e., greater activity during the resting state than during an attention-demanding cognitive task. The default system consists mainly of the medial cancer metabolism inhibitor prefrontal and medial parietal areas. It has been proposed that this default activity is concerned with internal thought processes. Here, I first describe activities observed in the human default
system measured by several methods, in relation task performance, development, aging and psychiatric disorder. I will then introduce recent nonhuman primate studies that indicate correlated low-frequency spontaneous brain activity within the default system, high metabolic levels in these medial brain areas during rest and task-induced suppression of neuronal activity in the medial parietal area. Furthermore, I will present our data in which we found selleckchem task-induced deactivation in the monkey default system, and will examine similarities and differences in default activity between the human and nonhuman primate. Finally. I will discuss the functional significance of the default system and consider the possibility of internal thought processes in the
monkey. (C) 2011 Elsevier B.V. All rights reserved.”
“BACKGROUND. Compartment-specific epithelial and stromal expression of the secreted glycoprotein Dickkopf-related protein (Dkk)-3 is altered in age-related proliferative disorders of the human prostate. This study aimed to determine the effect of Dkk-3 on prostate stromal remodeling that is stromal proliferation, fibroblast-to-myofibroblast differentiation and expression of angiogenic GNS-1480 mouse factors in vitro.\n\nMETHODS. Lentiviral-delivered overexpression and shRNA-mediated knockdown of DKK3 were applied to primary human prostatic stromal cells (PrSCs). Cellular proliferation was analyzed by BrdU incorporation ELISA. Expression of Dkk-3, apoptosis-related genes, cyclin-dependent kinase inhibitors and angiogenic factors were analyzed by qPCR, Western blot analysis or ELISA. Fibroblast-to-myofibroblast differentiation was monitored by smooth muscle cell actin and insulin-like growth factor binding protein
3 mRNA and protein levels. The relevance of Wnt/-catenin and PI3K/AKT signaling pathways was assessed by cytoplasmic/nuclear -catenin levels and phosphorylation of AKT.\n\nRESULTS. Knockdown of DKK3 significantly attenuated PrSC proliferation as well as fibroblast-to-myofibroblast differentiation and increased the expression of the vessel stabilizing factor angiopoietin-1. DKK3 knockdown did not affect subcellular localization or levels of -catenin but attenuated AKT phosphorylation in PrSCs. Consistently the PI3K/AKT inhibitor LY294002 mimicked the effects of DKK3 knockdown.\n\nCONCLUSIONS. Dkk-3 promotes fibroblast proliferation and myofibroblast differentiation and regulates expression of angiopoietin-1 in prostatic stroma potentially via enhancing PI3K/AKT signaling.