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PID: 19710487, COI: 1:CAS:528:DC%2BD1MXhtVKhtLrP
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Soluble ICAM-1 in CSF coincides with the extent of cerebral damage in patients with severe traumatic brain injury
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PID: 9624625, COI: 1:STN:280:DyaK1c3oslOhsw%3D%3D
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Pleines UE, Stover JF, Kossmann T, Trentz O, Morganti-Kossmann MC. Soluble ICAM-1 in CSF coincides with the extent of cerebral damage in patients with severe traumatic brain injury. J Neurotrauma. 1998;15:399–409.
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45
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5044223264
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Effect of intravenous corticosteroids on death within 14 days in 10008 adults with clinically significant head injury (MRC-CRASH trial): randomized placebo-controlled trial
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PID: 15474134
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Roberts I, Yates D, Sandercock P, Farrell B, Wasserberg J, Lomas G, et al. Effect of intravenous corticosteroids on death within 14 days in 10008 adults with clinically significant head injury (MRC-CRASH trial): randomized placebo-controlled trial. Lancet. 2004;364:1321–8.
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46
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Final results of MRC CRASH, a randomized placebo controlled trial of intravenous corticosteroids in adults with head injury—outcomes at 6 months
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PID: 15936423
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Edwards P, Arango M, Balica L, Cottingham R, El-Sayed H, Farrell B, et al. Final results of MRC CRASH, a randomized placebo controlled trial of intravenous corticosteroids in adults with head injury—outcomes at 6 months. Lancet. 2005;365:1957–9.
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A controlled trial of natalizumab for relapsing multiple sclerosis
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PID: 12510038, COI: 1:CAS:528:DC%2BD3sXhtlCntg%3D%3D
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Miller DH, Khan OA, Sheremata WA, Blumhardt LD, Rice GP, Libonati MA, et al. A controlled trial of natalizumab for relapsing multiple sclerosis. N Engl J Med. 2003;348:15–23.
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49
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A randomized, placebo-controlled trial of natalizumab for relapsing multiple sclerosis
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PID: 16510744, COI: 1:CAS:528:DC%2BD28XitVertL4%3D
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Polman CH, O'Connor PW, Havrdova E, Hutchinson M, Kappos L, Miller DH, et al. A randomized, placebo-controlled trial of natalizumab for relapsing multiple sclerosis. N Engl J Med. 2006;354:899–910.
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Miller, D.H.6
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50
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A role for leukocyte-endothelial adhesion mechanisms in epilepsy
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PID: 19029985, COI: 1:CAS:528:DC%2BD1cXhsVWhurnP
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Fabene PF, Navarro Mora G, Martinello M, Rossi B, Merigo F, Ottoboni L, et al. A role for leukocyte-endothelial adhesion mechanisms in epilepsy. Nat Med. 2008;14:1377–83.
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51
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Progressive multifocal leukoencephalopathy complicating treatment with natalizumab and interferon beta-1a for multiple sclerosis
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PID: 15947079, COI: 1:CAS:528:DC%2BD2MXms1KntrY%3D
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Kleinschmidt-DeMasters BK, Tyler KL. Progressive multifocal leukoencephalopathy complicating treatment with natalizumab and interferon beta-1a for multiple sclerosis. N Engl J Med. 2005;353:369–74.
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Progressive multifocal leukoencephalopathy in a patient treated with natalizumab
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PID: 15947078, COI: 1:CAS:528:DC%2BD2MXms1Kntrc%3D
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Langer-Gould A, Atlas SW, Green AJ, Bollen AW, Pelletier D. Progressive multifocal leukoencephalopathy in a patient treated with natalizumab. N Engl J Med. 2005;353:375–81.
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53
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Risk of natalizumab-associated progressive multifocal leukoencephalopathy
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PID: 22591293, COI: 1:CAS:528:DC%2BC38Xntlamu7Y%3D
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Bloomgren G, Richman S, Hotermans C, Subramanyam M, Goelz S, Natarajan A, et al. Risk of natalizumab-associated progressive multifocal leukoencephalopathy. N Engl J Med. 2012;366:1870–80.
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54
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Fingolimod and sphingosine-1-phosphate—modifiers of lymphocyte migration
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PID: 16971715, COI: 1:CAS:528:DC%2BD28XpsFKlsLs%3D
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Massberg S, von Andrian UH. Fingolimod and sphingosine-1-phosphate—modifiers of lymphocyte migration. N Engl J Med. 2006;355:1088–91.
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Massberg, S.1
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PID: 22276823, COI: 1:CAS:528:DC%2BC38Xhs1artLc%3D
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Pelletier D, Hafler DA. Fingolimod for multiple sclerosis. N Engl J Med. 2012;366:339–47.
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Recombinant human interleukin-1 receptor antagonist in severe traumatic brain injury: a phase II trial randomized control trial
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PID: 24569690, COI: 1:CAS:528:DC%2BC2cXjsFGlurw%3D, This is an exciting trial in humans demonstrating that subcutaneous administration of IL-1 receptor antagonist after TBI is safe, reaches therapeutic levels in the brain interstitial space, and alters cytokine profiles
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Helmy A, Guilfoyle MR, Carpenter KL, Pickard JD, Menon DK, Hutchison PJ. Recombinant human interleukin-1 receptor antagonist in severe traumatic brain injury: a phase II trial randomized control trial. J Cereb Blood Flow Metab. 2014;34:845–51. This is an exciting trial in humans demonstrating that subcutaneous administration of IL-1 receptor antagonist after TBI is safe, reaches therapeutic levels in the brain interstitial space, and alters cytokine profiles.
