Дисертації з теми "Bone anabolism"
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Fu, Xuekun. "The role of osteocyte Kindlin-2 in the anabolic actions of PTH in bone." HKBU Institutional Repository, 2020. https://repository.hkbu.edu.hk/etd_oa/741.
Повний текст джерелаSoon, Grace Ing. "The bone anabolic potential of dietary lysine and phytochemicals." Thesis, University of Cambridge, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.613967.
Повний текст джерела李振華. "Bone anabolic effect of flavonoids from Herba Epimedii in zebrafish and medaka." Thesis, University of Macau, 2010. http://umaclib3.umac.mo/record=b2454948.
Повний текст джерелаMiao, Dengshun. "Studies on the actions of bone anabolic drugs in vivo and in vitro." Thesis, University of Sheffield, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.300362.
Повний текст джерелаMatthies, Levi [Verfasser], and Eric [Akademischer Betreuer] Hesse. "The Role of Tgif1 in Bone Anabolic Signal Transduction / Levi Matthies ; Betreuer: Eric Hesse." Hamburg : Staats- und Universitätsbibliothek Hamburg, 2018. http://d-nb.info/116227526X/34.
Повний текст джерелаLiang, Chao. "Aptamer-functionalized lipid nanoparticles targeting osteoblasts as a novel RNA Interference-based bone anabolic strategy." HKBU Institutional Repository, 2016. https://repository.hkbu.edu.hk/etd_oa/325.
Повний текст джерелаMarcu, Jahan Phillip. "Novel Insights into CB1 Receptor Signaling and the Anabolic Role of Cannabinoid Receptors in Bone." Diss., Temple University Libraries, 2013. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/233543.
Повний текст джерелаPh.D.
Activation of the CB1 receptor is modulated by aspartate residue D2.63176 in transmembrane helix (TMH) II. Interestingly, D2.63 does not affect the affinity for ligand binding at the CB1 receptor. Studies in class A GPCRs have suggested an ionic interaction between residues of TMHII and VII. In this report, modeling studies identified residue K373, in the extracellular (EC)-3 loop, in charged interactions with D2.63. We investigated this possibility by performing reciprocal mutations and biochemical studies. D2.63176A, K373A, D2.63176A-K373A, and the reciprocal mutant with the interacting residues juxtaposed, D2.63176K-K373D were characterized using radioligand binding and guanosine 5'-3-O-(thio)triphosphate functional assays. None of the mutations resulted in a significant change in the binding affinity of CP55,940 or SR141716A. Computational results indicate that the D2.63176-K373 ionic interaction strongly influences the conformation(s) of the EC-3 loop, providing a structure-based rationale for the importance of the EC-3 loop to signal transduction in CB1. Specifically, the putative ionic interaction results in the EC-3 loop pulling over the top (extracellular side) of the receptor; this EC-3 loop conformation may serve protective and mechanistic roles. These results suggest that the ionic interaction between D2.63176 and K373 is crucial for CB1 signal transduction. This work may help to aide drug design efforts for the effective treatment of different diseases. The cannabinoid receptors of osteoblasts may represent a target for the treatment of bone disorders such as osteoporosis. Our research demonstrates that cannabinoids can affect important signaling molecules in osteoblasts. In MC3T3-E1 osteoblastic cells, the CB1 antagonist, AM251, has been reported to induce increases in Runx2 mRNA, mineralized bone nodule formation, and activation of signaling molecules such as ERK and AKT (Wu et al., 2011). Studies from our lab characterizing mice in which both CB1 and CB2 receptors were inactivated by homologous recombination have demonstrated increased bone mass coupled with enhanced osteoblast differentiation of bone marrow stromal cells in culture (manuscript in preparation). We explored the effect of antagonizing CB1 and CB2 cannabinoid receptors in osteoblastic cells to gain insights into molecular pathways that may help to explain the effects of the endocannabinoid system (ECS) in bone development. Our data was generated by running time course experiments with MC3T3-E1 cells under the influence of SR141716A, SR144528 or both in combination. The cells were harvested with a lysis buffer at specific time points and analyzed by western blot analysis. Quantification of protein activation was calculated using LiCor imaging equipment and software. Within 15 minutes, treatment with the CB1 receptor antagonist SR141716A resulted in several fold increases in pERK, pSMAD158, and pAKT. SR144528, a CB2 receptor antagonist, caused increases in pERK and pSMAD158, but not pAKT. When both antagonists were applied together, pERK and pSMAD158 levels increased, while pAKT signaling was diminished compared to SR141716A alone. The finding that cannabinoid receptor antagonists alter the activity of the SMAD158 complex is a novel finding, which suggests that cannabinoids can influence bone morphogenic signaling pathways, and therefore play a significant role in osteoblast differentiation and function.
