5 resultados para WADA

em Deakin Research Online - Australia


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Lifecycle approaches have found their wide applications in analyzing, evaluating and assessing technologies and management methods in the infrastructure systems. While environmental problems such as global warming have become a serious issue in the world, researchers and practicing engineers in civil engineering have to pay attention to environmental impacts as well as function, safety, cost and aesthetics in the
whole lifecycle of civil infrastructures. In addition to the normal lifecycle activities accompanied with operation and aging, the effects of natural hazards such as earthquakes with a low occurrence probability but a high
hazard loss require a full consideration in determining both lifecycle cost and lifecycle environmental impact. In this research, an approach is proposed to predetermine the lifecycle environmental impact and costs of bridges from their construction and maintenance as well as the losses and recovery after natural hazards. Based on this research, it becomes possible to quantitatively outline the roles of bridge construction, maintenance and earthquake in both environmental impact and cost in the whole lifetime of a bridge, especially their constituent parts from seismic losses and recoveries.

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The identification of microRNAs (miRNAs) has established new mechanisms that control skeletal muscle adaptation to exercise. The present study investigated the mRNA regulation of components of the miRNA biogenesis pathway (Drosha, Dicer and Exportin-5), muscle enriched miRNAs, (miR-1, -133a, -133b and -206), and several miRNAs dysregulated in muscle myopathies (miR-9, -23, -29, -31 and -181). Measurements were made in muscle biopsies from nine healthy untrained males at rest, 3 h following an acute bout of moderate-intensity endurance cycling and following 10 days of endurance training. Bioinformatics analysis was used to predict potential miRNA targets. In the 3 h period following the acute exercise bout, Drosha, Dicer and Exportin-5, as well as miR-1, -133a, -133-b and -181a were all increased. In contrast miR-9, -23a, -23b and -31 were decreased. Short-term training increased miR-1 and -29b, while miR-31 remained decreased. Negative correlations were observed between miR-9 and HDAC4 protein (r=-0.71; P= 0.04), miR-31 and HDAC4 protein (r =-0.87; P= 0.026) and miR-31 and NRF1 protein (r =-0.77; P= 0.01) 3 h following exercise. miR-31 binding to the HDAC4 and NRF1 3′ untranslated region (UTR) reduced luciferase reporter activity. Exercise rapidly and transiently regulates several miRNA species in muscle. Several of these miRNAs may be involved in the regulation of skeletal muscle regeneration, gene transcription and mitochondrial biogenesis. Identifying endurance exercise-mediated stress signals regulating skeletal muscle miRNAs, as well as validating their targets and regulatory pathways post exercise, will advance our understanding of their potential role/s in human health

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 As London 2012 starts to become a distant memory, and Sochi 2014 becomes a near reality, it is timely that Waddington, Christiansen, Gleaves, Hoberman, and Moller (2013) and Henne, Koh, and McDermott (2013) have brought to the fore the inconsistencies within the World Anti-Doping Agency's (WADA's) policies regarding drug use in sport. These inconsistencies are not new; Smith and Stewart (2008) highlighted the inconsistencies and ambiguities of WADA policy, but nothing has changed in this time. Why a substance is placed on the banned list is an important discussion that should be occurring; however, this discussion should not be occurring in the isolation of the sporting world.

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Skeletal muscles contain several subtypes of myofibers that differ in contractile and metabolic properties. Transcriptional control of fiber-type specification and adaptation has been intensively investigated over the past several decades. Recently, microRNA (miRNA)-mediated posttranscriptional gene regulation has attracted increasing attention. MiR-23a targets key molecules regulating contractile and metabolic properties of skeletal muscle, such as myosin heavy-chains and peroxisome proliferator-activated receptor gamma, coactivator 1 alpha (PGC-1α). In the present study, we analyzed the skeletal muscle phenotype of miR-23a transgenic (miR-23a Tg) mice to explore whether forced expression of miR-23a affects markers of mitochondrial content, muscle fiber composition, and muscle adaptations induced by 4 weeks of voluntary wheel running. When compared with wild-type mice, protein markers of mitochondrial content, including PGC-1α, and cytochrome c oxidase complex IV (COX IV), were significantly decreased in the slow soleus muscle, but not the fast plantaris muscle of miR-23a Tg mice. There was a decrease in type IId/x fibers only in the soleus muscle of the Tg mice. Following 4 weeks of voluntary wheel running, there was no difference in the endurance exercise capacity as well as in several muscle adaptive responses including an increase in muscle mass, capillary density, or the protein content of myosin heavy-chain IIa, PGC-1α, COX IV, and cytochrome c. These results show that miR-23a targets PGC-1α and regulates basal metabolic properties of slow but not fast twitch muscles. Elevated levels of miR-23a did not impact on whole body endurance capacity or exercise-induced muscle adaptations in the fast plantaris muscle.