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CircR-ZC3HC1 mediates MiR-384-5p/SIRT1 axis to promote neuronal autophagy and relieves ischemic stroke
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作者 MIN SHEN XIAOMAN XU +6 位作者 GUANGLING SUN LIANGZHU WANG TAO YING HANG SU WEI WANG QINGHUA CAO ZHEZHE SUN 《BIOCELL》 SCIE 2024年第3期491-499,共9页
Objective:Circular RNAs(circRNAs)have been shown to involve in pathological processes of ischemic stroke(IS),including autophagy.This study was designed to explore the effect of circR-ZC3HC1 on neuronal autophagy in I... Objective:Circular RNAs(circRNAs)have been shown to involve in pathological processes of ischemic stroke(IS),including autophagy.This study was designed to explore the effect of circR-ZC3HC1 on neuronal autophagy in IS and the related mechanisms.Methods:Expression of circR-ZC3HC1 in blood samples of IS patients and healthy controls was detected.Hippocampal neurons were treated with oxygen and glucose deprivation(OGD)to establish IS in vitro model.The expression of LC3 and p62 and the number of autophagosomes were examined to evaluate the autophagy level of OGD induced neurons using western blotting and transmission electron microscope.Cell apoptosis rate and the expression of cleaved caspase-3,Bax,and Bcl-2 were assessed byflow cytometry and western blotting.The binding relationships among circR-ZC3HC1,miR-384-5p,and SIRT1 were predicted and verified.Results:Low expression of circR-ZC3HC1 was found in blood samples of IS patients and OGD-treated neurons.Overexpressed circR-ZC3HC1 or inhibited miR-384-5p expression promoted autophagy and inhibited apoptosis of OGD-treated neurons,which could be reversed by further 3-MA treatment.Mechanistically,circR-ZC3HC1 targeted miR-384-5p to mediate SIRT1 expression.miR-384-5p overexpression or SIRT1 knockdown in the presence of circR-ZC3HC1 overexpression in OGD-treated neurons lead to reduced autophagy and enhanced apoptosis.Conclusion:Collectively,circR-ZC3HC1 promoted neuronal autophagy to attenuate IS via miR-384-5p/SIRT1 axis. 展开更多
关键词 Ischemic stroke circr-zc3hc1 miR-384-5p SIRT1 AUTOPHAGY
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MTSS1和RBCK1在卵巢癌组织中的表达及其与临床病理特征和预后的关系
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作者 徐琳琳 刘振娟 +1 位作者 张子轩 李彦霞 《临床和实验医学杂志》 2024年第17期1848-1852,共5页
目的 回顾性探讨卵巢癌组织中肿瘤转移抑制基因1(MTSS1)、ranbp2型和c3hc4型锌指1(RBCK1)表达、患者临床病理特征与预后的关系。方法 回顾性收集2021年8月至2023年8月期间青岛大学附属青岛市海慈医院(青岛市中医医院)收治的120例卵巢癌... 目的 回顾性探讨卵巢癌组织中肿瘤转移抑制基因1(MTSS1)、ranbp2型和c3hc4型锌指1(RBCK1)表达、患者临床病理特征与预后的关系。方法 回顾性收集2021年8月至2023年8月期间青岛大学附属青岛市海慈医院(青岛市中医医院)收治的120例卵巢癌患者在术中切除的卵巢癌癌组织及其癌旁组织标本。行免疫组织化学法检测卵巢癌组织和癌旁组织中MTSS1、RBCK1的表达,并收集患者的临床资料[年龄、分化程度、淋巴结转移、国际妇产科学联合会(FIGO)分期、病理类型、腹水];采用Spearman相关性分析卵巢癌组织中MTSS1与RBCK1表达的相关性;采用Kaplan-Meier法分析卵巢癌组织MTSS1、RBCK1表达与患者预后的关系;采用Cox回归分析卵巢癌患者预后的影响因素。结果 卵巢癌组织MTSS1、RBCK1阳性表达率分别为26.67%、23.33%,低于癌旁组织MTSS1、RBCK1阳性表达率(62.50%、74.17%),差异均有统计学意义(P<0.05)。临床资料比较显示,MTSS1、RBCK1表达水平与FIGO分期、淋巴结转移及分化程度有关(P<0.05);Spearman相关分析卵巢癌组织中MTSS1和RBCK1的之间表达呈正相关(r=0.812,P<0.05)。生存分析结果显示,卵巢癌组织MTSS1、RBCK1阳性表达患者5年生存率为84.37%、82.14%,均高于MTSS1、RBCK1阴性表达患者(55.68%、57.60%),差异均有统计学意义(P<0.05)。低分化程度、FIGO分期Ⅲ+Ⅳ期、淋巴结转移、RBCK1阴性表达和MTSS1阴性表达均是卵巢癌患者死亡的危险因素(P<0.05)。结论 MTSS1、RBCK1在卵巢癌患者中低表达,且两者表达水平与淋巴结转移、FIGO分期、分化程度有关,二者可能是影响卵巢癌患者预后的特异性指标。 展开更多
关键词 卵巢肿瘤 肿瘤转移抑制基因1 ranbp2型和c3hc4型锌指1 临床病理特征 预后
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浅析HClO HC1O_2 HC1O_3 HC1O_4的氧化性强弱顺序 被引量:1
