oalib
Search Results: 1 - 10 of 100 matches for " "
All listed articles are free for downloading (OA Articles)
Page 1 /100
Display every page Item
Resistencia a drogas en M. Tuberculosis: Bases moleculares
N Arráiz,V Bermúdez,B Urdaneta
Archivos Venezolanos de Farmacología y Terapéutica , 2005,
Abstract: La tuberculosis es una de las enfermedades infecciosas responsables de altas tasas de morbi-mortalidad a nivel mundial. La terapia de corta duración (DOTS) recomendada por la Organización de la Salud (OMS) incluye los antibióticos isoniazida, rifampicina, pirazinamida, estreptomicina y etambutol. Lamentablemente, la estrategia DOTS deja de ser la opción terapéutica para pacientes infectados con M. tuberculosis multirresistentes a drogas (TB-MDR) definidas como cepas resistentes al menos a isoniazida y rifampicina. La resistencia a drogas en M. tuberculosis se debe predominantemente a alteraciones en genes que codifican blancos de antibióticos y hasta el presente se han identificado múltiples mutaciones cromosomales asociadas al desarrollo de resistencia a antibióticos de primera línea. La caracterización de estas mutaciones ha conducido al desarrollo de nuevas estrategias de diagnóstico molecular que podrían acortar el periodo de reporte del patrón de resistencia a drogas en M. tuberculosis. La detección temprana de cepas resistentes a drogas de primera línea, contribuiría a un mejor manejo terapéutico del paciente con drogas de segunda línea y disminución del riesgo de propagación de cepas de TB-MDR. The tuberculosis is one of the infectious diseases responsible for high rates of morbi-mortality at world-wide level. The therapy of short duration (DOTS) recommended by the Organization of the Health (WHO) includes drugs isoniazid, rifampin, pyrazinamide, streptomycin and ethambutol. Unfortunately, strategy DOTS stops being the therapeutic option for patients infected with multidrug-resistant M.tuberculosis (MDR-TB) defined as TB resistant to at least isoniazid and rifampicin. The resistance to drugs in M. tuberculosis predominantly derives from alterations in genes that encodes antibiotic targets and until the present multiple chromosomal mutations associated to the development of resistance to first line drugs have been identified. The characterization of these mutations has lead to the development of new strategies for molecular diagnosis that could shorten the period of report of the drugs resistance pattern in M. tuberculosis. The early detection of resistant to first line drugs, provides useful insights for better therapeutic management of patient with second line drugs and decreasing the risk of propagation of TB-MDR strains.
RESISTANCE MECHANISMS OF ALUMINUM (Al3+)PHYTOTOXICITY IN CEREALS: PHYSIOLOGICAL, GENETIC AND MOLECULAR BASES Mecanismos de resistencia a la fítotoxicidad por aluminio (Al3+) en cereales: bases fisiológicas, genéticas y moleculares
Claudio Inostroza-Blancheteau,Braulio Soto,Pilar Ulloa,Felipe Aquea
Revista de la Ciencia del Suelo y Nutrición Vegetal , 2008,
Abstract: Aluminum (Al) toxicity is one of the main factors limiting crop productivity in acid soils around the world. In cereals, this problem can affect between 30 and 40% of crop yields. One way to reduce the toxic effect of Al is to neutralize the acidity with calcareous amendments. However, this practice is demanding and not very effective. An alternative is the search for genetic variability in the genome of cropping grasses and/or their wild relatives to resist Al. The development of biotechnology and molecular genetics approach has facilitated the understanding of the physiological, genetic and molecular bases in the process of ameliorating these species. This review presents the main physiological mechanisms of Al resistance and the genetic and molecular bases that explain the degree of resistance between different cereals species. La toxicidad por aluminio (Al), es uno de los principales factores que limitan la productividad de los cultivos en los suelos ácidos alrededor del mundo. En cereales este problema puede afectar entre 30 a 40% los rendimientos de los cultivos. Una de las opciones para reducir el efecto tóxico del Al, es neutralizar la acidez con el uso de enmiendas calcáreas. Sin embargo, esta es una práctica muy laboriosa y poco efectiva. Una alternativa es la búsqueda de variabilidad genética para la resistencia a Al en el genoma de gramíneas cultivadas y/o sus parientes silvestres. El desarrollo de la biotecnología y la genética molecular han facilitado el entendimiento de las bases fisiológicas, genéticas y moleculares en el proceso de mejoramiento de estas especies. En este review se presentan los principales mecanismos fisiológicos de la resistencia a la fitotoxicidad por Al y los fundamentos genéticos y moleculares que explican el grado de resistencia entre las diferentes especies de cereales.
Bases moleculares de las leucemias agudas
G. Martínez Antu?a
Iatreia , 2006,
Abstract: El gran desarrollo de la biología molecular en los últimos a os ha contribuido a un importante avance en los conocimientos relacionados con las bases moleculares de las leucemias agudas (LA). Ademas de profundizar en la biología de estas enfermedades y conocer las bases moleculares, ha renido también gran impacto en mejorar el resultado de los tratamientos y disminuir la toxicidad de las terapias.
