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Lucas, Gavin J. A. "Genetics of Paget's disease of bone". Thesis, University of Aberdeen, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.430978.
Pełny tekst źródłaHocking, Lynne J. "Genetics of Paget's disease of bone". Thesis, University of Aberdeen, 2002. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU160239.
Pełny tekst źródłaGood, David Andrew, i n/a. "Genetic Loci for Paget's Disease of Bone". Griffith University. School of Biomolecular and Biomedical Science, 2003. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20040319.125358.
Pełny tekst źródłaNajat, Dereen. "SQSTM1 mutations and Paget's disease of bone". Thesis, University of Nottingham, 2010. http://eprints.nottingham.ac.uk/11118/.
Pełny tekst źródłaBirch, Mark Andrew. "Investigations of bone cells in Paget's disease". Thesis, University of Liverpool, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.333632.
Pełny tekst źródłaGood, David Andrew. "Genetic Loci for Paget's Disease of Bone". Thesis, Griffith University, 2003. http://hdl.handle.net/10072/365759.
Pełny tekst źródłaThesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Biomolecular and Biomedical Sciences
Full Text
Numan, Mohamed. "Gene-environment interaction in Paget's disease of bone". Master's thesis, Université Laval, 2017. http://hdl.handle.net/20.500.11794/27518.
Pełny tekst źródłaPaget's disease of bone (PDB) is a metabolic bone disease. Although genetic factors play an important role in the pathogenesis of PDB, environmental factors such as rural residence and the exposure to wood heating was associated with PDB. In order to study the role of outdoor and indoor air pollutants on PDB, we performed a survey in 140 French-Canadian patients with PDB and 113 healthy controls. The survey covered the outdoor air pollution such as the residence near a highway, a bus station, a train or an airport or a gas station, and indoor air pollutants by focusing on heating fuels (carbon, wood, oil) and exposure to tobacco smoke. In a subgroup of patients, urinary concentration of 17 heavy metals and 11 polycyclic aromatic hydrocarbons was measured by mass spectrometry. In light of what we knew from the survey and urinary assays, we identified certain toxics that could be risk factors for PDB. To explore the in vitro effects of these toxics on osteoclasts in PDB, we conducted in vitro monocytes differentiation from peripheral blood of more than 40 participants, patients, healthy carriers of p.Pro392Leu mutation, and healthy controls, which osteoclasts were treated with or without the identified toxic. The morphology of osteoclasts, the percentage of bone resorption, gene expression level, and cellular oxidative stress levels were assayed. The results showed an inhibitory effect of cigarette smoke condensate and heavy metals on morphology and function of patients’ osteoclasts. Further, high levels of oxidative stress in patients’ osteoclasts were observed, and a heterogenic profile of heavy metals effect on gene expression was identified.
Billah, Ahmed Mohammed El-Motaz. "Markers of bone turnover in health and disease". Thesis, University of Nottingham, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.295769.
Pełny tekst źródłaTaggart, Frances Margaret. "The epidemiology of Paget's disease of bone in Europe". Thesis, University of Southampton, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.328623.
Pełny tekst źródłaRios, Visconti Micaela. "Genetic and environmental determinants of Paget's disease of bone". Thesis, University of Edinburgh, 2015. http://hdl.handle.net/1842/20421.
Pełny tekst źródłaObaid, 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 źródłaDaroszewska, A. "Role of osteoprotegerin and p62 in Paget's disease of bone". Thesis, University of Aberdeen, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.590957.
Pełny tekst źródłaNicholas, Richard Martin. "A laboratory and clinical study of Paget's disease of bone". Thesis, Queen's University Belfast, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.317547.
Pełny tekst źródłaGinty, Andrew Francis. "A study of cellular proliferation, plasminogen activator activity and cytokine expression in human osteoblasts and tumour cells". Thesis, University of Liverpool, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.261975.
Pełny tekst źródłaSimone, Bianciardi. "MicroRNAs expression profiling in Paget’s Disease of Bone, Osteoporosis and Hyperparathyroidism". Doctoral thesis, Università di Siena, 2021. http://hdl.handle.net/11365/1138295.
