期刊文献+
共找到36,807篇文章
< 1 2 250 >
每页显示 20 50 100
文章速递Ischemic Conditioning-Mediated Myocardial Protection in Relation to Duration of Coronary Occlusion 认领
1
作者 John G. Kingma Jr. 《心血管病(英文)》 2021年第3期210-222,共13页
<strong>Background</strong><span style="font-family:Verdana;"><b>:</b></span><span style="font-family:Verdana;"> Myocardial ischemia is a dynamic process w... <strong>Background</strong><span style="font-family:Verdana;"><b>:</b></span><span style="font-family:Verdana;"> Myocardial ischemia is a dynamic process whereby a cascade of events is initiated to stimulate transition from reversible to irreversible cellular injury. Non-pharmacologic approaches to cellular protection, such as ische</span><span style="font-family:;" "=""><span style="font-family:Verdana;">mic conditioning, delay onset of cellular injury in most organs in a host of animal species;however the degree of protection is limited to rather short durations of ischemia. In the present study, we examined whether protection afforded by ischemic conditioning could be extended beyond currently established limits of coronary occlusion in an </span><i><span style="font-family:Verdana;">in situ</span></i><span style="font-family:Verdana;"> animal model.</span></span><span style="font-family:Verdana;"> </span><span style="font-family:Verdana;"><b>Methods</b></span><span style="font-family:Verdana;"><b>:</b></span><span style="font-family:Verdana;"> </span><span style="font-family:Verdana;">Rabbits (n</span><span style="font-family:Verdana;"> </span><span style="font-family:Verdana;">=</span><span style="font-family:Verdana;"> </span><span style="font-family:Verdana;">106) were exposed to 30-, 60-, 120-, 180-, 240-, or 360-min coronary</span><span style="font-family:Verdana;"> </span><span style="font-family:;" "=""><span style="font-family:Verdana;">occlusion followed by 180-min coronary reperfusion (</span><i><span style="font-family:Verdana;">i</span></i><span style="font-family:Verdana;">.</span><i><span style="font-family:Verdana;">e</span></i><span style="font-family:Verdana;">. non-conditioned</span></span><span style="font-family:;" "=""><span style="font-family:Verdana;"> control groups). Ischemic conditioned rabbits were pre-treated by ischemic conditioning (</span><i><span style="font-family:Verdana;">i</span></i><span style="font-family:Verdana;">.</span><i><span style="font-family:Verdana;">e</span></i><span style="font-family:Verdana;">. 2-cycles of 5-min coronary occlusion and 5-min reperfusion) prior to a prolonged period of ischemia as described above. Area at risk (AR; by fluorescent microparticles) and area of necrosis (AN;by tetrazolium staining) were quantified by planimetry. Serum troponin I levels were assessed at baseline (</span><i><span style="font-family:Verdana;">i</span></i><span style="font-family:Verdana;">.</span><i><span style="font-family:Verdana;">e</span></i><span style="font-family:Verdana;">. before experimental protocol) and at the end of the experiment. </span></span><span style="font-family:;" "=""></span><span style="font-family:Verdana;"><b>Results</b></span><span style="font-family:Verdana;"><b>:</b></span><span style="font-family:;" "=""><span style="font-family:Verdana;"> Changes in heart rate and hemodyamic indices were similar for all groups regardless of duration of ischemia and regardless of treatment (</span><i><span style="font-family:Verdana;">i</span></i><span style="font-family:Verdana;">.</span><i><span style="font-family:Verdana;">e</span></i><span style="font-family:Verdana;">. non-conditioned vs. ischemic conditioned). Infarcts (as percent AR) were markedly smaller (~35%) in ischemic conditioned rabbits (vs. controls) for the 30-min coronary occlusion group. With longer durations of coronary occlusion (60</span></span><span style="font-family:Verdana;">-</span><span style="font-family:Verdana;">, 120-, 180-, 240-min) infarcts were smaller (~20%) in ischemic conditioned groups but protection afforded was not statistically significant. With 360-min coronary occlusion, infarct size was the same for both treatment groups. Serum troponin I levels were greater in relation to infarct size as expected but no differences were detected between treatments regardless of ischemic duration.</span><span style="font-family:Verdana;"> </span><span style="font-family:Verdana;"><b>Conclusions</b></span><span style="font-family:Verdana;"><b>: </b></span><span style="font-family:Verdana;">Ischemic conditioning limits infarct development;however, protection is limited when the duration of ischemia is extended beyond 4 hours. These findings provide further support for the concept that ischemic conditioning can delay, but does not limit myocyte necrosis. Underlying mechanisms for cellular protection remain to be established.</span> 展开更多
