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Finally, transgenic mouse studies demonstrate critical roles for PDGF in mesenchymal cell survival in the lung.
The human genetics of AD, combined with several lines of evidence in human and mouse studies demonstrate a pathogenic role for Aβ, and particularly for soluble, oligomeric assemblies of Aβ in synaptic and network dysfunction [ 10].
Recent mouse studies demonstrate for the first time that NaPi-IIb deletion attenuates hyperphosphatemia in models of CKD, supporting NaPi-IIb as a suitable treatment target for hyperphosphatemia in CKD.
It is, therefore, not entirely surprising that CDKN1A expression level may be predictive of radiation toxicity; a plausible biological explanation exists in that knockout mouse studies demonstrate CDKN1A, which plays a role in protecting intestinal epithelial cells from radiation-induced apoptosis (Wang et al, 1997).
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Epidemiological studies of MMA and DMA have been fewer, but mouse studies demonstrated that these compounds may be anorectic agents [ 13- 15].
In addition, several xenografts in NOD/SCID mouse studies demonstrated that LFM-A13 did not show notable levels of adverse effects in alone or in combination in-vivo.
Data from rat and mouse studies demonstrated an increased risk of C-cell carcinoma for liraglutide, although this has not been proven in humans [ 70].
Elegant mouse studies demonstrated that transfer of Th17 cells generated in the presence of IL-23, but not TGFβ, caused autoimmunity in mice (McGeachy et al., 2007; Ghoreschi et al., 2010).
Breast cancer cells with different levels of malignancy, according to in vitro and in vivo mouse studies, demonstrated invasive and metastatic properties within the embryonic zebrafish model that nicely correlated with their differential tumourigenicity in mouse models.
However, previous transgenic mouse studies demonstrated that the human TSPY promoter could be preferentially active in neurons of pre- and postnatal brains, suggesting a possible function of this Y chromosome gene in neural development [ 32].
For example, mouse studies demonstrated an inverse relationship between maternal alcohol dehydrogenase activity and maternal blood alcohol levels and consequent fetal abnormalities, but suggested that other inherited factors from both the mother and the fetus were also important [ 19, 21- 23].
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