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Given this fact, as well as homocystine’s proposed mechanisms of increasing endothelial dysfunction through oxidative damage, increased platelet coagulation and vascular smooth muscle cell proliferation, we recommend that homocysteine should be assessed and treated when levels rise, to reach a level of below 7 µmol/L
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Functional redundancy of type I and type II receptors in the regulation of skeletal muscle growth by myostatin and activin A
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