Purpose – This paper aims to present a holistic framework, termed ShaRInK (Sharer, Relations, Institution, Knowledge), that depicts key categories of influences that shape individual perceptions of knowledge sharing within an organisational setting. Design/methodology/approach – An exploratory and qualitative case study strategy in which empirical data were gathered from 24 interviewees that were based in four different branches (i.e. China, The Netherlands, the UK and the USA) of a single information technology services organisation. Findings – The findings led to a holistic framework that depicts four key categories of influences that shape knowledge sharing from an individual perspective: attitudes and characteristics of the sharers, relations between the sharers, institutions which act as a united entity on sharer perceptions and knowledge itself. Furthermore, the four key influences not only shape knowledge sharing independently but are intertwined and have a synergistic effect. The ShaRInK framework is formed by combining these. Originality/value – The findings indicate that knowledge sharing from an individual-level perspective is a more complex phenomenon than currently portrayed in the literature. All four key influences, each being fundamentally different in nature, and their relationships should be taken into account. Equally, the ShaRInK framework can be applied by organisations when developing a knowledge-sharing strategy or auditing existing strategies.
Regional differences in ion channel activity in the heart control the sequence of repolarization and may contribute to differences in contraction. Corticosteroids such as aldosterone or corticosterone increase the L-type Ca 2+ current (I CaL ) in the heart via the mineralocorticoid receptor (MR). Here, we investigate the differential impact of corticosteroid-mediated increase in I CaL on action potentials (AP), ion currents, intracellular Ca 2+ handling and contractility in endo- and epicardial myocytes of the rat left ventricle. Dexamethasone led to a similar increase in I CaL in endocardial and epicardial myocytes, while the K + currents I to and I K were unaffected. However, AP duration (APD) and AP-induced Ca 2+ influx (Q Ca ) significantly increased exclusively in epicardial myocytes, thus abrogating the normal differences between the groups. Dexamethasone increased Ca 2+ transients, contractility and SERCA activity in both regions, the latter possibly due to a decrease in total phospholamban (PLB) and an increase PLBpThr17. These results suggest that corticosteroids are powerful modulators of I CaL , Ca 2+ transients and contractility in both endo- and epicardial myocytes, while APD and Q Ca are increased in epicardial myocytes only. This indicates that increased I CaL and SERCA activity rather than Q Ca are the primary drivers of contractility by adrenocorticoids.
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