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And though we were anxious, though quivers of nervousness ran along our bodies like mice, we wanted to see whatever it was, we wanted to be there, since after all it was coming toward us, it was ours to witness, as if we were the ones they'd chosen, out there on the other side of the sky.
Since we had previously described preserved nephrin expression and reduced proteinuria in diabetic PKCα deficient mice we wanted to test whether chemical inhibition of PKCα would have a similar protective effect.
Having shown the recruitment and activation of T cells within tumors of α-TEA-treated mice, we wanted to determine whether T cells play a nonredundant role in α-TEA-mediated antitumor activity.
Because Gli1 and Gli3 were significantly down-regulated in SAC-KO mice, we wanted to know which Gli-factor is the predominant one responding immediately to the loss of Smo.
Having observed that the DENV2-specific antibodies promote increased MC degranulation and vascular leakage in infected WT mice, we wanted to investigate the contribution of MCs to the increased vascular pathology in the presence of a DENV-specific antibody.
As it is known that the M2 microglial response starts from 8-week-old of SOD1G93A mice, we wanted to see whether the antibiotic has any effects on M2 polarization in SOD1G93A mice.
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From the features that we generated for 1,200 mRNAs for humans and 4,000 mRNAs for mouse, we wanted to check how our method would perform on mRNAs that it had not seen before.
Finally, for mouse we want to return data annotated to Mus musculus and substrains thereof.
An ANOVA was conducted on the data from the first four test sessions in the older cohort of mice since we wanted to assess performance before significant mortality began to occur.
However, we chose to use stock C57BL/6 as controls for the experiments on M/Mt-CK−/−(129/Bl6) mice, because we wanted to emulate the conditions used in previous studies to determine whether we could recapitulate their findings.
After establishing the effects of the GHR mutations on the metabolite profile of mouse urine we wanted to determine if these mutations manifest in the metabolite profile of liver, as this was the subject of the microarray analysis and a major GH target tissue.
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Justyna Jupowicz-Kozak
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