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Tesi sul tema "Bones Pathophysiology"

Autore: Grafiati

Pubblicato: 4 giugno 2021

Ultima modifica: 3 febbraio 2022

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1

Anderson, Paul Hamill. "The regulation of Vitamin D metabolism in the kidney and bone." Title page, contents and abstract only, 2002. http://web4.library.adelaide.edu.au/theses/09PH/09pha5486.pdf.

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Abstract (sommario):

Includes bibliographical references (leaves 226-273.) Investigates the regulation of the expression of CYP27B1, CYP24 and vitamin D receptor (VDR) mRNA, both in the bone and in the kidney, with the aim to determine whether the regulation of the vitamin D metabolism in the bone is independent from that in the kidney. The effects of age, dietary calcium and vitamin D status on the expression of these genes in both the kidney and the bone, as well as on a number of biochemical factors known to regulate the renal metabolism of 1,25D, such as PTH, calcium and 1,25D itself, were examined. CYP27B1 mR

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2

Huang, 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.

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To enhance our understanding of the pathophysiology of bone disease associated with liver transplantation and of the mechanisms underlying bone loss in the three month period following transplantation, this prospective study was undertaken as follows: (1) bone pathophysiology was evaluated pre- and three months post-transplantation in transiliac biopsies using tetracycline-assisted histomorphometry; (2) cellular activities of bone formation and resorption pre- and post- transplantation were studied using quantitative enzyme cytochemistry in combination with histomorphometric methods; (3) cellu

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3

Chapurlat, Roland, Deborah Gensburger, Juan Jimenez-Andrade, Joseph Ghilardi, Marilyn Kelly, and Patrick Mantyh. "Pathophysiology and medical treatment of pain in fibrous dysplasia of bone." BioMed Central, 2012. http://hdl.handle.net/10150/610228.

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One of the most common complications of fibrous dysplasia of bone (FD) is bone pain. Usual pain killers are often of inadequate efficacy to control this bone pain. The mechanism of bone pain in FD remains uncertain, but by analogy with bone tumors one may consider that ectopic sprouting and formation of neuroma-like structures by sensory and sympathetic nerve fibers also occur in the dysplastic skeleton. Bone pain has been reported in up to 81% of adults and 49% of children. It affects predominantly the lower limbs and the spine. The degree of pain is highly variable and adults reports more pa

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4

Borazjani, Ali. "Pathophysiology of Pelvic Organ Prolapse." Cleveland State University / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=csu1432745397.

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5

Ismail, Medhat Mohamed. "Pathophysiology and therapy of bone marrow failure : studies of apoptosis and stem cell transplantation." Thesis, St George's, University of London, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.269742.

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6

Elkin, Sarah Louise. "The pathogenesis and pathophysiology of low bone mineral density in adults with cystic fibrosis." Thesis, Imperial College London, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.422707.

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7

Edwards, Sarah. "Investigating the role of a novel ER molecular chaperone : Creld2 in the physiology and pathophysiology of endochondral bone growth." Thesis, University of Manchester, 2015. https://www.research.manchester.ac.uk/portal/en/theses/investigating-the-role-of-a-novel-er-molecular-chaperone-creld2-in-the-physiology-and-pathophysiology-of-endochondral-bone-growth(6fd49909-beec-42d1-a546-8b2411616e59).html.

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Abstract (sommario):

Cysteine rich with EGF-like domains 2 (Creld2) is a novel endoplasmic reticulum (ER) resident molecular chaperone that has been recently implicated in the ER stress signalling response (ERSS) and the unfolded protein response (UPR). Global transcriptomic data derived from in vivo mouse models of rare chondrodysplasias; Multiple Epiphyseal Dysplasia (MED Matn3 p.V194D) and Metaphyseal chondrodysplasia type Schmid (MCDS Col10a1 p.N617K), identified a significant upregulation in Creld2 expression in mutant chondrocytes. These chondrodysplasias share a common disease signature consisting of aberra

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8

Davies, Matthew Rhys. "The role of bone morphogenetic protein 7 in the pathophysiology and treatment of vascular calcification associated with chronic renal failure." Thesis, University College London (University of London), 2006. http://discovery.ucl.ac.uk/1444711/.

