Why Do People With Schizophrenia Exercise? A Mixed Methods Analysis Among Community Dwelling Regular Exercisers.

Individuals with schizophrenia have reduced rates of physical activity, yet substantial proportions do engage in independent and regular exercise. Previous studies have shown improvement in symptoms and cognitive function in response to supervised exercise programs in people with schizophrenia. There is little data on motivations of individuals who exercise independently, or their chosen type, duration, or setting of exercise. This study explores motivational parameters and subjective experiences associated with sustained, independent exercise in outpatients with a diagnosis of schizophrenia or schizoaffective disorder. Participants completed a semi-structured interview and then were given a prospective survey containing visual analog scales of symptom severity and the Subjective Exercise Experiences Scales to complete immediately before and after three sessions of exercise. Results from the semi-structured interview were analyzed by modified content analysis. The most important reason for exercise was self-image, followed closely by psychological and physical health. Among psychological effects, participants reported exercise was most helpful for mood and cognitive symptoms. The prospective ratings demonstrated 10-15% average improvements in global well-being, energy, and negative, cognitive and mood symptoms, with almost no change in psychosis, after individual exercise sessions. This suggests that non-psychotic parameters are more susceptible to inter-session decay of exercise effects, which may reinforce continued exercise participation.

Hypermethylation of the promoter region is associated with the loss of MEG3 gene expression in human pituitary tumors.

MEG3 is a human homolog of the mouse maternal imprinted gene, Gtl2. Gtl2 has been suggested to be involved in fetal and postnatal development and to function as an RNA. Recently our laboratory demonstrated that a cDNA isoform of MEG3, MEG3a, inhibits cell growth in vitro. Interestingly, MEG3 is highly expressed in the normal human pituitary. In striking contrast, no MEG3 expression was detected in human clinically nonfunctioning pituitary tumors. These data indicate that this imprinted gene may be involved in pituitary tumorigenesis. In the present study we investigated the mechanism underlying the absence of MEG3 expression in human clinically nonfunctioning pituitary tumors. No genomic abnormality was detected in the tumors examined. Instead, we found that two 5'-flanking regions, immediately in front of and approximately 1.6-2.1 kb upstream of the first exon, respectively, were hypermethylated in tumors without MEG3 expression compared with the normal pituitary. Reporter assays demonstrated that these two regions are functionally important in gene expression activation. Furthermore, treatment of human cancer cell lines with a methylation inhibitor resulted in MEG3 expression. We conclude that hypermethylation of the MEG3 regulatory region is an important mechanism associated with the loss of MEG3 expression in clinically nonfunctioning pituitary tumors.