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Id: lil-748272
Autor: Lima, Tainah P.; Farinatti, Paulo T.V.; Rubini, Ercole C.; Silva, Elirez B.; Monteiro, Walace D..
Título: Hemodynamic responses during and after multiple sets of stretching exercises performed with and without the Valsalva maneuver
Fonte: Clinics;70(5):333-338, 05/2015. graf.
Idioma: en.
Resumo: OBJECTIVE: This study investigated the acute hemodynamic responses to multiple sets of passive stretching exercises performed with and without the Valsalva maneuver. METHODS: Fifteen healthy men aged 21 to 29 years with poor flexibility performed stretching protocols comprising 10 sets of maximal passive unilateral hip flexion, sustained for 30 seconds with equal intervals between sets. Protocols without and with the Valsalva maneuver were applied in a random counterbalanced order, separated by 48-hour intervals. Hemodynamic responses were measured by photoplethysmography pre-exercise, during the stretching sets, and post-exercise. RESULTS: The effects of stretching sets on systolic and diastolic blood pressure were cumulative until the fourth set in protocols performed with and without the Valsalva maneuver. The heart rate and rate pressure product increased in both protocols, but no additive effect was observed due to the number of sets. Hemodynamic responses were always higher when stretching was performed with the Valsalva maneuver, causing an additional elevation in the rate pressure product. CONCLUSIONS: Multiple sets of unilateral hip flexion stretching significantly increased blood pressure, heart rate, and rate pressure product values. A cumulative effect of the number of sets occurred only for systolic and diastolic blood pressure, at least in the initial sets of the stretching protocols. The performance of the Valsalva maneuver intensified all hemodynamic responses, which resulted in significant increases in cardiac work during stretching exercises. .
Descritores: Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Benzodioxóis/farmacologia
Neoplasias do Colo/tratamento farmacológico
Isoquinolinas/farmacologia
Inibidores de Proteínas Quinases/farmacologia
Tiofenos/farmacologia
Inibidores da Topoisomerase I/farmacologia
Ureia/análogos & derivados
-CHECKPOINT KINASE TEMEFOS
Replicação do DNA/efeitos dos fármacos
Sinergismo Farmacológico
HTABORTION, INCOMPLETE CELLS
Proteínas Quinases/metabolismo
Proteínas Serina-Treonina Quinases/metabolismo
Ureia/farmacologia
Limites: Humanos
Tipo de Publ: Research Support, N.I.H., Intramural
Research Support, Non-U.S. Gov't
Responsável: BR1.1 - BIREME


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Id: lil-677280
Autor: Monsalve Abaca, Francisco.
Título: Avances en los mecanismos moleculares del cáncer / Advances in the molecular mechanisms of cancer
Fonte: Rev. méd. Maule;28(1):40-55, jun. 2012. ilus.
Idioma: es.
Resumo: In this review, epidemiological, physiological, pathophysiological and pharmacological themes of cancer are dealt. So far, there are over 200types of cancers, which are linked to six key events that collectively lead to the formation of a malignance: self-sufficiency in growth signals, insensitivity to growth inhibitory signals, evasion of apoptosis, unlimited replication potential, sustained angiogenesis and invasion and metastasis. These six capabilities are possibly shared by most human tumors. In2000, there were 10 million new cancer cases and 6 million cancer deaths worldwide. According to estimates by the American Cancer Society, the disease produced approximately 556,000 deaths in 2003, corresponding to 1,500 deaths from cancer every day in America. Annually, in Chile, cancer is responsible for 23 percent of all deaths, constituting the second leading cause of death after cardiovascular diseases. They have identified several risk factors for cancer such as smoking, chronic infections, alcohol consumption, reproductive factors, hormone replacement therapy, dietary habits, sunlight, among others. These factors may cause multiple genetic alterations that involve activation of several oncogenes and the loss of two or more suppressor genes, but not a single change will lead to the formation of a neoplasm. The Knowledge of the molecular differences between normal and malignant cells could be used to target specific pathways and receptors of the latter, thus preventing normal cell death.
Descritores: Neoplasias/enzimologia
Neoplasias/patologia
Neoplasias/tratamento farmacológico
-Apoptose
Antineoplásicos/uso terapêutico
Ciclo Celular
Citotoxinas
CASPASA ABATTOIRS
Inibidores da Topoisomerase I
Limites: Humanos
Tipo de Publ: Revisão
Responsável: CL1.1 - Biblioteca Central


