<i>In Vivo</i> 9.4T MRI and <sup>1</sup>H MRS for Evaluation of Brain Structural and Metabolic Changes in the Ts65Dn Mouse Model for Down Syndrome

International audienceIn the present study we investigated structural and metabolic modifications of the brain in the Ts65Dn mouse model of Down syndrome(DS)using both in vivo magnetic resonance imaging(MRI)and proton magnetic resonance spectroscopy(MRS). MRI was performed for further texture analysis and changes in texture parameters, including mean grey levels, contrast and homogeneity, and they were found in Ts65Dn compared to diploid littermates (2n). These phenotypic changes were different in the hippocampus and cerebellum, since in Ts65Dn mean grey levels increased in the cerebellum and decreased in the hippocampus. In addition, proton NMR spectra revealed differences in metabolite ratios. Levels of N-acetylaspartate(NAA)and glutamate(Glu), were lower compared to total creatine levels (CX), in the Ts65Dn brain. However, the most striking finding was an increase in the concentration of myo-inositol(Ins)and choline(Cho)in the hippocampus, whereas the Ins concentration was reduced in the cerebellum. Overall, these data illustrate that MRI and MRS are valuable assesment tools sufficiently sensitive to detect associated changes in different brain areas, thus providing new insight into the causative role of dosage-sensitive genes in the Ts65Dn DS mouse model

Particle Production in a Hadron Collider Rapidity Gap: The Higgs Case

Production of rare particles within rapidity gaps has been proposed as a background-free signal for the detection of new physics at hadron colliders. No complete formalism accounts for such processes yet. We study a simple lowest-order QCD model for their description. Concentrating on Higgs production, we show that the calculation of the cross section pp -> pp H can be embedded into existing models which successfully account for diffractive data. We extend those models to take into account single and double diffractive cross sections pp -> H X1 X2 with a gap between the fragments X1 and X2. Using conservative scenarios, we evaluate the uncertainties in our calculation, and study the dependence of the cross section on the gap width. We predict that Higgs production within a gap of 4 units of rapidity is about 0.3 pb for a 100 GeV Higgs at the Tevatron, and almost 2 pb for a 400 GeV Higgs within a gap of 6 units at the LHC with 14 TeV beams.Comment: LaTeX file, 30 pages, 12 figures and psfig.sty included in a second uufile. The full ready-to-print postscript manuscript is available by anonymous ftp at ftp://lpsvsh.lps.umontreal.ca/ in theorie/hep-ph/Rapidity.ps (it's a VAX so you'll have to use the format theorie.hep-ph if you change by more than one directory at a time

Utilisation de la résonance magnétique pour l’exploration non invasive du microenvironnement tumoral

National audienc

IL-12Rβ2 Is Essential for the Development of Experimental Cerebral Malaria

International audienceA Th1 response is required for the development of Plasmodium berghei ANKA (PbA)-induced experimental cerebral malaria (ECM). The role of pro-Th1 IL-12 in malaria is complex and controversial. In this study, we addressed the role of IL-12Rβ2 in ECM development. C57BL/6 mice deficient for IL-12Rβ2, IL-12p40, or IL-12p35 were analyzed for ECM development after blood-stage PbA infection in terms of ischemia and blood flow by noninvasive magnetic resonance imaging and angiography, T cell recruitment, and gene expression. Without IL-12Rβ2, no neurologic sign of ECM developed upon PbA infection. Although wild-type mice developed distinct brain microvascular pathology, ECM-resistant, IL-12Rβ2-deficient mice showed unaltered cerebral microcirculation and the absence of ischemia after PbA infection. In contrast, mice deficient for IL-12p40 or IL-12p35 were sensitive to ECM development. The resistance of IL-12Rβ2-deficient mice to ECM correlated with reduced recruitment of activated T cells and impaired overexpression of lymphotoxin-α, TNF-α, and IFN-γ in the brain after PbA infection. Therefore, IL-12Rβ2 signaling is essential for ECM development but independent from IL-12p40 and IL-12p35. We document a novel link between IL-12Rβ2 and lymphotoxin-α, TNF-α, and IFN-γ expression, key cytokines for ECM pathogenesis