Mouse Tissue type Plasminogen Activator ELISA Kit

In utero alcohol exposure can induce severe neurodevelopmental disabilities leading to long-term behavioral deficits. Because alcohol induces brain defects, many studies have focused on nervous cells. However, recent reports have shown that alcohol markedly affects cortical angiogenesis in both animal models and infants with fetal alcohol spectrum disorder (FASD). In addition, the vascular system is known to contribute to controlling gamma-aminobutyric acid (GABA)ergic interneuron migration in the developing neocortex. Thus, alcohol-induced vascular dysfunction may contribute to the neurodevelopmental defects in FASD. The present study aimed at investigating the effects of alcohol on endothelial activity of pial microvessels. Ex vivo experiments on cortical slices from mouse neonates revealed that in endothelial cells from pial microvessels acute alcohol exposure inhibits both glutamate-induced calcium mobilization and activities of matrix metalloproteinase-9 (MMP-9) and tissue plasminogen activator (tPA). The inhibitory effect of alcohol on glutamate-induced MMP-9 activity was abrogated in tPA-knockout and Grin1(flox)/VeCad(cre) mice suggesting that alcohol interacts through the endothelial NMDAR/tPA/MMP-9 vascular pathway. Contrasting with the effects from acute alcohol exposure, in mouse neonates exposed to alcohol in utero during the last gestational week, glutamate exacerbated both calcium mobilization and endothelial protease activities from pial microvessels. This alcohol-induced vascular dysfunction was associated with strong overexpression of the N-methyl-D-aspartate receptor subunit GluN1 and mispositioning of the Gad67-GFP interneurons that normally populate the superficial cortical layers. By comparing several human control fetuses with a fetus chronically exposed to alcohol revealed that alcohol exposure led to mispositioning of the calretinin-positive interneurons, whose density was decreased in the superficial cortical layers II-III and increased in deepest layers. This study provides the first mechanistic and functional evidence that alcohol impairs glutamate-regulated activity of pial microvessels. Endothelial dysfunction is characterized by altered metalloproteinase activity and interneuron mispositioning, which was also observed in a fetus with fetal alcohol syndrome. These data suggest that alcohol-induced endothelial dysfunction may contribute in ectopic cortical GABAergic interneurons, that has previously been described in infants with FASD.

The possible pathways of sugars transformation into 1,2-propanediol (PDO) have been studied, using new bifunctional catalysts for this catalytic multistep reaction. The catalysts are based on an acidic active phase (polyoxometalates, POMs) and a metallic function (Ru nanoparticles) supported over activated carbon (AC, SBET = 1190 m(2)/g). This support was loaded with 15 wt% of polyoxometalate, either phosphotungstic acid (TPA) or tungstosilicic acid (STA), while the amount of loaded ruthenium was close to 2 wt%. The catalytic materials were characterized by X-ray diffraction and electron microscopy techniques (SEM and TEM), while the surface active sites were evaluated using model reaction tests: cyclohexane dehydrogenation for metallic surface sites and isomerization of 3,3-dimethyl-1-butene for acid sites. For different sugars (sucrose, pentoses or hexoses) hydrogenation/hydrogenolysis using these catalysts in batch reactor was studied. The higher PDO selectivity was obtained in ethanol:water media and this study aims to establish the possible ways that sugars follow to achieve this transformation. The best catalytic material, 2%Ru-15%STA supported on AC, yields up to 50% of PDO selectivity when fructose is used as reactant, under moderate reaction conditions (413 K and 30 bar H-2).