Rozprawy doktorskie na temat „Osteoclast”
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O'Brien, Elizabeth Ann. "Regulation of osteoclast activity : differential adhesion of osteoclasts to the bone surface". Thesis, University of Liverpool, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.343930.
Pełny tekst źródłaStephens, Sebastien. "Novel Osteoclast Signalling". Thesis, Griffith University, 2010. http://hdl.handle.net/10072/365823.
Pełny tekst źródłaThesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Medical Science
Griffith Health
Full Text
Wilkinson, Debbie Isabelle. "Visualisation of osteoclast membrane domains". Thesis, University of Aberdeen, 2010. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=158808.
Pełny tekst źródłaZaidi, Mone. "Novel mechanisms of osteoclast regulation". Thesis, University of London, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.411434.
Pełny tekst źródłaGu, Xiaomei Everett Eric T. "Physiopathology of osteoclast in bone". Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2008. http://dc.lib.unc.edu/u?/etd,1870.
Pełny tekst źródłaTitle from electronic title page (viewed Dec. 11, 2008). "... in partial fulfillment of the requirements for the degree of Master of Science in the Curriculum of Oral Biology." Discipline: Oral Biology; Department/School: Dentistry.
Barnes, Calvin Langston Toure. "C-mpl Expression in Osteoclast Progenitors: A Novel Role for Thrombopoietin in Regulating Osteoclast Development". Yale University, 2006. http://ymtdl.med.yale.edu/theses/available/etd-06262006-123750/.
Pełny tekst źródłaHale, Annette Julie. "The characterisation of the Pagetic osteoclast". Thesis, University of Nottingham, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.359919.
Pełny tekst źródłaLång, Johanna. "CCL11 and Effects on Pre-osteoclast Migration". Thesis, Umeå universitet, Institutionen för odontologi, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-143797.
Pełny tekst źródłaCombs, Charlotte Emma. "The role of urocortin in osteoclast physiology". Thesis, St George's, University of London, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.517193.
Pełny tekst źródłaMacQuarrie, Robyn Melanie. "Arthroplasty-derived wear particles effect osteoclast differentiation". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/MQ63539.pdf.
Pełny tekst źródłaSarma, Ushasri. "Regulation of human osteoclast formation 17β estradiol". Thesis, Imperial College London, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.312178.
Pełny tekst źródłaBerger, Christine Elizabeth Marie. "Superoxide anion in osteoclast and osteoblast function". Thesis, University of Newcastle Upon Tyne, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.265210.
Pełny tekst źródłaRathod, Hersha. "Osteoclast-extracellular matrix interaction and intracellular signalling". Thesis, University of Newcastle Upon Tyne, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.387474.
Pełny tekst źródłaMuguruma, Yukari. "The origin and differentiation of the osteoclast /". Thesis, Connect to this title online; UW restricted, 1998. http://hdl.handle.net/1773/5681.
Pełny tekst źródłaMcManus, Stephen. "Regulation of osteoclast activation and autophagy through altered protein kinase pathways in Paget's disease of bone". Thèse, Université de Sherbrooke, 2016. http://hdl.handle.net/11143/8960.
