The Experts below are selected from a list of 33555 Experts worldwide ranked by ideXlab platform
E Ferrer - One of the best experts on this subject based on the ideXlab platform.
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Should we perform ocular fundus in patients with severe Brain Trauma
Critical Care, 2006Co-Authors: R. Casado, J Abalo Lojo, J Chico, A Acevedo, S. Lange, E FerrerAbstract:The high incidence of intracraneal lesions of patients with Brain Trauma (BT) is well known. The aim of this study is to assess the incidence of an extracraneal injury: retinal haemorrhage (RH) in patients after BT.
Christophe Pellegrino - One of the best experts on this subject based on the ideXlab platform.
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Bumetanide Prevents Brain Trauma-Induced Depressive-Like Behavior
Frontiers in molecular neuroscience, 2019Co-Authors: Emmanuelle Goubert, Marc Altvater, Marie-noelle Rovira, Ilgam Khalilov, Morgane Mazzarino, Anne Sebastiani, Michael K. E. Schaefer, Claudio Rivera, Christophe PellegrinoAbstract:Brain Trauma triggers a cascade of deleterious events leading to enhanced incidence of drug resistant epilepsies, depression, and cognitive dysfunctions. The underlying mechanisms leading to these alterations are poorly understood and treatment that attenuates those sequels are not available. Using controlled-cortical impact as an experimental model of Brain Trauma in adult mice, we found a strong suppressive effect of the sodium-potassium-chloride importer (NKCC1) specific antagonist bumetanide on the appearance of depressive-like behavior. We demonstrate that this alteration in behavior is associated with an impairment of post-Traumatic secondary neurogenesis within the dentate gyrus of the hippocampus. The mechanism mediating the effect of bumetanide involves early transient changes in the expression of chloride regulatory proteins and qualitative changes in GABA(A) mediated transmission from hyperpolarizing to depolarizing after Brain Trauma. This work opens new perspectives in the early treatment of human post-Traumatic induced depression. Our results strongly suggest that bumetanide might constitute an efficient prophylactic treatment to reduce neurological and psychiatric consequences of Brain Trauma.
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Bumetanide prevents Brain Trauma-induced depressive-like behavior.
2018Co-Authors: Emmanuelle Goubert, Marc Altvater, Marie-noelle Rovira, Ilgam Khalilov, Morgane Mazzarino, Anne Sebastiani, Michael K. E. Schaefer, Claudio Rivera, Christophe PellegrinoAbstract:Brain Trauma triggers a cascade of deleterious events leading to enhanced incidence of drug resistant epilepsies, depression and cognitive dysfunctions. The underlying mechanisms leading to these alterations are poorly understood and treatment that attenuates those sequels not available. Using controlled-cortical impact (CCI) as experimental model of Brain Trauma in adult mouse we found a strong suppressive effect of the sodium-potassium-chloride importer (NKCC1) specific antagonist bumetanide on appearance of depression-like behavior. We demonstrate that this alteration in behavior is associated with a block of CCI-induced decrease in parvalbumin-positive interneurons and impairment of post-Traumatic secondary neurogenesis within the dentate gyrus of the hippocampus. The mechanism mediating the effect of bumetanide involves early transient changes in expression of chloride regulatory proteins and qualitative changes in GABA(A) mediated transmission after Brain Trauma. This work opens new perspectives in the early treatment of human post-Traumatic induced depression. Our results strongly suggest that bumetanide might constitute an efficient prophylactic treatment to reduce neurological and psychiatric consequences of Brain Trauma.
R. Casado - One of the best experts on this subject based on the ideXlab platform.
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Should we perform ocular fundus in patients with severe Brain Trauma
Critical Care, 2006Co-Authors: R. Casado, J Abalo Lojo, J Chico, A Acevedo, S. Lange, E FerrerAbstract:The high incidence of intracraneal lesions of patients with Brain Trauma (BT) is well known. The aim of this study is to assess the incidence of an extracraneal injury: retinal haemorrhage (RH) in patients after BT.
