The Experts below are selected from a list of 5697 Experts worldwide ranked by ideXlab platform
Susan C Fagan - One of the best experts on this subject based on the ideXlab platform.
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blood pressure lowering after Experimental Cerebral Ischemia provides neurovascular protection
Journal of Hypertension, 2007Co-Authors: Hazem Elewa, Susan C Fagan, Anna Kozak, Maribeth H Johnson, Adviye ErgulAbstract:BackgroundThere is evidence that acutely elevated blood pressure (BP) after stroke is associated with increased Cerebral hemorrhage and edema. Previous experiments in our laboratory have shown that candesartan 1 mg/kg administered after reperfusion in a model of hypertension after Experimental ische
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hypertension after Experimental Cerebral Ischemia candesartan provides neurovascular protection
Journal of Hypertension, 2006Co-Authors: Susan C Fagan, Anna Kozak, William D Hill, David M Pollock, Maribeth H Johnson, Adviye Ergul, David C HessAbstract:BackgroundAfter ischemic stroke, hypertension increases the risk of recurrence, hemorrhage and fatal Cerebral edema, but blood pressure (BP) lowering in the acute stroke period is controversial due to fears of infarct extension and worsened outcomes.ObjectiveTo determine whether BP lowering with can
Yu H Wu - One of the best experts on this subject based on the ideXlab platform.
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trefoil factor 3 as an endocrine neuroprotective factor from the liver in Experimental Cerebral Ischemia reperfusion injury
PLOS ONE, 2013Co-Authors: Derek Roberts, Brian Zhang, Liqun Zhang, Yu H WuAbstract:Cerebral Ischemia, while causing neuronal injury, can activate innate neuroprotective mechanisms, minimizing neuronal death. In this report, we demonstrate that Experimental Cerebral Ischemia/reperfusion injury in the mouse causes upregulation of the secretory protein trefoil factor 3 (TFF3) in the hepatocyte in association with an increase in serum TFF3. Partial hepatectomy (~60% liver resection) immediately following Cerebral injury significantly lowered the serum level of TFF3, suggesting a contribution of the liver to the elevation of serum TFF3. Compared to wild-type mice, TFF3-/- mice exhibited a significantly higher activity of caspase 3 and level of cell death in the ischemic Cerebral lesion, a larger fraction of Cerebral infarcts, and a smaller fraction of the injured Cerebral hemisphere, accompanied by severer forelimb motor deficits. Intravenous administration of recombinant TFF3 reversed changes in Cerebral injury and forelimb motor function due to TFF3 deficiency. These observations suggest an endocrine neuroprotective mechanism involving TFF3 from the liver in Experimental Cerebral Ischemia/reperfusion injury.
Derek Roberts - One of the best experts on this subject based on the ideXlab platform.
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trefoil factor 3 as an endocrine neuroprotective factor from the liver in Experimental Cerebral Ischemia reperfusion injury
PLOS ONE, 2013Co-Authors: Derek Roberts, Brian Zhang, Liqun Zhang, Yu H WuAbstract:Cerebral Ischemia, while causing neuronal injury, can activate innate neuroprotective mechanisms, minimizing neuronal death. In this report, we demonstrate that Experimental Cerebral Ischemia/reperfusion injury in the mouse causes upregulation of the secretory protein trefoil factor 3 (TFF3) in the hepatocyte in association with an increase in serum TFF3. Partial hepatectomy (~60% liver resection) immediately following Cerebral injury significantly lowered the serum level of TFF3, suggesting a contribution of the liver to the elevation of serum TFF3. Compared to wild-type mice, TFF3-/- mice exhibited a significantly higher activity of caspase 3 and level of cell death in the ischemic Cerebral lesion, a larger fraction of Cerebral infarcts, and a smaller fraction of the injured Cerebral hemisphere, accompanied by severer forelimb motor deficits. Intravenous administration of recombinant TFF3 reversed changes in Cerebral injury and forelimb motor function due to TFF3 deficiency. These observations suggest an endocrine neuroprotective mechanism involving TFF3 from the liver in Experimental Cerebral Ischemia/reperfusion injury.
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Trefoil Factor 3 as an Endocrine Neuroprotective Factor from the Liver in Experimental Cerebral Ischemia/Reperfusion Injury
PLoS ONE, 2013Co-Authors: Shu Q. Liu, Derek Roberts, Brian Zhang, Yupeng Ren, Liqun ZhangAbstract:Cerebral Ischemia, while causing neuronal injury, can activate innate neuroprotective mechanisms, minimizing neuronal death. In this report, we demonstrate that Experimental Cerebral Ischemia/reperfusion injury in the mouse causes upregulation of the secretory protein trefoil factor 3 (TFF3) in the hepatocyte in association with an increase in serum TFF3. Partial hepatectomy (~60% liver resection) immediately following Cerebral injury significantly lowered the serum level of TFF3, suggesting a contribution of the liver to the elevation of serum TFF3. Compared to wild-type mice, TFF3-/- mice exhibited a significantly higher activity of caspase 3 and level of cell death in the ischemic Cerebral lesion, a larger fraction of Cerebral infarcts, and a smaller fraction of the injured Cerebral hemisphere, accompanied by severer forelimb motor deficits. Intravenous administration of recombinant TFF3 reversed changes in Cerebral injury and forelimb motor function due to TFF3 deficiency. These observations suggest an endocrine neuroprotective mechanism involving TFF3 from the liver in Experimental Cerebral Ischemia/reperfusion injury.
Liqun Zhang - One of the best experts on this subject based on the ideXlab platform.
