All rights reserved.”
“A long RT-PCR method was developed to amplify the norovirus genome. Starting from RNA extracted directly from clinical samples

and using broadly reactive primers, it can generate near full-length amplicons that allow for easy Y 27632 determination of the near complete genomic sequence. Two norovirus isolates from Toronto, Canada, in 2002 and 2005 were sequenced. This approach will facilitate molecular epidemiology studies of noroviruses. (c) 2008 Elsevier B.V. All rights reserved.”
“Posttraumatic stress disorder (PTSD) is one of the most common psychiatric disorders. Despite the extensive study of the neurobiological correlates of this disorder, the underlying mechanisms of PTSD are still poorly understood. Recently, a study demonstrated that dexamethasone (Dex), a synthetic glucocorticoid, can up-regulate p11, known as S100A10-protein which is down-regulated in patients with depression, (Yao et al., 1999; Huang et al., 2003) a common comorbid disorder in PTSD. These observations led to our hypothesis that traumatic stress may alter expression of p11 mediated through a glucocorticold receptor. Here, we demonstrate that inescapable tail shock increased both prefrontal cortical pi 1 mRNA levels and plasma corticosterone Selleckchem SN-38 levels in rats. We also found that Dex up-regulated p11 expression in SH-SY5Y cells through glucocorticoid

response elements (GREs) within the p11 promoter. This response was attenuated by either RU486, a glucocorticoid receptor (GR) antagonist

or mutating two of three glucocorticoid response elements (GRE2 and GRE3) in the p11 promoter. Finally, we showed that p11 mRNA levels were increased in postmortem prefrontal cortical tissue (area 46) of patients with PTSD. The data obtained from our work in a rat model of inescapable tail shock, a p11-transfected cell line and postmortem brain tissue from PTSD patients outline a possible mechanism by which p11 is regulated tuclazepam by glucocorticoids elevated by traumatic stress. Published by Elsevier Ltd on behalf of IBRO.”
“Congenital human cytomegalovirus infections are the major infectious cause of birth defects in the United States. How this virus crosses the placenta and causes fetal disease is poorly understood. Guinea pig cytomegalovirus (GPCMV) is a related virus that provides an important model for studying cytomegaloviral congenital transmission and pathogenesis. In order to facilitate genetic analysis of GPCMV, the 232 kb GPCMV genome was cloned as an infectious bacterial artificial chromosome (BAC). The BAC vector sequences were flanked by LoxP sites to allow efficient excision using Cre recombinase. All initial clones contained spontaneous deletions of viral sequences and reconstituted mutant viruses with impaired growth kinetics in vitro. The deletions in one BAC were repaired using Escherichia coli genetics.