Humans ; Myocardial Infarction ; physiopathology ; Myocardial Reperfusion Injury

Objective:To observe the clinical efficacy of acupuncture with medication for post-stroke depression.Methods:A total of 96 patients with post-stroke depression were randomized into an observation group and a control group,with 48 cases in each group.The control group was treated with oral fluoxetine hydrochloride capsules,and the observation group was treated with acupuncture on the basis of the treatment of the control group.After 6 months of treatment,the traditional Chinese medicine (TCM) symptom scores,and Hamilton depression scale (HAMD) component scores and total scores of the two groups before and after treatment were observed,and the clinical efficacy and adverse reaction rate were compared between the two groups.Results:The total effective rate was 95.8％ in the observation group and 83.3％ in the control group,and the difference between the two groups was statistically significant (P＜0.05).After treatment,the intra-group differences in TCM symptom scores and HAMD score of both groups were statistically significant (all P＜0.01).In the observation group,the scores of indifferent expression,emotional restlessness,and sentimentality in the TCM symptoms were statistically different from those in the control group (all P＜0.01).The scores of desperate factor and sleep disorder factor and total score in HAMD in the observation group were significantly different from those in the control group (all P＜0.01).The incidence of adverse reactions was 6.3％ in the observation group and 4.2％ in the control group,and the difference was not significant between the two groups (P＞0.05).Conclusion:Acupuncture plus medication is an effective method for post-stroke depression,and it can further improve the patient's bad mood.

OBJECTIVETo discuss the effect of taurine (Tau) on the proliferation of hypoxia-induced pulmonary artery smooth muscle cells (PASMCs), and study whether the extracellular signal-regulated kinase 1/2 (ERK1/2) signal pathway participated in the Tau-inhibited PASMC proliferation process and the possible molecular mechanism.

METHODThe primary culture was performed for PASMCs in rats. The second to fifth generations were adopted for the experiment. The Tau concentration was 80 mmol x L(-1). The concentration of ERK1/2 blocker (PD98059) was 50 micromol x L(-1). The drug administration time was 24 h. The effect of Tau on the PASMC proliferation was detected by MTT assay, immunofluorescence staining method and western blot under different conditions. The PASMCs were growing were divided into four groups: the normoxia group, the normoxia + Tau group, the hypoxia group and the hypoxia + Tau group. The Western blot was adopted to detect whether the ERK1/2 signal pathway participated in the Tau-inhibited PASMC proliferation process. Subsequently, the PASMCs were divided into five groups: the normoxia group, the hypoxia group, the hypoxia + Tau group, the hypoxia + Tau + PD98059 group and the hypoxia + PD98059 group.

RESULTHypoxia could induce the PASMC proliferation. Under the conditions of normoxia, Tau had no effect on the PASMC proliferation. Under the conditions of normoxia and hypoxia, Tau had no effect on the expression of the tumor necrosis factor-alpha (TNF-alpha) among PASMCs. Tau could reverse the expression up-regulation of hypoxia-induced proliferative cell nuclear antigen (PCNA) (P < 0.01) and Cyclin A (Cyclin A) (P < 0. 05). Under the conditions of normoxia, Tau had no effect on the expression of phosphoryl extracellular signal-regulated kinase 1/2 (p-ERK1/2). Hypoxia could up-regulate the p-ERK1/2 expression (P < 0.01). Tau could reverse the up-regulation of the hypoxia-induced p-ERK1/2 expression(P < 0.01). Both PD98059 and Tau could inhibit the up-regulated expressions of PCNA, Cyclin A and p-ERK1/2. According to the comparison between the single addition of Tau and PD98059 under conditions of hypoxia, the hypoxia + Tau + PD98059 group showed more significant down-regulation in the expressions of PCNA, Cyclin A and p-ERK1/2.

CONCLUSIONTau could inhibit the hypoxia-induced PASMC proliferation, and may regulate it through ERK1/2 pathway.

Animals ; Cell Hypoxia ; drug effects ; Cell Proliferation ; drug effects ; Cells, Cultured ; MAP Kinase Signaling System ; drug effects ; Myocytes, Smooth Muscle ; cytology ; drug effects ; metabolism ; Oxygen ; metabolism ; Pulmonary Artery ; cytology ; drug effects ; metabolism ; physiopathology ; Rats ; Rats, Wistar ; Taurine ; pharmacology ; Tumor Necrosis Factor-alpha ; genetics ; metabolism

Aged, 80 and over ; Angioplasty, Balloon, Coronary ; methods ; Brachial Artery ; Humans ; Intra-Aortic Balloon Pumping ; Male

Adult ; Female ; Humans ; Myocardial Infarction ; complications ; Pregnancy ; Pregnancy Complications, Cardiovascular

