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Ex vivo mouse embryo models exhibited developmental and genetic toxicity after high doses of nano-TiO2.
Gene expression domains extracted from raw images are integrated spatially into a set of standard 3D virtual mouse embryo models at different stages of development.
These results are similar to those from previous studies that showed iAs-induced structural malformations in the chick (Han et al. 2011) and mouse embryo models (Chaineau et al. 1990; Tabocova et al. 1996).
Similar effects have been demonstrated in mouse embryo models (Hildebrand and Soriano, 2002): ctbp1−/− animals are small and have a significantly shorter life expectancy, whereas ctbp2−/− embryos die in utero.
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KSOM+AA is the standard medium used for in-vitro mouse embryo culture models and has been systematically optimized over the years.
Experiments examining the cooperation of c-Myc and knockouts of p19ARF and/or p53 in mouse embryo fibroblast models have suggested that suppression of c-Myc-induced apoptosis may facilitate malignant transformation and tumorigenesis (Zindy et al, 1998).
Recently, bax was determined to be transcriptionally regulated by c-Myc in a variety of human cell lines (including the SkBr3 human breast cancer cell line) and found to be critical for the induction of apoptosis by aberrant c-Myc expression in a mouse embryo fibroblast model system (Mitchell et al, 2000).
Hence, the amplicon may represent RNA from the few blood vessels that express BCAS3 as seen in mouse embryos and models of angiogenesis.
Here we test the hypothesis using the mouse embryo as a model system.
Microtitre plates were seeded with either HPRT1-deficient human HT1080 fibrosarcoma cells or HPRT1 null mouse embryo fibroblasts as model systems.
The asymmetric cell divisions observed during pre-implantation development of the mouse embryo differ from these models since centrosomes are absent until the blastocyst stage [3].
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