关键词 Ischemia Reperfusion Infarct Size Biomarkers Ischemic Conditioning Rab-bits
在线阅读 下载PDF
文章速递急性下肢动脉缺血的治疗策略 认领
2
作者 徐欣 周思远 方刚 《中国血管外科杂志:电子版》 2021年第1期13-16,20,共5页
急性下肢动脉缺血(acute lower limb ischemia,ALLI)指病程短于2周,由各种原因导致的急性下肢动脉灌注不足。ALLI是血管外科常见急症,如不及时处理可能会造成患者截肢或死亡的严重后果,其年发病率为1.0‰~1.5‰[1],30 d截肢率为10%~30%,... 急性下肢动脉缺血(acute lower limb ischemia,ALLI)指病程短于2周,由各种原因导致的急性下肢动脉灌注不足。ALLI是血管外科常见急症,如不及时处理可能会造成患者截肢或死亡的严重后果,其年发病率为1.0‰~1.5‰[1],30 d截肢率为10%~30%,30 d死亡率为15%[2]。一旦确诊为ALLI,需要尽可能快速恢复下肢动脉血流灌注[3]。 展开更多
关键词 下肢动脉 血管外科 灌注不足 治疗策略 截肢率 ischemia 血流灌注
在线阅读 下载PDF
文章速递Astragaloside IV suppresses post-ischemic natural killer cell infiltration and activation in the brain:involvement of histone deacetylase inhibition 认领
3
作者 Baokai Dou Shichun Li +6 位作者 Luyao Wei Lixin Wang Shiguo Zhu Zhengtao Wang Zunji Ke Kaixian Chen Zhifei Wang 《医学前沿:英文版》 SCIE CSCD 2021年第1期79-90,共12页
Natural killer(NK)cells,a type of cytotoxic lymphocytes,can infiltrate into ischemic brain and exacerbate neuronal cell death.Astragaloside IV(ASIV)is the major bioactive ingredient of Astragalus membranaceus,a Chines... Natural killer(NK)cells,a type of cytotoxic lymphocytes,can infiltrate into ischemic brain and exacerbate neuronal cell death.Astragaloside IV(ASIV)is the major bioactive ingredient of Astragalus membranaceus,a Chinese herbal medicine,and possesses potent immunomodulatory and neuroprotective properties.This study investigated the effects of ASIV on post-ischemic brain infiltration and activation of NK cells.ASIV reduced brain infarction and alleviated functional deficits in MCAO rats,and these beneficial effects persisted for at least 7 days.Abundant NK cells infiltrated into the ischemic hemisphere on day 1 after brain ischemia,and this infiltration was suppressed by ASIV.Strikingly,ASIV reversed NK cell deficiency in the spleen and blood after brain ischemia.ASIV inhibited astrocyte-derived CCL2 upregulation and reduced CCR2+NK cell levels in the ischemic brain.Meanwhile,ASIV attenuated NK cell activating receptor NKG2D levels and reduced interferon-γproduction.ASIV restored acetylation of histone H3 and the p65 subunit of nuclear factor-κB in the ischemic brain,suggesting inhibition of histone deacetylase(HDAC).Simultaneously,ASIV prevented p65 nuclear translocation.The effects of ASIV on reducing CCL2 production,restoring acetylated p65 levels and preventing p65 nuclear translocation were mimicked by valproate,an HDAC inhibitor,in astrocytes subjected to oxygen-glucose deprivation.Our findings suggest that ASIV inhibits post-ischemic NK cell brain infiltration and activation and reverses NK cell deficiency in the periphery,which together contribute to the beneficial effects of ASIV against brain ischemia.Furthermore,ASIV’s effects on suppressing NK cell brain infiltration and activation may involve HDAC inhibition. 展开更多
关键词 astragaloside IV brain ischemia natural killer cells histone deacetylase nuclear factor-κB
Hydroxyethylstarch revisited for acute brain injury treatment 认领
4
作者 Martin A.Schick Malgorzata Burek +3 位作者 Carola Y.Förster Michiaki Nagai Christian Wunder Winfried Neuhaus 《中国神经再生研究:英文版》 SCIE CAS 2021年第7期1372-1376,共5页
Infusion of the colloid hydroxyethylstarch has been used for volume substitution to maintain hemodynamics and microcirculation after e.g., severe blood loss.In the last decade it was revealed that hydroxyethylstarch c... Infusion of the colloid hydroxyethylstarch has been used for volume substitution to maintain hemodynamics and microcirculation after e.g., severe blood loss.In the last decade it was revealed that hydroxyethylstarch can aggravate acute kidney injury, especially in septic patients.Because of the serious risk for critically ill patients, the administration of hydroxyethylstarch was restricted for clinical use.Animal studies and recently published in vitro experiments showed that hydroxyethylstarch might exert protective effects on the blood-brain barrier.Since the prevention of blood-brain barrier disruption was shown to go along with the reduction of brain damage after several kinds of insults, we revisit the topic hydroxyethylstarch and discuss a possible niche for the application of hydroxyethylstarch in acute brain injury treatment. 展开更多
