Sentence examples for mice develop fatal from inspiring English sources

route has been used as a model that more closely approximates the route of infection with natural variola (smallpox) virus infections in humans; at high doses of VACV-WR i.n., mice develop fatal lung disease with high viral titers in lung tissue and the brain [6], [21].

Thus, T cell-specific TGF-β conditional knockout mice develop fatal autoimmune disease even though they survive longer than TGF-β−/− mice [11], and Th17 differentiation is hampered in these mice [11], indicating that TGF-β produced by T cells themselves is required for Th17 differentiation.

CTLA-4 knockout mice develop fatal autoimmunity resulting from unopposed T-cell activation and reaction to self-antigens.

These mice develop fatal anaphylactic reactions to hFIX protein following repeated exposures with a loss of ∼50% of the challenged mice by the fifth exposure (Fig 1C).

C3H/HeJ F9−/Y mice developed fatal anaphylactic reactions starting after the third hFIX injection (Fig. 1a) and required co-administration of antihistamine and platelet activating factor antagonist CV3988 to survive the challenge protocol.

CD22ΔE12xBCR-ABL CD22ΔE12xBCR-ABLpontaneously develop fatal BPL with lymphomatous features at a median of 78 days (Fig. S2).

CD22ΔE12 × BCR ABL double-Tg mice spontaneously develop fatal B-precursor leukemia with lymphomatous features at a median of 78 days.

Between postnatal day 10 and 13, Tk2 −/− mice rapidly develop fatal encephalomyopathy beginning with decreased ambulation, unstable gait, coarse tremor, and growth retardation that rapidly progress to early death at age 14 16 days (Dorado et al, 2011).

Both transgenic mouse lines develop fatal BPL.

In both instances the mice develop a fatal autoimmune lymphoproliferative disease [ 17].

Although cardiac-specific mTOR-deficient mice develop a fatal, dilated cardiomyopathy (27), partial loss of mTOR activity (27) and inhibition of mTOR by rapamycin (28) significantly impair hypertrophic cardiac growth.