The multi-terminal collaborative medical equipment acceptance management system was designed with the front-end and back-end separation mode.The front end was developed with Flutter framework and Dart language,the back end was implemented with Tornado 6.1 architecture and Python language,the communication between the front-end and the back-end service followed the RESTful design principle and the interaction was carried out through the hypertext transfer protocol(HTTP)request.There were three functional modules involved in the system for user management,basic information management and acceptance management.Results The system developed realized informatized management for medical equipment acceptance process,supported cross-platform management of acceptance reports,related attachments and medical device registration certificates and improved the quality and efficiency of medical equipment acceptance.Conclusion The system developed facilitates multi-terminal collaborative management for medical equipment acceptance,and lays a foundation for the digital and intelligent transformation of hospital medical equipment management.[Chinese Medical Equipment Journal,2025,46(7):39-44]

To screen potential drugs for the treatment of acute Liver Injury(ALI)through network pharmacology and mitochondrial dynamics,and to investigate their actions and mechanisms.Based on the commonly utilized Liver Pure Tablets and Liver-Protecting Capsules in the market,a com-ponent library of liver disease drugs was screened and established.Pharmacological anchoring anal-ysis was carried out.Potential liver disease therapeutic drugs were screened out through molecular docking,and feedback verification was performed using animal experiments.Acute liver injury mouse models were established through excessive induction with acetaminophen(APAP),and the histopathological changes of liver tissues were examined.The protective effect of the drug on ALI was evaluated by detecting alanine aminotransferase(ALT),aspartate aminotransferase(AST),superoxide dismutase(SOD),catalase(CAT),glutathione(GSH),and malondialdehyde(MDA)using enzyme-linked immunosorbent assay(ELISA).qRT-PCR was employed to detect peroxi-some proliferator-activated receptor gamma coactivator 1-alpha(PPARG1A),mitofusin 1(MFN1),mitofusin 2(MFN2),dynamin-related protein 1(DRP1),optic atrophy 1 protein(OP A1),Steroid receptor coactivator(SRC),and advanced glycosylation end-product specific re-ceptor(AGER)to explore the protective mechanism of the drug on ALI.The result showed that Network pharmacology identified a total of 662 intersection targets of three types of prescription drugs and ALI.Eventually,72 core targets were screened out.Pathway enrichment analysis indi-cates that the potential mechanism might be associated with the lipid and atherosclerosis signaling pathways.The results of the relevant molecular docking indicate that the most likely optimal drug might be emodin(EMO).EMO ameliorated the pathological damage in mice with acute liver inju-ry,significantly decreased the contents of transferase factors ALT and AST,simultaneously in-creased the contents of antioxidant enzymes CAT,GSH and SOD,and reduced the content of oxi-dative metabolic end product MDA.It also upregulated the mRNA expression levels of MFN1、MFN2,OPA1,DRP1,SRC and PPARGC1A proteins in liver tissue,and inhibited the mRNA ex-pression level of AGER protein.The drug EMO,jointly screened out by network pharmacology through anchoring and molecular docking,might promote mitochondrial fusion metabolism,allevi-ate liver oxidative stress,and improve liver injury in ALI mice via the Lipid and atherosclerosis pathway.

AIM To explore the clinical effects of Huayu Ditan Linao Decoction combined with Suhexiang Pills on elderly patients with cerebral hemorrhage in convalescent stage.METHODS One hundred and ten patients were randomly assigned into control group(55 cases)for 1-month intervention of both conventional treatment and rehabilitation training,and observation group(55 cases)for 1-month intervention of Huayu Ditan Linao Decoction,Suhexiang Pills,conventional treatment and rehabilitation training.The changes in clinical effects,TCM syndrome score,NIHSS score,FMA score,BI index,cerebrovascular function indices(dynamic resistance,average flow velocity,peripheral resistance,average flow rate),serum inflammatory indices(IL-6,hs-CPR,TNF-α)and serum oxidative stress indices(SOD,MDA)were detected.RESULTS The observation group demonstrated higher total effective rate than the control group(P＜0.05).After the treatment,the two groups displayed decreased TCM syndrome score,NIHSS score,dynamic resistance,peripheral resistance,serum inflammatory indices,MDA(P＜0.05),and increased FMA score,BI index,average flow velocity,average flow rate,SOD(P＜0.05),especially for the observation group(P＜0.05).CONCLUSION For the elderly patients with cerebral hemorrhage in convalescent stage,Huayu Ditan Linao Decoction combined with Suhexiang Pills can enhance clinical effects,improve limb functions and nerve functions,regulate serum inflammatory and oxidative stress indice,and promote prognosis.

Coronavirus,a major pathogen infecting humans,mammals,and birds,causes primarily respiratory diseases af-ter infecting humans.Seven coronaviruses have been found to infect humans and subsequently cause varying degrees of respira-tory symptoms.From 2019 to 2023,millions of people died from severe acute respiratory syndrome coronavirus 2 infections,and the virus continues to mutate.Therefore,drug screening research must urgently be expanded to develop more effective,broad-spectrum anti-coronavirus drugs.In-depth research has indicated that the coronavirus 3C-like protease and RNA polymer-ase are necessary for viral reproduction and are highly conserved among strains,and consequently are anti-virus targets of great interest.This article summarizes the enzymes encoded by coronaviruses and drug screening methods,to provide a reference for coronavirus prevention and control.

Body weight abnormalities, including overweight, obesity, and underweight, have become a dual public health challenge in Chinese adults: overweight and obesity lead to a variety of chronic complications, while underweight increases the risks of malnutrition, sarcopenia, and organ dysfunction. To systematically address these issues, multidisciplinary experts in endocrinology, sports science, nutrition, and psychiatry from various regions have held multiple weight management seminars. Based on the latest epidemiological data and clinical evidence, they expanded the guideline to include assessment and intervention strategies for underweight, in addition to the core content of obesity management. This guideline outlines the etiological mechanisms, evaluation methods, and multidimensional management strategies for overweight and obesity, covering key areas such as diagnosis and assessment, medical nutrition therapy, exercise prescription, pharmacological intervention, and psychological support. It is intended to provide a scientific and standardized approach to weight management across the adult population, aiming to curb the rising prevalence of obesity, mitigate complications associated with abnormal body weight, and improve nutritional status and overall quality of life.