38 resultados para Äetsä
em Repositório Institucional UNESP - Universidade Estadual Paulista "Julio de Mesquita Filho"
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Studies were carried out in Brazil to study the inheritance of tolerance to Zucchini yellow mosaic virus (ZYMV) in cucumber cv. Formosa. This cultivar was individually crossed with two cucumber lines from different varietal types (L(b) from a Brazilian type, and L(j) from a Japanese type), both susceptible to the virus. Two experiments, one for each line, were separately carried out, where 6 treatments (parents, generations F1, F2 and F1BC1 for both parents) were evaluated in a randomized block design with 5 repetitions. Cotyledons of 2-week-old cucumber seedlings were inoculated with ZYMV. Only the plants that did not show symptoms up to 63 days post inoculation were considered as tolerant. A chi-square (chi(2)) analysis for assessing segregation from F2 and both F1BC1, led to the conclusion that the tolerance found in cv. Formosa is determined by a recessive gene.
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The aim of this study was to evaluate the survival of a strain of Xanthomonas axonopodis pv. phaseoli var. fuscans (Xap), resistant to streptomycin sulphate, in common bean leaflets placed on the sod surface and buried at a depth of 10 and 15 cm. Four assays were carried out from November 1998 to December 2000 in Bandeirantes (Paran, Brazil). The leaflets were collected every 15 days, crushed and the dilution-plated on a semi-selective medium. Under mild temperatures and low rainfall, Xap survived for 65 to 180 days in the leaflets on the sod surface, and for 30 to 120 days in those incorporated in the soil, regardless of the depth. When higher rainfall and temperatures occurred, the survival was from 45 to 60 days in the leaflets on the sod surface and from 30 to 45 days in those buried 10 or 15 cm deep.
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
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CONTEXTO E OBJETIVO: Os tubos traqueais são dispositivos utilizados para manutenção da ventilação. A hiperinsuflação do balonete do tubo traqueal, causada pela difusão do óxido nitroso (N2O), pode determinar lesões traqueais, que se manifestam clinicamente como odinofagia, rouquidão e tosse. A lidocaína, quando injetada no balonete do tubo traqueal, difunde-se através de sua parede, determinando ação anestésica local na traquéia. O objetivo foi avaliar a efetividade e a segurança do balonete do tubo traqueal preenchido com ar comparado com o balonete preenchido com lidocaína, considerando os desfechos: sintomas cardiovasculatórios (HAS, taquicardia); odinofagia, tosse, rouquidão e tolerância ao tubo traqueal. TIPO DE ESTUDO E LOCAL: Estudo clínico prospectivo, realizado no Departamento de Anestesiologia da Faculdade de Medicina da Unesp, campus de Botucatu. MÉTODOS: A pressão do balonete do tubo traqueal foi medida, entre 50 pacientes, antes, 30, 60, 90 e 120 minutos após o início da inalação de N2O anestésico. As pacientes foram distribuídas aleatoriamente em dois grupos: Air, em que o balonete foi inflado com ar para obtenção de pressão de 20 cm H2O, e Lido, em que o balonete foi preenchido com lidocaína a 2% mais bicarbonato de sódio a 8,4% para obtenção da mesma pressão. O desconforto antes da extubação, e manifestações clínicas como dor de garganta, rouquidão e tosse foram registrados no momento da alta da unidade de cuidados pós-anestésicos, e dor de garganta e rouquidão foram avaliadas também 24 horas após a anestesia. RESULTADOS: Os valores da pressão no balonete em G2 foram significativamente menores do que os de Air em todos os tempos de estudo, a partir de 30 minutos (p < 0,001). A proporção de pacientes que reagiu ao tubo traqueal no momento da desintubação foi significantemente menor em Lido (p < 0,005). A incidência de odinofagia foi significantemente menor em Lido no primeiro dia de pós-operatório (p < 0,05). A incidência de tosse e rouquidão não diferiu entre os grupos. CONCLUSÕES: Durante ventilação artificial, empregando-se a mistura de oxigênio e N2O, a insuflação do balonete com lidocaína 2% alcalinizada impede que ocorra aumento significante da pressão no balonete e determina maior tolerância ao tubo traqueal e menor incidência de odinofagia no pós-operatório, podendo então ser considerada mais segura e com maior efetividade.
