Sentence examples for model mice that from inspiring English sources

To study these issues, appropriate model mice that show aberrant circadian rhythms are substantially useful.

The few EAD model mice that failed treatment to normalized BG levels following exogenous insulin (pellets) and anti-CD8 antibody injections (Figure 4C, 6, and data not shown), presumably because they had lost too many β-cells prior to treatment, also maintained increased β-cell proliferation.

In our recent study, we investigated the involvement of mitochondrial dysfunction in AD pathology by studying the offspring of Tg2576 AD model mice that were crossed with mice that overexpress SOD-2 [ 1].

Studying AD model mice that could overexpress SOD-2 at any age would permit one to determine whether diminishing mitochondrial superoxide after the onset of AD phenotypes could reverse symptoms of AD, such as cognitive dysfunction and plaque deposition.

In support of this model, mice that are deficient in UPR pathways, such as PERK-deficient mice [ 192], eIF2α mutant mice [ 98; 193] or mice with XBP1 haploinsufficiency deficiency [ 194], are prone to ER stress and develop metabolic disorders such as impaired glucose tolerance, insulin resistance, islet cell dysfunction, and increased adiposity.

In model mice that overexpress mutant human APP, synaptic dysfunction [ 22, 25], spine morphology alteration [ 26], and axonal transport defects [ 27] were observed in association with intracellular Aβ oligomers (iAβOs).

In experimental animal models, mice that lack p27 protein expression are larger than wild-type mice and develop large organs and pituitary tumours, most probably resulting from uncontrolled cell proliferation [ 24- 26].

We previously reported a mouse PD model (PD mice) that was produced by intraperitoneal injection of 60As6 cells [ 25]; in this study, we developed a viral therapeutic vector for the treatment of PD mice.

There are genetic models of mice that have abnormalities with drinking.

These assays will be suitable to assist in the characterization of cancer and other diseases modeled in mice that are associated with altered expression of cystatin genes.

Significantly, rescue experiments in DM1 model mice demonstrate that loss of Mbnl1 function is the key event of missplicing and myotonia [15].