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Bone phenotype of carbonic anhydrase...

The University of Arizona., Physiological Sciences.

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Bone phenotype of carbonic anhydrase II deficient and calbindin-D28k knockout mice and development of a method to measure in vivo bone strains in mice.

Record Type:	Language materials, printed : Monograph/item
Title/Author:	Bone phenotype of carbonic anhydrase II deficient and calbindin-D28k knockout mice and development of a method to measure in vivo bone strains in mice./
Author:	Margolis, David Stephen.
Description:	157 p.
Notes:	Adviser: Yeong-Hau H. Lien.
Contained By:	Dissertation Abstracts International69-03B.
Subject:	Biology, Physiology. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoeng/servlet/advanced?query=3303758
ISBN:	9780549505525

Bone phenotype of carbonic anhydrase II deficient and calbindin-D28k knockout mice and development of a method to measure in vivo bone strains in mice.
Margolis, David Stephen.

Bone phenotype of carbonic anhydrase II deficient and calbindin-D28k knockout mice and development of a method to measure in vivo bone strains in mice. - 157 p.

Adviser: Yeong-Hau H. Lien.

Thesis (Ph.D.)--The University of Arizona, 2008.

Since the development of knockout and transgenic mouse models, mice have become the most widely used mammalian animal model to study bone. Despite the advances in knowledge of bone biology and function that have occurred from use of mouse models, many studies use primarily qualitative techniques, which may result in overlooking important subtle pathophysiologic changes. The hypothesis of this dissertation is that quantitative techniques to measure bone structure and function could identify the physiologic role of carbonic anhydrase II and calbindin-D28k in mouse bone, despite earlier qualitative studies indicating mice without these proteins have normal bone structure and function. Furthermore, a method to quantify bone function in vivo will be tested in a mouse model.

ISBN: 9780549505525Subjects--Topical Terms:

1017816
Biology, Physiology.

Bone phenotype of carbonic anhydrase II deficient and calbindin-D28k knockout mice and development of a method to measure in vivo bone strains in mice.
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020 $a 9780549505525
035 $a (UMI)AAI3303758
035 $a AAI3303758
040 $a UMI $c UMI
100 1 $a Margolis, David Stephen. $3 1023507
245 1 0 $a Bone phenotype of carbonic anhydrase II deficient and calbindin-D28k knockout mice and development of a method to measure in vivo bone strains in mice.
300 $a 157 p.
500 $a Adviser: Yeong-Hau H. Lien.
500 $a Source: Dissertation Abstracts International, Volume: 69-03, Section: B, page: 1499.
502 $a Thesis (Ph.D.)--The University of Arizona, 2008.
520 $a Since the development of knockout and transgenic mouse models, mice have become the most widely used mammalian animal model to study bone. Despite the advances in knowledge of bone biology and function that have occurred from use of mouse models, many studies use primarily qualitative techniques, which may result in overlooking important subtle pathophysiologic changes. The hypothesis of this dissertation is that quantitative techniques to measure bone structure and function could identify the physiologic role of carbonic anhydrase II and calbindin-D28k in mouse bone, despite earlier qualitative studies indicating mice without these proteins have normal bone structure and function. Furthermore, a method to quantify bone function in vivo will be tested in a mouse model.
520 $a Although carbonic anhydrase II deficient mice are less severely affected than patients, the mice demonstrate features of osteopetrosis including metaphyseal widening and a 50% increase in trabecular bone volume. The mice partially compensate for inhibited osteoclast function by increasing osteoclast number.
520 $a Calbindin-D28k knockout mice demonstrated an increase in bone volume that results from additional bone at the endosteal surfaces. The higher bone volume results in increased stiffness and failure loads, highlighting the potential use of drugs that inhibit calbindin-D28k to treat diseases such as osteoporosis.
520 $a Finally, calcium phosphate ceramic and hydroxyapatite particles used as strain gauge coatings demonstrated bone bonding to mouse femora after two months in vivo. The use of hydroxyapatite particles to coat strain gauges is the first time this method has been used with all commercially available materials, and will allow other research groups to use this technique. The major limitation to in vivo bone strain measurement in mice is the relatively large size of the sensors, which resulted in increased second moments of inertia in the implanted bones.
520 $a Overall, this dissertation demonstrates that the use of quantitative techniques, including histology, histomorphometry, muCT imaging, and mechanical testing can measure subtle changes in bone properties that have been previously overlooked. Development of additional quantitative methods to study bone biomechanics in mouse models may encourage other research groups to quantify bone properties if no changes are noted using primarily qualitative methods.
590 $a School code: 0009.
650 4 $a Biology, Physiology. $3 1017816
650 4 $a Engineering, Biomedical. $3 1017684
650 4 $a Health Sciences, Medicine and Surgery. $3 1017756
690 $a 0541
690 $a 0564
690 $a 0719
710 2 $a The University of Arizona. $b Physiological Sciences. $3 1023472
773 0 $t Dissertation Abstracts International $g 69-03B.
790 $a 0009
790 1 0 $a Lien, Yeong-Hau H., $e advisor
791 $a Ph.D.
792 $a 2008
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoeng/servlet/advanced?query=3303758