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Aim: To investigate the role of MMP-2 and MMP-9 in cardiac remodelling induced by tobacco smoke exposure in rats.Methods: Rats were allocated into two groups: C (n = 9): control animals; ETS (n = 9): exposed to tobacco smoke. After 4months, the animals underwent echocardiography, morphometric study and determination of MMP-2 and MMP-9 activity.Results: ETS rats had larger diastolic (C= 15.6 +/- 1.2 mm/kg, ETS = 18.0 +/- 0.9 mm/kg; p < 0.001) and systolic (C= 7.3 +/- 1.2 mm/kg, ETS = 9.2 0.9 mm/kg; p = 0.001) ventricular diameters adjusted for body weight. Fractional shortening (C= 53 +/- 4.8%, ETS = 48 +/- 3.3%; p = 0.031) and ejection fraction (C= 0. 89 +/- 0.03 5 ETS = 0. 86 +/- 0.02; p = 0.03 0) were smaller in the ETS group. Myocyte cross-sectional area (C= 245 8 mu m(2), ETS=253 8 mu m(2); p = 0.028) was higher in ETS rats. There were no differences in MNtP-2 (C=50 +/- 14%; ETS 43 +/- 11%, p 0.22 +/- 8) or MMP-9 (C=0.36 +/- 0.3%; ETS=0.62 +/- 0.3%, p=0.630) activity between the groups.Conclusion: MMP-2 and MMP-9 did not participate in the remodelling process induced by tobacco smoke exposure. (c) 2007 European Society of Cardiology. Published by Elsevier B.V. All rights reserved.
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The objective of this study was to investigate the effects of exposure to tobacco smoke (ETS) in rats that were or were not supplemented with dietary beta-carotene (BC), on ventricular remodeling and survival after myocardial infarction (MI). Rats (n = 189) were allocated to 4 groups: the control group, n = 45; group BC administered 500 mg/kg diet, n = 49, BC supplemented rats; group ETS, n = 55, rats exposed to tobacco smoke; and group BC+ETS, n = 40. Wistar rats weighing 100 g were administered one of the treatments until they weighed 200 to 250 g (similar to 5 wk). The ETS rats were exposed to cigarette smoke for 30 min 4 times/d, in a chamber connected to a smoking device. After reaching a weight of 200-250 g, rats were subjected to experimental MI (coronary artery occlusion) and mortality rates were determined over the next 105 d. In addition, echocardiographic, isolated heart, morphometrical, and biochemical studies were performed. Mortality data were tested using Kaplan-Meyer curves and other data by 2-way ANOVA. Survival rates were greater in the ETS group (58.2%) than in the control (33.3%) (P = 0.001) and BC+ETS rats (30.0%) (P = 0.007). The groups did not differ in the other comparisons. Left ventricular end-diastolic diameter normalized to body weight was greater and maximal systolic pressures were lower in the ETS groups than in non-ETS groups. Previous exposure to tobacco smoke induced a process of cardiac remodeling after MI. There is a paradoxical protector effect with tobacco smoke exposure, characterized by lower mortality, which is offset by BC supplementation.
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Objective: the objectives were to analyze the cardiac effects of exposure to tobacco smoke (ETS), for a period of 30 days, alone and in combination with beta-carotene supplementation (BC). Research methods and procedures: Rats were allocated into: Air (control, n = 13); Air + BC (n = 11); ETS (n = 11); and BC + ETS (n = 9). In Air + BC and BC + ETS, 500 mg of BC were added to the diet. After three months of randomization, cardiac structure and function were assessed by echocardiogram. After that, animals were euthanized and morphological data were analyzed post-morten. One-way and two-way ANOVA were used to assess the effects of ETS, BC and the interaction between ETS and BC on the variables. Results: ETS presented smaller cardiac output (0.087 +/- 0.001 vs. 0.105 +/- 0.004 l/min; p = 0.007), higher left ventricular diastolic diameter (19.6 +/- 0.5 vs. 18.0 +/- 0.5 mm/kg; p = 0.024), higher left ventricular (2.02 +/- 0.05 vs. 1.70 +/- 0.03 g/kg; p < 0.001) and atrium (0.24 +/- 0.01 vs. 0.19 +/- 0.01 g/kg; p = 0.003) weight, adjusted to body weight of animals, and higher values of hepatic lipid hydroperoxide (5.32 +/- 0.1 vs. 4.84 +/- 0.1 nmol/g tissue; p = 0.031) than Air. However, considering those variables, there were no differences between Air and BC + ETS (0.099 +/- 0.004 l/min; 19.0 +/- 0.5 mm/kg; 1.83 +/- 0.04 g/kg; 0.19 +/- 0.01 g/kg; 4.88 +/- 0.1 nmol/g tissue, respectively; p > 0.05). Ultrastructural alterations were found in ETS: disorganization or loss of myofilaments, plasmatic membrane infolding, sarcoplasm reticulum dilatation, polymorphic mitochondria with swelling and decreased cristae. In BC + ETS, most fibers showed normal morphological aspects. Conclusion: One-month tobacco-smoke exposure induces functional and morphological cardiac alterations and BC supplementation attenuates this ventricular remodeling process.
