1000 resultados para Jean White-Haney
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Référence bibliographique : Rol, 55109
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Référence bibliographique : Rol, 55412
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Acquis le 9 mars 1836 d'Armans-Alexis Monteil pour le prix de 200 francs, parmi 52 volumes mss. y compris 3 rouleaux; cf. B.n.F., département des Manuscrits, registre des acquisitions 1833-1848, n° 1875 "16 terriers"
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Acquis le 2 avril 1743 de madame du Faÿ parmi 11 mss. pour le prix global de 1200 livres; cf. B.n.F., département des Manuscrits, Archives Ancien Régime 65, registre des acquisitions du département des Manuscrits 1667-1758, f. 291 "n° 87. Codex evangelii secundum Joannem, litteris auro depictis"; mention de la main de l'abbé Sallier "De madame du Fay. 12" (contreplat sup.); — note du XVe s. "Iste liber emptus fuit de precio scutorum LXV (...) M° CCCC° LXV°" (contreplat sup.); — anciennes cotes "87", "17" (Cv)
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Catalogue de l'abbaye de Corbie (éd. d'E. Coyecque, Cat des mss des bibliothèques de France, XIX, p.XI-XLVIII) XIIIe s.: n°246; 1621: n°420 Ex-libris : f.1 : « Sti Germani a Pratis »
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Activation of the peroxisome proliferator-activated receptor (PPAR)-alpha increases lipid catabolism and lowers the concentration of circulating lipid, but its role in the control of glucose metabolism is not as clearly established. Here we compared PPARalpha knockout mice with wild type and confirmed that the former developed hypoglycemia during fasting. This was associated with only a slight increase in insulin sensitivity but a dramatic increase in whole-body and adipose tissue glucose use rates in the fasting state. The white sc and visceral fat depots were larger due to an increase in the size and number of adipocytes, and their level of GLUT4 expression was higher and no longer regulated by the fed-to-fast transition. To evaluate whether these adipocyte deregulations were secondary to the absence of PPARalpha from liver, we reexpresssed this transcription factor in the liver of knockout mice using recombinant adenoviruses. Whereas more than 90% of the hepatocytes were infected and PPARalpha expression was restored to normal levels, the whole-body glucose use rate remained elevated. Next, to evaluate whether brain PPARalpha could affect glucose homeostasis, we activated brain PPARalpha in wild-type mice by infusing WY14643 into the lateral ventricle and showed that whole-body glucose use was reduced. Hence, our data show that PPARalpha is involved in the regulation of glucose homeostasis, insulin sensitivity, fat accumulation, and adipose tissue glucose use by a mechanism that does not require PPARalpha expression in the liver. By contrast, activation of PPARalpha in the brain stimulates peripheral glucose use. This suggests that the alteration in adipocyte glucose metabolism in the knockout mice may result from the absence of PPARalpha in the brain.
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Y chromosome variation is determined by several confounding factors including mutation rate, effective population size, demography, and selection. Disentangling these factors is essential to better understand the evolutionary properties of the Y chromosome. We analyzed genetic variation on the Y chromosome, X chromosome, and mtDNA of the greater white-toothed shrew, a species with low variance in male reproductive success and limited sex-biased dispersal, which enables us to control to some extent for life-history effects. We also compared ancestral (Moroccan) to derived (European) populations to investigate the role of demographic history in determining Y variation. Recent colonization of Europe by a small number of founders (combined with low mutation rates) is largely responsible for low diversity observed on the European Y and X chromosomes compared to mtDNA. After accounting for mutation rate, copy number, and demography, the Y chromosome still displays a deficit in variation relative to the X in both populations. This is possibly influenced by directional selection, but the slightly higher variance in male reproductive success is also likely to play a role, even though the difference is small compared to that in highly polygynous species. This study illustrates that demography and life-history effects should be scrutinized before inferring strong selective pressure as a reason for low diversity on the Y chromosome.
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Le complément de ce ms. se trouve dans le n. 15536.