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J Med Genet 1994;31: 872–874. 9 Kirkwood SC, Su JL, Conneally P, Foroud T: Progression of symptoms in the early and middle stages of Huntington disease. Arch Neurol 2001;58: 273–278. 10 Marder K, Zhao H, Myers RH, et al: Rate of functional decline in Huntington’s disease. Huntington study group. Neurology 2000;54:452–458. 11 Panov AV, Gutekunst CA, Leavitt BR, et al: Early mitochondrial calcium defects in Huntington’s disease are a direct effect of polyglutamines. Nat Neurosci 2002;5:731–736. 12 Sawa A, Wiegand GW, Cooper J, et al: Increased apoptosis of Huntington disease lymphoblasts associated with repeat length-dependent mitochondrial depolarization.

Enabling Technologies in GWAS Although the first GWAS appeared in the literature in 2003, the initial tools did not cover a representative area of the human genome. In 2004, Ishkanian et al. [10] described a tiling resolution DNA microarray that they described as showing ‘complete coverage’ of the human genome. Such tools are essential starting blocks for GWAS studies, which are based on enabling genotype-phenotype correlations, using the same principles as candidate gene studies. However, such studies are hypothesis free, since the variants measured span the entire human genome.

J Nutr Biochem 2003;14:717–726. 18 Lo CJ, Chiu KC, Fu M, Chu A, Helton S: Fish oil modulates macrophage P44/P42 mitogen-activated protein kinase activity induced by lipopolysaccharide. J Parenter Enteral Nutr 2000;24:159–163. CNV and EPA 19 Moon DO, Kim KC, Jin CY,et al: Inhibitory effects of eicosapentaenoic acid on lipopolysaccharideinduced activation in BV2 microglia. Int Immunopharmacol 2007;7:222–229. 20 Lynch AM, Loane DJ, Minogue AM, et al: Eicosapentaenoic acid confers neuroprotection in the amyloid-beta challenged aged hippocampus.

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3-scroll immersi in G (1,4) by Alzati A.

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