Pełny tekst źródłaAzzam, Eman. "The role of autophagy in the pathogenesis of Paget's disease of bone". Thesis, University of Aberdeen, 2013. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=203961.
Pełny tekst źródłaVallet, Mahéva. "The study of RIN3 : a susceptibility gene for Paget's disease of bone". Thesis, University of Edinburgh, 2017. http://hdl.handle.net/1842/28678.
Pełny tekst źródłaBell, Lynne Sevon. "Post mortem microstructural change to the skeleton". Thesis, University College London (University of London), 1995. http://discovery.ucl.ac.uk/1317796/.
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.
Rhodes, Emily C. "The role of sequestosome 1 (SQSTM1) in Paget's disease of bone a dissertation /". San Antonio : UTHSC, 2008. http://proquest.umi.com.libproxy.uthscsa.edu/pqdweb?did=1588776521&sid=2&Fmt=2&clientId=70986&RQT=309&VName=PQD.
Pełny tekst źródłaGoode, Alice. "Effects of Paget's disease of bone-associated P62 mutations on protein structure and function". Thesis, University of Nottingham, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.606813.
Pełny tekst źródłaHadi, Tamer. "THE ROLE OF p62 IN OSTEOCLASTOGENESIS AND PAGET’S DISEASE OF BONE". VCU Scholars Compass, 2012. http://scholarscompass.vcu.edu/etd/3312.
Pełny tekst źródłaConesa, Mateos Arántzazu. "Caracterización clínica, epidemiológica y molecular de la enfermedad Ósea de Paget". Doctoral thesis, Universitat Autònoma de Barcelona, 2021. http://hdl.handle.net/10803/673198.
Pełny tekst źródłaLa enfermedad ósea de Paget (EOP) se caracteriza por ser un trastorno crónico y focal del remodelado óseo que conlleva a la aparición de complicaciones como deformidades óseas, artropatía por vecindad y fracturas. La EOP presenta una gran variabilidad en su distribución en función de la edad, género, etnia y área geográfica. Recientes estudios han descrito cambios seculares en cuanto a la prevalencia, incidencia y gravedad al diagnóstico de la EOP, mostrando una disminución en las últimas décadas. La EOP se considera actualmente una enfermedad multifactorial con participación de factores ambientales y genéticos. El gen que ha mostrado mayor susceptibilidad es el Sequestosoma1(SQSMT1), las mutaciones descritas en él no explicarían de forma completa la patogenia de la EOP. En la actualidad, son escasos los estudios acerca de variaciones genéticas en los genes TNFRSF11B y TNFRSF11A asociados a EOP clásica así como la existencia de interacciones genéticas entre ambos genes y el gen SQSMT1, que conduzca a un incremento de riesgo de EOP e incluso que influya en el fenotipo. Con la finalidad de investigar el patrón de comportamiento clínico-epidemiológico como genético de la EOP de nuestra población de baja prevalencia, nos planteamos los siguientes objetivos. Los objetivos se centraron en evaluar cambios en la evolución del porcentaje de nuevos diagnósticos de EOP durante el periodo 1970-2009 y describir en dichos pacientes diferencias en cuanto a la severidad al diagnóstico. Así como así como analizar la importancia de alteraciones moleculares en el gen SQSTM1 y la presencia de variaciones alélicas en los genes TNFRSF11B y TNFRSF11A, tanto en la susceptibilidad para el desarrollo de la EOP como la influencia en su fenotipo. Pacientes y Métodos: Estudio descriptivo ambispectivo observacional de pacientes procedentes del Hospital del Mar-Parc de Salut Mar (Barcelona), un área de baja prevalencia. Se incluyeron 393 pacientes, diagnosticados entre 1970 y 2009. En base al estudio molecular se llevó a cabo el genotipado de las 21 variantes polimórfica para el estudio los genes TNFRSF11B y TNFRSF11A, así como la secuenciación del gen SQSTM1 en una población de 200 pacientes afectos de EOP y 200 controles hipernormales. Resultados: En el estudio se observa un descenso progresivo del porcentaje de nuevos diagnósticos de EOP en relación a la población de referencia, entre 1994 y 2009, más marcado en el grupo de ≥ de 65 años. Asimismo, se ha constatado que los pacientes afectos de EOP presentan una disminución en la actividad biológica de la enfermedad, una menor extensión de la enfermedad y una mayor edad de presentación al diagnóstico, en función del año de nacimiento y año del diagnóstico. En contraposición, se ha observado mayor severidad en el momento del diagnóstico en los pacientes con edades al diagnóstico de <45 años y ≥75 años. Se han identificado 5 factores