ObjectiveTo evaluate the therapeutic effects of Huanglian Jiedutang on cerebral infarction injury in a mouse model of middle cerebral artery occlusion （MCAO） and to explore its mechanism of action on oligodendrocytes， particularly its potential in myelin repair. MethodsMultiple experimental approaches were used to evaluate cerebral ischemic injury and the effects of drug intervention. Laser speckle imaging was used to detect changes in cerebral blood flow， 2，3，5-Triphenyltetrazolium chloride （TTC） staining was used to measure infarct volume， and neurological function was scored according to the Zea-Longa criteria. Brain tissues were routinely embedded in paraffin and subjected to HE and Nissl staining to observe tissue structure and neuronal damage. Animals were divided into a sham group （n=24）， model group （n=24）， Huanglian Jiedutang group （n=24）， and Ginkgo biloba extract （GBE） group （n=18）. After 1 week of acclimatization， intragastric administration was initiated. The sham and model groups received normal saline， the Huanglian Jiedutang group was administered 1.82 g·kg^-1， and the GBE group was administered 0.432 g·kg^-1 after preparation as a 2.16 g·L^-1 solution. All groups were treated for 5 consecutive days at a dose of 0.2 mL·（10 g）^-¹·d^-¹. The MCAO model was established after the final administration on day 6. Single-cell RNA sequencing was used to analyze brain tissue cellular composition and changes in oligodendrocyte subpopulations. Distinct subpopulations were identified by Uniform manifold approximation and projection （UMAP） dimensionality reduction and unsupervised clustering， and marker gene expression was analyzed. Pathway enrichment and causal inference were further performed using IPA. Finally， real-time quantitative PCR was used to verify mRNA expression changes of myelin-related genes. ResultsCompared with the sham group， the model group showed significantly increased neurological function scores （P<0.01）， significantly impaired blood flow （P<0.01）， significantly enlarged cerebral infarct area （P<0.01）， and pathological changes including disordered cortical structural arrangement， aggravated cytoplasmic vacuolization， and increased Nissl bodies. Compared with the model group， the Huanglian Jiedutang and GBE groups showed significantly decreased neurological function scores （P<0.01）， markedly restored blood flow levels （P<0.01）， significantly reduced cerebral infarct area （P<0.01）， and improvement in cortical structural disorder， alleviation of cytoplasmic vacuolization， and a reduction in Nissl bodies. Single-cell data showed that a myelin-associated oligodendrocyte （Mye-OL） subpopulation existed among oligodendrocytes， which was closely related to myelin generation. Compared with the sham group， the number of Mye-OL cells decreased in the model group. Compared with the model group， the number of Mye-OL cells increased in the Huanglian Jiedutang group. This subpopulation promoted the expression of myelin-related genes， including MOG， MBP， and MAG， via transcription factors such as OLIG1， OLIG2， NKX2-2， and SOX10， thereby regulating myelin generation， restoring cognition， and exerting therapeutic effects on acute cerebral infarction. Compared with the sham group， the mRNA expression levels of OLIG1， OLIG2， NKX2-2， and SOX10 were significantly downregulated in the model group （P<0.01）， and the mRNA expression levels of myelin-related genes， including MOG， MBP， and MAG， were also significantly downregulated （P<0.01）. In contrast， compared with the model group， the Huanglian Jiedutang and GBE groups showed significantly upregulated mRNA expression levels of OLIG1， OLIG2， NKX2-2， and SOX10 （P<0.01）， and significantly upregulated mRNA expression levels of myelin-related genes， including MOG， MBP， and MAG （P<0.01）. ConclusionHuanglian Jiedutang exerts therapeutic effects on acute cerebral infarction by regulating the OLIG1/2-NKX2-2-SOX10 signaling pathway to promote myelin generation by Mye-OL cells.