Temple University--Theses
Jay, Freya [Verfasser], and Marlon [Akademischer Betreuer] Schneider. "Role of amphiregulin in mediating the bone anabolic actions of parathyroid hormone / Freya Jay ; Betreuer: Marlon Schneider." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2016. http://d-nb.info/1117473953/34.
Повний текст джерелаAschenberg, Sophie [Verfasser], and Georg [Akademischer Betreuer] Schett. "Catabolic and anabolic periarticular bone changes in patients with rheumatoid arthritis: a computed tomography study on the role of age, disease duration and bone markers / Sophie Aschenberg. Gutachter: Georg Schett." Erlangen : Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), 2014. http://d-nb.info/1075741653/34.
Повний текст джерелаGuimarães, Ana Paula Franttini Garcia Moreno. "Decanoato de nandrolona, qualidade óssea e calo ósseo em fratura do fêmur de rato." Universidade de São Paulo, 2017. http://www.teses.usp.br/teses/disponiveis/17/17142/tde-29032018-100618/.
Повний текст джерелаThere has been a great interest in investigating systemic substances that can positively act on the musculoskeletal system to improve the bone quality thus avoiding osteoporotic fractures. The anabolic androgenic steroids have an important influence on general metabolism and can increase the bone resistance and bone mass. On muscle, it improves sarcopenic conditions. However, there is no consistent investigation of a possible action of these substances on bone callus. Thus, the aim of this study was to evaluate the effect of decanoate of nandrolone on fracture healing and bone quality of young adult male Wistar rats. One hundred animals were divided into 04 groups and 02 subgroups (14 and 28 days). A control group consisted of animals without any intervention (n=17). In the second group, a femoral shaft fracture was performed (n=26). In the third group, the animals received only decanoate of nandronole (n=23). In the fourth group, a fracture in the femoral shaft was performed and associated with administration of the same dose of decanoate of nandrolone (n=26). The fracture created in the femur was obtained by closed method and achieved with the aid of a blunt blade guillotine. After that, the fracture was fixed with a 1.0 mm thick Kirschner wire that was inserted into the medullary canal, and the limb was X-rayed in profile. Ten mg/kg of body mass of decanoate of nandrolone was administered intramuscularly, 02 times a week for 14 or 28 days, depending on the subgroup. After euthanasia, the right femurs were dissected and had the length measured. Bone mineral density and bone mineral content were determined by the dual-energy x-ray absorptiometry method (DXA). The mechanical properties maximum force and stiffness were determined by the twopoint bending test. The bone callus was evaluated microscopically in sections stained with hematoxylin and eosin and examined under ordinary light microscope to calculate the volume of bone callus by the morphometric technique. Other sections were stained in picrosirius red and examined under polarized light for quantification of type I collagen. The statistical significance was set at 5%. There was no significant difference between the animals treated and not treated with nandrolone decanoate for bone mass density, bone mineral content, mechanical resistance and type I collagen, both for the intact bone and for the bone callus. However, the body mass was higher in the groups that received nandrolone decanoate, although without statistical significance. The femur length was greater in the 28th day in the group treated with nandrolone decanoate. Callus mass also had significant increase at 28 days for animals that received nandrolone decanoate. Based on the results and under the experimental conditions and methods of evaluation, the decanoate of nandrolone did not cause significant benefit or harmfull effects both on callus and on bone qualities.