Emmanuelle Goubert - One of the best experts on this subject based on the ideXlab platform.
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Bumetanide Prevents Brain Trauma-Induced Depressive-Like Behavior
Frontiers in molecular neuroscience, 2019Co-Authors: Emmanuelle Goubert, Marc Altvater, Marie-noelle Rovira, Ilgam Khalilov, Morgane Mazzarino, Anne Sebastiani, Michael K. E. Schaefer, Claudio Rivera, Christophe PellegrinoAbstract:Brain Trauma triggers a cascade of deleterious events leading to enhanced incidence of drug resistant epilepsies, depression, and cognitive dysfunctions. The underlying mechanisms leading to these alterations are poorly understood and treatment that attenuates those sequels are not available. Using controlled-cortical impact as an experimental model of Brain Trauma in adult mice, we found a strong suppressive effect of the sodium-potassium-chloride importer (NKCC1) specific antagonist bumetanide on the appearance of depressive-like behavior. We demonstrate that this alteration in behavior is associated with an impairment of post-Traumatic secondary neurogenesis within the dentate gyrus of the hippocampus. The mechanism mediating the effect of bumetanide involves early transient changes in the expression of chloride regulatory proteins and qualitative changes in GABA(A) mediated transmission from hyperpolarizing to depolarizing after Brain Trauma. This work opens new perspectives in the early treatment of human post-Traumatic induced depression. Our results strongly suggest that bumetanide might constitute an efficient prophylactic treatment to reduce neurological and psychiatric consequences of Brain Trauma.
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Bumetanide prevents Brain Trauma-induced depressive-like behavior.
2018Co-Authors: Emmanuelle Goubert, Marc Altvater, Marie-noelle Rovira, Ilgam Khalilov, Morgane Mazzarino, Anne Sebastiani, Michael K. E. Schaefer, Claudio Rivera, Christophe PellegrinoAbstract:Brain Trauma triggers a cascade of deleterious events leading to enhanced incidence of drug resistant epilepsies, depression and cognitive dysfunctions. The underlying mechanisms leading to these alterations are poorly understood and treatment that attenuates those sequels not available. Using controlled-cortical impact (CCI) as experimental model of Brain Trauma in adult mouse we found a strong suppressive effect of the sodium-potassium-chloride importer (NKCC1) specific antagonist bumetanide on appearance of depression-like behavior. We demonstrate that this alteration in behavior is associated with a block of CCI-induced decrease in parvalbumin-positive interneurons and impairment of post-Traumatic secondary neurogenesis within the dentate gyrus of the hippocampus. The mechanism mediating the effect of bumetanide involves early transient changes in expression of chloride regulatory proteins and qualitative changes in GABA(A) mediated transmission after Brain Trauma. This work opens new perspectives in the early treatment of human post-Traumatic induced depression. Our results strongly suggest that bumetanide might constitute an efficient prophylactic treatment to reduce neurological and psychiatric consequences of Brain Trauma.
Lin Quning - One of the best experts on this subject based on the ideXlab platform.
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Clearance of Intracranial Hematoma plus Ventricular Drainage for Treating Severe Brain Trauma
The Journal of Medical Theory and Practice, 2001Co-Authors: Lin QuningAbstract:Objective: To determine the efficacy of clearance of intracranial hematoma plus ventricular drainage for treating the severe Brain Trauma.Methods: 67 patients with severe Brain Trauma from June, 1998 to June,2000 were treated by use of ventricular drainage and/or clearance of intracranial hematoma, and the clinical data were reviewed. Results: The mortality, disability rate and incidence of complication were lower in drainage group than these in non-drainage group, and the revival time and hospitalization time were shorter in drainage group. Conclusions: Clearance of intracranial hematoma plus ventricular drainage is a satisfactory method for treating severe Brain Trauma.