Thoracoabdominal aortic replacement,necessary in case of injuries,aneurysms and dissections,shows a high complication rate as a consequence of the perioperative ischemia/reperfusion-sequence（I/R）.Clamping above and ...Thoracoabdominal aortic replacement,necessary in case of injuries,aneurysms and dissections,shows a high complication rate as a consequence of the perioperative ischemia/reperfusion-sequence（I/R）.Clamping above and below the lesion leads to the spinal cord suffering from ischemia.Clamping times of less than 30 minutes show only a small risk of neurological deficit,展开更多
In the mammalian central nervous system（CNS）coupling of neurons by gap junctions and the expression of neuronal gap junction protein,connexin 36（Cx36）rapidly increases（usually during 1–2 hours）following a wide ...In the mammalian central nervous system（CNS）coupling of neurons by gap junctions and the expression of neuronal gap junction protein,connexin 36（Cx36）rapidly increases（usually during 1–2 hours）following a wide range of neuronal injuries,including ischemia,traumatic brain injury（TBI）,spinal cord injury and epilepsy（reviewed in Belousov and Fontes,2013）.Pharmacological blockade or genetic elimi-nation of Cx36-containing gap junctions dramatically re- duce neuronal death in animal models of ischemia, TBI and epilepsy and prevent NMDA receptor （NMDAR）-mediated excitotoxicity （Belousov and Fontes, 2014）.展开更多
文摘Thoracoabdominal aortic replacement,necessary in case of injuries,aneurysms and dissections,shows a high complication rate as a consequence of the perioperative ischemia/reperfusion-sequence（I/R）.Clamping above and below the lesion leads to the spinal cord suffering from ischemia.Clamping times of less than 30 minutes show only a small risk of neurological deficit,
基金supported by NIH (R21 NS076925)the University of Kansas Medical Center funds to A.B.B+1 种基金supported in part by NIH P20 GM104936, P30 AG035982 and UL1 TR000001Core support was provided by NIH HD002528
文摘In the mammalian central nervous system（CNS）coupling of neurons by gap junctions and the expression of neuronal gap junction protein,connexin 36（Cx36）rapidly increases（usually during 1–2 hours）following a wide range of neuronal injuries,including ischemia,traumatic brain injury（TBI）,spinal cord injury and epilepsy（reviewed in Belousov and Fontes,2013）.Pharmacological blockade or genetic elimi-nation of Cx36-containing gap junctions dramatically re- duce neuronal death in animal models of ischemia, TBI and epilepsy and prevent NMDA receptor （NMDAR）-mediated excitotoxicity （Belousov and Fontes, 2014）.
