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Biomedical subjects

M Castro

Publications and source records attributed to M Castro.

At least 145 records · Page 8Linked to original sources
PubMed1997

Relationship between microstructure and ductility of investment cast ASTM F-75 implant alloy.

Hip replacement implants fabricated using the ASTM F-75 alloy sometimes fail in a sudden catastrophic way. In general, fractures start at microstructural defects subjected to stress-corrosion under chemical attack by body fluids. In this paper the results of a study on the effect of casting parameters on the microstructure of ASTM F-75 are presented. The preheating mold temperature and the liquid temperature were varied between 900 and 1000 degrees C, and 1410 and 1470 degrees C, respectively. Optimum static strength and ductility were obtained when shrinkage microporosity and the volume fraction of M23C6 "eutectic" carbides precipitated at grain boundaries were minimized by increasing the preheating mold temperature to 1000 degrees C and by using intermediate pouring temperatures of 1455 degrees C. Under these casting conditions, however, the solidification rates are low, leading to large grain sizes, which, in turn, reduce the strength of the material under dynamic loading conditions. The volume fraction of the M23C6 "blocky" carbides appears to be independent of the casting conditions; however, their size and spatial distributions determine the strength of the as-cast alloys.

Alloys↗
PubMed1997

The hypothalamic-pituitary-adrenal axis of prairie voles (Microtus ochrogaster): evidence for target tissue glucocorticoid resistance.

Basal plasma corticosterone levels in prairie voles (Microtus ochrogaster) are extremely high, in the absence of any apparent negative consequences of glucocorticoid excess. We tested the hypothesis that prairie voles are a novel rodent model of target tissue resistance to glucocorticoids. Prairie voles had a significantly higher adrenal-to-body weight ratio, 5- to 10-fold greater basal plasma corticosterone, and 2- to 3-fold greater basal plasma ACTH concentrations than montane voles (Microtus montanus) and rats. While plasma corticosterone binding globulin (CBG) was 2-fold higher in prairie voles than in rats, both estimated and directly measured plasma free corticosterone were significantly higher in prairie voles than in rats. Plasma corticosterone levels in prairie voles were responsive to both circadian cues and a stressor, but were resistant to suppression by the synthetic glucocorticoid, dexamethasone (DEX). Western blots of brain and liver protein extracts, using a glucocorticoid receptor (GR) antibody, revealed the presence of a approximately 97 kDa immunoreactive band, the expected size for GR. Binding assays revealed significantly lower DEX affinity of corticosteroid receptors (CR) in cytosol of prairie vole brain and liver than that in the same tissues in rats. We conclude that prairie voles are a novel rodent model of glucocorticoid resistance, and that decreased affinity of CR for ligand might be partially responsible for this phenomenon.

Adrenocorticotropic Hormone↗
PubMed1997

Acrylic bone cement induces the production of free radicals by cultured human fibroblasts.

Arthroplasty with poly(methyl methacrylate) (PMMA) bone cement induces late loosening phenomena that compromise the prosthetic stability. As free radicals are inflammatory mediators and cytotoxic, it seemed useful to investigate whether PMMA induces the liberation of free radicals and/or cytotoxicity. The effect of PMMA interaction on cultured human fibroblasts was accessed by the cell viability test (MTT), and by the measurement of lipoperoxides in the incubation medium. The incubation with the medium exposed to PMMA induced a significant reduction in the viability and a significant increase in lipoperoxide liberation (vs control). These data suggest that PMMA is cytotoxic. This effect seems to be mediated by lipoperoxide and possibly by other free radicals, and may explain the peri-implant loosening phenomena that compromise the prosthetic stability.

Bone Cements↗
PubMed1997

Capsular type distribution and susceptibility to antibiotics of Streptococcus pneumoniae clinical strains isolated from Uruguayan children with systemic infections. Pneumococcus Study Group.

Children under 24 months of age are at high risk for serious infection with Streptococcus pneumoniae but they do not elicit effective immune responses to the currently available capsular polysaccharide vaccines. A polysaccharide protein conjugated vaccine involving the most frequent types has become an urgent need. To produce such a vaccine for Latin America, information on type distribution is required. Recently, Uruguay was 1 of the 6 countries in Latin America where surveillance for invasive pneumococcal infections in children under the age of 5 years was carried out. Seventy percent of the 182 invasive S. pneumoniae isolates were recovered from patients under 24 months of age, and 19% were recovered from infants under 6 months. The 7 most frequent types were 14, 5, 1, 6B, 3, 7F, and 19A; representing 80% of invasive isolates. Twenty-one types were identified, 16 in pneumonia and 14 in meningitis. Resistance to penicillin increased during the study period, from 29% in 1994, to 40% in 1995-1996, mainly because of the spread of type 14 strains resistant to penicillin and trimethoprim/sulphamethoxazol (89% of resistant isolates). The high proportion of systemic pneumococcal infections recorded in patients under 24 months of age and the increasing resistance of these agents to first-choice antibiotics point to an urgent need for a capsular polysaccharide protein conjugated vaccine.

