The Effects of Wearing a Portable Media Armband on Muscle Activation of the Biceps Brachii.

Portable media armbands are commonly used among the physically active population. Their effect on muscle function has not been established. The purpose of this study was to determine if muscle activation of the biceps brachii is influenced by wearing a portable media armband during an elbow flexion exercise. Eighteen participants (11 males: age = 22.5 ± 2.1 years, height = 178.3 ± 5.2 cm, mass = 85.0 ± 6.5 kg; 7 females: age = 22.9 ± 2.5 years, height = 168.3 ± 5.7 cm, mass = 72.3 ± 12.2 kg) with no history of upper extremity injury volunteered for the study. Participants performed elbow flexion trials with a hand-held dumbbell with and without wearing a portable media armband. Dumbbell weight was determined by an 8-10 repetition maximum, and the condition was counterbalanced. The average concentric and eccentric phases for five trials for each condition were normalized to a maximum voluntary isometric contraction using electromyography. The independent variable was condition (with-PMAB and without-PMAB). The dependent variable was the muscle activation of the biceps brachii. Mean data for each condition were analyzed using separate paired-samples t-tests for the concentric and eccentric phases (p < 0.05). Statistical analysis revealed a significant difference for the concentric phase (t17 = 2.905; p = 0.010). The with-PMAB condition elicited greater muscle activation (72.57 ± 36.31%) compared to the without-PMAB (63.67 ± 26.2%), with a medium effect size (d = 0.69). There was no statistical difference for the eccentric phase (t17 = 1.964; p = 0.066), and a small effect size (d = 0.46). The increase in muscle activation during the concentric phase is likely due to a change in the muscle properties due to the compressive force applied to the muscle fibers by the portable media armband.

Genetic variation in melatonin pathway enzymes in children with autism spectrum disorder and comorbid sleep onset delay.

Sleep disruption is common in individuals with autism spectrum disorder (ASD). Genes whose products regulate endogenous melatonin modify sleep patterns and have been implicated in ASD. Genetic factors likely contribute to comorbid expression of sleep disorders in ASD. We studied a clinically unique ASD subgroup, consisting solely of children with comorbid expression of sleep onset delay. We evaluated variation in two melatonin pathway genes, acetylserotonin O-methyltransferase (ASMT) and cytochrome P450 1A2 (CYP1A2). We observed higher frequencies than currently reported (p < 0.04) for variants evidenced to decrease ASMT expression and related to decreased CYP1A2 enzyme activity (p ≤ 0.0007). We detected a relationship between genotypes in ASMT and CYP1A2 (r(2) = 0.63). Our results indicate that expression of sleep onset delay relates to melatonin pathway genes.

KIAA1462, a coronary artery disease associated gene, is a candidate gene for late onset Alzheimer disease in APOE carriers.

Alzheimer disease (AD) is a devastating neurodegenerative disease affecting more than five million Americans. In this study, we have used updated genetic linkage data from chromosome 10 in combination with expression data from serial analysis of gene expression to choose a new set of thirteen candidate genes for genetic analysis in late onset Alzheimer disease (LOAD). Results in this study identify the KIAA1462 locus as a candidate locus for LOAD in APOE4 carriers. Two genes exist at this locus, KIAA1462, a gene associated with coronary artery disease, and "rokimi", encoding an untranslated spliced RNA The genetic architecture at this locus suggests that the gene product important in this association is either "rokimi", or a different isoform of KIAA1462 than the isoform that is important in cardiovascular disease. Expression data suggests that isoform f of KIAA1462 is a more attractive candidate for association with LOAD in APOE4 carriers than "rokimi" which had no detectable expression in brain.

No association between SNP rs498055 on chromosome 10 and late-onset Alzheimer disease in multiple datasets.

SNP rs498055 in the predicted gene LOC439999 on chromosome 10 was recently identified as being strongly associated with late-onset Alzheimer disease (LOAD). This SNP falls within a chromosomal region that has engendered continued interest generated from both preliminary genetic linkage and candidate gene studies. To independently evaluate this interesting candidate SNP we examined four independent datasets, three family-based and one case-control. All the cases were late-onset AD Caucasian patients with minimum age at onset >or= 60 years. None of the three family samples or the combined family-based dataset showed association in either allelic or genotypic family-based association tests at p < 0.05. Both original and OSA two-point LOD scores were calculated. However, there was no evidence indicating linkage no matter what covariates were applied (the highest LOD score was 0.82). The case-control dataset did not demonstrate any association between this SNP and AD (all p-values > 0.52). Our results do not confirm the previous association, but are consistent with a more recent negative association result that used family-based association tests to examine the effect of this SNP in two family datasets. Thus we conclude that rs498055 is not associated with an increased risk of LOAD.