Thematische Bibliographien / Bones Pathophysiology

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Zeitschriftenartikel
Dissertationen
Bücher
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Konferenzberichte
Berichte der Organisationen

Auswahl der wissenschaftlichen Literatur zum Thema „Bones Pathophysiology“

Autor: Grafiati

Veröffentlicht am 4. Juni 2021

Zuletzt aktualisiert am 3. Februar 2022

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Zeitschriftenartikel zum Thema "Bones Pathophysiology"

Wiegerinck, R. F., R. Schreurs, and F. W. Prinzen. "Pathophysiology of dyssynchrony: of squirrels and broken bones." Netherlands Heart Journal 24, no. 1 (December 10, 2015): 4–10. http://dx.doi.org/10.1007/s12471-015-0765-7.

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Shapkin, Yu G., P. A. Seliverstov, and E. A. Skripal. "THE PHENOMENON OF «SECOND HIT» AFTER OPERATIONS OF OSTEOSYNTHESIS IN CASE OF POLY-TRAUMA." Medical Journal of the Russian Federation 23, no. 6 (December 15, 2017): 331–36. http://dx.doi.org/10.18821/0869-2106-2017-23-6-331-336.

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In case of poly-trauma the early operations of osteosynthesis under fractures of long bones, unstable fractures of pelvis and backbone bones being an operational trauma, can provoke progression of inflammatory reaction, development of systemic complications and poly-organ inadequacy i.e. causing a «second hit» effect. The pathophysiologic mechanisms of «second hit» phenomenon are complicated and they are implementing by means of modulation of immune response. The risk of development of the given phenomenon depends on period of implementation and method of osteosynthesis, severity of injuries a

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Thévenin-Lemoine, C., J. Vial, J. L. Labbé, B. Lepage, B. Ilharreborde, and F. Accadbled. "MRI of acute osteomyelitis in long bones of children: Pathophysiology study." Orthopaedics & Traumatology: Surgery & Research 102, no. 7 (November 2016): 831–37. http://dx.doi.org/10.1016/j.otsr.2016.06.014.

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Tasis, Nikolaos, Ioannis Tsouknidas, Argyrios Ioannidis, Konstantinos Nassiopoulos, and Dimitrios Filippou. "Left Functional Pneumonectomy Caused by a Very Rare Giant Intrathoracic Cystic Lesion in a Patient with Gorham–Stout Syndrome: Case Report and Review of the Literature." Case Reports in Pulmonology 2018 (2018): 1–9. http://dx.doi.org/10.1155/2018/2406496.

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Gorham–Stout syndrome is an uncommon entity, with few cases reported in bibliography. It consists of osteolytic manifestations affecting various bones and replacing them with lymphangiomatous tissue. With pathophysiology unknown, Gorham–Stout disease affects also cardiorespiratory system usually causing lytic lesions to the bones of the thoracic cage or directly invading the thoracic duct. This is a case report of a unique respiratory manifestation of the disease and a review of its cardiorespiratory complications.

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Kuhweide, R., V. Van de Steene, S. Vlaminck, and J. W. Casselman. "Ramsay Hunt syndrome: pathophysiology of cochleovestibular symptoms." Journal of Laryngology & Otology 116, no. 10 (October 2002): 844–48. http://dx.doi.org/10.1258/00222150260293691.

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Ramsay Hunt’s hypothesis that herpes zoster oticus results from reactivation of the varicella zoster virus (VZV) in the geniculate ganglion is supported by the detection of viral genome in archival temporal bones of normals and Ramsay Hunt patients by the polymerase chain reaction. Ramsay Hunt syndrome is characterized by the presence of cochleovestibular symptoms in association with facial paralysis. VZV has also been demonstrated in the spiral and/or vestibular ganglion. Two cases are reported in which cochleovestibular symptoms outweighed the facial nerve symptoms, presumably representing V

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Puntillo, Filomena, Mariateresa Giglio, Antonella Paladini, Gaetano Perchiazzi, Omar Viswanath, Ivan Urits, Carlo Sabbà, Giustino Varrassi, and Nicola Brienza. "Pathophysiology of musculoskeletal pain: a narrative review." Therapeutic Advances in Musculoskeletal Disease 13 (January 2021): 1759720X2199506. http://dx.doi.org/10.1177/1759720x21995067.