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trefoil factor 3 as an endocrine neuroprotective factor from the liver in Experimental Cerebral Ischemia reperfusion injury
PLOS ONE, 2013Co-Authors: Derek Roberts, Brian Zhang, Liqun Zhang, Yu H WuAbstract:Cerebral Ischemia, while causing neuronal injury, can activate innate neuroprotective mechanisms, minimizing neuronal death. In this report, we demonstrate that Experimental Cerebral Ischemia/reperfusion injury in the mouse causes upregulation of the secretory protein trefoil factor 3 (TFF3) in the hepatocyte in association with an increase in serum TFF3. Partial hepatectomy (~60% liver resection) immediately following Cerebral injury significantly lowered the serum level of TFF3, suggesting a contribution of the liver to the elevation of serum TFF3. Compared to wild-type mice, TFF3-/- mice exhibited a significantly higher activity of caspase 3 and level of cell death in the ischemic Cerebral lesion, a larger fraction of Cerebral infarcts, and a smaller fraction of the injured Cerebral hemisphere, accompanied by severer forelimb motor deficits. Intravenous administration of recombinant TFF3 reversed changes in Cerebral injury and forelimb motor function due to TFF3 deficiency. These observations suggest an endocrine neuroprotective mechanism involving TFF3 from the liver in Experimental Cerebral Ischemia/reperfusion injury.
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Trefoil Factor 3 as an Endocrine Neuroprotective Factor from the Liver in Experimental Cerebral Ischemia/Reperfusion Injury
PLoS ONE, 2013Co-Authors: Shu Q. Liu, Derek Roberts, Brian Zhang, Yupeng Ren, Liqun ZhangAbstract:Cerebral Ischemia, while causing neuronal injury, can activate innate neuroprotective mechanisms, minimizing neuronal death. In this report, we demonstrate that Experimental Cerebral Ischemia/reperfusion injury in the mouse causes upregulation of the secretory protein trefoil factor 3 (TFF3) in the hepatocyte in association with an increase in serum TFF3. Partial hepatectomy (~60% liver resection) immediately following Cerebral injury significantly lowered the serum level of TFF3, suggesting a contribution of the liver to the elevation of serum TFF3. Compared to wild-type mice, TFF3-/- mice exhibited a significantly higher activity of caspase 3 and level of cell death in the ischemic Cerebral lesion, a larger fraction of Cerebral infarcts, and a smaller fraction of the injured Cerebral hemisphere, accompanied by severer forelimb motor deficits. Intravenous administration of recombinant TFF3 reversed changes in Cerebral injury and forelimb motor function due to TFF3 deficiency. These observations suggest an endocrine neuroprotective mechanism involving TFF3 from the liver in Experimental Cerebral Ischemia/reperfusion injury.
Brian Zhang - One of the best experts on this subject based on the ideXlab platform.
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trefoil factor 3 as an endocrine neuroprotective factor from the liver in Experimental Cerebral Ischemia reperfusion injury
PLOS ONE, 2013Co-Authors: Derek Roberts, Brian Zhang, Liqun Zhang, Yu H WuAbstract:Cerebral Ischemia, while causing neuronal injury, can activate innate neuroprotective mechanisms, minimizing neuronal death. In this report, we demonstrate that Experimental Cerebral Ischemia/reperfusion injury in the mouse causes upregulation of the secretory protein trefoil factor 3 (TFF3) in the hepatocyte in association with an increase in serum TFF3. Partial hepatectomy (~60% liver resection) immediately following Cerebral injury significantly lowered the serum level of TFF3, suggesting a contribution of the liver to the elevation of serum TFF3. Compared to wild-type mice, TFF3-/- mice exhibited a significantly higher activity of caspase 3 and level of cell death in the ischemic Cerebral lesion, a larger fraction of Cerebral infarcts, and a smaller fraction of the injured Cerebral hemisphere, accompanied by severer forelimb motor deficits. Intravenous administration of recombinant TFF3 reversed changes in Cerebral injury and forelimb motor function due to TFF3 deficiency. These observations suggest an endocrine neuroprotective mechanism involving TFF3 from the liver in Experimental Cerebral Ischemia/reperfusion injury.
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Trefoil Factor 3 as an Endocrine Neuroprotective Factor from the Liver in Experimental Cerebral Ischemia/Reperfusion Injury
PLoS ONE, 2013Co-Authors: Shu Q. Liu, Derek Roberts, Brian Zhang, Yupeng Ren, Liqun ZhangAbstract:Cerebral Ischemia, while causing neuronal injury, can activate innate neuroprotective mechanisms, minimizing neuronal death. In this report, we demonstrate that Experimental Cerebral Ischemia/reperfusion injury in the mouse causes upregulation of the secretory protein trefoil factor 3 (TFF3) in the hepatocyte in association with an increase in serum TFF3. Partial hepatectomy (~60% liver resection) immediately following Cerebral injury significantly lowered the serum level of TFF3, suggesting a contribution of the liver to the elevation of serum TFF3. Compared to wild-type mice, TFF3-/- mice exhibited a significantly higher activity of caspase 3 and level of cell death in the ischemic Cerebral lesion, a larger fraction of Cerebral infarcts, and a smaller fraction of the injured Cerebral hemisphere, accompanied by severer forelimb motor deficits. Intravenous administration of recombinant TFF3 reversed changes in Cerebral injury and forelimb motor function due to TFF3 deficiency. These observations suggest an endocrine neuroprotective mechanism involving TFF3 from the liver in Experimental Cerebral Ischemia/reperfusion injury.
