Necklace‐embedded electrocardiogram for the detection and diagnosis of atrial fibrillation

BackgroundAtrial fibrillation (AF) is the major cause of stroke since approximately 25% of all strokes are of cardioembolic‐origin. The detection and diagnosis of AF are often challenging due to the asymptomatic and intermittent nature of AF.HypothesisA wearable electrocardiogram (ECG)‐device could increase the likelihood of AF detection. The aim of this study was to evaluate the feasibility and reliability of a novel, consumer‐grade, single‐lead ECG recording device (Necklace‐ECG) for screening, identifying and diagnosing of AF both by a cardiologist and automated AF‐detection algorithms.MethodsA thirty‐second ECG was recorded with the Necklace‐ECG device from two positions; between the palms (palm) and between the palm and the chest (chest). Simultaneously registered 3‐lead ECGs (Holter) served as a golden standard for the final rhythm diagnosis. Two cardiologists interpreted independently in a blinded fashion the Necklace‐ECG recordings from 145 patients (66 AF and 79 sinus rhythm, SR). In addition, the Necklace‐ECG recordings were analyzed with an automatic AF detection algorithm.ResultsTwo cardiologists diagnosed the correct rhythm of the interpretable Necklace‐ECG with a mean sensitivity of 97.2% and 99.1% (palm and chest, respectively) and specificity of 100% and 98.5%. The automatic arrhythmia algorithm detected the correct rhythm with a sensitivity of 94.7% and 98.3% (palm and chest) and specificity of 100% of the interpretable measurements.ConclusionsThe novel Necklace‐ECG device is able to detect AF with high sensitivity and specificity as evaluated both by cardiologists and an automated AF‐detection algorithm. Thus, the wearable Necklace‐ECG is a new, promising method for AF screening. Clinical trial registration: Study was registered in the ClinicalTrials.gov database ({"type":"clinical-trial","attrs":{"text":"NCT03753139","term_id":"NCT03753139"}}NCT03753139).     

Psychosocial Group Intervention Among War‐Affected Children: An Analysis of Changes in Posttraumatic Cognitions

Cognitive theories point to reduction in dysfunctional posttraumatic cognitions (PTCs) as one mechanism involved in recovery from posttraumatic stress symptoms (PTSS), yet research findings have shown individual differences in the recovery process. We tested the cognitive mediation hypothesis above in a previously published psychosocial group intervention among war‐affected children. We also examined heterogeneity in children's PTCs during the intervention. We used a cluster randomized trial of Smith et al.'s (2002) teaching recovery techniques (TRT) intervention among 482 Palestinians 10–13 years of age (n = 242 for intervention group, n = 240 for control group). Children reported PTSS, PTCs, and depressive symptoms at baseline, midpoint, postintervention, and at 6‐month follow‐up. Path analysis results showed that TRT was not effective in reducing dysfunctional PTCs, and the reductions did not mediate intervention effects on PTSS. Using latent class growth analysis, we chose the model with 3 differing trajectories in the intervention group: high, decreasing, moderate, downward trending, and severe, stable levels of PTCs. Higher PTSS and depressive symptoms at baseline were associated with membership in the severe, stable trajectory. The intervention did not produce the kind of beneficial cognitive change needed in the cognitive mediation conceptualization. Nevertheless, cognitive changes differed substantially across children during the intervention, and were associated with their preintervention mental health status. These findings call for more detailed examination of the process of cognitive mediation.     

Solar activity during gestation does not affect human lifespan: evidence from national data

Human lifespan has been reported to relate to solar activity during prenatal development. The likely key mechanism behind this association is increased mutagenic ultraviolet (UVB) radiation during high solar activity that damages DNA. Here, the aim was to replicate the findings of those previous few studies that have suggested a reduced lifespan of individuals born during the years of high solar activity, measured as the sunspot numbers. We used data on annual cohort life expectancy at birth of both women and men born between 1751 and 1915, obtained from ten nations located mainly in Europe. These data, however, provided no evidence that human life expectancy at birth was related to solar activity during gestation among the countries studied.     

Variation and seasonal patterns of suicide mortality in Finland and Sweden since the 1750s

Objectives

Suicide mortality varies in both the short and long term. Our study examines suicide mortality in Finland and Sweden from the 1750s until today. The aim of our study is to detect any seasonal peaks in suicide rates and examine their temporal evolution to suggest a mechanism that may explain such peaks.

