A subsequent occurrence of MI, stroke, and cardiovascular death, as well as a combined cardiovascular outcome, was ascertained.
RESULTS: In analysis 1, women with preeclampsia or eclampsia were at significantly lower risk for combined cardiovascular outcome with all deaths (frequency of outcome 16.7%) and with cardiovascular deaths (10.6%) compared with women without preeclampsia or eclampsia after a first stroke
(33.8% and 23.5%, respectively). In analysis 2, women with preeclampsia or eclampsia and a first stroke during admission were at significantly higher risk of all death (11.1%) and the combined cardiovascular outcome with all deaths (11.1%) compared with women with preeclampsia or eclampsia without a stroke (1.9% and 2.7%, respectively) during that admission.
CONCLUSION: click here PX-478 concentration Our study indicates
that preeclampsia or eclampsia not complicated by MI or stroke during pregnancy may not confer a very high risk for subsequent MI and stroke in up to 16 years of follow-up. Our data suggest that other known risk factors put women at greater risk for stroke than preeclampsia or eclampsia complicated by a stroke. (Obstet Gynecol 2012; 120:823-31) DOI:http://10.1097/AOG.0b013e31826ae78a”
“During their development and administration, protein-based drugs routinely display suboptimal therapeutic efficacies due to their poor physicochemical and pharmacological properties. These innate liabilities have driven the development of molecular strategies to improve the therapeutic behavior of protein drugs. Among
the currently developed approaches, glycoengineering is one of the most promising, because it has been shown to simultaneously afford improvements in most of the parameters necessary for optimization of in vivo efficacy while allowing for targeting to the desired site of action. These include increased in vitro and in vivo molecular stability (due to reduced oxidation, cross-linking, XMU-MP-1 clinical trial pH-, chemical-, heating-, and freezing-induced unfolding/denaturation, precipitation, kinetic inactivation, and aggregation), as well as modulated pharmacodynamic responses (due to altered potencies from diminished in vitro enzymatic activities and altered receptor binding affinities) and improved pharmacokinetic profiles (due to altered absorption and distribution behaviors, longer circulation lifetimes, and decreased clearance rates). This article provides an account of the effects that glycosylation has on the therapeutic efficacy of protein drugs and describes the current understanding of the mechanisms by which glycosylation leads to such effects.