Pełny tekst źródłaAbstract : Paget’s disease of bone (PDB) is a skeletal disorder characterized by focal and disorganized increases in bone turnover. In PDB, osteoclasts are larger, more active, more numerous, and resistant to apoptotic stimuli. While no single root cause has been identified, mutations to the gene encoding the p62 protein, SQSTM1, have been described in a significant population of patients with PDB. Among these mutations, the P392L substitution is the most prevalent, and overexpression of p62P392L in osteoclasts generates at least a partial pagetic phenotype in vitro. Normally this protein mediates a number of cell functions, from control of NF-κB signaling to autophagy. In human osteoclasts, a multiprotein complex containing p62 and protein kinases PKCζ and PDK1 (the principal kinase of Akt), form in response to stimulation by receptor activator of nuclear factor kappa-B ligand (RANKL), the principal osteoclastogenic-signaling cytokine. We found that PKCζ is involved in RANKL-induced activation of NF-κB, and that it contributed to a basal activation of NF-κB observed in p62P392L mutants. This may be regulated in part by a PKCζ dependent increase in p65 phosphorylation at Ser536 which we characterized, independent of IκB. This could represent one alternative pathway by which mutant p62 leads to increased NF-κB activation. We observed increased basal phosphorylation of survival regulators ERK and Akt in PDB that was reduced upon PDK1 inhibition. The activity of 4EBP1 and Raptor, associated with mTOR activity, were also altered in pagetic osteoclasts and regulated by PDK1 inhibition. We then identified autophagic defects common to pagetic osteoclasts; with higher basal levels of LC3II (associated with autophagic structures), regardless of p62 mutation, and reduced sensitivity to autophagy induction in PDB. These results suggest an accumulation of non-degradative autophagosomes. Inhibition of PDK1 not only induced apoptosis in PDB and controls, but significantly reduced resorption in PDB, and with regards to autophagy, PDK1 inhibition was more potent in PDB than in controls. Therefore PDK1/Akt signaling represents an important checkpoint to PDB osteoclast activation. In sum, these results demonstrate the importance of several p62-associated kinases in the over-activation of pagetic osteoclasts, through increased survival and altered signaling. As p62 mutations alone do not account for most cases of PDB, the characterization of these pathways may identify a common factor linking pagetic osteoclasts. Therefore these studies represent a novel approach to osteoclast apoptosis, activation, and autophagy associated with PDB.
Tan, Jamie We-Yin. "The investigation of RANKL TNF-like core domain by truncation mutation". University of Western Australia. School of Surgery and Pathology, 2003. http://theses.library.uwa.edu.au/adt-WU2004.0032.
Pełny tekst źródłaMattsson, Jan P. "The osteoclast H⁺-ATPase isolation and initial characterization /". Göteborg, Sweden : Dept. of Biochemistry and Biophysics, Dept. of Cell Biology, University of Göteborg and Chalmers University of Technology, 1995. http://books.google.com/books?id=_85qAAAAMAAJ.
Pełny tekst źródłaDavey, 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.
Pełny tekst źródłaMoonga, Baljit Singh. "Studies on the intracellular mechanisms of osteoclast control". Thesis, St George's, University of London, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.411462.
Pełny tekst źródłaMorrison, Matthew Sam. "Osteoclast function : role of extracellular pH and ATP". Thesis, University College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.369218.
Pełny tekst źródłaTran, Anh Nhi. "Examining the role of autophagy in osteoclast function". Thesis, University of Aberdeen, 2018. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=238273.
Pełny tekst źródłaMoreira, Mariana Matheus. "Efeito do alendronato sódico sobre a atividade clástica na periodontite experimental em ratos". Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/23/23140/tde-18092014-133646/.
Pełny tekst źródłaPeriodontitis is an infectious disease of multifactor nature that results in the inflammation of the tissues supporting the teeth. This inflammation is caused by accumulation of biofilm and causes progressive insertion and bone loss. The bisphosphonates are drugs with the capability to inhibit the activity of clastic cells. The aim of this study was to investigate the effects of alendronate, a nitrogenated bisphosphonate with high antiresorptive power on experimental periodontal disease, and to analyze the possible presence of osteonecrosis in the rat alveolar process. Forty-eight male Wistar rats, three months old, with 250g weight were used. The animals were randomly divided into two groups: Alendronate (ALN) and Control (CON). The periodontitis was induced with a 4.0 silk wire inserted into the gingival sulcus around the right upper second molar. The ALN rats, received daily doses of 2.5 mg/kg alendronate (ALN) for 7 days before the induction of periodontitis; the treatment continued for additional 7, 14, 21 or 30 days. The CON rats, received sterile saline solution. In the time points cited, the maxillae were fixed, decalcified and embedded in Spurr resin or paraffin. The specimens were morphologically analyzed in HE stained sections, after which histomorphometry was carried out. Some stained sections were used for immunolabeling for RANKL and OPG. The osteoclasts were marker by tartrate-resistant acid phosphatase (TRAP) histochemistry. The ultrathin sections were examined in a transmission electron microscope. ALN reduced the activity of osteoclasts and significantly decreased the resorption of the alveolar crest. In the control group the alveolar crest appeared resorbed, while TRAP showed active osteoclasts, findings confirmed by transmission electron microscopy. The expression of RANKL, an osteoclast-activating molecule, was not inhibited by the drug. The expression of OPG was increased in the treated animals. The animals of the group treated for 21 and 30 days showed signs of osteonecrosis of the alveolar crest, as empty osteocyte lacunae in the exposed bone regions. The results showed that the use of ALN for periodontal disease inhibited bone resorption; when it was administered for prolonged periods it can cause osteonecrosis in the bone crest area.