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Vascular calcification (VC) is an important complication of chronic renal failure (CRF), and a risk factor for reduced survival. Osteoblast-like cells in the vessel wall derived from resident vascular smooth muscle cells (VSMC) are considered central to the pathogenesis of VC, which is exacerbated by mineral ion abnormalities inherent in renal osteodystrophy (ROD). Nevertheless, its aetiology is incompletely understood, and no effective therapies exist. Recently, CRF has been characterised as a state of Bone Morphogenetic Protein 7 (BMP7) deficiency, and animal studies have shown that administ

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9

Ho, Ken Choong Khoon School of Medicine UNSW. "Characterization of critical size sheep cranial defect model for study of bone graft substitute." 2007. http://handle.unsw.edu.au/1959.4/40499.

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This is an original study to quantify and grade defect healing in a large animal cranial bone substitute model. The study of various therapies to heal cranial defects requires an appropriate ?critical? animal model. An experimental animal model should be analogous and recognizable as an appropriate challenge to human physiology. In addition, the defect must fail to heal unless treated with the tissue engineering therapy under study. Sheep as a large animal model was chosen because of its ability to tolerate creation of large skull defects analogous to clinical scenario, and its biology of heal

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10

Dodge, Todd Randall. "Experimental and Computational Analysis of Dynamic Loading for Bone Formation." Thesis, 2013. http://hdl.handle.net/1805/3670.

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Abstract (sommario):

Indiana University-Purdue University Indianapolis (IUPUI)<br>Bone is a dynamic tissue that is constantly remodeling to repair damage and strengthen regions exposed to loads during everyday activities. However, certain conditions, including long-term unloading of the skeleton, hormonal imbalances, and aging can disrupt the normal bone remodeling cycle and lead to low bone mass and osteoporosis, increasing risk of fracture. While numerous treatments for low bone mass have been devised, dynamic mechanical loading modalities, such as axial loading of long bones and lateral loading of joints, have

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11

Weatherholt, Alyssa Marie. "Translational studies into the effects of exercise on estimated bone strength." 2015. http://hdl.handle.net/1805/8027.

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Indiana University-Purdue University Indianapolis (IUPUI)<br>Mechanical loading associated with exercise is known to benefit bone health; however, most studies explore exercise benefits on bone mass independent of bone structure and strength. The purpose of this dissertation is to explore the response of the skeleton to exercise across the translational divide between animal- and human-based studies, with a particular emphasis on exercise-induced changes in bone structure and estimated strength. To explore the skeletal benefits of exercise, models were used wherein loading is introduced

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12

Rhodes, Steven David. "Dissecting the cellular and molecular mechanisms mediating neurofibromatosis type 1 related bone defects." Thesis, 2014. http://hdl.handle.net/1805/3793.

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Abstract (sommario):

Indiana University-Purdue University Indianapolis (IUPUI)<br>Skeletal manifestations including short stature, osteoporosis, kyphoscoliosis, and tibial dysplasia cumulatively affect approximately 70% of patients with neurofibromatosis type 1 (NF1). Tibial pseudarthrosis, the chronic non-union of a spontaneous fracture, is a debilitating skeletal malady affecting young children with NF1. These non-healing fractures respond poorly to treatment and often require amputation of the affected limb due to limited understanding of the causative mechanisms. To better understand the cellular and molecula

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13

Baldock, Paul Andrew Jason. "Regional variation in oophorectomy induced trabecular bone osteopenia in the distal femur of the rat / Paul Andrew Jason Baldock." 2001. http://hdl.handle.net/2440/19901.

