Sentence examples for mouse models i from inspiring English sources

The thinner corneal epithelium in basonuclin-null mouse is similar to the phenotype of several recently described mouse models (i.e., null mutants of Pax6, KLF4, AP2-alpha and HMGN1).

However, there were several key differences in the mouse models; (i) in general, the mouse CIK cells expressed fewer CKRs on their surface, with CXCR3 being the only CKR that could be reliably and reproducibly detected on the cell surface by flow cytometry (N.B.

To better address how decline in serum IGF-1 affects aging, we used two mouse models: (i) congenital liver IGF-1-deficient (LID) mice, where serum IGF-1 is low throughout lifespan, and (ii) an inducible liver Igf1 gene-deleted (iLID) mouse model (Wu et al., 2010; Courtland et al., 2011), which allows temporal control of IGF-1.

This effect was then confirmed in two APP transgenic mouse models (i.e., Tg2576 and 5xFAD mice) in which pharmacological energy deprivation promoted amyloidogenesis via a BACE‐1‐dependent mechanism (O'Connor et al., 2008).

Many studies have been conducted on mice or humanized mouse models (i.e. germ-free mice administered human gut microbiota), which have been fed diets that are high in fat or saturated/unsaturated fat to investigate changes in the gut microbiota (Ley et al., 2006; Liu et al., 2012; Turnbaugh et al., 2009b; Wu et al., 2011; Zhang et al., 2012).

The fact that heterozygous COUP-TFII gene inactivation mouse models, i.e conditional beta cells [8] or complete invalidation [10] (50% decrease in COUP-TFII expression) displayed a strong phenotype suggests that any small variations of COUP-TFII expression does lead to a disturbed physiology.

We first performed passive immunization with MR16-1 in the bleomycin mouse model (i) to confirm previously reported findings in our in-house bleomycin-challenged mice and (ii) to obtain a range of effect of passive immunization efficacy, allowing further comparison with active immunization.

For this we used a double transgenic mouse model, i.e. apolipoprotein E3 Leiden cholesteryl ester transfer protein (ApoE*3Leiden.CETP) transgenic mice, that matches with human lipid metabolism as closely as possible.

In a xenograft mouse model, i.v. administration of tyropeptin-boronic acid derivatives inhibits proteasome in tumors and clearly suppresses tumor growth in mice bearing human multiple myeloma.

Of all these causative links potentially important for humans, likely only a few apply to our mouse model, i.e., the animals in our experiments all have equal access to food and an identical lifestyle (with the exception of chemical treatment).

However, we did not see any alterations of serotonin concentrations in dietary hypercholesterolemia mouse models, APP_SweDI animals and human patients with AD.