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Biomedical subjects

R C Pereira

Publications and source records attributed to R C Pereira.

31 records · Page 2Linked to original sources
PubMed1999

Cortisol enhances the expression of mac25/insulin-like growth factor-binding protein-related protein-1 in cultured osteoblasts.

Glucocorticoids inhibit the synthesis of insulin-like growth factor I (IGF-I) and regulate the expression of IGF-binding proteins (IGFBPs) in osteoblast cultures. IGFBP-related protein-1 (IGFBP-rP1), the product of the mac25 gene, binds IGF-I, IGF-II, and insulin, and we postulated that glucocorticoids regulate IGFBP-rP1 synthesis in osteoblasts. We tested the expression of mac25/IGFBP-rP1 in cultures of osteoblast-enriched cells from 22-day-old fetal rat calvariae (Ob cells). Cortisol treatment at 10 nM to 1 microM for 24-48 h caused a time- and dose-dependent increase in mac25/IGFBP-rP1 messenger RNA (mRNA) levels in Ob cells. Cycloheximide at 3.6 microM did not alter mac25/IGFBP-rP1 transcripts in control or cortisol-treated cells. Cortisol did not modify the decay of mac25/IGFBP-rP1 mRNA in transcriptionally arrested Ob cells and increased the rate of IGFBP-rP1 transcription as determined by nuclear run-on assays. Retinoic acid also increased mac25/IGFBP-rP1 mRNA levels, but 17beta-estradiol, testosterone, 5alpha-dihydrotestosterone, progesterone, and 1,25-dihydroxyvitamin D3 did not. In conclusion, cortisol stimulates mac25/IGFBP-rP1 expression in Ob cells by transcriptional mechanisms. As IGFBP-rP1 binds and possibly modifies the effects of IGFs and insulin, its increased expression could be relevant to the inhibitory actions of cortisol in bone.

Animals↗
PubMed1999

Parathyroid hormone increases mac25/insulin-like growth factor-binding protein-related protein-1 expression in cultured osteoblasts.

PTH induces the synthesis of insulin-like growth factor I (IGF-I) and regulates the expression of IGF-binding proteins (IGFBP) in osteoblast cultures. IGFBP-related protein-1 (IGFBP-RP-1), the product of the mac25 gene, binds IGF-I, IGF-II, and insulin. We tested the actions of PTH on the expression of mac25/IGFBP-RP-1 in cultures of osteoblast-enriched cells from 22-day-old fetal rat calvariae (Ob cells). PTH at 0.1-10 nM for 6-48 h increased mac25/IGFBP-RP-1 messenger RNA (mRNA) levels in Ob cells, an effect not altered by cycloheximide. PGE2 increased mac25/IGFBP-RP-1 mRNA levels, but indomethacin did not modify basal or PTH-stimulated mac25/IGFBP-RP-1 expression. The decay of mac25/IGFBP-RP-1 mRNA in transcriptionally arrested Ob cells was not modified by PTH, and PTH increased the rate of IGFBP-RP-1 transcription. GH, insulin, bone morphogenetic protein-2, fibroblast growth factor-2, platelet-derived growth factor BB, IGF-I, and IGF-II did not modify mac25/IGFBP-RP-1 expression, whereas transforming growth factor-beta1 was modestly stimulatory. In conclusion, PTH stimulates mac25/IGFBP-RP-1 transcription in osteoblasts, an effect that could be relevant to the actions of PTH in bone.

Animals↗
PubMed1994

Aluminium-related osteodystrophy and desferrioxamine treatment: role of phosphorus.

