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Objectives. The aim of the study was to assess self-reported medication adherence measure in patients selected during a health education and health promotion focused event held in the Campania region. The study also assessed sociodemographic determinants of adherence. Methods. An interviewer assisted survey was conducted to assess adherence using the Italian version of the 8-item Morisky Medication Adherence Scale (MMAS-8). Participants older than 18 years were interviewed by pharmacists while waiting for free-medical checkup. Results. A total of 312 participants were interviewed during the Health Campus event. A total of 187 (59.9%) had low adherence to medications. Pearson's bivariate correlation showed positive association between the MMAS-8 score and gender, educational level and smoking (P < 0.05). A multivariable analysis showed that the level of education and smoking were independent predictors of adherence. Individuals with an average level of education (odds ratio (OR), 2.21, 95% confidence interval (CI), 1.08-4.52) and nonsmoker (odds ratio (OR) 1.87, 95% confidence interval (CI), 1.04-3.35) were found to be more adherent to medication than those with a lower level of education and smoking. Conclusion. The analysis showed very low prescription adherence levels in the interviewed population. The level of education was a relevant predictor associated with that result.
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Frailty is a multifaceted condition that affects many older adults and marks decline on areas such as cognition, physical condition, and nutritional status. Frail individuals are at increased risk for the development of disability, dementia, and falls. There are hardly any health services that enable the identification of prefrail individuals and that focus on prevention of further functional decline. In this paper, we discuss the development of a community-based, technology-supported health service for detecting prefrailty and preventing frailty and further functional decline via participatory design with a wide range of stakeholders. The result is an innovative service model in which an online platform supports the integration of traditional services with novel, Information Communication Technology supported tools. This service is capable of supporting the different phases of screening and offers training services, by also integrating them with community-based services. The service model can be used as a basis for developing similar services within a wide range of healthcare systems. We present the service model, the general functioning of the technology platform, and the different ways in which screening for and prevention of frailty has been localized. Finally, we reflect on the added value of participatory design for creating such health services.
RESUMO
AIMS: Activation of Ca2+/Calmodulin protein kinase II (CaMKII) is an important step in signaling of cardiac hypertrophy. The molecular mechanisms by which CaMKII integrates with other pathways in the heart are incompletely understood. We hypothesize that CaMKII association with extracellular regulated kinase (ERK), promotes cardiac hypertrophy through ERK nuclear localization. METHODS AND RESULTS: In H9C2 cardiomyoblasts, the selective CaMKII peptide inhibitor AntCaNtide, its penetratin conjugated minimal inhibitory sequence analog tat-CN17ß, and the MEK/ERK inhibitor UO126 all reduce phenylephrine (PE)-mediated ERK and CaMKII activation and their interaction. Moreover, AntCaNtide or tat-CN17ß pretreatment prevented PE induced CaMKII and ERK nuclear accumulation in H9C2s and reduced the hypertrophy responses. To determine the role of CaMKII in cardiac hypertrophy in vivo, spontaneously hypertensive rats were subjected to intramyocardial injections of AntCaNtide or tat-CN17ß. Left ventricular hypertrophy was evaluated weekly for 3 weeks by cardiac ultrasounds. We observed that the treatment with CaMKII inhibitors induced similar but significant reduction of cardiac size, left ventricular mass, and thickness of cardiac wall. The treatment with CaMKII inhibitors caused a significant reduction of CaMKII and ERK phosphorylation levels and their nuclear localization in the heart. CONCLUSION: These results indicate that CaMKII and ERK interact to promote activation in hypertrophy; the inhibition of CaMKII-ERK interaction offers a novel therapeutic approach to limit cardiac hypertrophy.