Description of physical activity in outpatients with schizophrenia spectrum disorders

This study describes physical activity level in outpatients with schizophrenia spectrum disorders (SSD) using extended‐wear pedometers. Demographic data, body fat and body mass index (BMI) measures were obtained from 24 outpatients. Participants were provided extended‐wear pedometers and instructed to wear them during waking hours for 1 week. More than 79% of subjects met Centres for Disease Control (CDC) obesity criteria. Participants wore pedometers, on average, 6 days during the week. Men walked more steps, walked longer distances, and burned more calories each day; differences were statistically significant for steps and distance on days 3 (t = 2.12, P = 0.045) and 5 (t = 2.19, P = 0.04). Higher percent body fat and BMI were significantly associated with fewer steps walked on most days. Extended‐wear pedometers are an easy‐to‐use, cost‐effective way to document physical activity and evaluate efforts to help this vulnerable group achieve activity‐related health improvements.     

Characterization of a Factor H Mutation That Perturbs the Alternative Pathway of Complement in a Family with Membranoproliferative GN

Complement C3 activation is a characteristic finding in membranoproliferative GN (MPGN). This activation can be caused by immune complex deposition or an acquired or inherited defect in complement regulation. Deficiency of complement factor H has long been associated with MPGN. More recently, heterozygous genetic variants have been reported in sporadic cases of MPGN, although their functional significance has not been assessed. We describe a family with MPGN and acquired partial lipodystrophy. Although C3 nephritic factor was shown in family members with acquired partial lipodystrophy, it did not segregate with the renal phenotype. Genetic analysis revealed a novel heterozygous mutation in complement factor H (R83S) in addition to known risk polymorphisms carried by individuals with MPGN. Patients with MPGN had normal levels of factor H, and structural analysis of the mutant revealed only subtle alterations. However, functional analysis revealed profoundly reduced C3b binding, cofactor activity, and decay accelerating activity leading to loss of regulation of the alternative pathway. In summary, this family showed a confluence of common and rare functionally significant genetic risk factors causing disease. Data from our analysis of these factors highlight the role of the alternative pathway of complement in MPGN.