Older adults with weaker muscle strength stand up from a sitting position with more dynamic trunk use

The ability to stand up from a sitting position is essential for older adults to live independently. Body-fixed inertial sensors may provide an approach for quantifying the sit-to-stand (STS) in clinical settings. The aim of this study was to determine whether measurements of STS movements using body-fixed sensors yield parameters that are informative regarding changes in STS performance in older adults with reduced muscle strength. In twenty-seven healthy older adults, handgrip strength was assessed as a proxy for overall muscle strength. Subjects were asked to stand up from a chair placed at three heights. Trunk movements were measured using an inertial sensor fixed to the back. Duration, angular range, and maximum angular velocity of STS phases, as well as the vertical velocity of the extension phase, were calculated. Backwards elimination using Generalized Estimating Equations was used to determine if handgrip strength predicted the STS durations and trunk kinematics. Weaker subjects (i.e., with lower handgrip strength) were slower during the STS and showed a larger flexion angular range and a larger extension angular range. In addition, weaker subjects showed a greater maximum angular velocity, which increased with lower seat heights. Measurements with a single inertial sensor did reveal that older adults with lower handgrip strength employed a different strategy to stand up from a sitting position, involving more dynamic use of the trunk. This effect was greatest when elevating body mass. Trunk kinematic parameters were more sensitive to reduced muscle strength than durations

Feasibility of posture and movement detection by accelerometry

The discrimination of postures and movements using a minimal set of uniaxial accelerometers was investigated. Postures and movements were distinguished on the basis of the high-pass filtered, rectified and low-pass filtered signal of one accelerometer. Postures were discriminated by combining the constant valued signals of the accelerometers, mounted on different segments of the body. One sensor mounted radially on the trunk and one mounted radially or tangentially on the upper leg and lying. Methods are proposed for the discrimination of different cyclical movements

The Instrumented Sit-to-Stand Test (iSTS) Has Greater Clinical Relevance than the Manually Recorded Sit-to-Stand Test in Older Adults

10.1371/journal.pone.0157968PLOS ONE11

Discovery of a selective islet peptidome presented by the highest-risk HLA-DQ8trans molecule

Transplantation and autoimmunit

Human islets and dendritic cells generate post-translationally modified islet auto-antigens

Initiation of type 1 diabetes (T1D) requires a break in peripheral tolerance. New insights into neo-epitope formation indicate that post-translational modification of islet auto-antigens, for example via deamidation, may be an important component of disease initiation or exacerbation. Indeed, deamidation of islet auto-antigens increases their binding affinity to the T1D highest-risk HLA haplotypes HLA-DR3/DQ2 and -DR4/DQ8, increasing the chance that T-cells reactive to deamidated auto-antigens can be activated upon T-cell receptor ligation. Here we investigated human pancreatic islets and inflammatory and tolerogenic human dendritic cells (DC and tolDC) as potential sources of deamidated islet auto-antigens and examined whether deamidation is altered in an inflammatory environment. Islets, DC and tolDC contained tissue transglutaminase, the key enzyme responsible for peptide deamidation, and enzyme activity increased following an inflammatory insult. Islets treated with inflammatory cytokines were found to contain deamidated insulin C-peptide. DC, heterozygous for the T1D highest-risk DQ2/8, pulsed with native islet auto-antigens could present naturally processed deamidated neo-epitopes. HLA-DQ2 or -DQ8 homozygous DC did not present deamidated islet peptides. This study identifies both human islets and DC as sources of deamidated islet auto-antigens and implicates inflammatory activation of tissue transglutaminase as a potential mechanism for islet and DC deamidation. This article is protected by copyright. All rights reserved

Demographics, clinical characteristics, iSTS parameters and daily physical activity of the study population.

<p>Demographics, clinical characteristics, iSTS parameters and daily physical activity of the study population.</p