Response to Ballabh and LaGamma.
Response to Ballabh and LaGamma.
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对 Ballabh 和 LaGamma 的回应。
DOI：
10.1038/pr.2014.112
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发表时间：
2014
影响因子：
3.6
通讯作者：
Juul,SandraE
中科院分区：
文献类型：
--
作者：
Traudt,ChristopherM;Juul,SandraE
致编辑：我们要感谢 Ballabh 博士和 LaGamma 博士对我们关于甘油对大脑发育的影响的文章 (2) 的评论 (1)。我们同意甘油诱导的脑室内出血模型显示了血液在阻碍少突胶质细胞发育和白质损伤的原因中的重要性。他们在没有甘油的情况下使用脑切片进行的补充工作产生了与体内模型相似的结果，从而加强了甘油注射模型的发现。然而，我们不能排除甘油正在减少小脑增殖的可能性。甘油对许多细胞类型具有已知的抗增殖作用 (3, 4)。大脑内的神经发生大部分是在感兴趣的时间范围内完成的。相比之下，小脑在甘油暴露期间正在经历大量的神经发生。随着甘油剂量的增加，小脑尺寸减小，而暴露于甘油的试剂盒之间的脑室内出血或身体生长率没有差异，这使得甘油受到怀疑。小脑中甘油浓度的增加进一步支持甘油是罪魁祸首。我们很少看到不到 48 小时的早期死亡，因为大多数死亡发生在第 3 天至第 5 天之间。在我们的研究中，我们根本没有看到任何癫痫发作，这可能是由于超声和尸检证实的脑室内出血率较低。被发现死亡的动物都按照死前的情况用瓶装喂养。没有发现肺部有牛奶的证据。然而，肠道显示出积气的迹象。我们无法确定死亡时间，因此这些发现可能是正常的尸检变化，而不是坏死性小肠结肠炎。在幼崽之间清洁乳头，但事实上它们是瓶装喂养而不是强饲喂养，这可能是一个促成因素。我们并不是唯一发现兔子脑室内出血情况不一致的组。库尔特等人。在接受 225 个试剂盒（所有试剂盒均接受多剂量甘油和其他药物）后，未出现脑室内出血 (5)。事实上，我们从不同的供应商处获得动物可能是 Coulter 等人研究中最大的差异。总部设在犹他州，而洛伦佐等人。在波士顿 (5, 6)。在开发出新的后颅窝出血小鼠模型后，我们认为蛛网膜下腔出血可能解释或促成我们使用甘油模型注意到的小脑变化，因为我们在仅接触血液后看到了类似的小脑病理学。虽然我们承认 Ballabh 博士小组使用甘油诱导的 IVH 模型得出的脑部病理学和神经保护发现的重要性，但我们发现直接将血液注入后颅窝为研究小脑损伤提供了更一致的模型。
To the Editor: We would like to thank Drs Ballabh and LaGamma for their comments (1) regarding our article (2) on the effects of glycerol on the developing brain. We agree that the glycerol-induced intraventricular hemorrhage model has shown the importance of blood on hindering the development of oligodendrocytes and being a cause of white matter injury. Their complementary work using cerebral slices in the absence of glycerol has yielded similar results as the in vivo model thereby strengthening the findings of the glycerol injection model. However, we could not rule out the possibility that glycerol was decreasing proliferation in the cerebellum. Glycerol has known anti-proliferative effects on many cell types (3, 4). Neurogenesis within the cerebrum is for the most part completed by the time frame of interest. In contrast, the cerebellum is undergoing massive neurogenesis during the time of glycerol exposure. The decrease in cerebellar size as the dose of glycerol was increased, without differences in rates of intraventricular hemorrhage or body growth between glycerol-exposed kits makes glycerol suspect. The increase in glycerol concentration in the cerebellum further supports glycerol as a culprit. We saw very few early deaths at less than 48 h, as most of the deaths occurred between days 3 and 5. We did not see any seizures at all in our study and this is likely due to our low rate of intraventricular hemorrhage, confirmed by ultrasound and at necropsy. Animals that were found dead had bottled fed perfectly the feeding before death. No evidence of milk in the lungs was ever found. However, the intestines showed evidence of pneumatosis. We were unable to tell time of death so these findings may be normal post mortem changes and not necrotizing enterocolitis. Nipples were cleaned between pups, but the fact that they were bottled fed instead of gavage fed may have been a contributing factor.We are not the only group to see that intraventricular hemorrhage is not consistent in rabbits. Coulter et al. had no intraventricular hemorrhage after 225 kits with all of them receiving multiple doses of glycerol and additional agents (5). The fact that we obtained our animals from a different vendor may be the biggest difference in the study as Coulter et al. were based in Utah while Lorenzo et al. were in Boston (5, 6). After developing a new mouse model of posterior fossa hemorrhage, we believe that subarachnoid hemorrhages may account for or contribute to the cerebellar changes we noted using the glycerol model, as we are seeing similar cerebellar pathology after exposure to only blood. While we acknowledge the importance of cerebral findings of both pathology and neuroprotection by Dr Ballabh’group using the glycerol-induced IVH model, we have found that direct injection of blood into the posterior fossa provides a more consistent model for studying cerebellar injury.
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DOI：
10.1016/s0021-9258(17)42691-3
发表时间：
1984-12
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
J. V. van Mourik;D. Lawrence;D. Loskutoff
通讯作者：
J. V. van Mourik;D. Lawrence;D. Loskutoff
尿激酶催化 NH2 末端谷氨酸纤溶酶原转化为纤溶酶的动力学研究。
DOI：
10.1016/0005-2744(77)90297-2
发表时间：
1977
期刊：
Biochimica et biophysica acta
影响因子：
--
作者：
U. Christensen
通讯作者：
U. Christensen
内皮细胞产生纤溶酶原激活剂的潜在抑制剂，可以被变性剂激活。
DOI：
--
发表时间：
1985
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
Hekman,CM;Loskutoff,DJ
通讯作者：
Loskutoff,DJ
天然和重组组织型纤溶酶原激活剂激活纤溶酶原的动力学。
影响因子：
4.8
作者：
C. Zamarron;R. Lijnen;D. Collen
通讯作者：
D. Collen
从人血浆中分离组织型纤溶酶原激活剂-抑制剂复合物。
DOI：
10.1016/0304-4165(84)90040-0
发表时间：
1984
期刊：
Biochimica et biophysica acta
影响因子：
--
作者：
S. Thorsen;M. Philips
通讯作者：
M. Philips