Sentence examples for mice develop larger from inspiring English sources

COMP-deficient ApoE-KO mice develop larger plaques in the brachiocephalic artery.

ABCA1 knockout mice develop larger atherosclerotic lesions, and overexpression of ABCA1 inhibits the progression of atherosclerotic lesions [ 53- 55].

Since C57BL/6 mice develop larger infarcts after tMCAO than Sv129 mice [ 59, 66] and Sv129 mice exhibit higher levels of circulating PMNs compared with C57BL/6 mice [ 65], we studied tMCAO in both mouse strains in parallel (Table  1).

We have previously demonstrated that adiponectin-deficient (APN-KO) mice develop larger infarcts in the heart following ischemia-reperfusion injury [ 18], and that adiponectin administration leads to reduced myocardial injury and improved function following ischemia-reperfusion in mice and pigs [ 18, 19].

This seems to be an important pathogenic mechanism based on the findings that overexpression of ARC inhibits oxidant-induced apoptosis in isolated myocytes [244] and that ARC knockout mice develop larger infarcts after ischemia reperfusion and more rapidly develop pressure-overload-induced heart failure [245].

These mice develop large numbers of intestinal tumors at an early age and are thus used as a model for evaluating chemo-preventive interventions for humans with intestinal polyps.

Apc mutant mice develop large numbers of adenomas in their small intestine and fewer in the large intestine whereas; FAP patients develop low numbers of adenomas in their small intestine and large numbers of adenomas in their large intestine.

These changes are not typically observed in the transgenic primary tumor model, as the mice develop large multifocal luminal tumors that necessitate euthanizing the mice before these genetic and epigenetic alterations take place.

Consistent with the above findings, Rpn13−/− mice developed larger thymuses with more cellularity compared to Wt mice (Figure 7A and B).

For example, using a carcinogen induced colorectal cancer model, Nishihara et al. [25] showed that adiponectin knockout mice developed larger colorectal tumors.

155– 157 Homozygous mice developed larger cecal tumor and died due to gastrointestinal obstruction after some weeks.