RESUMEN
INTRODUCTION: Smartwatches have proven life-saving in medical specialties such as cardiology. Smartwatches actively warn us of arrhythmia risk and loud noise exposure. However, dermatologic health metrics are rarely monitored, and users are never alerted of potential skin health issues. Furthermore, the role of these devices within dermatology has not been evaluated in the literature. This study aims to analyze the current data points monitored by smartwatches and discuss potential adaptations to support dermatologic patient education and improve clinical management. Methods: The top three smartwatches per global market share were identified and analyzed to determine the health data points they monitor and the alerts they provide. These data points were grouped and compared based on their corresponding body systems. Results: Cardiovascular health comprises the highest percentage of data points collected with an average of 41% while dermatologic health averaged only 11%. Conclusion: Dermatology is grossly underrepresented in current smartwatch devices. There is an important need to expand the dermatologic health metrics tracked by adapting existing smartwatch technology. From proactive cancer prevention to disease-specific reactive interventions, smartwatches can play a significant role in improving dermatological health and reducing healthcare costs.
RESUMEN
Dysregulation of the renin-angiotensin II (AngII)-aldosterone system can contribute to cardiovascular disease, such that an understanding of this system is critical. Diacylglycerol-sensitive serine/threonine protein kinase D (PKD) is activated by AngII in several systems, including the human adrenocortical carcinoma cell line NCI H295R, where this enzyme enhances chronic (24h) AngII-evoked aldosterone secretion. However, the role of PKD in acute AngII-elicited aldosterone secretion has not been previously examined. In primary cultures of bovine adrenal glomerulosa cells, which secrete detectable quantities of aldosterone in response to secretagogues within minutes, PKD was activated in response to AngII, but not an elevated potassium concentration or adrenocorticotrophic hormone. This activation was time- and dose-dependent and occurred through the AT1, but not the AT2, receptor. Adenovirus-mediated overexpression of constitutively active PKD resulted in enhanced AngII-induced aldosterone secretion; whereas overexpression of a dominant-negative PKD construct decreased AngII-stimulated aldosterone secretion. Thus, we demonstrate for the first time that PKD mediates acute AngII-induced aldosterone secretion.
