A cycloisomerization reaction of Di-(p-halogenophenyl)-trifluoromethyl-carbinols

Résumé Une solution de di-(p-chlorophényl)-trifluorométhyl-carbinol dans l'acide sulfurique concentré, diluée à l'eau ou au méthanol, donne naissance à du chloro-3-hydroxy-(ou méthoxy-)-6-trifluorométhyl-9 fluorène. Le composé méthoxylé, après l'alcoolyse alcaline du groupement-CF₃, a été dégradé au fluorénone correspondant, dont la synthèse a été realisée indépendamment.     

A new quantitative relation between internal and external steady-state concentrations in active transport

Zusammenfassung Im aktiven Transport der Aminosäureanalogen (-Aminoisobuttersäure und Cyclopentan-1-aminocarbonsäure) in Gehirnschnitten folgt das Verhältnis im stationären Zustand zwischen der intrazellulären Konzentration und der Lösungskonzentration derFreundlich Adsorptionisotherme,C _i =AC ₀ ⁿ . Dieses Verhältnis stimmt mit dem Modell einer aktiven Pumpe, die der Michaelis-Menten Kinetik folgt und mit einer passiven Ausdiffusion ausgeglichen ist, nicht überein. Es wird vermutet, dass eine Kontrolle des aktiven Transports durch intra- und extrazelluläre Konzentrationen reguliert wird.     

Genetic variation in the 5q31 cytokine gene cluster confers susceptibility to Crohn disease

Linkage disequilibrium (LD) mapping provides a powerful method for fine-structure localization of rare disease genes, but has not yet been widely applied to common disease. We sought to design a systematic approach for LD mapping and apply it to the localization of a gene (IBD5) conferring susceptibility to Crohn disease. The key issues are: (i) to detect a significant LD signal (ii) to rigorously bound the critical region and (iii) to identify the causal genetic variant within this region. We previously mapped the IBD5 locus to a large region spanning 18 cM of chromosome 5q31 (P<10(-4)). Using dense genetic maps of microsatellite markers and single-nucleotide polymorphisms (SNPs) across the entire region, we found strong evidence of LD. We bound the region to a common haplotype spanning 250 kb that shows strong association with the disease (P< 2 x 10(-7)) and contains the cytokine gene cluster. This finding provides overwhelming evidence that a specific common haplotype of the cytokine region in 5q31 confers susceptibility to Crohn disease. However, genetic evidence alone is not sufficient to identify the causal mutation within this region, as strong LD across the region results in multiple SNPs having equivalent genetic evidence-each consistent with the expected properties of the IBD5 locus. These results have important implications for Crohn disease in particular and LD mapping in general.