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A I Martin

Publications and source records attributed to A I Martin.

5 recordsLinked to original sources
PubMed2002

Bioactivity of three CaO-P2O5-SiO2 sol-gel glasses.

Three gel glasses containing 25 mol % of CaO and SiO(2) + P(2)O(5) contents (in mol %): 75 + 0 (S75); 72.5 + 2.5 (S72.5P2.5); and 70 + 5 (S70P5), respectively, were obtained, characterized, and studied when soaked in a simulated body fluid (SBF). The influence of composition in both textural properties (surface area and porosity) and in vitro behavior of glasses was studied. In as prepared S72.5P2.5 and S70P5 glasses, crystalline phosphate nuclei were detected through XRD and FTIR. In addition, N(2) adsorption and Hg porosimetry measurements showed that the surface area increased, whereas the pore volume and the pore diameter decreased as P(2)O(5) in glasses increased. These variations were explained on the basis of the withdrawal of calcium from the glass silica network, due to the calcium-phosphorous bonding. In vitro studies showed that the three compositions were bioactive, because an apatite layer was formed after soaking in SBF. S75 presented the highest initial reactivity but the lowest crystallization rate of the apatite-like phase. For S72.5P2.5, and S70P5 the amorphous calcium phosphate formation was slower than for S75, but the crystallization of apatite was observed after shorter periods in SBF. Furthermore, after 7 days of soaking, the layer thickness decreased as P(2)O(5) in glasses increased.

Apatites↗
PubMed2001

The decrease in hepatic IGF-I gene expression in arthritic rats is not associated with modifications in hepatic GH receptor mRNA.

OBJECTIVE: Adjuvant-induced arthritis induces a catabolic response, and a decrease in circulating IGF-I. Hypermetabolism and GH insensitivity have been described in acute inflammation. The aim of this study was to analyze whether impaired IGF-I secretion in arthritic rats can be attributed to hepatic GH resistance. DESIGN AND METHODS: Male Wistar rats were injected with complete Freund's adjuvant, and 14 days afterwards arthritic and control rats were injected daily with recombinant human GH (rhGH) (3 IU/kg) or saline for 8 days. GH receptor (GHR) gene expression in the liver and the effect of rhGH on hepatic IGF-I synthesis in arthritic rats were examined. RESULTS: There was a significant decrease in hepatic concentrations of IGF-I (P < 0.01) as well as in the IGF-I gene expression in arthritic but not in pair-fed rats. In contrast, arthritis did not modify GHR mRNA levels in the liver. The 8 day administration of rhGH resulted in an increase in body weight gain in arthritic but not in control rats. There was an increase in hepatic IGF-I synthesis and in GHR mRNA levels after rhGH treatment, both in control and in arthritic rats. Two endotoxin lipopolysaccharide (LPS) (1 mg/kg) injections decreased hepatic concentrations of IGF-I and IGF-I mRNA (P < 0.01). Contrary to the results obtained in arthritic rats, mRNA expression of GHR in the liver was lower in LPS- than in saline-treated rats (P < 0.01). CONCLUSION: These data suggest that the decrease in IGF-I synthesis induced by chronic arthritis is not secondary to GH resistance.

Animals↗
PubMed2000

IGF-I and IGF-I-binding proteins in rats with adjuvant-induced arthritis given recombinant human growth hormone.

Adjuvant-induced arthritis in rats is associated with growth failure, hypermetabolism and accelerated protein breakdown. We have previously reported that adjuvant-induced arthritis in rats results in a decrease in body weight gain, pituitary GH mRNA, circulating GH and IGF-I together with an increase in serum IGF-binding proteins (IGFBPs). The aim of this study was to analyze the role of GH in the decrease in body weight and in the alterations in the IGF-I system observed in chronic inflammation. Male Wistar rats were injected with complete Freund's adjuvant and 16 days later arthritic rats were injected daily with recombinant human GH (rhGH) (3 IU/kg s.c.) for 8 days; control rats received 250 microl saline. Arthritis significantly decreased body weight gain and serum IGF-I. These decreases were not due to the reduced food intake, since in pair-fed rats they were not observed. Furthermore, administration of rhGH to arthritic rats increased body weight gain without modifying food intake. To further investigate the effect of GH administration, 14 days after adjuvant injection both control and arthritic rats were treated with 0, 1.5, 3 or 6 IU/kg of rhGH. GH treatment at the dose of 3 and 6 IU/kg significantly increased body weight gain in arthritic rats. GH administration, at the higher dose of 6 IU/kg, increased hepatic and serum concentrations of IGF-I in both control and arthritic rats. In control rats, rhGH at the three doses assayed increased circulating IGFBP-3. GH treatment in arthritic rats decreased IGFBP-1 and -2, and did not modify IGFBP-4. GH treatment at the dose of 3 IU/kg also decreased circulating IGFBP-3 in arthritic rats. These data suggest that GH treatment can ameliorate the catabolism observed in adjuvant-induced arthritis, an effect mediated, at least in part, by modifications in the circulating IGFBPs.

Animals↗