independientes de mal pronóstico al diagnóstico, que van a favorecer peores desenlaces. Por lo que podemos concluir, que en el momento de diagnóstico de EOP, la expresión de la enfermedad es menos severa y acontece de forma más tardía. Los resultados del estudio molecular destacan la asociación significativa entre los SNPs rs3018362 y rs1805034 del gen TNFRSF11A y rs11573871 del gen TNFRSF11B con el incremento de riesgo a desarrollar EOP así como la influencia en su fenotipo. Asimismo se observó que la presencia del alelo T en el polimorfismo rs6567274 del gen TNFRSF11A se asoció con una disminución de riesgo a desarrollar la EOP, así como a un fenotipo más leve. En el estudio molecular del gen SQSTM1 se identificaron seis variantes genéticas "missense" de nueva descripción, asociadas todas ellas a una mayor susceptibilidad en el desarrollo de la EOP.
Paget’s Disease of Bone (PDB) is characterized by a chronic and focal disorder of bone remodeling that leads to the appearance of complications as bone deformities, osteoarthritis and fractures. The PDB presents a great variability in its distribution depending on the age, gender, ethnics and geographic area. Recent studies have described secular changes in the prevalence, incidence and severity at diagnosis of PDB, showing a decline in the last decades. PDB is currently considered a multifactorial disease involving environmental and genetic factors. The gene which has shown higher susceptibility is the Sequestosome-1 (SQSTM1), the mutations described in it would not be able to explain completely the PDB pathogenesis. Nowadays, there are few studies on genetic variations in the TNFRSF11B and TNFRSF11A genes associated with classic PDB, as well as the existence of genetic interactions between both genes and the SQSMT1 gene, leading to an increased risk of PDB or even influencing the phenotype. To investigate the pattern of clinical-epidemiological and genetic behavior of the PDB in our low prevalence population, we propose the following objectives. The objectives were focused on evaluating changes in the evolution of the percentage of new PDB diagnoses during the period 1970-2009 and to describing in those patients differences in terms of severity at diagnosis. As well as to analyze the importance of molecular alterations in the SQSTM1 gene and the presence of allelic variations in the TNFRSF11B and TNFRSF11A genes, both in the susceptibility for the development of PDB and its influence on the phenotype. Patients and Methods: Descriptive, ambispective observational study of patients from Hospital del Mar-Parc de Salut Mar (Barcelona), a low prevalence area. 393 patients, diagnosed between 1970 and 2009, were included. Based on the molecular study, the genotyping of the 21 polymorphic variants was carried out for the study of the TNFRSF11B and TNFRSF11A genes, as well as the sequencing of the SQSTM1 gene in a population of 200 PDB affected patients and 200 hypernormal controls. Results: The study observed a progressive decrease in the percentage of new PDB diagnoses in relation to the reference population, between 1994 and 2009, more marked in the group ≥65 years old group. Thereby, it has been confirmed that the PDB-affected patients show a decrease in the biological activity of the disease, a lower extension of the disease, and a higher age of presentation at diagnosis, depending on the year of birth and the year of diagnosis. In contrast, it has been observed higher severity at diagnosis in patients with ages at diagnosis <45 years and ≥75 years. Five independent factors of poor prognosis at diagnosis have been identified, which will favor worse outcomes. We can conclude, that at the time of diagnosis of PDB, the expression of the disease is less severe and occurs later. The results of the molecular study highlight the significant association between SNPs rs3018362 and rs1805034 of the TNFRSF11A gene and rs11573871 of the TNFRSF11B gene with the increased risk of developing PDB as well as the influence on its phenotype. Thereby, it was observed that the presence of the T allele in the polymorphism rs6567274 of the TNFRSF11A gene was associated with a decreased risk of developing PDB, as well as a milder phenotype. In the molecular study of the SQSTM1 gene, six newly described “missense” genetic variants were identified, all associated with greater susceptibility in the development of PDB.
