ObjectiveTo explore the mechanism by which Sini San （SNS） inhibits ferroptosis， alleviates inflammation and myocardial injury， and improves myocardial infarction （MI）. MethodsThe active ingredients of SNS were obtained by searching the Traditional Chinese Medicine System Pharmacology Platform （TCMSP） database， its target sites were predicted using the SwissTargetPrediction Database， and the core components were screened out using the CytoNCA plug-in. The targets of MI and ferroptosis were obtained by using GeneCards， Online Mendelian Inheritance in Man （OMIM） database， DrugBank， Therapeutic Target Database （TTD）， FerrDb database and literature review， respectively. The intersection of these targets of SNS-MI-ferroptosis was plotted as a Venn diagram. The protein-protein interaction （PPI） network was constructed using the STRING database， and the visualization graph was prepared using Cytoscape. The core targets were screened out using the CytoNCA plug-in， and the biological functions were clustered by the MCODE plug-in. Gene Ontology （GO） functional enrichment analysis and Kyoto Encyclopedia of Genes and Genomes （KEGG） pathway enrichment analysis were performed using the David database. Molecular docking was performed using AutoDock and visualized with PyMOL2.5.2. The Kunming mice were randomly divided into the control group， the model group， the SNS group， and the trimetazidine （TMZ） group. The mice were subcutaneously injected with isoprenaline （ISO， 5 mg·kg^-1·d^-1） to establish an MI model. The drug was continuously intervened for 7 days. The ST-segment changes were recorded by electrocardiogram （ECG）， and the tissue morphology changes were observed by hematoxylin-eosin （HE） staining. Cardiomyocyte ferroptosis was investigated by transmission electron microscopy. Serum creatine kinase （CK）， creatine kinase isoenzyme （CK-MB）， lactate dehydrogenase （LDH）， reduced glutathione （GSH）， and malondialdehyde （MDA） levels were detected by biochemical assay. Enzyme-linked immunosorbent assay （ELISA） was used to detect serum levels of interleukin （IL）-6 and 4-hydroxynonenal （4-HNE）. Immunohistochemical staining was employed to detect IL-6 and phosphorylated signal transducer and transcription activator 3 （p-STAT3） in cardiac tissues. Western blot was used to detect STAT3 and p-STAT3 in cardiac tissues. Real-time PCR was used to detect the levels of IL-6， IL-18， solute carrier family 7 member 11 （SLC7A11）， arachidonic acid 15-lipoxygenase （ALOX15）， and glutathione peroxidase 4 （GPx4） in cardiac tissues. ResultsA total of 121 active ingredients of SNS were obtained， and 58 potential targets of SNS in the treatment of MI by regulating ferroptosis were screened. The three protein modules with a score5 were mainly related to the inflammatory response. The GO function was mainly related to inflammation， and KEGG enrichment analysis showed that SNS mainly regulated ferroptosis- and inflammation- related signaling pathways. Molecular docking indicated that the core component had a higher binding force to the target site. Animal experiments confirmed that SNS reduced the level of p-STAT3 （P0.01）， down-regulated the expression of ALOX15 mRNA （P0.01）， up-regulated the level of serum GSH， and the expressions of SLC7A11 and GPx4 mRNA， reduced MDA and 4-HNE levels （P0.05， P0.01）. Additionally， SNS improved the mitochondrial injury induced by cardiomyocyte ferroptosis， reduced the area of MI， alleviated inflammation and myocardial injury， lowered the levels of serum CK， CK-MB， LDH， IL-6， and the mRNA expression levels of IL-16 and IL-18 （P0.05）， and improved ST segment elevation. ConclusionSNS can reduce ISO-induced STAT3 phosphorylation levels， inhibit ferroptosis in cardiomyocytes， alleviate inflammation and myocardial injury， thereby improving MI.

