Polycystic ovary syndrome （PCOS） is a common endocrine and metabolic disorder among women of reproductive age. Hyperandrogenism （HA）， one of its core pathological features， is closely associated with the clinical manifestations and metabolic complications of the disease. Current western medical treatments for PCOS-HA mainly include anti-androgen therapy and ovulation induction， such as short-acting oral contraceptives like Diane-35 and Yasmin. However， long-term use of these medications may result in adverse reactions like increasing the risk of liver dysfunction and exacerbating lipid metabolism disorders， with unsatisfactory long-term efficacy when used alone. Traditional Chinese medicine offers unique advantages in the treatment of PCOS-HA due to its holistic approach and multi-target regulatory mechanisms. In the view of traditional Chinese medicine， PCOS-HA is classified under the categories such as "delayed menstruation"， "amenorrhea"， and "infertility"， with kidney deficiency as the root， as well as liver stagnation and spleen deficiency as the manifestations. Phlegm and blood stasis are considered to be intertwined throughout the disease course. Modern studies have shown that traditional Chinese medicine is significantly effective in improving the androgen levels， restoring ovulation， and improving insulin resistance in PCOS-HA patients. Representative prescriptions， such as Erxian Tang， Jiawei Xiaoyaosan， Guizhi Fulingwan， and Cangfu Daotantang， exert therapeutic effects through various mechanisms including regulation of the hypothalamic-pituitary-ovarian axis， reduction of ovarian androgen synthase activity， improvement of insulin signaling pathways， and inhibition of inflammation and oxidative stress， which demonstrates the characteristics of comprehensive treatment with traditional Chinese medicine. Based on the perspectives of etiology and pathogenesis of traditional Chinese medicine， modern medical cognition， typical prescriptions， and action mechanisms， this paper reviewed the research progress of traditional Chinese medicine in the treatment of PCOS-HA， aiming to provide a reference for in-depth research and clinical applications in this field.

Polycystic ovary syndrome （PCOS） is a common endocrine and metabolic disorder among women of reproductive age. Hyperandrogenism （HA）， one of its core pathological features， is closely associated with the clinical manifestations and metabolic complications of the disease. Current western medical treatments for PCOS-HA mainly include anti-androgen therapy and ovulation induction， such as short-acting oral contraceptives like Diane-35 and Yasmin. However， long-term use of these medications may result in adverse reactions like increasing the risk of liver dysfunction and exacerbating lipid metabolism disorders， with unsatisfactory long-term efficacy when used alone. Traditional Chinese medicine offers unique advantages in the treatment of PCOS-HA due to its holistic approach and multi-target regulatory mechanisms. In the view of traditional Chinese medicine， PCOS-HA is classified under the categories such as "delayed menstruation"， "amenorrhea"， and "infertility"， with kidney deficiency as the root， as well as liver stagnation and spleen deficiency as the manifestations. Phlegm and blood stasis are considered to be intertwined throughout the disease course. Modern studies have shown that traditional Chinese medicine is significantly effective in improving the androgen levels， restoring ovulation， and improving insulin resistance in PCOS-HA patients. Representative prescriptions， such as Erxian Tang， Jiawei Xiaoyaosan， Guizhi Fulingwan， and Cangfu Daotantang， exert therapeutic effects through various mechanisms including regulation of the hypothalamic-pituitary-ovarian axis， reduction of ovarian androgen synthase activity， improvement of insulin signaling pathways， and inhibition of inflammation and oxidative stress， which demonstrates the characteristics of comprehensive treatment with traditional Chinese medicine. Based on the perspectives of etiology and pathogenesis of traditional Chinese medicine， modern medical cognition， typical prescriptions， and action mechanisms， this paper reviewed the research progress of traditional Chinese medicine in the treatment of PCOS-HA， aiming to provide a reference for in-depth research and clinical applications in this field.