Drug Resistance, Microbial↗
PubMed1997

Neutrophil phagocytosis in AIDS patients with azole resistant candidiasis.

OBJECTIVE AND SUBJECTS: This study aimed to evaluate phagocytosis of C. albicans by neutrophils in 10 AIDS patients and 50 control subjects. Five of the AIDS patients were colonised with azole-resistant C. albicans isolates and five with azole-sensitive isolates. RESULTS AND CONCLUSIONS: Percentage phagocytosis was within normal limits for seven of the 10 AIDS patients and was reduced in the remaining three patients. Phagocytosis was unaffected by the carriage of azole resistant C. albicans, and the patients' own strains were phagocytosed as readily as a standard strain of C. albicans. This study suggests that azole resistance is not related to impaired phagocytosis in AIDS patients.

AIDS-Related Opportunistic Infections↗
PubMed1997

Strength, skeletal muscle composition, and enzyme activity in multiple sclerosis.

This study examined functional, biochemical, and morphological characteristics of skeletal muscle in nine multiple sclerosis (MS) patients and eight healthy controls in an effort to ascertain whether intramuscular adaptations could account for excessive fatigue in this disease. Analyses of biopsies of the tibialis anterior muscle showed that there were fewer type I fibers (66 +/- 6 vs. 76 +/- 6%), and that fibers of all types were smaller (average downward arrow26%) and had lower succinic dehydrogenase (SDH; average downward arrow40%) and SDH/alpha-glycerol-phosphate dehydrogenase (GPDH) but not GPDH activities in MS vs. control subjects, suggesting that muscle in this disease is smaller and relies more on anaerobic than aerobic-oxidative energy supply than does muscle of healthy individuals. Maximal voluntary isometric force for dorsiflexion was associated with both average fiber cross-sectional area (r = 0.71, P = 0.005) and muscle fat-free cross-sectional area by magnetic resonance imaging (r = 0.80, P < 0. 001). Physical activity, assessed by accelerometer, was associated with average fiber SDH/GPDH (r = 0.78, P = 0.008). There was a tendency for symptomatic fatigue to be inversely associated with average fiber SDH activity (r = -0.57, P = 0.068). The results of this study suggest that the inherent characteristics of skeletal muscle fibers per se and of skeletal muscle as a whole are altered in the direction of disuse in MS. They also suggest that changes in skeletal muscle in MS may significantly affect function.

Adult↗
PubMed1997

[Molecular analysis of glucose-6-dehydrogenase deficiency in Spain].

PURPOSE: G6PD deficiency is the most frequent enzymopathy-producing genetic polymorphism in humans. Up to now, over 400 putative variants of G6PD have been distinguished on the basis of biochemical characterization of the deficient enzyme. Analysis of the G6PD gene has made possible a precise classification of the G6PD molecular variants by identification of about 80 different point mutations causing much of the phenotypic heterogeneity. In the Spanish population, the analysis of G6PD has led to the identification of 15 different point mutations that underlay the phenotypic heterogeneity of G6PD previously reported by biochemical analysis. The purpose of the study has been to identify the genetic mutation responsible of the G6PD deficiency and to improve the knowledge of its genetic homogeneity. PATIENTS AND METHODS: From 50 Spanish males with G6PD deficiency 34 came from out consultation and 16 from the Spanish Study Group on Red Cell Pathology (GEHBTA-Eritropatología) The methods employed included screening of prevalent mutations by ER-PCR, SSCP-PCR, genetic segmentation and biochemical characterization of the deficient enzyme. RESULTS: In 31 cases the mutations were characteristic of the four most frequent polymorphic variants found in Spain (G6PD A-376G/202A, G6PD Mediterranean 563T G6PD Union 1360T and G6PD Seattle 344C). Since these mutations either create or abolish a specific site recognized by a restriction endonuclease (RE), they can be rapidly detected by RE digestion of a PCR-amplified product (PCR-RE). In patients where none of these mutations were present (17 cases), the G6PD gene was subjected to PCR single-strand conformation polymorphism (PCR-SSCP) analysis combined with direct PCR-sequencing. By using this procedure, 9 new mutations have been identified, five of them have been also found in other geographical areas and were associated with favism (G6PD A-376G/968C, G6PD Santamaria 376G/542T, G6PD Aures 143C and G6PD Chatham 1003A) or chronic haemolytic anaemia (G6PD Tomah 1153C). The other four mutations are unique and not reported so far: Three of them are associated with favism (G6PD Málaga 542T, G6PD Murcia 209G and G6PD Valladolid 406T) and one with chronic haemolytic anaemia (G6PD Madrid 1155G). The remaining eight cases are under study. CONCLUSION: The present study confirms the marked genetic heterogeneity of G6PD deficiency in Spain and demonstrate that the PCR-RE analysis is an easy tool for rapid diagnosis of the molecular defect in subjects with the common forms of G6PD deficiency. Furthermore the fact that G6PD A-376G/202A is the most common variant within Spanish population and the finding of G6PD Aures 43C and G6PD Santamaría 76G/542T, who are polymorphic in Algeria is consistent with a significant gene flow from Africa to Europe through Spain.

