Publications by authors named "Sarah J Watkins"

Cardiac hypertrophy occurs as an adaptation to hypertension but a sustained hypertrophic response can ultimately lead to heart failure. Angiotensin-II (Ang II) is released following hemodynamic overload and stimulates a cardiac hypertrophic response. AngII also increases expression of the regulatory cytokine, transforming growth factor-β1 (TGFβ1), which is also implicated in the cardiac hypertrophic response and can stimulate activation of Smad2/3 as well as TGFβ-activated kinase 1 (TAK1) signaling mediators.

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Cardiac hypertrophy is a major risk factor for heart failure and associated patient morbidity and mortality. Research investigating the aberrant molecular processes that occur during cardiac hypertrophy uses primary cardiomyocytes from neonatal rat hearts as the standard experimental in vitro system. In addition, some studies make use of the H9C2 rat cardiomyoblast cell line, which has the advantage of being an animal-free alternative; however, the extent to which H9C2 cells can accurately mimic the hypertrophic responses of primary cardiac myocytes has not yet been fully established.

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The authors determined whether results of experiments on copulatory and affiliative behavior of pairs of Japanese quail (Coturnix japonica) conducted in a closely confining apparatus would predict behavior in a large enclosure in which female quail could avoid contact with male quail. As found previously in studies of closely confined quail, in a large enclosure containing numerous barriers, both unmated female quail and mated female quail laying unfertilized eggs were more likely to remain near a confined male quail than were mated female quail laying fertilized eggs. Furthermore, the number of copulations that a pair engaged in when closely confined predicted the number of copulations that they engaged in when they were in the large enclosure.

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Objective: Transforming growth factor beta (TGFbeta)-activated kinase 1 (TAK1) is a MAP kinase kinase kinase involved in numerous signalling pathways and is strongly implicated in cardiac hypertrophy and heart failure. TGFbeta is also associated with hypertension and heart disease, and evidence suggests that TGFbeta1 and TAK1 act together in a cardiac stress signalling pathway. Canonical TGFbeta signalling is mediated through Smad transcription factors, but TGFbeta can also rapidly activate TAK1.

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