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作者 贺金虎 《安庆师范学院学报(自然科学版)》 2004年第1期115-116,119,共3页
关键词 hcIO hc1O2 hc1O3 hc1O4 氧化性 无机含氧酸
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HCl Dry Removal with Modified Ca-Based Sorbents at Moderate to High Temperatures 被引量:3
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作者 DezhenChen XiongpingWang +1 位作者 TongZhu HeshengZhang 《Journal of Thermal Science》 SCIE EI CAS CSCD 2003年第3期283-288,203,共7页
Modified Ca-based sorbents were obtained by adding sodium alkali into Ca(OH)2 and CaCO3. Reactive properties of modified Ca-based sorbents with acidic gases were investigated through reacting with gaseous HC1 at 450-... Modified Ca-based sorbents were obtained by adding sodium alkali into Ca(OH)2 and CaCO3. Reactive properties of modified Ca-based sorbents with acidic gases were investigated through reacting with gaseous HC1 at 450-760℃, and SEM and XRD technologies were adopted to get information on the reaction mechanism. Experimental data showed that HC1 dry removal efficiencies increased with temperature before 700℃ for all of the investigated sorbents, and there existed improved sorbents that corresponded to the highest removal efficiencies under the similar conditions. SEM photographs exhibited morphology difference between original and improved sorbents both before and after the reaction; and displayed that improved sorbents formed more porous product layers than original sorbents especially at higher temperature when product sintering became heavier, which is favorable to HC1 dry removal. XRD analysis showed that (1) improved Ca(OH)2 and CaCO3 were less crystalline than original lime and limestone; (2) the reaction product species of improved Ca(OH)2 changed with reaction temperature, while for original Ca(OH)2 the same product species appeared for all of the tested temperatures; and (3) for improved CaCO3, the only product at lower temperatures was CaCl2.2H2O and more product species were produced when temperature was higher than 650℃, but no CaCl2.Ca(OH)2.H2O formed at 700℃, while for the case of original CaCO3, the undesired CaCl2.Ca(OH)2.H2O appeared at 700℃. Presently, reaction temperature interval of 650-700℃ is recommended for improved Ca(OH2) to get the highest efficiency, for improved CaCO3 reaction at higher temperature deserves further investigation to make a good choice. 展开更多
关键词 hc1 dry removal improved Ca(OH)2 and CaCO3 Ca-based sorbent reaction temperature product species
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Zosuquidar逆转肝癌患者多药耐药性
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作者 王海 刘巧玉 +1 位作者 邵文雨 黄志勇 《江苏医药》 CAS CSCD 北大核心 2011年第7期809-811,共3页
目的利用第三代P糖蛋白(Pgp)抑制剂zosuquidar.3HC1(LY335979)逆转人肝癌化疗耐药性。方法 60例未经治疗的原发性肝癌患者先后行两次99mTc-甲氧基异丁基异腈(99mTc-MIBI)单光子发射计算机断层成像术(SPECT)检测:经外周静脉注射20 mCi99m... 目的利用第三代P糖蛋白(Pgp)抑制剂zosuquidar.3HC1(LY335979)逆转人肝癌化疗耐药性。方法 60例未经治疗的原发性肝癌患者先后行两次99mTc-甲氧基异丁基异腈(99mTc-MIBI)单光子发射计算机断层成像术(SPECT)检测:经外周静脉注射20 mCi99mTc-MIBI后15、120 min行平面显像,半定量分析肿物部位的摄取比值(UR)。第1次SPECT检测后,口服zosuquidar.3HC1 500 mg/d,连续3 d后进行第2次SPECT检测,两次检测结果进行对照比较。结果 60例中,肿瘤部位99mTc-MIBI被排空50例(83.3%),经zosuquidar.3HC1治疗后第2次SPECT检测发现,肿瘤部位出现明显的99mTc-MIBI浓聚。结论 Zosuquidar.3HC1作为一种新型Pgp逆转剂可有效逆转临床肝癌患者的多药耐药性。 展开更多
关键词 肝癌 多药耐药 99mTc-甲氧基异丁基异腈 Zosuquidar.3hc1
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