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OBJECTIVE: To evaluate the roles of oxidative stress and lipid peroxidation in the ventricular remodeling that is induced by tobacco smoke exposure after myocardial infarction.METHODS: After induced myocardial infarction, rats were allocated into two groups: C (control, n=25) and ETS (exposed to tobacco smoke, n=24). After 6 months, survivors were submitted to echocardiogram and biochemical analyses.RESULTS: Rats in the ETS group showed higher diastolic (C = 1.52 +/- 0.4 mm(2), ETS = 1.95 +/- 0.4 mm(2); p=0.032) and systolic (C = 1.03 +/- 0.3, ETS = 1.36 +/- 0.4 mm(2)/g; p=0.049) ventricular areas, adjusted for body weight. The fractional area change was smaller in the ETS group (C = 30.3 +/- 10.1 %, ETS = 19.2 +/- 11.1 %; p=0.024) and E/A ratios were higher in ETS animals (C = 2.3 +/- 2.2, ETS = 5.1 +/- 2.5; p=0.037). ETS was also associated with a higher water percentage in the lung (C = 4.8 (4.3-4.8), ETS = 5.5 (5.3-5.6); p=0.013) as well as higher cardiac levels of reduced glutathione (C = 20.7 +/- 7.6 nmol/mg of protein, ETS = 40.7 +/- 12.7 nmol/mg of protein; p=0.037) and oxidized glutathione (C = 0.3 +/- 0.1 nmol/g of protein, ETS = 0.9 +/- 0.3 nmol/g of protein; p=0.008). No differences were observed in lipid hydroperoxide levels (C = 0.4 +/- 0.2 nmol/mg of tissue, ETS = 0.1 +/- 0.1 nmol/mg of tissue; p=0.08).CONCLUSION: In animals exposed to tobacco smoke, oxidative stress is associated with the intensification of ventricular re-remodeling after myocardial infarction.
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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
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Background/Aims: To investigate the effect of taurine on cardiac remodeling induced by smoking. Methods: In the first step, rats were allocated into two groups: Group C (n=14): control; Group T (n=14): treated with taurine (3% in drinking water), for three months. In the second step, rats were allocated into two groups: Group ETS (n=9): rats exposed to tobacco smoke; Group ETS-T (n=9): rats exposed to tobacco smoke and treated with taurine for two months. Results: After three months, taurine presented no effects on morphological or functional variables of normal rats assessed by echocardiogram. on the other hand, after two months, ETS-T group presented higher LV wall thickness (ETS=1.30 (1.20-1.42); ETS-T=1.50 (1.40-1.50); p=0.029), E/A ratio (ETS=1.13 +/- 0.13; ETS-T=1.37 +/- 0.26; p=0.028), and isovolumetric relaxation time normalized for heart rate (ETS=53.9 +/- 4.33; ETS-T=72.5 +/- 12.0; p<0.001). The cardiac activity of the lactate dehydrogenase was higher in the ETS-T group (ETS=204 +/- 14 nmol/mg protein; ETS-T=232 +/- 12 nmol/mg protein; p<0.001). ETS-T group presented lower levels of phospholamban (ETS=1.00 +/- 0.13; ETS-T=0.82 +/- 0.06; p=0.026), phosphorylated phospholamban at Ser16 (ETS=1.00 +/- 0.14;ETS-T=0.63 +/- 0.10;p=0.003), and phosphorylated phosfolamban/phospholamban ratio (ETS=1.01 +/- 0.17; ETS-T=0.77 +/- 0.11; p=0.050). Conclusion: In normal rats, taurine produces no effects on cardiac morphological or functional variables. on the other hand, in rats exposed to cigarette smoke, taurine supplementation increases wall thickness and worsens diastolic function, associated with alterations in calcium handling protein and cardiac energy metabolism. Copyright (C) 2011 S. Karger AG, Basel