Objective:To explore the effect of inhibiting miR-203a-3p gene expression on proliferation and apoptosis of rheu-matoid arthritis(RA)synovial fibroblasts.Methods:Divided fibroblast-like synovial cells MH7A into Control group(untransfected cells),anti-miR-NC group(transfected with anti-miR-NC),anti-miR-203a-3p group(transfected with anti-miR-203a-3p),anti-miR-203a-3p+LiCl group(transfected with anti-miR-203a-3p+signal pathway activator LiCl).qRT-PCR was used to detect expression level of miR-203a-3p;clone formation experiment,MTT experiment were used to detect cell proliferation;flow cytometry was used to de-tect cell apoptosis;Western blot was used to detect protein expressions of PCNA,Bcl-2,Bax,Wnt1,β-catenin.Results:Transfec-tion of miR-203a-3p reduced the number of clones and survival rate of MH7A cells,increased rate of apoptosis,reduced expression levels of PCNA,Bcl-2,Wnt1,β-catenin protein,increased expression level of Bax protein.The signaling pathway activator LiCl in-creases the number of clones and survival rate of MH7A cells transfected with miR-203a-3p,reduces the rate of apoptosis,increases the expression level of Wnt1,β-catenin,PCNA,Bcl-2 protein,and reduces expression level of Bax protein.Conclusion:miR-203a-3p may promote proliferation of RA synovial fibroblasts and inhibit cell apoptosis by activating Wnt/β-catenin.

Objective Prepubertal mice are administered subcutaneously with letrozole sustained-release pellets behind the neck and treated with a high-fat diet to establish a mouse model of polycystic ovary syndrome(PCOS).The liver transcriptomes of the model mice are compared with those of the placebo control mice to investigate the underlying mechanisms of liver involvement in the pathogenesis of PCOS.Methods A customized 2 mg dose of letrozole sustained-release pellets with a 40-day release period was used.The control placebo and letrozole pellets were implanted subcutaneously in the dorsal cervical region of 3-4-week-old C57BL/6J mice(8 mice per group)to establish the control group and letrozole-induced PCOS model group.Both groups were treated with a high-fat diet starting the day after administration.The modeling period lasted for 5 weeks,during which body weight and 24-hour food intake were monitored in each group every week.When samples were collected,liver weight was recorded.Pathological changes in ovarian and hepatic tissues were examined by hematoxylin-eosin(HE)staining,while hepatic lipid deposition was observed by Oil Red O staining.The extent of macrophage infiltration in the liver was evaluated via F4/80 immunohistochemical staining,and hepatic fibrosis levels were observed by Masson's trichrome staining.Transcriptomic sequencing was performed to analyze differentially expressed genes(DEGs)in liver tissues between the control and model groups,followed by enrichment analysis of significant DEGs.Quantitative real-time fluorescent quantitative PCR(qPCR)was subsequently used to validate the expression of significant DEGs in liver tissues of both groups.Results Compared with the control group,the model group which received subcutaneous letrozole sustained-release pellets combined with a high-fat diet exhibited significantly increased body weight(P＜0.001),prominent polycystic ovarian morphology,and significantly decreased liver-to-body weight ratio(P＜0.05).However,no significant changes were observed in absolute liver weight(P＞0.05),hepatic histomorphology,or lipid deposition.Transcriptome sequencing identified 119 upregulated and 217 downregulated DEGs in the liver tissues of letrozole-treated mice,which were predominantly enriched in pathways related to cholesterol and steroid biosynthesis,steroid hormone metabolism,and inflammatory responses.qPCR validation demonstrated that mRNA expression of HSD3B2 and HMGCR was significantly upregulated in liver(P＜0.01),while mRNA expression of IL4,CCL2 and COL1A1 was downregulated(P＜0.05)in the model group compared with the control group.However,Masson's trichrome staining and F4/80 immunohistochemical analysis showed no significant changes in hepatic fibrosis or macrophage infiltration.Conclusion Subcutaneous administration of letrozole sustained-release pellets combined with a high-fat diet successfully establishes a mouse model of PCOS.The model mice exhibited significant changes in hepatic gene expression.Liver may contribute to PCOS pathogenesis through regulating cholesterol and steroid metabolism.

