21 research outputs found
Constituição cidadã e representações sociais: uma reflexão sobre modelos de assistência à saúde
Ocorrência de bactérias clinicamente relevantes nos resíduos de serviços de saúde em um aterro sanitário brasileiro e perfil de susceptibilidade a antimicrobianos
Modulation of 11β-hydroxysteroid dehydrogenase as a strategy to reduce vascular inflammation
Atherosclerosis is a chronic inflammatory disease in which initial vascular damage leads to extensive macrophage and lymphocyte infiltration. Although acutely glucocorticoids suppress inflammation, chronic glucocorticoid excess worsens atherosclerosis, possibly by exacerbating systemic cardiovascular risk factors. However, glucocorticoid action within the lesion may reduce neointimal proliferation and inflammation. Glucocorticoid levels within cells do not necessarily reflect circulating levels due to pre-receptor metabolism by 11β-hydroxysteroid dehydrogenases (11β-HSDs). 11β-HSD2 converts active glucocorticoids into inert 11-keto forms. 11β-HSD1 catalyses the reverse reaction, regenerating active glucocorticoids. 11β-HSD2-deficiency/ inhibition causes hypertension, whereas deficiency/ inhibition of 11β-HSD1 generates a cardioprotective lipid profile and improves glycemic control. Importantly, 11β-HSD1-deficiency/ inhibition is atheroprotective, whereas 11β-HSD2-deficiency accelerates atherosclerosis. These effects are largely independent of systemic risk factors, reflecting modulation of glucocorticoid action and inflammation within the vasculature. Here, we consider whether evidence linking the 11β-HSDs to vascular inflammation suggests these isozymes are potential therapeutic targets in vascular injury and atherosclerosis
Electrochemotherapy in the Treatment of Cutaneous Metastases from Breast Cancer: A Multicenter Cohort Analysis
Bioequivalence of two lithium formulations in healthy volunteers
Objective. The purpose of this study was to compare the maximum exposure and extent of bioavailability of two lithium carbonate (CAS 554-13-2) containing 300 mg tablet formulations (test and reference) for oral administration. Method. This bioequivalence study was conducted in a 2-period crossover design with a washout phase of 7 days. Plasma samples were obtained by blood sampling over 72 h in each period. Twenty-four healthy volunteers of both genders participated in the trial. Samples were analyzed by a flame atomic absorption spectrometer. Resulting Li+ concentrations were used for determination of the pharmacokinetic parameters AUC(last), AUC(inf) and C-max. Results: 90 % confidence intervals for AUC(last), AUC(inf), and C-max were 96.81-107.44 98.44-109.54 % and 98.60-111.33 respectively. Conclusion: All 90 % and 95 % confidence intervals were inside the limits defined by the FDA Guidance for Industry (80 %-125 %) and thus stated that test and reference formulation may be accepted as bioequivalent, with regard to both, maximum exposure and extent of bioavailability.56752452