Recent studies have suggested the beneficial effects of GH treatment in patients with dilated cardiomyopathy. We have treated with recombinant human growth hormone (rhGH) a 6-year-old female with a complex congenital heart defect (severe tricuspid hypoplasia and malposition of the great arteries), who developed a progressive dilated cardiomyopathy of unknown etiology. rhGH treatment (0,1 U/kg/day, for 3 months) did not improve cardiac function, nor clinical symptoms, although we have no clear explanations for this. However, a trial with rhGH may be offered to children with dilated cardiomyopathy and waiting for heart transplantation.
We evaluated growth hormone binding protein (GHBP) activity in a group of obese children (12 boys and 12 girls, age 3.1-14.7 years, BMI 21.1-33.3, 11 prepubertal and 13 early pubertal) and in 26 age-matched normal weight children (14 boys and 12 girls, age 2.1-16.0 years, BMI 14.2-21.4, 18 prepubertal and 8 early pubertal). All children were of normal stature. GHBP activity was significantly higher in the obese (39.1 +/- 1.1%) than in the control children (28.3 +/- 1.0%, p < 0.0001). Mean serum GHBP was not different between boys and girls or between prepubertal and pubertal subjects. A positive correlation was found between BMI and GHBP levels only in the normal weight children (r = 0.425, p < 0.05). Baseline insulin concentrations in the obese children were 97.6 +/- 7.9 pmol/l (normal values, 45.0 +/- 18.6 pmol/l), and the mean insulin AUC following OGTT in the obese was 811.3 +/- 160.7 pmol/l (normal values, 373.1 +/- 150.1 pmol/l). Serum GHBP activity in the obese was not correlated with baseline serum insulin concentrations or with the insulin AUC following OGTT. In conclusion, we found that obese children have elevated GHBP activity, and speculate that this phenomenon may serve to compensate for their reduced GH secretion and accelerated GH clearance.
Objective: To analyze the effects of melatonin administration on the periodontal tissues of rats, linked or not with ligature-induced periodontal disease. Materials and Methods: 40 male Wistar rats aged eight weeks, divided into Control Group (GCON), Ligature Group (GLIG), Melatonin Group (GMEL) and Ligature and Melatonin Group (GLIGMEL). GLIG and GLIGMEL were induced to experimental periodontitis by placing a ligature on the lower molars for 30 days. During the experiment, after 16 days with the ligature, melatonin was administered orally for 10 mg/kg for 14 days in GMEL and GLIGMEL. In the end, euthanasia was performed and the hemi-mandibles were collected for the respective histological and radiographic analyzes; for the results, Shapiro-Wilk, ANOVA-One-Way and Tukey's multiple comparison tests were used. Results: A significantly lower alveolar bone loss (p<0.05) was demonstrated in the animals that received the administration of melatonin, in which it had a prophylactic function against the effects of the disease, evidenced in radiographic, histomorphometric and histological analyzes in the bone cell count. Conclusion: Results show that the therapy with administration of melatonin promotes a protective effect on the alveolar bone tissue of rats with induced experimental periodontitis.
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