Multimodel Approach for Intelligent Control and Applications

IntroductionThemultimodelapproachappearsasapowerfultechniquetodealwithcomplex,nonlinearand/orilldefinedsystemsrepresentedusingasetofsimplelinearorsmoothlynonlinearmodelseachofthemallowingthegenerationofapartialcontroller.Differentapproachesexistintheliterature[1,2]tocopewiththetwokeypointsofthemultimodel/multicontrolstrategy:themodelbasisdeterminationandtheuseofpartialcontrollersinordertoderiveaglobalone.Hence,itappearsobviousthatoneofthemainobjectstofocusoninthemultimodel/multicontrolapproach…     

Variation in FTO contributes to childhood obesity and severe adult obesity

We identified a set of SNPs in the first intron of the FTO (fat mass and obesity associated) gene on chromosome 16q12.2 that is consistently strongly associated with early-onset and severe obesity in both adults and children of European ancestry with an experiment-wise P value of 1.67 x 10(-26) in 2,900 affected individuals and 5,100 controls. The at-risk haplotype yields a proportion of attributable risk of 22% for common obesity. We conclude that FTO contributes to human obesity and hence may be a target for subsequent functional analyses.     

Drosophila and the genetics of the internal milieu

'Homeostasis', from the Greek words for 'same' and 'steady', refers to ways in which the body acts to maintain a stable internal environment despite perturbations. Recent studies in Drosophila exemplify the conservation of regulatory mechanisms involved in metabolic homeostasis. These new findings underscore the use of Drosophila as a model for the study of various human disorders.     

Truncating mutations in the last exon of NOTCH2 cause a rare skeletal disorder with osteoporosis

Hajdu-Cheney syndrome is a rare autosomal dominant skeletal disorder with facial anomalies, osteoporosis and acro-osteolysis. We sequenced the exomes of six unrelated individuals with this syndrome and identified heterozygous nonsense and frameshift mutations in NOTCH2 in five of them. All mutations cluster to the last coding exon of the gene, suggesting that the mutant mRNA products escape nonsense-mediated decay and that the resulting truncated NOTCH2 proteins act in a gain-of-function manner.