英[dɪˈɡreɪdɪŋ ] 美[dɪˈɡreɪdɪŋ ]






adj. 丧失体面的,可耻的,不名誉的


  • 1.Furthermore, senescent activated stellate cells exhibit gene expression profile consistent with cell-cycle exit, reduced secretion of extracellular matrix components, enhanced secretion of extracellular matrix-degrading enzymes, and enhanced immune surveillance.


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  • 2.Methods and Results— Atherosclerotic carotid plaques were obtained from 804 symptomatic (stroke=204 and TIA=426) and asymptomatic (n=174) patients undergoing carotid endarterectomy. The presence of macrophages, smooth muscle cells (SMC), collagen, calcification, and lipid-core size were assessed histologically. At protein level, inflammatory mediators (interleukin [IL]-2, IL-4, IL-5, IL-8, IL-10, IL-12p70, interferon-gamma [INF- ], tumor necrosis factor-alpha [TNF- ], matrix degrading proteinases (MMPs), and an apoptosis marker (caspase-3) were determined. We associated plaque characteristics with time elapsed between the latest event and surgery. Early after stroke and TIA, plaques revealed an unstable phenotype. After stroke, the content of macrophages decreased significantly with time (P=0.02), whereas SMC contenttended to increase. At protein level, IL-6, IL-8 expression levels and caspase activity strongly decreased after stroke or TIA.

    方法和结果:颈动脉粥样硬化斑块来自于804名有症状(中风=204和短暂性脑缺血发作=426)和无症状的病人(n=174),他们都接受了动脉内膜剥脱术。从组织学的角度对巨噬细胞、平滑肌细胞(SMC)、胶原、钙化和脂核的大小都被评价。在蛋白水平,炎症介质如白介素(IL-2、4、5、8、10和12p70,干扰素γ [INF-γ],肿瘤坏死因子α[TNF-α],基质金属蛋白酶(MMPs)以及凋亡标志物(caspase-3)被进行了检测。我们将斑块的特征与最后一次事件与手术之间的时间联系后进行观察。在中风和短暂性脑缺血发作的早期,斑块显示出一个不稳定的状态。在中风后,随着时间推移,巨噬细胞的数目明显下降(P=0.02),而SMC上升。在蛋白水平,在中风或TIA后,IL-6、IL-8的表达水平和激酶活性强烈的下降。

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  • 3.Hyperglycaemia and hyperinsulinaemia:is insulin-degrading enzyme the missing link?


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  • 4.Autophagy is a process by which a cell responds to starvation and other stresses by degrading damaged or unneeded parts of itself to produce energy. It is sometimes called the cell's housekeeping pathway.


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  • 5.Castration-resistant prostate cancer (CRPC) is an advanced form of prostate cancer that occurs when the disease progresses after treatment with androgen deprivation therapy. Galeterone works against CRPC by blocking the androgen receptor, reducing levels of the ligand that binds to the receptor and degrading the androgen receptor protein.


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