ObjectiveTo investigate the characteristics of metabolic reprogramming during cerebral ischemia-reperfusion injury using single-cell transcriptome sequencing， analyze the heterogeneity of microglial populations， and evaluate the interventional effects of Huanglian Jiedutang on metabolic abnormalities and neuroinflammation. MethodsA transient middle cerebral artery occlusion （tMCAO） model was used to establish ischemic stroke in mice. Local cerebral blood flow changes were monitored by laser speckle imaging. Neurological impairment was evaluated using the Zea-Longa score， and histopathological damage in brain tissue was observed by HE and Nissl staining. Animals were divided into a sham group， model group， Huanglian Jiedutang group， and Ginkgo biloba extract （GBE） group. After 1 week of acclimatization， intragastric administration was initiated. The sham and model groups received normal saline， the Huanglian Jiedutang group was administered 1.82 g·kg^-1， and the GBE group was administered 0.432 g·kg^-1 after preparation as a 2.16 mg/mL solution. All groups were treated for 5 consecutive days （0.2 mL/10 g/day）， and the tMCAO model was established on day 6 after the final administration. At the molecular level， single-cell RNA sequencing was performed on ischemic hemisphere tissue. Non-negative matrix factorization （NMF） was used to cluster microglial subpopulations， combined with differential expression analysis， metabolic reprogramming assessment， and inflammatory factor correlation analysis to elucidate their functional characteristics in ischemia-reperfusion injury. Transcription factor enrichment analysis was further conducted to identify key regulatory nodes. Finally， PCR was used to detect mRNA expression changes of relevant genes to validate the single-cell sequencing results. ResultsCompared with the sham group， the model group showed increased neurological function scores （P<0.01）， decreased blood flow levels （P<0.01）， disordered cortical structure， increased cytoplasmic vacuolization， and increased Nissl bodies. Compared with the model group， the Huanglian Jiedutang and GBE groups showed decreased neurological function scores （P<0.01）， increased blood flow levels （P<0.01）， alleviated cortical structural disorder， reduced cytoplasmic vacuolization， and decreased Nissl bodies. Single-cell analysis showed that microglia could be divided into five subpopulations. Among them， clusters 3 and 5 exhibited significant pro-inflammatory phenotypes， with marked activation of hypoxia and NF-κB signaling pathways， and were identified as pro-inflammatory subpopulations. Clusters 1 and 2 were enriched in Wnt/β-catenin and transforming growth factor（TGF）-β signaling pathways and exhibited prominent anti-inflammatory and reparative characteristics. Meanwhile， glycolysis-related genes， such as HK2， PFKP， and LDHA， were significantly upregulated in the pro-inflammatory subpopulations. Correlation analysis showed that the expression levels of inflammatory molecules were positively correlated with glycolysis-related gene expression levels， whereas the expression levels of reparative and anti-inflammatory molecules were negatively correlated with glycolysis-related gene expression levels， indicating that microglia rely on the glycolytic pathway for energy acquisition under ischemic conditions. Further single-cell transcriptome analysis revealed that Huanglian Jiedutang effectively downregulated key genes driving metabolic reprogramming （such as HK2， PFKP， and LDHA）， significantly reduced the proportion of microglial subpopulations accompanied by glycolytic reprogramming， and inhibited their transformation toward a damage phenotype， thereby reducing inflammatory injury. Meanwhile， compared with the sham group， the mRNA expression levels of interleukin （IL）-1β， IL-6， tumor necrosis factor（TNF）-α， CCL2， CXCL2， and CSF3 were significantly upregulated （P<0.01） in the model group， whereas the mRNA expression levels of endothelial- and pericyte-related functional genes， including RGS5， PECAM1， VEGFB， and NOS3， were significantly downregulated （P<0.01）. In contrast， compared with the model group， the Huanglian Jiedutang and GBE groups showed significantly decreased mRNA expression levels of IL-1β， IL-6， TNF-α， CCL2， CXCL2， and CSF3 （P<0.01）， and significantly increased mRNA expression levels of endothelial- and pericyte-related functional genes， including RGS5， PECAM1， VEGFB， and NOS3 （P<0.01）. ConclusionHuanglian Jiedutang exerts neuroprotective effects by regulating the metabolic reprogramming state of microglia and modulating their inflammatory levels， thereby inhibiting neuroinflammatory injury.

