[Soluble proteins in feces of children with chronic nutritional disorders].
Explore the source record for details and available documents.
SEARCH · Search PubMed
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Cardiac cachexia is divided into two types, i.e., the classic type, which occurs in patients with severe heart failure, and the nosocomial type, which develops in the postoperative state. Cardiac cachexia is due both to a decrease in nutrient intake (anorexia, malabsorption) and to specific metabolic alterations (hypercatabolism with increased energy expenditure, response to hypoxia, inflammatory status, etc). Among the various mechanisms involved in the pathogenesis of cachexia, cellular hypoxia has long been recognized. The chronic activation of the endogenous neurohormonal system is another specific feature of such patients; a striking relationship was found between cardiac cachexia and hormonal levels which correlate better than the classical parameters of cardiac failure severity. Finally, inflammatory syndrome has been known to occur frequently in patients with cardiac cachexia. Several studies have shown that tumor necrosis factor-alpha was significantly increased in cachectic patients and that chronic activation of the systemic immune response might be a common and unifying factor.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
OBJECTIVES: We studied the effect of a low-quality dietary protein on cellular proliferation and maturation in the thymus of growing rats over time. METHODS: After weaning Wistar rats were fed a diet containing 6.5 g/100 g of corn flour for 6, 10, 18, and 45 d (M groups). For comparison, other rats were fed a diet containing 6.5 g/100 g of casein (Cas groups), and well-nourished age-matched control rats were fed a commercial laboratory diet (C groups). Food intake, body weight, thymus weight, total number of thymocytes, and the percentages of CD43(+) and Thy1(+) thymocyte phenotypic antigen determinants were measured. RESULTS: M versus Cas and C groups showed significant differences (P < 0.01) in body and thymus weights after 6 d of feeding, and the total number of thymocytes and the percentages of CD43(+) and Thy1(+) were significantly lower after 10 d of feeding. The results indicated that consuming a cereal diet for short or long periods causes thymus atrophy in growing rats, with significant reductions in the total number of T-cells concomitant with increases in the number of immature thymocytes. CONCLUSIONS: The data showed that, in addition to low-protein concentration, low-quality dietary protein is a limiting factor in certain steps of cellular intrathymic pathways, probably related to the requirement of specific amino acids for optimal immune response.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.