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The objectives of this study were to evaluate 11 muscle electromyograms (EMGs) while performing force application tasks in a 3D workspace, and to identify challenging regions within the workspace in which subjects had difficultly generating forces in desired directions. Each subject (4 young healthy adults, 4 older with stroke-induced disability, 4 age-matched older) applied forces (8 lbs desired) in 6 directions at 19 locations spatially distributed in the workspace. The normals could meet the force threshold levels except for the 2 female aged participants for the Right force direction. The stroke group had common difficult directions of Up and Right. The muscle activations were dependent upon the applied force direction, with Up force being associated with maximum EMGs. Maximum variation in the EMGs was in the right and far region for the young adults and in far and low region for the older adults. The stroke subjects' shoulder-arm EMGs showed less directional variability in the regions of workspace, and considerable compensatory trunk movement, unlike the normals.

Aims: In humans, genetic variation in endocannabinergic signaling has been associated with anthropometric measures of obesity. In randomized trials, pharmacological blockade at the level of the cannabinoid receptor 1 (CNR1) receptor not only facilitates weight reduction, but also improves insulin sensitivity and clinical measures of lipid homeostasis. We therefore tested the hypothesis that genetic variation in CNR1 is associated with common obesity-related metabolic disorders., Materials & Methods: A total of six haplotype tagging SNPs were selected for CNR1, using data available within the Human HapMap (Centre d'Etude du Polymorphisme Humain population) these included: two promoter SNPs, three exonic SNPs, and a single SNP within the 3'-untranslated region. These tags were then genotyped in a rigorously phenotyped family-based collection of obese study subjects of Northern European origin., Results & Conclusions: A common CNR1 haplotype (H4; prevalence 0.132) is associated with abnormal lipid homeostasis. Additional statistical tests using single tagging SNPs revealed that these associations are partly independent of body mass index.

Although the head is more closely represented as an ellipsoid than a sphere, calculation in ellipsoidal coordinates is difficult. This paper presents a four shell ellipsoidal model, employing multipole expansion in ellipsoidal coordinates, for EEG, MEG, and evoked potential applications. Computational detail and insight into efficient calculation of the Lamé functions of the first and second kind are provided to demonstrate feasibilty. The Lamé function of the second kind, derived from the Lamé function of the first kind, can be computed at higher degrees by means of partial fraction expansion.

Background and Aims: Our studies of the standard neurological examination on 66 middle-aged (50-64 yrs) and elderly subjects (65-84 yrs) demonstrate that healthy elders have neurological deficits (or "signs") that are not associated with specific known neurological disease. The purpose of the current study is to describe this loss of neurological function in healthy aging subjects as seen through accumulated subclinical neurological signs present., Methods: Logistic regression is applied to the data on each of six signs. Parameters determined are used to describe the distribution of first occurrence times for each sign. The results are then used to construct a Poisson-like model that describes the accumulation in the number of signs present over time on average. This model is also used to simulate a longitudinal population to explore the variability in the number of signs present over time in an aging population., Results: As the rate of arrival of the signs is heterogeneous, as determined through logistic regression, and the number of signs detected is finite, the resulting distributions of the number of signs over time have a different nature than Poisson. Our results suggest that we can expect to see on average one neurological deficit in healthy people by the age of 62, and that the expected number of deficits increases linearly at the rate of 1 additional sign every 12 years over a wide age range (age 70-90). The distribution of the number of deficits over time is also described., Conclusions: The linearity in the average rate at which signs appear in this population is somewhat of a surprise, in that an increasing (accelerating) rate might be anticipated. In addition to characterizing the neurological exam results in this group, we demonstrate a methodology that allows the comparison of groups and defines a rate of neurological aging.

Multiple studies have identified resting heart rate as a risk factor for cardiovascular disease independent of other cardiovascular disease risk factors (such as dyslipidemia and hypertension). Previous studies have examined heart rate in hypertensive individuals, but little is known about the genetic determination of resting heart rate in a normal population. Therefore, our objective was to perform a genome screen on a population containing normotensive and hypertensive individuals. We performed variance decomposition linkage analysis using maximum likelihood methods at approximately 10 cM intervals in 2209 individuals of predominantly North European ancestry. We estimated the heritability of resting heart rate to be 26% and obtained significant evidence of linkage (logarithm of the odds [LOD]=3.9) for resting heart rate on chromosome 4q. This signal is in the same region as a quantitative trait locus (QTL) for long QT syndrome 4 and a QTL for heart rate in rats. Within the 1-LOD unit support interval, there are 2 strong candidates: ankyrin-B and myozenin 2.