BackgroundThe recent increase in childhood obesity is expected to add significantly to the prevalence of chronic diseases. We used multivariate multilevel analysis to examine associations between parks/green space and childhood overweight/obesity across communities in Calgary, Canada, a city characterized by intensified urban sprawl and high car use.MethodsBody Mass Index was calculated from measured height and weight data obtained from 6,772 children (mean age = 4.95 years) attending public health clinics for pre-school vaccinations. Each child's home postal code was geocoded using ESRI ArcGIS 9.2. We examined four measures of spatial access to parks/green space (based on Geographic Information Systems): 1) the number of parks/green spaces per 10,000 residents, 2) the area of parks/green space as a proportion of the total area within a community, 3) average distance to a park/green space, and 4) the proportion of parks/green space service area as a proportion of the total area within a community. Analyses were adjusted for dissemination area median family income (as a proxy for an individual child's family income) community-level education, and community-level proportion of visible minorities.ResultsIn general, parks/green space at the community level was not associated with overweight/obesity in Calgary, with the exception of a marginally significant effect whereby a moderate number of parks/green spaces per 10,000 residents was associated with lower odds of overweight/obesity. This effect was non-significant in adjusted analyses.ConclusionOur null findings may reflect the popularity of car travel in Calgary, Canada and suggest that the role built environment characteristics play in explaining health outcomes may differ depending on the type of urban environment being studied.

No abstract

No abstract

Different synthetic forms of supplemental methionine (Met) are produced commercially by various manufacturers. Limited information exists on the bioavailability of these different forms in commercially relevant fish species. The objective of this study was to compare the relative bioavailability of L-methionine and a methionine hydroxy analogue calcium salt (MHA-Ca) to DL-methionine in a commercially relevant species, rainbow trout, using a linear slope-ratio assay. In addition, the ability of the rainbow trout to effectively convert the D-isomer of methionine into the biologically active L-isomer was studied by comparing the relative bioavailability of L-methionine to DL-methionine. Nine (9) diets were created from a methionine-deficient basal diet which was supplemented with graded equimolar levels of methionine (0.1%, 0.2%, 0.3% of diet by weight) from either DL-methionine, L-methionine and methionine hydroxy analogue calcium salt (MHA-Ca). Diets were fed in triplicate (IBW = 24.0 AE 0.6 g) for 12 weeks using a pair-feeding protocol. The basal diet was formulated to be deficient in both methionine (0.5%) and cysteine (0.3%), whereas meeting all other known nutritional requirements of rainbow trout. MHA-Ca was found to be less available (P < 0.05) than DL-methionine with relative bioavailability values of 69%, 60% and 73% based upon weight gain, growth rate (TGC) and retained nitrogen values respectively. No significant differences (P > 0.05) in bioavailability were found between DL-methionine and L-methionine.These findings lead to the conclusion that differences in bioavailability do exist between sources of synthetic methionine, additionally findings suggest that rainbow trout are able to effectively convert the D-isomer of methionine into the L-isomer without significantly affecting fish performance.

Ageing in Saccharomyces cerevisiae is a finite phenomenon, determined by replicative, rather than chronological lifespan. Yeast physiological condition is known to influence industrial fermentation performance, however, until recently cellular senescence has not been considered as a brewing yeast stress factor. A polyploid lager yeast (BB11) and a brewery isolate, exhibiting petite mutation were analysed for longevity. It was observed that mitochondrial deficiency induced a reduction in lifespan. In addition, replicative capacity was perceived to be dependent on environmental conditions.