Bewegungsförderung : evidenzen und perspektiven

Angesichts der gut dokumentierten gesundheitlichen Konsequenzen körperlicher Inaktivität besteht ein wachsendes Interesse an der Förderung regelmäßiger körperlicher Aktivität und an entsprechenden Interventionen. Die wissenschaftliche Evidenz hinsichtlich der Effektivität von Interventionen zur Änderung des körperlichen Aktivitätsverhaltens Erwachsener lässt sich anhand der Ergebnisse randomisierter Kontrolluntersuchungen einschätzen. Interventionsansätze zur Förderung der körperlichen Aktivität lassen sich dabei voneinander unterschieden in: • Individuumsbezogene Interventionen • Bevölkerungsbezogene Interventionen Die nachfolgende Zusammenfassung bietet einen ersten Überblick über die Evidenzlage zu beiden Ansätzen. Vorliegende Forschungsergebnisse werden miteinander verglichen und die forschungsbezogenen sowie praktischen Stärken, aber auch Schwächen der entsprechenden Interventionsansätze werden aufgezeigt.

The reduced expression of the HADH2 protein causes X-linked mental retardation, choreoathetosis, and abnormal behavior

Recently, we defined a new syndromic form of X-linked mental retardation in a 4-generation family with a unique clinical phenotype characterized by mild mental retardation, choreoathetosis, and abnormal behavior (MRXS10). Linkage analysis in this family revealed a candidate region of 13.4 Mb between markers DXS1201 and DXS991 on Xp11; therefore, mutation analysis was performed by direct sequencing in most of the 135 annotated genes located in the region. The gene (HADH2) encoding L-3-hydroxyacyl-CoA dehydrogenase II displayed a sequence alteration (c.574 C-->A; p.R192R) in all patients and carrier females that was absent in unaffected male family members and could not be found in 2,500 control X chromosomes, including in those of 500 healthy males. The silent C-->A substitution is located in exon 5 and was shown by western blot to reduce the amount of HADH2 protein by 60%-70% in the patient. Quantitative in vivo and in vitro expression studies revealed a ratio of splicing transcript amounts different from those normally seen in controls. Apparently, the reduced expression of the wild-type fragment, which results in the decreased protein expression, rather than the increased amount of aberrant splicing fragments of the HADH2 gene, is pathogenic. Our data therefore strongly suggest that reduced expression of the HADH2 protein causes MRXS10, a phenotype different from that caused by 2-methyl-3-hydroxybutyryl-CoA dehydrogenase deficiency, which is a neurodegenerative disorder caused by missense mutations in this multifunctional protein.

ACE Research Vignette 047: What is the hard evidence on innovation and business productivity

This series of research vignettes is aimed at sharing current and interesting research findings from our team of international Entrepreneurship researchers. This vignette, written by Professor Beth Webster at Swinburne University of Technology, examines how innovation in small and medium size businesses affect their productivity.