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Search Results: 1 - 10 of 512899 matches for " A. I.; Morbidoni "
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Mecanismos de acción y de resistencia a rifampicina e isoniacida en Mycobacterium tuberculosis: nueva información sobre viejos conocidos
De la Iglesia,A. I.; Morbidoni,Y H. R.;
Revista argentina de microbiolog?-a , 2006,
Abstract: human tuberculosis is still one of the most frequent causes of death worldwide. despite the implementation of therapeutic regimes combining four drugs, the rise of resistant and multidrug-resistant mycobacterium tuberculosis strains has compromised their efficacy. two of the most effective anti-tubercular drugs in use, rifampicin and isoniazid, have been closely studied due to their therapeutic importance. these studies have led to the identification of the genes involved in resistance mechanisms and of those encoding the molecular targets for these drugs. rifampicin is an inhibitor of the b-subunit of the rna polymerase of prokaryotes, including m. tuberculosis. resistance to rifampicin is mediated by mutations clustered in a small region of the rpob gene. a fraction of resistant strains showed no mutations in rpob, suggesting that other mechanisms of resistance, possibly efflux pumps, may exist. isoniazid is a pro-drug activated by katg, a catalase-peroxidase. mutations in katg, the most commonly found in m. tuberculosis clinical isolates, give high levels of resistance. in spite of this, the molecular target for isoniazid is inha, an enoyl-acp-reductase involved in the biosynthesis of mycolic acids. other mutations causing resistance to isoniazid have been mapped to ndh, a gene encoding the nadh dehydrogenase.
Mecanismos de acción y de resistencia a rifampicina e isoniacida en Mycobacterium tuberculosis: nueva información sobre viejos conocidos Mechanisms of action of and resistance to rifampicin and isoniazid in Mycobacterium tuberculosis: new information on old friends
A. I. De la Iglesia,Y H. R. Morbidoni
Revista argentina de microbiolog?-a , 2006,
Abstract: La tuberculosis constituye todavía una de la causas más frecuentes de mortalidad en el mundo. A pesar de la implementación de tratamientos con cuatro drogas antituberculosas, la aparición de cepas resistentes y multirresistentes ha comprometido la eficacia de los mismos. Dos de las drogas en uso, la rifampicina y la isoniacida, recibieron gran atención por su importancia terapéutica, incluso se han identificado los genes involucrados en los mecanismos de resistencia y los que codifican para sus blancos moleculares. La rifampicina es un inhibidor de la subunidad beta de la ARN polimerasa de procariotas, incluido Mycobacterium tuberculosis. La resistencia a esta droga está principalmente mediada por mutaciones agrupadas en una región del gen rpoB. Una peque a fracción de cepas resistentes no mostró mutaciones en rpoB, lo que sugiere la existencia de otros mecanismos de resistencia, posiblemente eflujo de la droga. La isoniacida es una prodroga que se activa por la catalasa-peroxidasa KatG. Mutaciones en katG son las más comúnmente identificadas en cepas clínicas de M. tuberculosis resistentes a isoniacida, confiriendo altos niveles de resistencia. Sin embargo, el blanco molecular de acción para la isoniacida es la InhA, una enoil-ACP reductasa involucrada en la vía de síntesis de los ácidos micólicos. Otras mutaciones involucradas en la resistencia a la isoniacida afectan al gen ndh, que codifica para la NADH deshidrogenasa. Human tuberculosis is still one of the most frequent causes of death worldwide. Despite the implementation of therapeutic regimes combining four drugs, the rise of resistant and multidrug-resistant Mycobacterium tuberculosis strains has compromised their efficacy. Two of the most effective anti-tubercular drugs in use, rifampicin and isoniazid, have been closely studied due to their therapeutic importance. These studies have led to the identification of the genes involved in resistance mechanisms and of those encoding the molecular targets for these drugs. Rifampicin is an inhibitor of the beta-subunit of the RNA polymerase of prokaryotes, including M. tuberculosis. Resistance to rifampicin is mediated by mutations clustered in a small region of the rpoB gene. A fraction of resistant strains showed no mutations in rpoB, suggesting that other mechanisms of resistance, possibly efflux pumps, may exist. Isoniazid is a pro-drug activated by KatG, a catalase-peroxidase. Mutations in katG, the most commonly found in M. tuberculosis clinical isolates, give high levels of resistance. In spite of this, the molecular target for isoniazid is Inh
