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Although there was limited tau pathology, the mice displayed frequent neurites that were both ubiquitin- and α-synuclein-positive.
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The subject and the mouse model both displayed frequent interictal spikes as well as ictal patterns consisting of high-amplitude discharges followed by background suppression.
Cancer cells were small, surrounded by interstitial fibrosis, and displayed frequent mitosis.
In this test, mutant mice displayed a more-frequent repetitive stumble (i.e., multiple attempts to place the same paw on or near the same spot) and a shortening of step length compared to the normal controls (Fig. 5A, B).
Consistent with our light microscopy data, CHMP2BIntron5 mice displayed numerous large aggregates within neurons (asterisks, Fig. 4), whilst smaller and less frequent lipofuscin-like deposits were observed in non-transgenic mice (average areas: CHMP2BIntron5 3.99 ± 3.33 μm, n = 38 deposits; non-transgenic 0.77 ± 0.42 μm, n = 35 deposits, mean ± SD).
Following sepsis induction, however, HDC−/− mice displayed an evidently lower levels of those cytokines compared with WT mice.
In contrast, both mice displayed increased expression of NR1, but Prnp −/− displayed enhanced NR2B expression.
Additionally, the mice displayed no overt phenotypic differences.
Treated mice displayed slightly lower parasitemia levels (Fig. 4D).
Oprm1 knockout mice displayed a remarkable decrease in motor impulsivity.
The hSAA transgenic mice displayed no visible phenotype.
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