关键词 acute subarachnoid hemorrhage ASTROCYTE chronic kidney disease delayed cerebral ischemia MICROGLIA neurovascular unit osmotic pressure PERICYTE STROKE traumatic brain injury
在线阅读 下载PDF
Genes associated with Alzheimer's disease affecting ischemic neurodegeneration of the hippocampal CA3 region 认领
5
作者 Ryszard Pluta Marzena Ułamek-Kozioł 《中国神经再生研究:英文版》 SCIE CAS 2021年第7期1392-1393,共2页
Neurodegeneration in the brain after ischemia with reperfusion mimicking the neuropathology of Alzheimer's disease:Brain ischemia with reperfusion,which is one of the main causes of morbidity and mortality in the ... Neurodegeneration in the brain after ischemia with reperfusion mimicking the neuropathology of Alzheimer's disease:Brain ischemia with reperfusion,which is one of the main causes of morbidity and mortality in the world,triggers various neuropathological changes characteristic for Alzheimer's disease(AD)such as increased blood-brain barrier permeability,excitotoxicity,necrosis,autophagy,mitophagy,apoptosis,neuroinflammation,amyloid plaques,neurofibrillary tangles,cerebral vessel pathology,and brain atrophy that lead to the death of neurons,deteriorating motor,sensory and cognitive functions(Figure 1)(Kato et al.,1988;Wisniewski et al.,1995;Van Groen et al.,2005;Kocki et al.,2015;Ułamek-Koziołet al.,2016,2017,2019).Brain ischemia is recognized as a major contributor to the dysfunction of an aging brain and the development of neurodegenerative diseases,including AD(Pluta,2019). 展开更多
关键词 ALZHEIMER ISCHEMIA cerebral
在线阅读 下载PDF
MicroRNA-670 aggravates cerebral ischemia/reperfusion injury via the Yap pathway 认领
6
作者 Shi-Jia Yu Ming-Jun Yu +2 位作者 Zhong-Qi Bu Ping-Ping He Juan Feng 《中国神经再生研究:英文版》 SCIE CAS 2021年第6期1024-1030,共7页
Apoptosis is an important programmed cell death process involved in ischemia/reperfusion injury.MicroRNAs are considered to play an important role in the molecular mechanism underlying the regulation of cerebral ische... Apoptosis is an important programmed cell death process involved in ischemia/reperfusion injury.MicroRNAs are considered to play an important role in the molecular mechanism underlying the regulation of cerebral ischemia and reperfusion injury.However,whether miR-670 can regulate cell growth and death in cerebral ischemia/reperfusion and the underlying mechanism are poorly understood.In this study,we established mouse models of transient middle artery occlusion and Neuro 2a cell models of oxygen-glucose deprivation and reoxygenation to investigate the potential molecular mechanism by which miR-670 exhibits its effects during cerebral ischemia/reperfusion injury both in vitro and in vivo.Our results showed that after ischemia/reperfusion injury,miR-670 expression was obviously increased.After miR-670 expression was inhibited with an miR-670 antagomir,cerebral ischemia/reperfusion injury-induced neuronal death was obviously reduced.When miR-670 overexpression was induced by an miR-670 agomir,neuronal apoptosis was increased.In addition,we also found that miR-670 could promote Yap degradation via phosphorylation and worsen neuronal apoptosis and neurological deficits.Inhibition of miR-670 reduced neurological impairments after cerebral ischemia/reperfusion injury.These results suggest that microRNA-670 aggravates cerebral ischemia/reperfusion injury through the Yap pathway,which may be a potential target for treatment of cerebral ischemia/reperfusion injury.The present study was approved by the Institutional Animal Care and Use Committee of China Medical University on February 27,2017(IRB No.2017PS035K). 展开更多
关键词 APOPTOSIS cerebral ischemia and reperfusion injury MICRORNA miR-670 neurological function NEURON non-coding RNA PATHWAY
在线阅读 下载PDF
Strategies to prevent and detect intraoperative spinal cord ischemia during complex aortic surgery:from drainages and biomarkers 认领
7
作者 Alexander Gombert Florian Simon 《中国神经再生研究:英文版》 SCIE CAS 2021年第4期678-679,共2页
Spinal cord ischemia(SCI),a frequent complication following open and endovascular thoracoabdominal aortic aneurysm(TAAA)repair,is a feared complication with relevant impact on a patient's quality of life.In the ea... Spinal cord ischemia(SCI),a frequent complication following open and endovascular thoracoabdominal aortic aneurysm(TAAA)repair,is a feared complication with relevant impact on a patient's quality of life.In the early days of open TAAA repair,more than one third of the patients suffered from SCI.Nowadays,due to improved preventive measures and the option of staged endovascular TAAA repair,10%of all patients are affected by spinal cord problems after TAAA repair(Rocha et al.,2020). 展开更多
