Objective: To explore influence of urokinase on expression of soluble CD40 ligand (sCD40L) in patients with acute coronary syndrome (ACS).Methods: A total of 94 ACS patients diagnosed and treated in our hospital from Aug 2013 to Aug 2015 were selected.According to random number table, they were randomly and equally divided into routine treatment group and urokinase group (received small dose urokinase intravenous drip based on routine treatment group).Levels of sCD40L and cardiac troponin T (cTnT) before and after treatment, therapeutic effect and incidence rate of major adverse cardiovascular events (MACE) were measured and compared between two groups.Results: Compared with before treatment, there were significant reductions in levels of sCD40L and cTnT in both groups after treatment, P<0.01 all;compared with routine treatment group after treatment, there were significant reductions in levels of sCD40L [(2.92±0.36) ng/ml vs.(2.58±0.18) ng/ml] and cTnT [(0.10±0.02) μg/L vs.(0.04±0.01) μg/L] in urokinase group, P=0.013, 0.001 successively.Compared with routine treatment group, there was significant rise in total effective rate (76.6% vs.95.7%),and significant reduction in incidence rate of MACE (34.0% vs.4.3%) within six months in urokinase group (P<0.01 both).Conclusion: Urokinase can significantly inhibit expression of sCD40L and reduce release of cTnT, and improve therapeutic effect, and prevent major adverse cardiovascular events in patients with acute coronary syndrome.

Objective To investigate the effects of intervention of information literacy education on the feeling of uncertainty of patients with percutaneous coronary intervention.Methods A total of 228 cases of patients with percutaneous coronary intervention who were hospitalized during July 2010 to June 2012 were selected.The patients were divided into two groups by means of random numbers table:the experimental group (including 119 cases) and the control group (including 109 cases).The patients of the control group received traditional nursing intervention,while the patients of the experimental group received additional information literacy education intervention besides the traditional nursing.The change of feeling of uncertainty and state anxiety level of patients under two kinds of nursing interventions was analyzed and compared.Results The patients of the experimental group had high uncertainty level on the day of admission,(99.17-4.46) points.It was obviously higher than the total score (80) by 50％.Compared with that on the day of admission,the uncertainty level on the night before surgery and on the day of patient discharge significantly declined.The state anxiety level of the patients of the experimental group was (52.97±5.91) points,higher than the normative level of Chinese normal people.Compared with that on the day of admission,the state anxiety level on the night before surgery and on the day of patient discharge significantly declined,and it was lower than the normative level.Compared with those of the control group,the MUIS and SAI assessment of the experimental group on the night before surgery and the day of patient discharge obviously declined.Conclusions The information literacy education intervention was able to reduce the uncertainty level and state anxiety level of patients with percutaneous coronary intervention.Therefore,the nursing quality of patients was enhanced.

Objective To evaluate the effect of a vasoactive substance urotensin Ⅱ on the expression of type Ⅰ collagen and migration of human skin fibroblasts,and to explore the underlying mechanisms of signal transduction.Methods Fibroblasts were isolated from human foreskin tissues and subjected to primary culture.After a series of subculture,fibroblasts were classified into several groups to be treated with different concentrations (10-10 to 10-6 mol/L) of urotensin lⅡ for 24 hours,urotensin Ⅱ of 10-s mol/L for different durations (0,4,12,24 hours),or pretreated with PD98059 (a mitogen-activated protein kinase kinase inhibitor),nicardipine (a calcium channel blocker) and ciclosporin (a calcineurin inhibitor) of 10-5 mol/L respectively for 30 minutes followed by treatment with urotensin Ⅱ of 10-8 mol/L for 24 hours.The cells receiving no treatment served as the control.Subsequently,enzyme-linked immunosorbent assay was performed to determine the level of urotensin Ⅱ in the supernatant of fibroblasts,and Transwell assay to estimate the migration activity of fibroblasts.Statistical analysis was carried out by t test and analysis of variance.Results Urotensin Ⅱ promoted the expression of type Ⅰ collagen in a time-and concentrationdependent manner.The level of type Ⅰ collagen was increased by 21.2％ (P ＞ 0.05),52.2％ (P ＜ 0.05),84.4％ (P ＜0.05),83.6％ (P ＜ 0.05) and 77.1％ (P ＜ 0.05) in the supernatant of fibroblasts treated with 10-10,10-9,10-8,10-7 and 10-6 mol/L of urotensin Ⅱ for 24 hours respectively,by 23.2％ (P ＞ 0.05),69.5％ (P ＜ 0.05) and 84.1％ (P ＜0.05) in the supernatant of fibroblasts treated with urotensin Ⅱ of 10-8 mol/L for 4,12 and 24 hours respectively,compared with the untreated control fibroblasts.The migration activity was markedly enhanced in fibroblasts treated with urotensin Ⅱ of 10-8 mol/L for 24 hours compared with the control fibroblasts (P ＜ 0.05).PD98059,nicardipine and cyclosporin A inhibited the secretion of type Ⅰ collagen by 18.2％,15.9％ and 19.7％ respectively,and suppressed the migration of fibroblasts by 38.3％ (P ＜ 0.05),20.7％ (P ＜ 0.05) and 81.4％ (P ＜ 0.05) respectively in the groups receiving pretreatment compared with those treated with urotensin Ⅱ alone.Conclusions Urotensin Ⅱ can promote the secretion of type Ⅰ collagen by and migration of fibroblasts,which may be realized through the Ca2+,calmodulin kinase,and mitogen-activated protein kinase pathways.

