当适应度函数和突变、重组及水平基因转移率已知时，该项新的数学上的结果可以使这一机制运算化。

The new mathematical results allow calculation of this mechanism when the fitness function and the mutation, recombination and horizontal gene transfer rates are known.

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接受了转移来的肠道微生物的普通小鼠也开始表现出进食更多的食物并像突变的小鼠一样，也逐步表现出代谢综合征症状。

When these animals received the teeming gut world of the TLR5-deficient mice, they too began eating more and developed the same metabolic-syndrome symptoms that their donors had.

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在小鼠模型中，GNA11突变诱导了自发转移性肿瘤，激活了丝裂原活化蛋白激酶途径。

Mutations in GNA11 induced spontaneously metastasizing tumors in a mouse model and activated the mitogen-activated protein kinase pathway.

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