001-0.2 mg/kg, i.v.) and noradrenergic (0.025-0.05 mg/kg i.v.) neuronal firing, and PI3K inhibitor asenapine (0.1-0.2 mg/kg, s.c) increased cortical noradrenaline and

serotonin output. Local asenapine administration increased all three monoamines in the cortex but did not affect accumbal dopamine output. Intra-VTA tetrodotoxin perfusion blocked asenapine-induced accumbal but not cortical dopamine outflow.

Asenapine at doses associated with antipsychotic activity enhanced cortical monoamine efflux. Whereas the asenapine-induced dopamine increase in nucleus accumbens is dependent on activation of dopaminergic neurons in the VTA, the increase of cortical dopamine outflow involves largely a local action at nerve terminals. Our data provide further insight on the pharmacologic characteristics of asenapine that may have bearing on its clinical efficacy in the treatment of schizophrenia and bipolar disorder.”
“Kaposi’s MEK162 purchase sarcoma-associated herpesvirus (KSHV) encodes 12 pre-microRNAs (pre-miRNAs).

Current studies have shown that these miRNAs are involved in regulation of viral and host gene expression, implicating a role in the maintenance of viral latency and suppression of antiviral innate immunity. However, the functions of these miRNAs remain largely unknown. On the basis of the sequence homology between oncogenic miR-155 and KSHV-encoded miR-K12-11, we hypothesized that miR-K12-11 could attenuate transforming growth factor beta (TGF-beta) signaling, facilitating viral infection and tumorigenesis. In the present study, we demonstrated that ectopic expression of miR-K12-11 in Ramos, a TGF-beta-sensitive cell line, downregulated TGF-beta signaling and facilitated cell proliferation upon TGF-beta treatment by directly targeting SMAD5, an important mediator in TGF-beta signaling. In

addition, the downregulation of SMAD5 by miR-K12-11 was further confirmed in a de novo KSHV infection system or latently infected KSHV-positive B-lymphoma cell lines. More importantly, repression of miR-K12-11 by a specific sponge inhibitor restored the MycoClean Mycoplasma Removal Kit expression of SMAD5 in both de novo-infected and latently infected cells. Finally, we found that restoration of SMAD5, in addition to the TGF-beta type II receptor, which was epigenetically silenced by the latent viral protein latency-associated nuclear antigen, sensitized BC3 cells to the cytostatic effect of TGF-beta signaling. Taken together, our findings highlight a novel mechanism in which miR-K12-11 downregulates TGF-beta signaling and suggest that viral miRNAs and proteins may exert a dichotomy regulation in virus-induced oncogenesis by targeting the same signaling pathway.”
“BACKGROUND: Endovascular therapy is now the preferred treatment option for basilar tip aneurysms (BTAs).

OBJECTIVE: To compare the safety and efficacy of common endovascular techniques in the treatment of BTAs.