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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Effects of treatments with cyclooxygenase inhibitors on chickens infected with Eimeria acervulina.

Reduced weight gains and feed conversions are major sources of economic losses from avian coccidiosis. Experiments were conducted to determine possible involvement of up-regulation of cyclooxygenase (COX) activity during coccidia infections that might contribute to reduced weight gain. In a series of trials, young (3 to 5 wk of age) cockerels infected with Eimeria acervulina, a duodenal parasite, received oral treatments with indomethacin (IM), an inhibitor of both COX-1 and COX-2, or nimesulide (NIM), a specific inhibitor of COX-2. Infection doses varied with experiment (from 10(5) to 10(6) oocysts per chick). Effects of infection on weight gain, duodenal lesions, plasma carotenoids, and levels of NO2+ NO3- were determined at 6 d postinoculation. Total oocysts were enumerated in feces collected from 5 through 8 d postinoculation from separate replicate groups. In no trials did treatment with IM reverse effects of infection on weight gain or significantly reduce lesion scores. However, in all trials, IM treatment reduced oocyst output per chick (Trial 1, 15%; Trial 2, 19%; Trial 3, 53%; Trial 4, 29%; Trial 5, 28.5%). Supplementation of feed with 400 and 100 ppm NIM significantly reduced weight gain of, and increased oocyst output from, infected chicks, whereas supplementation with 50 ppm NIM had no beneficial effects on weight gain or lesion scores, but reduced oocyst shedding. The inability of the IM and NIM treatments to reverse infection-associated weight gain suppression suggests that this pathological effect is not linked to increased prostanoid synthesis as a result of COX-2 up-regulation during infection. The inhibitory effects of IM treatment on oocyst shedding suggest that COX-2 products may have immunosuppressive effects in coccidia infection at local sites of infection. The stimulating effects of high-dose NIM treatments on oocyst shedding suggest that this compound may inhibit synthesis of other prostanoids as well.[1]


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