3D RENDITION/QUANTITATIVE ANALYSIS GI2 DEFICIENT MICE

该子项目是利用NIH/NCRR资助的中心赠款提供的资源的许多研究子项目之一。子项目和研究者（PI）可能从另一个NIH来源获得主要资金，因此可以在其他CRISP条目中表示。所列机构为中心，不一定是研究者所在机构。编码（Gi 2信号传导蛋白的α亚基）的基因被破坏的小鼠发生类似于人类溃疡性结肠炎（UC; 1，2）的炎性肠病，并表现出肠道派尔集合淋巴结数量减少。 MRM成像提供了一个独特的机会，以获得相关的形态学数据。这些变化是100%渗透性的，这意味着它们发生在所有突变动物中，这使得Gi 2小鼠成为开发和微调技术和计算改进的良好模型，使MRM成为科学界可用的工具。 从野生型小鼠中制备组织学切片与从Gi 2小鼠中制备的组织学切片在登记中的问题使得很难定性和定量地描述Gi 2小鼠小脑中的结构改变。使用传统的连续组织学方法，如果不付出巨大的努力，不花费大量的人力，不手工记录容易出现与手工annotation相关的错误的数据，就不可能获得深入的了解。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Mice with a disrupted gene encoding (alpha subunit of Gi2 signaling protein) develop inflammatory bowel disease resembling human ulcerative colitis (UC; 1,2) and exhibit reduced number of intestinal Peyers patches. MRM imaging offers a unique opportunity to obtain relevant morphometric data. The changes are 100% penetrant, meaning they occur in all mutant animals, which makes the Gi2 mouse a good model for development and fine tuning of technical and computational refinements needed to make MRM an accessible tool to the scientific community. Problems preparing histological cuts from wild type mice in registry with those prepared from Gi2 mice make it very difficult to both qualitatively and quantitatively describe structural alterations in cerebellums of Gi2 mice. Insight is impossible to obtain using conventional serial histology without a major effort, innumerable manpower hours and manual recording of the data susceptible to errors associated with manual anno