关键词 ISCHEMIA AORTIC SCI
在线阅读 下载PDF
益气活血中药联合骨髓间充质干细胞促进缺血性脑卒中血管新生的作用与机制 认领
8
作者 樊飞燕 张运克 《中国组织工程研究》 CAS 北大核心 2021年第13期2060-2069,共10页
背景:骨髓间充质干细胞具有促进血管新生的作用,治疗缺血性脑卒中效果良好,益气活血类中药在促进血管新生方面亦存在显著疗效。目的:综述益气活血类中药联合骨髓间充质干细胞促进缺血性脑卒中血管新生的机制,以期为缺血性脑卒中的研究... 背景:骨髓间充质干细胞具有促进血管新生的作用,治疗缺血性脑卒中效果良好,益气活血类中药在促进血管新生方面亦存在显著疗效。目的:综述益气活血类中药联合骨髓间充质干细胞促进缺血性脑卒中血管新生的机制,以期为缺血性脑卒中的研究及治疗提供参考。方法:以“bone marrow mesenchymal stem cells,angiogenesis,ischemic stroke,traditional chinese medicine”为英文关键词,以“骨髓间充质干细胞,血管新生,缺血性脑卒中,中药”为中文关键词,检索2009至2020年期间收录在PubMed、中国知网、万方数据库中的文献,纳入血管新生相关机制及中药联合骨髓间充质干细胞促进血管新生相关的文献,排除重复与相关性弱的文献,对145篇文献进行总结分析。结果与结论:①梳理了骨髓间充质干细胞、血管新生的定义及血管新生的机制;②总结了益气活血类中药联合骨髓间充质干细胞促进血管新生的相关因子及信号通路,如血管内皮生长因子、脑源性神经营养因子、碱性成纤维细胞生长因子、缺氧诱导因子1α、血管生成素、整合素αvβ3、基质金属蛋白酶9及Wnt信号通路、Notch信号通路、PI3K/Akt信号通路和SDF-1/CXCR4信号轴;③总结发现益气活血类中药与骨髓间充质干细胞联合应用能增强血管新生作用,提升缺血性脑卒中的治疗效果。 展开更多
关键词 干细胞 骨髓间充质干细胞 血管新生 脑卒中 缺血性 中药 复方 综述
在线阅读 下载PDF
急性肠系膜缺血合并肠坏死的预测因素分析 认领
9
作者 董天庚 龚昱达 +2 位作者 高卫东 张波 盛卫忠 《中华普通外科杂志》 北大核心 2021年第2期98-101,共4页
目的探讨急性肠系膜缺血性疾病合并肠坏死的预测因素。方法回顾性分析2012年11月至2017年5月在复旦大学附属中山医院普外科诊治的81例肠系膜缺血患者的临床资料。根据单因素及多因素Logistic回归分析预测肠坏死发生的相关因素。结果本... 目的探讨急性肠系膜缺血性疾病合并肠坏死的预测因素。方法回顾性分析2012年11月至2017年5月在复旦大学附属中山医院普外科诊治的81例肠系膜缺血患者的临床资料。根据单因素及多因素Logistic回归分析预测肠坏死发生的相关因素。结果本组81例患者中49例(60%)发生肠坏死,32例(40%)无肠坏死行保守治疗。单因素分析结果显示:腹膜刺激征(P<0.001)、外周血白细胞总数(P<0.001)、血清白蛋白(P=0.028)、肌酐(P=0.025)、乳酸(P=0.008)、D-二聚体水平(P=0.037).CT检查发现肠壁积气改变(P=0.017)、肠璧强化减弱或消失(P<0.001)及肠腔扩张>2.5cm(P=0.01)均与肠坏死有关。多因索回归分析结果显示:外周血白细胞总数(OR=3.60,95%CI:1.51-5.47,P=0.007)、血清乳酸(OR=4.80,95%CI:1.36~9.89,P=0.032)及CT检查发现肠壁增强减弱或消失(OR=10.57.95%CI:1.82-61.10,P=0.008)为急性肠系膜缺血发生肠坏死的独立预测因素。结论肠系膜缺血发生肠坏死的预测危险因素为外周血白细胞计数升高.血清乳酸水平升高以及CT检查提示肠壁强化减弱或消失。 展开更多
关键词 肠系膜血管闭塞 缺血 坏死 危险因素
Extremely low frequency electromagnetic fields promote cognitive function and hippocampal neurogenesis of rats with cerebral ischemia 认领
10
作者 Qiang Gao Aaron Leung +5 位作者 Yong-Hong Yang Benson Wui-Man Lau Qian Wang Ling-Yi Liao Yun-Juan Xie Cheng-Qi He 《中国神经再生研究:英文版》 SCIE CAS 2021年第7期1252-1257,共6页
Extremely low frequency electromagnetic fields(ELF-EMF) can improve the learning and memory impairment of rats with Alzheimer's disease, however, its effect on cerebral ischemia remains poorly understood.In this s... Extremely low frequency electromagnetic fields(ELF-EMF) can improve the learning and memory impairment of rats with Alzheimer's disease, however, its effect on cerebral ischemia remains poorly understood.In this study, we established rat models of middle cerebral artery occlusion/reperfusion.One day after modeling, a group of rats were treated with ELF-EMF(50 Hz, 1 mT) for 2 hours daily on 28 successive days.Our results showed that rats treated with ELF-EMF required shorter swimming distances and latencies in the Morris water maze test than those of untreated rats.The number of times the platform was crossed and the time spent in the target quadrant were greater than those of untreated rats.The number of BrdU~+/NeuN~+ cells, representing newly born neurons, in the hippocampal subgranular zone increased more in the treated than in untreated rats.Up-regulation in the expressions of Notch1, Hes1, and Hes5 proteins, which are the key factors of the Notch signaling pathway, was greatest in the treated rats.These findings suggest that ELF-EMF can enhance hippocampal neurogenesis of rats with cerebral ischemia, possibly by affecting the Notch signaling pathway.The study was approved by the Institutional Ethics Committee of Sichuan University, China(approval No.2019255A) on March 5, 2019. 展开更多
关键词 cerebral ischemia cognitive function electromagnetic fields HIPPOCAMPUS NEUROGENESIS PLASTICITY repair signaling pathway STROKE rat
在线阅读 下载PDF
Effect of electroacupuncture on glial fibrillary acidic protein and nerve growth factor in the hippocampus of rats with hyperlipidemia and middle cerebral artery thrombus 认领
11
作者 Na-Ying Xue Dong-Yu Ge +3 位作者 Rui-Juan Dong Hyung-Hwan Kim Xiu-Jun Ren Ya Tu 《中国神经再生研究:英文版》 SCIE CAS 2021年第1期137-142,共6页
