The intra-class correlation coefficient (ICC) for independent ROI measurements was 0.90 (genu) and 0.90 (splenium). There were no regions where FA values were significantly higher in the patients than in the healthy controls.

Conclusions. Widespread structural dysconnectivity, including the subcortical region, is already present

this website in neuroleptic-naive patients in their first episode of illness.”
“Although the intermediary role of central neurons in the hypertensive and sympathoexcitatory actions of cyclosporine (CSA) has been recognized in previous studies including our own, the underlying mechanism remains obscure. In this study, we tested the hypothesis that central pathways of nitric oxide (NO) and carbon monoxide (CO) modulate the blood pressure (BP) response elicited by CSA in conscious rats. Hemodynamic effects of CSA were evaluated in absence and presence of maneuvers that inhibit or facilitate biosynthesizing enzymes of NO (NOS) or CO (heme oxygenase, HO). CSA (20 mg/kg i.v.) produced abrupt increases in BP that peaked in 5 min and maintained for at least 45 min. The hypertensive effect

of CSA disappeared in rats pretreated intracisternally (i.c.) with N-omega-nitro-L-arginine methyl ester (L-NAME, nonselective NOS inhibitor), N-5-(1-iminoethyl)-L-ornithine (L-NIO, selective eNOS inhibitor), N-omega-propyl-L-arginine (NPLA, selective nNOS inhibitor), or 1H-[1,2,4] oxadiazolo[4,3-a] quinoxalin-1-one (ODQ, guanylate cyclase inhibitor), suggesting the importance of central eNOS/nNOS/GC selleck cascade in CSA-induced hypertension. L-NAME Avelestat (AZD9668) also abolished the hypotension caused by the sympatholytic drug moxonidine, indicating a tonic sympathoinhibitory action for NO. The inhibition of HO activity by zinc protoporphyrin IX (ZnPP) abrogated the hypertensive action of CSA. The abolition by L-NAME or ZnPP of CSA hypertension was compromised upon simultaneous i.c. exposure to hemin (HO substrate) and L-arginine (NOS substrate), respectively. Together, the interruption of the mutually facilitated NOS/NO and HO/CO pathways and coupled GC/cGMP in central neuronal pools

accounts, at least partly, for the hypertensive and perhaps sympathoexcitatory actions of CSA. (C) 2011 Elsevier Ltd. All rights reserved.”
“The thyroid hormone receptors, encoded by the TR alpha and TR beta genes, are ligand-dependent transcription factors that belong to the nuclear receptor superfamily. In addition to the role of these receptors in growth, development and metabolism, there is increasing evidence that they also inhibit transformation and act as tumor suppressors. Aberrant TR action, as well as receptor silencing, are common events in human cancer, and TRs also have an important role in tumor progression in experimental animal models, suggesting that these receptors constitute a novel therapeutic target in cancer.