Dissertations / Theses on the topic 'Bones – Growth'
To see the other types of publications on this topic, follow the link: Bones – Growth.
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the top 50 dissertations / theses for your research on the topic 'Bones – Growth.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Browse dissertations / theses on a wide variety of disciplines and organise your bibliography correctly.
1
Yadav, Priti. "Modelling loading and growth of long bones Modelling loading and growth of long bones." Licentiate thesis, KTH, Biomekanik, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-177913.
Full textAbstract:
The long bones grow by the process of endochondral ossification, which occurs at the growth plate. This process is regulated by biological factors and mechanical factors. The biological factors which contribute to endochondral ossification process are genes, hormones, nutrients etc. The mechanical factor is the load acting on the bone. The major forces on the bone are due to joint contact load and muscle forces, which induce stresses in the bone. Carter and Wong proposed in a theory that cyclic or intermittent octahedral shear stress promotes the bone growth and cyclic or intermittent hydrostatic compressive stress inhibits the bone growth. Previously this theory has been used to predict the morphological development of long bones, but with studies using simplified femur and growth plate models. Furthermore, the Carter and Wong theory has a limitation that it does not intrinsically incorporate the resulting growth direction.In the first study, the importance of a subject-specific growth plate over a simplified growth plate has been studied, and growth has been simulated using two different growth direction models: Femoral neck shaft deformation direction and minimum shear stress direction. This study favors the minimum shear stress growth direction model, as it is less sensitive to applied boundary condition than the femoral neck shaft deformation direction model.The second study aims to understand how different muscle groups affect the bone growth tendency. Subject-specific femur and growth plate models of able-bodied children were used. The muscle forces and associated hip contact force from specific muscle groups were applied, and neck shaft angle and femoral anteversion growth tendencies were predicted. This study indicated a tendency for reduction of neck shaft angle and femoral anteversion. Hip abductor muscle forces contribute most, and hip adductor muscle forces least, to bone growth rate.Accurate prediction of bone growth tendency and knowledge of the influence of different muscle groups on bone growth tendency may help in better treatment planning for children at risk of developing bone deformity problems.QC 20151201
2
Chim, Shek Man. "Identification and characterization of novel secreted factors involved in bone remodeling." University of Western Australia. School of Surgery, 2009. http://theses.library.uwa.edu.au/adt-WU2010.0110.
Full textAbstract:
[Truncated abstract] Bone remodeling is an important process to maintain mechanical integrity. It is accomplished by two important steps, bone resorption followed by new bone formation. Osteoclasts and osteoblasts are the principal cells in bone resorption and bone formation, respectively. A multitude of local and systemic factors regulates this process by controlling the cellular activities in bone remodeling compartments (BRC). An imbalance of osteoblastic bone formation and osteoclastic bone destruction will result in the development of skeletal diseases. Recent studies suggested that angiogenesis is closely associated with bone remodeling. The vasculature in bone is important for skeletal development, growth and repair. During endochondral ossification, cartilage is invaded by blood vessels which bring in osteoblast and osteoclast precursor cells, nutrients, growth factors and differentiation factors. During fracture repair, it has been demonstrated that mature osteoclasts produce heparanase which can degrade heparin sulfate proteoglycans, a major component in extracellular matrix (ECM). The process leads to the release of heparin-binding growth factors including vascular endothelial growth factor (VEGF), a potent angiogenic factor which contributes largely to local angiogenesis. In recent studies, endothelial cells have been found to produce bone morphogenetic protein (BMP)-2 and BMP-4 when they are subjected to mechanical stimuli, or a hypoxia environment. Conversely, inhibition of angiogenesis has been shown to prevent fracture healing. In a distraction osteogenesis model, either inhibition of angiogenesis or disruption of the mechanical environment prevents normal osteogenesis and results in fibrous nonunion. .... A total of 42 mice from F1 and F2 generations were genotyped as transgene positive. Preliminary analysis using radiography did not reveal any difference between the gross structures of transgenic and wild type mice. Interestingly, the preliminary histology revealed a decrease in trabecular bone and an increase of lipid space in metaphysis of transgenic mice overexpressing EGFL6. However, further studies will need to be carried out to investigate the role of EGFL6 in angiogenesis and adipogenesis using a transgenic mice model. This will be a prime focus of future work. Collectively, the results presented in this thesis have identified EGFL6, a member of the EGF-like family, as a potential angiogenic factor which may play an important role in bone remodeling. EGFL6 has been found to be expressed highly in calvarial osteoblasts and upregulated during primary murine osteoblast differentiation. EGFL6 has been 8 characterized to be a secreted homomeric complex. More importantly, EGFL6 has been shown to induce angiogenic activity in endothelial cell migration, tube formation and in vivo chick embryo chorioallantoic membrane assay. Furthermore, conditioned medium containing the EGFL6 recombinant protein was shown to induce phosphorylation of ERK in endothelial cells. Inhibition of ERK impaired EGFL6-induced ERK activation and endothelial cell migration. Taken together these studies raise the possibility that EGFL6 has a potential role in angiogenesis, and mediates a paracrine mechanism of cross-talk between vascular endothelial cells and osteoblasts during osteogenesis. An understanding of this process offers the potential to facilitate the development of therapeutic treatments for bone disease.
3
Ma, Li, and 马丽. "The influence of nicotine on angiogenesis and osteogenesis in bone regeneration." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B41508440.
Full text
4
Oest, Megan Elizabeth. "Dual Osteogenic and Angiogenic Growth Factor Delivery as a Treatment for Segmental Bone Defects." Diss., Georgia Institute of Technology, 2007. http://hdl.handle.net/1853/16264.
Full textAbstract:
A new model of a critically-sized segmental femoral bone defect in rats was developed to enable in vivo imaging and facilitate post-mortem mechanical testing of samples. The critically-sized nature of the model was assessed and confirmed. The efficacy of sustained co-delivery of osteogenic (BMP-2 and TGF- Ò3) and angiogenic (VEGF) growth factors in promoting functional bone repair was assessed. Effects of scaffold modification in terms of geometry and composition were evaluated. The results indicated that co-delivery of BMP-2 and TGF- Ò3 resulted in a dose-dependent improvement in functional bone repair. Modification of the polylactide scaffold to include an absorbable ceramic component and a cored out geometry enhanced rate of union. Addition of VEGF to the scaffold treatment did not significantly impact revascularization of the defect site or functional repair of the bone defect. These data demonstrate that the complex environment of an acute bone defect requires different treatment strategies than simple ectopic models would suggest. A positive predictive correlation between bone repair parameters measured in vivo and mechanical functionality was established. The novel defect model demonstrated robustness and reproducibility. Implications for further research are discussed.
5
關健明 and Kin-ming Kwan. "Defining the function of type X collagen in skeletal development." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1997. http://hub.hku.hk/bib/B31237162.
Full text
6
Foster, Bruce Kristian. "Epiphyseal plate repair using fat interposition to reverse physeal deformity : an experimental study." Title page, contents and summary only, 1989. http://web4.library.adelaide.edu.au/theses/09MD/09mdf754.pdf.
Full textAbstract:
Bibliography: leaves 169-197. Hypothesises that the physis has an internal mechanism of repair to restore physeal function. Aims to establish a defined degree of deformity by partial growth plate excision, then to examine different methods of reversal of such deformity to observe the process of growth plate repair. A secondary aim was to define the percentage of physis that could be resected yet still enable reversal of deformity.
7
Chayanupatkul, Atinooch. "Bone formation in the temporomandibular joint in response to forward mandibular positioning." Thesis, Hong Kong : University of Hong Kong, 2002. http://sunzi.lib.hku.hk/hkuto/record.jsp?B25598776.
Full text
8
Cha, Ming Chuan 1955. "The effect of zinc deficiency on the growth promoting actions of growth hormone and insulin-like growth factor-I /." Thesis, McGill University, 1994. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=55484.
Full textAbstract:
The effect of zinc deficiency on the growth promoting effect of circulating IGF-I and the direct growth effect of GH on long bone growth were investigated. Food intake was decreased by lack of zinc in the diet. Tissue zinc content and plasma alkaline phosphatase activity were reduced by zinc deficiency. Systemic administration of human IGF-I increased the body weight, tail length and tibia epiphyseal cartilage width of control animals. This somatogenic action was impaired by zinc deficiency, as evidenced by continued weight loss, no increase in tail length and decreased tibial epiphyseal cartilage width of zinc deficient animals. Unilateral arterial infusion of GH increased the tibial epiphyseal width of the treated limb but not of the non-treated limb in control rats. However, no difference was found between the infused and the non-infused limb of zinc deficient animals, suggesting the occurrence of GH resistance on long bone growth in zinc deficiency. We conclude that zinc deficiency inhibits the growth promoting action of circulating IGF-I and the direct growth effect of GH on long bone growth.
9
Dai, Zhijie, and 戴志洁. "The role of sodium/myo-inositol cotransporter 1 and myo-inositol in osteogenesis and bone formation." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B43783533.