Universitat Autònoma de Barcelona. Programa de Doctorat en Medicina
Nazari, Shekeba. "Maladie de Paget : résistance à l'apoptose et défaut de l'autophagie". Mémoire, Université de Sherbrooke, 2017. http://hdl.handle.net/11143/11869.
Pełny tekst źródłaAbstract : Paget's disease is an osteopathy characterized by a multifocal increase in bone remodeling, which begins with excessive bone resorption followed by increased bone formation. Osteoclasts "OCs" were incriminated in the initiation of the pagetic process. Pagetic OCs are characterized by a resistance to apoptosis, and abnormalities in the process of autophagy “in particular induction defect”. In order to define whether these two characteristics were linked, we hypothesized the role of Bcl2-Beclin1 complexes. Beclin-1 is an autophagy-inducing protein that can bind anti-apoptotic proteins of the Bcl-2 family; Bcl-2 then inhibits Beclin-1 "and thus the induction of autophagy" while retaining its anti-apoptotic functions. To study the impact of Bcl2 expression on autophagy in human OCs, we used an in vitro differentiation model that uses monocytes, which are derived from umbilical cord blood and grown in the presence of RANKL and MCSF for 21 days. These conditions make it possible to obtain multinucleated cells with an osteoclastic phenotype. To increase the expression of Bcl-2 in OCs and analyze its impact on autophagy due to its interaction with Beclin-1, cultures were stimulated with TNFα or RANKL in order to induce NF-κB activation. The expression of Beclin1 and Bcl2 was confirmed by immunoblotting of Ocs cell lysates. Autophagy was induced in cultures carried out under stringent conditions "nutriment-deprived mediun", but we did not observe any variation in the expression of Bcl2 or Beclin 1 according to the culture conditions or TNFα or RANKL stimulation. TNFα significantly stimulated the activation of NF-κB in HEK cells but not in OCs. However, whatever the conditions, results from immunoprecipitaion experiments did not reveal any association between Beclin1 and Bcl2. On the other hand, the classic interaction partner of Beclin1, PI3K type III, was associated with Beclin1. In conclusion, our work did not allow us to demonstrate the formation of Beclin1 / Bcl2 complexes and the relationship between apoptosis and autophagy, partly because of the complexity of the model "multiple effects of NF-κB and TNFα". Our initial hypothesis should thereby be re-evaluated using a more appropriate methodology. On the other hand, the different techniques are now ready for further study.
Materozzi, 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 źródłaLiu, Xiaoyan. "IDENTIFICATION OF SUMOYLATED PROTEINS AND INVESTIGATION OF PROTEIN UBIQUITINATION IN THE NF-κB PATHWAY". UKnowledge, 2012. http://uknowledge.uky.edu/biochem_etds/4.
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 źródłaEllis, Patricia Elizabeth. "The molecular pathology of Paget's disease of the vulva and the breast". Thesis, University College London (University of London), 2007. http://discovery.ucl.ac.uk/1444443/.
Pełny tekst źródłaWatson, Nicola Sophia Alexandra. "Identification of novel genes involved in Paget's disease by Differential Display PCR". Thesis, University of Aberdeen, 1999. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU535579.
Pełny tekst źródłaWedin, Rikard. "Metastatic bone disease /". Stockholm, 2000. http://diss.kib.ki.se/2000/91-628-3829-6/.
Pełny tekst źródłaAndrade, José Costa de. "Perfil imunoistoquímico do carcinoma de Paget da mama /". Botucatu : [s.n.], 2004. http://hdl.handle.net/11449/103714.
