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However, ablation of MAPK14 in the epithelial cells of the digestive tract of another mouse strain caused development of significantly more tumours [ 16].
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In 129 strain mice, inactivation of Dnd1, as in the 129-Ter mouse strain, causes loss of germ cells and in addition, development of testicular germ cell tumors [3].
A mutation found in the lpr (lymphoproliferation) mouse strain causes defective expression of CD95.
For example, Npc1-null mutations put into the C57BL/6 mouse strain cause a more severe early defect (leading to premature death prior to obvious neurodegeneration) than in FVB/N, Balb/c or mixed genetic backgrounds.
In wild-type mice, neither strain caused mortality or weight loss, though one mouse inoculated with WNV-MADIC showed mild signs of disease.
Taken together, infection of mouse brain by the mutant strain caused a more wide spread activation of astrocytes and microglial cells, which is consistent with our transcriptome data.
As shown in Figure 7A, the NIH230 strain caused bacteremia in mice 24 h after intraperitoneal injection whereas the bacteremia was barely detected in mice infected with NIH230::csrS+as well as the 1566 strain (p = 0.005 compared with non-invasive isolates, and p = 0.005 compared with invasive isolates +CsrS).
We found that the STM-WT virulent strain caused the death of four mice and induced abortion in three others.
Compared to the wild-type strain, a H201R isogenic mutant strain caused significantly larger skin lesions in mice.
When injected into the brains of susceptible mice, the MSA strain causes a fatal disease similar to human MSA.
Accordingly, it seemed possible that the genetic manipulations used for preparation of either of these mouse strains might have caused a change in the expression pattern.
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