Analytical Modelling of No-Load Density in Surface Mounted Permanent Magnet Motor

International audienceIn this paper, the authors present an analytical calculation in order to predict the no-load flux density in surface mounted synchronous permanent magnet machines. This analytical model is based on two-dimensional analysis in polar coordinates and has been developed for both parallel and radial magnetization of the magnets. The no-load magnetic vector potential is established by solving Laplace/Poisson's equations using the Fourier's series and the method of separating variables. Two circular regions are considered: the Region.I, which is the air-gap modified by Carter's coefficient, and the Region.II, which includes the magnets and the air-spaces between magnets. The analytical results are compared with the ones obtained by a numerical analysis using the finite-element method (FEM)

Maximization of No-Load Density in Surface Mounted Permanent Magnet Motor

International audienceAn exact two-dimensional (2-D) analytical model (AM) of slotless permanent magnet (PM) machines in polar coordinates is used to determine the analytical equations of the air-gap flux density at no-load operation. The authors show that, for a radial magnetization, there is an optimal magnet thickness which permits to maximize the noload flux density. In order to use easily and directly this optimal value during the design of surface mounted PM motors (SMPMM), the authors propose an original analytical expression of this maximum magnet thickness that have been obtained by interpolation of the values given by several analytical computations. This interpolation function could be applied to SMPMM having a parallel or radial magnetization direction

Design of a High-Speed Permanent Magnet Motor for the Drive of a Fuel Cell Air-Compressor

International audienceThis paper deals with the design of a 500 W permanent magnet (PM) machine used to drive the aircompressor of a 5 kW fuel cell (FC). The authors focus on the optimization of the motor efficiency in order to minimize the energy consumption of the air-compressor which can represent up to 30 % of the electrical energy delivered by the FC. The authors justify the use of a PM machine by the fact that, by using rare earth Nd-Fe-B magnets, such a type of machine makes it possible to reach a high efficiency as well as a high power density. The optimized machine presented in this paper have theoretically more than 25 % of its working area with an efficiency higher than 90 % and the efficiency at the rated point equals to 92 %. Those promising results of computation are confirmed by the first experimental results obtained with a prototype

Étude de la Désaimantation dans l'Air d'un Inducteur Cylindrique de Machines à Aimants permanents montés en Surface

National audienceCet article traite de la démagnétisation dans l'air des aimants permanents (AP) d'un inducteur cylindrique de machines à AP montés en surface. Les auteurs présentent d'abord un calcul analytique exact du champ pour une telle structure, puis les résultats obtenus sont confirmés par des simulations numériques 2D et 3D. Les auteurs déterminent ainsi, dans un cas concret, les limites en température et en épaisseur d'aimants pour se prémunir de la désaimantation dans l'air

Artificial Neural Networks to aid defferentiation of Benign and Malignant Breast Tumors by Microwave Imaging

In this paper, we propose a method for discriminating between malignant and benign breast tumors, by exploiting the dielectric properties of these tumors. The proposed technique is based on neural networks approach. Simulation results are presented on a model developed using EM simulator (CST)

Effects of Thyroxine Exposure on Osteogenesis in Mouse Calvarial Pre-Osteoblasts

The incidence of craniosynostosis is one in every 1,800-2500 births. The gene-environment model proposes that if a genetic predisposition is coupled with environmental exposures, the effects can be multiplicative resulting in severely abnormal phenotypes. At present, very little is known about the role of gene-environment interactions in modulating craniosynostosis phenotypes, but prior evidence suggests a role for endocrine factors. Here we provide a report of the effects of thyroid hormone exposure on murine calvaria cells. Murine derived calvaria cells were exposed to critical doses of pharmaceutical thyroxine and analyzed after 3 and 7 days of treatment. Endpoint assays were designed to determine the effects of the hormone exposure on markers of osteogenesis and included, proliferation assay, quantitative ALP activity assay, targeted qPCR for mRNA expression of Runx2, Alp, Ocn, and Twist1, genechip array for 28,853 targets, and targeted osteogenic microarray with qPCR confirmations. Exposure to thyroxine stimulated the cells to express ALP in a dose dependent manner. There were no patterns of difference observed for proliferation. Targeted RNA expression data confirmed expression increases for Alp and Ocn at 7 days in culture. The genechip array suggests substantive expression differences for 46 gene targets and the targeted osteogenesis microarray indicated 23 targets with substantive differences. 11 gene targets were chosen for qPCR confirmation because of their known association with bone or craniosynostosis (Col2a1, Dmp1, Fgf1, 2, Igf1, Mmp9, Phex, Tnf, Htra1, Por, and Dcn). We confirmed substantive increases in mRNA for Phex, FGF1, 2, Tnf, Dmp1, Htra1, Por, Igf1 and Mmp9, and substantive decreases for Dcn. It appears thyroid hormone may exert its effects through increasing osteogenesis. Targets isolated suggest a possible interaction for those gene products associated with calvarial suture growth and homeostasis as well as craniosynostosis. © 2013 Cray et al

