1000 resultados para early


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Early growth response-1 (Egr-1) is expressed in human airways and found to modulate tumor necrosis factor, immunoglobulin E (IgE), airway responsiveness, and interleukin-13-induced inflammation in mice. We investigated the effects of Chinese-tagging singl

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Toxicological effects of Asulox-40 and Emisan-6 to eggs and early life history stages of Sarotherodon mossambicus were reported. 80% of egg hatching occurred in the controls, 1 p.p.m and 5 p.p.m concentrations of Asulox-40. 10 p.p.m. and 50 p.p.m. concentrations of the same toxicants had 70% and 60% hatchings while in Emisan-6 in the same concentrations the hatching were 70% and! 40%. In 100 p.p.m. concentration of both toxicants 20% incomplete hatching occurred. In Emisan-6 Lc 50 and Lc 100 values were recorded at 32 hand 96h respectively in 10 p.p.m. concentrations. In Asulox-40 the same values were recorded in 24h and 40h respectively at 50 p.p.m. concentration. The fish activity during the experimental period showed initial hyper activity. It was established that the Emisan-6 is more harmful to S. mossambicus than Asulox-40. The harmless concentrations of these chemicals were 1.2 p.p.m. for Asulox-40 and 0.6 p.p.m. for Emisan-6.

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为了探讨早期饲养环境对成年后大鼠条件化恐惧的影响,实验采用巴氏恐惧条件化的方法对不同饲养环境下的大鼠进行了行为检测.具体操作为:把断奶后的大鼠饲养在3个不同的人工控制的环境中(丰富环境、社群环境和贫瘠环境);8周后进行恐惧条件化训练和测试(指标为僵直百分比),以及检测不同饲养环境下的大鼠的体重、自发活动和足部电击敏感性.结果显示:与社群组相比,丰富组的大鼠条件化僵直水平明显增加,而贫瘠组的明显减少;丰富和贫瘠环境明显的影响了大鼠的体重;不同环境对自发活动和足部电击敏感性没有影响.这些结果说明幼年期的丰富环境能提高成年后大鼠的由声音诱发的条件化恐惧反应,而贫瘠环境则削弱了这种反应.

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We compared early stages of face processing in young and older participants as indexed by ERPs elicited by faces and non-face stimuli presented in upright and inverted orientations. The P1 and N170 components were larger in older than in young participant

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Stress in early life is believed to cause cognitive and affective disorders, and to disrupt hippocampal synaptic plasticity in adolescence into adult, but it is unclear whether exposure to enriched environment (EE) can overcome these effects. Here, we rep

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Sequence analysis of the mitochondrial genome has become a routine method in the study of mitochondrial diseases. Quite often, the sequencing efforts in the search of pathogenic or disease-associated mutations are affected by technical and interpretive pr