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Journal Article

Citation

Roberts BR, Hare DJ, McLean CA, Conquest A, Lind M, Li QX, Bush AI, Masters CL, Morganti-Kossmann MC, Frugier T. Metallomics 2014; 7(1): 66-70.

Affiliation

The Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Parkville, Victoria, Australia.

Copyright

(Copyright © 2014, RSC Publishing)

DOI

10.1039/c4mt00258j

PMID

25424382

Abstract

Traumatic brain injury (TBI) is the most common cause of death and disability in young adults, yet the molecular mechanisms that follow TBI are poorly understood. We previously reported a perturbation in iron (Fe) levels following TBI. Here we report that the distribution of cobalt (Co) is modulated in post-mortem human brain following injury. We also investigated how the distribution of other biologically relevant elements changes in TBI. Cobalt is increased due to TBI while copper (Cu), magnesium (Mg), manganese (Mn), phosphorus (P), potassium (K), rubidium (Rb), selenium (Se) and zinc (Zn) remain unchanged. The elevated Co has important implications for positron emission tomography neuroimaging. This is the first demonstration of the accumulation of Co in injured tissue explaining the previous utility of (55)Co-PET imaging in TBI.


Language: en

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