Pełny tekst źródłaResumo: O objetivo deste trabalho foi estudar através do exame Imunoistoquimico, a correlação entre alguns fatores Anatomopatológicos (tipo histológico e grau nuclear) e alguns fatores biológicos (receptores hormonais de estrógeno e de progesterona, proteína c-erbB-2 e proteína p53, no carcinoma de Paget da mama, doença rara e especial. No período entre Janeiro de 1980 a Dezembro de 1998 foram tratados no Instituto Brasileiro de Controle do Câncer, 6.303 casos de câncer de mama, deste total 98 casos foram diagnosticados como carcinoma de Paget, cuja incidência foi de 1,55%. Estudamos retrospectivamente 60 casos, sendo que 38 deles foram excluídos da análise, devido a limitação e escassez da amostra no material disponível, a idade das pacientes variou entre 26 e 84 anos, com média de 55,4 anos, as informações clínicas e terapêuticas foram obtidas dos prontuários das pacientes considerando, idade na época do diagnóstico, tamanho do tumor quando palpável, estadiamento clínico, e o tipo de cirurgia realizada. As amostras de tecido mamário foram recuperadas dos arquivos do Departamento de Anatomia Patológica do I.B.C.C. / MATTOSINHO. Após a revisão histológica, realizada por dois patologistas os casos foram classificados em quatro grupos: Grupo A- Doença de Paget (forma pura) n = 09 Grupo B- Doença de Paget + neoplasia ductal "in situ", n = 12 Grupo C- Doença de Paget, neoplasia ductal invasora, n = 30 Grupo D- Doença de Paget + neoplasia ductal "in situ"+ neoplasia ductal invasora, n = 09. Entre as variáveis anatomopatológicas, o grupo C prevaleceu com 30 casos (50%). O grau nuclear (GN-II) predominou com 45 casos (75%). Em relação as variáveis biológicas o receptor de estrógeno negativo predominou com 41 casos (68,3%), seguido pelo receptor de progesterona negativo com 40 casos (66,7%), podemos dizer que... (Resumo completo, clicar acesso eletrônico abaixo)
Abstract: The objective of this paper was to study the immunohistochemical efects of Paget's disease, a rare and special carcinoma of the breast, by correlating anatomopathological (histological and nuclear grade) and biological (estrogen and progesterone hormonal receptors, c-erbB-2 protein and p53 protein) factors. Between January 1980 and December 1998, 6303 cases of breast cancer were treated at the Brazilian Institute of Cancer Control; 98 of these were diagnosed with Paget's carcinoma, an incidence of 1.55%. We retrospectively studied 60 of these cases; 38 were excluded due to lack of available sample material. Patient age varied between 26 and 84 years (mean 55.4), clinical and therapeutic information were obtained from patient's medical records considering age at time of diagnosis, tumor size when palpable, clinical stage, and type of surgery performed. Samples of breast tissue were retrieved the Anatomical Pathology Department, I.B.C.C. / MATTOSINHO. After histological review, by two different pathologists, they were classified into four groups: Group A- Paget's disease (pure form) n = 09 Group B- Paget's disease + "in situ" duct neoplasia n = 12 Group C- Paget's disease, invasive duct neoplasia n = 30 Group D- Paget's disease + "in situ" duct neoplasia + invasive duct neoplasia n = 09.Invasive duct neoplasia was the most prevalent anatomopathological variable (Group C, n = 30, 50%). Nuclear grade (GNII) was found in 45 cases (75%). In relation to the biological variables, the negative estrogen receptor was predominant with 41 cases (68.3%), followed by the negative progesterone receptor with 40 cases (66.7%); this correlation had good concordance by the Kappa test. The c-erbB-2 protein was positive in 53 cases (88.3%) and p53 was negative in 47 cases (78.3%). From these results, we concluded that there was no statistical... (Complete abstract click electronic address below)
Doutor
Бугайов, Володимир Іванович, Владимир Иванович Бугаев, Volodymyr Ivanovych Buhaiov i Н. А. Лисенко. "Хвороба Педжета". Thesis, Видавництво СумДУ, 2009. http://essuir.sumdu.edu.ua/handle/123456789/6641.
Pełny tekst źródłaМолодан, Д. В., Н. С. Куфтеріна, Г. О. Гладкова, Н. І. Завгородня i О. Я. Гречаніна. "Оцінка стану кісткової системи у пацієнтів з хворобою педжета". Thesis, Видавництво СумДУ, 2005. http://essuir.sumdu.edu.ua/handle/123456789/12698.
