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We also show that clonal somatic CNVs exist both in normal brain and in HMG.
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Much of this debate comes down to the fact that we don't yet have a real understanding of neurogenesis, how it works, and how it is controlled both in normal brains and in the presence of antidepressants.
Previous reports have described the expression of both RAAS and AT1 in normal brain tissue as well as their possible participation in cerebral vascular regulation (Ganong, 1984).
In brain tumour imaging FET and MET both have an advantage over FDG, as they do not accumulate in normal brain cells.
Increased lapatinib uptake was observed in brain metastases but not in normal brain.
In comparison, the uptake in normal brain was less than 0.08% ID/g.
Minimal variability in lapatinib uptake is seen in normal brain between subjects.
In normal brain, various dystrophin isoforms are expressed, but little is known about their function.
In contrast to Morikawa et al., we were also able to evaluate lapatinib uptake in normal brain and observed a consistent lack of lapatinib uptake in normal brain, in patients with and without brain metastases.
The radioactivity observed in normal brain was due to brain vasculature activity and not due to brain tissue uptake.
PET signal in the brain corresponded to circulating radioactivity levels, with no [11C]lapatinib uptake observed in normal brain tissue.
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