Sentence examples for mouse is supported from inspiring English sources

The increase in inflammation at 'peak' BP in the BPH/2J mouse is supported by our GO and GST analyses, and the higher levels of inflammatory markers that have been reported in hypertensive patients during the morning BP surge [39].

The predicted TSS in mouse is supported by 3 FANTOM 5'CAGE tags at 7,651 bp from the start of mmu-miR-23a.

The circadian rhythmicity of many cartilage specific genes found in mouse is supported by microarray studies in rat cartilage under diurnal (LD cycle) conditions [ 72].

The salt dependant phenotype of the SPAK243A/243A mouse is supported by the abolition of hypotension following a high salt (3% Na+) diet (Fig 2E).

Our proposal that aging of the gastrocnemius progenitor cells and myofibers is delayed by reducing the levels of P-p38α activity in the DN-p38αAF/+ mouse is supported by the demonstration that its attenuation reduces the level of activation of cell cycle inhibitors of the Cdkn2a and Cdkn2b tumor suppressor loci in multiple organs (kidney, spleen, lung, liver) [ 24].

The notion that most CD8α+ HY-TCR-expressing cells in IEL have a different origin than CD8α+ IEL of WT mice is supported by the finding that only the former expressed uniformly low levels of CD5 (data not shown).

The hypothesis that Dbh −/− mice lose more heat through the periphery than control mice is supported by the observation that these mice eat similar amounts of food (Fig. 1) relative to their controls (Dbh −/− compared to control and DBL MUT compared to ob/ob), yet have a cooler body temperature (Table).

Our conclusion that the Snord116 deletion is responsible for the phenotypes in the mice is supported by a recently presented individual with PWS who has a paternally derived small genomic deletion comprising the entire SNORD116 cluster and half of the SNORD115 cluster.

A key role for neuroinflammation in cognitive dysfunction in AD mice is supported by previous studies (Wirths et al., 2010).

Regardless, the notion that impaired activation of AKT in osteoclast precursors contributes to the osteopetrotic phenotype of induced SHP-2-deficient mice is supported by findings in ovariectomized female NF1 +/− mice.

Mutant K58I with the lowest threshold for fusion of pH 5.4 demonstrated increased replication and virulence, suggesting that adaptation of avian H5N1 influenza virus for replication in mice is supported by a low pH threshold for fusion.