|
|
|
题名
|
作者
|
年代
|
出处
|
被引量
|
| 1 | Epidemiology of severe sepsis in critically ill surgical patients in ten university hospitals in China显示文摘 | Baoli Cheng Guohao Xie ShangLong Yao Xinmin Wu Qulian Guo Miaoning Gu Qiang Fang Qiuping Xu Dongxin Wang Yuhong Jin ShiYing Yuan Junlu Wang Zhaohui Du Yunbo Sun XiangMing Fang | 2007 | Critical Care Medicine2007，，11： | 2 |
| 2 | 中度低温对心脏停跳复苏后脑组织PGI_2及TXA_2含量的影响显示文摘心脏停跳复苏后将脑温降低至30~32℃时,测定脑组织PGI2及TXA2含量。结果表明:全脑中度低温可明显抑制TXA2的产生,而PGI2含量无明显变化。提示中度低温能早期有效地抑制脑内花生四烯酸环氧酶途径代谢,减轻缺血后脑损伤。 | Guo Qulian Tan Xiujuan Cai Hongwei Lei Baiping Xu Qiming(Department of Anesthesiology, Xiangya Hospital, Hunan Medical University, Changsha 410008) | 1998 | 湖南医科大学学报1998，23，4： | 1 |
| 3 | Repeated intrathecal administration of ropivacaine causes neurotoxicity in rats显示文摘 | Zhong Z Qulian G Yuan Z | 2009 | Anaesth Intensive Care2009，37，11： | 1 |
| 4 | Downstream signaling of reactive oxygen species,protein kinase C epsilon translocation and delayed neuroprotection in sevoflurane preconditioned rats following cerebral ischemia/reperfusion显示文摘BACKGROUND:Brief exposure to the anesthetic sevoflurane results in delayed neuroprotection. However,few studies have addressed delayed neuroprotection after preconditioning with a single administration of sevoflurane. OBJECTIVE:To explore the relationship between a single preconditioning administration of sevoflurane and reactive oxygen species production and protein kinase C-epsilon(PKC-ε) translocation. DESIGN,TIME,AND SETTING:The randomized,controlled,animal experiment was conducted at the Central Laboratory,Xiangya Hospital,Central South University,China from November 2007 to April 2008. MATERIALS:A total of 120 healthy,male,Sprague Dawley rats were equally and randomly assigned into five groups:sham operation,ischemia/reperfusion,sevoflurane,2-mercaptopropionylglycine (2-MPG,a selective reactive oxygen species scavenger) + sevoflurane(MPG + sevoflurane),and MPG.Sevoflurane(Baxter,USA) and MPG(Sigma,USA) were used in this study. METHODS:Intervention consisted of three procedures.(1) MPG injection:a selective reactive oxygen species scavenger,MPG(20 mg/kg),was infused into the rat caudal vein in the MPG and MPG + sevoflurane groups.(2) Sevoflurane preconditioning:30 minutes following MPG injection, rats in the sevoflurane and MPG + sevoflurane groups breathed a mixed gas of 2.4%sevoflurane and 97.6%oxygen for 60 minutes.Rats in the sham operation,ischemia/reperfusion,and MPG groups breathed 100%pure oxygen for 60 minutes.(3) Ischemia/reperfusion:24 hours after sevoflurane or pure oxygen preconditioning,middle cerebral artery occlusion models were established in the ischemia/reperfusion,sevoflurane,MPG + sevoflurane,and MPG groups. Following 2 hours ischemia/6 hours and 24 hours reperfusion,the carotid artery was separated,but the middle cerebral artery was not occluded,in the sham operation group. MAIN OUTCOME MEASURES:In the ischemic hemisphere,PKC-εtranslocation in the rat parietal cortex was measured by Western blot analysis.Infarct volume was calculated using the TTC assay.Neurological deficits were evaluated in rats using a scoring system of 8 points. RESULTS:After 6 hours reperfusion,the ratio of PKC-εin membrane/(cytosol + membrane) was significantly less in the sham operation group than in the ischemia/reperfusion,sevoflurane,MPG + sevoflurane),and MPG groups(P<0.05).The ratio of PKC-εin