Full text
10
Dahlgren, Emma. "Effects of Different Load Magnitudes on Longitudinal Growth of Immature Bones." Thesis, KTH, Skolan för kemi, bioteknologi och hälsa (CBH), 2018. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-230885.
Full textAbstract:
In vivo studies of mechanical loading on bone have suggested that load magnitude is one of the parameters that play a vital role in bone adaptation. This study examined how longitudinal growth of immature rat metatarsals is affected by different load magnitudes. The main hypotheses were that the longitudinal growth of immature bone would decrease with increased compressive load magnitude, and that the longitudinal growth would be more decelerated the higher the load mag- nitude. The three middle metatarsal bones in the back paws of 19-20 days old Sprague-Dawley rat fetuses were extracted. Metatarsal bones were loaded with 0.05 N, 0.25 N, 1.25 N and 6.25 N. Loading rate and number of cycles were constant at 0.01 mm/sec and 10 cycles respectively. Length measurements occurred every 2-3 day. Concluded from the study was that a load magni- tude of 0.05 N resulted in an increased longitudinal growth, compared to unloaded bones. For the other load magnitudes the results were insufficient and inconsistent and therefore nothing could be suggested for them. The problem remained as before and further studies are needed.
11
Wong, Hoi-leong Xavier, and 王凱亮. "The functional crosstalk between MT1-MMP and ADAMs in craniofacial & vascular development." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/197072.
Full text
12
Saxon, Leanne, and mikewood@deakin edu au. "The role of exercise in the development of bone strength during growth." Deakin University. School of Health Sciences, 2002. http://tux.lib.deakin.edu.au./adt-VDU/public/adt-VDU20051125.095337.
Full textAbstract:
Exercise during growth may increase peak bone mass; if the benefits are maintained it may reduce the risk of fracture later in life (1). It is hypothesised that exercise will preferentially enhance bone formation on the surface of cortical bone that is undergoing bone modeling at the time (2). Therefore, exercise may increase bone mass accrual on the outer periosteal surface during the pre- and peri-pubertal years, and on the inner endocortical surface during puberty (3). An increase in bone formation on the periosteal surface is, however, more effective for increasing bone strength than medullary contraction (4).
While exercise may have a role in osteoporosis prevention, there is little evidential basis to support this notion. It is generally accepted that weight-bearing exercise is important, but it is not known how much, how often, what magnitude or how long children need to exercise before a clinically important increase in bone density is obtained.
In this thesis, the effect of exercise on the growing skeleton is investigated in two projects. The first quantifies the magnitude and number of loads associated with and in a moderate and low impact exercise program and non-structured play. The second project examines how exercise affects bone size and shape during different stages of growth.
Study One: The Assessment of the Magnitude of Exercise Loading and the Skeletal Response in Girls
Questions: 1) Does moderate impact exercise lead to a greater increase in BMC than low impact exercise? 2) Does loading history influence the osteogenic response to moderate impact exercise? 3) What is the magnitude and number of loads that are associated with a moderate and low impact exercise program?
Methods: Sixty-eight pre-and early-pubertal girls (aged 8.9±0.2 years) were randomised to either a moderate or low impact exercise regime for 8.5-months. In each exercise
group the girls received either calcium fortified (-2000 mg/week) or non-fortified foods for the duration of the study. The magnitude and number of loads associated with the exercise programs and non-structured play were assessed using a Pedar in-sole mobile system and video footage, respectively.
Findings: After adjusting for baseline BMC, change in length and calcium intake, the girls in the moderate exercise intervention showed greater increases in BMC at the tibia (2.7%) and total body (1.3%) (p ≤0.05). Girl's who participated in moderate impact sports outside of school, showed greater gains in BMC in response to the moderate impact exercise program compared to the low impact exercise program (2.5 to 4.5%, p ≤0.06 to 0.01). The moderate exercise program included -400 impacts per class, that were applied in a dynamic manner and the magnitude of impact was up to 4 times body weight.
Conclusion: Moderate-impact exercise may be sufficient to enhance BMC accrual during the pre-pubertal years. However, loading history is likely to influence the osteogenic response to additional moderate impact exercise. These findings contribute towards the development of school-based exercise programs aimed at improving bone health of children.
Study Two: Exercise Effect on Cortical Bone Morphology During Different Stages of Maturation in Tennis Players
Questions: 1) How does exercise affect bone mass (BMC) bone geometry and bone strength during different stages of growth? 2) Is there an optimal stage during growth when exercise has the greatest affect on bone strength?
Methods: MRI was used to measure average total bone, cortical and medullary areas at the mid- and distal-regions of the playing and non-playing humerii in 47 pre-, peri- and post-pubertal competitive female tennis players aged 8 to 17 years. To assess bone rigidity, each image was imported into Scion Image 4.0.2 and the maximum, minimum
and polar second moments of area were calculated using a custom macro. DXA was used to measure BMC of the whole humerus. Longitudinal data was collected on 37 of the original cohort.
Findings: Analysis of the entire cohort showed that exercise was associated with increased BMC and cortical area (8 to 14%), and bone rigidity (11 to 23%) (all p ≤0.05). The increase in cortical bone area was associated with periosteal expansion in the pre-pubertal years and endocortical contraction in the post-pubertal years (p ≤0.05). The exercise-related gains in bone mass that were accrued at the periosteum during the pre-pubertal years, did not increase with advanced maturation and/or additional training.
Conclusion: Exercise increased cortical BMC by enhancing bone formation on the periosteal surface during the pre-pubertal years and on the endocortical surface in the post-pubertal years. However, bone strength only increased in response to bone acquisition on the periosteal surface. Therefore the pre-pubertal years appear to be the most opportune time for exercise to enhance BMC accrual and bone strength
13
Wong, Wing-Kit Ricky, and 黃永傑. "Bone induction using Simvastatin and Gusuibu." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2004. http://hub.hku.hk/bib/B31246126.
Full text
14
Brooker, Molly J. "The effect of acute exercise on bone metabolism in the pre-pubertal child." Virtual Press, 2000. http://liblink.bsu.edu/uhtbin/catkey/1164852.
Full textAbstract:
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
15
Liu, Jin. "Increased CKIP-1 suppresses Smad-dependent BMP signaling to inhibit bone formation during aging." HKBU Institutional Repository, 2016. https://repository.hkbu.edu.hk/etd_oa/327.
Full textAbstract:
Emerging evidence indicates that the dysregulation of protein ubiquitination plays a crucial role in aging-associated diseases. Smad-dependent canonical BMP signaling pathway is indispensable for osteoblastic bone formation, which could be disrupted by the ubiquitination and subsequent proteasomal degradation of Smad1/5, the key molecules for BMP signaling transduction. However, whether the dysregulation of Smad1/5 ubiquitination and disrupted BMP signaling pathway are responsible for the age-related bone formation reduction is still underexplored. Casein kinase-2 interacting protein-1 (CKIP-1), also known as Pleckstrin homology domain-containing family O member 1 (PLEKHO1), is a previously identified ubiquitination-related molecule that could specifically target the linker region between the WW domains of Smurf1 to promote the ubiquitination of Smad1/5. Here, we found an age-related increase in the expression of CKIP-1 in bone specimens from either fractured patients or aging rodents, which was associated with the age-related reduction in Smad-dependent BMP signaling and bone formation. By genetic approach, we demonstrated that loss of Ckip-1 in osteoblasts could promote the Smad-dependent BMP signaling and alleviated the age-related bone formation reduction. In addition, osteoblast-specific Smad1 overexpression had beneficial effect on bone formation during aging, which could be counteracted after overexpressing Ckip-1 within osteoblasts. By pharmacological approach, we showed that osteoblast-targeted CKIP-1 siRNA treatment could enhance Smad-dependent BMP signaling and promote bone formation in aging rodents. Taken together, it suggests that the increased CKIP-1 could suppress Smad-dependent BMP signaling to inhibit bone formation during aging, indicating the translational potential of targeting CKIP-1 in osteoblast as a novel bone anabolic strategy for reversing established osteoporosis during aging.
16
Zheng, Liwu, and 鄭立武. "Biochemical modulation of mandibular distraction osteogenesis." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2004. http://hub.hku.hk/bib/B31246308.
Full text
17
Alfonso, Durruty Marta Pilar. "Biosignificance of Harris lines as stress markers in relation to moderate undernutrition and bone growth velocity a New Zealand white rabbit model for the study of bone growth /." Diss., Online access via UMI:, 2008.
Find full text
18
Gan, Huiyan, and 甘慧妍. "Understanding the role of KIF5B in long bone development and chondrocyte cytokinesis." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hdl.handle.net/10722/211554.
Full textAbstract:
Kinesins are motor proteins responsible for the anterograde transport on microtubules. Kinesin-1 is the first characterized kinesin, and it consists of two heavy chains and two light chains. KIF5B is a form of Kinesin-1 heavy chains that is ubiquitously expressed in mammals. The head domain of KIF5B is responsible for ATP-dependent mechanical movement along microtubules, while the tail region is well-known for its interaction with cell specific cargos. Recent studies reveal a second microtubule binding site in the tail, suggesting special functions of KIF5B in microtubule sliding and bundling.
