Karger AG, Basel.”
“Changes in the interactions between intestinal cells and their surrounding environment during virus infection have not been well documented. The growth and survival of intestinal

epithelial cells, the main targets of rotavirus infection, are largely dependent on the interaction of cell surface integrins with the extracellular matrix. In this study, we detected alterations in cellular integrin expression following rotavirus infection, identified the signaling components required, and analyzed Selleckchem GDC-0994 the subsequent effects on cell binding to the matrix component collagen. After rotavirus infection of intestinal cells, expression of alpha 2 beta 1 and beta 2 integrins was up-regulated, whereas that of alpha V beta 3, alpha V beta 5, and alpha 6 beta 1 integrins, if present, was down-regulated. This differential regulation of integrins was reflected

at the transcriptional level. It was unrelated to the use of integrins as rotavirus receptors, as both integrin-using and integrin-independent viruses induced integrin regulation. Using pharmacological agents that inhibit kinase activity, integrin regulation was shown to be dependent on phosphatidylinositol 3-kinase (PI3K) but independent of the activities of the mitogen-activated protein kinases p38 and ERK1/2, and cyclooxygenase-2. Replication-dependent activation of the PI3K/Akt pathway was observed following infection of intestinal and nonintestinal cell lines. Rotavirus activation of PI3K was important for regulation of alpha 2 beta 1 expression. Blockade

of integrin regulation Daporinad research buy by PI3K inhibition led to decreased adherence of infected intestinal cells to collagen and a concomitant decrease in virus titer. These findings indicate that rotavirus-induced PI3K activation causes regulation of integrin expression in intestinal cells, leading to prolonged adherence of infected cells to collagen and increased virus production.”
“Impaired working memory processing is one of the broad range of cognitive deficits in patients with Alzheimer’s disease (AD). We aimed to elucidate the differences in brain activities involved in the process of working memory between AD patients and healthy comparison selleck chemical subjects. Twelve patients with AD were recruited along with 12 healthy volunteers as a comparison group. Functional magnetic resonance imaging was employed to assess cortical activities during the performance of a 1-back working memory paradigm using the Korean alphabet as mnemonic content. Subsequently, the difference in neural activities between the 2 groups was analyzed. The AD group performed the tasks with reduced accuracy. Group comparison analysis revealed that the AD group showed decreased brain activity in the left frontal pole ( Brodmann area, BA, 10), the left ventrolateral prefrontal cortex (BA47), the left insula (BA13) and the right premotor cortex (BA6) compared to the control group.