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We were able to identify PTAX and its metabolites in mouse brains after a cycle of 5 injections of p97-PTAX (Table 1).
Samples obtained from mouse brains after perfusion and craniotomy were cut into small fragments and immersed for 2 h in a fixative solution containing 2.5% glutaraldehyde in 0.1 M PBS, pH 7.2, at room temperature.
Compromised capillaries were found with variable frequency at different time points in Gcdh−/− mouse brains after protein diet exposure.
In this study we first compared the lesion profile and extent of tissue damage in Prnp+/+ and Prnp−/− mouse brains after transient focal ischemia.
It remains to be determined if the survival and differentiation rates are different in adult mouse brains after IR, given the protracted inflammatory reaction.
It also reflects PBDE accumulation in postnatal day 10 and 19 mouse brains after 7 days in vivo (20- to 140-fold) that we calculated from a study of Viberg et al. (2003).
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Autoradiographic picture of mouse brain after intraperitoneal injection of [3H]prazosin.
In order to reconcile our results with those of Kirkham et al. we analyzed mouse brain after 24 h of full starvation (fasting).
We find no qualitative or quantitative differences in these parameters between the transthyretin-null and the wild-type mouse brain after either [125I]thyroxine or [125I]triiodothyronine administration.
Here we show that there is massive accumulation of Treg cells in the mouse brain after ischaemic stroke, and this potentiates neurological recovery during the chronic phase of ischaemic brain injury.
We have shown that the endocannabinoid 2-arachidonoyl glycerol (2-AG) is released in mouse brain after closed head injury (CHI), and treatment with exogenous 2-AG exerts neuroprotection via the central cannabinoid receptor CB1.
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