Accurate and ongoing assessments of physical activity (PA) and sedentary time (SED) are needed to support public health surveillance, evaluate interventions, and advance the understanding of how movem Show more
Accurate and ongoing assessments of physical activity (PA) and sedentary time (SED) are needed to support public health surveillance, evaluate interventions, and advance the understanding of how movement behaviours relate to health. After six cycles of data collection (2007 to 2019) using the Actical (AC) accelerometer, the Canadian Health Measures Survey (CHMS) transitioned to the ActiGraph wGT3X-BT (AG). To understand how estimates from the AC accelerometer may compare with those from the AG in the context of the CHMS, this study compares AC and AG accelerometer estimates of PA, step counts, and SED using CHMS protocols. A convenience sample of 47 adults (aged 18 to 79 years) and 36 children and youth (aged 3 to 17 years) wore both AC and AG accelerometers on their waist for seven consecutive days. Estimates of PA and SED, step counts, and the percentage of those meeting PA recommendations were compared between the devices using descriptive, correlation, and agreement statistics. Agreement ranged from poor to excellent, with variability across PA intensities and age groups. Significant absolute differences in SED and light PA (LPA) were observed across all age groups, and in step counts among children and youth. Agreement was good to excellent across most age groups for moderate-to-vigorous PA (MVPA), and among adults for step counts. While the percentage of those meeting PA recommendations was higher with the AG, results were not statistically different. Similar comparisons could be made with the AG device when using the normal and low frequency extension filters. The results of the present study provide data users and researchers with an indication of the expected differences between the devices across various movement behaviour outcomes in the context of the CHMS. Results suggest that comparisons between cycles 1 to 6 and Cycle 7 onward of the CHMS for MVPA are acceptable, but they should be carried out with caution. Comparisons of SED, LPA, vigorous PA, and step counts are not recommended. Show less
Mutations that inactivate LET-767 are shown to affect growth, reproduction, and development in Caenorhabditis elegans. Sequence analysis indicates that LET-767 shares the highest homology with human t Show more
Mutations that inactivate LET-767 are shown to affect growth, reproduction, and development in Caenorhabditis elegans. Sequence analysis indicates that LET-767 shares the highest homology with human types 3 and 12 17beta-hydroxysteroid dehydrogenases (17beta-HSD3 and 12). Using LET-767 transiently transfected into human embryonic kidney-293 cells, we have found that the enzyme catalyzes the transformation of both 4-androstenedione into testosterone and estrone into estradiol, similar to that of mouse 17beta-HSD12 but different from human and primate enzymes that catalyze the transformation of estrone into estradiol. Previously, we have shown that amino acid F234 in human 17beta-HSD12 is responsible for the selectivity of the enzyme toward estrogens. To assess whether this amino acid position 234 in LET-767 could play a role in androgen-estrogen selectivity, we have changed the methionine M234 in LET-767 into F. The results show that the M234F change causes the loss of the ability to transform androstenedione into testosterone, while conserving the ability to transform estrone into estradiol, thus confirming the role of amino acid position 234 in substrate selectivity. To further analyze the structure-function relationship of this enzyme, we have changed the three amino acids corresponding to lethal mutations in let-767 gene. The data show that these mutations strongly affect the ability of LET-767 to convert estrone in to estradiol and abolish its ability to transform androstenedione into testosterone. The high conservation of the active site and amino acids responsible for enzymatic activity and substrate selectivity strongly suggests that LET-767 shares a common ancestor with human 17beta-HSD3 and 12. Show less