Pełny tekst źródłaPutman, Melissa. "Cystic Fibrosis Related Bone Disease". Thesis, Harvard University, 2015. http://nrs.harvard.edu/urn-3:HUL.InstRepos:17613728.
Pełny tekst źródłaNixon, Matthew Frank. "Metabolic bone disease and arthroplasty loosening". Thesis, University of Leicester, 2009. http://hdl.handle.net/2381/8448.
Pełny tekst źródłaIga, Natsuko. "Accumulation of exhausted CD8+ T cells in extramammary Paget’s disease". Kyoto University, 2019. http://hdl.handle.net/2433/242908.
Pełny tekst źródłaHaarhaus, Mathias. "Bone alkaline phosphatase isoforms in chronic kidney disease : mineral and bone disorder". Doctoral thesis, Linköpings universitet, Avdelningen för mikrobiologi och molekylär medicin, 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-111870.
Pełny tekst źródłaPorter, Ryan Michael. "Examination of Glucocorticoid Treatment on Bone Marrow Stroma: Implications for Bone Disease and Applied Bone Regeneration". Thesis, Virginia Tech, 2002. http://hdl.handle.net/10919/36365.
Pełny tekst źródłaMaster of Science
Amofah, Eunice. "Bone marrow stem cells in liver disease". Thesis, Imperial College London, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.497234.
Pełny tekst źródłaOgilvie, D. J. "The genetics of collagen in brittle bone disease". Thesis, University of Oxford, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.235046.
Pełny tekst źródłaGowers, Kate Hayley Christine. "Characterisation of bone marrow progenitor cells in disease". Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/11068.
Pełny tekst źródłaAbdelhadi, Mohamed Mohamed. "Posttransplantation bone disease : the effect of immunosuppressive drugs on bone: clinical and experimental studies /". Stockholm, 2002. http://diss.kib.ki.se/2002/91-7349-384-8/.
Pełny tekst źródłaHuang, C. C. "Pathophysiology of post-transplantation bone disease : mechanisms of bone loss after orthotopic liver transplantation". Thesis, University of Cambridge, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.604707.
Pełny tekst źródłaMacPherson, Heather. "Role of the nitric oxide synthase pathway in bone cell function and bone disease". Thesis, University of Aberdeen, 1999. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU112398.
Pełny tekst źródłaOrmarsdóttir, Sif. "Osteoporosis in chronic liver disease /". Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2001. http://publications.uu.se/theses/91-554-5021-0/.
Pełny tekst źródłaPAOLETTI, Nicola. "Formal Computational Modelling of Bone Physiology and Disease Processes". Doctoral thesis, Università degli Studi di Camerino, 2014. http://hdl.handle.net/11581/401835.
Pełny tekst źródłaBurdon, Peter Charles Edward. "Regulation of neutrophil mobilisation from the bone marrow". Thesis, Imperial College London, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.289739.
Pełny tekst źródłaMurata, Teruasa. "Three-dimensional evaluation of subclinical extension of extramammary Paget’s disease: Visualization of histological border and its comparison to clinical border". 京都大学 (Kyoto University), 2017. http://hdl.handle.net/2433/225470.
Pełny tekst źródłaKawai, Shunsuke. "In vitro bone-like nodules generated from patient-derived iPSCs recapitulate pathological bone phenotypes". Doctoral thesis, Kyoto University, 2020. http://hdl.handle.net/2433/245828.
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新制・課程博士
博士(医学)
甲第22143号
医博第4534号
新制||医||1039(附属図書館)
京都大学大学院医学研究科医学専攻
(主査)教授 妻木 範行, 教授 森本 尚樹, 教授 別所 和久
学位規則第4条第1項該当
Doctor of Medical Science
Kyoto University
DFAM
Uno, Jennifer Kikue. "Bone Mineralization in a Murine Model of Inflammatory Bowel Disease". Diss., Tucson, Arizona : University of Arizona, 2006. http://etd.library.arizona.edu/etd/GetFileServlet?file=file:///data1/pdf/etd/azu%5Fetd%5F1650%5F1%5Fm.pdf&type=application/pdf.
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