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Biomedical subjects

C O Silva

Publications and source records attributed to C O Silva.

8 recordsLinked to original sources
PubMed2006

Purification of a beta-galactosidase from cotyledons of Hymenaea courbaril L. (Leguminosae). Enzyme properties and biological function.

Beta-galactosidases are enzymes that can be found in most living beings and in the plant kingdom its activity and genes have been detected in several tissues such as ripening fruits, developing leaves and flowers and storage tissues such as cotyledons. In plants, their activities are usually associated with the secondary metabolism or with oligosaccharide or polysaccharide degradation. Polysaccharide specific beta-galactosidases include beta-galactanases, which attack pectic polymers and beta-galactosidases that attack xyloglucans (XG). In the present work we purified an XG-specific beta-galactosidase (named hcbetagal) from cotyledons of developing seedlings of Hymenaea courbaril, a legume tree from the Neotropical region of the world. The enzyme has a molecular weight of 52-62 kDa and was shown to attack specifically xyloglucan oligosaccharides (XGOs) but not the polymer. It has a pH optimum between 3 and 4 and at this pH range the enzyme increases activity linearly up to 50 degrees C. Kinetic studies showed that hcbetagal is inhibited competitively by free galactose (K(i) = 3.7). The biochemical properties of hcbetagal as a whole suggest that it is involved in storage xyloglucan mobilisation during seedling development. Its high specificity towards XGOs, the low pH optimum and the fact that it is inhibited by its product (galactose) suggest that hcbetagal might be one of the biochemical control points in xyloglucan catabolism in vivo. A possible relationship with functional stability of the wall during cell death as cotyledons undergo senescence is discussed.

Cell Death↗
PubMed2005

Hereditary gingival fibromatosis: report of a five-generation family using cellular proliferation analysis.

BACKGROUND: Hereditary gingival fibromatosis (HGF) is an uncommon condition characterized by an accumulation of extracellular matrix resulting in a fibrotic enlargement of the gingiva. The goal of this article is to describe one kindred affected with HGF and discuss the diagnosis, treatment, and control of the disease. The pattern of inheritance, histopathologic characteristics, and proliferative potential of epithelial and mesenchymal cells of HGF are also emphasized. METHODS: To characterize the pattern of inheritance and the clinical appearance of gingival overgrowth, 117 family members were examined. The recurrence risk was estimated by the use of a genetic analysis program. Immunohistochemistry against the proliferating cell nuclear antigen (PCNA) and pKi-67 was performed to assess cellular proliferation of normal gingiva (NG) and HGF cells. RESULTS: Examination of the family pedigree demonstrated an autosomal dominant trait of inheritance, and a sibling recurrence risk of 0.085 and an offspring recurrence risk of 0.078, indicating that HGF was a consequence of genetic alteration with low penetrance. Unaffected and affected members transmitted the disease to their offspring. The affected patients showed a generalized but mild gingival overgrowth. Surgical treatment consisted of a combination of gingivectomy and gingivoplasty. Histologic examination showed that the gingival lesions of all patients were quite similar, with increased amounts of collagen fiber bundles in the connective tissue. Immunohistochemistry revealed that the proliferative potential of epithelial cells was significantly higher in the HGF group compared to the NG group, whereas mesenchymal cells from both groups were negative for the proliferative markers. CONCLUSION: Our data demonstrated that, in the studied family, HGF is transmitted by an autosomal dominant pattern with incomplete disease penetrance, and although the gingival enlargement resulted from an excessive accumulation of collagen fibers, HGF is characterized by an increase in the proliferation rate of epithelial cells.

Cell Proliferation↗
PubMed2001

Effects of long-term pretreatment with isoproterenol on inotropic responsiveness to alpha-adrenoceptor stimulation: study in isolated perfused rat hearts.

