Changes from 1986 to 2006 in reasons for liking leisure-time physical activity among adolescents

Reasons for participating in physical activity (PA) may have changed in accordance with the general modernization of society. The aim is to examine changes in self-reported reasons for liking leisure-time physical activity (LTPA) and their association with self-reported LTPA over a 20-year period. Data were collected among nationally representative samples of 13-year-olds in Finland, Norway, and Wales in 1986 and 2006 (N = 9252) as part of the WHO cross-national Health Behaviour in School-aged Children (HBSC) study. Univariate ANOVAs to establish differences according to gender, year, and country were conducted. In all countries, 13-year-olds in 2006 tended to report higher importance in terms of achievement and social reasons than their counterparts in 1986, while changes in health reasons were minor. These reasons were associated with LTPA in a similar way at both time points. Health reasons for liking LTPA were considered most important, and were the strongest predictor of LTPA. The findings seem robust as they were consistent across countries and genders. Health education constitutes the most viable strategy for promoting adolescents' motivation for PA, and interventions and educational efforts could be improved by an increased focus on LTPA and sport as a social activity

Skeletal muscle phenotypes initiated by ectopic MyoD in transgenic mouse heart

Forced expression of the myogenic regulatory gene MyoD in many types of cultured cells initiates their conversion into skeletal muscle. It is not known, however, if MyoD expression serves to activate all or part of the skeletal muscle program in vivo during animal development, nor is it known how limiting the influences of cellular environment may be on the regulatory effects of MyoD. To begin to address these issues, we have produced transgenic mice which express MyoD in developing heart, where neither MyoD nor its three close relatives—myogenin, Myf-5, and MRF4/herculin/Myf-6—are normally expressed. The resulting gross phenotype in offspring from multiple, independent transgenic founders includes abnormal heart morphology and ultimately leads to death. At the molecular level, affected hearts exhibit activation of skeletal muscle-specific regulatory as well as structural genes. We conclude that MyoD is able to initiate the program that leads to skeletal muscle differentiation during mouse development, even in the presence of the ongoing cardiac differentiation program. Thus, targeted misexpression of this tissue-specific regulator during mammalian embryogenesis can activate, either directly or indirectly, a diverse set of genes normally restricted to a different cell lineage and a different cellular environment

MyoD−/− Satellite Cells in Single-Fiber Culture Are Differentiation Defective and MRF4 Deficient

AbstractMyoD-deficient mice are without obvious deleterious muscle phenotype during embryogenesis and fetal development, and adults in the laboratory have grossly normal skeletal muscle and life span. However, a previous study showed that in the context of muscle degeneration on a mdx (dystrophin null) genetic background, animals lacking MyoD have a greatly intensified disease phenotype leading to lethality not otherwise seen in mdx mice. Here we have examined MyoD−/− adult muscle fibers and their associated satellite cells in single myofiber cultures and describe major phenotypic differences found at the tissue, cellular, and molecular levels. The steady-state number of satellite cells on freshly isolated MyoD−/− fibers was elevated and abnormal branched fiber morphologies were observed, the latter suggesting chronic muscle regeneration in vivo. Single-cell RNA coexpression analyses were performed for c-met, m-cadherin, and the four myogenic regulatory factors (MRFs.) Most mutant satellite cells entered the cell cycle and upregulated expression of myf5, both characteristic early steps in satellite cell maturation. However, they later failed to normally upregulate MRF4, displayed a major deficit in m-cadherin expression, and showed a significant diminution in myogenin-positive status compared with wildtype. MyoD−/− satellite cells formed unusual aggregate structures, failed to fuse efficiently, and showed greater than 90% reduction in differentiation efficiency relative to wildtype. A further survey of RNAs encoding regulators of growth and differentiation, cell cycle progression, and cell signaling revealed similar or identical expression profiles for most genes as well as several noteworthy differences. Among these, GDF8 and Msx1 were identified as potentially important regulators of the quiescent state whose expression profile differs between mutant and wildtype. Considered together, these data suggest that activated MyoD−/− satellite cells assume a phenotype that resembles in some ways a developmentally “stalled” cell compared to wildtype. However, the MyoD−/− cells are not merely developmentally immature, as they also display novel molecular and cellular characteristics that differ from any observed in wild-type muscle precursor counterparts of any stage