Electroacupuncture(EA)has been shown to reduce blood lipid level and improve cerebral ischemia in rats with hyperlipemia complicated by cerebral ischemia.However,there are few studies on the results and mechanism of t... Electroacupuncture(EA)has been shown to reduce blood lipid level and improve cerebral ischemia in rats with hyperlipemia complicated by cerebral ischemia.However,there are few studies on the results and mechanism of the effect of EA in reducing blood lipid level or promoting neural repair after stroke in hyperlipidemic subjects.In this study,EA was applied to a rat model of hyperlipidemia and middle cerebral artery thrombosis and the condition of neurons and astrocytes after hippocampal injury was assessed.Except for the normal group,rats in other groups were fed a high-fat diet throughout the whole experiment.Hyperlipidemia models were established in rats fed a high-fat diet for 6 weeks.Middle cerebral artery thrombus models were induced by pasting 50%FeCl3 filter paper on the left middle cerebral artery for 20 minutes on day 50 as the model group.EA1 group rats received EA at bilateral ST40(Fenglong)for 7 days before the thrombosis.Rats in the EA1 and EA2 groups received EA at GV20(Baihui)and bilateral ST40 for 14 days after model establishment.Neuronal health was assessed by hematoxylin-eosin staining in the brain.Hyperlipidemia was assessed by biochemical methods that measured total cholesterol,triglyceride,low-density lipoprotein and high-density lipoprotein in blood sera.Behavioral analysis was used to confirm the establishment of the model.Immunohistochemical methods were used to detect the expression of glial fibrillary acidic protein and nerve growth factor in the hippocampal CA1 region.The results demonstrated that,compared with the model group,blood lipid levels significantly decreased,glial fibrillary acidic protein immunoreactivity was significantly weakened and nerve growth factor immunoreactivity was significantly enhanced in the EA1 and EA2 groups.The repair effect was superior in the EA1 group than in the EA2 group.These findings confirm that EA can reduce blood lipid,inhibit glial fibrillary acidic protein expression and promote nerve growth factor expression in the hippocampal CA1 region after 展开更多
关键词 ASTROCYTES CA1 cerebral ischemia ELECTROACUPUNCTURE glial fibrillary acidic protein hematoxylin-eosin staining HIPPOCAMPUS HYPERLIPIDEMIA immunohistochemistry nerve growth factor
在线阅读 下载PDF
ROS-responsive capsules engineered from EGCG-Zinc networks improve therapeutic angiogenesis in mouse limb ischemia 认领
12
作者 Zuoguan Chen Jianwei Duan +9 位作者 Yongpeng Diao Youlu Chen Xiaoyu Liang Huiyang Li Yuqing Miao Qing Gao Liang Gui Xiaoli Wang Jing Yang Yongjun Li 《生物活性材料》 SCIE 2021年第1期1-11,共11页
The successful treatment of limb ischemia requires that promote angiogenesis along with microenvironment improvement.Zinc ions have been reported to stimulate angiogenesis,but application was limited to the toxicity c... The successful treatment of limb ischemia requires that promote angiogenesis along with microenvironment improvement.Zinc ions have been reported to stimulate angiogenesis,but application was limited to the toxicity concerns.We hypothesized that zinc based metal-EGCG capsule(EGCG/Zn Ps)can achieve sustained release Zn2+resulting in reduced toxicity and improve angiogenesis as well as the improvement of microenvironment by ROS scavenging of EGCG.The surface morphology,zeta potential,infrared absorbance peaks and zinc ion release profile of the EGCG/Zn Ps were measured.In vitro,EGCG/Zn showed significantly antioxidant,antiinflammatory and induced cell migration effect.In addition,EGCG/Zn Ps enabled the sustained release of zinc ions,which reduced cytotoxicity and enhanced the secretion of vascular endothelial growth factor(VEGF)in vitro and in vivo.In mouse models of limb ischemia,EGCG/Zn Ps promoted angiogenesis and cell proliferation in ischemic tissues.Moreover,EGCG/Zn Ps group exhibited the most significant recovery of limb ischemic score,limb temperature and blood flow than other groups.In conclusion,EGCG/Zn Ps is a safe and promising approach to combine the merit of Zn2+and EGCG,thus enabling the direct application to limb ischemia. 展开更多
关键词 Polyphenol metal networks Green tea polyphenol ZINC ANGIOGENESIS Limb ischemia disease
Modeling subcortical ischemic white matter injury in rodents:unmet need for a breakthrough in translational research 认领
13
作者 Yuexian Cui Xuelian Jin +1 位作者 Jun Young Choi Byung Gon Kim 《中国神经再生研究:英文版》 SCIE CAS 2021年第4期638-642,共5页
