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本文引用的文献

1
Deficiency in Six2 during prenatal development is associated with reduced nephron number, chronic renal failure, and hypertension in Br/+ adult mice.产前发育期间Six2的缺乏与Br/+成年小鼠的肾单位数量减少、慢性肾衰竭和高血压有关。
Am J Physiol Renal Physiol. 2009 May;296(5):F1166-78. doi: 10.1152/ajprenal.90550.2008. Epub 2009 Feb 4.
2
Misexpression of Six2 is associated with heritable frontonasal dysplasia and renal hypoplasia in 3H1 Br mice.Six2的错误表达与3H1 Br小鼠的遗传性额鼻发育异常和肾发育不全有关。
Dev Dyn. 2008 Jul;237(7):1767-79. doi: 10.1002/dvdy.21587.
3
Stem cells in the embryonic kidney.胚胎肾中的干细胞。
Kidney Int. 2008 Apr;73(8):913-7. doi: 10.1038/sj.ki.5002784. Epub 2008 Jan 16.
4
Six2 is required for suppression of nephrogenesis and progenitor renewal in the developing kidney.Six2对于发育中的肾脏中肾发生的抑制和祖细胞更新是必需的。
EMBO J. 2006 Nov 1;25(21):5214-28. doi: 10.1038/sj.emboj.7601381. Epub 2006 Oct 12.
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Renal branching morphogenesis: concepts, questions, and recent advances.肾分支形态发生:概念、问题及最新进展
Differentiation. 2006 Sep;74(7):402-21. doi: 10.1111/j.1432-0436.2006.00106.x.
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The cellular basis of kidney development.肾脏发育的细胞基础。
Annu Rev Cell Dev Biol. 2006;22:509-29. doi: 10.1146/annurev.cellbio.22.010305.104340.
7
Methods of studying the planar distribution of objects in histological sections of brain tissue.研究脑组织组织学切片中物体平面分布的方法。
J Microsc. 2006 Mar;221(Pt 3):153-8. doi: 10.1111/j.1365-2818.2006.01559.x.
8
Explorative statistical analysis of planar point processes in microscopy.显微镜下平面点过程的探索性统计分析。
J Microsc. 2005 Dec;220(Pt 3):131-9. doi: 10.1111/j.1365-2818.2005.01521.x.
9
Quantitative spatial analysis of the distribution of NADPH-diaphorase-positive neurons in the developing and mature rat retina.发育中和成年大鼠视网膜中NADPH-黄递酶阳性神经元分布的定量空间分析
Brain Res Bull. 2005 Apr 30;65(4):349-60. doi: 10.1016/j.brainresbull.2005.01.011.
10
Pathways to nephron loss starting from glomerular diseases-insights from animal models.从肾小球疾病开始的肾单位丢失途径——来自动物模型的见解
Kidney Int. 2005 Feb;67(2):404-19. doi: 10.1111/j.1523-1755.2005.67097.x.

遗传性肾发育不全小鼠肾小球空间排列的镶嵌分析。

Tessellation analysis of glomerular spatial arrangement in mice with heritable renal hypoplasia.

机构信息

Department of Anatomy, Biochemistry and Physiology, University of Hawaii School of Medicine, Honolulu, Hawaii.

出版信息

Anat Rec (Hoboken). 2010 Feb;293(2):280-90. doi: 10.1002/ar.21038.

DOI:10.1002/ar.21038
PMID:19937638
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3162479/
Abstract

Renal hypoplasia results from an insufficient kidney volume caused, in part, by a deficient number of glomeruli. The purpose of this study was to apply tessellation analysis to determine whether glomerular point patterns differed between adult normal (WT) and mutant (Br) mice with heritable renal hypoplasia and to delineate a spatial distribution accounting for the observed patterns. Kidneys from adult WT and Br mice were collected, processed with routine light histology and representative transverse sections were photographed. Cortical area and perimeter were calculated from traced tissue contours and glomeruli were identified and digitized. Voronoi tessellations were constructed and average parameters for Voronoi polygon number, area, perimeter and edge counts as well as spatial metrics comprising nearest neighbor and centroidal distances were calculated and compared. Point distributions were simulated by randomizing glomerular coordinates from each section and plotting the new points utilizing uniform random, Gaussian random, or isotropic functions. Average nearest neighbor distances were generated for each specimen and ranked with respect to corresponding values generated from 1,000 iterations for each simulated set. Results showed that WT and Br were significantly different for each parameter suggesting that WT kidneys possessed more glomeruli, but these were less clustered compared to Br. Simulations suggested that WT and Br demonstrated similar, but not identical, underlying glomerular spatial distributions. Defective gene expression in Br is important for determining glomerular number and the defective pattern likely results from a heterochronic disturbance consisting of a truncated growth trajectory during embryonic kidney development.

摘要

肾发育不全是由于肾小球数量不足导致的肾脏体积不足引起的。本研究旨在应用镶嵌分析来确定遗传性肾发育不全的成年正常(WT)和突变(Br)小鼠的肾小球点模式是否存在差异,并描绘出一个能够解释观察到的模式的空间分布。收集成年 WT 和 Br 小鼠的肾脏,进行常规光组织学处理,并拍摄代表性的横切面照片。从追踪的组织轮廓计算皮质面积和周长,并识别和数字化肾小球。构建 Voronoi 镶嵌,并计算 Voronoi 多边形数量、面积、周长和边缘计数的平均参数,以及包含最近邻和质心距离的空间度量,并进行比较。通过从每个切片随机化肾小球坐标并利用均匀随机、高斯随机或各向同性函数绘制新点来模拟点分布。为每个标本生成平均最近邻距离,并根据每个模拟集的 1000 次迭代生成的相应值进行排序。结果表明,WT 和 Br 在每个参数上都有显著差异,这表明 WT 肾脏具有更多的肾小球,但与 Br 相比,这些肾小球的聚类程度较低。模拟表明,WT 和 Br 表现出相似但不完全相同的肾小球空间分布。Br 中的缺陷基因表达对于确定肾小球数量很重要,缺陷模式可能是由于胚胎肾脏发育过程中生长轨迹缩短导致的异时性干扰所致。