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https://www.selleckchem.com/products/spautin-1.html Open comments from respondents further revealed that, although indicators which indicate openness, transparency, and quality (e.g., publishing open access, publishing negative findings, sharing data, etc.) should ultimately be valued more in research assessments, the resources and support currently in place were insufficient to allow researchers to endorse such practices. In other words, current research assessments are inadequate and ignore practices which are essential in contributing to the advancement of science. Yet, before we change the way in which researchers are being assessed, supporting infrastructures must be put in place to ensure that researchers are able to commit to the activities that may benefit the advancement of science. To determine the direct effect of pravastatin on angiogenesis and to study the interaction between pravastatin and maternal sera from women with early- or late-onset pre-eclampsia (PE), intrauterine growth restriction, or healthy pregnancy. We collected 5 maternal serum samples from each group. The effect of pravastatin on angiogenesis was assessed with and without maternal sera by quantifying tubule formation in a human-based in vitro assay. Pravastatin was added at 20, 1,000, and 8,000 ng/mL concentrations. Concentrations of angiogenic and inflammatory biomarkers in serum and in test medium after supplementation of serum alone and with pravastatin (1,000 ng/mL) were measured. Therapeutic concentration of pravastatin (20 ng/mL) did not have significant direct effect on angiogenesis, but the highest concentrations inhibited angiogenesis. Pravastatin did not change the levels of biomarkers in the test media. There were no changes in angiogenesis when therapeutic dose of pravastatin was added with maternal sera, but there was a trend to wide individual variation towards enhanced angiogenesis, particularly in the early-onset PE group. At therapeutic concentration, pravastatin alone

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