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Thus AR [41] or ERa [42] knockout mice develop several physio-pathological features characteristic of the metabolic syndrome including body weight gain, hyperphagia and increased visceral adipose tissue.
IκBζ-deficient mice develop several signs of autoimmune syndromes.
Injected with the same amount of cells, some mice develop several lung tumors, whereas other mice obviously are able to clear G-2 cells.
However, these mice develop several types of neoplastic lesions that are rarely seen in MEN1 patients, such as high frequency sex-cord stromal cell tumours in 88% of aged male mice and 50% of female mice [ 6, 8].
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A cohort of Sdhd/H19 KO mice developed several cases of profound cardiac hypertrophy, but showed no evidence of PGL/PC.
Pten+/− mice are viable but develop several hyperplastic and dysplastic lesions in different organs [10], [11].
The YAC128 mouse model carries 128 CAG repeats and is known to develop several HD-like symptoms.
Applying the gavage antibiotic depletion protocol had a profound effect on the phenotype of the mice as they developed several characteristics typical of germ-free mice.
IL-10−/− mice develop a chronic colitis over several weeks following weaning that is characterized by a patchy transmural inflammation limited to the colon [22].
In mice, homozygous deletion of VHL is embryonic lethal due to vascular abnormalities in the placenta; and, VHL+/− mice develop proliferative vascular lesions in several major organs, most prominently the liver.
Pathologically, Ercc1 Δ/ − mice develop mild histological abnormalities in several tissues, in particular liver and kidney, consistent with previous reported findings in Ercc1 Δ/Δ and Ercc1− / − mice [ 38, 49, 55, 65].
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