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J Cereb Blood Flow Metab
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Helmy, A.1
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Hutchison, P.J.6
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57
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Neutralization of interleukin-1β modifies the inflammatory response and improves histological and cognitive outcome following traumatic brain injury in mice
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PID: 19614750
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Clausen F, Hånell A, Björk M, Hillered L, Mir AK, Gram H, et al. Neutralization of interleukin-1β modifies the inflammatory response and improves histological and cognitive outcome following traumatic brain injury in mice. Eur J Neurosci. 2009;30:385–96.
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58
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Neutralization of interleukin-1beta reduces cerebral edema and tissue loss and improves late cognitive outcome following traumatic brain injury in mice
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PID: 21623956
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Clausen F, Hånell A, Björk M, Hillered L, Mir AK, Gram H, et al. Neutralization of interleukin-1beta reduces cerebral edema and tissue loss and improves late cognitive outcome following traumatic brain injury in mice. Eur J Neurosci. 2011;34:110–23.
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Minocycline effects on cerebral edema: relations with inflammatory and oxidative stress markers following traumatic brain injury in mice
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PID: 19631631, COI: 1:CAS:528:DC%2BD1MXhtVKls7%2FN
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Homsi S, Federico F, Croci N, Palmier B, Plotkine M, Marchand-Leroux C, et al. Minocycline effects on cerebral edema: relations with inflammatory and oxidative stress markers following traumatic brain injury in mice. Brain Res. 2009;1291:122–32.
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62
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CB1 and CB2 cannabinoid receptor antagonists prevent minocycline-induced neuroprotection following traumatic brain injury in mice
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PID: 23960212
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Lopez-Rodriguez AB, Siopi E, Finn DP, Marchand-Leroux C, Garcia-Segura LM, Jafarian-Tehrani M, et al. CB1 and CB2 cannabinoid receptor antagonists prevent minocycline-induced neuroprotection following traumatic brain injury in mice. Cereb Cortex. 2013. doi:10.1093/cercor/bht202.
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Lopez-Rodriguez, A.B.1
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63
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PID: 22915134, COI: 1:CAS:528:DC%2BC38XhsVentb7J, Administering a monoclonal anti-HMGB1 antibody after fluid percussion injury caused a dramatic reduction in lesion volume and cerebral edema, as well as significant functional improvement. This study paves the way for human trials investigating whether inhibiting HMGB1 signaling may improve outcomes after TBI
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Okuma Y, Liu K, Wake H, Zhang J, Maruo T, Date I, et al. Anti-high mobility group box-1 antibody therapy for traumatic brain injury. Ann Neurol. 2012;72:373–84. Administering a monoclonal anti-HMGB1 antibody after fluid percussion injury caused a dramatic reduction in lesion volume and cerebral edema, as well as significant functional improvement. This study paves the way for human trials investigating whether inhibiting HMGB1 signaling may improve outcomes after TBI.
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PID: 10398600, COI: 1:CAS:528:DyaK1MXks1Sjtb0%3D
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65
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A Drosophila model of closed head injury
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PID: 24127584, The authors developed a simple, reproducible model of TBI in Drosophila, paving the way for forward genetic screens that can identify genes that may protect against secondary brain injury. Susceptibility to TBI in flies was shown to depend on genetic background and components of the innate immune system. Similar approaches have identified numerous important clinical targets in a variety of other diseases
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Katzenberger RJ, Loewen CA, Wassarman DR, Petersen AJ, Ganetzky B, Wassarman DA. A Drosophila model of closed head injury. Proc Natl Acad Sci U S A. 2013. doi:10.1073/pnas.1316895110. The authors developed a simple, reproducible model of TBI in Drosophila, paving the way for forward genetic screens that can identify genes that may protect against secondary brain injury. Susceptibility to TBI in flies was shown to depend on genetic background and components of the innate immune system. Similar approaches have identified numerous important clinical targets in a variety of other diseases.
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Proc Natl Acad Sci U S A
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Katzenberger, R.J.1
Loewen, C.A.2
Wassarman, D.R.3
Petersen, A.J.4
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Wassarman, D.A.6
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66
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Günther M, Al Nimer F, Gahm C, Piel F, Mathiesen T. iNOS-mediated secondary inflammatory response differs between rat strains following experimental brain contusion. Acta Neurochir. 2012;154:689–97.
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They showed early changes in microglial morphology followed by infiltration of neutrophils, Adding blockers of reactive oxygen species to the surface of the thinned skull remarkably blocked most of the inflammatory response
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Roth TL, Nayak D, Atanasijevic T, Koretsky AP, Latour LL, McGavern DB. Transcranial amelioration of inflammation and cell death after brain injury. Nature. 2014;505223-8. The authors used in vivo multiphoton microscopy to study the dynamics of immune cell activation after a concussion-type injury in mice. They showed early changes in microglial morphology followed by infiltration of neutrophils. Adding blockers of reactive oxygen species to the surface of the thinned skull remarkably blocked most of the inflammatory response.
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505223-8. The authors used in vivo multiphoton microscopy to study the dynamics of immune cell activation after a concussion-type injury in mice
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Roth, T.L.1
Nayak, D.2
Atanasijevic, T.3
Koretsky, A.P.4
Latour, L.L.5
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