To understand the role of KIF5B in long bone development, a conditional knockout mouse model was generated, in which Kif5b is deleted in early limb mesenchyme using Prx1-cre/LoxP mediated recombination. Unlike Col2a1-cre directed Kif5b knockout in chondrocytes, the expression of Prx1-cre in limb mesenchyme results in Kif5b knockout in both chondrocyte and osteoblast lineages. The Prx1-cre mediated Kif5b conditional knockout mice develop malformed long bones characterized by their bowed shape, shortened length and multiple fractures, which reflects a combination of defects in bone matrix and growth plate. The mutant mice demonstrate impaired bone matrix formation, as indicated by both collagen density reduction and collagen matrix disorganization. Also, the growth plate does not retain its normal organization, and the hypertrophic zone is absent. The KIF5B deficient chondrocytes not only lose planar cell polarity, but also undergo early apoptosis and fail in terminal differentiation. Interestingly, the binucleation rate is significantly increased in these chondrocytes, suggesting a severe cytokinesis defect. Besides, the intracellular retention of extracellular matrix (ECM) molecules and the uneven distribution of ECM in the cartilage imply both blockage and inappropriate direction of secretion.
Cytokinetic defect in chondrocytes is closely associated with growth plate abnormality and growth retardation. In Kif5b knockout chondrocytes, cytokinetic defect is also one of the earliest and principal phenotypes. Therefore the underlying mechanism of cytokinetic defect was further investigated at cellular level. Since Kif5b knockout chondrocytes cannot survive in primary culture, RNA interference approach was adopted to generate a Kif5b-knockdown chondrogenic cell line. As expected, the Kif5b knockdown cells demonstrate cytokinetic defects characterized by increased binucleation rate and prolonged cytokinesis phase. In control cells, KIF5B becomes concentrated in the midbody during cytokinesis, and the midbody organization is disrupted in Kif5b knockdown cells. Furthermore, transient expression of full-length KIF5B significantly reduces the binucleation rate of these KIF5B deficient cells, whereas over-expression of a truncated KIF5B (without microtubule binding sites in tail region) cannot rescue the defect. Additionally, KIF5B is found to interact with midbody components PRC1 and Aurora B kinase by GST pull-down assay.
This study demonstrates the multiple functions of KIF5B in long bone development and emphasizes its significant role as a key modulator in chondrocyte cytokinesis. More importantly, the study also brings new insights into the mechanisms of cytokinesis: we propose that KIF5B may participate in cytokinesis by regulating the midbody organization and stability via microtubule bundling and transporting or anchoring important components to the midbody.published_or_final_version
Biochemistry
Doctoral
Doctor of Philosophy
19
Gluck, Beth. "The Effects of Physical Activity on Bone Density in Adolescent Females." Fogler Library, University of Maine, 2004. http://www.library.umaine.edu/theses/pdf/GluckB2004.pdf.
Full text
20
Blostein, Ashley C. "Effects of running on hormonal growth factors." Virtual Press, 1993. http://liblink.bsu.edu/uhtbin/catkey/865946.
Full textAbstract:
To determine the influence of running on certain blood-born parameters that are involved in bone metabolism, serum levels of calcium, alkaline phosphatase (ALP, a marker of bone formation), growth hormone (hGH), and parathyroid hormone (PTH), were analyzed in 10 male subjects following a 40 min. run at 70% VO2max. Each trial was preceeded by 1 day of inactivity, a 8-12 hr. fast, and drawing of a baseline blood sample by venipuncture. All other blood samples were taken via an indwelling catheter which was inserted in an antecubital vein immediately following the completion of the exercise bout. When the catheter was in place, an "immediate post" sample was drawn. Subsequent samples were taken at 1, 2, 3, 4, 5, 10, 15, 20, 30, 45, and 60 min. after the immediate post sample. Analysis of serum calcium concentrations demonstrated that levels were significantly elevated by 12% following exercise, going from a fasted level of 9.7 ± .53 mg/dl to post-exercise levels of 11.8 ± .73 mg/dl. Serum calcium remained elevated during the first 4 min. following exercise. By 5 min. post-exercise, calcium levels dropped to levels that were significantly lower than the post-exercise sample. However, serum alkaline phosphatase did not change significantly following exercise, as the values remained within normal range throughout the experimental period. Concentrations tended to decrease over time but were not significantly lower than the preor post-exercise levels by the end of the sampling period. Serum concentrations of hGH were more than doubled following a single bout of exercise, going from 4.0 ± 0.98 ng/ml before exercise to 8.8 ± 1.6 ng/ml immediately post-exercise. Following this initial rise, hGH progressively declined and returned to baseline values by 30 min. post-exercise. The concentrations of PTH did not change significantly following exercise. The postexercise sample tended to be higher than baseline values but were not significantly different. The results presented here indicate that an exercise bout 40 min. at 70% V02max results in an elevation of serum calcium and hGH, but does not alter PTH secretion or ALP activity. The data presented in this study indicate that the temporary rise in calcium following exercise is unrelated to PTH. It is hypothesized that the increase in calcium that we observed is attributable to lactate accumulation that would result from an exercise bout of this nature. The buildup of lactic acid and drop in pH causes a dissolution of the crystaline calcium hydroxyapatite compartment of the skeleton, thus causing an increase in ionized calcium. It is not known whether a single bout of exercise can influence hormonal secretion to a sufficient degree to affect bone density, but the hormonal changes demonstrated here could be involved in long-term effects of training.School of Physical Education
21
Zhong, Ming. "Apoptotic signaling pathways in mammalian growth plate chondrocytes." Diss., Georgia Institute of Technology, 2010. http://hdl.handle.net/1853/33993.
Full textAbstract:
The growth plate resting zone consists of hyaline-like chondrocytes disbursed in a proteoglycan rich extracellular matrix. These cells give rise to the columns of the growth zone, consisting of progressively hypertrophic cells. Proliferation of resting zone chondrocytes induced by systemic and local stimuli is the driving force of longitudinal growth of long bones. Therefore, homeostasis of this cell population has great importance. Although the regulation of proliferation and differentiation of these cells has been well studied, little is known about the regulation of their apoptosis. We have previously shown that chelerythrine and tamoxifen induce apoptosis in resting zone chondrocytes in a nitric oxide (NO)-dependent pathway. In this study we explored two physiological apoptogens: inorganic phosphate (Pi) and 17β-estradiol (E₂). We found NO production is necessary in Pi-induced apoptosis. We also found that NO donors induced chondrocyte apoptosis by up-regulating p53 expression, Bax/Bcl-2 expression ratio and cytochrome C release from mitochondria, as well as caspase-3 activity, indicating that NO induces chondrocyte apoptosis in a mitochondrial pathway. Mitogen activated protein kinase (MAPK) activity was involved. A c-Jun N-terminal kinase (JNK) inhibitor, but not inhibitors of p38 or extracellular signal-regulated kinase (ERK1/2), was able to block NO-induced apoptosis, indicating that JNK is necessary in this pathway. Taken together, Pi elevates NO production, which leads to a mitochondrial apoptotic pathway dependent on JNK. On the other hand, although E₂caused apoptosis in resting zone chondrocytes in a dose-dependent manner, up-regulated p53 and Bax, and induced release of cytochrome C from the mitochondria, which indicated a mitochondrial apoptotic pathway, the apoptosis did not involve elevated nitric oxide production or MAPK as was found in Pi-induced apoptosis. This study elucidates the signaling pathway underlying Pi and E₂-induced chondrocyte apoptosis. It has important implications on understanding the development of mammalian growth plate. It also provides further information about the physiological functions of estrogen on longitudinal bone growth.
22
Kar, Archana. "Hydroxyapatite deposition onto nanoporous TiO2 and assessment of bone cell growth and proliferation." abstract and full text PDF (free order & download UNR users only), 2007. http://0-gateway.proquest.com.innopac.library.unr.edu/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:1447622.
Full text
23
Mohamad, Yusof Loqman. "Longitudinal growth of mammalian bones : a possible role for membrane transporters in mediating chondrocyte hypertrophy." Thesis, University of Edinburgh, 2012. http://hdl.handle.net/1842/6481.
