[The impact of retirement on the quality of life of the elderly]. / Repercussões da aposentadoria na qualidade de vida do idoso.

The purpose of this qualitative study was to understand how the elderly experience retirement and the effects of retirement on quality of life. Content analysis was on thematic categories obtained through semistructured interviews with elderly retirees who attended the Geriatrics Department at Hospital do Servidor Público Estadual--São Paulo (Brazil). Six individuals were interviewed. Positive attitudes facing retirement were predominant. The meaning given to retirement and planning skills were essential to understand the retirement experience. Furthermore, the change in environments, emptying of routines, and the availability of food are factors that appear closely related to the changes in eating habits and in body weight. Therefore, retirement is a time marked by changes in the social, emotional and nutritional aspects of life for the elderly, with either positive or negative effects, depending on the meanings that were attributed.

In vivo effects of TGFbeta1 on the growth of gastric epithelium in suckling rats.

As the content of Transforming Growth Factor-beta (TGFbeta) wanes in the milk of lactating rat, an increase in TGFbeta is observed in the gastric epithelia concomitant with differentiation of the glands upon weaning. Whereas TGFbeta has been shown to inhibit the proliferation of gastrointestinal cells in vitro, its functional significance and mechanisms of action have not been studied in vivo. Therefore, we administered TGFbeta1 (1 ng/g body wt.) to 14-day-old rats in which the gastric epithelium was induced to proliferate by fasting, and determined the involvement of signaling through Smads and the impact on epithelial cell proliferation and apoptosis. After the gavage, we observed the progressive increase of active TGFbeta1 while TbetaRII-receptor remained constant in the gastric mucosa. By immunohistochemistry, we showed Smad2/3 increase at 60 min (p<0.05) and Smad2 phosphorylation/activation and translocation to the nucleus most prominently between 0 and 30 min after treatment (p<0.05). Importantly, TGFbeta1 inhibited cell proliferation (p<0.05), which was estimated by BrDU pulse-labeling 12 h after gavage. Lower proliferation was reflected by increased p27(kip1) at 2 h (p<0.05). Also, TGFbeta1 increased apoptosis as measured by M30 labeling at 60 and 180 min (p<0.001), and by morphological features at 12 h (p<0.05). In addition, we observed higher levels of activated caspase 3 (17 kDa) from 0 to 30 min. Altogether, these data indicate a direct effect of TGFbeta1 signaling through Smads on both inhibiting proliferation, through alteration of cycle proteins, and inducing apoptosis of gastric epithelial cells in vivo. Further, the studies suggest a potential role for both milk and tissue-expressed TGFbeta1 in gastric growth during postnatal development.

Corticosteroids induce the differential expression of TGFbeta isoforms, receptors and signaling in the gastric mucosa of suckling rats.

Glucocorticoids inhibit the cell proliferation in the gastric epithelium, and induce differentiation, migration and death. The mechanism by which these effects are triggered and controlled is still discussed and can involve the transcription and activation of transforming growth factor beta (TGFbeta). The present study was conducted to evaluate the effect of hydrocortisone short-term treatment on tissue level and distribution of TGFbeta isoforms, receptors and signaling through Smad2/3. To achieve that, 18-day-old rats were injected with hydrocortisone (50 mg/Kg b.wt.) for 0, 1 and 3 h. The stomachs were collected and processed for immunohistochemistry and western blotting. We observed that the treatment for 3 h increased the number of labeled epithelial cells for TGFbeta1 (p < 0.05), decreased the distribution of TGFbeta2 (p < 0.05) and did not alter TGFbeta3, TbetaRI and TbetaRII status. The levels of TGFbeta1 and receptors were checked by western blotting and results corroborate the immunodetection. We also found that phosphorylation of Smad2/3 into Smad2P increased after 3 h (p < 0.05), indicating that the high level TGFbeta1 was active on the cells. We suggest that glucocorticoids differentially regulate the expression of TGFbeta isoforms, receptors and signaling, and so TGFbeta1 might be involved in the inhibitory pathway triggered by the hormone.