Mutations in FGF17, IL17RD, DUSP6, SPRY4, and FLRT3 Are Identified in Individuals with Congenital Hypogonadotropic Hypogonadism

Congenital hypogonadotropic hypogonadism (CHH) and its anosmia-associated form (Kallmann syndrome [KS]) are genetically heterogeneous. Among the >15 genes implicated in these conditions, mutations in FGF8 and FGFR1 account for ∼12% of cases; notably, KAL1 and HS6ST1 are also involved in FGFR1 signaling and can be mutated in CHH. We therefore hypothesized that mutations in genes encoding a broader range of modulators of the FGFR1 pathway might contribute to the genetics of CHH as causal or modifier mutations. Thus, we aimed to (1) investigate whether CHH individuals harbor mutations in members of the so-called "FGF8 synexpression" group and (2) validate the ability of a bioinformatics algorithm on the basis of protein-protein interactome data (interactome-based affiliation scoring [IBAS]) to identify high-quality candidate genes. On the basis of sequence homology, expression, and structural and functional data, seven genes were selected and sequenced in 386 unrelated CHH individuals and 155 controls. Except for FGF18 and SPRY2, all other genes were found to be mutated in CHH individuals: FGF17 (n = 3 individuals), IL17RD (n = 8), DUSP6 (n = 5), SPRY4 (n = 14), and FLRT3 (n = 3). Independently, IBAS predicted FGF17 and IL17RD as the two top candidates in the entire proteome on the basis of a statistical test of their protein-protein interaction patterns to proteins known to be altered in CHH. Most of the FGF17 and IL17RD mutations altered protein function in vitro. IL17RD mutations were found only in KS individuals and were strongly linked to hearing loss (6/8 individuals). Mutations in genes encoding components of the FGF pathway are associated with complex modes of CHH inheritance and act primarily as contributors to an oligogenic genetic architecture underlying CHH

KLB , encoding β‐Klotho, is mutated in patients with congenital hypogonadotropic hypogonadism

Congenital hypogonadotropic hypogonadism (CHH) is a rare genetic form of isolated gonadotropin‐releasing hormone (GnRH) deficiency caused by mutations in > 30 genes. Fibroblast growth factor receptor 1 (FGFR1) is the most frequently mutated gene in CHH and is implicated in GnRH neuron development and maintenance. We note that a CHH FGFR1 mutation (p.L342S) decreases signaling of the metabolic regulator FGF21 by impairing the association of FGFR1 with β‐Klotho (KLB), the obligate co‐receptor for FGF21. We thus hypothesized that the metabolic FGF21/KLB/FGFR1 pathway is involved in CHH. Genetic screening of 334 CHH patients identified seven heterozygous loss‐of‐function KLB mutations in 13 patients (4%). Most patients with KLB mutations (9/13) exhibited metabolic defects. In mice, lack of Klb led to delayed puberty, altered estrous cyclicity, and subfertility due to a hypothalamic defect associated with inability of GnRH neurons to release GnRH in response to FGF21. Peripheral FGF21 administration could indeed reach GnRH neurons through circumventricular organs in the hypothalamus. We conclude that FGF21/KLB/FGFR1 signaling plays an essential role in GnRH biology, potentially linking metabolism with reproduction

Addressing gaps in care of people with conditions affecting sex development and maturation

Differences of sex development are conditions with discrepancies between chromosomal, gonadal and phenotypic sex. In congenital hypogonadotropic hypogonadism, a lack of gonadotropin activity results primarily in the absence of pubertal development with prenatal sex development being (almost) unaffected in most patients. To expedite progress in the care of people affected by differences of sex development and congenital hypogonadotropic hypogonadism, the European Union has funded a number of scientific networks. Two Actions of the Cooperation of Science and Technology (COST) programmes - DSDnet (BM1303) and GnRH Network (BM1105) - provided the framework for ground-breaking research and allowed the development of position papers on diagnostic procedures and special laboratory analyses as well as clinical management. Both Actions developed educational programmes to increase expertise and promote interest in this area of science and medicine. In this Perspective article, we discuss the success of the COST Actions DSDnet and GnRH Network and the European Reference Network for Rare Endocrine Conditions (Endo-ERN), and provide recommendations for future research