The catalytic properties of modified Au/TiO₂ catalysts for low-temperature CO oxidation are affected by deactivation and reactivation after long-term storage and by redox treatments. The effect of these phenomena on the catalysts was studied by HRTEM, BET, SEM, FTIR CO, XPS and H₂ TPR methods. The main cause for the deactivation and reactivation of catalytic properties is the variation in the e...

Zorflex® activated carbon fibers (ACF), reference FM100 198B, are used before and after an oxidizing procedure with H3PO4 to study the adsorption of Pb 2+. The point of zero charge was determined for the modified and unmodified fiber giving values of 2.3 and 4.3, respectively. After oxidizing the ACF, the fiber showed to have a greater Pb2+ adsorption capacity in comparison with the unmodified ...

Natural killer (NK) cells play critical roles in host defense against tumors and intracellular pathogens. Various transcription factors have been reported to alter NK cell development, but the definitive transcriptional program governing this process is not well understood. Our laboratory has shown previously that the T-box transcription factors T-bet and Eomesodermin (Eomes) direct fate and fu...

Beyond its critical role in T cells, T-bet regulates the functions of APCs including dendritic cells and B cells, as well as NK cells. Given that recipient APCs are essential for priming allogeneic T cells and recipient NK or T cells are able to reject allogeneic donor cells, we evaluated the role of T-bet on the host in acute graft-versus-host disease (GVHD) using murine models of allogeneic b...

Preeclampsia is a leading cause of maternal and fetal morbidity/ mortality; however, the pathophysiological mechanisms are poorly understood. Vascular endothelial dysfunction in preeclampsia has been partially attributed to changes in endothelin-1 (ET-1). Several enzymes, including matrix metalloproteinases (MMPs, particularly MMP-2), cleave the inactive precursor bigET-1 (bET-1) to active ET-1...

Preeclampsia is a leading cause of maternal and fetal morbidity/ mortality; however, the pathophysiological mechanisms are poorly understood. Vascular endothelial dysfunction in preeclampsia has been partially attributed to changes in endothelin-1 (ET-1). Several enzymes, including matrix metalloproteinases (MMPs, particularly MMP-2), cleave the inactive precursor bigET-1 (bET-1) to active ET-1...

Preeclampsia is a leading cause of maternal and fetal morbidity/ mortality; however, the pathophysiological mechanisms are poorly understood. Vascular endothelial dysfunction in preeclampsia has been partially attributed to changes in endothelin-1 (ET-1). Several enzymes, including matrix metalloproteinases (MMPs, particularly MMP-2), cleave the inactive precursor bigET-1 (bET-1) to active ET-1...

Preeclampsia is a leading cause of maternal and fetal morbidity/ mortality; however, the pathophysiological mechanisms are poorly understood. Vascular endothelial dysfunction in preeclampsia has been partially attributed to changes in endothelin-1 (ET-1). Several enzymes, including matrix metalloproteinases (MMPs, particularly MMP-2), cleave the inactive precursor bigET-1 (bET-1) to active ET-1...

Preeclampsia is a leading cause of maternal and fetal morbidity/ mortality; however, the pathophysiological mechanisms are poorly understood. Vascular endothelial dysfunction in preeclampsia has been partially attributed to changes in endothelin-1 (ET-1). Several enzymes, including matrix metalloproteinases (MMPs, particularly MMP-2), cleave the inactive precursor bigET-1 (bET-1) to active ET-1...

Preeclampsia is a leading cause of maternal and fetal morbidity/ mortality; however, the pathophysiological mechanisms are poorly understood. Vascular endothelial dysfunction in preeclampsia has been partially attributed to changes in endothelin-1 (ET-1). Several enzymes, including matrix metalloproteinases (MMPs, particularly MMP-2), cleave the inactive precursor bigET-1 (bET-1) to active ET-1...