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Similar results were observed in HDM-exposed PARP-1−/− mice, which provide evidence for the specificity of such protective effects.

This notion is supported by the results obtained from gonadectomized mice, which provide an experimental model of high FSH levels observed in aging populations (Hsueh & Erickson, 1979).

In apolipoprotein-E deficient mice, which provide a valid research model for atherosclerosis, inactivation of the gene encoding TNFα significantly reduces the size of atheroma plaques [ 8, 9].

Thus, we generated the Ppt1-KI mice, which provide a platform for evaluating not only PTC124, but also other nonsense suppressors alone or in combination with a recently characterized thioesterase-mimetic small molecule, N-tert (Butyl) hydroxylamine (NtBuHA).

To examine the importance of direct effects of leptin on lymphopoiesis and immune response, we generated bone marrow chimeras by transplantation of db/db bone marrow cells into lethally irradiated normal recipient mice, which provide a normal environment for the grafted cells.

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injection in mice, which provided 6d in a high protective index (TD50/ED50) of 37.4 comparable to the reference drugs.

It is suggested that the favorably altered stools as shown in the microbiome might promote the inflammation and proteinuria in ADR-sensitive mice, which provides a new insight on the pathogenicity of chronic kidney disease.

Atherosclerosis research using mice began with the invention of traditional atherosclerotic mice including low-density lipoprotein receptor knockout (LDLR−/−) and apolipoprotein E knockout (apoE−/−) mice, which provided tremendous progress in atherosclerosis research.

The most active compound 8f has shown the MES-induced seizures with ED50 value of 28.05 mg/kg and TD50 value of 561 mg/kg after intraperitoneal injection to mice, which provided compound 8f with a protective index (TD50/ED50) of 20 in the MES test.

Similarly, B16 melanoma, previously reported to engage a vascular component in response to single dose radiotherapy[6], is radiosensitized by DC101 (Figure S11), but when implanted in bak−/− mice, which provides radioresistant vasculature [8], similarly exhibited resistance to DC101-induced radiosensitization.

OA progression was significantly enhanced in the Tfap2e−/− mice, which provided evidence for in vivo relevance.

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