𝔖 Bobbio Scriptorium
✦   LIBER   ✦

MRI assessment of lung parenchymal motion in normal mice and transgenic mice with sickle cell disease

✍ Scribed by Shigeru Kiryu; Tessa Sundaram; Shigeto Kubo; Kuni Ohtomo; Toshio Asakura; James C. Gee; Hiroto Hatabu; Masaya Takahashi


Publisher
John Wiley and Sons
Year
2007
Tongue
English
Weight
244 KB
Volume
27
Category
Article
ISSN
1053-1807

No coin nor oath required. For personal study only.

✦ Synopsis


Abstract

Purpose

To test the feasibility of a method to quantify regional pulmonary parenchymal motion via nonrigid registration algorithm at small animal scales.

Materials and Methods

Voxel‐wise displacement vector field maps were generated between end‐inspiratory and end‐expiratory coronal thoracic MR images on normal mice (N = 5) to analyze the magnitude and direction of parenchymal motion in the segmented regions. The analysis was repeated before and after short‐term exposure to hypoxia to demonstrate the effect of hypoxia on the respiratory motion in transgenic (Tg) mice with sickle cell disease (SCD) (N = 4).

Results

Normal mice revealed that the right and left lungs moved symmetrically but that there was greater movement in the lower regions than in the upper regions. Calculated strain was uniform in the entire lung. In the Tg mice, the pulmonary motion before hypoxia was similar to that observed in the normal mice. Upon exposure to hypoxia, the displacement magnitude reduced and the direction of motion in some areas became distorted.

Conclusion

MR quantification of pulmonary motion was feasible in mice and the principle that the method could detect mechanical abnormalities due to pathologic changes was proven. Quantification of pulmonary motion has the potential to lead to earlier disease diagnosis and better monitoring of disease treatments. J. Magn. Reson. Imaging 2007. © 2007 Wiley‐Liss, Inc.


📜 SIMILAR VOLUMES


Noninvasive in vivo MRI detection of neu
✍ G. Vanhoutte; I. Dewachter; P. Borghgraef; F. Van Leuven; A. Van der Linden 📂 Article 📅 2005 🏛 John Wiley and Sons 🌐 English ⚖ 255 KB

## Abstract Transgenic mice overexpressing the London mutant of human amyloid precursor protein (APP[V717I]) in neurons develop amyloid plaques in the brain, thus demonstrating the most prominent neuropathological hallmark of Alzheimer's disease. In vivo 3D __T__~2~\*‐weighted MRI on these mice (24