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As a simple example, mice in the wild rarely live past one year, and most age-associated tissue decline and increased cancer incidence occur well past this natural lifespan [ 20].
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b, Pupil size at different tone intensities, with and without laser activation, for the example mouse in a using a 7-s averaging window after tone onset.
For example, mice deficient in the dominant NHEJ pathway and in telomere maintenance mechanisms get lymphoma and infections more often, and, as a consequence, have shorter lifespans than wild-type mice.
For example, mice deficient in TRAIL had a severe defect in thymic deletion of T cells and were hypersensitive to collagen-induced arthritis [ 31].
For example, mice tested in Muenster were, on average, less active than those tested in other labs (measured by 'total path moved in the open field test' or 'total path moved in the novel object test').
104 For example, mice deficient in 11β-hydroxysteroid dehydrogenase type I fail to develop marrow fat in the proximal tibia, yet maintain the same skeletal architecture and rate of bone loss with age when compared to wild-type mice.
For example, mice exposed in utero even to low doses of endocrine disruptors appear normal at first but develop excess abdominal body fat as adults.
For example, mice deficient in Fas - FasL develop autoimmunity [30].
For example, mice defective in DNA-binding by NR3C1 are viable while those deleted for NR3C1 die at birth [ 29].
For example, mice deficient in secreted (but not membrane bound) IgM develop autoantibodies and deposition of immunoglobulin and C3 in their kidneys [ 5].
IFN-γ is essential for controlling intracellular bacterial infection; for example, mice deficient in IFN-γ or its cognate receptors are more susceptible to Listeria monocytogenes (LM) infection.
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