Sentence examples for mouse which exhibits from inspiring English sources

The importance of α-dystrobrevin in maintaining healthy muscle is demonstrated by the α-dystrobrevin null (adbn−/−) mouse, which exhibits extensive myofiber degeneration [13].

This is similar to the Hspg2 homozygous knockout mouse, which exhibits significant kyphoscoliosis and skeletal defects (Costell et al. 1999).

One commonly used mouse model of dyslipidemia is the apolipoprotein E-deficient (apoE-/) mouse, which exhibits the typical features of dyslipidemia seen in humans, including elevations in LDL cholesterol and triglyceride levels and reductions in HDL cholesterol levels [ 12, 13].

Similar results were obtained in the  db/ db mouse, which exhibits key characteristics of T2DM, namely hyperinsulinaemia, insulin resistance, hyperglycaemia, and develops diabetic cardiomyopathy with decreased cardiac function (Battiprolu et al, 2012).

In the SOD1 G 93 A gene transgenic mouse, which exhibits a disease phenotype similar to that of familial ALS patients, the accumulation of SOD1 G93andnd the interaction between Derlin-1 and SOD1 G93A were observed along with the onset of the disease [ 60].

This phenotype is reminiscent of male androgen receptor knockout (ARKO) mice, which exhibits severe developmental defects and spermatogenesis arrest [42].

A transplantable carcinoma of spontaneous origin in CBA mice which exhibits a large WBI effect was assayed quantitatively in mice which had been immunologically crippled in terms of allograft acceptance by depletion of thymus derived lymphocytes.

The X-ALD mouse model is a classic Abcd1 gene knockout model (Abcd1− mice), which exhibits late-onset axonopathy in the spinal cord without overt inflammation or demyelination; thus, it resembles adult onset adrenomyeloneuropathy in humans [ 65].

Using gene microarrays, we compared gene expression patterns in the somatosensory cortex of wild type and ephrinA5 deficient mice, which exhibit subtle, but highly reproducible alterations of thalamocortical projections and intrinsic cortical circuits.

To investigate this, opiate-induced brain metabolomic responses were profiled using a semi-targeted method in C57BL/6 and 129Sv1 mice, which exhibit extreme differences in their tendency to become opiate dependent.

Escalating morphine doses (10 40 mg/kg) administered over a 4-day period selectively induced a twofold decrease (p < 0.00005) in adenosine abundance in the brainstem of C57BL/6 mice, which exhibited symptoms of narcotic drug dependence; but did not decrease adenosine abundance in 129Sv1 mice, which do not exhibit symptoms of dependence.