Genetica de la resistencia cuantitativa a la roya amarilla  [cached]
Josu00E9 Sergio Sandoval Islas,Leonardus Hendricus Broers,Hugo Vivar Flores
Revista fitotecnia mexicana , 2002,
Abstract: A la fecha existe muy poca información acerca de la resistencia cuantitativa a la roya amarilla en cebada (Puccinia striiformis f. sp. hordei). Para auxiliar a los programas de mejoramiento es necesario conocer más sobre la genética de la resistencia. Por esta razón, se cruzaron tres cultivares de cebada con resistencia cuantitativa (Calicuchima- 92, Gloria/Copal y Alelí) procedentes del programa de cebada del ICARDA-CIMMYT (International Center for Agricultural Research in Dry Areas-Centro Internacional de Mejoramiento de Maíz y Trigo) y un cultivar susceptible (Apizaco). La respuesta de la F1, F2, F3 se evaluó después de que fueron inoculdadas con una variante de la raza 24 de Puccinia striiformis f. sp. hordei. La F1 reveló recesividad parcial en todas las cruzas. La F2 y F3 revelaron segregación para dos loci en Calicuchima-92 y Gloria/Copal y para tres loci en Alelí. En cada cruza de resistente por resistente se encontró un locus común, sugiriendo que en estas tres poblaciones existen de cuatro a cinco genes que pueden ser acumulados mediante técnicas de hibridación y selección.
Resistencia a drogas en M. Tuberculosis: Bases moleculares
Arráiz,N; Bermúdez,V; Urdaneta,B;
Archivos Venezolanos de Farmacología y Terapéutica , 2005,
Abstract: the tuberculosis is one of the infectious diseases responsible for high rates of morbi-mortality at world-wide level. the therapy of short duration (dots) recommended by the organization of the health (who) includes drugs isoniazid, rifampin, pyrazinamide, streptomycin and ethambutol. unfortunately, strategy dots stops being the therapeutic option for patients infected with multidrug-resistant m.tuberculosis (mdr-tb) defined as tb resistant to at least isoniazid and rifampicin. the resistance to drugs in m. tuberculosis predominantly derives from alterations in genes that encodes antibiotic targets and until the present multiple chromosomal mutations associated to the development of resistance to first line drugs have been identified. the characterization of these mutations has lead to the development of new strategies for molecular diagnosis that could shorten the period of report of the drugs resistance pattern in m. tuberculosis. the early detection of resistant to first line drugs, provides useful insights for better therapeutic management of patient with second line drugs and decreasing the risk of propagation of tb-mdr strains.
Bases moleculares del cáncer
Meza-Junco, Judith;Monta?o-Loza, Aldo;Aguayo-González, Alvaro;
Revista de investigación clínica , 2006,
Abstract: cancer is a group of diseases characterized by an autonomous proliferation of neoplastia cells which have a number of alterations, including mutations and genetic instability. cellular functions are controlled by proteins, and because these proteins are encoded by dna organized into genes, molecular studies have shown that cancer is a paradigm of acquired genetic disease. the process of protein production involves a cascade of several different steps, each with its attendant enzymes, which are also encoded by dna and regulated by other proteins. most steps in the process can be affected, eventually leading to an alteration in the amount or structure of proteins, which in turn affects cellular function. however, whereas cellular function may be altered by disturbance of one gene, malignant transformation is thought to require two or more abnormalities occurring in the same cell. although there are mechanisms responsible for dna maintenance and repair, the basic structure of dna and the order of the nucleotide bases can be mutated. these mutations can be inherited or can occur sporadically, and can be present in all cells or only in the tumor cells. at the nucleotide level, these mutations can be substitutions, additions or deletions. several of the oncogenes discussed below, including the pb3, c-fms, and ras genes, can be activated by point mutations that lead to aminoacid substitution in critical portions of the protein. this article examines the current concepts relating to cellular mechanism that underlie the molecular alterations that characterize the development of cancer.
Bases Moleculares da Hiperplasia Adrenal Congênita
Mello Maricilda Pallandi de,Bachega Tania A.S.S.,Costa-Santos Marivania da,Mermejo Lívia Mara
Arquivos Brasileiros de Endocrinologia & Metabologia , 2002,
Abstract: Hiperplasia adrenal congênita (HAC) é uma doen a autoss mica recessiva decorrente da altera o de enzimas que participam da síntese do cortisol. As manifesta es podem ser causadas pela deficiência do cortisol e, em alguns casos, aldosterona e pelo acúmulo de precursores. O objetivo desta revis o é apresentar os mecanismos moleculares dos principais defeitos enzimáticos envolvidos na etiopatogênese da HAC. A deficiência da 21-hidroxilase (21OH) ocorre em 95% dos casos de HAC. Existem dois genes que codificam o P450c21: um ativo, CYP21, e um pseudogene CYP21P. Ambos s o altamente homólogos (98%), o que favorece o emparelhamento desigual dos cromossomos homólogos durante a meiose, levando a duplica es e/ou dele es ou convers es desses genes. Adicionalmente, foram também descritas muta es de ponto, muitas delas presentes no pseudogene sugerindo microconvers es. Muta es no gene CYP11B1 causam HAC por deficiência da 11beta-hidroxilase, forma esta que corresponde a 5% dos casos. Algumas muta es s o recorrentes, situando-se principalmente entre os exons 6-8 que representaria uma área hot-spot no gene CYP11B1. A deficiência de 17-hidroxilase é causada por muta es no gene CYP17, que codificam uma proteína alterada, levando a deficiência total ou parcial de 17-hidroxila o e 17,20-liase ou deficiência isolada de 17,20-liase. Finalmente, deficiência de 3beta-HSD é causada por muta es no gene HSD3B2, que codifica a enzima 3beta-HSD tipo II e estas muta es têm sido associadas tanto com a forma clássica como com a forma n o clássica da deficiência da 3beta-HSD.
