Here we demonstrate by high temperature quench experiments that platinum and arsenic self-organize to nanoparticles, well before the melt has reached a Pt-As concentration at which discrete Pt arsenide minerals become stable phases. If all highly siderophile elements associate to nanophases in undersaturated melts, the distribution of the noble metals between silicate, sulphide and metal melts will be controlled by the surface properties of nano-associations, more so than by the chemical properties of the elements.”
“We have previously shown that immunization with SIV, SHIV-, or HA (influenza

hemagglutinin)-virus-like particles (VLPs) elicits a strong humoral immune response in mice. However, little is known about the action VLPs exert on immune effector cells, including B cells. In this study, we found that all three types of VLPs this website could directly bind and activate B cells in vitro. VLPs stimulated GSK1210151A purchase the proliferation

of B220(+)IgM(+)CD43(-)CD5(-) B2 cells and their differentiation to plasma cells that preferentially produce lgG2a antibodies. Up-regulation of Blimp-1, XBP-1, IRF4, and AID genes, which are responsible for class-switch recombination and somatic hypermutation, was observed in VLP-activated B2 cells. Stimulation of naive splenocytes with VLPs led to a high expression of IL-12, RANTES and MIP, the cytokine milieu that favors B cell differentiation into IgG2a secreting cells. VLP immunization of C57BL/6 click here mice corroborated our in vitro data showing enlarged germinal centers and expanded conventional B2 cells, but no

enlarged marginal zone B1 cells, in the spleen. Enhanced antigen-specific plasma cell formation, antibody production, and IgG2a class switching were found in VLP-immunized groups. The current study details the interaction between VLPs and B cells which result in preferential IgG2a antibody production following VLP immunization. (C) 2009 Elsevier Ltd. All rights reserved.”
“Schizophrenia patients exhibit increased hippocampal activity that is correlated with positive symptoms. Although the cause of this hippocampal hyperactivity has not been demonstrated, it likely involves a decrease in GABAergic signaling. Thus, we posit that restoring GABAergic function may provide a novel therapeutic approach for the treatment of schizophrenia. It has been demonstrated that transplanted GABAergic precursor cells from the medial ganglionic eminence (MGE) can migrate and differentiate into mature interneurons. Here, we demonstrate that ventral hippocampal MGE transplants can restore hippocampal function and normalize downstream dopamine neuron activity in a rodent model of schizophrenia. Furthermore, MGE transplants also reverse the hyper-responsive locomotor response to amphetamine.