membrane/(cytosol + membrane) was significantly greater in the sevoflurane group than in the sham operation,ischemia/reperfusion, MPG + sevoflurane,and MPG groups(P<0.05).No significant differences were observed in the ischemia/reperfusion,MPG + sevoflurane,and MPG groups(P>0.05).Following 24 hours reperfusion, the ratio of PKC-εin membrane/(cytosol + membrane) was significantly less in the sham operation group than in the ischemia/reperfusion,sevoflurane,MPG + sevoflurane,and MPG groups(P<0.05). No significant differences were detected in the ischemia/reperfusion,sevoflurane,MPG + sevoflurane, and MPG groups(P>0.05).Compared with the ischemia/reperfusion,MPG + sevoflurane,and MPG groups,infarct volume was significantly smaller,and neurological deficits were significantly improved, in the sevoflurane group(P<0.05).No significant differences in infarct volume and neurological deficits were observed among the ischemia/reperfusion,MPG + sevoflurane,and MPG groups(P>0.05).Infarcts or neurological deficits were not detected in the sham operation group. CONCLUSION:A single preconditioning administration of sevoflurane reduced infarct volumes and improved neurological deficits in ischemic rats.Delayed neuroprotection may be mediated by reactive oxygen species and correlated to PKC-εactivation. | Zhi Ye Qulian Guo E Wang Yundan Pan Qing Li Honghao Zhou | 2009 | Neural Regeneration Research2009，4，3： | 1 |
| 5 | Epidemiology of severe sepsis in critically ill surgical patients in ten university hospitals in China显示文摘 | Baoli Cheng Guohao Xie ShangLong Yao Xinmin Wu Qulian Guo Miaoning Gu Qiang Fang Qiuping Xu Dongxin Wang Yuhong Jin ShiYing Yuan Junlu Wang Zhaohui Du Yunbo Sun XiangMing Fang | 2007 | Critical Care Medicine2007，，11： | 1 |
| 6 | N-methyl-D-aspartate receptor expression in the spinal dorsal horn of a rat model of formalin-induced inflammatory pain following intrathecal injection of butorphanol显示文摘Clinical and animal experiments have proved that intrathecal injection of butorphanol has an analgesic effect. However, whether the analgesic effect is associated with activation of the N-methyl-D-aspartate (NMDA) receptor remains unclear. This study presumed that intrathecal injection of butorphanol has an analgesic effect on formalin-induced inflammatory pain in rats, and its analgesic effect is associated with inhibition of NMDA receptors. Concurrently, ketamine was injected into the intrathecal space, which is a non-competitive NMDA receptor antagonist, to determine the analgesic mechanism of butorphanol. The total reflection time in phase 1 and phase 2 of rat hind paws carding action was reduced when the butorphanol dose was increased to 25 μg, or a low dose of butorphanol was combined with ketamine. Intrathecal injection of a high dose of butorphanol alone or a low dose of butorphanol combined with ketamine can remarkably reduce NMDA receptor expression in the L5 spinal dorsal horn of formalin-induced pain rats. The results suggest that intrathecal injection of butorphanol has analgesic effects on formalin-induced inflammatory pain, and remarkably reduces NMDA receptor expression in the rat spinal dorsal horn. Ketamine strengthens this analgesic effect. The analgesic mechanism of intrathecal injection of butorphanol is associated with inhibition of NMDA receptor activation. | Yichun Wang Yuan Zhang Qulian Guo Xiaohong Liu Mingde Wang Hui Luo | 2010 | Neural Regeneration Research2010，5，21： | 1 |
