The molecular changes did not, though, seem to change the aminothiazoles prion-killingattributes.
氨噻唑分子的改变似乎并没有改变其杀灭朊病毒的特性。
When tested in Petri dishes, the new molecules were as good as their precursors.
在培养皿实验中,修饰后的分子与其前体一样有效。
More importantly, preliminary results suggest they are effective at extending the lives ofprion-infected mice.
更重要的是,初步的实验结果提示这些分子能有效延长朊病毒感染小鼠的寿命,
Such mice lived for 100 days longer when treated with the new molecules than they didwhen untreated.
用这些新分子治疗的小鼠比不治疗的小鼠多存活100天。
That is a significant fraction of the two to three years a healthy laboratory mouse might beexpected to survive if it is not experimented on.
考虑到实验室中未受试的健康小鼠的预期寿命是2到3年,染毒小鼠获得延长的这部分存活期显得很显著了。
Trials in mice are, of course, just the beginning. But breaching the blood-brain barrier in thisway is a crucial step, and one that might be generalised to potential treatments for otherbrain diseasesAlzheimer s, for example.
当然,用小鼠进行的试验只是个开始。但药物以这种方式突破血脑屏障确实是个关键步骤,在此基础上,人们还可能找到治疗阿尔茨海默尔病这样的其他脑部疾病的良方。
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