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31.
32.
Rainbow trout (Oncorhynchus mykiss) were fed three different diets for 110 days — a basal dry diet with 8.4% oil content (BD8), a basal dry diet with 11.1%; oil content (BD11) a nd an expanded diet with 20.7% oil content (ED) — to investigate the influence of high fish oil exp anded diet on fatty acid composition of muscle, and to evaluate nutritional properties of edible tissue. I n fact, the experimental diets were also different in their component fatty acids, with an in creasing content of 3 highly unsaturated fatty acids (3 HUFA) from BD8 to ED. As regards biomet rics data, the condition factor and the coefficient of fatness were higher in fish fed ED in com parison with groups BD8 and BD11 (p < 0.05 ED vs. BD8). On the other hand, hepatosomatic index in group ED was markedly lower than those in groups BD8 and BD11 (p < 0.05 ED vs. BD8 and E D vs. BD11). This could be explained by the lower amount of crude protein in ED or it may indicate an excess amount of essential fatty acids (EFA) in ED. As regards fatty acid composition of fish m uscle, there were only slight differences in fatty acid composition of the edible tissue of fish wh en compared with the differences in fatty acid composition of the diets. The increased amount of fish oil in ED had a positive influence on the final weight of fish (p < 0.05 ED vs. BD8 and ED vs. BD11), but did not affect proportionately the percentage of 3 HUFA (20:53, 22:53, 22:63) and therefore the derived indices of lipid quality: so it appears possible to partially substitute fish oil in the diet with other lipid as a source of dietary fat.  相似文献   
33.
Porencephaly is a rare neurological disease, typically manifest in infants, which is characterized by the existence of degenerative cavities in the brain. To investigate the molecular pathogenesis of porencephaly, we studied a mouse mutant that develops porencephaly secondary to focal disruptions of vascular basement membranes. Half of the mutant mice died with cerebral hemorrhage within a day of birth, and approximately 18% of survivors had porencephaly. We show that vascular defects are caused by a semidominant mutation in the procollagen type IV alpha 1 gene (Col4a1) in mice, which inhibits the secretion of mutant and normal type IV collagen. We also show that COL4A1 mutations segregate with porencephaly in human families. Because not all mutant mice develop porencephaly, we propose that Col4a1 mutations conspire with environmental trauma in causing the disease.  相似文献   
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