ObjectiveTo explore the mechanism by which Sini San （SNS） inhibits ferroptosis， alleviates inflammation and myocardial injury， and improves myocardial infarction （MI）. MethodsThe active ingredients of SNS were obtained by searching the Traditional Chinese Medicine System Pharmacology Platform （TCMSP） database， its target sites were predicted using the SwissTargetPrediction Database， and the core components were screened out using the CytoNCA plug-in. The targets of MI and ferroptosis were obtained by using GeneCards， Online Mendelian Inheritance in Man （OMIM） database， DrugBank， Therapeutic Target Database （TTD）， FerrDb database and literature review， respectively. The intersection of these targets of SNS-MI-ferroptosis was plotted as a Venn diagram. The protein-protein interaction （PPI） network was constructed using the STRING database， and the visualization graph was prepared using Cytoscape. The core targets were screened out using the CytoNCA plug-in， and the biological functions were clustered by the MCODE plug-in. Gene Ontology （GO） functional enrichment analysis and Kyoto Encyclopedia of Genes and Genomes （KEGG） pathway enrichment analysis were performed using the David database. Molecular docking was performed using AutoDock and visualized with PyMOL2.5.2. The Kunming mice were randomly divided into the control group， the model group， the SNS group， and the trimetazidine （TMZ） group. The mice were subcutaneously injected with isoprenaline （ISO， 5 mg·kg^-1·d^-1） to establish an MI model. The drug was continuously intervened for 7 days. The ST-segment changes were recorded by electrocardiogram （ECG）， and the tissue morphology changes were observed by hematoxylin-eosin （HE） staining. Cardiomyocyte ferroptosis was investigated by transmission electron microscopy. Serum creatine kinase （CK）， creatine kinase isoenzyme （CK-MB）， lactate dehydrogenase （LDH）， reduced glutathione （GSH）， and malondialdehyde （MDA） levels were detected by biochemical assay. Enzyme-linked immunosorbent assay （ELISA） was used to detect serum levels of interleukin （IL）-6 and 4-hydroxynonenal （4-HNE）. Immunohistochemical staining was employed to detect IL-6 and phosphorylated signal transducer and transcription activator 3 （p-STAT3） in cardiac tissues. Western blot was used to detect STAT3 and p-STAT3 in cardiac tissues. Real-time PCR was used to detect the levels of IL-6， IL-18， solute carrier family 7 member 11 （SLC7A11）， arachidonic acid 15-lipoxygenase （ALOX15）， and glutathione peroxidase 4 （GPx4） in cardiac tissues. ResultsA total of 121 active ingredients of SNS were obtained， and 58 potential targets of SNS in the treatment of MI by regulating ferroptosis were screened. The three protein modules with a score5 were mainly related to the inflammatory response. The GO function was mainly related to inflammation， and KEGG enrichment analysis showed that SNS mainly regulated ferroptosis- and inflammation- related signaling pathways. Molecular docking indicated that the core component had a higher binding force to the target site. Animal experiments confirmed that SNS reduced the level of p-STAT3 （P0.01）， down-regulated the expression of ALOX15 mRNA （P0.01）， up-regulated the level of serum GSH， and the expressions of SLC7A11 and GPx4 mRNA， reduced MDA and 4-HNE levels （P0.05， P0.01）. Additionally， SNS improved the mitochondrial injury induced by cardiomyocyte ferroptosis， reduced the area of MI， alleviated inflammation and myocardial injury， lowered the levels of serum CK， CK-MB， LDH， IL-6， and the mRNA expression levels of IL-16 and IL-18 （P0.05）， and improved ST segment elevation. ConclusionSNS can reduce ISO-induced STAT3 phosphorylation levels， inhibit ferroptosis in cardiomyocytes， alleviate inflammation and myocardial injury， thereby improving MI.

ObjectiveTo systematically investigate the discrepancies between employment preferences and actual job placements among postgraduate students in rehabilitation medicine, explore the influencing factors, and elucidate the underlying mechanisms of their employment decisions. MethodsA cross-sectional questionnaire survey was conducted among 100 full-time postgraduate students who had graduated from Capital Medical University School of Rehabilitation in the past six years. A self-designed questionnaire was used to collect information on personal background, self-assessed competencies, employment preferences, and actual job placements. Logistic regression models were employed to analyze the factors influencing employment preferences and actual job placements, respectively. ResultsEmployment preferences among rehabilitation medicine postgraduates were highly concentrated on large tertiary hospitals (79.0%), yet the actual placement rate (61.0%) showed a significant gap. Preference for tertiary hospitals showed no significant association with individual factors such as gender, degree type or self-assessed competencies (P > 0.05). Univariate analysis revealed that those who entered tertiary hospitals scored significantly higher in self-assessed clinical skills, research ability, communication and coordination, and resource integration (|t| > 3.661, P < 0.001), and demonstrated clearer career planning (P = 0.012). Multivariate logistic regression analysis did not identify any independent predictors of actual employment within the context of this study sample (P > 0.05). ConclusionEmployment among rehabilitation medicine postgraduates is characterized by highly homogeneous preferences coexisting with complexity of factors influencing actual employment. It is recommended to optimize the training system, deepen personalized career education, and establish diversified employment guidance mechanisms to promote rational talent flow and facilitate the balanced development of the rehabilitation medical service system.