Full textAbstract:
Long bone lengthening occurs at the growth plate (GP) by well-regulated chondrocyte proliferation, hypertrophy and terminal matrix deposition. GP chondrocyte (GPC) hypertrophy has been implicated to be the main determinant of bone growth rate; however the mechanism is poorly understood. The work of this thesis examined some of the cellular process that drives the chondrocyte swelling or hypertrophy particularly in a mammalian post natal GPs using living in situ GPC and fixed GP tissues. Confocal scanning microscopy (CLSM) was used to determine living in situ GPC volume and dimension changes in proliferative zone (PZ) through to hypertrophic zone (HZ) chondrocytes of different GPs of various bones. While PZ cells showed similar volumes and dimensions, HZ cells varied in different GPs, even within the same long bone but at opposite ends. However, the hypertrophic cell volume measured at a single post natal age (day 7) was independent of the corresponding bone length. This could reflect a complex interplay between local and systemic factors in different GPs, which occurs throughout the active phase of bone growth. Maintaining GPC morphology was critical in studying GPC hypertrophy using fixed tissues. This work highlighted a problem caused by conventional fixative solutions, which caused up to 44% hypertrophic GPC shrinkage following GP fixation. This artifact appeared to be associated with the hyperosmotic nature of the fixatives used and could be abolished by adjusting the fixative osmolarity close to physiological level (280 mOsm), or could be significantly reduced by bisecting bone tissues prior to tissue fixation. This thesis proposed roles for plasma membrane transporter(s) in mediating GPC hypertrophy. This hypothesis was tested by examining roles of sodium-hydrogen exchanger (NHE) and anion exchanger (AE) in GPC hypertrophy using an ex vivo bone growth inhibition model. Inhibition of bone growth by inhibitors of NHE (EIPA) and AE (DIDS) respectively was shown to be dose-dependent. The histology of bones demonstrated that the late HZ width was significantly reduced in GPs treated with EIPA or DIDS. Although in situ GPC volumes in the PZ and HZ were not notably different in DIDS-treated GP, the cell volumes in both zones were significantly reduced by EIPA treatment. Fluorescence immunohistochemistry revealed distinctive cellular localisations of NHE1 and AE2 in the PZ and early HZ. These results suggest a possible role of AE in mediating GPC volume increase in PZ chondrocytes and those in the early stages of cell hypertrophy, whereas NHE could possibly maintain intracellular pH of GPC throughout all GP zones. This thesis has characterized various changes in volume and dimensions of living in situ GPC from PZ through to HZ of different GPs of postnatal rats. This work emphasized the importance of fixative osmolarity in order to accurately preserve the normal volume/morphology of cells within tissues. Most importantly, this thesis confirmed a potential role of the plasma membrane transporters, AE and NHE in GPC hypertrophy of growing bones.
24
Moore, Alison Jane. "Quantitative histomorphometric analysis of the bone growth plate in infancy : a comparative study between SIDS and normal subjects /." Title page, contents and abstract only, 1998. http://web4.library.adelaide.edu.au/theses/09MSM/09msmm821.pdf.
Full text
25
Serrat, Maria A. "Environmentally-determined tissue temperature modulates extremity growth in mammals a potential comprehensive explanation of Allen's Rule /." [Kent, Ohio] : Kent State University, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=kent1185486409.
Full textAbstract:
Thesis (Ph.D.)--Kent State University, 2007.Title from PDF t.p. (viewed Mar. 5, 2009). Advisor: C. Owen Lovejoy. Keywords: temperature, bone growth, Allen's Rule, skeletal morphology, limb proportions, environmental effects on bone growth. Includes bibliographical references (p. 157-176).
26
Zhu, Guixia, and 朱貴霞. "Study of the function of Kinesin-1 (KIF5B) in long bone development." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B41757919.
Full text
27
Zierath, Juleen R. "Bone mineral content in laboratory rats following swim and run training." Virtual Press, 1986. http://liblink.bsu.edu/uhtbin/catkey/472942.
Full textAbstract:
Increased bone density has been observed following physical training. However, it is not known whether the mechanical forces of muscular contraction, gravitational pull, or a combination of these forces are required to cause this adaptation. Therefore, the purpose of this study was to determine which mechanical force, muscular contraction or gravitational pull, offered the greatest contribution to increased bone mineral content observed following either swim or run training. METHODS: Female Wistar rats were randomly assigned to one of three groups: 1) Sedentary Control (SC; n = 12), 2) Run Trained (RT; 27.7 m/m, 8% incline, 2 hrs/day; n = 20), and 3) Swim Trained (ST; 2 hrs/day, 2Y/ body weight; n = 14). The animals were sacrificed after 9 weeks of training and the humeri and femurs were removed for analysis.RESULTS: Femur weight, length, diameter, and ponderal index (a measure of robustness), and bone mineral content (BMC) were not different between the three treatment groups. However, femur cortical thickness was significantly (p < 0.01) smaller in the RT when compared to ST and SC rats. The ST humeri were significantly (p < 0.05) heavier, wider, and had a greater BMC when compared with those of the RT and SC rats, while cross sectional area was unaffected by physical training. CONCLUSION: The results of this study indicate that the mechanical forces applied by the swim training protocol produced marked bone adaptation in the ST animals following 9 weeks of physical training. Whereas, the combined mechanical and gravitational forces applied during running by the RT rats produced minimal adaptation of bone following 9 weeks of physical training.
28
Li, Gang Gang. "Biological studies of distraction osteogenesis." Thesis, University of Oxford, 1997. http://ora.ox.ac.uk/objects/uuid:d2976713-d0f6-439a-a70c-9183d44cff81.
Full text
29
Tsai, Ming-ju Marjorie. "Replicating mesenchymal cells in the condyle in response to normal growth and mandibular protrusion." Hong Kong : University of Hong Kong, 2002. http://sunzi.lib.hku.hk/hkuto/record.jsp?B25575995.
Full text
30
Valverde, Franco Gladys 1972. "The role of fibroblast growth factor receptor 3 in post-natal cartilage and bone metabolism /." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=115917.
Full textAbstract:
FGFR 3 is one of a family of four high affinity receptors for FGF ligands. Activating mutations in FGFR 3 result in skeletal dysplasias that vary in severity from undetectable to neonatal lethal. Mice with congenital deficiency of FGFR3 develop severe kyphosis and skeletal overgrowth. FGFR3 is also expressed in calvarial pre-osteoblasts, osteoblast and articular chondrocytes, although it biological role in these cells remains undefined. By changing the genetic background of the Fgfr3-/- mice we were able to extend their lifespan and examine its impact on post-natal skeletal growth. To investigate the implication of FGFR 3 in post-natal cartilage and bone metabolism we used a combination of imaging, classic histology, molecular biology and biomechanical testing. The results demonstrated that the synovial joints of young adult Fgfr3-/- mice revealed a progressive deterioration, loss of the joint space width and changes in the subchondral bone. These alterations were accompanied by an increase of cartilage matrix degradation. Increased aggrecan and collagen type II degradation products, generated by MMPs were detected with DIAPEN and COL2-3/4C antibodies. Increased collagen type X, cellular hypertrophy and loss of proteoglycan at the articular surface were also demonstrated. A novel micro-mechanical indentation protocol revealed that the humeral heads of Fgfr3-/- mice were less stiff than those of wild type littermates. On the other hand, young adult Fgfr3-/- mice are osteopenic due to reduced cortical bone thickness and defective trabecular bone mineralization. The reduction in mineralized bone and lack of trabecular connectivity observed by micro-computed tomography were confirmed by histological and histomorphometric analyses, which revealed a significant decrease in calcein labeling of mineralizing surfaces and a significant increase in osteoid in the long bones of 4-month-old Fgfr3-/- mice. Primary cultures of adherent bone marrow-derived cells from Fgfr3-/- mice expressed markers of differentiated osteoblasts but developed fewer mineralized nodules than Fgfr3+/+ cultures of the same age. These data point to a major role for FGFR3 signaling in development and homeostatic maintenance of cartilage and bone post-natally and identify FGFR3 as a potential target for intervention in degenerative disorders of cartilage, osteopenia and those associated with defective bone mineralization.
31
Langeveldt, Carmen Ronel. "Alternative insulin mitogenic signaling pathways in immature osteoblast cell lines." Thesis, Stellenbosch : Stellenbosch University, 2002. http://hdl.handle.net/10019.1/52646.