Wang, Ee Jen Wilson. "The effects of infection-related factors on bone resorption". Thesis, University of Oxford, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.365291.
Pełny tekst źródłaPhan, Tuan (Tony). "Functional characterisation of an osteoclast-derived osteoblastic factor (ODOF)". University of Western Australia. School of Surgery and Pathology, 2004. http://theses.library.uwa.edu.au/adt-WU2005.0028.
Pełny tekst źródłaJones, Gemma. "Optimisation and characterisation of osteoblast : osteoclast growth in biomaterials". Thesis, Keele University, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.505664.
Pełny tekst źródłaO'Grádaigh, Donncha. "Osteoclast regulation in the erosive process in rheumatoid arthritis". Thesis, University of Cambridge, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.615638.
Pełny tekst źródłaWalsh, Catherine Ann. "The study of tumour stimulated osteoclast activity in vitro". Thesis, University of Liverpool, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.317317.
Pełny tekst źródłaLuchin, Alexander I. "Regulation of Osteoclast differentiation by Microphthalmia-associated transcription factor /". The Ohio State University, 2001. http://rave.ohiolink.edu/etdc/view?acc_num=osu1486399451961539.
Pełny tekst źródłaMartin, Joanne. "In vitro osteoclast resorption of calcium phosphate bone substitutes". Thesis, Queen's University Belfast, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.695663.
Pełny tekst źródłaZhu, Min. "Regulation of osteoclast maturation and function by resolvin E1". Thesis, Boston University, 2012. https://hdl.handle.net/2144/12701.
Pełny tekst źródłaInnate and adaptive immunity actively interact with bone and play an important role in bone physiology and pathology. Acute inflammation is a physiologic response that represents the hosts' first line of defense. Failure to resolve the acute inflammatory lesion leads to a chronic pathologic lesion including bone destructive conditions such as periodontitis and arthritis. Resolution of inflammation is now known to be an active process with highly coordinated interaction of cells and soluble mediators leading to the return of tissues to homeostasis, rather than a passive decay of pro-inflammatory signals as previously supposed. The ω-3 polyunsaturated fatty acid derivative resolvin E1 (RvE1) is a novel lipid mediator shown to be actively involved in the resolution of inflammation. The goal of the current studies was to determine the cellular and molecular mechanism of RvE1 impact on osteoclasts. Investigation of the actions of RvE1 treatment on the specific stages of osteoclast maturation revealed that RvE1 targeted late stages of osteoclast maturation. Observations with time-lapse vital microscopy revealed that RvE1 inhibited migration and fusion of osteoclast precursors. Migration assays confirmed that chemotactic migration of osteoclast precursors was significantly inhibited by RvE1. To determine the molecular basis of RvE1 actions, fusion proteins that mediate the migration, fusion and function of osteoclasts and the essential transcription factor NFATc1 were examined. RvE1 specifically down-regulated the pivotal osteoclast fusion protein DC-STAMP (dendritic cell specific transmembrane protein) through the receptor BLT-1. RvE1 did not impact the induction of NFATc1 nor its nuclear translocation; however, NFATc1 binding to the DC-STAMP promoter was inhibited by RvE1 treatment. The results suggest that RvE1 inhibits migration and fusion of osteoclast precursors leading to decreased numbers of mature osteoclasts. On the molecular level, RvE1 binds to the cell surface receptor BL T-1 inhibiting the downstream binding of the transcription factor NFATc1 to the fusion protein DC-STAMP promoter, leading to a reduction in the number of functioning multinucleated osteoclasts and reduced bone resorption. These observations further establish a dual role for inflammation resolution in innate immunity as well as bone preservation through the direct regulation of bone cell function.
