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In vivo studies of mice supported this potential, but clinical approaches using TAMs are few at present.
Interestingly, expression analysis of Abhd5 tm1aWtsi/+ mice supported this testicular defect and demonstrated the extent to which lacZ was also expressed in the skin (pinna and tail), the major tissue affected in individuals with Chanarin-Dorfman syndrome, and in white and brown adipose tissues (Fig. 7J-L), where Abhd5 could play additional functional roles.
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The data obtained in our G2019S LRRK2 mice supports this assertion.
The structural defects observed in the calvaria of pRb knockout mice support this hypothesis and are suggestive of osteoblasts that are incapable of adhering to each other.
Our laboratory adaptation strategy in quail and chickens using a duck H9N2 virus and the subsequent realization that the virus replicated more efficiently in mice supports this hypothesis.
Indeed, the finding that LPS was able to restore IgA production in cultures containing DC from GF mice supports this hypothesis.
The histological evidence of βgal activity in the retinal ganglion cell layer of AAV-treated GM1 mice supports this notion, and could be the basis for preservation of some visual function in these mice.
The evidence that mutations in PSEN1/PSEN2 that cause Familial Alzheimer's disease are loss of function mutants, and that loss of PSEN1/PSEN2 function causes neurodegeneration in mice, supports this hypothesis [49], [50], [51], [52], [53].
Cav1.4 knock-out mice support this view as these mice show severe visual deficiencies [13,14].
Studies of CBP/p300 individual domain knock-in mutations in mice support this idea.
Our finding of increased granuloma size in SOM−/− mice supports this hypothesis.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com