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In aged Ncadk.i and Ncadk.i. p53 mice with numerous lactation cycles, we observed a histological transition from benign to malignant structures.
In more recent work, Mathias Jucker and Larry Walker showed in collaboration that brain homogenates from Alzheimer's disease and mice with numerous amyloid-β plaques accelerated the deposition of amyloid-β in the brains of mice transgenic for human mutant amyloid precursor protein.
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One group of 20 mice was placed in an enriched environment, which consisted of a large cage (surface area of 231 cm per mouse) with numerous pieces of stimulatory equipment (exercise wheels, tunnels, refuges, tissues), and the 18 mice in the other group were placed in four standard cages (4 5 mice/cage with surface area of 78 cm per mouse) with tissues only.
Other studies using CX3CR1-deficient mice showed exacerbated levels of phospho-Tau and elevated Tau pathology in Tau transgenic mice [ 9, 22], while CX3CR1 deficiency reduced amyloid load in AD mouse models with numerous Aβ deposits [ 71, 74].
Endothelial cell sprouting is also reduced in tumor vessels in the NG2 null mouse, consistent with numerous studies demonstrating the importance of extracellular matrix attachment for activation of key signaling pathways in endothelial cells [ 46- 48].
The cellular structure of RPE in aging cKO mice is disorganized with numerous vacuole-like structures, undigested phagosomes, autophagosomes, cellular materials, and increased lipid deposition compared with the floxed controls.
Our results in control mice are in agreement with numerous studies on NOD.scid.IL2RγcKO mice showing human T cell functional impairment [15], [18], [20] [22].
Analysis of TLQP21-treated mice revealed a phenotype with numerous additional similarities to VGF knockout mice including increased energy expenditure, increased WAT β2-adrenergic receptor mRNA levels, increased WAT UCP1 mRNA levels, normal locomotor activity, and decreased WAT weight {see Results and [ 21]}.
In contrast, the lungs from TN3-19.12-treated mice were strikingly enlarged, with numerous large granulomatous lesions not seen in the IgG1 control or CC-3052-treated CC-3052-treated CC-3052-treated
In addition to epidemiological studies, dietary studies with mice and humans, combined with numerous tissue culture studies, have substantiated the beneficial role of DHA in breast cancer [ 17- 20].
Likewise, 80% of aberrations detected by array CGH in tumour cells of the mouse model for epithelial ovarian cancer are conserved in human epithelial ovarian cancer [281] and epithelial carcinomas in mice with telomere dysfunction show numerous copy number changes in regions syntenic to those in human cancers [282].
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