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Propagation of the three types of clone in mouse brain resulted in swa-resistant 22L prions (Fig 1Ai).

More importantly, direct in vivo expression of WNV-Cp protein in mouse brain resulted in an induction of apoptosis similar to what is observed in natural infection.

Interestingly, infusion of zebularine, a DNA methyltransferase inhibitor, into mouse brain resulted in immediate DNA demethylation of several genes leading to enhanced transcription [ 52].

Additionally, conditional ablation of HIF1-α in adult mouse brain resulted in hydrocephalus, decreased neurogenesis (partly due to an increase in apoptosis) and deficits in spatial memory (Tomita et al., 2003).

DeGiorgio et al. showed that injection of anti-NR2 glutamate receptor binding antibodies (purified antibodies from the sera of SLE patients or one CSF sample from an SLE patient with progressive cognitive decline) into the mouse brain resulted in apoptosis of the neuronal cells without signs of inflammation [ 22].

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The lower limit of detection was identified through amplification of targets known not to be expressed in mouse brain resulting in Ct values >32 corresponding to copy numbers <10 per ng total RNA.

The increase in RAGE expression is correlated with the ribosylation-induced AGE elevation both in astrocytoma cells and in the mouse brain, resulting in RAGE-dependent NF- κB activation and astrocyte activation and subsequent impairment of spatial learning and memory ability.

Together, these results indicate that the tumor cells with long-term self-renewing capacities we engrafted in mouse brains resulted in the in vivo development of tumors that recapitulated the histological and molecular profile of the original human tumor.

The CD133+ cells can differentiate in vitro to neurons and glial cells, and their transplantation into the lateral ventricles of newborn NOD-SCID mouse brains resulted in specific engraftment in numerous sites of the brain [ 20, 21, 23].

Thus, DeGiorgio et al. showed that injection of anti-NR2 glutamate receptor binding antibodies (purified antibodies from the sera or CSF from NPSLE patients) into mice brain resulted in apoptosis of the neuronal cells without signs of inflammation [ 6].

Knockdown of DISC1 in the adult mouse brain results in a cellular phenotype very similar to that of phosphatase and tensin homologue (PTEN) suppressed mice.

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