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Includes articles co-authored by the author during the preparation of this thesis.<br>Includes erratum on back leaf.<br>Includes bibliographical references (leaves 257-299).<br>xvii, 300 [27] leaves : ill. (some col.) ; 30 cm.<br>Title page, contents and abstract only. The complete thesis in print form is available from the University Library.<br>Examines regional variations in trabecular bone remodelling and bone loss following oophorectomy in the distal femur of the rat. The studies reveal a complex interaction between weight bearing and ovarian hormone deficiency, and show that physiologica

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14

Martins, Ana Isabel Barros Ramos. "Aplastic anemia: from pathophysiology to diagnosis, management and treatment." Master's thesis, 2015. http://hdl.handle.net/10316/30585.

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Trabalho final de mestrado integrado em Medicina (Hematologia), apresentado à Faculdade de Medicina da Universidade de Coimbra.<br>Aplastic anemia (AA) is a rare hematopoietic disease characterized by a pancytopenia and a hypoplastic bone marrow. AA can be congenital (CAA) or acquired (AAA). Acquired AA comprises those cases where a causative factor is identified (Secondary AA) and also idiopathic cases (Idiopathic AA). There was a marked improvement on treatment options in the last years that had resulted on increased overall survival rates. It is known that a correct management of this entit

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15

Unthan, Mark. "Die Rolle des Bone morphogenetic protein 2 in der Pathophysiologie der Adipositas." 2017. https://ul.qucosa.de/id/qucosa%3A23456.

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16

Sousa, Cristina Maria Peixoto de. "Contribution to the study of bone turnover markers for assessment of the pathophysiology of normal and disturbed fracture healing process." Doctoral thesis, 2016. http://hdl.handle.net/10348/5717.

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Tese de Doutoramento em Ciências Veterinárias<br>Os biomarcadores de remodelagem óssea (BTM) são produtos da actividade celular e são geralmente subdivididos em três categorias: biomarcadores de reabsorção óssea, formação óssea e proteínas reguladoras da actividade dos osteoclastos. Em vários estudos foi demonstrado que s BTM são capazes de reflectir o processo de cicatrização óssea, com os seus níveis dependentes da localização, tamanho e tipo da fractura. Além disso, a variação dos seus níveis tem, também, sido avaliada por alguns autores quanto à sua capacidade de prever precocemente

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17

"The role of mechanical loading, bone morphogenetic proteins and erroneous differentiation of tendon-derived stem cells in the pathogenesis of patellar tendinopathy: a potential mechanism for the chondron-ossification and failed healing in patellar tendinopathy." Thesis, 2011. http://library.cuhk.edu.hk/record=b6075353.

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Chronic patellar tendinopathy is a degenerative tendon disorder characterized by chronic activity-related, anterior knee pain associated with localized tenderness, swelling and impaired performance, which is a common clinical problem in athletes. The pathogenesis of patellar tendinopathy is still largely unknown, although tendon overuse is the most commonly suggested etiological factor, and treatment is usually symptomatic.<br>Histopathologically, the predominant feature of patellar tendinopathy is tendinosis, which is characterized by progressive tissue degeneration with a failed healing resp

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18

Dharmarajan, Subramanian. "BMP Pathway and Reactive Retinal Gliosis." 2013. http://hdl.handle.net/1805/3247.

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Abstract (sommario):

Indiana University-Purdue University Indianapolis (IUPUI)<br>Reactive gliosis is known to have a beneficial and a degenerative effect following injury to neurons. Although many factors have been implicated in reactive gliosis, their role in regulating this change is still unclear. We investigated the role of bone morphogenetic proteins in reactive gliosis in vivo and in vitro. In vivo, IHC analysis indicated reactive gliosis in the 6 week Ins2Akita mouse and WPK rat retinas. Expression of BMP7 was upregulated in these models, leading to an increase in the phosphorylation of downstream SMAD1. I

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