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Coauthors
Sonia Villapol Department of Neuroscience, Georgetown University, United States, United States,
1 protocol

Mark Burns Department of Neuroscience, Georgetown University, United States, United States,
1 protocol

Italo Mocchetti Department of Neuroscience, Georgetown University, United States, United States,
1 protocol

Maria Fe Lanfranco Department of Neuroscience, Georgetown University, United States, United States,
1 protocol

David J Loane
  • Department of Anesthesiology, Center for Shock, Trauma, and Anesthesiology Research (STAR), University of Maryland School of Medicine, United States, United States,
  • 1 Author merit

Education

Ph.D., University of Bristol, United Kingdom, 2004

Current position

Associate Professor, Department of Anesthesiology, University of Maryland School of Medicine, USA

Publications

  1. Google Scholar: https://scholar.google.com/citations?user=dznbdfYAAAAJ&hl=en&oi=sra
  2. Villapol, S., Loane, D. J. and Burns, M. P. (2017). Sexual dimorphism in the inflammatory response to traumatic brain injury. Glia 65(9): 1423-1438.
  3. Barrett, J. P., Henry, R. J., Villapol, S., Stoica, B. A., Kumar, A., Burns, M. P., Faden, A. I. and Loane, D. J. (2017). NOX2 deficiency alters macrophage phenotype through an IL-10/STAT3 dependent mechanism: implications for traumatic brain injury. J Neuroinflammation 14(1): 65.
  4. Kumar, A., Alvarez-Croda, D. M., Stoica, B. A., Faden, A. I. and Loane, D. J. (2016). Microglial/Macrophage Polarization Dynamics following Traumatic Brain Injury. J Neurotrauma 33(19): 1732-1750.
  5. Kumar, A., Barrett, J. P., Alvarez-Croda, D. M., Stoica, B. A., Faden, A. I. and Loane, D. J. (2016). NOX2 drives M1-like microglial/macrophage activation and neurodegeneration following experimental traumatic brain injury. Brain Behav Immun 58: 291-309.
  6. Loane, D. J., Kumar, A., Stoica, B. A., Cabatbat, R. and Faden, A. I. (2014). Progressive neurodegeneration after experimental brain trauma: association with chronic microglial activation. J Neuropathol Exp Neurol 73(1): 14-29.
  7. Kumar, A., Stoica, B. A., Sabirzhanov, B., Burns, M. P., Faden, A. I. and Loane, D. J. (2013). Traumatic brain injury in aged animals increases lesion size and chronically alters microglial/macrophage classical and alternative activation states. Neurobiol Aging 34(5): 1397-1411.
  8. Kumar, A. and Loane, D. J. (2012). Neuroinflammation after traumatic brain injury: opportunities for therapeutic intervention. Brain Behav Immun 26(8): 1191-1201.
  9. Loane, D. J., Pocivavsek, A., Moussa, C. E., Thompson, R., Matsuoka, Y., Faden, A. I., Rebeck, G. W. and Burns, M. P. (2009). Amyloid precursor protein secretases as therapeutic targets for traumatic brain injury. Nat Med 15(4): 377-379.
  10. Loane, D. J., Deighan, B. F., Clarke, R. M., Griffin, R. J., Lynch, A. M. and Lynch, M. A. (2009). Interleukin-4 mediates the neuroprotective effects of rosiglitazone in the aged brain. Neurobiol Aging 30(6): 920-931.
1 Protocol published
Combination of Fluorescent in situ Hybridization (FISH) and Immunofluorescence Imaging for Detection of Cytokine Expression in Microglia/Macrophage Cells
Authors:  Maria Fe Lanfranco, David J. Loane, Italo Mocchetti, Mark P. Burns and Sonia Villapol, date: 11/20/2017, view: 329, Q&A: 0
Microglia and macrophage cells are the primary producers of cytokines in response to neuroinflammatory processes. But these cytokines are also produced by other glial cells, endothelial cells, and neurons. It is essential to identify the cells that ...