Cheng, Tak Sum. "Molecular identification and characterization of novel osteoclast V-ATPase subunits". University of Western Australia. School of Surgery and Pathology, 2008. http://theses.library.uwa.edu.au/adt-WU2008.0068.
Pełny tekst źródłaZhao, Yuming. "Phenotypic analysis of osteoclast lineage in c-fos mutant mice". Thesis, King's College London (University of London), 2003. https://kclpure.kcl.ac.uk/portal/en/theses/phenotypic-analysis-of-osteoclast-lineage-in-cfos-mutant-mice(fafcec7f-6480-4f8c-87b6-3cca60a475fb).html.
Pełny tekst źródłaJames, Ian Edward. "The production and characterization of human osteoclast-reactive monoclonal antibodies". Thesis, University of Bath, 1992. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.303100.
Pełny tekst źródłaMcDermott, Emma. "Characterisation of the osteoclast ruffled border using advanced imaging techniques". Thesis, University of Aberdeen, 2018. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=236980.
Pełny tekst źródłaTai, Victoria. "The effects of leukotriene B¦4 on osteoclast formation and osteoclastic bone resorption and the role of osteoblastic cells in these processes". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ28805.pdf.
Pełny tekst źródłaMcMichael, Brooke Kristin Trinrud. "Tropomyosin 4, myosin IIA, and myosin X enhance osteoclast function through regulation of cellular attachment structures". Columbus, Ohio : Ohio State University, 2008. http://rave.ohiolink.edu/etdc/view.cgi?acc%5Fnum=osu1206052974.
Pełny tekst źródłaMaterozzi, Maria. "Molecular biology of Paget’s Disease of Bone: role of p62 and novel genes". Doctoral thesis, Università di Siena, 2020. http://hdl.handle.net/11365/1104964.
Pełny tekst źródłaLees, Rita L. "Osteoclast heterogeneity, the importance of cell size and phase of activity". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0016/NQ53821.pdf.
Pełny tekst źródłaBrunton, Fiona. "Targeting the osteoclast alpha v beta 3 integrin by phage display". Thesis, Queen Mary, University of London, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.511761.
Pełny tekst źródłaAl-Hadi, Hadil. "The effect of Hyperbaric Oxygen Therapy on osteoclast and osteoblast function". Thesis, University of Plymouth, 2013. http://hdl.handle.net/10026.1/1614.
Pełny tekst źródłaHuber, Dustin Michael. "ANDROGENS SUPPRESS OSTEOCLAST FORMATION INDUCED BY RANK LIGAND AND M-CSF". University of Cincinnati / OhioLINK, 2001. http://rave.ohiolink.edu/etdc/view?acc_num=ucin999020063.
Pełny tekst źródłaSelinger, Christina Imanta. "Identification of RANKL-Regulated Genes Involved in Osteoclast Differentiation and Resorption". Thesis, Griffith University, 2008. http://hdl.handle.net/10072/367396.
Pełny tekst źródłaThesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Medical Science
Griffith Health
Full Text
Obaid, Rami Abdulhadi Abdulmajeed. "Investigating the role of optineurin in bone biology and Paget's disease of bone". Thesis, University of Edinburgh, 2016. http://hdl.handle.net/1842/23419.
Pełny tekst źródłaRezende, Eloiza de. "Estudo do efeito de bisfosfonatos nas células clásticas durante a ossificação endocondral do joelho de ratos e em cultura primária: abordagens morfológicas e moleculares". Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/42/42134/tde-29052014-151314/.
