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Sökning: id:"swepub:oai:DiVA.org:oru-113590" > Human traumatic bra...

Human traumatic brain injury induces autoantibody response against glial fibrillary acidic protein and its breakdown products

Zhang, Zhiqun (författare)
Banyan Biomarkers Inc., Alachua, Florida, United States of America
Zoltewicz, J. Susie (författare)
Department of Psychiatry, Center for Neuroproteomics and Biomarker Research, University of Florida, Gainesville, Florida, United States of America
Mondello, Stefania (författare)
University of Messina, Messina, Italy
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Newsom, Kimberly J. (författare)
Department of Psychiatry, Center for Neuroproteomics and Biomarker Research, University of Florida, Gainesville, Florida, United States of America
Yang, Zhihui (författare)
Banyan Biomarkers Inc., Alachua, Florida, United States of America
Yang, Boxuan (författare)
Department of Psychiatry, Center for Neuroproteomics and Biomarker Research, University of Florida, Gainesville, Florida, United States of America
Kobeissy, Firas (författare)
Banyan Biomarkers Inc., Alachua, Florida, United States of America
Guingab, Joy (författare)
Department of Psychiatry, Center for Neuroproteomics and Biomarker Research, University of Florida, Gainesville, Florida, United States of America
Glushakova, Olena (författare)
Department of Psychiatry, Center for Neuroproteomics and Biomarker Research, University of Florida, Gainesville, Florida, United States of America
Robicsek, Steven (författare)
Department of Anesthesiology, University of Florida, Gainesville, Florida, United States of America
Heaton, Shelley (författare)
Clinical and Health Psychology, University of Florida, Gainesville, Florida, United States of America
Büki, Andras, 1966- (författare)
Department of Neurosurgery, University of Pécs and Clinical Neuroscience Image Center of Hungarian Academy of Sciences (HAS) Pécs, Hungary
Hannay, Julia (författare)
Department of Psychology, University of Houston, Houston, Texas, United States of America
Gold, Mark S. (författare)
University of Messina, Messina, Italy
Rubenstein, Richard (författare)
Laboratory of Neurodegenerative Disease and CNS Biomarkers, Departments of Neurology and Physiology/Pharmacology, SUNY Downstate Medical Center, Brooklyn, New York, United States of America
Lu, Xi-chun May (författare)
Center for Military Psychiatry and Neuroscience, Walter Reed Army Institute of Research, Silver Spring, Maryland, United States of America
Dave, Jitendra R. (författare)
Center for Military Psychiatry and Neuroscience, Walter Reed Army Institute of Research, Silver Spring, Maryland, United States of America
Schmid, Kara (författare)
Center for Military Psychiatry and Neuroscience, Walter Reed Army Institute of Research, Silver Spring, Maryland, United States of America
Tortella, Frank (författare)
Center for Military Psychiatry and Neuroscience, Walter Reed Army Institute of Research, Silver Spring, Maryland, United States of America
Robertson, Claudia S. (författare)
Department of Neurosurgery, Baylor College of Medicine, Houston, Texas, United States of America
Wang, Kevin K. W. (författare)
Banyan Biomarkers Inc., Alachua, Florida, United States of America
visa färre...
Banyan Biomarkers Inc, Alachua, Florida, United States of America Department of Psychiatry, Center for Neuroproteomics and Biomarker Research, University of Florida, Gainesville, Florida, United States of America (creator_code:org_t)
2014-03-25
2014
Engelska.
Ingår i: PLOS ONE. - San Francisco, USA : Public Library of Science (PLoS). - 1932-6203. ; 9:3
  • Tidskriftsartikel (refereegranskat)
Abstract Ämnesord
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  • The role of systemic autoimmunity in human traumatic brain injury (TBI) and other forms of brain injuries is recognized but not well understood. In this study, a systematic investigation was performed to identify serum autoantibody responses to brain-specific proteins after TBI in humans. TBI autoantibodies showed predominant immunoreactivity against a cluster of bands from 38-50 kDa on human brain immunoblots, which were identified as GFAP and GFAP breakdown products. GFAP autoantibody levels increased by 7 days after injury, and were of the IgG subtype predominantly. Results from in vitro tests and rat TBI experiments also indicated that calpain was responsible for removing the amino and carboxyl termini of GFAP to yield a 38 kDa fragment. Additionally, TBI autoantibody staining co-localized with GFAP in injured rat brain and in primary rat astrocytes. These results suggest that GFAP breakdown products persist within degenerating astrocytes in the brain. Anti-GFAP autoantibody also can enter living astroglia cells in culture and its presence appears to compromise glial cell health. TBI patients showed an average 3.77 fold increase in anti-GFAP autoantibody levels from early (0-1 days) to late (7-10 days) times post injury. Changes in autoantibody levels were negatively correlated with outcome as measured by GOS-E score at 6 months, suggesting that TBI patients with greater anti-GFAP immune-responses had worse outcomes. Due to the long lasting nature of IgG, a test to detect anti-GFAP autoantibodies is likely to prolong the temporal window for assessment of brain damage in human patients. 

Ämnesord

MEDICIN OCH HÄLSOVETENSKAP  -- Klinisk medicin -- Neurologi (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Clinical Medicine -- Neurology (hsv//eng)

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