Full textAbstract:
Thesis (MSc)--University of Stellenbosch, 2002.ENGLISH ABSTRACT: Insulin is a mitogen for many cells and commonly signals through the classical, mitogenic Raf- MEK-ERK or metabolic PB-kinase pathways. Insulin deficiency or type I diabetes causes severe osteopenia. Obese patients with type II diabetes or insulin resistance, a disease associated with defective insulin signaling pathways and high levels of circulating insulin, have increased or normal bone mineral density. The question of whether hyperinsul inemia preserves bone mass is frequently raised. However, there is still a lot of controversy on the role of insulin as an osteoanabolic agent and this question still remains unanswered. A critical role for insulin signaling in bone building osteoblasts has recently been demonstrated with IRS-l knock-out mice. These mice developed low-turnover osteopenia due to impaired proliferation and differentiation, stressing the importance of osteoblastic IRS-l for maintaining normal bone formation. In the present study it was found that insulin does function in vitro as an osteoblast mitogen. This was illustrated in three relatively immature osteoblast (MBA-15.4, -15.6 mouse and MG- 63 human) cell lines, which responded to insulin with significant increases in proliferation. In the MBA -15.4 preosteoblasts insulin stimulation of proliferation was comparable to the welldescribed mitogen, TPA. The UMR-I06 cell line expresses markers of differentiated osteoblasts, and was much less responsive to insulin treatment. The difference in proliferative potential may be due to differences between spontaneously transformed cell lines, or the stage of cell differentiation. UOI26, a MEKI/2 inhibitor and wortmannin, a PB-kinase inhibitor, were used to investigate the pathway used by insulin to signal and activate ERK and osteoblast proliferation. In MBA-15.4 mouse preosteoblasts, GF-containing FCS was completely dependent on MEK for DNA synthesis. In contrast, in both MBA-15.4 and more mature MBA-15.6 osteoblasts, insulininduced proliferation was resistant to the inhibitors alone or in combination. Higher MEKinhibitor concentrations had no effect, and proliferation was also increased by the inhibitors in several experiments. This indicated that the classical, insulin mitogenic pathway was not involved in MBA-15.4 proliferation. Wortmannin had no effect on either insulin- or 20% FCSstimulated proliferation, but inhibited activation of Akt/PKB, the metabolic downstream target of PI3-kinase. Insul in signal ing to ERK was both MEK-and PI3-kinase- dependent, but this had no effect on proliferation. In contrast, FCS-stimulated ERK activation and proliferation was almost completely dependent on MEK-ERK activation. Proliferative signaling in the MG-63 human osteoblastic cell line in response to insulin was partially dependent on MEK and partially dependent on PB-kinase. In contrast, signaling in response to the phorbol ester, TPA, was partially dependent on PI3K but totally dependent on MEK-ERK. This indicates that the signal converges on ERK, suggesting the involvement of a PB-kinase upstream of a dominant MEK-ERK pathway. The differences found here between mouse and human insulin mitogenic signaling pathways indicate that there may be species differences between osteoblast signaling pathways, with mouse cells being independent and human cells being dependent on MEK for DNA synthesis in response to insulin. The effects of glucocorticoids on insulin mitogenic signaling in osteoblasts were also investigated, because chronic long-term steroid use results in excessive bone loss. The PTP inhibitor, sodium orthovanadate, reversed GC-impaired TPA- and FCS- induced proliferation in MBA-1SA and MG-63 preosteoblasts. PTPs, such as SHP-l and PTP-IB, dephosphorylate and inactivate phosphorylated kinases. Both SHP-l and PTPlB associated with kinases in the mitogenic signaling cascade of MBA-lS.4 preosteoblasts growing rapidly in 10% FCS. Further, SHP-I co-irnmunoprecipitated with active, tyrosine phosphorylated ERK, which may indicate that it can dephosphorylate and inactivate ERK. However, since the MEK-ERK or PB-kinase pathways are not important in insulin-induced proliferation in mouse osteoblasts, the PTPs are unlikely to be role players in the negative regulation of this signaling pathway. This was confirmed by the finding that vanadate was unable to reverse GC-induced decreases in insulinstimulated DNA synthesis. This suggests that vanadate-sensitive PTPs may not be important in the negative regulation of insulin-induced mouse osteoblast proliferation, and provides further evidence of a novel insulin mitogenic pathway in the MBA-lSA but not MG-63 osteoblastic cell line.
AFRIKAANSE OPSOMMING: Insulien is 'n mitogeen vir baie selle en gelei na binding aan die insulien reseptor, intrasellulêre seine via die klassieke, mitogeniese Raf-MEK-ERK of die metaboliese PB-kinase seintransduksie pad. 'n Insulien gebrek of tipe I diabetes veroorsaak osteopenie. Vetsugtige pasiënte met insulien weestandigheid of tipe II diabetes, 'n siekte wat geassosieer word met foutiewe insulien seintransduksie en hoë vlakke van sirkuierende insulien, het verhoogde of normale been mineraal digtheid (BMD). Die vraag of hiper insulin ernie 'n verlies aan beenmassa teëwerk word dikwels gevra. Teenstrydigheid oor die rol van insulien as 'n osteo-anaboliese stof bestaan egter steeds en hierdie vraag bly dus onbeantwoord. Dat insulien seintransduksie wel 'n kritiese rol speel in beenvormende osteoblaste is onlangs bevestig in studies met muise waarvan die geen vir IRS-l uitgeslaan is. Hierdie muise ontwikkel 'n lae omset osteopenie weens verswakte proliferasie en differensiasie. fn hierdie studie is gevind dat insulien wel in vitro as 'n osteoblast mitogeen kan funksioneer. Dit is in drie relatief onvolwasse (MBA-15.4, -15.6 muis en MG-63 mens) sellyne geillistreer, deur betekenisvolle verhogings in insulien-geaktiveerde proliferasie. In MBA-15.4 preosteoblaste is die persentasie verhoging in insulien-gestimuleerde proliferasie vergelykbaar met dié van die bekende mitogeniese forbolester, TPA. Die UMR-I06 sellyn het kenmerke van gedifferensieerde osteoblaste, en was baie minder responsief op insulien behandeling. Die verskil in die proliferasie vermoë van die verskillende sellyne kan die gevolg wees van verskille wat bestaan tussen spontaan getransformeerde sellyne of die stadium van sel differensiasie. 'n MEK 1/2 inhibitor, UO126 en 'n PB-kinase inhibitor, wortmannin, is gebruik om die insulien seintransduksie pad noodsaaklik vir die aktivering van ERK en osteoblast proliferasie te bepaal. In MBA-1S.4 muis pre-osteoblaste, was fetale kalf SenlTI1(FKS)-geinduseerde DNA sintese totaal afhanklik van MEK. Beide die MBA-15.4 en die meer volwasse MBA-15.6 muis osteoblaste was weerstandig teen die inhibitors op hulle eie, of in kombinasie. Verhoogde MEK-inhibitor konsentrasies het geen verdere effek gehad nie en in verskeie eksperimente is 'n verhoging in preliferasie selfs waargeneem met MEK-inhibisie. Hierdie resultate dui aan dat die klassieke insulien mitogeniese pad nie betrokke is in MBA-I5.4 gestimuleerde selproliferasie nie. Wortmannin het geen effek gehad op insulien- of20% FKS-gestimuleerde DNA sintese nie, maar het wel die aktivering van PB-kinase se metaboliese teiken, AktJPKB geinhibeer. Insulien seintransduksie aktiveer dus ERK deur beide MEK en PB-kinase, maar het geen effek op proliferasie gehad nie. FKS-gestimuleerde ERK aktivering en proliferasie was totaal afhanlik van MEK-ERK aktivering. Insulien-geaktiveerde DNA sintese in die mens MG-63 osteoblaste was gedeeltelik afhanklik van beide MEK en PB-kinase. Alhoewel IPA ook PB-kinase kon aktiveer, was dit totaal afhanklik van MEK vir DNA sintese. Dit dui aan dat daar 'n PB-kinase stroom-op van 'n dominante MEK-ERK seintransduksie pad voorkom. Die verskille wat ons dus waargeneem het in insulien mitogeniese seintransduksie tussen muis en mens, kan aandui dat insuliengestimuleerde seintranduksie paaie kan verskil van spesie tot spesie. Dit is bevestig met die muisselle wat onafhanklik is en mens selle wat afhanklik is van MEK aktivering vir insuliengeaktiveerde DNA sintese. Kroniese, langtermyn steroied behandeling kan beenverlies veroorsaak en die effek van glukokortikoide (GK) op die insulien mitogeniese pad in osteoblaste is dus ook ondersoek. Natrium-ortovanadaat, 'n proteien tirosien fosfatase (PIP) inhibitor het GK-verlaagde proliferasie in repons tot beide IPA- en FKS behandeling herstel in MBA-lSA en MG-63 preosteoblaste. PIPs soos SHP-l en PIP-l B funksioneer deur gefosforileerde kinases te defosforileer en dus te inaktiveer. Beide SHP-l and PIP-lB kon assosieer met kinases in die mitogeniese insulien seintransduksie pad van vinnig groeiende MBA-IS A preosteoblaste in 10% FKS. Verder het SHP-I ook geko-immunopresipiteer met aktiewe, tirosien-gefosforileerde ERK, wat aandui dat SHP-I met ERK assosieer om dit te defosforileer en inaktiveer. Die MEKERK of PB-kinase paaie is nie belangrik vir insulien-geaktiveerde seintransduksie in muis osteoblaste nie. Dit is dus onwaarskynlik dat die PIPs 'n rol sal speel in die negatiewe regulering van hierdie seintransduksie paaie. Die ontdekking dat vanadaat nie glukokortikoiedverlaagde insulien-geaktiveerde DNA sintese kan herstel nie, toon dat vanadaat-sensitiewe PIPs nie 'n rol speel in insulien-geaktiveerde proliferasie in muisselle nie. Hierdie bevinding het verder bevestig dat 'n nuwe insulien mitogeniese pad in die MBA-ISA, maar nie die MG-63 selle moontlik bestaan.