Subcortical ischemic white matter injury(SIWMI),pathological correlate of white matter hyperintensities or leukoaraiosis on magnetic resonance imaging,is a common cause of cognitive decline in elderly.Despite its high... Subcortical ischemic white matter injury(SIWMI),pathological correlate of white matter hyperintensities or leukoaraiosis on magnetic resonance imaging,is a common cause of cognitive decline in elderly.Despite its high prevalence,it remains unknown how various components of the white matter degenerate in response to chronic ischemia.This incomplete knowledge is in part due to a lack of adequate animal model.The current review introduces various SIWMI animal models and aims to scrutinize their advantages and disadvantages primarily in regard to the pathological manifestations of white matter components.The SIWMI animal models are categorized into 1)chemically induced SIWMI models,2)vascular occlusive SIWMI models,and 3)SIWMI models with comorbid vascular risk factors.Chemically induced models display consistent lesions in predetermined areas of the white matter,but the abrupt evolution of lesions does not appropriately reflect the progressive pathological processes in human white matter hyperintensities.Vascular occlusive SIWMI models often do not exhibit white matter lesions that are sufficiently unequivocal to be quantified.When combined with comorbid vascular risk factors(specifically hypertension),however,they can produce progressive and definitive white matter lesions including diffuse rarefaction,demyelination,loss of oligodendrocytes,and glial activation,which are by far the closest to those found in human white matter hyperintensities lesions.However,considerable surgical mortality and unpredictable natural deaths during a follow-up period would necessitate further refinements in these models.In the meantime,in vitro SIWMI models that recapitulate myelinated white matter track may be utilized to study molecular mechanisms of the ischemic white matter injury.Appropriate in vivo and in vitro SIWMI models will contribute in a complementary manner to making a breakthrough in developing effective treatment to prevent progression of white matter hyperintensities. 展开更多
关键词 animal model axonal degeneration DEMYELINATION hypertension ischemia OLIGODENDROCYTES subcortical ischemic white matter injury vascular cognitive impairment white matter hyperintensities
在线阅读 下载PDF
Exosomes derived from human induced pluripotent stem cell-derived neural progenitor cells protect neuronal function under ischemic conditions 认领
14
作者 Wen-Yu Li Qiong-Bin Zhu +3 位作者 Lu-Ya Jin Yi Yang Xiao-Yan Xu Xing-Yue Hu 《中国神经再生研究:英文版》 SCIE CAS 2021年第10期2064-2070,共7页
Compared with other stem cells,human induced pluripotent stem cells-derived neural progenitor cells(iPSC-NPCs)are more similar to cortical neurons in morphology and immunohistochemistry.Thus,they have greater potentia... Compared with other stem cells,human induced pluripotent stem cells-derived neural progenitor cells(iPSC-NPCs)are more similar to cortical neurons in morphology and immunohistochemistry.Thus,they have greater potential for promoting the survival and growth of neurons and alleviating the proliferation of astrocytes.Transplantation of stem cell exosomes and stem cells themselves have both been shown to effectively repair nerve injury.However,there is no study on the protective effects of exosomes derived from iPSC-NPCs on oxygen and glucose deprived neurons.In this study,we established an oxygen-glucose deprivation model in embryonic cortical neurons of the rat by culturing the neurons in an atmosphere of 95%N2 and 5%CO2 for 1 hour and then treated them with iPSC-NPC-derived exosomes for 30 minutes.Our results showed that iPSC-NPC-derived exosomes increased the survival of oxygen-and glucose-deprived neurons and the level of brain-derived neurotrophic factor in the culture medium.Additionally,it attenuated oxygen and glucose deprivation-induced changes in the expression of the PTEN/AKT signaling pathway as well as synaptic plasticity-related proteins in the neurons.Further,it increased the length of the longest neurite in the oxygen-and glucose-deprived neurons.These findings validate the hypothesis that exosomes from iPSCNPCs exhibit a neuroprotective effect on oxygen-and glucose-deprived neurons by regulating the PTEN/AKT signaling pathway and neurite outgrowth.This study was approved by the Animal Ethics Committee of Sir Run Run Shaw Hospital,School of Medicine,Zhejiang University,China(approval No.SRRSH20191010)on October 10,2019. 展开更多
关键词 AKT cortical neurons EXOSOME ischemia neural progenitor cells neuronal protection oxygen and glucose deprivation pluripotent stem cells PTEN signaling pathway
在线阅读 下载PDF
急性心肌梗死并发缺血性二尖瓣反流的相关因素分析 认领
15
作者 张华 张宇 +3 位作者 张申伟 王明杰 夏开 厉菁 《中国实用医刊》 2021年第2期12-16,共5页