Percutaneous coronary intervention(PCI) can effectively restore reperfusion of ischemic myocardium in patients with coronary artery disease.But currently PCI treatment is just available for a small proportion of the patients with coronary artery disease,so there was an insufficiency of PCI in patients with coronary artery disease.From the perspective of ethics,the reasons for the phenomenon and some feasible strategies for the problem are also analyzed in this paper.

Objective To explore the association between folic acid supplementation during periconcerptional period and congenital heart disease in newborns to provide scientific evidence for making intervening measures.Methods Using stratified random cluster sampling,a total of 30 counties were sampled from Shaanxi Province.A questionnaire survey was conducted among childbearing-aged women pregnant between January 2010 and November 2013.All of the included women had definite pregnancy outcomes and had signed the consent form.Logistic regression was performed to investigate the association between folic acid supplementation during pregnancy and congenital heart disease in newborns.Results In total,28 354 questionnaires were available for analysis.The overall prevalence of congenital heart disease among live-birth neonates in the present study was 7.3‰.The percentage of childbearing-age women who had taken folic acid supplementation during pregnancy was 64.4％,while only 17.2％ of them took folic acid according to the specification.Taking folic acid regularly during pregnancy was associated with a lower risk of congenital heart disease among the newborns (OR 0.502,95％ CI:0.279 0.902).The multiple-factor analysis results also showed that taking folic acid regularly during periconcerptional period could reduce the risk of congenital heart disease (adjusted OR=0.512,P=0.046) when we controlled the family background factors,mother factors and exposure risk factors during pregnancy.However,no association was found between irregularly taking folic acid during periconcerptional period and the risk of congenital heart disease.Conclusion Taking folic acid according to the specification during periconcerptional period (taking folic acid during 3 months before pregnancy to 3 months after pregnancy with a daily dose of 0.4mg for more than 90 days) may prevent congenital heart disease of newborns.

OBJECTIVES: In this study, we explored how adiponectin mediated urotensin II (UII)‍-induced tumor necrosis factor-‍α (TNF-‍α) and α‍-smooth muscle actin (α‍-SMA) expression and ensuing intracellular signaling pathways in adventitial fibroblasts (AFs). METHODS: Growth-arrested AFs and rat tunica adventitia of vessels were incubated with UII and inhibitors of signal transduction pathways for 1‍‒‍24 h. The cells were then harvested for TNF-α receptor (TNF-‍α-R) messenger RNA (mRNA) and TNF-‍α protein expression determination by reverse transcription-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA), respectively. Adiponectin and adiponectin receptor (adipoR) expression was measured by RT-PCR, quantitative real-time PCR (qPCR), immunohistochemical analysis, and cell counting kit-8 (CCK-8) cell proliferation experiments. We then quantified TNF-α and α-SMA mRNA and protein expression levels by qPCR and immunofluorescence (IF) staining. RNA interference (RNAi) was used to explore the function of the adipoR genes. To investigate the signaling pathway, we applied western blotting (WB) to examine phosphorylation of adenosine 5'-monophosphate (AMP)‍-activated protein kinase (AMPK). In vivo, an adiponectin (APN)‍-knockout (APN-KO) mouse model mimicking adventitial inflammation was generated to measure TNF-α and α‍-SMA expression by application of qPCR and IF, with the goal of gaining a comprehensive atlas of adiponectin in vascular remodeling. RESULTS: In both cells and tissues, UII promoted TNF-α protein and TNF-α-R secretion in a dose- and time-dependent manner via Rho/protein kinase C (PKC) pathway. We detected marked expression of adipoR1, T-cadherin, and calreticulin as well as a moderate presence of adipoR2 in AFs, while no adiponectin was observed. Globular adiponectin (gAd) fostered the growth of AFs, and acted in concert with UII to induce α-SMA and TNF-α through the adipoR1/T-cadherin/calreticulin/AMPK pathway. In AFs, gAd and UII synergistically induced AMPK phosphorylation. In the adventitial inflammation model, APN deficiency up-regulated the expression of α-SMA, UII receptor (UT), and UII while inhibiting TNF-‍α expression. CONCLUSIONS From the results of our study, we can speculate that UII induces TNF‍-‍α protein and TNF-‍α‍-R secretion in AFs and rat tunica adventitia of vessels via the Rho and PKC signal transduction pathways. Thus, it is plausible that adiponectin is a major player in adventitial progression and could serve as a novel therapeutic target for cardiovascular disease administration.
Mice ; Rats ; Animals ; Adventitia/metabolism* ; Tumor Necrosis Factor-alpha/metabolism* ; Calreticulin/metabolism* ; Vascular Remodeling ; AMP-Activated Protein Kinases/metabolism* ; Cells, Cultured ; RNA, Messenger/genetics* ; Inflammation