依据上述论点，本研究利用AT2受体基因敲出小鼠，观察了AT2受体缺失后是否造成肾素-血管紧张素系统其它成分代偿性紊乱。
In the present study, we investigated whether gene deletion of AT2 receptor causes the compensatory chaos of renin-angiotensin system in mice.
符合条件的患者乙肝表面抗原阳性的代偿性肝脏疾病的男性和女性谁是至少6个月以上的，给予拉米夫定和HBV聚合酶基因突变。
Eligible patients were hepatitis B surface antigen-positive men and women with compensated liver disease who were given lamivudine at least more than 6 months and had HBV polymerase gene mutation.
结论DPR基因敲除型小鼠脑中组胺能神经活性显著降低，这一变化可能是该种小鼠尚能维持正常睡眠的代偿机制之一。
Conclusion The activity of the histaminergic system decreased and the decrease might be one of the compensatory mechanisms for maintenance of the normal sleep in the null mice lacking DPR.
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