Pełny tekst źródłaIn endochondral ossification, clastic cells (Oc) resorb the calcified cartilage, while osteoblasts (Ob) form new bone. Bisphosphonates (Bps) inhibit the action of Oc. The effect of the Bps alendronate (Aln) and etidronate (Etn) on the knees of young rats (in vivo) and in primary cultures of Oc (in vitro) was evaluated. The specimens were analyzed by SEM, TEM, and LM or TRAP histochemistry. RNA was extracted to analysis by RT-PRC and protein to analysis by WB. RNA and protein were also extracted after the treatment of cultures with Bps. Rats treated with Etn exhibited a disorganized epiphyseal plate containing large area of cartilage; SEM showed few bone trabeculae with resorption lacunae, which were not observed in Aln specimens. Aln showed numerous latent Oc by TRAP histochemistry and TEM. In vivo, the Bps decreased the expression of all analyzed genes; in vitro, Aln decreased only the expression of Runx2 as well as SPP1, which expression was less with Etn. Protein expression varied among the groups. Aln is more potent for inhibiting the Oc, while Etn acts on Ob.
Marques, Natasha D'Andrea Mateus. "Estudo da expressão das moléculas reguladoras da remodelação do osso alveolar durante a movimentação ortodôntica com força contínua em ratos tratados com alendronato sódico". Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/23/23140/tde-25022016-165617/.
Pełny tekst źródłaOrthodontic tooth movement occurs through two processes in which the alveolar bone is resorbed in the pressure areas, whereas new bone is formed in the tension area. The bone resorption occurs by multinucleated cell, the osteoclasts. The bisphosphonates are drugs with capability to inhibit clastic activity were used in the present study in order to interfere with the bone remodeling induced orthodontic. For this continuous force of 15 cN was applied to the first molars of Wistar male rats of 2 1/2 months, using a biomechanical with superelastic wire. The animals were randomly divided into 4 groups: 1) The control group consisted of eighteen mice, which received sterile saline solution saline for 7 days prior to installation of passive biomechanics, which remained for 3, 10 and 18 days; 2) Eighteen animals were treated with ALN (dose 2.5 mg / kg) for 7 days prior to installation of the passive biomechanical to remain for 3, 10 and 18 days; 3) Eighteen animals were treated with alendronate with the same dose quoted above for 7 days prior to the biomechanical installation that remains active for 3, 10 and 18 days; 4) Eighteen animals were injected with sterile saline solution 7 days prior to the biomechanical installation that remains active for 3, 10 and 18 days. The maxillae were fixed with 4% formaldehyde + 0.1% glutaraldehyde, decalcified in EDTA 4.13% and embedded in paraffin or Spurr resin. The specimens were morphologically analyzed in HE stained sections. Some stained sections were used for immunolabeling for RANKL and OPG. The osteoclasts were marked by tartrate-resistant acid phosphatase (TRAP) histochemistry. The ultrathin sections were examined in a trasnmission electron micrsocpe. Some specimens were frozen in liquid nitrogen for protein extraction and Western Blotting protein expression analyzes. The ALN inhibited bone resorption and root of all the treated groups. The clastic cells present in a latent state. In the orthodontic movement group alveolar bone was remodeled with 18 days to root surface presented itself reabsorbed and the TRAP revealed clasts assets, findings confirmed by transmission electron microscopy. Expression of RANKL activating molecule clastic cells was not inhibited by the drug. The OPG expression was increased in treated animals. The results demonstrate that the use of alendronate in the orthodontic movement does not interfere with osteoclast recruitment, it apparently inhibits their activation, which can interfere in the bone remodeling process and may reduce the amount of tooth movement.
Hu, Rong. "Regulation of osteoclast differentiation by transcription factors MITF, PU.1 and EOS". Columbus, Ohio : Ohio State University, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1166644761.
Pełny tekst źródłaDossa, Tanya. "Osteoclast-specific inactivation of the Integrin-Linked Kinase (ILK) inhibits bone resorption". Thesis, McGill University, 2006. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=99336.
Pełny tekst źródłaMellis, David. "The study of RANK mutations associated with the diseases of osteoclast dysfunction". Thesis, University of Aberdeen, 2010. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=166647.
Pełny tekst źródłaWani, Mohan Ramchandra. "Regulation of osteoclast formation and activation by TRANCE and prostaglandin Eâ†2". Thesis, St George's, University of London, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.341938.
Pełny tekst źródłaAlthnaian, Thnaian Ali. "Factors that regulate osteoclast formation and bone resorption in regenerating deer antlers". Thesis, Royal Veterinary College (University of London), 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.439832.
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