Osteoarthritis （OA） and stroke are common clinical diseases that reduce patients' quality of life and place a burden on families and society. Ruyi Zhenbaowan， a classic prescription in Tibetan medicine， have the functions of clearing heat， awakening the brain and opening orifices， relaxing tendons and promoting meridian circulation， and eliminating yellow water. Clinically， they are used to treat osteoarthritis， post-stroke sequelae， neuropathic pain， and other related conditions. Modern pharmacological studies have demonstrated their anti-inflammatory， analgesic， and nerve-repairing effects. However， current research remains insufficient regarding the appropriate indications， timing， and efficacy of this medicine in treating relevant diseases. To enhance clinicians' understanding of this medicine and promote its standardized and rational clinical use， a panel of national experts， including clinical specialists， Tibetan medicine practitioners， pharmacologists， and methodologists， formulated this consensus based on clinical experience and evidence-based practice. The Cochrane systematic review framework， the Grading of Recommendations Assessment， Development and Evaluation （GRADE） system， and the nominal group method were employed to generate seven graded recommendations and 19 consensus-based suggestions. These recommendations clearly define the key points in the clinical application of Ruyi Zhenbaowan， including therapeutic indications， dosage and administration， treatment duration， and medication safety. The consensus specifically addresses the clinical efficacy， appropriate timing of administration， dosage strategies， treatment cycles， and combination medication strategies for treating osteoarthritis and stroke and provides an overview of safety considerations. The aim is to provide standardized guidance for hospitals and healthcare institutions nationwide to ensure the rational application of Ruyi Zhenbaowan in the treatment of osteoarthritis and stroke， reduce medication-related risks， and further leverage its clinical advantages. This consensus has been approved and issued by the China Association of Chinese Medicine， with the standard number GS/CACM 369-2024.

Objective To investigate the effect of triptolide on cerebral ischemia- reperfusion injury （CIRI） and explore its molecular mechanism. Methods One hundred and forty-four Wistar rats were randomly divided into sham operation group, model group, low, medium, high dose of triptolide group and butylphthalide group, with 24 rats in each group. The CIRI rat model was established by blocking the middle cerebral artery for 2 hours. 3 days before modeling, the rats in each group were ip administration once a day. 24 hours after reperfusion, the neurological deficit score was detected, the rate of cerebral infarction was measured by TTC staining, the blood brain barrier （BBB） permeability was detected by EB penetration test. The pathological changes neurons in the ischemic penumbra cortex were observed by HE and TUNEL staining. The content of inflammatory factors in ischemic cerebral cortex were detected by Elisa method. The expression of TLR4/NF-κB pathway related proteins were detected by Western blot. Results Compared with the model group, the neurological deficit score, cerebral infarction rate and EB content in the triptolide middle, high dose groups and the butylphthalide group were significantly decreased （P<0.05）. The pathological changes of cortical neurons in the ischemic penumbra were significantly improved, and the apoptosis rate of neurons was significantly decreased （P<0.05）. The content of TNF-α, IL-1β and the expression of TLR4, p-NF-κB, cleaved caspase-3, Bax were significantly decreased, the expression of Bcl-2 was significantly increased, the ratio of p-NF-κB/NF-κB and Bax/Bcl-2 were significantly decreased （P<0.05）. The regulatory effect of the high dose triptolide group on various detection indexes were better than that of the butylphthalide group （P<0.05）. Conclusion Triptolide could protect the permeability of BBB, improve the neurological deficit and neuropathy in CIRI rats, and reduce the rate of cerebral infarction, its mechanism may be related to the inhibition of TLR4/NF-κB pathway and which mediated inflammatory response and neuronal apoptosis.