ObjectiveTo evaluate the therapeutic effects of Huanglian Jiedutang on cerebral infarction injury in a mouse model of middle cerebral artery occlusion （MCAO） and to explore its mechanism of action on oligodendrocytes， particularly its potential in myelin repair. MethodsMultiple experimental approaches were used to evaluate cerebral ischemic injury and the effects of drug intervention. Laser speckle imaging was used to detect changes in cerebral blood flow， 2，3，5-Triphenyltetrazolium chloride （TTC） staining was used to measure infarct volume， and neurological function was scored according to the Zea-Longa criteria. Brain tissues were routinely embedded in paraffin and subjected to HE and Nissl staining to observe tissue structure and neuronal damage. Animals were divided into a sham group （n=24）， model group （n=24）， Huanglian Jiedutang group （n=24）， and Ginkgo biloba extract （GBE） group （n=18）. After 1 week of acclimatization， intragastric administration was initiated. The sham and model groups received normal saline， the Huanglian Jiedutang group was administered 1.82 g·kg^-1， and the GBE group was administered 0.432 g·kg^-1 after preparation as a 2.16 g·L^-1 solution. All groups were treated for 5 consecutive days at a dose of 0.2 mL·（10 g）^-¹·d^-¹. The MCAO model was established after the final administration on day 6. Single-cell RNA sequencing was used to analyze brain tissue cellular composition and changes in oligodendrocyte subpopulations. Distinct subpopulations were identified by Uniform manifold approximation and projection （UMAP） dimensionality reduction and unsupervised clustering， and marker gene expression was analyzed. Pathway enrichment and causal inference were further performed using IPA. Finally， real-time quantitative PCR was used to verify mRNA expression changes of myelin-related genes. ResultsCompared with the sham group， the model group showed significantly increased neurological function scores （P<0.01）， significantly impaired blood flow （P<0.01）， significantly enlarged cerebral infarct area （P<0.01）， and pathological changes including disordered cortical structural arrangement， aggravated cytoplasmic vacuolization， and increased Nissl bodies. Compared with the model group， the Huanglian Jiedutang and GBE groups showed significantly decreased neurological function scores （P<0.01）， markedly restored blood flow levels （P<0.01）， significantly reduced cerebral infarct area （P<0.01）， and improvement in cortical structural disorder， alleviation of cytoplasmic vacuolization， and a reduction in Nissl bodies. Single-cell data showed that a myelin-associated oligodendrocyte （Mye-OL） subpopulation existed among oligodendrocytes， which was closely related to myelin generation. Compared with the sham group， the number of Mye-OL cells decreased in the model group. Compared with the model group， the number of Mye-OL cells increased in the Huanglian Jiedutang group. This subpopulation promoted the expression of myelin-related genes， including MOG， MBP， and MAG， via transcription factors such as OLIG1， OLIG2， NKX2-2， and SOX10， thereby regulating myelin generation， restoring cognition， and exerting therapeutic effects on acute cerebral infarction. Compared with the sham group， the mRNA expression levels of OLIG1， OLIG2， NKX2-2， and SOX10 were significantly downregulated in the model group （P<0.01）， and the mRNA expression levels of myelin-related genes， including MOG， MBP， and MAG， were also significantly downregulated （P<0.01）. In contrast， compared with the model group， the Huanglian Jiedutang and GBE groups showed significantly upregulated mRNA expression levels of OLIG1， OLIG2， NKX2-2， and SOX10 （P<0.01）， and significantly upregulated mRNA expression levels of myelin-related genes， including MOG， MBP， and MAG （P<0.01）. ConclusionHuanglian Jiedutang exerts therapeutic effects on acute cerebral infarction by regulating the OLIG1/2-NKX2-2-SOX10 signaling pathway to promote myelin generation by Mye-OL cells.

