Increasing rates of diabetes and cardiovascular risk in Métis Settlements in northern Alberta.

OBJECTIVES: To determine the prevalence of diabetes (using secondary data analysis), as well as undiagnosed diabetes and pre-diabetes (using primary research methods) among adult Métis Settlement dwellers in northern Alberta. We also sought to identify cardiovascular risk factors. STUDY DESIGN: Quantitative research study utilizing both population census and community-based diabetes screening data. METHODS: Self-reported diabetes was analyzed from the results of the Métis Settlement specific censuses in 1998 and 2006. Mobile clinics travelled into each of the 8 Métis Settlement communities in Alberta recruiting 693 subjects for screening for undiagnosed diabetes, pre-diabetes and metabolic syndrome. Logistic regression analyses (adjusted for age and sex) were used to identify associated factors. RESULTS: According to the censuses, 4,312 Métis individuals were living on Settlements in 1998 and 5,059 in 2006. Self-reported age-adjusted prevalence of diabetes increased significantly from 5.1% in 1998 to 6.9% in 2006 (p < 0.01), with a crude prevalence increase of 66% (p < 0.01). In 2006, diabetes prevalence was higher among females than males, 7.8% vs. 6.1% respectively (p < 0.05). Of the 266 adults screened in the fasting state, 5.3% had undiagnosed diabetes, whereas 20.3% (Canadian Diabetes Association criteria) and 51.9% (American Diabetes Association criteria) had pre-diabetes. Rates of obesity and metabolic syndrome were 49.4% (n = 693) and 46.4% (n = 266), respectively. Hemoglobin A1c > 6.1% was strongly associated with diabetes, pre-diabetes and metabolic syndrome. CONCLUSIONS: Our results indicate high rates of diabetes, undiagnosed diabetes, pre-diabetes and metabolic syndrome among adult Alberta Métis Settlement dwellers.

Whole-genome analysis of 60 G protein-coupled receptors in Caenorhabditis elegans by gene knockout with RNAi.

G protein-coupled receptors (GPCRs) are the largest family of genes in animal genomes and represent more than 2% of genes in humans and C. elegans. These evolutionarily conserved seven-transmembrane proteins transduce a diverse range of signals. In view of their pivotal role in cell signaling, it is perhaps surprising that decades of genetic analysis in C. elegans, and recent genome-wide RNAi screens, have identified very few GPCR mutants. Therefore, we screened all GPCRs predicted to bind either small-molecule neurotransmitters or neuropeptides by using RNAi and quantitative behavioral assays. This shows that C16D6.2, C25G6.5, C26F1.6, F35G8.1, F41E7.3, and F59C12.2 are likely to be involved in reproduction, whereas C15B12.5, C10C6.2, C24A8.4, F15A8.5, F59D12.1, T02E9.1, and T05A1.1 have a role in locomotion. Gene deletions for F35G8.1 and T05A1.1 resulted in the same phenotype as that seen with RNAi. As some GPCRs may be resistant to RNAi, or may result in abnormalities not screened for here, the actual proportion of nonredundant receptors with an assayable function is probably greater. Strikingly, most phenotypes were observed for NPY-like receptors that may bind neuropeptides. This is consistent with the known actions of neuropeptides on the body wall muscle and reproductive tract in nematodes.

Serotype 14 variants of the Spanish penicillin-resistant serotype 9V clone of Streptococcus pneumoniae arose by large recombinational replacements of the cpsA-pbp1a region.

The high prevalence of penicillin resistance among Streptococcus pneumoniae isolates from Uruguay has been associated with the emergence of a penicillin-resistant clone of serotype 14. Isolates of this clone were identical by multilocus sequence typing to members of the Spanish penicillin-resistant serotype 9V clone and possessed indistinguishable forms of the penicillin-binding protein 2b and 2x genes. Their pbp1a genes were also identical, except at the 3' end. The serotype 14 isolates were shown to be a variant of the Spanish serotype 9V clone which arose by a 22.2 kb recombinational replacement that introduced the capsular biosynthetic locus, and part of the neighbouring pbp1a gene, from a serotype 14 isolate. One end of the recombinational replacement was within the first gene of the capsular polysaccharide operon, cpsA, as the sequence of the upstream dexB gene, through most of cpsA, was identical in the penicillin-resistant serotype 9V and 14 isolates, but the sequences differed in the rest of cpsA and in cpsB. The other recombinational junction was at the end of the divergently transcribed pbp1a gene, which is approximately 11.6 kb downstream of the capsular biosynthetic locus. Isolates of this serotype variant were also detected in Spain and Denmark. Penicillin-resistant serotype 14 isolates from Poland were also closely related to the penicillin-resistant serotype 9V clone, but have emerged independently, as one end of the recombinational replacement was upstream of dexB and the other was within pbp1a, but at a different position from that in the serotype 14 variants from Uruguay, Spain and Denmark. Serotype 14 variants of the Spanish serotype 9V clone have therefore arisen on more than one occasion by large recombinational replacements that extend from the start of the cps region into the pbp1a gene.