Exercise is known to have a long-term benefit on bone mass in children, but little is known about the underlying mechanisms. The purpose of this investigation was to determine the acute effect of exercise on bone metabolism in pre-pubertal children. Biochemical markers of bone formation were measured in 4 male and 4 female children, 8 to 11 years of age. Each subject performed 50 vertical jumps. Serum osteocalcin and C-telopeptide of type I collagen (CTx), were determined prior to exercise and at 24 and 72 hours post exercise as indicators of bone formation and bone resorption. Osteocalcin concentration was 8.20 ± 3.65 ng•mL"' before exercise, and was 7.1 ± 3.7 ng•mL-' and7.4 ± 3.7 ng•mL-' at 24 hours and 72 hours post exercise, respectively (P > 0.05). CTx concentrations were 11632 ± 4093 pmol•L-' before exercise, and was 9831 ± 3159 pmol•L-' at 24 hours and 9722 ± 2426 pmol•L7' at 72 hours post exercise (P > 0.05). In conclusion an acute bout of ballistic exercise appears to have no effect on bone metabolism in pre-pubertal children. / School of Physical Education

This thesis has evaluated if housing is a feasible alternative for vacant upper floor space in the central business district of small towns in general and in downtown Burlington, Iowa, specifically. The study required discussing the issue of housing in vacant upper floor spaces in general, establishing if there was a need for additional multi-use housing in the Burlington, Iowa housing market, and finally determining if there was vacant upper floor space that would fulfill this need.The analysis determined that housing was indeed a feasible and practical use for vacant upper floor space in downtown areas in general and in Burlington, Iowa specifically. The study provided a method that could be used to ascertain the feasibility of this type of housing in other towns as well. / Department of Urban Planning

Chromatin remodeling enzymes are instrumental for neural development as evidenced by their identification as disease genes underlying human disorders characterized by intellectual-disability. In this regard, the murine Snf2h and Snf2l genes show differential expression patterns during embryonic development, with a unique pattern in the brain where Snf2h is predominant in neural progenitors, while Snf2l expression peaks at the onset of differentiation. These observations led me to investigate the role of Snf2h and Snf2l in brain development by using conditionally targeted Snf2h and Snf2l mice. I selectively ablated Snf2h expression in cortical progenitors, cerebellar progenitors, or postmitotic Purkinje neurons of the cerebellum, while Snf2l was deleted in the germline. I found that Snf2h plays diverse roles in neural progenitor expansion and postmitotic gene expression control, while Snf2l is involved in the precise timing of neural differentiation onset. Gene expression studies revealed that Snf2h and Snf2l co-modulate the FoxG1 and En1 transcription factors during cortical and cerebellar neurogenesis, respectively, to precisely control the transition from a progenitor to a differentiated neuron. Moreover, Snf2h is essential for the postmitotic neural activation of the clustered protocadherin genes, and does so by functionally interacting with the matrix-attachment region protein Satb2. My neurobehavioral studies also provided insight into how Snf2h loss in cerebellar progenitors results in cerebellar ataxia, while Snf2h loss in cortical progenitors, or in postmitotic Purkinje neurons of the cerebellum, resulted in learning and memory deficits, and hyperactive-like behavior. Molecularly, Snf2h plays an important role in linker histone H1e dynamics and higher order chromatin packaging, as evidenced by loss of chromatin ultrastructure upon Snf2h deletion in progenitor and postmitotic neurons. I further demonstrated that Snf2h loss in a neuronal cell culture model results in reduced H1e deposition, and that overexpression of human SNF2H or SNF2L upon Snf2h knockdown rescues this biochemical dysfunction. My experiments suggest that Snf2h and Snf2l are regulatory nucleosome remodeling engines that co-modulate the gene expression programs necessary for proper brain development, maturation and function.

The osteoclasts, the bone cells responsible for bone degradation, have a crucial role in the age-related bone loss and post-menopause osteoporosis. Rac1 and Rac2, members of the Rho-family of small GTPases, are known for having a key role in osteoclast formation and activity, which could be translated to bone quality. In this study, we characterize the roles of Rac1 and Rac2 on bone quality using an aged and osteoporotic mouse model. Bones from wild type, Rac1KO and Rac2KO mice were harvested for mechanical tests, bone densitometry, micro-computed tomography and histomorphometric analyses to evaluate bone mineralization and architecture. We observed that the deletion of Rac1 or Rac2 in pre-osteoclasts minimized bone loss in both age-related and post-menopause osteoporosis. These results highlight the importance of the two small GTPases in bone remodeling and identify Rac1 and Rac2 as potential targets for the development of new therapies for the treatment of osteoporosis.

The osteoclasts, the bone cells responsible for bone degradation, have a crucial role in the age-related bone loss and post-menopause osteoporosis. Rac1 and Rac2, members of the Rho-family of small GTPases, are known for having a key role in osteoclast formation and activity, which could be translated to bone quality. In this study, we characterize the roles of Rac1 and Rac2 on bone quality using an aged and osteoporotic mouse model. Bones from wild type, Rac1KO and Rac2KO mice were harvested for mechanical tests, bone densitometry, micro-computed tomography and histomorphometric analyses to evaluate bone mineralization and architecture. We observed that the deletion of Rac1 or Rac2 in pre-osteoclasts minimized bone loss in both age-related and post-menopause osteoporosis. These results highlight the importance of the two small GTPases in bone remodeling and identify Rac1 and Rac2 as potential targets for the development of new therapies for the treatment of osteoporosis.

Thesis (M.Sc.)--York University, 2006. Graduate Programme in Biology. / Typescript. Includes bibliographical references. Also available on the Internet. MODE OF ACCESS via web browser by entering the following URL: http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&res_dat=xri:pqdiss&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&rft_dat=xri:pqdiss:MR19720

Diss. (sammanfattning) Stockholm : Karol. inst., 2004. / Härtill 4 uppsatser.

Thesis (M. S.)--Mechanical Engineering, Georgia Institute of Technology, 2009. / Committee Chair: Vito, Raymond; Committee Member: Gleason, Rudolph; Committee Member: Rachev, Alexander. Part of the SMARTech Electronic Thesis and Dissertation Collection.

Dissertation (Ph.D.)--Auburn University, 2009. / Abstract. Vita. Includes bibliographic references (p.94-115).

Thesis (Ph.D)--Biomedical Engineering, Georgia Institute of Technology, 2009. / Committee Chair: Yoganathan, Ajit; Committee Member: Fogel, Mark; Committee Member: Kanter, Kirk; Committee Member: Oshinski, John; Committee Member: Skrinjar, Oskar. Part of the SMARTech Electronic Thesis and Dissertation Collection.