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Id: lil-633501
Autor: Reguera, Rosa M; Pérez-Pertejo, Yolanda; Redondo, Cármen M; Díaz-González, Rosario; Balaña-Fouce, Rafael.
Título: La ADN topoisomerasa tipo I de protozoos patógenos como Diana terapéutica de fármacos antitumorales / Type I DNA topoisomerase from protozoan pathogens as a potential target for anti-tumoral drugs
Fonte: Medicina (B.Aires);67(6):747-757, nov.-dic. 2007. ilus, graf.
Idioma: es.
Resumo: La utilización intensiva de fármacos antiparasitarios es la causa principal de la aparición de microorganismos parásitos multirresistentes en las regiones del planeta donde son precisamente endémicos. Los agentes etiológicos de las denominadas enfermedades tropicales -malaria, criptosporiodiosis, enfermedad del sueño, enfermedad de Chagas o los distintos tipos de leishmaniosis- son protozoos unicelulares sobre los que no se ha desarrollado en la actualidad ninguna vacuna eficaz y cuyo tratamiento se basa en medidas sanitarias preventivas y en el uso de medicamentos. La quimioterapia antiparasitaria actual es cara, no está ausente de efectos adversos y no supone beneficios a las empresas que la comercializan, por lo que la inversión en I & D es marginal comparada con la llevada a cabo para otros procesos patológicos de menor relevancia médica. La identificación de las ADN topoisomerasas como dianas farmacológicas se basa en los excelentes resultados obtenidos en los ensayos clínicos llevados a cabo con los derivados de la camptotecina en la terapia antitumoral. Las importantes diferencias estructurales entre las ADN topoisomerasas de tipo I de tripanosomas y leishmanias con respecto a sus homólogas de mamífero ha abierto un nuevo campo de investigación que combina las técnicas de biología molecular con la cristalización de proteínas para poder diseñar nuevos fármacos dirigidos específicamente a su inhibición. Revisamos aquí las características de estas nuevas dianas farmacológicas, así como los compuestos que en el momento están siendo utilizados para su inhibición en los agentes parasitarios que causan las principales enfermedades tropicales.

The intensive use of antiparasitic drugs is the main cause of the emergence of multiresistant parasite strains on those regions where these parasites are endemic. The aetiological agents of the so-called tropical diseases viz. malaria, cryptosporidiosis, sleeping sickness, Chagas disease or leishmaniasis, among others, are unicellular protozoan parasites with no immune-prophylactic treatment and where the chemotherapeutical treatment is still under controversy. At present, the chemotherapeutic approach to these diseases is expensive, has side or toxic effects and it does not provide economic profits to the Pharmaceuticals which then have no or scarce enthusiasm in R & D investments in this field. The identification of type I DNAtopoisomerases as promising drug targets is based on the excellent results obtained with camptothecin derivatives in anticancer therapy. The recent finding of significant structural differences between human type I DNAtopoisomerase and their counterparts in trypanosomatids has open a new field in drug discovery, the aim is to find structural insights to be targeted by new drugs. This review is an update of DNA-topoisomerases as potential chemotherapeutic targets against the most important protozoan agents of medical interest.
Descritores: Antineoplásicos/farmacologia
Eucariotos/enzimologia
Inibidores da Topoisomerase I
-Antineoplásicos/química
Reparo do DNA
DNA Topoisomerases Tipo I/genética
DNA Topoisomerases Tipo I/metabolismo
Desenho de Fármacos
Eucariotos/genética
Leishmania/enzimologia
Leishmania/genética
Neoplasias/tratamento farmacológico
Infecções por Protozoários/parasitologia
Relação Estrutura-Atividade
Trypanosoma/enzimologia
Trypanosoma/genética
Limites: Animais
Humanos
Tipo de Publ: Research Support, Non-U.S. Gov't
Revisão
Responsável: AR1.2 - Instituto de Investigaciónes Epidemiológicas



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