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4篇 您的检索式:作者名="Adam Timmis"
    题名 作者 年代 出处 被引量
1冠状动脉介入治疗稳定性心绞痛ORBITA挑战心脏病专家,在选择经皮冠状动脉介入治疗的患者时要更加严格显示文摘十余年前,随机临床试验COURAGE研究显示,经皮冠状动脉介入治疗(PCI)未能降低已接受最佳药物治疗的稳定性冠心病患者的死亡或心肌梗死风险。PCI对延缓动脉粥样硬化病变进展无效,但却成为临床最常用的恢复冠状动脉灌注和缓解劳力性心绞痛的治疗方法。Adam Timmis Andrew Wragg 刘冬(译) 袁建松(校) 2019英国医学杂志中文版2019,22,4:0
2治疗心绞痛的新药显示文摘心绞痛是心肌缺血所致的疼痛,通常由阻塞性冠状动脉疾病所致.虽然典型心绞痛表现为劳力性胸痛,但患者也可有不典型症状,Daniel A Jones Adam Timmis Andrew Wragg 苏冠华(译) 李景东(校) 2014英国医学杂志中文版2014,,1:0
3急性冠状动脉综合征显示文摘急性冠状动脉综合征(ACS),或称“心脏病突发”,包括不稳定性心绞痛(UA)和急性心肌梗死(AMI)。后者根据心电图改变进一步分为非sT段抬高型心肌梗死(NSTEMI)和ST段抬高型心肌梗死(STEMI),英国国家急性心肌梗死入院注册登记显示两者所占比例分别为61%和39%。Adam Timmis 徐娜 2016英国医学杂志中文版2016,0,2:0
4Chimera RNA interference knockdown of γ-synuclein in human cortical astrocytes results in mitotic catastrophe显示文摘Elevated levels of γ-synuclein(γ-syn)expression have been noted in the progression of glioblastomas,and also in the cerebrospinal fluid of patients diagnosed with neurodegenerative diseases.γ-Syn can be either internalized from the extracellular milieu or expressed endogenously by human cortical astrocytes.Internalizedγ-syn results in increased cellular proliferation,brain derived neurotrophic factor release and astroprotection.However,the function of endogenousγ-syn in primary astrocytes,and the relationship to these two opposing disease states are unknown.γ-Syn is expressed by astrocytes in the human cortex,and to gain a better understanding of the role of endogenous γ-syn,primary human cortical astrocytes were treated with chimera RNA interference(RNAi)targeting γ-syn after release from cell synchronization.Quantitative polymerase chain reaction analysis demonstrated an increase in endogenousγ-syn expression 48 hours after release from cell synchronization,while RNAi reduced γ-syn expression to control levels.Immunocytochemistry of Ki67 and 5-bromodeoxyuridine showed chimera RNAi γ-syn knockdown reduced cellular proliferation at 24 and 48 hours after release from cell synchronization.To further investigate the consequence of γ-syn knockdown on the astrocytic cell cycle,phosphorylated histone H3 pSer10(pHH3)and phosphorylated cyclin dependent kinase-2 pTyr15(pCDK2)levels were observed via western blot analysis.The results revealed an elevated expression of pHH3,but not pCDK2,indicating γ-syn knockdown leads to disruption of the cell cycle and chromosomal compaction after 48 hours.Subsequently,flow cytometry with propidium iodide determined that increases in apoptosis coincided with γ-syn knockdown.Therefore,γ-syn exerts its effect to allow normal astrocytic progression through the cell cycle,as evidenced by decreased proliferation marker expression,increased pHH3,and mitotic catastrophe after knockdown.In this study,we demonstrated that the knockdown of γ-syn within primary human cortical astrocytes using chimera RNAi leads to cell cycle disruption and apoptosis,indicating an essential role for γ-syn in regulating normal cell division in astrocytes.Therefore,disruption to γ-syn function would influence astrocytic proliferation,and could be an important contributor to neurological diseases.Timmy Le Cynthia L.Winham Fotis Andromidas Adam C.Silver Evan R.Jellison Aime A.Levesque Andrew O.Koob 2020Neural Regeneration Research2020,15,10:0
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