The neuroprotective effect against spinal cord ischemia/reperfusion injury in rats exerted by delayed xenon post-conditioning is stronger than that produced by immediate xenon post-conditioning. However, the mechanism...The neuroprotective effect against spinal cord ischemia/reperfusion injury in rats exerted by delayed xenon post-conditioning is stronger than that produced by immediate xenon post-conditioning. However, the mechanisms underlying this process remain unclear. Activated microglia are the main inflammatory cell type in the nervous system. The release of pro-inflammatory factors following microglial activation can lead to spinal cord damage, and inhibition of microglial activation can relieve spinal cord ischemia/reperfusion injury. To investigate how xenon regulates microglial activation and the release of inflammatory factors, a rabbit model of spinal cord ischemia/reperfusion injury was induced by balloon occlusion of the infrarenal aorta. After establishment of the model, two interventions were given： （1） immediate xenon post-conditioning—after reperfusion, inhalation of 50% xenon for 1 hour, 50% N2/50%O2 for 2 hours; （2） delayed xenon post-conditioning—after reperfusion, inhalation of 50% N2/50%O2 for 2 hours, 50% xenon for 1 hour. At 4, 8, 24, 48 and 72 hours after reperfusion, hindlimb locomotor function was scored using the Jacobs locomotor scale. At 72 hours after reperfusion, interleukin 6 and interleukin 10 levels in the spinal cord of each group were measured using western blot assays. Iba1 levels were determined using immunohistochemistry and a western blot assay. The number of normal neurons at the injury site was quantified using hematoxylin-eosin staining. At 72 hours after reperfusion, delayed xenon post-conditioning remarkably enhanced hindlimb motor function, increased the number of normal neurons at the injury site, decreased Iba1 levels, and inhibited interleukin-6 and interleukin-10 levels in the spinal cord.Immediate xenon post-conditioning did not noticeably affect the above-mentioned indexes. These findings indicate that delayed xenon post-conditioning after spinal cord injury improves the recovery of neurological function by reducing microglial activation and the release of interleukin-6 and interleukin-10.展开更多
The signaling mechanisms underlying ischemia-induced nerve cell apoptosis are poorly understood.We investigated the effects of apoptosis-related signal transduction pathways following ischemic spinal cord injury,inclu...The signaling mechanisms underlying ischemia-induced nerve cell apoptosis are poorly understood.We investigated the effects of apoptosis-related signal transduction pathways following ischemic spinal cord injury,including extracellular signal-regulated kinase(ERK),serine-threonine protein kinase(Akt)and c-Jun N-terminal kinase(JNK)signaling pathways.We established a rat model of acute spinal cord injury by inserting a catheter balloon in the left subclavian artery for 25 minutes.Rat models exhibited notable hindlimb dysfunction.Apoptotic cells were abundant in the anterior horn and central canal of the spinal cord.The number of apoptotic neurons was highest 48 hours post injury.The expression of phosphorylated Akt(pAkt)and phosphorylated ERK(p-ERK)increased immediately after reperfusion,peaked at 4 hours(p-Akt)or 2 hours(p-ERK),decreased at 12 hours,and then increased at 24 hours.Phosphorylated JNK expression reduced after reperfusion,increased at 12 hours to near normal levels,and then showed a downward trend at 24 hours.Pearson linear correlation analysis also demonstrated that the number of apoptotic cells negatively correlated with p-Akt expression.These findings suggest that activation of Akt may be a key contributing factor in the delay of neuronal apoptosis after spinal cord ischemia,particularly at the stage of reperfusion,and thus may be a target for neuronal protection and reduction of neuronal apoptosis after spinal cord injury.展开更多
BACKGROUND Since the outbreak of the coronavirus disease 2019(COVID-19)pandemic,the exclusion of a patient from COVID-19 should be performed before surgery.However,patients with type A acute aortic dissection(AAD)duri...BACKGROUND Since the outbreak of the coronavirus disease 2019(COVID-19)pandemic,the exclusion of a patient from COVID-19 should be performed before surgery.However,patients with type A acute aortic dissection(AAD)during pregnancy can seriously endanger the health of either the mother or fetus that requires emergency surgical treatment without the test for COVID-19.CASE SUMMARY A 38-year-old woman without Marfan syndrome was admitted to the hospital because of chest pain in the 34th week of gestation.She has diagnosed as having a Stanford type-A AAD involving an aortic arch and descending aorta via aortic computed tomographic angiography.The patient was transferred to the isolated negative pressure operating room in one hour and underwent cesarean delivery and ascending aorta replacement.All medical staff adopted third-level medical protection measures throughout the patient transfer and surgical procedure.After surgery,the patient was transferred to the isolated negative pressure intensive care unit ward.The nucleic acid test and anti-COVID-19 immunoglobulin(Ig)G and IgM were performed and were negative.The patient and infant were discharged without complication nine days later and recovered uneventfully.CONCLUSION The results indicated that the procedure that we used is feasible in patients with a combined cesarean delivery and surgery for Stanford type-A AAD during the COVID-19 outbreak,which was mainly attributed to rapid multidisciplinary consultation,collaboration,and quick decision-making.展开更多
An electrophoresis device was used to separate hydrophobic gold nanoparticles with particle size less than 10 nm dispersed in organic solvent. Image of transmission electron microscope (TEM) and UV-Vis spectra showed ...An electrophoresis device was used to separate hydrophobic gold nanoparticles with particle size less than 10 nm dispersed in organic solvent. Image of transmission electron microscope (TEM) and UV-Vis spectra showed that the particles in the vicinity of cathode have a smaller mean diameter than those near the anode. This result indicates that the nanogolds in chloroform bring a positive charge in oppo-sition to what is predicted by Coehn rule, and provides an electrophrosis method for separating hydrophobic nanogold particles of different sizes.展开更多
