Combined antihypertensive and statin therapy for the prevention of cardiovascular events in patients with hypertension without complications: protocol for a systematic review and meta-analysis.

INTRODUCTION: High blood pressure (BP) affects over 40% of adults over the age of 25 worldwide and is the leading global risk factor for death or disability. Hypertension is also the most important risk factor for endovascular atherosclerosis, which, when combined with other cardiovascular risk factors, leads to atherosclerotic cardiovascular disease (ASCVD). Statins are one of the most widely used drugs for the prevention of ASCVD. The recently announced study of Heart Outcomes Prevention Evaluation-3 suggests that cholesterol-lowering agents combined with antihypertensive therapy can prevent cardiovascular events and reduce the combined endpoint. We plan to conduct a systematic review and meta-analysis to evaluate whether combined antihypertensive and statin therapy is more beneficial than antihypertensive therapy alone in patients with hypertension without complications. METHODS AND ANALYSIS: We will perform a comprehensive search for randomised controlled trials evaluating combined antihypertensive and statin therapy for the treatment of patients with hypertension. The following English electronic databases will be searched: The Cochrane Library, EMBASE and PubMed. Outcomes will be categorised as short-term (≤6 months) or long-term (>6 months). When evaluating the effects of combined antihypertensive and statin therapy, a short-term outcome is usually defined as a change in BP or lipid levels, while a long-term outcome is usually defined as cardiovascular benefits or risks. The data screening and extraction will be conducted by two different reviewers. The quality of the RCTs will be assessed according to the Cochrane handbook risk of bias tool. ETHICS AND DISSEMINATION: This review does not require ethics approval and the results of the meta-analysis will be submitted to a peer-review journal. PROSPERO REGISTRATION NUMBER: CRD42017071935.

Competence of clinical teachers: A survey on perception of masters of nursing specialist postgraduates, their clinical teachers, and head nurses.

OBJECTIVES: To explore the current admittance situation of clinical teachers for masters of nursing specialist (MNS) postgraduates and to test the competence of clinical teachers in self-evaluation and other evaluations. METHODS: In this cross-sectional study, using a random number table, we chose 80 MNS postgraduates under clinical practice, their clinical teachers, and head nurses each from six hospitals in Hunan and Guangdong. The participants were tested on the basis of the Clinical Teachers' Competence Inventory of MNS Postgraduates. The competences of clinical teachers were evaluated by the three groups of participants. RESULTS: The aggregated scores of teacher competence as evaluated by the MNS postgraduates (181.33 ± 24.95) were lower than those assigned by both clinical teachers (190.75 ± 24.30) and their head nurses (198.53 ± 18.90), with significant differences in all dimensions except for clinical managing ability. The five highest rated items from all participants focused on the teachers' clinical nursing ability, and the five lowest rated items were mainly about their clinical research ability. CONCLUSION: The evaluation from MNS postgraduates is obviously lower than the self-evaluation of clinical teachers, and all participants are aware of the deficiency in research ability of the teachers. Thus, the admittance and examination of clinical teachers should be controlled strictly. Training should be carried out immediately to strengthen their comprehensive abilities, especially their research ability.

Mesenchymal stem cells promote pancreatic adenocarcinoma cells invasion by transforming growth factor-ß1 induced epithelial-mesenchymal transition.

Mesenchymal stem cells (MSCs) could be ideal delivery vehicles for antitumor biological agents in pancreatic adenocarcinoma (PA). While the role of MSCs in tumor growth is elusive. Inflammation is an important feature of PA. In this study, we reported that MSCs pre-stimulated with the combination of TNF-α and IFN-γ promote PA cells invasion. The invasion of PA cell lines were evaluate by wound healing assay and transwell assay in vitro and liver metastasis in nude mice. We observed MSCs pre-stimulated with the combination of TNF-α and IFN-γ promoted PA cells invasion in vitro and in vivo. Consistent with MSCs promoting PA cells invasion, PA cells were found undergo epithelial-mesenchymal transition (EMT). We demonstrated that MSCs pre-stimulated with both of TNF-α and IFN-γ provoked expression transforming growth factor-ß1 (TGF-ß1). MSCs promoting EMT-mediated PA cells invasion could be reversed by short interfering RNA of TGF-ß1. Our results suggest that MSCs could promote PA cells invasion in inflammation microenvironment and should be cautious as delivery vehicles in molecular target therapy.

Upregulation of Sestrin2 expression protects against macrophage apoptosis induced by oxidized low-density lipoprotein.

Sestrin2 is involved in a different cellular response to stress conditions. However, the function of Sestrin2 in the cardiovascular system remains unknown. In the present study, we tested whether Sestrin2 has a beneficial effect on macrophage cell apoptosis induced by oxidized low-density lipoprotein (oxLDL). We found that oxLDL induces expression of Sestrin2 in RAW264.7 cells in a time-dependent and dose-dependent manner. We also found that knockdown of Sestrin2 using small RNA interference promotes cell apoptosis and reactive oxygen species production induced by oxLDL. In addition, our results show that the c-Jun NH(2)-terminal kinase (JNK)/c-Jun pathway is activated by oxLDL. Inhibiting the activity of the JNK pathway abolishes the increase of Sestrin2 induced by oxLDL. These findings suggest that the inductive effect of Sestrin2 is mediated by the JNK/c-Jun pathway. Our results indicate that the induction of Sestrin2 acts as a compensatory response to oxLDL for survival, implying that stimulating expression of Sestrin2 might be an effective pharmacological target for the treatment of lipid-related cardiovascular diseases.