Gene expression profiling identifies distinct molecular signatures in thrombotic and obstetric antiphospholipid syndrome.

Antiphospholipid antibodies (aPL) cause vascular thrombosis (VT) and/or pregnancy morbidity (PM). Differential mechanisms however, underlying the pathogenesis of these different manifestations of antiphospholipid syndrome (APS) are not fully understood. Therefore, we compared the effects of aPL from patients with thrombotic or obstetric APS on monocytes to identify different molecular pathways involved in the pathogenesis of APS subtypes.

A Functional Model of [Fe]-Hydrogenase.

[Fe]-Hydrogenase catalyzes the hydrogenation of a biological substrate via the heterolytic splitting of molecular hydrogen. While many synthetic models of [Fe]-hydrogenase have been prepared, none yet are capable of activating H2 on their own. Here, we report the first Fe-based functional mimic of the active site of [Fe]-hydrogenase, which was developed based on a mechanistic understanding.

Chemoselective Alkene Hydrosilylation Catalyzed by Nickel Pincer Complexes.

Chemoselective hydrosilylation of functionalized alkenes is difficult to achieve using base-metal catalysts. Reported herein is that well-defined bis(amino)amide nickel pincer complexes are efficient catalysts for anti-Markovnikov hydrosilylation of terminal alkenes with turnover frequencies of up to 83,000 per hour and turnover numbers of up to 10,000. Alkenes containing amino, ester, amido, ketone, and formyl groups are selectively hydrosilylated.

Autophagy and pancreatic β-cells.

Autophagy plays a key role in maintaining pancreatic β-cell homeostasis. Deregulation of this process is associated with loss of β-cell mass and function, and it is likely to be involved in type 2 diabetes development and progression. Evidence that modulation of autophagy may be beneficial to preserve β-cell mass and function is beginning to accumulate although the complexity of this process, the intricate link between autophagy and apoptosis, and the fine balance between the protective and the disruptive role of autophagy make it very difficult to develop interventional strategies.

Class II phosphoinositide 3-kinase C2alpha: what we learned so far.

More than fifteen years after the first identification of a class II isoform of phosphoinositide 3-kinase (PI3K) in Drosophila melanoǵaster this subfamily remains the most enigmatic among all PI3Ks. What are the functions of these enzymes? What are their mechanisms of activation? Which downstream effectors are specifically regulated by these isoforms? Are class I and class II PI3Ks redundant or do they control different intracellular processes? And, more important, do class II PI3Ks have a role in human diseases? The recent increased interest on class II PI3Ks has started providing some answers to these questions but still a lot needs to be done to completely uncover the contribution of these enzymes to physiological processes and possibly to pathological conditions. Here we will summarise the recent findings on the alpha isoform of mammalian class II PI3Ks (PI3K-C2α ) and we will discuss the potential involvement of this enzyme in human diseases.