32
Duvall, Craig L. "The Role of osteopontin in postnatal vascular growth functional effects in ischemic limb collateral vessel formation and long bone fracture healing /." Available online, Georgia Institute of Technology, 2006, 2006. http://etd.gatech.edu/theses/available/etd-01102007-130423/.
Full textAbstract:
Thesis (Ph. D.)--Biomedical Engineering, Georgia Institute of Technology, 2007.David Harrison, Committee Member ; Ravi Bellamkonda, Committee Member ; Larry McIntire, Committee Member ; Oskar Skrinjar, Committee Member ; W. Robert Taylor, Committee Chair ; Robert Guldberg, Committee Chair.
33
陳卓榮 and Cheuk-wing Wilson Chan. "Molecular basis for increased bone formation in a mouse expressing mutant collagen X." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2003. http://hub.hku.hk/bib/B31227132.
Full text
34
曹凱韻 and Hoi-wan Tso. "Effects of phagocytosis of apoptotic cells by mesenchymal stem cells on osteogenesis and T cells responses." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B39707520.
Full text
35
Xu, Wei. "The impact of rhizoma chuanxiong in fetal bone development." HKBU Institutional Repository, 2016. https://repository.hkbu.edu.hk/etd_oa/253.
Full textAbstract:
Background and purpose: Rhizoma Chuanxiong (CX), the dry rhizome of Ligusticum chuanxiong Hort., is a commonly used Chinese herbal medicine to treat gynecological diseases. So far, more than 60 chemical components have been identified from CX such as volatile oils (ligustilide, etc.), phenolic acids (ferulic acid, etc.) and alkaloids (chuanxiongzine, etc.). These components in CX are the basis of its wide pharmacodynamic actions including estrogen-like, progesterone-like and anti-coagulant/anti- platelet effects. In our recent survey based on previous published clinical trials, CX was ranked as one of the top 20 herbs commonly used for anti-miscarriages amongst Chinese pregnant women. However, CX should be used with caution during pregnancy as its property of 2invigorating blood circulation and removing blood stagnation3. Despite its wide applications, the safe dosage of CX in pregnant women remains unclear with no records found in the current Chinese Pharmacopoeia or other guidelines. Thus, verification regarding the impacts of CX preparations and its components in embryonic development is urgently required. In view of the limited experimental evidence that is currently available to assess the safety of CX, this project aims to (1) identify the general impacts of CX aqueous extract in maternal function and fetal development with an in vivo mouse model; and to (2) investigate the adverse impacts and underlying mechanisms of CX aqueous extract in fetal bone development with a biomarker assay and metabolomics analysis.;Concusion: CX aqueous extract at a low dosage of 2 g/kg/day (equals to the daily dosage of human adults) did not cause adverse effect in pregnant mice, and it suggested that this dosage of CX preparations should be safe for pregnant women. Our data demonstrated that high dosage and long-term use of CX aqueous extract might result in embryonic toxicities including fetal bone malformations for the first time. As the CX aqueous extract in this study was not contaminated by pesticide residues and heavy metals, the adverse impacts of CX aqueous extract should be considered as a result of its intrinsic components in the herb. Furthermore, CX aqueous extract might significantly down-regulate biomarkers related to bone formation and metabolism during osteogenesis. It is therefore valuable to establish a practical approach to systematically assess the safety of CX and other herbal medicines.;Method: Referred to the guidelines of WHO, the Chinese Pharmacopoeia and the Hong Kong Chinese Materia Medica Standards, CX aqueous extract was prepared, and its reference marker (ligustilide and ferulic acid) were quantitatively authenticated by HPLC analysis. LC/MS fingerprint analysis was performed for the quality control purposes. In addition, pesticide residues and heavy metals found in CX aqueous extract were examined using GC-MS and ICP-MS analysis. In the Segment II study as per FDA and OECD guidelines, pregnant mice were randomly assigned into 6 groups (n=18 per group): i.e. mice were orally administrated with distilled water as the negative controls (Group 1); or CX aqueous extract of 2, 16, 24 and 32 g/kg/day respectively from the gestation day (GD)6 to 16(Group 2, 3, 4 and 5); or vitamin A (200,000 IU) on GD7, 9 and 11 as the positive controls (Group 6). All mice were sacrificed to assess maternal and fetal parameters on the GD18. In the mechanistic study, the expressions of biomarkers related to fetal bone development including PICP, ICTP, B-ALP, BGP, Gdf-5, BMPs, BMP-6, BMP-8, BMP-11, IL-4, IL-4r, IL-10 and IL-10r in fetal tissue samples of the Group 1 and 5 (32 g/kg/day, n=18) were measured using ELISA analyses on GD16. Meanwhile, the metabolites of two-group samples were also analyzed by the UHD Accurate-Mass Q- TOF LC/MS, and profiling data was further analyzed by specific software. During statistical analysis, measurement data from G1, 2, 3 4 and 5 groups were analyzed using one-way ANOVA(SPSS software, version 16.0). LSD test in Post hoc method was applied to compare differences between every two groups. Pearsons x 2 - test was used to analyze category data from G1, 2, 3, 4 and 5 groups, and Fishers exact test was applied to compare differences between different groups. The student t-test was also used to compare differences between G1 and G6 groups in animal studies as well as G1 and G5 groups using ELISA or metabolomics results. An intragroup difference with a p-value less than 0.05 was considered as statistical significant.;Resutt:(1) There was no statistical significant difference in maternal and fetal parameters found between the Group 1 and 2 (p> 0.05). However, the maternal body weight (BW), gravid uterine weight, corrected BW change, live fetus/litter, mean fetal BW in the Group 4 and 5 were significantly lower than those in the Group 1(p
36
Dang, Lei. "Osteoblastic PLEKHO1 contributes to joint inflammation in rheumatoid arthritis." HKBU Institutional Repository, 2019. https://repository.hkbu.edu.hk/etd_oa/687.
Full textAbstract:
Background: Osteoblasts participating in the inflammation regulation gradually obtain concerns. However, its role in joint inflammation of rheumatoid arthritis (RA) is largely unknown. Here, we investigated the role of osteoblastic pleckstrin homology domain-containing family O member 1 (PLEKHO1), a negative regulator of osteogenic lineage activity, in regulating joint inflammation in RA. Methods: The level of osteoblastic PLEKHO1 in RA patients and collagen-induced arthritis (CIA) mice was examined. The role of osteoblastic PLEKHO1 in joint inflammation was evaluated by a CIA mice model which was induced in osteoblast-specific Plekho1 conditional knockout mice and mice expressing high Plekho1 exclusively in osteoblasts, respectively. The effect of osteoblastic PLEKHO1 inhibition was explored in a CIA mice model. The mechanism of osteoblastic PLEKHO1 in regulating joint inflammation was performed by a series of in vitro studies. Results: PLEKHO1 was highly expressed in osteoblasts from RA patients and CIA mice. Osteoblastic Plekho1 deletion ameliorated joint inflammation, whereas overexpressing Plekho1 only within osteoblasts exacerbated local inflammation in CIA mice. PLEKHO1 was required for TNF receptor-associated factor 2 (TRAF2)-mediated the ubiquitination of receptor-interacting serine/threonine-protein kinase 1 (RIP1) to activate nuclear factor kappa-light-chain-enhancer of activated B (NF-kB) pathway for inducing inflammatory cytokines production in osteoblasts. Moreover, osteoblastic PLEKHO1 inhibition improved joint inflammation and attenuated bone formation reduction in CIA mice. Conclusions: These data strongly suggest that highly expressed PLEKHO1 in osteoblasts mediates joint inflammation in RA. Targeting osteoblastic PLEKHO1 may exert dual therapeutic action of alleviating joint inflammation and promoting bone repair in RA.
37
蔡明汝 and Ming-ju Marjorie Tsai. "Replicating mesenchymal cells in the condyle in response to normal growth and mandibular protrusion." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2002. http://hub.hku.hk/bib/B31973127.
Full text
38
Essman, Stephanie Christine. "Effects of ¹⁵³samarium-ethylenediaminetetramethylene phosphonate on physeal and articular cartilage in juvenile rabbits /." Free to MU Campus, others may purchase, 2003. http://wwwlib.umi.com/cr/mo/fullcit?p1418016.
Full text
39
黃淑興 and Shu-hing Louise Wong. "Replicating mesenchymal cells in the glenoid fossa in response to mandibular advancement." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2002. http://hub.hku.hk/bib/B31973140.
Full text
40
Xiong, Hui, and 熊暉. "Condylar adaptation to active mandibular forward positioning in non-growing rats." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2004. http://hub.hku.hk/bib/B31374220.
Full text
41
Poon, Chin-ho, and 潘展豪. "Pushing stem cells toward bone lineage through ultrasound stimulation." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B47849824.
Full textAbstract:
When human mesenchymal stem cells (hMSCs) are cultured inside a 3D collagen meshwork, they become a potential tissue engineering bone graft alternative. However, the in vitro osteogenesis rate of hMSCs is slow, leading to a low mineral deposition.