| 7 | Repeated intrathecal administration of ropivacaine causes neurotoxicity in rats 显示文摘 | Zhong Z Qulian G Yuan Z | 2009 | Anaesth Intensive Care2009，37，6： | 1 |
| 8 | Repeated intrathecal adminis- tration of ropivacaine causes neurotoxicity in rats 显示文摘 | Zhong Z Qulian G Yuan Z | 2009 | Anaesth In- tensive Care2009，37，： | 1 |
| 9 | Parecoxib Suppresses CHOP and Foxo1 Nuclear Translocation, but Increases GRP78 Levels in a Rat Model of Focal Ischemia显示文摘 | Zhi Ye Na Wang Pingping Xia E. Wang Juan Liao Qulian Guo | 2013 | Neurochemical Research2013，，4： | 1 |
| 10 | Sevoflurane postconditioning involves an up-regulation of HIF-1α and HO-1 expression via PI3K/Akt pathway in a rat model of focal cerebral ischemia显示文摘 | Zhi Ye Qulian Guo Pingping Xia Na Wang E. Wang Yajing Yuan | 2012 | Brain Research2012，，： | 1 |
| 11 | Delayed Administration of Parecoxib, a Specific COX-2 Inhibitor, Attenuated Postischemic Neuronal Apoptosis by Phosphorylation Akt and GSK-3β显示文摘 | Zhi Ye Na Wang Pingping Xia E. Wang Yajing Yuan Qulian Guo | 2012 | Neurochemical Research2012，，2： | 1 |
| 12 | Studies on HoxB4 expression during differentiation of human cytomegalovirus-infected hematopoietic stem cells into lymphocyte and erythrocyte progenitor cells显示文摘 | Liu Wenjun Guo Qulian Chen Hongying | 2012 | Cell Bioch-emistry and Biophysics2012，61，3： | 1 |
| 13 | Effect of human cytomegalovirus infection on the expression of HoxB2 and HoxB4 genes in the developmental process of cord blood erythroid progenitors显示文摘 | Liu Wenjun Huang Meixian Guo Qulian | 2011 | Molecular Medicine Reports2011，4，6： | 1 |
| 14 | Repeated intratheeal administrationof ropvaeaine causes neurotoxieity in rats显示文摘 | Zhong Z Qulian G Yuan Z | 2009 | AnaesthIntensive Care2009，37，6： | 1 |
| 15 | Glial Activation and Segmental Upregulation of Interleukin-1β (IL-1β) in the Rat Spinal Cord after Surgical Incision显示文摘 | Di Fu Qulian Guo Yuhang Ai Hongwei Cai Jianqin Yan Ruping Dai | 2006 | Neurochemical Research2006，，3： | 1 |
| 16 | Berberine targets the electron transport chain complex I and reveals the landscape of OXPHOS dependency in acute myeloid leukemia with IDH1 mutation显示文摘Metabolic reprogramming,a newly recognized trait of tumor biology,is an intensively studied prospect for oncology medicines.For numerous tumors and cancer cell subpopulations,oxidative phosphorylation(OXPHOS)is essential for their biosynthetic and bioenergetic functions.Cancer cells with mutations in isocitrate dehydrogenase 1(IDH1)exhibit differentiation arrest,epigenetic and transcriptional reprogramming,and sensitivity to mitochondrial OXPHOS inhibitors.In this study,we report that berberine,which is widely used in China to treat intestinal infections,acted solely at the mitochondrial electron transport chain(ETC)complex I,and that its association with IDH1 mutant inhibitor(IDH1^(m)i)AG-120 decreased mitochondrial activity and enhanced antileukemic effect in vitro and in vivo.Our study gives a scientific rationale for the therapy of IDH1 mutant acute myeloid leukemia(AML)patients using combinatory mitochondrial targeted medicines,particularly those who are resistant to or relapsing from IDH1m i. | HUANG Zhe SHEN Yunfu LIU Wenjun YANG Yan GUO Ling YAN Qin WEI Chengming GUO Qulian FAN Xianming MA Wenzhe | 2023 | Chinese Journal of Natural Medicines2023，21，2： | 0 |
您所在的机构暂未开通此部分的功能，请联系管理员