"Combination of vitamins K₂ & D₃ supplementation enhances bone anabolism in type 2 diabetes-associated osteoporosis." 2014. http://repository.lib.cuhk.edu.hk/en/item/cuhk-1290651.
Повний текст джерела儘管大量研究已證明第二類型糖尿病和骨質疏鬆症的關聯,連接這兩個病症的基本機制仍然是難以捉摸的。在臨床上,鈣和維生素D的綜合補充劑是最常見的骨質疏鬆症治療,然而最近的研究卻表明服用鈣和維生素D的綜合補充劑會增加患者的心血管風險,因此急切需要尋找可以給予同時患有骨質疏鬆症和第二類型糖尿病患者的替代治療。在本研究中,我們假設甲萘醌-4(維生素K₂,維生素K生物活性形式)和1α,25 - 二羥基維生素D₃(維生素D₃,維生素D的生物活性形式)可以嘗試在同時患有骨質疏鬆症和第二類型糖尿病患者身上作為一種革新的療法。本研究從C57BL/KsJ瘦削/非糖尿病 (db⁺/m⁺) 的小鼠和肥胖/帶有第二類型糖尿病基因 (db⁺/db⁺) 兼有瘦素受體缺陷的小鼠的髂嵴原始成骨細胞上對維生素K₂和維生素D₃單獨或組合使用的合成代謝作用進行了評估。此外,我們也對該成骨細胞的底層機制進行了一系列的研究。
在肥胖/帶有第二類型糖尿病基因的小鼠血清內低羧骨鈣素水平(維生素K₂水平的指標)較高而維生素D水平較低,另外,它們的髂嵴的部分與瘦削/非糖尿病的小鼠相比,呈現出比較廣泛的多孔結構並填滿了擴大的脂肪細胞。從肥胖/帶有第二類型糖尿病基因的小鼠的成骨細胞中,可以觀察到它們的骨合成代謝的標誌物和骨骼形成的轉錄因子 (骨鈣蛋白,Runx2,Dlx5,ATF4,第一類型骨膠原,OSX,鹼性磷酸酶 (ALP) 活性,p-Smad1/5/8和p-ERK1/2) 的水平比較低。急性維生素D₃ (10 nM) 的應用在瘦削/非糖尿病小鼠的成骨細胞比起在肥胖/帶有第二類型糖尿病基因的小鼠的成骨細胞引起更持續和更大幅度的細胞內鈣變化增加。在瘦削/非糖尿病小鼠的成骨細胞中比起在肥胖/帶有第二類型糖尿病基因的小鼠的成骨細胞有顯著較高的鈣沉積形成。維生素K₂ (10 nM) 和維生素D₃ (10 nM) 的綜合藥在兩種小鼠的成骨細胞中可以有效地增強鈣沉積的形成。維生素K₂和維生素D₃的綜合藥對增加骨合成代謝的標誌物和骨形成轉錄因子的水平有時間依賴性 (7,14和21日),療程越長至21日,在肥胖/帶有第二類型糖尿病基因小鼠的成骨細胞中有更大的幅度的增加。合併維生素治療能部分有效地逆轉在肥胖/帶有第二類型糖尿病基因小鼠的成骨細胞中被抑制表達的鈣敏感受體 (CASR),F-肌動蛋白,V-ATP酶,維生素D受體 (VDR) 和孕烷X受體 (PXR)。此外,結合維生素K₂加維生素D₃治療顯著增強了肥胖/帶有第二類型糖尿病基因小鼠的成骨細胞的細胞遷移和增加了成骨細胞表面外觀的微絨毛和褶皺。在瘦削/非糖尿病小鼠的成骨細胞及肥胖/帶有第二類型糖尿病基因的小鼠的成骨細胞上結合維生素K₂加維生素D₃的治療效果被華法林 (20 μM,維生素K環氧化物還原酶抑製劑) 根除。因此,我們的結果証明了維生素K₂加維生素D₃補充劑的結合使用可有效地作為治療第二類型糖尿病患者並患有骨質疏鬆症的一種新的治療策略。
Poon, Chui Wa Christina.