ObjectiveTo investigate the characteristics of metabolic reprogramming during cerebral ischemia-reperfusion injury using single-cell transcriptome sequencing， analyze the heterogeneity of microglial populations， and evaluate the interventional effects of Huanglian Jiedutang on metabolic abnormalities and neuroinflammation. MethodsA transient middle cerebral artery occlusion （tMCAO） model was used to establish ischemic stroke in mice. Local cerebral blood flow changes were monitored by laser speckle imaging. Neurological impairment was evaluated using the Zea-Longa score， and histopathological damage in brain tissue was observed by HE and Nissl staining. Animals were divided into a sham group， model group， Huanglian Jiedutang group， and Ginkgo biloba extract （GBE） group. After 1 week of acclimatization， intragastric administration was initiated. The sham and model groups received normal saline， the Huanglian Jiedutang group was administered 1.82 g·kg^-1， and the GBE group was administered 0.432 g·kg^-1 after preparation as a 2.16 mg/mL solution. All groups were treated for 5 consecutive days （0.2 mL/10 g/day）， and the tMCAO model was established on day 6 after the final administration. At the molecular level， single-cell RNA sequencing was performed on ischemic hemisphere tissue. Non-negative matrix factorization （NMF） was used to cluster microglial subpopulations， combined with differential expression analysis， metabolic reprogramming assessment， and inflammatory factor correlation analysis to elucidate their functional characteristics in ischemia-reperfusion injury. Transcription factor enrichment analysis was further conducted to identify key regulatory nodes. Finally， PCR was used to detect mRNA expression changes of relevant genes to validate the single-cell sequencing results. ResultsCompared with the sham group， the model group showed increased neurological function scores （P<0.01）， decreased blood flow levels （P<0.01）， disordered cortical structure， increased cytoplasmic vacuolization， and increased Nissl bodies. Compared with the model group， the Huanglian Jiedutang and GBE groups showed decreased neurological function scores （P<0.01）， increased blood flow levels （P<0.01）， alleviated cortical structural disorder， reduced cytoplasmic vacuolization， and decreased Nissl bodies. Single-cell analysis showed that microglia could be divided into five subpopulations. Among them， clusters 3 and 5 exhibited significant pro-inflammatory phenotypes， with marked activation of hypoxia and NF-κB signaling pathways， and were identified as pro-inflammatory subpopulations. Clusters 1 and 2 were enriched in Wnt/β-catenin and transforming growth factor（TGF）-β signaling pathways and exhibited prominent anti-inflammatory and reparative characteristics. Meanwhile， glycolysis-related genes， such as HK2， PFKP， and LDHA， were significantly upregulated in the pro-inflammatory subpopulations. Correlation analysis showed that the expression levels of inflammatory molecules were positively correlated with glycolysis-related gene expression levels， whereas the expression levels of reparative and anti-inflammatory molecules were negatively correlated with glycolysis-related gene expression levels， indicating that microglia rely on the glycolytic pathway for energy acquisition under ischemic conditions. Further single-cell transcriptome analysis revealed that Huanglian Jiedutang effectively downregulated key genes driving metabolic reprogramming （such as HK2， PFKP， and LDHA）， significantly reduced the proportion of microglial subpopulations accompanied by glycolytic reprogramming， and inhibited their transformation toward a damage phenotype， thereby reducing inflammatory injury. Meanwhile， compared with the sham group， the mRNA expression levels of interleukin （IL）-1β， IL-6， tumor necrosis factor（TNF）-α， CCL2， CXCL2， and CSF3 were significantly upregulated （P<0.01） in the model group， whereas the mRNA expression levels of endothelial- and pericyte-related functional genes， including RGS5， PECAM1， VEGFB， and NOS3， were significantly downregulated （P<0.01）. In contrast， compared with the model group， the Huanglian Jiedutang and GBE groups showed significantly decreased mRNA expression levels of IL-1β， IL-6， TNF-α， CCL2， CXCL2， and CSF3 （P<0.01）， and significantly increased mRNA expression levels of endothelial- and pericyte-related functional genes， including RGS5， PECAM1， VEGFB， and NOS3 （P<0.01）. ConclusionHuanglian Jiedutang exerts neuroprotective effects by regulating the metabolic reprogramming state of microglia and modulating their inflammatory levels， thereby inhibiting neuroinflammatory injury.

