“
“To investigate the effects of early life stress on the development of social behaviors in male mice, we examined

behavioral responses toward same sex stimulus mice in the social investigation test and aggressive behaviors check details in peripubertal male mice exposed to maternal separation ( MS) during the first 2 weeks of life. MS suppressed aggressive behaviors from 5-9 weeks of age, but had no effect on social investigative behaviors in the social investigation test. Investigation of neuroendocrine bases of behavioral effects of MS showed that MS reduced plasma testosterone levels and decreased arginine vasopressin and increased oxytocin immunoreactivity in the paraventricular nucleus of peripubertal males. These results collectively suggest that early life stress disrupts the development of male aggressive behaviors and associated neuroendocrine systems. NeuroReport 22:259-263 (C) 2011 Wolters Kluwer Health | Lippincott Williams & Wilkins.”
“Infection of resting primary human B cells by Epstein-Barr virus (EBV) results in their transformation into indefinitely proliferating lymphoblastoid cell

lines (LCLs). LCL formation serves as a model for lymphomagenesis, and LCLs are phenotypically https://www.selleckchem.com/products/bay-11-7082-bay-11-7821.html similar to EBV-positive diffuse large B-cell lymphomas (DLBCLs), which represent a common AIDS-associated malignancy. B-cell infection by EBV induces the expression of several cellular microRNAs (miRNAs), most notably miR-155, which is overexpressed in many tumors and can induce B-cell lymphomas when overexpressed in animals. Here, we demonstrate that miR-155

is the most highly expressed miRNA in LCLs and that the selective inhibition of miR-155 function specifically inhibits the growth of both LCLs and the DLBCL cell line IBL-1. Cells lacking miR-155 are inefficient in progressing through S phase and spontaneously undergo apoptosis. In contrast, three other B-cell lymphoma lines, including two EBV-positive Burkitt’s lymphoma cell lines, grew normally in the absence of miR-155 function. These data identify AZD5582 molecular weight the induction of cellular miR-155 expression by EBV as critical for the growth of both laboratory-generated LCLs and naturally occurring DLBCLs and suggest that targeted inhibition of miR-155 function could represent a novel approach to the treatment of DLBCL in vivo.”
“The phenotype loss of parvalbumin-containing interneurons, characterized by decreased parvalbumin expression, has been observed in schizophrenic patients. Overproduction of intraneuronal reactive oxygen species leads to such a phenotype loss. Nuclear factor-kappa B (NF-kappa B) activation is both a target and a regulator of intracellular oxidative stress response, suggesting its involvement in the parvalbumin regulation. This study was carried out to investigate the role of the NF-kappa B activation in the ketamine-induced phenotype loss of parvalbumin-interneurons in vitro.