The Role of Oxidative Stress and Lipid Peroxidation in Ventricular Remodeling Induced by Tobacco Smoke Exposure after Myocardial Infarction

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

Genome of the Avirulent Human-Infective Trypanosome—Trypanosoma rangeli

Background: Trypanosoma rangeli is a hemoflagellate protozoan parasite infecting humans and other wild and domestic mammals across Central and South America. It does not cause human disease, but it can be mistaken for the etiologic agent of Chagas disease, Trypanosoma cruzi. We have sequenced the T. rangeli genome to provide new tools for elucidating the distinct and intriguing biology of this species and the key pathways related to interaction with its arthropod and mammalian hosts.  Methodology/Principal Findings: The T. rangeli haploid genome is ,24 Mb in length, and is the smallest and least repetitive trypanosomatid genome sequenced thus far. This parasite genome has shorter subtelomeric sequences compared to those of T. cruzi and T. brucei; displays intraspecific karyotype variability and lacks minichromosomes. Of the predicted 7,613 protein coding sequences, functional annotations could be determined for 2,415, while 5,043 are hypothetical proteins, some with evidence of protein expression. 7,101 genes (93%) are shared with other trypanosomatids that infect humans. An ortholog of the dcl2 gene involved in the T. brucei RNAi pathway was found in T. rangeli, but the RNAi machinery is non-functional since the other genes in this pathway are pseudogenized. T. rangeli is highly susceptible to oxidative stress, a phenotype that may be explained by a smaller number of anti-oxidant defense enzymes and heatshock proteins.  Conclusions/Significance: Phylogenetic comparison of nuclear and mitochondrial genes indicates that T. rangeli and T. cruzi are equidistant from T. brucei. In addition to revealing new aspects of trypanosome co-evolution within the vertebrate and invertebrate hosts, comparative genomic analysis with pathogenic trypanosomatids provides valuable new information that can be further explored with the aim of developing better diagnostic tools and/or therapeutic targets

Ventricular remodeling after myocardial infarction: Concepts and clinical implications

Submitted by Vitor Silverio Rodrigues ([email protected]) on 2014-05-27T11:23:52Z No. of bitstreams: 0Bitstream added on 2014-05-27T14:35:26Z : No. of bitstreams: 1 2-s2.0-65949107311.pdf: 834581 bytes, checksum: 500b0ac4dfcc294d8c614e6c44776bdc (MD5)Made available in DSpace on 2014-05-27T11:23:52Z (GMT). No. of bitstreams: 0 Previous issue date: 2009-02-01Faculdade de Medicina de Botucatu, SPFaculdade de Medicina de Botucatu Departamento de Clínica Médica, Distrito de Rubião Jr, s/n, Botucatu, SPFaculdade de Medicina de Botucatu, SPFaculdade de Medicina de Botucatu Departamento de Clínica Médica, Distrito de Rubião Jr, s/n, Botucatu, S

Comparação de diferentes métodos para medida do tamanho do infarto experimental crônico em Ratos Comparison of different methods to measure experimental chronic infarction size in the rat model

OBJETIVO: Avaliar as diferenças entre três métodos para medida do infarto experimental em ratos, em relação ao método tradicional. MÉTODOS: A área infartada por histologia (AREA), o perímetro interno da cavidade infartada por histologia (PER) e o perímetro interno por ecocardiograma (ECO) foram comparados ao método tradicional (análise histológica das circunferências epicárdicas e endocárdicas da região infartada - CIR). Utilizaram-se ANOVA de medidas repetidas, complementada com o teste de comparações múltiplas de Dunn, o método de concordância de Bland & Altman e o teste de correlação de Spearman. A significância foi p < 0,05. RESULTADOS: Foram analisados dados de 122 animais, após 3 a 6 meses do infarto. Houve diferença na avaliação do tamanho do infarto entre CIR e os outros três métodos (p < 0,001): CIR = 42,4% (35,9-48,8), PER = 50,3% (39,1-57,0), AREA = 27,3% (20,2-34,3), ECO = 46,1% (39,9-52,6). Assim, a medida por área resultou em subestimação de 15% do tamanho do infarto, enquanto as medidas por ecocardiograma e pelo perímetro interno por meio de histologia resultaram em superestimação do tamanho do infarto de 4% e 5%, respectivamente. Em relação ao ECO e PER, apesar de a diferença entre os métodos ser de apenas 1,27%, o intervalo de concordância variou de 24,1% a -26,7%, sugerindo baixa concordância entre os métodos. Em relação às associações, houve correlações estatisticamente significativas entre: CIR e PER (r = 0,88 e p < 0,0001); CIR e AREA (r = 0,87 e p < 0,0001) e CIR e ECO (r = 0,42 e p < 0,0001). CONCLUSÃO: Na determinação do tamanho do infarto, apesar da alta correlação, houve baixa concordância entre os métodos.<br>OBJECTIVE: To evaluate the differences between three methods for the measurement of experimental infarction in rats in comparison to the traditional method. METHODS: Histological analysis of the infarction area (AREA), histological analysis of the internal cavity perimeter (PER) and echocardiogram analysis of the internal perimeter (ECHO) were compared to the traditional method (histological analysis of the epicardial and endocardial circumferences of the infarction region - CIR). Repeated ANOVA measurements were used in conjunction with the Dunn multiple comparison test, the Bland and Altman concordance method and the Spearman correlation test. Significance was established as p < 0.05. RESULTS: The data of 122 animals were analyzed, 3 to 6 months after the infarction. Infarction size assessments revealed differences between CIR and the other three methods (p < 0.001): CIR = 42.4% (35.9-48.8), PER = 50.3% (39.1-57.0), AREA = 27.3% (20.2-34.3), ECHO = 46.1% (39.9-52.6). Therefore, measurement by area underestimated the infarct size by 15%, whereas the echocardiogram and histological internal perimeter measurements overestimated the infarct size by 4% and 5%, respectively. In relation to ECHO and PER, even though the difference between the methods was only 1.27%, the concordance interval ranged from 24.1% to -26.7%, suggesting a low level of concordance between the methods. In relation to associations, statistically significant correlations were found between: CIR and PER (r = 0.88 and p < 0.0001); CIR and AREA (r = 0.87 and p < 0.0001) and CIR and ECHO (r = 0.42 and p < 0.0001). CONCLUSION: Despite the high level of correlation, there was a low level of concordance between the methods to define infarct size