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Moreover, embryonic lethality and development of non-epithelial tumours are another important limitation of genetically mutated Brca2 mice.
Furthermore, certain hospitals have reported nosocomial outbreaks in crowded conditions, which are associated with high case lethality and development of lung sequelae [ 9].
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As another example, the inactivation of the Retinoblastoma tumor suppressor (Rb) in Gfap expressing cells led to perinatal lethality and astrocytoma development in mice [50].
These two populations exhibit substantial genetic divergence, with nucleotide substitutions occurring on average every 163 bp (Koboldt et al. 2010), and also show some evidence of mild hybrid dysfunction, including an increase in hybrid embryonic lethality and hybrid development rate (Dolgin et al. 2008; Ross et al. 2011; Baird and Stonesifer 2012).
In the case of PLCB3, discordant results have been reported when the gene is knocked out in mice producing both embryonic lethality and normal development in different studies [ 23, 24]; however, it has been found that the knockout of a related gene, the PLCB1, developed epilepsy in mice [ 25].
Here, we show that hppy overexpression results in partial lethality during development and that the surviving flies have smaller wings due to the loss of epithelial cells.
Knockdown of PDCD2 in Danio rerio results in embryonic lethality and defects in HSC development (Kramer et al., 2013).
There is some evidence that the global and endothelial cell-specific knockout of HDAC 7, a class II HDAC, is associated with embryonic lethality and required for the development of a normal vasculature [ 60].
In experimental studies it was found that exposure to NO2 during gestation induced increased lipid peroxidation in the placenta, elevated postimplantation embryonic lethality, and disturbances of postnatal development [ 27].
Bar-Ilan et al. [ 9] demonstrated that various sized gold and silver particles were able to affect zebrafish development, causing lethality and developmental anomalies in body axis shape and heart functionality.
Gli1 homozygous null mice have reduced body weight, increased postnatal lethality, and defects in T-cell development, while heterozygotes are of normal weight but have reduced bone mass, reflecting the importance of normal levels of GLI1 for bone homeostasis and immune function (Kitaura et al., 2014, Drakopoulou et al., 2010).
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