Method

We acquired the study material from the Finnish and Swedish cause of death statistics (257,341 deaths by suicide) and the relevant population gender structure data. We then separately calculated the annual male and female suicide rates per 100,000 inhabitants. We analysed the suicide peaks, calculating factors of proportionality for the available data by dividing the suicide rates in the peak months (May and October) by the annual suicide rates.

Results

Suicide rates in Finland and Sweden peak twice a year. Both men and women in both countries most often commit suicide in May. There is another peak in October, with the exception of Finnish men. These suicide peaks coincide with a temperature increase in May and the biggest annual drop in temperature in October. We also observed a monotonic long-term change in the Swedish statistics, but not in the Finnish data. Our hypothesis is that seasonal variation in suicide rates may be caused by abrupt temperature changes twice a year that trigger the activity in brown adipose tissue and deepen depression.

Conclusion

While the overall suicide mortality rates varied considerably, the monthly proportions in May did not. This finding suggests a routine factor underlying the spring peak in suicide mortality.     

Genetic variants and blood pressure in a population-based cohort: the Cardiovascular Risk in Young Finns study

Clinical relevance of a genetic predisposition to elevated blood pressure was quantified during the transition from childhood to adulthood in a population-based Finnish cohort (N=2357). Blood pressure was measured at baseline in 1980 (age 3-18 years) and in follow-ups in 1983, 1986, 2001, and 2007. Thirteen single nucleotide polymorphisms associated with blood pressure were genotyped, and 3 genetic risk scores associated with systolic and diastolic blood pressures and their combination were derived for all of the participants. Effects of the genetic risk score were 0.47 mm Hg for systolic and 0.53 mm Hg for diastolic blood pressures (both P<0.01). The combination genetic risk score was associated with diastolic blood pressure from age 9 years onward (β=0.68 mm Hg; P=0.015). Replications in 1194 participants of the Bogalusa Heart Study showed essentially similar results. The participants in the highest quintile of the combination genetic risk score had a 1.82-fold risk of hypertension in adulthood (P<0.0001) compared with the lowest quintile, independent of a family history of premature hypertension. These findings show that genetic variants are associated with preclinical blood pressure traits in childhood; individuals with several susceptibility alleles have, on average, a 0.5-mm Hg higher blood pressure, and this trajectory continues from childhood to adulthood.     

Support for involvement of glutamate decarboxylase 1 and neuropeptide Y in anxiety susceptibility

Genetic mapping efforts have identified putative susceptibility genes for human anxiety disorders. The most intensively studied genes are involved in neurotransmitter metabolism and signaling or stress response. In addition, neuropeptides and targets of anxiolytics have been examined. It has become apparent that gene?×?environment interactions may explain individual variation in stress resilience and predisposition to mental disorders. We aimed to replicate previous genetic findings in 16 putative anxiety susceptibility genes and further test whether they modulate the risk for developing an anxiety disorder in adulthood after childhood stress exposure. We tested 93 single-nucleotide polymorphisms (SNPs) for genetic association to anxiety disorders in the Finnish population-based Health 2000 sample (282 cases and 575 matched controls). In addition, we examined by logistic regression modeling whether the SNP genotypes modified the effect of the number of self-reported childhood adversities on anxiety disorder risk. The most significant evidence for association was observed in glutamate decarboxylase 1 (GAD1) with phobias (P?=?0.0005). A subsequent meta-analysis (N?=?1985) incorporating previously published findings supported involvement of a single GAD1 risk haplotype in determining susceptibility to a broad range of internalizing disorders (P?=?0.0009). We additionally found that SNPs and haplotypes in neuropeptide Y (NPY) modified the effect of childhood adversities on anxiety susceptibility (P?=?0.003). In conclusion, we provide further support for involvement of mainly GAD1, but also NPY in determining predisposition to anxiety disorders.     

Transected myofibres may remain permanently divided in two parts

During regeneration of transected myofibres a scar is formed between their stumps. Myofibres restore their tendon-muscle-tendon continuity and contractile function by attaching to the scar with new myotendinous junctions. The scar contracts with time, and thereby the stumps are pulled close to each other. During early regeneration, myoblasts and myotubes can fuse with the surviving parts of the transected myofibres. However, it is not known whether it is possible that the opposite stumps could eventually fuse to reunite the divided parts of the transected fibres. In this study, we show in rat that even after 12 months the stumps remain attached to the separating scar by myotendinous junctions without showing definite fusion of the stumps. We conclude that transected myofibres probably remain permanently divided in two consecutive tendon-muscle-tendon units.