Sentence examples for mutant mice aged from inspiring English sources

As the mutant mice aged past 5 months, convulsions appeared, often elicited by handling.

The ventricle size of control and mutant mice (aged 1, 3, and 24 months) was assessed using micro-MRI.

As ankyrin-B mutant mice aged we noticed a consistent pattern of kyphosis, hair loss and general deterioration compared to their littermates.

Control and mutant mice aged 20∼24 months were subjected to mild stress on rotarod at a fixed speed of 4 rpm for 2 min. The amount of voided urine was collected on a piece of Whatman chromatography paper (3 mm thick, 52.5 cm2) placed on top of the sensor plate of the rotarod.

To further characterize the skeletal abnormalities, we performed radiography on wild-type and mutant mice aged 6 wk.

However, analysis of older mice aged between 8 and 18 months revealed evidence of a focal osteolytic lesion in the left femur in one Optn D477N/D477N mutant mouse aged 15 months.

As the majority of IIS mutant mouse aging studies are based on lifespan curves derived from single experimental cohorts, several authors (e.g. [13], [14]) have suggested that replication and validation of these experiments is necessary in order to use these models with confidence in our quest to understand the aging process.

Precise diagnostic criteria that are used to identify the disease in man are not used in the mouse; instead wild-type and mutant mice (age- and sex-matched individuals, which are ideally littermates) are compared with one another.

The gait of control (n = 5) and mutant (n = 10) mice aged 20∼24 months was analyzed using a CatWalk gait automatic analyzer (Noldus Information Technology, Leesburg, VA, USA).

Consistent with data from younger mice, aged 5A3 mutant BM displayed markedly reduced lymphoid repopulating potential, but efficiently contributed to myeloid reconstitution.

The development of a focal osteolytic lesion in one Optn D477N/D477N mutant mouse (∼10% of mice aged ≥15 months), but not in Optn ΔEx12/ΔEx12, supports the hypothesis that loss of function in optineurin can lead to a PDB-like phenotype while illustrating that additional factors must also be present for focal osteolytic lesions to become fully penetrant.