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Objectives: Working Alliance (WA) is important in the care of patients with Schizophrenia Spectrum Disorders (SSD). This study aims to determine which sociodemographic and clinical factors are associated with WA, as assessed by patients and staff members in Residential Facilities (RFs), and may predict WA dyads' discrepancies. Methods: Three hundred and three SSD patients and 165 healthcare workers were recruited from 98 RFs and characterized for sociodemographic features. WA was rated by the Working Alliance Inventory (WAI) for patients (WAIP) and staff members (WAI- T). SSD patients were assessed for the severity of psychopathology and psychosocial functioning. Results: Pearson's correlation revealed a positive correlation (ρ = .314; p < .001) between WAI- P and WAI- T ratings. Linear regression showed that patients with higher education reported lower WAI- P ratings (β = -.50, p = .044), while not being engaged in work or study was associated with lower WAI- T scores (β = -4.17, p = .015). A shorter lifetime hospitalization was associated with higher WAI- P ratings (β = 5.90, p = .008), while higher psychopathology severity negatively predicted WAI- T (β = -.10, p = .002) and WAI- P ratings (β = -.19, p < .001). Better functioning level positively foresaw WAI- T (β = .14, p < .001) and WAI- P ratings (β = .12, p < .001). Regarding discrepancies, staff members' age was associated with higher dyads discrepancy in Total scale and Agreement subscale scores, which were also associated with more severe negative symptoms, while patients' age was negatively correlated to Relationship subscale discrepancy. Conclusions: This study provides insight into the factors that influence WA in SSD patients and health workers in RFs. The findings address interventions to improve WA and ultimately patient outcomes. [ABSTRACT FROM AUTHOR]

Clinical and experimental evidence indicates that atypical antipsychotics impair glucose metabolism. We investigated whether clozapine may directly affect insulin action by analyzing insulin signaling in vitro and in vivo. Clozapine reduced insulin-stimulated glucose uptake in PC12 and in L6 cells, representative models of neuron and skeletal muscle, respectively. Consistently, clozapine reduced insulin effect on insulin receptor (IR) by 40% and on IR substrate-1 (IRS1) tyrosine phosphorylation by 60%. Insulin-stimulated Akt phosphorylation was also reduced by about 40%. Moreover, insulin-dependent phosphorylation of protein kinase C-ζ (PKC-ζ) was completely blunted in clozapine-treated cells. Interestingly, clozapine treatment was accompanied by an insulin-independent increase of Akt phosphorylation, with no change of IR, IRS1, and PKC-ζ basal phosphorylation. The cellular abundance of Ped/Pea-15, an Akt substrate and inducer of insulin resistance, was also increased following clozapine exposure, both in the absence and in the presence of cyclohexymide, a protein synthesis inhibitor. Similar as in cellular models, in the caudate-putamen and in the tibialis muscle of clozapine-treated C57/BL/KsJ mice, Akt phosphorylation and Ped/Pea-15 protein levels were increased and PKC-ζ phosphorylation was decreased. Thus, in these experimental models, clozapine deranged Akt function and up-regulated Ped/Pea-15, thereby inhibiting insulin stimulation of PKC-ζ and of glucose uptake. J. Cell. Physiol. 227: 1485-1492, 2012. © 2011 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

Neuronal expression of immediate-early genes in response to a drug is a powerful screening tool for dissecting anatomical and functional brain circuitry affected by psychoactive compounds. We examined the effect of dopaminergic perturbation on two Homer 1 gene splice variants, Homer 1a and ania-3, in rat forebrain. Rats were treated with the 'typical' antipsychotic haloperidol, the 'atypical' quetiapine, or the selective dopamine transporter (DAT) inhibitor GBR 12909 in acute and chronic paradigms. Our results show that the high affinity dopamine D2 receptor antagonist haloperidol strongly induces Homer 1 gene expression in the caudate-putamen, whereas quetiapine, a fast D2R dissociating antagonist, does not. This confirms that Homer 1 may be considered a predictor of 'atypicality' of antipsychotic compounds in acute and also chronic regimens. Chronic treatment with GBR 12909 showed a strong induction in the parietal cortex, resembling the activation of 'sensitization' circuitry by stimulants. Finally, we describe a differential spatial induction pattern of Homer 1 gene within the caudate-putamen by typical antipsychotics and DAT blockers, and propose a novel method to quantitate it. Synapse 61:429-439, 2007. © 2007 Wiley-Liss, Inc. [ABSTRACT FROM AUTHOR]