Publications by authors named "C William Balke"

Purpose: This study used a collaborative approach to explore the needs, barriers, and facilitators to developing cochlear implant referral information material that would be valuable for hard of hearing adults and referring audiologists.

Method: During the development of a prototype referral aid to be used within the Australian context, a multistage qualitative study was conducted using a consultative process, informal and semistructured interviews, as well as online surveys. A deductive directed content analysis approach was applied to assess respondents' perspectives.

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Tetrodotoxin (TTX) sensitive inward Ca currents, I, have been identified in cardiac myocytes from several species, although it is unclear if I is expressed in all cardiac cell types, and if I reflects Ca entry through the main, Nav1.5-encoded, cardiac Na (Nav) channels. To address these questions, recordings were obtained with 2 mm Ca and 0 mm Na in the bath and 120 mm Cs in the pipettes from myocytes isolated from adult mouse interventricular septum (IVS), left ventricular (LV) endocardium, apex, and epicardium and from human LV endocardium and epicardium.

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Nurturing the development of cardiovascular physician-scientist investigators is critical for sustained progress in cardiovascular science and improving human health. The transition from an inexperienced trainee to an independent physician-scientist is a multifaceted process requiring a sustained commitment from the trainee, mentors, and institution. A cornerstone of this training process is a career development (K) award from the National Institutes of Health (NIH).

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It is well known that spontaneously hypertensive rats (SHR) develop muscle pathologies with hypertension and heart failure, though the mechanism remains poorly understood. Woon et al. (2007) linked the circadian clock gene Bmal1 to hypertension and metabolic dysfunction in the SHR.

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An altered cardiac myofilament response to activating Ca(2+) is a hallmark of human heart failure. Phosphorylation of cardiac troponin I (cTnI) is critical in modulating contractility and Ca(2+) sensitivity of cardiac muscle. cTnI can be phosphorylated by protein kinase A (PKA) at Ser(22/23) and protein kinase C (PKC) at Ser(22/23), Ser(42/44), and Thr(143).

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