The expert consensus on the clinical treatment of herpes zoster with fire needling was developed, and the commonly used fire needling treatment scheme verified by clinical research was selected to form a standardized diagnosis and treatment scheme for acute herpes zoster and postherpetic neuralgia (PHN), so as to answer the core problems in clinical application. The consensus focuses on patients with herpes zoster, and forms recommendations for 9 key clinical issues, covering simple fire needling and TCM comprehensive therapy based on fire needling, including fire needling combined with cupping, fire needling combined with Chinese herb, fire needling combined with cupping and Chinese herb, fire needling combined with filiform needling, fire needling combined with moxibustion, and provides specific recommendations and operational guidelines for various therapies.
Humans ; Herpes Zoster/therapy* ; Acupuncture Therapy/instrumentation* ; Consensus ; Clinical Protocols

Objectives:This study aims to establish a calcified aortic valve disease(CAVD)-related gene regulatory network,and clarify the impact of interactions between CAVD-related genes on CAVD.Methods:Differential expression gene method was used to screen candidate genes,and STRING software was used to construct protein-protein interaction networks for screened genes.The networks and genes with the highest scores were obtained.Monte Carlo method was used to rank the importance of genes in CAVD,and the top 1%genes were identified.Genes identified by these two methods are intersected to obtain the key genes.The correlation between the key genes and CAVD were confirmed by biological verification method.Then,key genes were used as query genes to establish CAVD gene regulatory module with a co-expression patterns-based gene regulatory network identifying method.Specifically,we first detected the underlying co-expression patterns of the seemingly uncorrelated genes,and then pieced the isolated gene pairs up into gene regulatory network with the help of the bridging genes.Finally,we verified the function of the established gene regulatory network through enrichment analysis and literature analysis.Results:We identified the CAVD gene regulatory network containing 211 genes from 18 084 candidate genes.Functional enrichment analysis indicate that the established gene regulatory network included genes with both known interactions and potential novel pathway interactions related to CAVD,serving as candidates for further experimental CAVD studies.Conclusions:Methodologically,the proposed method avoids the problem of complex computation,and relies only on available biological priors.It is also able to detect underlying co-expression patterns.The results will advance the understanding of the interactions of the CAVD-related genes and this method provides a novel way to identify underlying gene co-expression patterns in the setting of CAVD.

Objective To investigate the effect of intravenous flurbiprofen axetil on the incidence and severity of catheter-related bladder discomfort(CRBD)after transurethral resection of the prostate(TURP).Methods The elderly patients undergoing TURP under general anesthesia were enrolled,and randomly divided into two groups:flurbiprofen axetil group(group F)and control group(group C).Ten minutes before the end of surgery,group F was given 50 mg of flurbiprofen axetil intravenously,group C was given an equal amount of 0.9％sodium chloride injection.The primary outcome indicator was the incidence of moderate to severe CRBD immediately after entering the resuscitation room(T0).Secondary indicators included the incidence and severity of CRBD at 1 h(T1),2 h(T2),and 6 h(T3)after entering the resuscitation room,the amount of sufentanil used within 24 hours after surgery,postoperative NRS score,flurbiprofen axetil-related and analgesic adverse reactions 24 hours after surgery,and patient satisfaction.Results A total of 90 patients were included and each group was 45 patients.The incidence of moderate to severe CRBD at T0 was significantly lower in group F than that in group C(8.9％vs.33.3％,P=0.004).The incidence of CRBD in T1,T2,and T3 was lower in group F than in group C(P＜0.05).The incidence of mild CRBD at T3 in group F was lower than that in group C(P＜0.05).The incidence of moderate to severe CRBD at T1 and T2 in groups F was lower than that in group C(P＜0.05).The amount of sufentanil used in group F at 24 hours after surgery was significantly lower than that in group C(P=0.001).The pain scores in group F at T0,T1,T2,and T3 were lower than those in group C(P＜0.05);The postoperative patient satisfaction score in group F was higher than that in group C(P=0.001).However,there were no significant differences between the two groups in postoperative anesthesia resuscitation time and 24-hour adverse reactions incidence(P＞0.05).Conclusion Intravenous flurbiprofen axetil can safely and effectively reduce the incidence and severity of CRBD after TURP.It can significantly relieve pain,reduce sufentanil use,and have high clinical application value.

