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Doreen A. Ezeife MD Francois Dionne PhD Aline Fusco Fares MD Ellen Laura Rose Cusano MD Rouhi Fazelzad BSc MISt Wenzie Ng BSc MPharm RPh Don Husereau BSc Pharm MSc Farzad Ali BPharm MSc Christina Sit MSc Barry Stein B.Com BCL LLB Jennifer H. Law MSc Lisa Le MSc Peter Michael Ellis MD MMed PhD Scott Berry MD Stuart Peacock PhD Craig Mitton PhD Craig C. Earle MD Kelvin K. W. Chan MD PhD Natasha B. Leighl MD MMSc 《Cancer》2020,126(7):1530-1540
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Krishnan Radhakrishnan Mihaela Aslan Kelly M. Harrington Robert H. Pietrzak Grant Huang Sumitra Muralidhar Kelly Cho Rachel Quaden David Gagnon Saiju Pyarajan Ning Sun Hongyu Zhao Michael Gaziano John Concato Murray B. Stein Joel Gelernter 《International journal of methods in psychiatric research》2019,28(1)
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M. Risling D. Smith T. D. Stein E. P. Thelin E. R. Zanier M. Ankarcrona P. Nilsson 《Journal of internal medicine》2019,285(6):594-607
Traumatic brain injury (TBI) is caused by a head impact with a force exceeding regular exposure from normal body movement which the brain normally can accommodate. People affected include, but are not restricted to, sport athletes in American football, ice hockey, boxing as well as military personnel. Both single and repetitive exposures may affect the brain acutely and can lead to chronic neurodegenerative changes including chronic traumatic encephalopathy associated with the development of dementia. The changes in the brain following TBI include neuroinflammation, white matter lesions, and axonal damage as well as hyperphosphorylation and aggregation of tau protein. Even though the human brain gross anatomy is different from rodents implicating different energy transfer upon impact, especially rotational forces, animal models of TBI are important tools to investigate the changes that occur upon TBI at molecular and cellular levels. Importantly, such models may help to increase the knowledge of how the pathologies develop, including the spreading of tau pathologies, and how to diagnose the severity of the TBI in the clinic. In addition, animal models are helpful in the development of novel biomarkers and can also be used to test potential disease‐modifying compounds in a preclinical setting. 相似文献
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Antoinette Burger Maritha J. Kotze Dan J. Stein Susan Janse van Rensburg Fleur M. Howells 《The European journal of neuroscience》2020,51(4):984-990
Fundamental human studies which address associations between glutamate and iron metabolism are needed. Basic research reports associations between glutamate and iron metabolism. Human studies report sex differences in iron metabolism and glutamate concentrations, which suggest that these relationships may differ by sex. We hypothesised associations would be apparent between in vivo glutamate and peripheral markers of iron metabolism, and these associations would differ by sex. To test this, we recruited 40 healthy adults (20 men, 20 women) and measured (a) standard clinical biomarker concentrations for iron metabolism and (b) an in vivo proxy for glutamate concentration, glutamate with glutamine in relation to total creatine containing metabolites using proton magnetic resonance spectroscopy studies with a two‐dimensional chemical shift imaging slice, with voxels located in bilateral dorsolateral prefrontal cortices, anterior cingulate cortices and frontal white matter. Only the female group reported significant associations between peripheral markers of iron metabolism and Glx:tCr concentration: (a) right dorsolateral prefrontal cortex Glx:tCr associated positively with serum transferrin (r = .60, p = .006) and negatively with transferrin saturation (r = ?.62, p = .004) and (b) right frontal white matter Glx:tCr associated negatively with iron concentration (r = ?.59, p = .008) and transferrin saturation (r = ?.65, p = .002). Our results support associations between iron metabolism and our proxy for in vivo glutamate concentration (Glx:tCr). These associations were limited to women, suggesting a stronger regulatory control between iron and glutamate metabolism. These associations support additional fundamental research into the molecular mechanisms of this regulatory control. 相似文献
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