Multidimensional collocation stochastic method to evaluate the Whole Specific Absorption Rate for a given population

To protect people from Electromagnetic Fields (EMF), ICNIRP has defined limits [1]. The Basic Restrictions (BR) set the maximum values of Specific Absorption Rate (SAR). Since BR are complex to assess ICNIRP has also derived the reference levels (RL) from BR. These RL were established to guaranty the compliance to BR. Several studies with human model (phantoms) show that even below the RL, the WBSAR (Whole Body averaged SAR) may exceed the BR due to the variability of human morphology [2]. The number of phantoms is very limited. Hence, t e characterization of the WBSAR for a given using usual methods such as Monte Carlo is not possible. To bridge this lack of phantoms a model for the WBSAR as a function of morphology is suitable. However, this model requires knowledge on internal morphology (proportion of fat, muscle...) and external ones (mainly height and weight) [5]. Due to the absence of statistical data concerning the internal morphology, the statistical distribution of the WBSAR is difficult to obtain. In this paper, the internal morphology is released by considering one equivalent tissue for the whole body. The stochastic collocation is used to characterize the distribution of the WBSAR for a given population. The study is conducted in the case of a plane wave operating at 2.1 GHz, vertically polarized and frontally oriented on phantoms. The incident power is equal to 1W/m²

Added Value of Assessing Adnexal Masses with Advanced MRI Techniques

International audienceThis review will present the added value of perfusion and diffusion MR sequences to characterize adnexal masses. These two functional MR techniques are readily available in routine clinical practice. We will describe the acquisition parameters and a method of analysis to optimize their added value compared with conventional images. We will then propose a model of interpretation that combines the anatomical and morphological information from conventional MRI sequences with the functional information provided by perfusion and diffusion weighted sequences

Interaction Between ALK1 Signaling and Connexin40 in the Development of Arteriovenous Malformations

International audienceOBJECTIVE:To determine the role of Gja5 that encodes for the gap junction protein connexin40 in the generation of arteriovenous malformations in the hereditary hemorrhagic telangiectasia type 2 (HHT2) mouse model.APPROACH AND RESULTS:We identified GJA5 as a target gene of the bone morphogenetic protein-9/activin receptor-like kinase 1 signaling pathway in human aortic endothelial cells and importantly found that connexin40 levels were particularly low in a small group of patients with HHT2. We next took advantage of the Acvrl1(+/-) mutant mice that develop lesions similar to those in patients with HHT2 and generated Acvrl1(+/-); Gja5(EGFP/+) mice. Gja5 haploinsufficiency led to vasodilation of the arteries and rarefaction of the capillary bed in Acvrl1(+/-) mice. At the molecular level, we found that reduced Gja5 in Acvrl1(+/-) mice stimulated the production of reactive oxygen species, an important mediator of vessel remodeling. To normalize the altered hemodynamic forces in Acvrl1(+/-); Gja5(EGFP/+) mice, capillaries formed transient arteriovenous shunts that could develop into large malformations when exposed to environmental insults.CONCLUSIONS:We identified GJA5 as a potential modifier gene for HHT2. Our findings demonstrate that Acvrl1 haploinsufficiency combined with the effects of modifier genes that regulate vessel caliber is responsible for the heterogeneity and severity of the disease. The mouse models of HHT have led to the proposal that 3 events-heterozygosity, loss of heterozygosity, and angiogenic stimulation-are necessary for arteriovenous malformation formation. Here, we present a novel 3-step model in which pathological vessel caliber and consequent altered blood flow are necessary events for arteriovenous malformation development

Interaction Between ALK1 Signaling and Connexin40 in the Development of Arteriovenous Malformations

Nephrolog