The effects of chronic pretreatment with isoproterenol (5 mg kg(-1)) daily for 10 days on cardiac alpha-adrenergic responsiveness in Langendorff heart preparations were investigated. Isoproterenol pretreatment caused cardiac hypertrophy (29%) as shown by a significant increase in the ratio of ventricular dry weight to body weight. In preparations from isoproterenol-pretreated rats, both maximum increases in left ventricular systolic pressure and heart rate elicited by isoproterenol (10(-12) to 10(-4) M) were significantly reduced (the isoproterenol concentration producing 50% of the maximum positive inotropic and chronotropic responses was enhanced almost 32- and 4-fold, respectively), while the positive inotropic response to phenylephrine (10(-12) to 10(-4) M) was significantly enhanced (the phenylephrine concentration producing 50% of the maximum positive inotropic effect was reduced almost 100-fold), compared with saline-pretreated rats. In preparations from both groups, phenylephrine infusion induced non-significant changes in heart rate and its positive inotropic response was reduced in the presence of propranolol (10(-7) M) in the perfusion medium. Even under beta-adrenoceptor blockade, the curve for the phenylephrine-induced positive inotropic effect remained shifted upward after isoproterenol pretreatment. Chronic isoproterenol pretreatment induces the expected cardiac beta-adrenoceptor desensitization while simultaneously enhancing the positive inotropic responsiveness to phenylephrine in Langendorff heart preparations. These findings support the hypothesis that cardiac alpha1-adrenoceptor stimulation may contribute to the maintenance of myocardial function under conditions in which beta-adrenoceptor function is compromised.

Adrenergic alpha-Agonists↗
PubMed1999

Comparison of spiramycin and clarithromycin for community-acquired lower respiratory tract infections.

This open multicentre study compared the efficacy and tolerability of clarithromycin and spiramycin in the treatment of lower respiratory tract infections in Brazil and Colombia. A total of 125 patients with a clinical and radiological diagnosis of pneumonia, acute bronchitis or exacerbation of chronic bronchitis were randomised to receive oral doses of either clarithromycin (500 mg) or spiramycin (3 MIU) every 12 hours for courses of 5-10 days. Patients were assessed before the start of treatment, and at days 3-4 and days 9-17. Twenty-six (26) patients (16 in the spiramycin group and 10 in the clarithromycin group) reported adverse events, seven of whom withdrew from the trial. Statistical analysis detected no significant differences between efficacy (p = 0.768) or tolerability (p = 0.236) for the two treatment groups. Spiramycin therefore has similar efficacy to clarithromycin in the treatment of community-acquired lower respiratory tract infections.

Adolescent↗
PubMed1991

[The effect of nifedipine on hemodynamics and gas exchange in dogs with experimental acute respiratory insufficiency].

PURPOSE: Evaluate the action of nifedipine, a calcium channel blocking agent, on the hemodynamics and gas exchange experimental acute respiratory failure. METHODS: Lung injury was provoked in sixteen mongrel dogs with intratracheal instillation of hydrochloric acid (HC1) (0.1N; pH = 2.0; 2.0 ml/kg body weight). As steady state was achieved after HC1 instillation (maintenance of a stable arterial PO2), saline 1 ml (six dogs) or nifedipine (ten dogs) 30 micrograms/kg for body weight were intravenously injected. The hemodynamic variables and gas exchange parameters were analyzed before HC1, after HC1 and 10 and 30 minutes after nifedipine or saline. RESULTS: The intratracheal instillation of HC1 provoked significant drop of PaO2, of systemic oxygen transport index (ITO2S), and increase of venous admixture (QVA/Q). Nifedipine provoked significant reduction of the mean systemic arterial pressure (Pas), and of the systemic (IRVS) and pulmonary vascular resistance index (IRVP), with significant increase of cardiac (IC) and systolic index (IS), with no changes ot the mean arterial pulmonary (Pap) and capillary pressures (Pcap). After nifedipine there was a significant increase of PaO2, PvO2, and ITO2S, with no significant variations of QVA/Q and alveolar arterial O2 difference (P(A-a)O2). CONCLUSION: Nifedipine promoted systemic vasodilation, and probably by increasing the venous return and/or by a reflex mechanism, the cardiac output increased, augmenting the ITO2S. The IRVP decreased in the nifedipine group, with no significant alterations of Pap and Pcap, probably consequent to the systemic vasodilation provoked by the drug. The arterial PO2 augmented in the nifedipine group, as a consequence of mixed venous PO2 increase, since no changes occurred in QVA/Q, P(A-a)O2, inspired fraction of O2 and alveolar ventilation.

Acute Disease↗