Las Bases Moleculares del Cáncer Las Bases Moleculares del Cáncer
Juan Carlos Raya Pérez
Acta Universitaria , 2012,
Abstract: El estudio del cáncer a nivel molecular ha permitido el descubrimiento de gran cantidad de genes mutados relacionados con esta enfermedad. Estos genes son supresores de tumores u oncogenes, que tienen con ver la proliferación celular, la metástasis y/o la capacidad de las células para inducir la vascularización del tejido. La búsqueda de terapias ha llevado al descubrimiento de muchas moléculas capaces de inhibir el crecimiento de las células cancerosas, aunque la mejor opción sigue siendo la revisión periódica y la prevención. Al parecer, pese a los avances, los marcadores moleculares fallan en un alto porcentaje al tratar de diagnosticar un cáncer, así como al tratar de dar un pronóstico. Esto podría deberse al hecho de que se esta abordando el problema a nivel de célula. Cancer research has allowed us to discover many genes implied in development of this disease. These genes are suppressors or oncogenes that participate in cellular proliferation, methastasis and/or capacity of cell to induce vascularization of the tissue. Also, it has allowed the discovery of molecules able to inhibit the growth of cells cancerous. However, periodic checkups continues to be the best prevention against cancer. At molecular level is difficult to diagnose it, perhaps because is necessary to go to the tissue level. Molecular markers are not yet a reliable method in order to obtain a diagnosis or forecast cancer, maybe because one forgets the tissue level.
Bases moleculares del cáncer oral: Revisión bibliográfica  [cached]
V García García,MA González-Moles,A Bascones Martínez
Avances en Odontoestomatología , 2005,
Abstract: El cáncer oral representa del 2 al 4% de todos los cánceres diagnosticados, con un incremento anual de 5000 nuevos casos por a o, aunque cabe destacar la marcada variabilidad geográfica respecto a su incidencia. Histológicamente, el carcinoma de células escamosas o epidermoide es el tumor más común encontrado en la cavidad oral. Es indiscutible el papel del odontólogo en la prevención primaria (promocionando un estilo de vida saludable) y secundaria (diagnóstico precoz) del cáncer oral. Entender las bases moleculares del cáncer oral supone una tarea ardua que trataremos de resolver simplificando lo máximo posible y ayudándonos de esquemas esclarecedores para comprender la raíz de esta inquietante y desconocida enfermedad. Oral cancer represents 2%-4% of the all types of cancer that are diagnosed with an annual increment of 5000 new cases per year, and it′s related to the variety that exist in the different geographical areas. Histologically, escamous cell carcinoma or epidermal carcinoma is the most common tumour found in the oral cavity. The dentist has a very important role about primary prevention (by promoting a health life style ) and about secondary prevention( early diagnose) of oral cancer. To simplify the knowledge of molecular bases of oral cancer we will use diagrams to clarify this disturbing and unknown illnesses.
Staphylococcus aureus resistente a meticilina: bases moleculares de la resistencia, epidemiología y tipificación
Jiménez Quiceno,Judy Natalia; Correa Ochoa,Margarita María;
Iatreia , 2009,
Abstract: staphylococcus aureus is responsible for a wide variety of clinical manifestations ranging from skin and soft tissue infections to severe systemic and life threatening diseases; it is of relevance in the community and is commonly associated with nosocomial infections. additionally, a high percentage of the population is colonized by s. aureus, which constitutes a risk factor for its dissemination. s. aureus has great capacity to acquire antimicrobial resistance, and currently there are resistant strains to the majority of available antibiotics; in particular, its resistance to methycillin, initially in the hospital environment (hospital associated methycillin resistant s. aureus, ha-mrsa) and later in the community (community acquired methycillin resistant s. aureus, ca-mrsa), has made even more difficult the worldwide control of this microorganism. molecular epidemiological studies have provided a better understanding of the evolutionary relationships of the strains, and the definition of the clonal source during epidemic outbreaks. in colombia, very little is known about s. aureus epidemiology and even less about its behavior in the community. therefore, studies based on epidemiological surveillance, involving molecular typing, will lead to a better understanding of its epidemiology, making it possible the design of more assertive control strategies.
Page 1 /100
Display every page Item


Home
Copyright © 2008-2017 Open Access Library. All rights reserved.