Objective:To investigate the clinicopathological features, immunohistochemical characteristics, and differential diagnosis of low-grade adenosquamous carcinoma of the breast arising from benign sclerosing lesions.Methods:Twelve cases of low-grade adenosquamous carcinoma arising from benign sclerosing lesions of the breast were collected, which were diagnosed from January 2010 to December 2023 at the Seventh Medical Center of the Chinese People′s Liberation Army General Hospital. Their clinical manifestations, histopathological morphology, and immunohistochemical characteristics were analyzed and related literatures were reviewed.Results:All the 12 patients were females with a median age of 42 years (21-60 years). Five of the 12 cases had coexisting complex sclerosing lesions, 5 with sclerosing adenosis, 1 with sclerosing intraductal papilloma, and 1 with ductal adenoma. Microscopically, low-grade adenosquamous carcinoma grew infiltratively in multinodular and sclerosing lesions. The carcinomatous component was characterized by small irregular glandular structures, tubular formations, solid nests, clusters, or a single tumor cell. The epithelium showed varying degrees of squamous differentiation. The carcinoma was surrounded by fibroadenomatoid and desmoplastic lesions. The invasive neoplastic component typically infiltrated normal breast structures, and might infiltrate nerves and adipose tissue. There were lymphocytic aggregates commonly seen at the periphery. By immunohistochemistry, the tumor cells of all 12 cases showed diffuse and strong immunopositivity for CK5/6; negative expression of ER, PR and HER2; and variable expression of myoepithelial markers such as SMA, calponin, SMMHC and others. There was varied staining pattern of tumor cells for p63. CK8/18 (or CK7) was variably positive or negative. The proliferative index measured by Ki-67 was low.Conclusions:Low-grade adenosquamous carcinoma of the breast is a rare variant, which is found to coexist with other benign sclerosing lesions and can be easily missed and/or misdiagnosed. Their invasive growth pattern, presence of sweat duct-like structures and immunophenotypic profile are key features for appropriate diagnosis.

BACKGROUND:Myocardial cell hypoxic injury is closely associated with oxidative stress and ferroptosis.Previous studies have shown that aloin has various effects such as antioxidant,anti-inflammatory,and anti-tumor activities.OBJECTIVE:To investigate the effects of aloin on oxidative stress and ferroptosis in hypoxia-induced H9C2 cells.METHODS:A hypoxia model was established using H9C2 myocardial cells.Firstly,cell viability was determined to confirm the lack of cytotoxicity of aloin and to determine its optimal therapeutic concentration.Subsequently,the effects of aloin on hypoxia-induced lactate dehydrogenase release,reactive oxygen species production,and mitochondrial oxidative stress in H9C2 cells were evaluated using assay kits,dihydroethidium fluorescent probes,and MitoSOX?Red fluorescent probes,respectively.To verify the effect of aloin on ferroptosis,intracellular Fe2+content and lipid peroxidation level were detected using fluorescence staining and flow cytometry,respectively.Then,the expression levels of ferroptosis regulatory factors glutathione peroxidase 4,acyl-CoA synthetase long-chain family member 4,and nuclear factor E2-related factor 2 were detected using western blot assay and real-time fluorescence quantitative PCR techniques.Finally,the role of ferroptosis in aloin-mediated myocardial protection was further confirmed by using the ferroptosis inducer Erastin.RESULTS AND CONCLUSION:(1)Compared with the control group,the viability of H9C2 cells in the hypoxia group was significantly decreased,lactate dehydrogenase release,reactive oxygen species level,mitochondrial oxidative stress degree,Fe2+content,and lipid peroxidation degree were significantly increased,while glutathione peroxidase 4 and nuclear factor E2-related factor 2 mRNA and protein expression levels were significantly decreased,and acyl-CoA synthetase long-chain family member 4 mRNA and protein expression were significantly increased(all P＜0.05).(2)Compared with the hypoxia group,both low and high doses of aloin reversed the changes in above indicators(all P＜0.05).(3)Compared with the hypoxia+aloin group,the hypoxia+aloin+Erastin group showed a significant decrease in H9C2 cell viability and a significant increase in lactate dehydrogenase release(both P＜0.01).The results indicate that aloin has a protective effect on hypoxia-treated H9C2 cells in a dose-dependent manner,mainly achieved by inhibiting oxidative stress and ferroptosis.