Mycobacteriophages as versatile tools for genetic manipulation of mycobacteria and development of simple methods for diagnosis of mycobacterial diseases
Stella,E. J.; De La Iglesia,A. I.; Morbidoni,H. R.;
Revista argentina de microbiolog?-a , 2009,
Abstract: tuberculosis, caused by mycobacterium tuberculosis, is responsible for over two million deaths per year worldwide. due to its long doubling time (18 h), the microbiological detection of m. tuberculosis by conventional methods takes up to one month, unless the number of bacilli in the biological sample is high enough. thus, drug resistance assessment requires at least one month for obtaining the primary culture and another month to determine its susceptibility to antimycobacterial drugs. moreover, for a long time, the lack of genetic tools for mycobacteria has been a barrier for undertaking studies aimed at understanding the mechanisms of drug resistance and drug target identification, being all these topics of utmost importance considering the increase in the number of drug-resistant clones and the few therapeutic options available. mycobacteriophages are promising as a novel source of genetic elements for mycobacteria manipulation, as well as for the development of versatile, simple, fast and cheap methods for drug resistance assessment of m. tuberculosis clinical isolates. we herein describe the background related to the use of mycobacteriophages, with emphasis placed on their utilization for drug resistance analysis in our country.
Mycobacteriophages as versatile tools for genetic manipulation of mycobacteria and development of simple methods for diagnosis of mycobacterial diseases Micobacteriófagos como herramientas versátiles para la manipulación genética y el desarrollo de métodos simples para el diagnóstico de enfermedades micobacterianas
E. J. Stella,A. I. De La Iglesia,H. R. Morbidoni
Revista argentina de microbiolog?-a , 2009,
Abstract: Tuberculosis, caused by Mycobacterium tuberculosis, is responsible for over two million deaths per year worldwide. Due to its long doubling time (18 h), the microbiological detection of M. tuberculosis by conventional methods takes up to one month, unless the number of bacilli in the biological sample is high enough. Thus, drug resistance assessment requires at least one month for obtaining the primary culture and another month to determine its susceptibility to antimycobacterial drugs. Moreover, for a long time, the lack of genetic tools for mycobacteria has been a barrier for undertaking studies aimed at understanding the mechanisms of drug resistance and drug target identification, being all these topics of utmost importance considering the increase in the number of drug-resistant clones and the few therapeutic options available. Mycobacteriophages are promising as a novel source of genetic elements for mycobacteria manipulation, as well as for the development of versatile, simple, fast and cheap methods for drug resistance assessment of M. tuberculosis clinical isolates. We herein describe the background related to the use of mycobacteriophages, with emphasis placed on their utilization for drug resistance analysis in our country. La tuberculosis, enfermedad causada por el bacilo Mycobacterium tuberculosis, es responsable de más de dos millones de muertes anuales en el mundo. Debido a su largo tiempo de duplicación (18 h), la detección bacteriológica de M. tuberculosis por métodos convencionales necesita de un mes o aun más, a menos que el número de bacilos en la muestra clínica sea suficientemente alto. Por consiguiente, se necesita un mínimo de dos meses para determinar la resistencia de este microorganismo a las drogas antituberculosas: uno para obtener el cultivo primario y otro para ensayar la sensibilidad frente a aquellas. La falta de herramientas para la manipulación genética de micobacterias ha dificultado la identificación de los blancos de acción de las drogas y el estudio de los mecanismos de resistencia a éstas, tópicos de la mayor relevancia dado el aumento mundial del número de aislamientos clínicos multirresistentes y las pocas opciones terapéuticas disponibles. Los micobacteriófagos son considerados nuevas herramientas para la manipulación de las micobacterias, así como para el desarrollo de métodos simples, rápidos y económicos para determinar la sensibilidad a drogas de los aislamientos clínicos de M. tuberculosis. En esta revisión se describen los antecedentes del uso de micobacteriófagos con énfasis en su utilización para el aná
La moral de Tartufo?