Objective Prepubertal mice are administered subcutaneously with letrozole sustained-release pellets behind the neck and treated with a high-fat diet to establish a mouse model of polycystic ovary syndrome(PCOS).The liver transcriptomes of the model mice are compared with those of the placebo control mice to investigate the underlying mechanisms of liver involvement in the pathogenesis of PCOS.Methods A customized 2 mg dose of letrozole sustained-release pellets with a 40-day release period was used.The control placebo and letrozole pellets were implanted subcutaneously in the dorsal cervical region of 3-4-week-old C57BL/6J mice(8 mice per group)to establish the control group and letrozole-induced PCOS model group.Both groups were treated with a high-fat diet starting the day after administration.The modeling period lasted for 5 weeks,during which body weight and 24-hour food intake were monitored in each group every week.When samples were collected,liver weight was recorded.Pathological changes in ovarian and hepatic tissues were examined by hematoxylin-eosin(HE)staining,while hepatic lipid deposition was observed by Oil Red O staining.The extent of macrophage infiltration in the liver was evaluated via F4/80 immunohistochemical staining,and hepatic fibrosis levels were observed by Masson's trichrome staining.Transcriptomic sequencing was performed to analyze differentially expressed genes(DEGs)in liver tissues between the control and model groups,followed by enrichment analysis of significant DEGs.Quantitative real-time fluorescent quantitative PCR(qPCR)was subsequently used to validate the expression of significant DEGs in liver tissues of both groups.Results Compared with the control group,the model group which received subcutaneous letrozole sustained-release pellets combined with a high-fat diet exhibited significantly increased body weight(P＜0.001),prominent polycystic ovarian morphology,and significantly decreased liver-to-body weight ratio(P＜0.05).However,no significant changes were observed in absolute liver weight(P＞0.05),hepatic histomorphology,or lipid deposition.Transcriptome sequencing identified 119 upregulated and 217 downregulated DEGs in the liver tissues of letrozole-treated mice,which were predominantly enriched in pathways related to cholesterol and steroid biosynthesis,steroid hormone metabolism,and inflammatory responses.qPCR validation demonstrated that mRNA expression of HSD3B2 and HMGCR was significantly upregulated in liver(P＜0.01),while mRNA expression of IL4,CCL2 and COL1A1 was downregulated(P＜0.05)in the model group compared with the control group.However,Masson's trichrome staining and F4/80 immunohistochemical analysis showed no significant changes in hepatic fibrosis or macrophage infiltration.Conclusion Subcutaneous administration of letrozole sustained-release pellets combined with a high-fat diet successfully establishes a mouse model of PCOS.The model mice exhibited significant changes in hepatic gene expression.Liver may contribute to PCOS pathogenesis through regulating cholesterol and steroid metabolism.

Objective:To explore the effect of inhibiting miR-203a-3p gene expression on proliferation and apoptosis of rheu-matoid arthritis(RA)synovial fibroblasts.Methods:Divided fibroblast-like synovial cells MH7A into Control group(untransfected cells),anti-miR-NC group(transfected with anti-miR-NC),anti-miR-203a-3p group(transfected with anti-miR-203a-3p),anti-miR-203a-3p+LiCl group(transfected with anti-miR-203a-3p+signal pathway activator LiCl).qRT-PCR was used to detect expression level of miR-203a-3p;clone formation experiment,MTT experiment were used to detect cell proliferation;flow cytometry was used to de-tect cell apoptosis;Western blot was used to detect protein expressions of PCNA,Bcl-2,Bax,Wnt1,β-catenin.Results:Transfec-tion of miR-203a-3p reduced the number of clones and survival rate of MH7A cells,increased rate of apoptosis,reduced expression levels of PCNA,Bcl-2,Wnt1,β-catenin protein,increased expression level of Bax protein.The signaling pathway activator LiCl in-creases the number of clones and survival rate of MH7A cells transfected with miR-203a-3p,reduces the rate of apoptosis,increases the expression level of Wnt1,β-catenin,PCNA,Bcl-2 protein,and reduces expression level of Bax protein.Conclusion:miR-203a-3p may promote proliferation of RA synovial fibroblasts and inhibit cell apoptosis by activating Wnt/β-catenin.