To enhance the osteogenic differentiation of hMSCs, low intensity pulsed ultrasound (LIPUS) was employed as an external stumulus. The present study demonstrated the feasibility of employing daily LIPUS exposure for enhancing osteogenesis in vitro. Exposure of seven consecutive days LIPUS, each of 30 minutes duration, did not affect the cell viability, and the organization of hMSCs within the collagen meshwork was not disturbed. The calcium deposition within the collagen meshwork was enhanced after seven days of exposure. The osteoinductivity was also upregulated at the early period of culture.
In order to optimizing the enhancement effects of LIPUS, various ultrasound parameters, including intensity, exposure duration and exposure repetition were investigated. Results showed the LIPUS enhancement effects are dose dependent, LIPUS exposure should be longer than 10 minutes/day in order to elicit a significant effect. Calcium deposition was higher when LIPUS exposure was done twice per day instead of one. Although individual variation exists, optimal LIPUS intensity range was between 60-120 mW/cm2 ISATA (Spatial Average Temporal Average Intensity).
The interaction mechanism between LIPUS and cells was also investigated. Microbubbles were added to the culture during LIPUS exposure to find out whether cavitation is involved in the interaction. Flow sensor primary cilium was also studied in order to verify that ultrasound is transduced through fluid flow. Results showed cavitation may not be a contributing factor to osteogenesis, and primary may be involved in the transduction of LIPUS stimulation.
This study demonstrated that osteogenesis of hMSCs encapsulated in collagen constructs could be enhanced by LIPUS. The LIPUS parameters were also optimized. The LIPUS interaction pathways were also being better understood. This thesis study will be a paradigm for cellular mechanotransduction studies and put an important step forward for therapeutic ultrasound.published_or_final_version
Electrical and Electronic Engineering
Master
Master of Philosophy
42
Monegue, James S. "EVALUATION OF THE EFFECTS OF VITAMIN K ON GROWTH PERFORMANCE AND BONE HEALTH IN SWINE." UKnowledge, 2013. http://uknowledge.uky.edu/animalsci_etds/26.
Full textAbstract:
The role of vitamin K in the blood clotting cascade has been well documented. Vitamin K has recently been implicated in improving bone health. The current studies were conducted to determine the effects of vitamin K in diets with and without mycotoxin contaminated corn on growth performance, bone characteristics, and related blood metabolites in pigs from weaning to market. Menadione sodium bisulfite complex (MSBC, 33% vitamin K) was chosen as the source of supplemental vitamin K because it is the most common form fed to swine. Vitamin K was tested at 0, 0.5, and 2.0 ppm in a corn-soybean meal based diets on two generations of pigs to evaluate any time and dose responses. The first generation of pigs was subjected to mycotoxin contaminated corn in the nursery phase to test for any interactions between the toxins and vitamin K. The addition of 0.5 ppm vitamin K reduced (P < 0.0001) prothrombin time. No additional decrease in prothrombin time was detected when increasing vitamin K inclusion from 0.5 to 2.0 ppm. With regard to growth performance, daily gain, feed intake, and feed efficiency were unaffected (P > 0.10) by supplemental vitamin K. However, pigs fed mycotoxin contaminated corn ate less (P = 0.005) and grew slower (P = 0.015) compared to those receiving good corn. The addition of vitamin K did not alleviate the negative growth effects in response to corn type. Vitamin K did not affect bone characteristics (P > 0.10), blood Ca (P > 0.05) or OC (P > 0.10). Other than blood clotting it does not appear that dietary vitamin K provides any additional benefits at these levels of inclusion and stages of swine production.
43
Moreira, Alessandra Arnaud. ""Estudo da utilização clínica das proteínas ósseas morfogenéticas em cirurgia buco-maxilo-facial no Brasil"." Universidade de São Paulo, 2004. http://www.teses.usp.br/teses/disponiveis/23/23143/tde-16032005-161053/.
Full textAbstract:
A recuperação de partes deficientes do corpo humano por substitutos funcionais, tem suscitado questionamentos por parte de profissionais cirurgiões e pesquisadores da área de cirurgia e traumatologia Bucomaxilofacial. Na tentativa de recuperar o contorno anatômico natural e restaurar a função de áreas com deficiência de tecido ósseo, optou-se inicialmente pela utilização de enxertos ósseos autógenos. Apesar de suas inúmeras vantagens, o uso de enxertos autógenos na reconstrução da face apresenta certos inconvenientes, como a necessidade de hospitalização, intervenção em outra área do organismo, morbidade da área doadora, maior período de convalescença, susceptibilidade a infecções, e ainda, uma possível reabsorção progressiva e constante. Um questionamento ainda maior gira em torno das cirurgias para enxerto ósseo na face já que os ossos da face são curtos e não justifica a morbidade de uma outra região do organismo para suprir sua necessidade. Na tentativa de substituir o uso de enxertos autógenos, cirurgiões começaram a optar por materiais sintéticos ou similares orgânicos, associadas com o uso das proteínas ósseas morfogenéticas, que são fatores de crescimento responsáveis pela indução da formação óssea no organismo humano desde sua fase fetal até a idade madura. A proposta deste estudo é fazer uma avaliação sobre o conhecimento e o uso clínico pelos cirurgiões buco-maxilo-faciais, no Brasil, de proteínas ósseas morfogenéticas no auxílio à reparos de defeitos ósseos da face.The use of alloplastic materials for bone replacement has been extensively debated lately by surgeons and researchers in the Oral and Maxillofacial field. In the attempt to reconstruct bone defects anatomically and functionally autogenous bone grafts have been the preferred option. Although being considered the gold standard in craniofacial reconstruction, there are some inconveniences in the use of bone autografts. Among them the need of hospitalization, the need of a donor site usually in a different area than the bone defect, donor area morbidity, longer recovery time, increased risk of infection, and the possibility of bone resorption over time. When the face is operated the use of autogenous bone is even more questionable. Usually small amounts of bone grafts are necessary in the face, and might not justify the morbidity of the donor site. In an attempt to avoid the use of bone autografts, allografts and alloplastic materials have been advertised, in association with bone morphogenetic proteins. These proteins are growth factors involved in the osteogenesis in humans from the fetus up to the adult age. The aim of this study is to evaluate the knowledge and the clinical use of bone morphogenetic proteins in the repair of facial bone defects by Brazilian Oral and Maxillofacial surgeons.
44
Seo, Hwa-Seon. "The role of TGFß signaling in skeletal development." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2008. https://www.mhsl.uab.edu/dt/2008p/seo.pdf.
Full text
45
Burr, Laura Lynn. "Diet enrichment with arachidonic and docosahexaenoic acid during the lactation period attenuates the effects of intrauterine growth restriction from birth to maturity in the guinea pig and improves maternal bone mass." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=112384.
Full textAbstract:
Intrauterine growth restriction (IUGR) reduces bone mass by 10-30% and impairs arachidonic (AA) and docosahexaenoic (DHA) acid status in infants. Because AA and DHA enhance neonatal bone mass, the aim of this study was to determine the effects of dietary 0.5% AA and 0.2% DHA (w/w) prior to weaning on bone and growth. 40 guinea pigs were randomized to either a control (C) or low-protein diet (LP) during pregnancy and the C diet or the C diet with AA+DHA during lactation. Measurements included bone mass, metabolism, and strength, and erythrocyte lipid of sows and offspring from birth to 16 wk post-partum. The LP diet induced IUGR, while the AA+DHA increased bone mass by 5-20% in sows and offspring and corrected growth and bone mass in IUGR pups. Thus, AA+DHA provided in lactation rescues the growth trajectory in an IUGR state and is beneficial to maternal and neonatal bone mass.
46
Davey, Tamara. "Functional characterisation of a novel osteoclast-derived factor." University of Western Australia. School of Surgery and Pathology, 2008. http://theses.library.uwa.edu.au/adt-WU2008.0219.