基金supported by the National Natural Science Foundation of China,No.81271387the Research Special Fund of Public Welfare and Health Department of China,No.201402009a grant form the National Key Technology R&D Program in China,No.Z141107002514031
文摘The neuroprotective effect against spinal cord ischemia/reperfusion injury in rats exerted by delayed xenon post-conditioning is stronger than that produced by immediate xenon post-conditioning. However, the mechanisms underlying this process remain unclear. Activated microglia are the main inflammatory cell type in the nervous system. The release of pro-inflammatory factors following microglial activation can lead to spinal cord damage, and inhibition of microglial activation can relieve spinal cord ischemia/reperfusion injury. To investigate how xenon regulates microglial activation and the release of inflammatory factors, a rabbit model of spinal cord ischemia/reperfusion injury was induced by balloon occlusion of the infrarenal aorta. After establishment of the model, two interventions were given： （1） immediate xenon post-conditioning—after reperfusion, inhalation of 50% xenon for 1 hour, 50% N2/50%O2 for 2 hours; （2） delayed xenon post-conditioning—after reperfusion, inhalation of 50% N2/50%O2 for 2 hours, 50% xenon for 1 hour. At 4, 8, 24, 48 and 72 hours after reperfusion, hindlimb locomotor function was scored using the Jacobs locomotor scale. At 72 hours after reperfusion, interleukin 6 and interleukin 10 levels in the spinal cord of each group were measured using western blot assays. Iba1 levels were determined using immunohistochemistry and a western blot assay. The number of normal neurons at the injury site was quantified using hematoxylin-eosin staining. At 72 hours after reperfusion, delayed xenon post-conditioning remarkably enhanced hindlimb motor function, increased the number of normal neurons at the injury site, decreased Iba1 levels, and inhibited interleukin-6 and interleukin-10 levels in the spinal cord.Immediate xenon post-conditioning did not noticeably affect the above-mentioned indexes. These findings indicate that delayed xenon post-conditioning after spinal cord injury improves the recovery of neurological function by reducing microglial activation and the release of interleukin-6 and interleukin-10.
基金supported by the National Natural Science Foundation of ChinaNo.81271387+3 种基金the Research Special Fund of Public Welfare and Health Department of ChinaNo.201402009the National Key Technology R&D Program in ChinaNo.Z141107002514031
文摘The signaling mechanisms underlying ischemia-induced nerve cell apoptosis are poorly understood.We investigated the effects of apoptosis-related signal transduction pathways following ischemic spinal cord injury,including extracellular signal-regulated kinase(ERK),serine-threonine protein kinase(Akt)and c-Jun N-terminal kinase(JNK)signaling pathways.We established a rat model of acute spinal cord injury by inserting a catheter balloon in the left subclavian artery for 25 minutes.Rat models exhibited notable hindlimb dysfunction.Apoptotic cells were abundant in the anterior horn and central canal of the spinal cord.The number of apoptotic neurons was highest 48 hours post injury.The expression of phosphorylated Akt(pAkt)and phosphorylated ERK(p-ERK)increased immediately after reperfusion,peaked at 4 hours(p-Akt)or 2 hours(p-ERK),decreased at 12 hours,and then increased at 24 hours.Phosphorylated JNK expression reduced after reperfusion,increased at 12 hours to near normal levels,and then showed a downward trend at 24 hours.Pearson linear correlation analysis also demonstrated that the number of apoptotic cells negatively correlated with p-Akt expression.These findings suggest that activation of Akt may be a key contributing factor in the delay of neuronal apoptosis after spinal cord ischemia,particularly at the stage of reperfusion,and thus may be a target for neuronal protection and reduction of neuronal apoptosis after spinal cord injury.
文摘BACKGROUND Since the outbreak of the coronavirus disease 2019(COVID-19)pandemic,the exclusion of a patient from COVID-19 should be performed before surgery.However,patients with type A acute aortic dissection(AAD)during pregnancy can seriously endanger the health of either the mother or fetus that requires emergency surgical treatment without the test for COVID-19.CASE SUMMARY A 38-year-old woman without Marfan syndrome was admitted to the hospital because of chest pain in the 34th week of gestation.She has diagnosed as having a Stanford type-A AAD involving an aortic arch and descending aorta via aortic computed tomographic angiography.The patient was transferred to the isolated negative pressure operating room in one hour and underwent cesarean delivery and ascending aorta replacement.All medical staff adopted third-level medical protection measures throughout the patient transfer and surgical procedure.After surgery,the patient was transferred to the isolated negative pressure intensive care unit ward.The nucleic acid test and anti-COVID-19 immunoglobulin(Ig)G and IgM were performed and were negative.The patient and infant were discharged without complication nine days later and recovered uneventfully.CONCLUSION The results indicated that the procedure that we used is feasible in patients with a combined cesarean delivery and surgery for Stanford type-A AAD during the COVID-19 outbreak,which was mainly attributed to rapid multidisciplinary consultation,collaboration,and quick decision-making.
基金This work was supported by the National Natural Science Foundation of China(Grant No.90207026).
文摘An electrophoresis device was used to separate hydrophobic gold nanoparticles with particle size less than 10 nm dispersed in organic solvent. Image of transmission electron microscope (TEM) and UV-Vis spectra showed that the particles in the vicinity of cathode have a smaller mean diameter than those near the anode. This result indicates that the nanogolds in chloroform bring a positive charge in oppo-sition to what is predicted by Coehn rule, and provides an electrophrosis method for separating hydrophobic nanogold particles of different sizes.