Héctor R. Morbidoni,Gerardo A. Leotta
Revista argentina de microbiolog?-a , 2010,
Abstract:
Tuberculosis: un viejo enemigo
Hector Ricardo Morbidoni
Química Viva , 2004,
Abstract: Mycobacterium tuberculosis, agente causal de la tuberculosis humana, es responsable de casi tres millones de muertes por a o en el mundo, siendo además uno de los patógenos oportunistas de mayor incidencia en pacientes HIV+. El tratamiento de la tuberculosis requiere varios antibióticos durante por lo menos seis meses, lo cual causa un elevado grado de incumplimiento. Esta situación favorece la aparición de cepas clínicas resistentes a una o más drogas. Estudios llevados a cabo durante los últimos a os han identificado los blancos moleculares de las drogas corrientemente en uso y sus mecanismos de resistencia mas frecuentes. La información generada ha evidenciado un dato de gran interés: la mayoría de las drogas especificas activas contra M. tuberculosis (como Isoniacida, Etionamida, o Pirazinamida) afectan la síntesis de ácidos grasos (incluyendo los ácidos micólicos, ácidos grasos de cadena muy larga presentes en micobacterias) o de componentes de la pared celular como el caso arabinogalactano cuya síntesis es inhibida por la droga Etambutol. Estos resultados han generado un gran interés en el estudio de la síntesis de estos componentes celulares para identificar nuevos blancos aptos para el dise o de fármacos, lo cual trae esperanza para lograr mejores drogas para el tratamiento de la tuberculosis
Transferencia e intercambio de conocimiento a través de reuniones científicas: cerca del corazón de los amigos, lejos de las arcas del Estado
Héctor Ricardo Morbidoni
Revista argentina de microbiolog?-a , 2009,
Abstract:
Círculo vicioso vs. círculo virtuoso: cómo mantener a la RAM en el SCIE
Héctor Ricardo Morbidoni
Revista argentina de microbiolog?-a , 2009,
Abstract:
La "nano", el "Mano" y la microbiologia clinica The nanotech, the "Mano" and the clinical microbiology
Hector R Morbidoni,Ana M Jar
Revista argentina de microbiolog?-a , 2012,
Abstract:
Cyclosporin A promotes in vivo myogenic response in collagen VI deficient myopathic mice
Francesca Gattazzo,Sibilla Molon,Valeria Morbidoni,Braghetta Paola,Paolo Bonaldo
Frontiers in Aging Neuroscience , 2014, DOI: 10.3389/fnagi.2014.00244
Abstract: Mutations of genes encoding for collagen VI cause various muscle diseases in humans, including Bethlem myopathy and Ullrich congenital muscular dystrophy. Collagen VI null (Col6a1–/–) mice are affected by a myopathic phenotype with mitochondrial dysfunction, spontaneous apoptosis of muscle fibers and defective autophagy. Moreover, Col6a1–/– mice display impaired muscle regeneration and defective self-renewal of satellite cells after injury. Treatment with cyclosporin A (CsA) is effective in normalizing the mitochondrial, apoptotic and autophagic defects of myofibers in Col6a1–/– mice. A pilot clinical trial with CsA in Ullrich patients suggested that CsA may increase the number of regenerating myofibers. Here we report the effects of CsA administration at 5 mg/kg body weight every 12 hr in Col6a1–/– mice on muscle regeneration under physiological conditions and after cardiotoxin (CdTx)-induced muscle injury. Our findings indicate that CsA influences satellite cell activity and triggers the formation of regenerating fibers in Col6a1–/– mice. Data obtained on injured muscles show that under appropriate administration regimens CsA is able to stimulate myogenesis in Col6a1–/– mice by significantly increasing the number of myogenin (MyoG)-positive cells and of regenerating myofibers at the early stages of muscle regeneration. CsA is also able to ameliorate muscle regeneration of Col6a1–/– mice subjected to multiple CdTx injuries, with a concurrent maintenance of the satellite cell pool. Our data show that CsA is beneficial for muscle regeneration in Col6a1–/– mice.
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