We investigated (1) the prevalence of aluminium overload among 96 patients with symptomatic bone disease haemodialysed from 1987 to 1989 in the Sao Paulo area, Brazil; (2) the effect of 6 months desferrioxamine (DFO) treatment (1-2g/week). All patients underwent a first bone biopsy. Aluminium overload (extent of stainable bone aluminium more than 20% trabecular surface) was observed in 74 of 96 patients. Forty overloaded patients were divided into patients with high bone formation rate (BFR) (group 1; n = 17) and patients with low BFR (group 2; n = 23), and had a second biopsy after DFO therapy. In both groups aluminium surface was reduced after treatment (P < 0.001), osteoblast surface (P < 0.02-P < 0.01) and plasma parathyroid hormone (iPTH) (P < 0.01) increased. In group 1 BFR remained high. In group 2 BFR remained low in 16 patients (2a) and increased in seven (P < 0.02) (2b). In group 2a plasma phosphorus was below that in group 2b patients, before (P < 0.03) and after (P < 0.01) DFO. The histological features of group 2a patients resembled hypophosphataemic osteomalacia, those of group 2b patients aluminium osteodystrophy. These data show a high prevalence of aluminium overload in Brazilian patients. Low-dose DFO therapy was safe, decreased bone pain, prevented fractures, and reduced stainable bone aluminium. Bone lesions only partially improved, suggesting that low phosphorus intake and/or plasma calcitriol concentrations may have prevented improvement of bone formation and mineralization.

Adolescent↗
PubMed1993

Reversal of aluminum-related bone disease after renal transplantation.

We evaluated the course of severe aluminum-related bone disease (ARBD) after the first year of a successful renal transplantation (RTx) in 11 adult patients. Bone pain and muscle weakness, presented in all patients previously to RTx, subsided, and all were able to walk, even the ones who were confined to wheelchairs. Bone necrosis developed in 6 patients, but none required surgical repair. Serum alkaline phosphatase activity increased 2.5 times the upper normal level, up to the 5th month and then declined to normal levels up the 12th month (p < 0.05). The inverse profile was observed in both serum calcium and phosphorus levels. In bone biopsies, there was a significant decrease in all of the following histomorphometric static parameters: osteoid volume, thickness and surface and also in aluminum surface. Also, there was a significant increase in all the dynamic parameters of mineralization: mineral apposition rate, mineralization surface, bone formation rate and adjusted apposition rate. In conclusion, ARBD remarkably improves after 1 year of successful RTx.

Adult↗
PubMed1992

[Health promotion and disease prevention: an individual responsibility or social responsibility].

This article is about some theoretical assumptions that have guided health promotion and disease prevention strategies. Some questions are raised in relation to the professional's interventions that consider health promotion as an individual responsibility. It is suggested that the focus should be on social changes through the professionals' consciousness in social, political, behavioral and economic aspects that exert influences over the population's health. These ideas ought to be incorporated to the nurse-client interaction.

Brazil↗
PubMed1981

Possible mechanism of action of cholesterol enriched diet on the thyroid.

Groups of male Sprague Dawley rats aged 60 days were fed either a control diet (CD) or the same diet enriched with 1% cholesterol (CHD) for 30 days. In CHD fed animals an increase of 131I uptake by thyroid, PB131I and TSH level in plasma was found, while the level of thyroxine (T4) was unchanged and that of triiodothyronine (T3) was decreased. In the animals treated with T3 (20 micrograms i.p. daily) a decrease of 131I uptake by thyroid and of T4 and TSH level in plasma was found irrespectively of a cholesterol content in the diet. However, PB131I level was decreased in CHD fed and T3 treated animals compared to those fed CD under the same treatment. Finally, in the animals treated with cimetidine (10 mg i.p. daily) no changes of any measure was found after CD feeding as compared to untreated ones, while CHD in such animals resulted in a decreased of T3 level. The site of cholesterol action appears to be at the hypothalamus-pituitary system since TSH suppressed animals (i.e. T3 treated) did not show any thyroid stimulation when fed with a cholesterol excess. Furthermore, thyroidectomized animals showed increased TSH in plasma after cholesterol feeding. In the present study, chronic administration of cimetidine completely abolished thyroid gland stimulation promoted by cholesterol feeding thus suggesting that central histamine may play a considerable role in this process.

Animals↗