The influence of plasma 25-(OH) vitamin D levels in acute ST elevation myocardial infarction

Background: The preventive role of acute occurring of collateral circulation (AOCC) to infarct related artery (IRA) in patients presenting with acute ST-segment elevation myocardial infarction (STEMI) is well known. Therefore, we aimed to investigate whether there is an association between admission plasma 25-hydroxyvitamin D (25(OH)D3) levels and grade of collateralization in patients with STEMI. Methods: We prospectively included 369 STEMI patients within the first 12 h of symptoms onset. Patients were divided into two groups according to their Rentrop collateralization grade to IRA: poorly developed collateral (PDC) group (Rentrop grade ≤ 1, 272 patients) and well developed collateral (WDC) group (Rentrop grade ≥ 2, 97 patients). Results: We observed that AOCC grade to IRA was negatively correlated with high sensitive C-reactive protein (hs-CRP), N terminal pro-B-type natriuretic peptide (NT-proBNP), as well as peak troponin T levels, yet positively correlated with admission plasma 25(OH)D3 level (p < 0.05, for all). In multi¬variate analysis, 25(OH)D3 levels (OR 1.246, 95% CI 1.185–1.310, p < 0.001), together with hs-CRP, NT-proBNP, and peak troponin T levels were found independent predictors of AOCC to IRA in patients with acute STEMI. Conclusions: Admission level of plasma 25(OH)D3 levels together with cardiac risk biomarkers (troponin T, NT-proBNP, hs-CRP) are associated with collateralization grade to IRA in acute STEMI patients. In addition, 25(OH)D3 may be a promoter of AOCC in patients with acute STEMI

Morphine counteracts the effects of paclitaxel in triple-negative breast cancer cells

MDA.MB.231 cells were treated with paclitaxel in the presence or absence of morphine and examined for cell proliferation by the MTT assay. In addition, the effect of morphine on paclitaxel-induced apoptosis was investigated by flow cytometric assay and by the ratio of Bax/Bcl-2 mRNA expression levels with quantitative real-time (qRT)-PCR.Morphine significantly increased the proliferation of breast cancer cells at low concentrations (0.1-2.5 µM) but higher concentrations showed cytotoxic effect. Pre-treatment with 0.1 or 1 µM of morphine decreased the paclitaxel-induced cytotoxicity, the proportion of apoptotic cell, and the ratio of Bax/Bcl-2 mRNA expressions.Our data suggest that morphine promotes breast cancer cell viability at clinically relevant plasma concentrations and reduces the apoptotic effect of paclitaxel. This interaction may be very important in clinical settings; however, more studies are needed to explore the plausible mechanisms of interaction and to correlate such findings through&nbsp;in vivo&nbsp;animal studies as well as clinically.</h3