Africa, Northern↗
PubMed1996

Candida albicans induces the release of inflammatory mediators from human peripheral blood monocytes.

Candida albicans (C. albicans) is a major nosocomial pathogen. We examined arachidonic acid (AA) and cytokine production by monocytes stimulated with C. albicans. [14C]-AA labeled monocytes released 8.9 +/- 2.3% of the incorporated AA following stimulation with live C. albicans (C. albicans: monocyte of 16:1) (P = 0.0002). Prior studies indicate that soluble alpha-mannans and beta-glucans antagonize mannose and beta-glucan receptors, respectively. Preincubation of monocytes with alpha-mannan (100 micrograms/ml) caused 45.8 +/- 5.7% inhibition of [14C]-AA release, whereas beta-glucan (100 micrograms/ml) yielded 43.7 +/- 6.0% inhibition (P < 0.05 for each compared to control). Additionally, monocytes stimulated with C. albicans also released interleukin-1 beta (IL-1 beta), tumor necrosis factor-alpha (TNF alpha), interleukin-6 (IL-6) and interleukin-8 (IL-8). However, alpha-mannan or beta-glucan failed to inhibit IL-1 beta release. These data indicate that C. albicans induces monocytes to release AA and inflammatory cytokines. Furthermore, AA, but not cytokine liberation, is partially mediated by alpha-mannan and beta-glucan components of the fungus.

Arachidonic Acid↗
PubMed1996

In vitro effects of a flavonoid-rich extract on LDL oxidation.

Flavonoids are phenolic compounds of vegetable origin with antioxidant effects. The present study aimed to determine their properties as LDL antioxidants. LDL were incubated with increasing concentrations of flavonoids (0-16 micrograms/ml) and LDL oxidation was started by adding CuCl2 (2 microM) to the media. When flavonoids were present in the media, vitamin E consumption, the lag phase of conjugated diene formation, LDL electrophoretic mobility in agarose gels and the appearance of thiobarbituric acid reacting substances (TBARS) were delayed in a concentration-dependent manner. To determine whether flavonoids could terminate LDL oxidation once initiated, two sets of experiments were performed. In the first, LDL oxidation was initiated as described above. At 2 or 4 h of incubation, flavonoids were added (4 micrograms/ml) and their effect compared to samples where butylated hydroxytoluene or EDTA were added. At 5 h, in the LDL samples where flavonoids were added, the electrophoretic mobility and TBARS production were the same as those present in LDL samples incubated for the whole period in the absence of flavonoids. However, when either butylate hydroxytoluene or EDTA was added, as would be expected, the LDL oxidation process was completely arrested as shown by a reduction in the appearance of TBARS and a lower LDL electrophoretic mobility. In the second experiment, LDL oxidation was initiated as described above and at 0, 10 and 20 min, flavonoids were added (4 micrograms/ml). When vitamin E was still present in the LDL solution, the flavonoids were able to both increase the lag phase in the formation of conjugated dienes and to delay the consumption of vitamin E. The present results show that in vitro, flavonoids prevent LDL oxidation in a concentration-dependent manner, delaying the consumption of vitamin E, but they cannot terminate or delay LDL oxidation once vitamin E in LDL is consumed.

Antioxidants↗
PubMed1996

Hepatopulmonary syndrome. A pulmonary vascular complication of liver disease.

Hepatopulmonary syndrome is part of the spectrum of pulmonary vascular disorders seen in advanced liver disease. The pathophysiology of these entities likely is dependent on the degree of pulmonary vasoconstriction or vasodilation that occurs. Our understanding of hepatopulmonary syndrome has helped further our knowledge of the interaction of the liver and the lung. Advances in the management of this disorder, especially liver transplantation, finally have allowed us to offer some hope to patients with this disease.

Hemodynamics↗