Second order verbal stories and a non-verbal picture-sequencing task were used as ToM Measures. Results Showed no differences in ToM performance between patients and controls on either measure. Subsequent Subgrouping of patients into remitted and non-remitted showed a worse performance of non-remitted patients Selleck AG14699 only on second order ToM tasks. Specific ToM deficits were found associated with delusions. Association with negative symptoms was found to be less specific and accounted for by illness chronicity and general cognitive impairment. The results from the present Study are in line with models which hypothesise that specific ToM
deficits in schizophrenia are state dependent and associated with delusions. Such associations may also be task specific. (c) 2006 Elsevier Ireland Ltd. All rights reserved.”
“Glioblastoma multiforme (GBM) is the most aggressive and common kind of primary brain tumor in adults, and is thought to be driven by a subpopulation of glioma stem cells (GSCs). GSCs reside in a specialized hypoxic niche, which can regulate the tumorigenic capacity of GSCs primarily through the hypoxia-inducible factors (HIFs), HIF1 alpha and HIF2 alpha. ZNF217 is an oncogene frequently amplified in many kinds of tumors. It
is associated with aggressive tumor behavior and poor clinical prognosis, but its role in gliomas is poorly known. Gene expression and copy number analysis from TCGA data reveal that ZNF217 is amplified in 32% and overexpressed in 71.2% of GBMs. Quantitative RT-PCR and western blotting of a cohort of glioma samples showed that ZNF217 was highly expressed in gliomas BIBF 1120 and increased with tumor grade. Analysis of a molecular database demonstrated that ZNF217 expression correlated with poor survival of glioma patients. Investigation of ZNF217 expression in GSCs, non-GSCs and normal neural stem cells (NSCs) indicated that ZNF217 was more highly expressed in GSCs than in non-GSCs and NSCs. Knockdown of ZNF217 in GSCs by small-interfering RNA (siRNA) inhibited their growth and promoted their differentiation. Interestingly, ZNF217 was
upregulated in GSCs and the GBM cell line U87 when exposed to the hypoxic environment of 1% oxygen. Knockdown of either HIF1 alpha or HIF2 alpha, which has a central PX-478 nmr role in the hypoxia-induced responses of these cells, inhibited ZNF217 expression. In addition, ZNF217 upregulation was compromised under hypoxia in U87 and GSCs when either HIF1 alpha or HIF2 alpha was targeted by siRNA. HIF2 alpha knockdown inhibited ZNF217 expression more efficiently in both normoxia and hypoxia than HIF1 alpha knockdown. Therefore, ZNF217 is overexpressed in GBMs and contributes to the maintenance of GSCs, which is regulated by HIFs released by the hypoxic environment of the tumor. Laboratory Investigation (2011) 91, 1068-1078; doi:10.1038labinvest.2011.