Objective: To explore the peri-operative treatment and 3 years post-operative outcome in patients with rheumatic mitral valve stenosis and small left ventricle. Methods: A total of 152 patients with rheumatic mitral valve stenosis and severe pulmonary hypertension were studied. According to left ventricular end diastolic index (LVEDI) value, the patients were divided into 2 groups: Small left ventricle (Small) group, the patients with LVEDI value≤60 mm, n=67 and Non-small left ventricle (Non-small) group, the patients with LVEDI value>60 mm,n=85. Peri-operative condition and follow-up parameters were compared between 2 groups. Results: Compared with Non-small group, Small group had increased pre-operative CVP, SPAP and decreased LVEDV, LVEDVI and RVEF at admission, all P<0.05. All patients had liver damage at admission, the indexes (except alkaline phosphatase) were higher in Small group than Non-small group, and the function was recovered prior operation by proper treatment. The immediate post-operative SPAP in Small group and Non-small group were (67.3.1±23.4) mmHg and (61.3±26.9) mmHg, P>0.05. There were 52 severe pulmonary hypertension patients received iloprost inhalation, their SPAP was decreased than non-inhalation patients at incision closing; SPAP was lower in Small group inhalation patients than Non-small group inhalation patients, all P<0.05. Post-operative LVEDVI was lower and SPAP was higher in Small group than Non-small group. At 3 years post-operation, LVEDVI, RVEF increased, NYHA classification decreased and 6MWT prolonged in both groups; while LVEDVI was lower and 6MWT was shorter in Small group than Non-small group, P<0.05. The median survival time at (3.7±1.6) years post-operation was shorter in Small group than Non-small group,P<0.05, while the mortality was similar between 2 groups (2.6% vs 2.0%),P>0.05. Conclusion: The patients with mitral valve stenosis and small left ventricle had the worse pre-operative condition and higher risk in surgery; peri-operative treatment could improve their cardiac and liver function, but they still had the shorter post-operative median survival time.

Objective To investigate the expression of lncRNA SENCR in aortic dissection(AD)tissues of AD patients and its effect on and mechanism in the proliferation apoptosis of human vascular smooth muscle cells(HVSMCs).Methods HE staining was done to detect the pathological changes of AD tissues.Fluorescence in situ hybridization(FISH)and RT-qPCR were used to determine the expression of SENCR in the AD tissue and HVSMCs and the expression of SENCR and miR-206 in the tissues,respectively.HVSMCs were cultured and trans-fected with pcDNA3.1-SENCR overexpression plasmids,or pcDNA3.1 blank plasmid.Then cell proliferation and apoptosis were detected by CCK-8 method and Annexin V/PI double staining flow cytometry assay,respectively.Double luciferase report verified the targeting relationship between SENCR and miR-206.Results SENCR was mainly located in the cytoplasm and nucleus of HVSMCs.Compared with the normal tissue,the expression of SENCR in the AD tissues was down-regulated(P＜0.01),but the expression of miR-206 was up-regulated(P＜0.01).Overexpressed SENCR decreased the cell proliferation of HVSMCs(P＜0.01),but significantly increased the cell apoptosis of HVSMCs(P＜0.01).SENCR could target and negatively regulate miR-206.Conclusion The expression of SENCR is down-regulated in AD tissues,and overexpressed SENCR may inhibit the proliferation and promote the apoptosis of HVSMCs by targeting down-regulated miR-206.

OBJECTIVE To investigate the mechanisms of rutin in alleviating depressive symptoms associated with premenstrual dysphoric disorder （PMDD） characterized by liver qi stagnation syndrome. METHODS Network pharmacology was employed to identify the intersecting targets of action between PMDD and rutin. A protein-protein interaction network was constructed to screen core targets， followed by gene ontology （GO） and Kyoto Encyclopedia of Genes and Genomes （KEGG） pathway enrichment analysis. Molecular docking simulations validated rutin’s binding affinity to core targets. The bilateral ovaries of female Wistar rats were removed， followed by artificial hormone induction. The rats were then randomly divided into normal group （10 rats） and modeling group （50 rats）. PMDD rat model with liver qi stagnation syndrome was established via restraint stress. The successfully modeled rats were further divided into model group， fluoxetine group （positive control） and rutin group， with 12 rats in each group. The corresponding drug solutions or water were administered by gavage at 9：00 a.m. every day， continuing for two estrous cycles. The open-field test， forced swimming test and Y-maze test were utilized to evaluate the effects of rutin on the behavioral indexes of model rats. Additionally， the density of neuronal dendritic spines in the hippocampal tissues of the rats was observed. Serum brain-derived neurotrophic factor （BDNF） levels and the expressions of BDNF， tyrosine kinase receptor type B （TrkB）， synuclein （Syn）， and postsynaptic density protein 95 （PSD95） in hippocampal tissues were quantified， respectively. RESULTS Network pharmacology and molecular docking revealed the core targets through which rutin ameliorated PMDD characterized by liver qi stagnation syndrome included BDNF， TrkB， PSD65， Syn， etc. The results of experimental validation demonstrated that rutin significantly increased the spontaneous alternation behavior scores of PMDD model rats with liver qi stagnation syndrome during the non-receptive phase， shortened their immobility time during the forced swimming test， and enhanced the density of neuronal dendritic spines in the hippocampal tissues. Additionally， rutin upregulated the levels of serum BDNF and the protein expressions of BDNF， TrkB and Syn in the hippocampal tissues （P＜0.05）. However， it had no significant effect on the above indexes in model rats during the receptive phase （P＞0.05）. CONCLUSIONS Rutin ameliorates depressive symptoms， enhances spatial memory capabilities， and reduces neuronal damage in PMDD model rats with liver qi stagnation syndrome. These effects may be associated with the activation of BDNF/TrkB signaling pathway and upregulation of Syn protein expression.