Aberrant intra- and internetwork functional connectivity patterns of the anterior and posterior hippocampal networks in schizophrenia.

AIM: Schizophrenia is associated with abnormal hippocampal structure and function. Available evidence suggests that the anterior and posterior hippocampus are differentially affected by schizophrenia pathology. This study was designed to provide new insight into the anterior and posterior hippocampus in schizophrenia from the perspective of functional connectivity. METHODS: Based on resting-state functional magnetic resonance imaging data of 71 schizophrenia patients and 74 normal controls, we utilized a data-driven approach to functionally segment the hippocampus into anterior and posterior segments and then investigated the functional connectivity patterns within and between the two hippocampal networks at the network, edge, and nodal levels. RESULTS: We found that schizophrenia patients showed hyperconnectivity of both the anterior and posterior hippocampal networks. We also observed that the network alterations appear somewhat greater in the anterior hippocampal network than the posterior network, the left side than the right, and the intranetwork connectivity than the internetwork connectivity. CONCLUSION: The results reveal convergent and divergent intranetwork and internetwork connectivity patterns of the anterior and posterior hippocampus in schizophrenia, providing novel and important insights into the mechanisms of hippocampal pathology in schizophrenia.

[Lentivirus-mediated shRNA targeting ZNF217 suppresses cell growth, migration, and invasion of glioma cells in vitro].

OBJECTIVE: To explore the role of ZNF217 in regulating cell proliferation, migration and invasion in glioma cells. METHDOS: A lentivirus-mediated shRNA-ZNF217 vector was infected into glioma U251 cells, and the interference efficiency was examined by Western blotting. MTT assay, flow cytometry, Transwell assay, and Boyden chamber assay were used to analyze the changes in cell proliferation, migration and invasion. Western blotting was used to detect the changes in ZNF217-related genes in the cells. RESULTS: shRNA-ZNF217 transfection significantly inhibited the expression of ZNF217 in U251 cells and suppressed the cell migration, invasion, growth, and cell cycle transition. ZNF217 knockdown downregulated the expression of pPI3, pAKT, C-Myc, and the mesenchyme biomarker N-cadherin, and stimulated the expression of the epithelium biomarker E-cadherin. CONCLUSION: ZNF217 promotes cell migration, invasion, and growth by activating PI3K/AKT signal to upregulate C-Myc and by modulating the genes associated with epithelial-mesenchymal transition in glioma cells.

Interleukin-16 polymorphism is associated with an increased risk of glioma.

OBJECTIVE: Previous studies have shown that interleukin (IL)-16 is overexpressed in human and rat gliomas. Potential links between IL-16 polymorphisms and glioma risk are currently unclear. The aim of this study was to investigate the association between IL-16 polymorphisms and glioma risk. METHODS: We examined IL-16 gene polymorphisms (i.e., rs 4778889, rs 11556218, and rs 4072111) in 216 patients with glioma and 275 controls in a Chinese population. Genotypes were determined using a polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) assay. Odds ratios (OR) and their corresponding 95% confidence intervals (CI) were used to evaluate the effect of the IL-16 polymorphisms on glioma risk. RESULTS: The rs 11556218TG genotype is associated with an increased risk of glioma compared with the TT genotype (OR=1.76; 95% CI, 1.22-2.54; p=0.002). Similarly, the rs 11556218G allele is associated with an increased risk of glioma compared with the T allele (OR=1.41; 95% CI, 1.06-1.87; p=0.017). However, no significant association was observed between the IL-16 rs 4778889 and rs 4072111 polymorphisms and the risk of glioma. CONCLUSION: These findings suggest that the IL-16 rs 11556218 polymorphism may be used as a susceptibility marker for glioma.