目的探讨急性心肌梗死并发缺血性二尖瓣反流(IMR)的相关因素。方法回顾性分析2017年5月至2020年6月郑州市第七人民医院心内科收治的急性心肌梗死患者360例。根据心脏超声心动图检查结果显示的二尖瓣反流情况将其分为两组:IMR组(108例)和... 目的探讨急性心肌梗死并发缺血性二尖瓣反流(IMR)的相关因素。方法回顾性分析2017年5月至2020年6月郑州市第七人民医院心内科收治的急性心肌梗死患者360例。根据心脏超声心动图检查结果显示的二尖瓣反流情况将其分为两组:IMR组(108例)和非IMR组(252例)。比较两组患者的基本信息、心肌梗死相关指标、血检结果、治疗及院内死亡情况。结果360例急性心肌梗死患者中,合并IMR共108例,IMR发生率为30%。IMR组患者年龄为(65.37±10.42)岁,大于非IMR组的(56.35±10.23)岁,差异有统计学意义(P<0.05);与非IMR组比较,IMR组Killip分级≥3级、三支病变、梗死位置在前壁心肌梗死患者所占比例较高(分别为9.26%比1.98%,39.81%比21.03%,45.37%比25.00%),但行血运重建患者比例较低(60.19%比86.90%),差异均有统计学意义(P<0.05);与非IMR组比较,IMR组左房内径(LA)、左室舒末内径(LVDD)、室壁运动计分(WMSI评分)、心率、二尖瓣反流程度(中-重度患者所占比例)明显偏高,分别为(42.01±5.43)mm比(36.54±3.54)mm,(58.01±5.34)mm比(51.03±4.02)mm,(2.62±0.42)分比(2.13±0.35)分,(75.60±11.24)次/min比(69.30±10.23)次/min,9.26%比1.98%,而左心室射血分数(LVEF)偏低,差异有统计学意义(P<0.05)。住院期间,两组B型尿钠肽(BNP)峰值、血红蛋白(HB)最低值分别为(1077.42±103.52)pg/ml比(358.48±57.32)pg/ml,(115.23±12.44)g/L比(123.01±13.51)g/L,经比较差异有统计学意义(P<0.05),两组直接经皮冠状动脉介入治疗(PCI)、血管紧张素转化酶抑制剂/血管紧张素Ⅱ受体拮抗剂(ACEI/ARB)、β受体阻滞剂、院内死亡所占比例分别为27.78%比57.14%,78.70%比88.10%,63.89%比75.00%,4.63%比1.19%,经比较差异有统计学意义(P<0.05)。Logistics多因素回归分析结果显示,年龄大、梗死位置在前壁、LVDD增大、心率增高、未行PCI是急性心肌梗死并发IMR的独立危险因素(P<0.05)。结论年龄、梗死位置、LVDD、心率、PCI是急性� 展开更多
关键词 心肌梗死 二尖瓣 反流 缺血性
激素性股骨头缺血坏死发病机制中的内质网应激 认领
16
作者 张煦坚 赵振群 刘万林 《中国组织工程研究》 CAS 北大核心 2021年第11期1759-1765,共7页
背景:激素性股骨头缺血坏死的发病机制尚不明确,可能与内质网应激有关,控制内质网应激信号通路可能调控细胞的自噬与凋亡,对该病具有一定的防治作用。目的:通过探讨内质网应激与激素引起的细胞自噬、细胞凋亡的相互关系,总结内质网应激... 背景:激素性股骨头缺血坏死的发病机制尚不明确,可能与内质网应激有关,控制内质网应激信号通路可能调控细胞的自噬与凋亡,对该病具有一定的防治作用。目的:通过探讨内质网应激与激素引起的细胞自噬、细胞凋亡的相互关系,总结内质网应激在激素性股骨头缺血坏死发病机制中的研究进展。方法:检索2000至2020年相关文献,以“内质网应激,股骨头坏死,未折叠蛋白反应,糖皮质激素,自噬,凋亡,缺血”为中文检索词检索CNKI、万方、维普数据库;以“endoplasmic reticulum stress,femur head necrosis,unfolded protein response,glucocorticoid,autophagy,apoptosis,ischaemia”为英文检索词检索PubMed、Web of science数据库。排除重复和较陈旧的文献及Meta分析,共81篇文献符合纳入标准。结果与结论:①未折叠蛋白反应为缓解内质网应激引发的3条下游信号通路可使细胞发生自噬和凋亡;②内质网应激与激素诱导的细胞自噬和凋亡及股骨头缺血有密切联系;③内质网应激可能是激素性股骨头缺血坏死发生过程中的病理环节,激素通过让细胞缺血缺氧激发内质网应激进而诱导细胞的自噬与凋亡,最终导致股骨头坏死。 展开更多
关键词 内质网应激 股骨头坏死 未折叠蛋白反应 糖皮质激素 自噬 凋亡 缺血
在线阅读 下载PDF
血管腔内介入治疗下肢严重缺血后急性肾损伤危险因素 认领
17
作者 梁永红 冯超 +2 位作者 梁顺添 陈清 周忠信 《中国介入影像与治疗学》 北大核心 2021年第2期91-94,共4页
目的探讨血管腔内介入治疗下肢严重肢体缺血(CLI)后急性肾损伤(AKI)危险因素。方法回顾性分析168例接受血管腔内介入治疗的下肢CLI患者,对比剂均为低渗型碘克沙醇,统计发生术后AKI例数,以单因素及多因素Logistic分析筛选AKI危险因素。结... 目的探讨血管腔内介入治疗下肢严重肢体缺血(CLI)后急性肾损伤(AKI)危险因素。方法回顾性分析168例接受血管腔内介入治疗的下肢CLI患者,对比剂均为低渗型碘克沙醇,统计发生术后AKI例数,以单因素及多因素Logistic分析筛选AKI危险因素。结果168例CLI患者中,42例(42/168,25.00%)术后发生AKI,其中1级AKI 31例,2级6例,3级5例;AKI与无AKI患者间年龄、合并糖尿病及慢性肾衰竭、术前糖化血红蛋白、血肌酐及肾小球滤过率(eGFR)差异均有统计学意义(P均<0.05)。多元Logistic回归分析结果显示,年龄及合并慢性心力衰竭、慢性肾衰竭、糖尿病均与AKI独立相关(P均<0.05)。结论血管腔内介入治疗CLI后发生AKI与患者年龄及术前并发慢性心力衰竭、慢性肾衰竭、糖尿病均有关。 展开更多
关键词 下肢 缺血 急性肾损伤 血管内治疗
在线阅读 下载PDF
Teriflunomide provides protective properties after oxygen-glucose-deprivation in hippocampal and cerebellar slice cultures 认领
18
作者 Anna Wolters Judith Reuther +4 位作者 Philipp Gude Thomas Weber Carsten Theiss Heike Vogelsang Veronika Matschke 《中国神经再生研究:英文版》 SCIE CAS 2021年第11期2243-2249,共7页
One of the major challenges in emergency medicine is out-of-hospital cardiac arrest(OHCA).Every year,about 53–62/100000 people worldwide suffer an out-of-hospital cardiac arrest with serious consequences,whereas pers... One of the major challenges in emergency medicine is out-of-hospital cardiac arrest(OHCA).Every year,about 53–62/100000 people worldwide suffer an out-of-hospital cardiac arrest with serious consequences,whereas persistent brain injury is a major cause of morbidity and mortality of those surviving a cardiac arrest.Today,only few and insufficient strategies are known to limit neurological damage of ischemia and reperfusion injury.The aim of the present study was to investigate whether teriflunomide,an approved drug for treatment of relapsing-remitting-multiple-sclerosis,exerts a protective effect on brain cells in an in vitro model of ischemia.Therefore,organotypic slice cultures from rat hippocampus and cerebellum were exposed to oxygen-glucose-deprivation and subsequently treated with teriflunomide.The administration of teriflunomide in the reperfusion time on both hippocampal and cerebellar slice cultures significantly decreased the amount of detectable propidium iodide signal compared with an untreated culture,indicating that more cells survive after oxygen-glucosedeprivation.However,hippocampal slice cultures showed a higher vulnerability to ischemic conditions and a more sensitive response to teriflunomide compared with cerebellar slice cultures.Our study suggests that teriflunomide,applied as a post-treatment after an oxygenglucose-deprivation,has a protective effect on hippocampal and cerebellar cells in organotypic slice cultures of rats.All procedures were conducted under established standards of the German federal state of North Rhine Westphalia,in accordance with the European Communities Council Directive 2010/63/EU on the protection of animals used for scientific purposes. 展开更多
