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The Apert syndrome Fgfr2+/S252W mouse model exhibits perinatal lethality.
Furthermore, the PRKAG2 mouse model exhibits myocardial insulin resistance.
The Calsequestrin (CSQ) mouse model exhibits extreme variation in the phenotype progression and severity highly dependent on the genetic background.
The ARTE10 mouse model exhibits a neuropathological phenotype that mimics several characteristics of human AD.
We have previously reported that a Comt−/− mouse model exhibits a preeclampsia phenotype that is reversed by administration of 2-ME[27].
Given that our LID mouse model exhibits a constitutive serum IGF-1 deficiency (from birth) we could not rule out an accumulating effect of IGF-1 on bone development in these animals.
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However, our Rag2-R229Q mouset model modexhibitedted a milder immunological phenotype in lymphocyte development than in the previous Rag2 KI/EGFP mouse model13.
The impairment of neurogenesis in a mouse model exhibiting progressive amyloid deposition was reflected by a reduction in the number of neural stem cells, progenitor cells and neuroblasts in the dentate gyrus [13].
These results extend previous findings by demonstrating that in a mouse model exhibiting hyper-cholesterolemia and atherosclerosis, marked elevations in serum cholesterol concentrations are induced by PCB-77.
Here, using geometric morphometrics, we analyzed facial outgrowth and shape change over time in a novel mouse model exhibiting fully penetrant bilateral CL/P.
In a mouse model exhibiting disrupted TGFβ signaling, spontaneous liver cancer development and activation of IL6 signaling were observed [ 115], whereas in cell lines, the modulation of JAK/STAT was able to promote differentiation and elimination of CSCs [ 133].
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