ObjectiveTo investigate the regulatory effects of Huanglian Jiedutang （HLJDT） on immune cell migration， blood-brain barrier protection， and cellular functional recovery in a model of ischemic stroke. MethodsA transient middle cerebral artery occlusion （tMCAO） model was established in mice to induce ischemic stroke. Cerebral blood flow and neurological function were evaluated using laser speckle imaging and neurological deficit scoring. Histopathological damage in brain tissues was assessed by hematoxylin-eosin （HE） and Nissl staining. Mice were divided into a sham group， a model group， an HLJDT group， and a Ginkgo biloba extract （GBE） group. After one week of acclimatization， intragastric administration was initiated. The sham and model groups received normal saline， the HLJDT group received HLJDT at 1.82 g·kg^-¹， and the GBE group received GBE at 0.432 g·kg^-¹. Administration was continued for 5 consecutive days， and the tMCAO model was established after the final dose on day 6. Single-cell RNA sequencing was performed on brain tissues and peripheral immune cells. UMAP and odds ratio （OR） indices were used to analyze cell distribution. Differential expression analysis was conducted to evaluate the effects of HLJDT on endothelial cells， pericytes， and macrophages， combined with CellChat and decoupler to analyze cell-cell communication and transcription factor regulation. Finally， PCR and ELISA were used to validate the mRNA and protein expression of relevant genes. ResultsCompared with the sham group， the model group showed significantly increased neurological deficit scores （P<0.01） and significantly decreased cerebral blood flow （P<0.01）， accompanied by cortical structural disorder， aggravated cytoplasmic vacuolization， and increased numbers of Nissl bodies. Compared with the model group， both the HLJDT and GBE groups exhibited significantly reduced neurological deficit scores （P<0.01） and markedly improved cerebral blood flow （P<0.01）， along with amelioration of cortical structural disorder， alleviated cytoplasmic vacuolization， and reduced numbers of Nissl bodies. Single-cell analysis showed that HLJDT protected endothelial cells and pericytes by preventing their reduction， restored the expression of functional genes in these cells （e.g.， PECAM1 and NOS3）， and downregulated the expression of chemokines and adhesion-related factors （e.g.， CCL2 and CXCL2）. In macrophages， HLJDT reduced their recruitment to the central nervous system and downregulated the expression of chemokine receptors and inflammatory factors （e.g.， IL-6， CCR2， and CXCR2）. Cell-cell communication analysis further indicated that HLJDT， through the above mechanisms， alleviated damage to pericytes and endothelial cells， reduced their recruitment of macrophages， and decreased ligand-receptor interactions in chemokine signaling pathways （including CCL， CXCL， and CSF3） between pericytes/endothelial cells and macrophages， thereby preventing secondary injury. Compared with the sham group， the model group showed significantly upregulated mRNA expression levels of IL-1β， IL-6， TNF-α， CCL2， CXCL2， and CSF3 （P<0.01）， while mRNA expression levels of endothelial- and pericyte function-related genes （RGS5， PECAM1， VEGFB， and NOS3） were significantly downregulated （P<0.01）. In contrast， compared with the model group， the HLJDT and GBE groups exhibited significantly decreased mRNA expression levels of IL-1β， IL-6， TNF-α， CCL2， CXCL2， and CSF3 （P<0.01）， and significantly increased expression of RGS5， PECAM1， VEGFB， and NOS3 （P<0.01）. At the protein level， compared with the sham group， the model group showed significantly increased expression of IL-1β， IL-6， and TNF-α （P<0.01）， whereas these protein levels were significantly reduced in the HLJDT and GBE groups compared with the model group （P<0.01）. ConclusionHLJDT reduces neuronal damage in ischemic stroke by protecting endothelial cells and pericytes， while inhibiting their interaction with macrophages， thereby mitigating secondary injury in the central nervous system.

