Mapping the Mayo-Portland adaptability inventory to the international classification of functioning, disability and health

Objective: To examine the contents of the Mayo-Portland Adaptability Inventory (MPAI-4) by mapping it to the International Classification of Functioning, Disability and Health (ICF). Methods: Each of the 30 scoreable items in the MPAI-4 was mapped to the most precise ICF categories. Results: All 30 items could be mapped to components and categories in the ICF. A total of 88 meaningful concepts were identified. There were, on average, 2.9 meaningful concepts per item, and 65% of all concepts could be mapped. Items in the Ability and Adjustment subscales mapped to categories in both the Body Functions and Activity/Participation components of the ICF, whereas all except 1 in the Participation subscale were to categories in the Activity/Participation component. The items could also be mapped to 34 (13%) of the 258 Environmental Factors in the ICF. Conclusion: This mapping provides better definition through more concrete examples (as listed in the ICF) of the types of body functions, activities, and participation indicators that are represented by the 30 scoreable MPAI-4 items. This may assist users throughout the world in understanding the intent of each item, and support further development and the possibility to report results in the form of an ICF categorical profile, making it universally interpretable

Age-related differences in adaptation during childhood: The influences of muscular power production and segmental energy flow caused by muscles

Acquisition of skillfulness is not only characterized by a task-appropriate application of muscular forces but also by the ability to adapt performance to changing task demands. Previous research suggests that there is a different developmental schedule for adaptation at the kinematic compared to the neuro-muscular level. The purpose of this study was to determine how age-related differences in neuro-muscular organization affect the mechanical construction of pedaling at different levels of the task. By quantifying the flow of segmental energy caused by muscles, we determined the muscular synergies that construct the movement outcome across movement speeds. Younger children (5-7 years; n = 11), older children (8-10 years; n = 8), and adults (22-31 years; n = 8) rode a stationary ergometer at five discrete cadences (60, 75, 90, 105, and 120 rpm) at 10% of their individually predicted peak power output. Using a forward dynamics simulation, we determined the muscular contributions to crank power, as well as muscular power delivered to the crank directly and indirectly (through energy absorption and transfer) during the downstroke and the upstroke of the crank cycle. We found significant age × cadence interactions for (1) peak muscular power at the hip joint [Wilks' Lambda = 0.441, F(8,42) = 2.65, p = 0.019] indicating that at high movement speeds children produced less peak power at the hip than adults, (2) muscular power delivered to the crank during the downstroke and the upstroke of the crank cycle [Wilks' Lambda = 0.399, F(8,42) = 3.07, p = 0.009] indicating that children delivered a greater proportion of the power to the crank during the upstroke when compared to adults, (3) hip power contribution to limb power [Wilks' Lambda = 0.454, F(8,42) = 2.54, p = 0.023] indicating a cadence-dependence of age-related differences in the muscular synergy between hip extensors and plantarflexors. The results demonstrate that in spite of a successful performance, children construct the task of pedaling differently when compared to adults, especially when they are pushed to their performance limits. The weaker synergy between hip extensors and plantarflexors suggests that a lack of inter-muscular coordination, rather than muscular power production per se, is a factor that limits children's performance ranges

Human sarcopenia reveals an increase in SOCS-3 and myostatin and a reduced efficiency of Akt phosphorylation

Age-related skeletal muscle sarcopenia is linked with increases in falls, fractures, and death and therefore has important socioeconomic consequences. The molecular mechanisms controlling age-related muscle loss in humans are not well understood, but are likely to involve multiple signaling pathways. This study investigated the regulation of several genes and proteins involved in the activation of key signaling pathways promoting muscle hypertrophy, including GH/STAT5, IGF-1/Akt/GSK-3&beta;/4E-BP1, and muscle atrophy, including TNF&alpha;/SOCS-3 and Akt/FKHR/atrogene, in muscle biopsies from 13 young (20 &plusmn; 0.2 years) and 16 older (70 &plusmn; 0.3 years) males. In the older males compared to the young subjects, muscle fiber cross-sectional area was reduced by 40&ndash;45% in the type II muscle fibers. TNF&alpha; and SOCS-3 were increased by 2.8 and 1.5 fold, respectively. Growth hormone receptor protein (GHR) and IGF-1 mRNA were decreased by 45%. Total Akt, but not phosphorylated Akt, was increased by 2.5 fold, which corresponded to a 30% reduction in the efficiency of Akt phosphorylation in the older subjects. Phosphorylated and total GSK-3&beta; were increased by 1.5 and 1.8 fold, respectively, while 4E-BP1 levels were not changed. Nuclear FKHR and FKHRL1 were decreased by 73 and 50%, respectively, with no changes in their atrophy target genes, atrogin-1 and MuRF1. Myostatin mRNA and protein levels were significantly elevated by 2 and 1.4 fold. Human sarcopenia may be linked to a reduction in the activity or sensitivity of anabolic signaling proteins such as GHR, IGF-1, and Akt. TNF&alpha;, SOCS-3, and myostatin are potential candidates influencing this anabolic perturbation.<br /

Serum Concentrations of Myostatin and Myostatin-Interacting Proteins do not differ between young and Scarcopenic elderly men

Peer reviewedPostprin

Spatiotemporal analysis of the runaway distribution function from synchrotron images in an ASDEX Upgrade disruption

Synchrotron radiation images from runaway electrons (REs) in an ASDEX Upgrade discharge disrupted by argon injection are analysed using the synchrotron diagnostic tool Soft and coupled fluid-kinetic simulations. We show that the evolution of the runaway distribution is well described by an initial hot-tail seed population, which is accelerated to energies between 25-50 MeV during the current quench, together with an avalanche runaway tail which has an exponentially decreasing energy spectrum. We find that, although the avalanche component carries the vast majority of the current, it is the high-energy seed remnant that dominates synchrotron emission. With insights from the fluid-kinetic simulations, an analytic model for the evolution of the runaway seed component is developed and used to reconstruct the radial density profile of the RE beam. The analysis shows that the observed change of the synchrotron pattern from circular to crescent shape is caused by a rapid redistribution of the radial profile of the runaway density