A 31-year-old man sought medical evaluation for a 2-year history of edema and proteinuria, with prior pathology suggesting atypical membranous nephropathy (MN). Despite treatment with a combination of steroids, calcineurin inhibitors, and four courses of rituximab (1 g, intravenous injection), the patient′s nephrotic syndrome showed no relief (24 h urine protein peaked at 31.18 g/d), indicating refractory nephrotic syndrome. Later in the disease course, a sudden surge of creatinine level (322.5 μmol/L) prompted a renal biopsy, which revealed concurrent acute interstitial nephritis. Further treatment involving steroids, cyclophosphamide, and a fifth rituximab infusion (1 g, intravenous injection) resulted in improvement in renal function (serum creatinine: 322.5?147 μmol/L), but the MN failed to achieve partial relief. Subsequent treatment with the novel humanized CD20 monoclonal antibody obinutuzumab (1 g, intravenous injection) was initiated. In the latest follow-up, anti-phospholipase-A2-receptor antibody (PLA2R) antibody were negative, B cells were eliminated, serum albumin was 36 g/L, urine protein-to-creatinine ratio was 4 810 mg/g, and serum creatinine was 162 μmol/L. This case underscores the potential efficacy of obinutuzumab in refractory MN. For advanced MN cases, prompt identification of the cause of acute kidney injury is crucial, emphasizing the need for targeted interventions to potentially stall renal function decline.

Objective To analyze the clinical characteristics and prognosis of patients with coronary slow flow(CSF)or no reflow(CNR)after emergency PCI.Methods A total of 443 elderly STEMI patients who underwent emergency PCI in Department of Cardiology of the First Affilia-ted Hospital of Tsinghua University from January 2017 to August 2023 were recruited,and ac-cording to thrombolysis in myocardial infarction(TIMI)flow grading after operation,they were divided into CSF/CNR group(TIMI grade≤2 flow,n=40)and normal flow(NCF)group(TIMI grade 3 flow,n=403).Logistic regression analysis was used to analyze the risk factors for CSF/CNR in STEMI patients after PCI.The prognosis was analyzed in the two groups.Results The CSF/CNR group had advanced age,longer durations from onset to admission and from onset to balloon opening,higher mortality rate,and larger proportions of chronic heart failure(CHF),type 2 diabetes mellitus(T2DM),pulse rate＞100 times/min,SBP＜100 mm Hg(1 mm Hg=0.133 kPa),Killip grade＞1,left anterior descending artery disease,LVEF＜50％,and using glycopro-tein Ⅱb/Ⅲa inhibitors and intraaortic balloon counterpulsation,but lower male ratio and DBP when compared with the control group(P＜0.05,P＜0.01).Multiple logistic regression analysis revealed that T2DM(OR=1.320,95％CI:0.618-2.123,P=0.046),mean SBP(OR=1.239,95％CI:0.752-1.525,P=0.04)and SBP＜100 mm Hg(OR=1.330,95％CI:0.836-1.675,P=0.013)were independent risk factors,while male was a protective factor(OR=-1.755,95％CI:-2.338--1.171,P=0.002)for CSF/CNR in STEMI patients after PCI.Conclusion T2DM and lower SBP are independent risk factors,while male is a protective factor for CSF/CNR in STEMI patients after emergency PCI.