BACKGROUND:At present,the treatment of infected bone defects has the problems of long course of disease,poor treatment effect and high cost.The osteogenic effect of personalized bone replacement materials in clinical treatment is limited.Therefore,a 3D-printed bone graft material with both good osteogenic effect and antibacterial effect is urgently needed for clinical treatment. OBJECTIVE:To summarize the research status of 3D-printed scaffolds loaded with antimicrobial agents for the treatment of infected bone defects. METHODS:PubMed,Web of Science,Elsevier,and CNKI databases from January 2010 to June 2022 were searched for related articles.The Chinese search terms were"bone defect,3D printing,scaffold material,antibacterial,animal experiments,in vitro experiments".English search terms were"bone defect,3D printing,scaffold,antibiosis,animal experiment,in vitro".Finally,60 articles were included for review and analysis. RESULTS AND CONCLUSION:The 3D scaffolds made of titanium,magnesium,tantalum and other metals and their alloys have certain osteogenic properties,but do not have antibacterial function.Hydroxyapatite and other bioceramic materials have good biocompatibility and are prone to be degraded,whereas due to the lack of strength,they are usually combined with artificial polymer materials to form composite materials,which respectively mimic the inorganic and organic components in natural bone,and play their respective excellent functions.Antibiotics,silver/copper nanoparticles,antimicrobial peptides,gallium and other antibacterial agents play an antibacterial role by destroying bacterial cell membrane,producing reactive oxygen species to interfere with bacterial DNA replication,inhibiting iron absorption and other mechanisms.As a result,the 3D-printed scaffold has both antibacterial and osteogenic effects.However,there are still some problems such as drug resistance and difficult to control effective concentrations.3D-printed scaffolds are often loaded with antibacterial agents by loading drug-loaded microspheres on scaffolds,preparing antibacterial coating on the scaffold surface,and participating in joint 3D printing with drugs.The loading mode of antibacterial coating prepared on the scaffold surface is the most widely used,and its antibacterial effect is more stable.Nonetheless,the selection of the most suitable loading mode for antibacterial agents needs to be further discussed and summarized.It is a future research prospect to optimize the mechanical properties of composite scaffolds and prepare biomimetic bone scaffolds so that the degradation rate is consistent with the bone reconstruction rate in infected bone defects.The ideal antibacterial agents may play a role through a variety of antibacterial mechanisms,thus being expected to play a good antibacterial effect through low antibacterial concentration,which should be a hot spot of anti-bone infection research.After loading antibacterial agents on the surface of the scaffold,antibacterial agents can"intelligently"react to the local microenvironment,achieving controlled release,and regulating the osteogenesis,vascularization and immune response of the microenvironment,which is the focus of current research.

ObjectiveTo screen out the transcriptomes related to the intervention of Wuzi Yanzongwan on the spermatogenic function of semi-castrated male mice， and to explore its potential mechanism in the intervention of the progress of low spermatogenic function. MethodBalb/c mice were randomly divided into sham-operated group， model group， testosterone propionate group（0.2 mg·kg^-1·d^-1， intramuscular injection） and Wuzi Yanzongwan group（1.56 g·kg^-1·d^-1， intragastric administration） according to body weight， with 12 mice in each group. The right testicle and epididymis were extracted from the model group and the drug administration group to construct the semi-castrated model of low spermatogenic function， while the fur and the right scrotum of the sham-operated group were only cut and immediately sterilized and sutured. At the end of the intervention， hematoxylin-eosin（HE） staining was used to observe the histopathology of testis， enzyme-linked immunosorbent assay（ELISA） was used to detect the levels of serum testosterone（T）， luteinizing hormone（LH） and follicle stimulating hormone（FSH）. The sperm count and motility of epididymis were measured by automatic sperm detector of small animal. Transcriptomic microarray technology was used to detect the mRNA expression level of testicular tissue in each group， the transcriptome of genes related to the regulation of Wuzi Yanzongwan was screened， and three mRNAs were selected for Real-time fluorescence quantitative polymerase chain reaction（Real-time PCR） to verify the transcriptome data. Through the annotation analysis of Gene Ontology（GO） and the signaling pathway analysis of Kyoto Encyclopedia of Genes and Genomes（KEGG）， the related functions of drugs regulating transcriptome were analyzed. ResultCompared with the sham-operated group， the testicular tissue of mice in the model group showed spermatogenic