Thesis (Ph.D.)--Chinese University of Hong Kong, 2014.n5203
Includes bibliographical references (leaves 135-151).
Abstracts also in Chinese.
Title from PDF title page (viewed on 26, October, 2016).
Detailed summary in vernacular field only.
Detailed summary in vernacular field only.
Welldon, Katie Jane. "The effect of bone anabolic stimuli on human osteoblast to osteocyte transition." Thesis, 2012. http://hdl.handle.net/2440/86832.
Повний текст джерелаThesis (M.Phil.) -- University of Adelaide, School of Medicine, 2012
Kamikovski, Ivan. "Does the growth hormone-derived peptide AOD9604 have an anabolic effect on bone?" 2009. http://link.library.utoronto.ca/eir/EIRdetail.cfm?Resources__ID=958095&T=F.
Повний текст джерелаTsai, Jhih-Jie, and 蔡志杰. "Forced expression of Notch signaling induces osteogenesis and hyperosteogeny in zebrafish Screen and evaluation of bone anabolic and cata bolic compounds in zebrafish." Thesis, 2013. http://ndltd.ncl.edu.tw/handle/47153474044588448062.
Повний текст джерелаHum, Julia M. "Signaling mechanisms that suppress the anabolic response of osteoblasts and osteocytes to fluid shear stress." Thesis, 2014. http://hdl.handle.net/1805/4652.
Повний текст джерелаBone is a dynamic organ that responds to its external environment. Cell signaling cascades are initiated within bone cells when changes in mechanical loading occur. To describe these molecular signaling networks that sense a mechanical signal and convert it into a transcriptional response, we proposed the mechanosome model. “GO” and “STOP” mechansomes contain an adhesion-associated protein and a nucleocytoplasmic shuttling transcription factor. “GO” mechanosomes functions to promote the anabolic response of bone to mechanical loading, while “STOP” mechanosomes function to suppress the anabolic response of bone to mechanical loading. While much work has been done to describe the molecular mechanisms that enhance the anabolic response of bone to loading, less is known about the signaling mechanisms that suppress bone’s response to loading. We studied two adhesion-associated proteins, Src and Pyk2, which may function as “STOP” mechanosomes. Src kinase is involved in a number of signaling pathways that respond to changes in external loads on bone. An inhibition of Src causes an increase in the expression of the anabolic bone gene osteocalcin. Additionally, mechanical stimulation of osteoblasts and osteocytes by fluid shear stress further enhanced expression of osteocalcin when Src activity was inhibited. Importantly, fluid shear stress stimulated an increase in nuclear Src activation and activity. The mechanism by which Src participates in attenuating anabolic gene transcription remains unknown. The studies described here suggest Src and Pyk2 increase their association in response to fluid shear stress. Pyk2, a protein-tyrosine kinase, exhibits nucleocytoplasmic shuttling, increased association with methyl-CpG-binding protein 2 (MBD2), and suppression of osteopontin expression in response to fluid shear stress. MBD2, known to be involved in DNA methylation and interpretation of DNA methylation patterns, may aid in fluid shear stress-induced suppression of anabolic bone genes. We conclude that both Src and Pyk2 play a role in regulating bone mass, possibly through a complex with MBD2, and function to limit the anabolic response of bone cells to fluid shear stress through the suppression of anabolic bone gene expression. Taken together, these data support the hypothesis that “STOP” mechanosomes exist and their activity is simulated in response to fluid shear stress.
Liu, Careesa Chang. "Effects of a New Conjugate Drug in a Rat Model of Postmenopausal Osteoporosis." Thesis, 2013. http://hdl.handle.net/1807/43088.
Повний текст джерела