Albrightknudsen7767
BACKGROUND This study explored both the evolution of the information needs and the perceived relevance of different health information sources in patients with essential hypertension. It also investigated the relationships between information needs and the perceived relevance of information sources with socio-demographic and clinical variables. METHODS Two hundred and two patients with essential arterial hypertension were enrolled in the study and evaluated at baseline and during three follow-ups at 6, 12 and 24 months after baseline. Patients had a mean age of 54.3 years [range 21-78; SD = 10.4], and 43% were women. Repeated measures ANOVA, Bonferroni post hoc tests, and Cochran's Q Test were performed to test differences in variables of interest over time. RESULTS It was observed a significant reduction in all the domains of information needs related to disease management except for pharmacological treatment and risks and complications. At baseline, patients reported receiving health information primarily from specialists, general practitioners, relatives, and television, but the use of these sources decreased over time, even if the decrease was significant only for relatives. Multiple patterns of relationships were found between information needs and the perceived relevance of sources of information and socio-demographics and clinical variables, both at baseline and over time. CONCLUSIONS The findings showed a general decrease in both the desire for information and the perceived relevance of different information sources. Hypertensive patients appeared to show little interest in health communication topics as their disease progressed. Understanding patients' information needs and the perceived relevance of different information sources is the first step in implementing tailored communication strategies that can promote patients' self-management skills and optimal clinical outcomes.BACKGROUND The voltage-gated potassium channel Kv7.1 encoded by KCNQ1 is located in both cardiac myocytes and insulin producing beta cells. Loss-of-function mutations in KCNQ1 causes long QT syndrome along with glucose-stimulated hyperinsulinemia, increased C-peptide and postprandial hypoglycemia. The KCNE1 protein modulates Kv7.1 in cardiac myocytes, but is not expressed in beta cells. Gain-of-function mutations in KCNQ1 and KCNE1 shorten the action potential duration in cardiac myocytes, but their effect on beta cells and insulin secretion is unknown. CASE PRESENTATION Two patients with atrial fibrillation due to gain-of-function mutations in KCNQ1 (R670K) and KCNE1 (G60D) were BMI-, age-, and sex-matched to six control participants and underwent a 6-h oral glucose tolerance test (OGTT). During the OGTT, the KCNQ1 gain-of-function mutation carrier had 86% lower C-peptide response after glucose stimulation compared with matched control participants (iAUC360min = 34 pmol/l*min VS iAUC360min = 246 ± 71 pmol/l*min). The KCNE1 gain-of-function mutation carrier had normal C-peptide levels. CONCLUSIONS This case story presents a patient with a gain-of-function mutation KCNQ1 R670K with low glucose-stimulated C-peptide secretion, additionally suggesting involvement of the voltage-gated potassium channel KCNQ1 in glucose-stimulated insulin regulation.BACKGROUND Type 2 diabetes mellitus (T2DM) comprises the vast majority of all diabetes cases in adults, with alarmingly increasing prevalence over the past few decades worldwide. A particularly heavy healthcare burden of diabetes is noted in Europe, where 8.8% of the population aged 20-79 years is estimated to have diabetes according to the International Diabetes Federation. Multiple risk factors are implicated in the pathogenesis of T2DM with complex underlying interplay and intricate gene-environment interactions. Thus, intense research has been focused on studying the role of T2DM risk factors and on identifying vulnerable groups for T2DM in the general population which can then be targeted for prevention interventions. METHODS For this narrative review, we conducted a comprehensive search of the existing literature on T2DM risk factors, focusing on studies in adult cohorts from European countries which were published in English after January 2000. RESULTS Multiple lifestyle-related and sociodemographic fa T2DM prevention.BACKGROUND Emotional symptoms are increasingly considered a core feature of attention deficit/hyperactivity disorder (ADHD). We aimed to quantify the evidence of emotional dysregulation and its respective facets in individuals with adult ADHD compared to healthy controls using meta-analysis. METHODS Two electronic databases (PubMed, PsycINFO) were reviewed to identify studies. Studies were eligible for inclusion that had reports on any measure of emotion (dys) regulation in adults (> 18 years of age) in clinically diagnosed patients with ADHD as well as healthy control participants. We included a total of 13 studies (N = 2535) to assess (1) the standardized mean difference in emotion dysregulation (ED) as a general factor and its specific facets (i.e., emotional lability, negative emotional responses, and emotion recognition) between adults with ADHD and healthy controls; and (2) the association between ADHD symptom severity and ED. RESULTS Compared to healthy controls, adults with ADHD revealed significantly higher levels of general ED (Hedges' g = 1.17, p less then 0.001; Hedges' g is the adjusted effect size). With regard to intermediate dimensions of ED, emotional lability exhibited the strongest weighted effect (Hedges' g = 1.20, CI [0.57, 1.83], p less then 0.001). Erastin Ferroptosis activator Furthermore, symptom severity and general ED correlated significantly (r = 0.54, p less then 0.001). Regarding intermediate dimensions of ED, negative emotional responses correlated closely with ADHD symptom severity (r = 0.63, p less then 0.001) and emotional lability (r = 0.52, p less then 0.001). CONCLUSIONS Our findings support ED symptoms as a core feature of ADHD's psychopathology. With respect to dimensions of ED, emotional lability, and negative emotional responses play a more definitive role in the psychopathology of adults with ADHD. Due to insufficient statistical reports in the included studies, we could not perform meta-regressions to control the role of moderator variables.