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AZRA RAZA Professor of medicine and director of the MDS Centre, Columbia University, New York An obvious truth that is either being ignored or going unaddressed in cancer research is that mouse models do not mimic human disease well and are essentially worthless for drug development.
Recent results from PDE3B transgenic mouse models do indicate that PDE3B plays an important role in overall regulation of energy metabolism [10], [11].
Transgenic mouse models do not resolve this problem conclusively, i.e. the relative hierarchy of amyloid and tau pathology depends on the actual model and the genes expressed or inactivated.
However, the current mouse models do not exhibit overt neuronal loss and have failed to recapitulate the progressive degeneration of nigrostriatal dopaminergic neurons; the hallmark pathology underlying the clinical motor symptoms of PD.
The fact that germline mutations of NDRG1 in humans and NDRG1 knockout mouse models do not develop cancers suggests that NDRG1 may not be involved with cancer initiation but at a later event in cancer progression which includes metastasis [14], [15].
Most FA mouse models do not show any gross, FA-specific developmental abnormalities.
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Preclinical success in AD transgenic mouse models does not imply that successful translation to human subjects will occur.
Of note, the degree of steatosis in our different genetically modified mouse models did not strictly correlate with the extent of liver injury upon MCD-diet feeding.
In accord with their longer latency, the great majority of tumors arising in our mouse models did not display any of the cardinal features of PABC, including aggressive growth rate, high Ki67, and stromal involvement (data not shown) (Schedin, 2006).
Sholl analysis for other four mouse models did not show similar arborization defects, as shown in Figure 6 figure supplement 1. (B ) Spine density defects are present in Shank3+/ΔC and Mecp2 R308/Y.
Even though the mouse model do not reproduce actual clinical manifestation of the disease, in our previous studies, selection did influenced the outcome of inflammation and tissue damage [2], [3].
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