Sentence examples for mouse demonstrated that from inspiring English sources

In vivo efficacy study on human gastric (MKN-45) and human non-small cell lung NCI-H19933) tumor xenograft in nude mouse demonstrated that 4d·CH3SO3H had a better inhibiting activity than SGX-523 in a dose-dependent manner.

Towards this end, the progesterone receptor knockout (PRKO) mouse demonstrated that progesterone is essential for pregnancy-associated mammary gland ductal side-branching and alveologenesis and that these morphological changes are dependent on progesterone-induced mammary epithelial proliferation.

The failure to generate an IKBKAP KO mouse demonstrated that the gene is essential [12] as are the IKBKAP orthologs of C. elegans and Drosophila [11].

Our previous work in the hippocampus of the mouse demonstrated that recombinant NMDAR with NR2B overexpression enhanced both synaptic plasticity in the hippocampus and hippocampal-dependent learning [38].

The mouse Smyd1/Bop gene is also strongly expressed in skeletal and heart muscle; studies with Smyd1/Bop knockout mouse demonstrated that it is essential for cardiogenesis [61].

Studies of intra/interspecific crossings in mouse demonstrated that paternal mitochondrial DNA (mtDNA) is selectively eliminated during early embryogenesis in intraspecific crossings, whereas 50% of paternal mtDNA are transmitted to progeny in interspecifc crossings [5], [6].

p65EHT mice developed papillomas similarly to p65FL mice demonstrating that heterozygous loss of p65 in the epidermis was not sufficient to prevent tumour development (Fig 1D and E).

The researchers imaged particles accumulating in the liver of the mouse, demonstrating that the technique could visualize structures within the body.

Here a combined approach of multicolor stimulated emission depletion microscopy (STED) and confocal imaging in rat and mouse demonstrates that structural plasticity is linked to the addition of unitary synaptic nanomodules to spines.

Studies in Drosophila, zebrafish and mouse demonstrate that the neuronal dysfunction of TDP-43 is causally related to disease formation.

The failure to generate a p53 and ASPP2 double knockout mouse demonstrates that ASPP2 and p53 deficiency are synthetic lethal.