Thus, NEFL mRNA expression level could be a potential prognosis prediction marker in breast cancer patients. Metallothionein is a 6�C7 kDa, cysteine rich, metal binding protein that has been shown to be Rimonabant Hydrochloride neuroprotective during central nervous system insults in studies utilising transgenic MT-I over-expressing animals and MT-I/II2/2 mice. Interestingly, it is not MT-III, the brain-specific isoform of MT, that provides neuroprotection but the MT-I and MT-II isoforms that provide the most neuroprotection after brain injury. The MT-I and MT-II isoforms are often considered as a single species due to their high homology and the inability of primary antibodies to differentiate between the two forms. The mechanism by which MT-I/II imparts protection to the injured CNS is yet to be fully elucidated. MT-I/II is expressed in many organs throughout the murine body. Numerous studies have shown that after brain injury, the level of MT-I/II expression in the brain is increased. MT is chiefly a cytoplasmic protein but increased levels have been observed in the blood of brain injured patients. The expression levels of MT-I/II in other organs after brain injury have not been reported previously and the origin of the MT found in the blood has not been determined. Up-regulation of MT-I/II expression in the liver occurs in Pantoprazole sodium response to many stressful stimuli such as burn injury, restraint stress, zinc challenge, fasting and lipopolysaccharide challenge. The induction of liver MT-I/II expression has been shown to cause increases in hepatic zinc content, a response that does not occur in MT-I/II2/2 mice. Therefore, it appears that the induction of hepatic MT-I/II expression results in the sequestration of zinc to the liver. Zinc sequestration from the plasma is a characteristic of the acute phase response which is typically induced by the cytokine interleukin-6. MT-I/II expression is induced by increased intracellular zinc concentration, glucocorticoids and IL-6 which indicates that MT-I/II expression may occur in conjunction with the acute phase response. Altered zinc homeostasis and raised concentrations of IL-6 in serum have been observed in patients suffering the early stages of brain injury. The process of hepatic MT-I/II mediated zinc sequestration has been proposed to explain these alterations in plasma zinc concentrations but hepatic MT-I/II expression has not been experimentally quantified after brain injury. There is some evidence that systemic zinc status may affect the outcome of brain injury because rats with dietary zinc deficiency preceding experimental brain injury have greater microglial activation and neuron death compared to injured rats on zinc-sufficient diets. There is also a positive association between zinc supplementation after hospital admission and neurologic recovery rate in head injured patients. The aim of this study was to determine whether brain injury in mice causes an increase in hepatic MT-I/II expression.