Measurement of the local Jahn-Teller distortion in LaMnO_3.006

The atomic pair distribution function (PDF) of stoichiometric LaMnO_3 has been measured. This has been fit with a structural model to extract the local Jahn-Teller distortion for an ideal Mn(3+)O_6 octahedron. These results are compared to Rietveld refinements of the same data which give the average structure. Since the local structure is being measured in the PDF there is no assumption of long-range orbital order and the real, local, Jahn-Teller distortion is measured directly. We find good agreement both with published crystallographic results and our own Rietveld refinements suggesting that in an accurately stoichiometric material there is long range orbital order as expected. The local Jahn-Teller distortion has 2 short, 2 medium and 2 long bonds.Comment: 5 pages, 3 postscript figures, minor change

Use of near infrared reflectance spectroscopy to predict nitrogen uptake by winter wheat within fields with high variability in organic matter

In this study, the ability to predict N-uptake in winter wheat crops using NIR-spectroscopy on soil samples was evaluated. Soil samples were taken in unfertilized plots in one winter wheat field during three years (1997-1999) and in another winter wheat field nearby in one year (2000). Soil samples were analyzed for organic C content and their NIR-spectra. N-uptake was measured as total N-content in aboveground plant materials at harvest. Models calibrated to predict N-uptake were internally cross validated and validated across years and across fields. Cross-validated calibrations predicted N-uptake with an average error of 12.1 to 15.4 kg N ha-1. The standard deviation divided by this error (RPD) ranged between 1.9 and 2.5. In comparison, the corresponding calibrations based on organic C alone had an error from 11.7 to 28.2 kg N ha-1 and RPDs from 1.3 to 2.5. In three of four annual calibrations within a field, the NIR-based calibrations worked better than the organic C based calibrations. The prediction of N-uptake across years, but within a field, worked slightly better with an organic C based calibration than with a NIR based one, RPD = 1.9 and 1.7 respectively. Across fields, the corresponding difference was large in favour of the NIR-calibration, RPD = 2.5 for the NIR-calibration and 1.5 for the organic C calibration. It was concluded that NIR-spectroscopy integrates information about organic C with other relevant soil components and therefore has a good potential to predict complex functions of soils such as N-mineralization. A relatively good agreement of spectral relationships to parameters related to the N-mineralization of datasets across the world suggests that more general models can be calibrated

Skeletal muscle phenotypes initiated by ectopic MyoD in transgenic mouse heart

Forced expression of the myogenic regulatory gene MyoD in many types of cultured cells initiates their conversion into skeletal muscle. It is not known, however, if MyoD expression serves to activate all or part of the skeletal muscle program in vivo during animal development, nor is it known how limiting the influences of cellular environment may be on the regulatory effects of MyoD. To begin to address these issues, we have produced transgenic mice which express MyoD in developing heart, where neither MyoD nor its three close relatives—myogenin, Myf-5, and MRF4/herculin/Myf-6—are normally expressed. The resulting gross phenotype in offspring from multiple, independent transgenic founders includes abnormal heart morphology and ultimately leads to death. At the molecular level, affected hearts exhibit activation of skeletal muscle-specific regulatory as well as structural genes. We conclude that MyoD is able to initiate the program that leads to skeletal muscle differentiation during mouse development, even in the presence of the ongoing cardiac differentiation program. Thus, targeted misexpression of this tissue-specific regulator during mammalian embryogenesis can activate, either directly or indirectly, a diverse set of genes normally restricted to a different cell lineage and a different cellular environment