关键词 brain damage cardiac arrest cell death hypoxic chamber ischemia organotypic slice cultures POST-TREATMENT RESUSCITATION
在线阅读 下载PDF
Effect of remote ischemic preconditioning among donors and recipients following pediatric liver transplantation:A randomized clinical trial 认领
19
作者 Bo Qi Xiao-Qiang Wang +5 位作者 Shu-Ting Pan Pei-Ying Li Ling-Ke Chen Qiang Xia Li-Qun Yang Wei-Feng Yu 《世界胃肠病学杂志:英文版》 SCIE CAS 2021年第4期345-357,共13页
BACKGROUND Studies suggested that remote ischemic preconditioning(RIPC)may effectively lessen the harmful effects of ischemia reperfusion injury during organ transplantation surgery.AIM To investigate the protective e... BACKGROUND Studies suggested that remote ischemic preconditioning(RIPC)may effectively lessen the harmful effects of ischemia reperfusion injury during organ transplantation surgery.AIM To investigate the protective effects of RIPC on living liver donors and recipients following pediatric liver transplantation.METHODS From January 2016 to January 2019 at Renji Hospital Affiliated with Shanghai Jiao Tong University School of Medicine,208 donors were recruited and randomly assigned to four groups:S-RIPC group(no intervention;n=55),D-RIPC group(donors received RIPC;n=51),R-RIPC group(recipients received RIPC,n=51)and DR-RIPC group(both donors and recipients received RIPC;n=51).We primarily evaluated postoperative liver function among donors and recipients and incidences of early allograft dysfunction,primary nonfunction and postoperative complications among recipients.RESULTS RIPC did not significantly improve alanine transaminase and aspartate aminotransferase levels among donors and recipients or decrease the incidences of early allograft dysfunction,primary nonfunction,and postoperative complications among recipients.Limited protective effects were observed,including a lower creatinine level in the D-RIPC group than in the S-RIPC group on postoperative day 0(P<0.05).However,no significant improvements were found in donors who received RIPC.Furthermore,RIPC had no effects on the overall survival of recipients.CONCLUSION The protective effects of RIPC were limited for recipients who received living liver transplantation,and no significant improvement of the prognosis was observed in recipients. 展开更多
关键词 Pediatric liver transplantation Remote ischemic preconditioning Postoperative complications Ischemia reperfusion injury Primary nonfunction HEPATOLOGY
在线阅读 免费下载
Microglial activation and adult neurogenesis after brain stroke 认领
20
作者 Ijair R.C.dos Santos Michelle Nerissa C.Dias Walace Gomes-Leal 《中国神经再生研究:英文版》 SCIE CAS 2021年第3期456-459,共4页
The discovery that new neurons are produced in some regions of the adult mammalian brain is a paradigm-shift in neuroscience research.These new-born cells are produced from neuroprogenitors mainly in the subventricula... The discovery that new neurons are produced in some regions of the adult mammalian brain is a paradigm-shift in neuroscience research.These new-born cells are produced from neuroprogenitors mainly in the subventricular zone at the margin of the lateral ventricle,subgranular zone in the hippocampal dentate gyrus and in the striatum,a component of the basal ganglia,even in humans.In the human hippocampus,neuroblasts are produced even in elderlies.The regulation of adult neurogenesis is a complex phenomenon involving a multitude of molecules,neurotransmitters and soluble factors released by different sources including glial cells.Microglia,the resident macrophages of the central nervous system,are considered to play an important role on the regulation of adult neurogenesis both in physiological and pathological conditions.Following stroke and other acute neural disorders,there is an increase in the numbers of neuroblast production in the neurogenic niches.Microglial activation is believed to display both beneficial and detrimental role on adult neurogenesis after stroke,depending on the activation level and brain location.In this article,we review the scientific evidence addressing the role of microglial activation on adult neurogenesis after ischemia.A comprehensive understanding of the microglial role after stroke and other neural disorders it is an important step for development of future therapies based on manipulation of adult neurogenesis. 展开更多
关键词 adult neurogenesis HIPPOCAMPUS ISCHEMIA MICROGLIA NEUROINFLAMMATION NEUROPROTECTION STROKE subventricular zone therapy
在线阅读 下载PDF
上一页 1 2 250 下一页 到第
使用帮助 返回顶部 意见反馈