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Measurement of the inclusive charmless semileptonic branching ratio of B mesons and determination of vertical bar V-ub vertical bar
We report a measurement of the inclusive charmless semileptonic branching fraction of B mesons in a sample of 89x10(6) B(b) over bar events recorded with the BABAR detector at the Y(4S) resonance. Events are selected by fully reconstructing the decay of one B meson and identifying a charged lepton from the decay of the other B meson. The number of signal events is extracted from the mass distribution of the hadronic system accompanying the lepton and is used to determine the ratio of branching fractions B((B) over bar --> X(u)l (v) over bar)/B((B) over bar --> Xl (v) over bar) = [2.06 +/- 0.25(stat) +/- 0.23(syst) +/- 0.36(theo)] x 10(-2). Using the measured branching fraction for inclusive semileptonic B decays, we find B((B) over bar --> X(u)l (V) over bar) = [2.24+/-0.27(stat) +/- 0.26(syst) +/- 0.39(theo)] x 10(-3) and derive the Cabibbo-Kobayashi-Maskawa matrix element parallel toV(ub)parallel to = [4.62 +/- 0.28(stat) +/- 0.27(syst) +/- 0.48(theo)] x 10(-3)
Efeitos do exercício físico sobre o estado redox cerebral Effects of physical exercise over the redox brain state
A atividade física é conhecida por promover saúde e bem-estar. O exercício também é responsável por aumentar a produção de Espécies Reativas de Oxigênio (ERO) pelo acréscimo do consumo de oxigênio mitocondrial nos tecidos. O desequilíbrio entre a produção de EROs e as defesas oxidantes dos tecidos pode provocar danos oxidativos a proteínas, lipídios e DNA. O dano oxidativo cerebral é um mecanismo etiopatológico comum da apoptose e da neurodegeneração. O fator de crescimento cérebro-derivado desempenha um importante papel neste contexto. Nesta revisão, apresentamos os resultados de diferentes modelos de exercício físico no metabolismo oxidativo e neurotrófico do Sistema Nervoso Central (SNC). Também revisamos estudos que utilizaram suplementação antioxidante para prevenir danos oxidativos exercício-induzido ao SNC. Os modelos de exercício físico mais comuns foram as rodas de correr, a natação e a esteira com configurações de treinamento muito diferentes como a duração e a intensidade. Os resultados do treinamento físico no tecido cerebral são muito controversos, mas geralmente demonstram ganhos na plasticidade sináptica e na função cognitiva com exercícios de intensidade moderada e baixa.<br>Physical activity is known for promoting health and well-being. Exercise is also responsible for increasing the production of Oxygen Reactive Species (ORS) by increasing mitochondrial oxygen consumption causing tissue oxidative stress. The imbalance between ORS production and tissue antioxidant defenses can cause oxidative damage to proteins, lipids and DNA. Brain oxidative damage is a common etiopathology mechanism of apoptosis and neurodegeneration. The brain-derived neurotrophic factor plays an important role in this context. In this review, we showed the results of different models and configurations of physical exercise in oxidative and neurotrophic metabolism of the Central Nervous System (CNS). We also reviewed studies that utilized antioxidant supplementation to prevent exercise-induced oxidative damage to CNS. The commonest physical exercise models were running wheels, swimming and treadmill with very different configurations of physical training such as duration and intensity. The results of physical training on brain tissues are very controversial, but generally show improvement in synaptic plasticity and cognition function with low and moderate intensity exercises