Anatomical phenotyping in the brain and skull of a mutant mouse by magnetic resonance imaging and computed tomography
Anatomical phenotyping in the brain and skull of a mutant mouse by magnetic resonance imaging and computed tomography
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DOI：
10.1152/physiolgenomics.00217.2005
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发表时间：
2006-01-12
影响因子：
4.6
通讯作者：
Sled, JG
中科院分区：
文献类型：
--
作者：
Nieman, BJ;Flenniken, AM;Sled, JG
由于转基因小鼠作为人类疾病的模型在生物医学研究中变得越来越普遍，因此对评估小鼠表型的有效和定量方法的需求也在增长。表型分型的一种有力手段是对突变体与正常群体的解剖特征进行表征。解剖表型需要对原位结构进行可视化，对小鼠群体之间复杂形状差异进行量化，并在高通量调查工作中检测细微或弥漫性异常。这些目标可以通过临床放射学的成像技术来实现，例如磁共振成像和计算机断层扫描。这些成像技术为活体个体或标本的解剖可视化提供了一种极好的非破坏性方法。然后，对这些图像进行基于计算机的分析，可以进行彻底的解剖表征。我们提出了一种自动分析多图像数据集的方法。该方法利用图像配准来识别对照组和突变组之间对应的解剖结构。组内和组间的形状差异用于绘制解剖结构显著不同的区域。这些区域被突出显示，并用位移和体积变化定量地表示。该方法在由n -乙基-n -亚硝基脲诱变产生的部分特征小鼠突变中得到了证明，该突变是人类眼齿发育不良综合征的假定模型，由编码连接蛋白43的基因的点突变引起。
Since genetically modified mice have become more common in biomedical research as models of human disease, a need has also grown for efficient and quantitative methods to assess mouse phenotype. One powerful means of phenotyping is characterization of anatomy in mutant vs. normal populations. Anatomical phenotyping requires visualization of structures in situ, quantification of complex shape differences between mouse populations, and detection of subtle or diffuse abnormalities during high-throughput survey work. These aims can be achieved with imaging techniques adapted from clinical radiology, such as magnetic resonance imaging and computed tomography. These imaging technologies provide an excellent nondestructive method for visualization of anatomy in live individuals or specimens. The computer-based analysis of these images then allows thorough anatomical characterizations. We present an automated method for analyzing multiple-image data sets. This method uses image registration to identify corresponding anatomy between control and mutant groups. Within-and between-group shape differences are used to map regions of significantly differing anatomy. These regions are highlighted and represented quantitatively by displacements and volume changes. This methodology is demonstrated for a partially characterized mouse mutation generated by N-ethyl-N-nitrosourea mutagenesis that is a putative model of the human syndrome oculodentodigital dysplasia, caused by point mutations in the gene encoding connexin 43.