However, levels of SSTR2 mRNA were significantly 37.6% lower in monkeys exposed chronically to low dose haloperidol, suggesting that the lower levels of SSTR2 mRNA selectively in pyramidal neurons in DLPFC layers 5-6 in schizophrenia should be interpreted with caution. In concert with prior findings of lower SST mRNA expression in the same subjects, the results of this study suggest the convergence of pre- and post-synaptic mechanisms to reduce inhibitory inputs to pyramidal neurons in the infragranular layers of the DLPFC.
This article is part of a Special Issue entitled ‘Schizophrenia’.
(C) 2010 Elsevier Ltd. All rights reserved.”
“Clozapine is known to be effective in treating schizophrenia patients with comorbid alcohol use
disorders (AUD). However, few prospective Veliparib studies have examined the effect of clozapine on community survival of the patient, which is one of the most important indicators of E7080 chemical structure success for patients with schizophrenia. In this prospective, naturalistic, observational, community-survival-analysis study, we compared the effect of clozapine and risperidone on two-year psychiatric hospitalization rate and time to hospitalization in the treatment of patients with schizophrenia and comorbid AUD. We found that the clozapine treated patients were readmitted to hospital significantly later (mean survival=526.5 days, n=25 patients) than the risperidone treated patients (mean survival=420.4 days, n=36 patients). The survival curve for the clozapine-treated patients was significantly different from that of the risperidone treated patients
(log-rank test, df=1, p=.045). At the end of the two-year study period, 75% of the risperidone treated patients had been admitted to the hospital, compared to only 48% of the clozapine treated patients. These findings suggest that clozapine should be considered for the treatment of schizophrenia patients with comorbid AUD. However, due to the limitations of this study, further studies will be required to confirm these findings. (C) 2008 Elsevier Inc. All rights reserved.”
“Glycogen storage disease type BAY 63-2521 supplier I (GSD I) is caused by deficiency of the glucose-6-phosphatase catalytic subunit in type la or of glucose-6-phosphate transporter in type lb. The cellular bases for disruptions of homeostasis have been increasingly understood in GSD I, including those for anemia, renal failure and neutropenia. Advances in the understanding of cellular abnormalities in GSD I have provided rationales for new therapy, and recent developments in gene therapy have led to potential curative treatments for GSD I. These advances will benefit patients with GSD I in the future, improving both quality of life and survival, as well as illuminating the molecular effects of altered metabolism upon multiple organ systems.