injury， contraction and vacuolization of the seminiferous tubules， reduction of spermatogenic cells at all levels， widening of the interstitial space， obstruction of spermatogonial cell development and other morphological abnormalities， and serum T significantly decreased， LH significantly increased（P<0.01）， and FSH elevated but no statistically significant difference， the count and vitality of epididymal sperm significantly decreased（P<0.01）. There were 882 differentially expressed mRNAs in the testicular tissues， of which 565 were up-regulated and 317 were down-regulated. Cluster analysis showed that these differentially expressed mRNA could effectively distinguish between the sham-operated group and the model group. Compared with the model group， the damage to testicular tissue in the Wuzi Yanzongwan group was reduced， the structure of the seminiferous tubules was intact， vacuolization was reduced， and the number of spermatogenic cells at all levels was significantly increased and arranged tightly. The serum T significantly increased， LH significantly decreased（P<0.01）， and FSH decreased but the difference was not statistically significant. The count and vitality of sperm in the epididymis were significantly increased（P<0.01）. Moreover， Wuzi Yanzongwan could regulate 159 mRNA levels in the testes of semi-castrated mice， of which 32 were up-regulated and 127 were down-regulated， and the data of the transcriptome assay was verified to be reliable by Real-time PCR. GO and KEGG analysis showed that the transcriptome functions regulated by Wuzi Yanzongwan were involved in the whole cell cycle process of sperm development such as sex hormone production of interstitial cells in testis， renewal， differentiation， metabolism， apoptosis and signal transduction of spermatogenic cells， and were closely related to the biological behaviors of signaling pathways such as spermatogenic stem cell function， endoplasmic reticulum protein processing and metabolic program. ConclusionWuzi Yanzongwan can effectively improve the low spermatogenic function of semi-castrated male mice， and its mechanism may be related to the regulation of testicular transcriptional regulatory network， the synthesis of sex hormones in testicular interstitial cells， the function of spermatogenic stem cells， the whole cell cycle process of spermatogenesis， as well as the expression of endoplasmic reticulum protein processing and metabolic program related genes transcription.

Objective:To investigate the carriage status of Neisseria meningitidis ( Nm) among the healthy population in Hebei Province for the prevention and control of meningitis. Methods:From 2015 to 2022, throat swabs were collected from health people, which were selected by cluster random sampling in 11 cities of Hebei.The positive rate of Nm was detected by bacterial culture. The serogroups of isolated strains were identified.The laboratory detection results of Nm strains, combined with epidemiological survey data, were synthetically analyzed. Results:A total of 20 245 people were investigated; 249 strains of Nm were isolated; the overall Nm carriage rate was 1.23%. The carriage rate was significantly higher in men than in women(χ 2=28.831, P<0.05). The positive rates of Nm in different age groups were significantly different(χ 2=428.018, P<0.05), with the highest rates in the 15-19 year-old group(4.90%, 149/3 042). The positive rates of Nm were significantly different in different regions(χ 2=177.512, P<0.05), with the highest positive rate of Nm in Xingtai, Shijiazhuang, Chengde and Baoding city in sequence. Among the isolated Nm strains, ungroupable serogroups, serogroup B, serogroup C, and serogroup W accounted for 71.49%(178/249), 13.65%(34/249), 6.83%(17/249) and 4.42%(11/249), respectively. Conclusions:The carriage rate of Nm among healthy population is generally low in Hebei Province. It is recommended to continue to strengthen monitoring, pay attention to the changes and distribution characteristics of Nm, and formulate scientific and targeted prevention and control measures of meningococcal disease.

Patellofemoral pain syndrome(PFPS)is one of the main diseases leading to patellofemoral joint dysfunction,which seriously affects the quality of life of patients.This disease is classified as"knee impediment"and"tendon impediment"in TCM,and acupuncture treatment has a significant effect on this disease.This article combed the clinical studies on acupuncture treatment of PFPS in recent years around filiform needling,warm acupuncture and moxibustion,fire needle,needle knife,electro-acupuncture and other acupuncture treatments,and discussed the clinical effects and application scope of different treatments.Studies have shown that acupuncture therapy can effectively improve the symptoms and function of PFPS through a variety of mechanisms,such as regulating the function of the central nervous system,promoting the absorption of inflammatory factors and the clearance of joint effusion,and improving local blood circulation.These findings provide an important reference for the clinical treatment of PFPS.