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Gonzalez, J. A.

Publications and source records attributed to Gonzalez, J. A..

2 recordsLinked to original sources

Strengthening Bolivian Pharmacovigilance system: new therapeutic strategies to improve health of Chagas Disease and Tuberculosis patients

IntroductionChagas disease (CD) and Tuberculosis (TB) are important health problems in Bolivia. Current treatments for both infections require a long period of time, and unwanted drug-related adverse events (ADRs) are frequent.\n\nPurposeThis study aims to strengthen the Bolivian Pharmacovigilance system, focusing on CD and TB.\n\nMethodsA situational diagnosis of Pharmacovigilance in the Department of Cochabamba was performed. The use of a new Local Case Report Form (CRF) was implemented, together with the CRF established by the Unidad de Medicamentos y Tecnologia en Salud (UNIMED), in several health care centers. Training and follow-up on drug safety monitoring and ADR reporting was provided to all health professionals involved in CD and TB treatment. A comparative analysis of the reported ADRs using the CRF provided by UNIMED, the new CRF proposal, and medical records, was performed.\n\nResultsOut of the total patients starting treatment for CD, 35,35% suffered ADR according to the information collected in the medical records, and 25% of them were classified as moderate/severe (MS) types. Only 51,43% of MS ADRs were reported to UNIMED. Regarding TB treatment, 9,89% of the total patients suffered ADR, 44% of them were classified as MS, and 75% of MS ADRs were reported to UNIMED.\n\nConclusionsThe reinforcement of the Bolivian Pharmacovigilance system is an ambitious project that should take a long-term perspective and the engagement of national health workers and other stake holders at all levels. Continuity and perseverance are essential to achieve a solid ADR reporting system, improving patient safety, drug efficacy and adherence to treatment.

pharmacology and toxicology

Orexin/Hypocretin Immunoreactivity In The Lateral Hypothalamus Is Reduced In Genetically Obese But Not In Diet-Induced Obese Mice

The mechanisms that link diet and body weight are not fully understood. A diet high in fat often leads to obesity, and this in part is the consequence of diet-induced injury to specific hypothalamic nuclei. It has been suggested that a diet high in fat leads to cell loss in the lateral hypothalamus, which contains specific populations of neurones that are essential for regulating energy homoeostasis; however, we do not know which cell types are affected by the diet. We studied the possibility that high-fat diet leads to a reduction in orexin/hypocretin (O/H) and/or melanin-concentrating hormone (MCH) immunoreactivity in the lateral hypothalamus. We quantified immuno-labelled O/H and MCH cells in brain sections of mice fed a diet high in fat for up to 12 weeks starting at 4 weeks of age and found that this diet did not modify the number of O/H- or MCH-immunoreactive neurones. By contrast, there were fewer O/H- (but not MCH-) immunoreactive cells in geneticallyobese db/db mice compared to wild-type mice. Non-obese, heterozygous db/+ mice also had fewer O/H-immunoreactive cells. Differences in the number of O/H-immunoreactive cells were only a function of the db genotype but not of diet or body weight. Our findings show that the lateral hypothalamus is affected differently in genetic and in diet-induced obesity, and support the idea that hypothalamic neurones involved in energy balance regulation are not equally sensitive to the effects of diet.

neuroscience