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本文引用的文献

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A Gamma-Knife-Enabled Mouse Model of Cerebral Single-Hemisphere Delayed Radiation Necrosis.一种用于脑单半球延迟性放射性坏死研究的伽玛刀小鼠模型。
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2
Perilesional edema in radiation necrosis reflects axonal degeneration.放射性坏死中的病灶周围水肿反映了轴突退变。
Radiat Oncol. 2015 Jan 31;10:33. doi: 10.1186/s13014-015-0335-6.
3
Toward distinguishing recurrent tumor from radiation necrosis: DWI and MTC in a Gamma Knife--irradiated mouse glioma model.针对复发性肿瘤与放射性坏死的鉴别:伽玛刀照射的小鼠脑胶质瘤模型中的 DWI 和 MTC。
Int J Radiat Oncol Biol Phys. 2014 Oct 1;90(2):446-53. doi: 10.1016/j.ijrobp.2014.06.015. Epub 2014 Aug 4.
4
A GSK-3β inhibitor protects against radiation necrosis in mouse brain.GSK-3β 抑制剂可预防小鼠脑辐射坏死。
Int J Radiat Oncol Biol Phys. 2014 Jul 15;89(4):714-21. doi: 10.1016/j.ijrobp.2014.04.018.
5
Anti-VEGF antibodies mitigate the development of radiation necrosis in mouse brain.抗血管内皮生长因子(VEGF)抗体可减轻小鼠脑部放射性坏死的发展。
Clin Cancer Res. 2014 May 15;20(10):2695-702. doi: 10.1158/1078-0432.CCR-13-1941. Epub 2014 Mar 19.
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Radiation-induced brain injury: A review.放射性脑损伤:综述。
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7
Assessment of MRI parameters as imaging biomarkers for radiation necrosis in the rat brain.评估 MRI 参数作为大鼠脑放射性坏死的影像学生物标志物。
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8
Development of a novel animal model to differentiate radiation necrosis from tumor recurrence.开发一种新型动物模型以区分放射性坏死与肿瘤复发。
J Neurooncol. 2012 Jul;108(3):411-20. doi: 10.1007/s11060-012-0846-z. Epub 2012 Mar 10.
9
Radiation necrosis following treatment of high grade glioma--a review of the literature and current understanding.高级别脑胶质瘤治疗后放射性坏死——文献复习与目前认识。
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10
Evaluation of radiation necrosis and malignant glioma in rat models using diffusion tensor MR imaging.应用弥散张量磁共振成像评价大鼠模型中的放射性坏死和恶性胶质瘤。
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辐射剂量对大鼠模型中辐射诱导的脑坏死的发生和进展的影响。

The effect of radiation dose on the onset and progression of radiation-induced brain necrosis in the rat model.

作者信息

Hartl Brad A, Ma Htet S W, Hansen Katherine S, Perks Julian, Kent Michael S, Fragoso Ruben C, Marcu Laura

机构信息

a Department of Biomedical Engineering , University of California Davis , Davis , CA , USA.

b Department of Surgical and Radiological Sciences , University of California Davis School of Veterinary Medicine , Davis , CA , USA.

出版信息

Int J Radiat Biol. 2017 Jul;93(7):676-682. doi: 10.1080/09553002.2017.1297902. Epub 2017 Mar 17.

DOI:10.1080/09553002.2017.1297902
PMID:28306402
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5751742/
Abstract

PURPOSE

To provide a comprehensive understanding of how the selection of radiation dose affects the temporal and spatial progression of radiation-induced necrosis in the rat model.

MATERIALS AND METHODS

Necrosis was induced with a single fraction of radiation exposure, at doses ranging between 20 and 60 Gy, to the right hemisphere of 8-week-old Fischer rats from a linear accelerator. The development and progression of necrosis in the rats was monitored and quantified every other week with T1- and T2-weighted gadolinium contrast-enhanced MRI studies.

RESULTS

The time to onset of necrosis was found to be dose-dependent, but after the initial onset, the necrosis progression rate and total volume generated was constant across different doses ranging between 30 and 60 Gy. Radiation doses less than 30 Gy did not develop necrosis within 33 weeks after treatment, indicating a dose threshold existing between 20 and 30 Gy.

CONCLUSION

The highest dose used in this study led to the shortest time to onset of radiation-induced necrosis, while producing comparable disease progression dynamics after the onset. Therefore, for the radiation-induced necrosis rat model using a linear accelerator, the most optimum results were generated from a dose of 60 Gy.

摘要

目的

全面了解辐射剂量的选择如何影响大鼠模型中辐射诱导坏死的时间和空间进展。

材料与方法

使用直线加速器对8周龄的Fischer大鼠右半球进行单次辐射暴露,剂量范围为20至60 Gy,诱导坏死。每隔一周通过T1加权和T2加权钆对比增强MRI研究监测和量化大鼠坏死的发生和进展。

结果

发现坏死开始时间与剂量相关,但在最初发病后,坏死进展率和产生的总体积在30至60 Gy的不同剂量范围内是恒定的。小于30 Gy的辐射剂量在治疗后33周内未发生坏死,表明在20至30 Gy之间存在剂量阈值。

结论

本研究中使用的最高剂量导致辐射诱导坏死的发病时间最短,同时在发病后产生相当的疾病进展动态。因此,对于使用直线加速器的辐射诱导坏死大鼠模型,60 Gy的剂量产生了最理想的结果。