Morphees+:Studying Everyday Reconfigurable Objects for the Design and Taxonomy of Reconfigurable Uls

International audienc

The production of a machine designed for the cold radial cyclic forging of solid and tube billets

This paper gives an account of a new project for the design and production of a radial cyclic forging machine. This new design considers the advantages of its predecessor and of modern trends within the engineering industry. The use of this machine could enable the considerable reduction of production wastes. Besides the cold cyclic technology implemented in this machine, it will also allow for the increase in energy efficiency, for the minimum capital investments. © 2014 WIT Press.International Journal of Safety and Security Engineering;International Journal of Sustainable Development and Planning;WIT Transactions on Ecology and the Environmen

Assessing socioeconomic health care utilization inequity in Israel: impact of alternative approaches to morbidity adjustment

<p/> <p>Background</p> <p>The ability to accurately detect differential resource use between persons of different socioeconomic status relies on the accuracy of health-needs adjustment measures. This study tests different approaches to morbidity adjustment in explanation of health care utilization inequity.</p> <p>Methods</p> <p>A representative sample was selected of 10 percent (~270,000) adult enrolees of Clalit Health Services, Israel's largest health care organization. The Johns-Hopkins University Adjusted Clinical Groups^®were used to assess each person's overall morbidity burden based on one year's (2009) diagnostic information. The odds of above average health care resource use (primary care visits, specialty visits, diagnostic tests, or hospitalizations) were tested using multivariate logistic regression models, separately adjusting for levels of health-need using data on age and gender, comorbidity (using the Charlson Comorbidity Index), or morbidity burden (using the Adjusted Clinical Groups). Model fit was assessed using tests of the Area Under the Receiver Operating Characteristics Curve and the Akaike Information Criteria.</p> <p>Results</p> <p>Low socioeconomic status was associated with higher morbidity burden (1.5-fold difference). Adjusting for health needs using age and gender or the Charlson index, persons of low socioeconomic status had greater odds of above average resource use for all types of services examined (primary care and specialist visits, diagnostic tests, or hospitalizations). In contrast, after adjustment for overall morbidity burden (using Adjusted Clinical Groups), low socioeconomic status was no longer associated with greater odds of specialty care or diagnostic tests (OR: 0.95, CI: 0.94-0.99; and OR: 0.91, CI: 0.86-0.96, for specialty visits and diagnostic respectively). Tests of model fit showed that adjustment using the comprehensive morbidity burden measure provided a better fit than age and gender or the Charlson Index.</p> <p>Conclusions</p> <p>Identification of socioeconomic differences in health care utilization is an important step in disparity reduction efforts. Adjustment for health-needs using a comprehensive morbidity burden diagnoses-based measure, this study showed relative underutilization in use of specialist and diagnostic services, and thus allowed for identification of inequity in health resources use, which could not be detected with less comprehensive forms of health-needs adjustments.</p

A Duplication CNV That Conveys Traits Reciprocal to Metabolic Syndrome and Protects against Diet-Induced Obesity in Mice and Men

The functional contribution of CNV to human biology and disease pathophysiology has undergone limited exploration. Recent observations in humans indicate a tentative link between CNV and weight regulation. Smith-Magenis syndrome (SMS), manifesting obesity and hypercholesterolemia, results from a deletion CNV at 17p11.2, but is sometimes due to haploinsufficiency of a single gene, RAI1. The reciprocal duplication in 17p11.2 causes Potocki-Lupski syndrome (PTLS). We previously constructed mouse strains with a deletion, Df(11)17, or duplication, Dp(11)17, of the mouse genomic interval syntenic to the SMS/PTLS region. We demonstrate that Dp(11)17 is obesity-opposing; it conveys a highly penetrant, strain-independent phenotype of reduced weight, leaner body composition, lower TC/LDL, and increased insulin sensitivity that is not due to alteration in food intake or activity level. When fed with a high-fat diet, Dp(11)17/+ mice display much less weight gain and metabolic change than WT mice, demonstrating that the Dp(11)17 CNV protects against metabolic syndrome. Reciprocally, Df(11)17/+ mice with the deletion CNV have increased weight, higher fat content, decreased HDL, and reduced insulin sensitivity, manifesting a bona fide metabolic syndrome. These observations in the deficiency animal model are supported by human data from 76 SMS subjects. Further, studies on knockout/transgenic mice showed that the metabolic consequences of Dp(11)17 and Df(11)17 CNVs are not only due to dosage alterations of Rai1, the predominant dosage-sensitive gene for SMS and likely also PTLS. Our experiments in chromosome-engineered mouse CNV models for human genomic disorders demonstrate that a CNV can be causative for weight/metabolic phenotypes. Furthermore, we explored the biology underlying the contribution of CNV to the physiology of weight control and energy metabolism. The high penetrance, strain independence, and resistance to dietary influences associated with the CNVs in this study are features distinct from most SNP–associated metabolic traits and further highlight the potential importance of CNV in the etiology of both obesity and MetS as well as in the protection from these traits

Following the genes: a framework for animal modeling of psychiatric disorders

The number of individual cases of psychiatric disorders that can be ascribed to identified, rare, single mutations is increasing with great rapidity. Such mutations can be recapitulated in mice to generate animal models with direct etiological validity. Defining the underlying pathogenic mechanisms will require an experimental and theoretical framework to make the links from mutation to altered behavior in an animal or psychopathology in a human. Here, we discuss key elements of such a framework, including cell type-based phenotyping, developmental trajectories, linking circuit properties at micro and macro scales and definition of neurobiological phenotypes that are directly translatable to humans

The 16p11.2 locus modulates brain structures common to autism, schizophrenia and obesity

Anatomical structures and mechanisms linking genes to neuropsychiatric disorders are not deciphered. Reciprocal copy number variants at the 16p11.2 BP4-BP5 locus offer a unique opportunity to study the intermediate phenotypes in carriers at high risk for autism spectrum disorder (ASD) or schizophrenia (SZ). We investigated the variation in brain anatomy in 16p11.2 deletion and duplication carriers. Beyond gene dosage effects on global brain metrics, we show that the number of genomic copies negatively correlated to the gray matter volume and white matter tissue properties in cortico-subcortical regions implicated in reward, language and social cognition. Despite the near absence of ASD or SZ diagnoses in our 16p11.2 cohort, the pattern of brain anatomy changes in carriers spatially overlaps with the well-established structural abnormalities in ASD and SZ. Using measures of peripheral mRNA levels, we confirm our genomic copy number findings. This combined molecular, neuroimaging and clinical approach, applied to larger datasets, will help interpret the relative contributions of genes to neuropsychiatric conditions by measuring their effect on local brain anatomy