Obesity prevalence estimates in a Canadian regional population of preschool children using variant growth references

<p>Abstract</p> <p>Background</p> <p>Childhood obesity is a public health problem in Canada. Accurate measurement of a health problem is crucial in defining its burden. The objective of this study is to compare the prevalence estimates of overweight and obesity in preschool children using three growth references.</p> <p>Methods</p> <p>Weights and heights were measured on 1026 preschool children born in Newfoundland and Labrador (NL), Canada, and body mass index calculated. The prevalence of overweight and obesity was determined and statistical comparisons conducted among the three growth references; the Centres for Disease Control (CDC), the International Obesity Task Force (IOTF) and the World Health Organization (WHO).</p> <p>Results</p> <p>CDC and IOTF produced similar estimates of the prevalence of overweight, 19.1% versus 18.2% while the WHO reported a higher prevalence 26.7% (p < .001). The CDC classified twice as many children as obese compared to the IOTF 16.6% versus 8.3% (p < .001) and a third more than the WHO 16.6% versus 11.3% (p < .01). There was variable level of agreement between methods.</p> <p>Conclusions</p> <p>The CDC reported a much higher prevalence of obesity compared to the other references. The prevalence of childhood obesity is dependent on the growth reference used.</p

Association of the T-cell regulatory gene CTLA4 with susceptibility to autoimmune disease

Genes and mechanisms involved in common complex diseases, such as the autoimmune disorders that affect approximately 5% of the population, remain obscure. Here we identify polymorphisms of the cytotoxic T lymphocyte antigen 4 gene (CTLA4)—which encodes a vital negative regulatory molecule of the immune system—as candidates for primary determinants of risk of the common autoimmune disorders Graves' disease, autoimmune hypothyroidism and type 1 diabetes. In humans, disease susceptibility was mapped to a non-coding 6.1 kb 3' region of CTLA4, the common allelic variation of which was correlated with lower messenger RNA levels of the soluble alternative splice form of CTLA4. In the mouse model of type 1 diabetes, susceptibility was also associated with variation in CTLA-4 gene splicing with reduced production of a splice form encoding a molecule lacking the CD80/CD86 ligand-binding domain. Genetic mapping of variants conferring a small disease risk can identify pathways in complex disorders, as exemplified by our discovery of inherited, quantitative alterations of CTLA4 contributing to autoimmune tissue destruction.<br/

Potential damaging mutation in LRP5 from genome sequencing of the first reported chimpanzee with the Chiari malformation

The genus Pan is the closest related to humans (Homo sapiens) and it includes two species: Pan troglodytes (chimpanzees) and Pan paniscus (bonobos). Different characteristics, some of biomedical aspect, separate them from us. For instance, some common human medical conditions are rare in chimpanzees (menopause, Alzheimer disease) although it is unclear to which extent longevity plays an active role in these differences. However, both humans and chimpanzees present similar pathologies, thus, understanding traits in chimpanzees can help unravel the molecular basis of human conditions. Here, we sequenced the genome of Nico, a central chimpanzee diagnosed with a particular biomedical condition, the Chiari malformation. We performed a variant calling analysis comparing his genome to 25 whole genomes from healthy individuals (bonobos and chimpanzees), and after predicting the effects of the genetic variants, we looked for genes within the OMIM database. We found a novel, private, predicted as damaging mutation in Nico in LRP5, a gene related to bone density alteration pathologies, and we suggest a link between this mutation and his Chiari malformation as previously shown in humans. Our results reinforce the idea that a comparison between humans and chimpanzees can be established in this genetic frame of common diseases.M.S.-M. is supported by the Ministerio de Economía y Competitividad, Spain (Maria de Maetzu grant MDM-2014-0370-16-3). M.d.M. is supported by a Formació de personal Investigador fellowship from Generalitat de Catalunya (FI_B01111). J.H.-R. is supported by the Ministerio de Economía y Competitividad, Spain (FPI grant BES-2013-064333). C.F. is supported by La Caixa Foundation. A.N. is funded by MINECO BFU2015-68649-P. T.M.-B. is supported by MINECO BFU2014-55090- P (FEDER), U01 MH106874 grant, Howard Hughes International Early Career, La Caixa Foundation and Secretaria d'Universitats i Recerca del Departament d'Economia i Coneixement de la Generalitat de Catalunya