6-OHDA showed similar toxicity pattern in differentiated compared to undifferentiated NPCs. By evaluating the toxicity of MPP+ on MAP2ab(+) neurons derived from both mNPCs and sNPCs as well as tyrosine hydroxylase (TH)(+) dopaminergic cells from mNPCs, we found concentration-dependent cell death of all cell types with no increased vulnerability of TH+ cells. Primary TH+ neurons showed significantly higher vulnerability to MPP+. Together, we demonstrated stage-dependent vulnerability of NPCs towards dopaminergic neurotoxins,

but no selective vulnerability of NPC-derived TH+ dopaminergic cells towards MPP+. This cell system seems not suitable as a screening tool for selective dopaminergic toxicity. (C) 2008 Elsevier Inc. All rights reserved.”
“Sulfatide is abundantly expressed in various mammalian organs, including the intestines and trachea, in SB203580 datasheet which influenza A viruses (IAVs) replicate. However, the function of sulfatide in IAV infection remains unknown. Sulfatide is synthesized by two transferases, ceramide galactosyltransferase (CGT) and cerebroside sulfotransferase (CST), and is degraded by arylsulfatase A (ASA). In this study, we demonstrated that sulfatide enhanced Omipalisib solubility dmso IAV replication through efficient translocation of the newly synthesized IAV nucleoprotein

(NP) from the nucleus to the cytoplasm, by using genetically produced cells in which sulfatide expression was down-regulated by RNA interference against CST mRNA or overexpression of the ASA gene and in which sulfatide expression was up-regulated by overexpression of both the CST and CGT genes. Treatment of IAV-infected cells with an antisulfatide monoclonal antibody (MAb) or an anti-hemagglutinin (HA) MAb, which

blocks the binding of IAV and sulfatide, resulted in a significant reduction in IAV replication and accumulation of the viral NP in the nucleus. Furthermore, antisulfatide MAb protected mice against lethal challenge Selleck BMS-777607 with pathogenic influenza A/WSN/33 (H1N1) virus. These results indicate that association of sulfatide with HA delivered to the cell surface induces translocation of the newly synthesized IAV ribonucleoprotein complexes from the nucleus to the cytoplasm. Our findings provide new insights into IAV replication and suggest new therapeutic strategies.”
“Previous studies have suggested that prenatal exposure to nicotine is associated with abnormal development in fetuses, including fetal brain damage. The present study determined the effect of maternal administration of nicotine during different gestational periods on brain nicotine receptor subunits in fetal rats. Subcutaneous injections of nicotine in maternal rats from the early and middle gestation decreased fetal blood PO2, increased fetal blood PCO2 and hemoglobin, and decreased fetal brain weight. The nicotinic acetylcholine receptor (nAChRs) mRNA abundance in the fetal brain was significantly changed by prenatal treatment with nicotine during pregnancy.