Objective:To construct acute ST-segment elevation myocardial infarction (STEMI) percutaneous coronary intervention (PCI) by using lipoprotein-associated phospholipase A2 (Lp-PLA2) and D-dimer to fibrinogen ratio (D/F) and other indicators postoperative patient prognosis nomogram model and evaluation of its predictive value.Methods:A total of 291 acute STEMI patients admitted to the BenQ Hospital Affiliated to Nanjing Medical University from January 2017 to January 2020 were retrospectively selected, including but not limited to Lp-PLA2 and D/F, were collected. Receiver operating characteristic (ROC) curve and multivariate Logistic regression were used to analyze the risk factors of death within 90 d after PCI in STEMI patients, and Kaplan-Meier survival curves were drawn to compare the survival of patients in different Lp-PLA2 and D/F groups. The R language software was used to build nomogram model and decision curve.Results:The AUCs of LpPLA2 and D/F for predicting the risk of death from cardiac causes at 90 s after PCI in patients with acute STEMI were 0.896 (95% CI 0.850 to 0.932) and 0.884 (95% CI 0.837 to 0.922), respectively. The values were 59.50 μg/L and 0.46 respectively ( P<0.05); the mortality rates of acute STEMI patients in LpPLA2>59.50 μg/L and D/F>0.46 groups after PCI were higher than those in LpPLA2≤59.50 μg/L group and D/F≤0.46 group ( P<0.05); age (>66 years), left ventricular ejection fraction (LVEF) (≤45%), LpPLA2 (>59.50 μg/L), D/F (>0.46), N-terminal brain natriuretic peptide precursor (>1.55 μg/L) and fasting blood glucose (>7.00 mmol/L) were the risk of death from cardiac causes at 90 d after PCI in patients with acute STEMI ( P<0.05); when the risk thresholds were >0.24, the nomogram model could provide significant additional net clinical benefit. Conclusions:Lp-PLA2 and D/F are closely related to the prognosis of patients with acute STEMI after PCI, and the nomogram model constructed in combination with other clinical indicators can effectively predict the risk of death within 90 d after PCI.

OBJECT IVE To evaluate the application effect of the whole cour se medication management mode led by pharmacists in rheumatic immune diseases. METHODS A total of 122 patients treated with tacrolimus or cyclosporine in the department of rheumatology and immunology of Wuhan No. 1 Hospital from 2018 to 2020 were selected as the study subjects. Among them ，44 cases in the control group were under the traditional supervision mode ；78 patients in the observation group adopted the whole course medication management mode led by pharmacists ，that was ，individual pharmacists and specialist clinical pharmacists cooperated and led ，and not only participated in the whole process of drug treatment but also involved in the whole process of therapeutic drug monitoring （TDM）. On the basis of the control group ，the division of labor and cooperation among medical，pharmaceutical and nursing parties were strengthened ，and the homogeneous supervision was carried out for the outpatients and inpatients from admission to discharge . The daily dose of medication ，the rate of reaching the standard of blood drug concentration ，the incidence of problematic samples （the sample was calculated by the number of times ），the average hospitalization days ，the re-admission rate within 6 months after discharge ，the medication compliance score and the patient ’s satisfaction rate were compared between the two groups. RESULTS In the control group ，53 times of TDM were performed ， including 18 times of tacrolimus monitoring and 35 times of cyclosporine monitoring ；in the observation group ，123 timesof TDM were performed ，including 55 times of tacrolimus monitoring and 68 times of cyclosporine monitoring. The daily dose of tacrolimus ，the daily dose of cyclosporine ，the rate of reaching the standard of cyclosporine blood drugconcentration，the inc idence of problematic samples ，the rate of re-admission within 6 months after discharge ， the medication compliance score and the patient ’s satisfaction rate in the observation group were significantly better than those in the control group （P＜0.05）. CONCLUSIONS It can effectively improve the effect of the quality of pharmaceutical care to implement whole course and homogeneous medication management led by pharmacists and provide precise drug guidance for patients with rheumatic and immune diseases.