Drug-Eluting Stents ; adverse effects ; Humans ; Male ; Middle Aged ; Thrombosis ; etiology

Objective To explore the expression of PRR11(Proline-rich protein 11) in human osteosarcoma and investigate the effect of PRR11 on the proliferation of human osteosarcoma cells.Methods Immunohistochemical staining was applied to detect the PRR11 expression in 75 cases of osteosarcoma and corresponding normal tissues.Western blotting was used to examine PRR11 protein expression levels in osteosarcoma cell lines.We used siRNA to knock down the expression of PRR11 and tested the effects of PRR11 down-regulation on the proliferation in SaOS2 cells.Results PRR11 was overexpressed in osteosarcoma specimens compared to their paired normal tissues,the over expression rate of PRR11 in osteosarcoma and corresponding paracancerous tissues were 76％(57/75) and 9.33％(7/75) with statistical difference(P<0.05).The high expression of PRR11 was correlated with tumor pathological grade and lymphatic metastasis(P<0.05).PRR11 was expressed in 4 osteosarcoma cell lines which were SaOS2,143B,U2OS and MG63 respectively,the expression was highest in SaOS2 cells.Silencing PRR11 inhibited cell growth as compared with control cells(P<0.05).Conclusion PRR11 is overexpression in human osteosarcoma and promotes its progression by enhancing proliferation.The increased expression of PRR11 in osteosarcoma is a new target for treatment and early diagnosis of human osteosarcoma patients.

OBJECTIVE To investigate the expression of PTEN and VEGF gene in laryngeal squamous cell carcinoma and their clinical significance. METHODS The expression of PTEN and VEGF gene were examined by using immunohistochemical S-P staining method in 10 cases of normal tissues, 20 cases of para-tumor tissues and 60 cases of LSCC. RESULTS The positive rates of PTEN in normal tissues, para-tumor tissues and LSCC were 100.0 %, 95.0 %, and 70.0 % respectively (P＜0.05),and VEGF protein showed positive expression of 20.0 %,50.0 %,73.3% in normal, para-tumor and LSCC tissues with statistical significance(P＜0.05), In LSCC, the expression of PTEN and VEGF was positively correlated with TNM stage, differentiation of tumor, cervical and distant metastasis of lymph node, 3-year survive rate of patients(P＜0.05),No significant association was observed in expression of PTEN and VEGF with tumor location,patient's age and sex(P＞0.05). Spearman correlation analysis revealed that PTEN was negatively correlated with VEGF expression(?=-0.3948, P=0.0018). CONCLUSION The aberrant expression of PTEN and VEGF may play a role in occurrence, progression and metastasis of LSCC.

Objective: To study the chemical constituents in the stems of Trigonostemonlutescens. Methods:Silica gel column chromatography and semi-preparative high performance liquid chromatography were used for separation and purification. The structures were identified by NMR, IR, MS and other spectral techniques. Toxicity of compounds 1-4 on human lung cancer A549 cells, cervical cancer Hela cells and breast cancer MCF-7 cells was determined by the MTT method. Results: Four lignans were isolated from the stems of T. lutescens. The structures were identified as 5,5'-dimethoxylclemaphenol A (1), syringaresinol (2), lirioresinol B dimethyl ether (3) and clemaphenol A (4). Conclusion:Compound1 is a new compound, and compounds 2-4 are isolated from this genus for the first time. Compounds 1-4 have certain cytotoxic activity on A549, HeLa and MCF-7 human tumor cells.

ObjectiveTo investigate the mechanism of cerebral white matter damage in premature rats induced by intrauterine infection.Methods30 mature pregnant Wistar-Imamichi rats were divided into the experimental group (n=18) and control group (n=12). The rats of the experimental group were injected with lipopolysaccharide (LPS) 0.2 mg/kg in abdomen on 15th and 16th day after gestation. Those of the control group were injected with distilled water in equal volume. 45 premature rats born in the experimental group and 45 full-term rats born in the control group were tested with RIA for interleukin-6 (IL-6). The brain tissues of another 47 premature rats and 41 full-term rats were stained with HE method. Finally water content in brain tissue were tested in 50 premature rats and 50 full-term rats.ResultsIL-6 concentration of brain tissue of the premature rats in the experimental group was significantly higher than that in the control group ( P<0.01); and water content of the premature rats' brain was also higher than that of the full-term rats ( P<0.01). The edema of periventricular white matter, loose neuropil, decreased cell numbers, broaden intercellular space, and cell swelling and rupture were found in the brain tissue of the premature rats, no abnormal form and structure were found in the control group.ConclusionWhite matter damage of premature rats can be caused by endotoxin, and accompanied by IL-6 and water contents increasing.