Full textAbstract:
[Truncated abstract] Intracellular communication between osteoclasts and osteoblasts is imperative to maintain bone integrity. A myriad of molecules are responsible for regulating osteoblast and osteoclast activity. In particular, it is well documented that osteoblast-derived factors are crucial in directly controlling osteoclast formation and function. Since bone formation is coupled to bone resorption, it would be expected that osteoclasts also have some role in regulating the growth and function of osteoblast cells. However, despite extensive research upon osteoclast and osteoblast biology, the mechanisms by which osteoclasts regulate osteoblast growth and function is not well understood. In an attempt to further elucidate the mechanisms by which osteoclasts and osteoblasts communicate, the technique of subtractive hybridisation was used to identify a novel osteoclastderived factor identical to that of mouse Seminal Vesicle Secretion VII (SVS VII). Previous characterisation of the gene in bone demonstrated that SVS VII was abundantly and specifically expressed by mature osteoclasts (Phan, 2004). Additional research hinted that SVS VII acted as a novel osteoclast-derived factor, that by paracrine mechanisms, targeted osteoblast function (Phan, 2004). However, it remained open as to whether the SVS VII molecule did uniquely target the osteoblast, and whether this interaction influenced bone formation in vivo. Therefore, this thesis endeavoured to functionally characterise the role of the SVS VII molecule in the bone environment. ... Further work is needed to identigy a clear consensus binding sequence, to determine the specificity of the interaction between SVS VII protein and each phage clone, and to isolate a specific binding partner for SVS VII. In conclusion, the studies of this thesis sought to characterise the significance of SVS VII expression by mature osteoclasts, relative to its effects on osteoblast behaviour, but failed to conclusively determine a role for SVS VII in bone. Given that the effects of SVS VII on in vitro osteoblast activity and function are minimal, it is doubtful that SVS VII primarily acts as a paracrine factor integral to osteoblast function. Therefore, these findings conflict with those presented previously (Phan, 2004). However, it was demonstrated that SVS VII treatment was associated with in vivo effect on the skeleton, suggesting that SVS VII may target other elements of the bone microenvironment. Via mechanisms not yet understood, which possibly involves additional factors of the bone 11 extracellular matrix, SVS VII may target a subset of osteoprogenitor cells within the bone environment and act to regulate their proliferation. Therefore, SVS VII may enhance osteogenic precursor cell number at sites of bone formation which would increase the pool of cells that can differentiate down the osteoblast linage and contribute to bone formation. In this regard, SVS VII might function in a manner homologous to the Ly-6 molecule Sca-1 and act as an important factor that maintains a balance between the bone formation and resorption process. Clearly, more work focusing on alternative facets of bone biology is needed to identify whether there is a significant role for SVS VII in skeletal tissue.
47
Schwartz, Filho Humberto Osvaldo [UNESP]. "Osteogênese sobre titânio com nanotopografia." Universidade Estadual Paulista (UNESP), 2011. http://hdl.handle.net/11449/110660.
Full textAbstract:
Made available in DSpace on 2014-11-10T11:09:56Z (GMT). No. of bitstreams: 0
Previous issue date: 2011-09-19Bitstream added on 2014-11-10T11:57:36Z : No. of bitstreams: 1
000697140_20151015.pdf: 232164 bytes, checksum: 0bed7471a6786fe38e3164319d6deb3e (MD5) Bitstreams deleted on 2015-08-07T12:19:55Z: 000697140_20151015.pdf,. Added 1 bitstream(s) on 2015-08-07T12:20:58Z : No. of bitstreams: 1
000697140.pdf: 6167998 bytes, checksum: bf8732b598c57469944be2ab9eac1b0c (MD5)Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
Os objetivos deste estudo foram avaliar a influência da nanotopografia de superfícies de titânio no processo de osteogênese por meio de avaliação histológica do contato osso-implante, em ratos, sob efeito da inalação forçada da fumaça de cigarro; Avaliar a osteogênese e a expressão de citocinas em cultura de células primárias sobre discos de titânio com nanotopografia; E avaliar o efeito morfológico e molecular da incorporação da laminina-1 (LN-1) em superfícies com nanotopografia, em coelhos. Implantes e discos de titânio foram especialmente produzidos e submetidos a diferentes métodos para a obtenção de superfícies: usinada, micro e nanotopografia. As superfícies foram devidamente caracterizadas quanto a sua topografia, morfologia e química. Os resultados mostraram que: a nanotopografia é capaz de aumentar o contato osso-implante (BIC) mesmo na presença da inalação intermitente da fumaça de cigarro, e foi capaz de reduzir, porem não totalmente, seus efeitos deletérios e uma menor formação óssea; A nanotopografia de titânio pode ter papel importante no processo de mineralização da matriz extracelular e na modulação da expressão de citocinas; E que a incorporação de LN-1 a superfície de titânio com nanotopografia demonstrou favorecer uma maior expressão de importantes genes envolvidos na cascata da osseointegração.
The aims of this study were to evaluate the influence of nanotopography of titanium surfaces in the process of osteogenesis by means of histological assessment of bone-implant contact, in rats, under the effect of forced inhalation of cigarette smoke; To assess the osteogenesis process and the expression of cytokines in primary cell culture on titanium disks with nanotopography; And evaluate morphological and molecular the effect of incorporation of laminin-1 (LN-1) surfaces with nanotopography, in rabbits. Implants and titanium disks were specially produced and submitted to different methods for obtaining surfaces with turned, micro and nanotopography. The surfaces have been properly characterized as its topography, morphology and chemistry. The results showed that: nanotopography is able to increase bone-implant contact (BIC) even in the presence of intermittent inhalation of cigarette smoke, and was able to reduce, although not entirely, their harmful effects and a lower bone formation; Nanotopography may play a important role in mineralization process and in cytokine expression.; And the incorporation of LN-1 on titanium surface with nanotopography favor a higher expression of important genes involved in the cascade of osseointegration.
48
Chan, Cheuk-wing Wilson, and 陳卓榮. "ER stress in the pathogenesis of osteochondrodysplasia." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B43085192.
Full text
49
Turner, Justine Marie. "Adolescent onset anorexia nervosa : a model for the effects of inadequate nutrition upon bone size and development." University of Western Australia. School of Paediatrics and Child Health, 2006. http://theses.library.uwa.edu.au/adt-WU2006.0131.
Full textAbstract:
Despite usual onset during adolescence the cause of low bone density in adolescent onset anorexia nervosa is incompletely understood. Puberty is known to be a crucial time for the development of peak bone mass, due principally to growth plate bone formation and modelling on preformed surfaces. This results in bone formation uncoupled from bone resorption leading to increased bone size due to increase in matrix and bone mineral content. It was hypothesized that low bone density in adolescent anorexia nervosa was caused by malnutrition during puberty suppressing normal bone matrix formation at all sites of bone formation thus arresting bone mineralization. Method 49 female adolescents with anorexia nervosa and 109 healthy female adolescent controls were studied. 22 of the anorexia nervosa subjects were studied again a year later. Bone area, mineral content and density were measured using Dual Xray Absorptiometry at the spine, hip and whole body sites, including body composition assessment. Estimated volumetric bone density was calculated using published equations in order to study bone density independent of bone size. Height, weight and Tanner stage in puberty were measured. Dietary intake and physical exercise were assessed using questionnaires. In a subset of anorexia nervosa and control subjects bone age was measured. In a subset of anorexia nervosa subjects bone formation was assessed using serum bone specific alkaline phosphatase and osteocalcin, and bone resorption was assessed using urine N-telopeptide.
50
Mason, Shelley S. "Exploring Tissue Engineering: Vitamin D3 Influences on the Proliferation and Differentiation of an Engineered Osteoblast Precursor Cell Line During Early Bone Tissue Development." PDXScholar, 2013. https://pdxscholar.library.pdx.edu/open_access_etds/1000.
Full textAbstract:
Most of the load-bearing demand placed on the human body is transduced by skeletal tissue, and the capacity of the skeleton to articulate in various opposing directions is essential for body movement and locomotion. Consequently, cartilage and bone defects due to trauma, disease, and developmental abnormalities result in disabling pain and immobility for millions of people worldwide. A novel way of promoting cartilage and bone regeneration is through the incorporation of either primary cells or multipotent progenitor cells in a three-dimensional (3D) biomaterial scaffold, and/or the addition of exogenous growth and differentiation factors. The first part of this study reports a protocol for using freshly isolated mature chondrocytes seeded in a 3D hydrogel biomaterial scaffold, developed to explore mechanotransduction of engineered cartilage constructs cultured in a designed bioreactor. The bioreactor was designed to allow the application of physiological mechanical forces (compression and fluid flow), as well as a non-invasive/non-destructive method for analyzing regenerating tissue in real time through ultrasound transducers and a computerized monitoring system. In the second part of this study, an engineered immortalized osteoprecursor cell line, designated OPC1 (osteoblastic precursor cell line 1), was used as a culture model system for exploring the effects of exogenous growth and differentiation factors, mainly vitamin D, on early bone development. OPC1 was previously designed to provide a consistent reproducible culture system for direct comparisons of engineered bone constructs, evaluating bone development and cell/biomaterial interactions, and for investigating putative bone differentiating factors. One of the objectives of this research effort was to explore tissue development and regeneration by culturing OPC1 in the presence of vitamin D metabolites vitaD3 and 1,25OH2D3, while assaying the concomitant biological response. Results indicate that OPC1 is capable of metabolizing the parental metabolite vitaD3, and thus 25OHD3, to the active vitamin D form 1,25OH2D3. The metabolism of vita3 resulted in an anti-proliferative and pro-differentiative influence on OPC-1. These results support the hypothesis that extra-endocrine synthesis of 1,25OH2D3 functions in a tissue specific manner to regulate growth and differentiation, in addition to the classic calcimic actions of the vitamin D endocrine pathway. Understanding the influence of vitamin D on bone development will have significant implications on healthy aging, including the susceptibility to skeletal disorders involved in development and aging, such as osteoarthritis (OA) and osteoporosis.