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Musculoskeletal pain (excluding bone cancer pain) affects more than 30% of the global population and imposes an enormous burden on patients, families, and caregivers related to functional limitation, emotional distress, effects on mood, loss of independence, and reduced quality of life. The pathogenic mechanisms of musculoskeletal pain relate to the differential sensory innervation of bones, joints, and muscles as opposed to skin and involve a number of peripheral and central nervous system cells and mediators. The interplay of neurons and non-neural cells (e.g. glial, mesenchymal, and immune

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Shams, Ramsha, Kelsey P. Drasites, Vandana Zaman, Denise Matzelle, Donald C. Shields, Dena P. Garner, Christopher J. Sole, Azizul Haque, and Narendra L. Banik. "The Pathophysiology of Osteoporosis after Spinal Cord Injury." International Journal of Molecular Sciences 22, no. 6 (March 17, 2021): 3057. http://dx.doi.org/10.3390/ijms22063057.

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Spinal cord injury (SCI) affects approximately 300,000 people in the United States. Most individuals who sustain severe SCI also develop subsequent osteoporosis. However, beyond immobilization-related lack of long bone loading, multiple mechanisms of SCI-related bone density loss are incompletely understood. Recent findings suggest neuronal impairment and disability may lead to an upregulation of receptor activator of nuclear factor-κB ligand (RANKL), which promotes bone resorption. Disruption of Wnt signaling and dysregulation of RANKL may also contribute to the pathogenesis of SCI-related os

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Gore, Ashwini P., Soon Ho Kwon, and Antine E. Stenbit. "A Roadmap to the Brittle Bones of Cystic Fibrosis." Journal of Osteoporosis 2011 (2011): 1–10. http://dx.doi.org/10.4061/2011/926045.

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Cystic fibrosis (CF) is an autosomal recessive disorder which despite advances in medical care continues to be a life-limiting and often fatal disease. With increase in life expectancy of the CF population, bone disease has emerged as a common complication. Unlike the osteoporosis seen in postmenopausal population, bone disease in CF begins at a young age and is associated with significant morbidity due to fractures, kyphosis, increased pain, and decreased lung function. The maintenance of bone health is essential for the CF population during their lives to prevent pain and fractures but also

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Assi, Tarek, Sarah Watson, Bachar Samra, Elie Rassy, Axel Le Cesne, Antoine Italiano, and Olivier Mir. "Targeting the VEGF Pathway in Osteosarcoma." Cells 10, no. 5 (May 18, 2021): 1240. http://dx.doi.org/10.3390/cells10051240.

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Osteosarcoma is the most common primary tumor of the bones affecting mainly young adults. Despite the advances in the field of systemic anticancer therapy, the prognosis of relapsed of metastatic osteosarcoma patients remain dismal with very short survival. However, the better understanding of the pathophysiology of this subtype of sarcoma has led to the identification of new targeted agents with significant activity. In fact, increased angiogenesis plays a major role in the tumor growth and survival of osteosarcoma patients. Several targeted agents have demonstrated a significant anti-tumor a

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Golovach, I. Yu. "Clinical significance of spondyloarthritis-attended enthesites: from pathophysiology to treatment (review)." PAIN, JOINTS, SPINE 11, no. 1 (April 1, 2021): 17–27. http://dx.doi.org/10.22141/2224-1507.11.1.2021.226905.

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The article presents the latest views on enthesites’ anatomy and pathogenesis, clinical features, diagnostic and therapeutic options. The enthesis lesions are considered an outstanding pathologic and clinical manifestation of spondyloarthritis group; this symptom is included into the classification criteria by the Assessment of SpondyloArthritis International Society for the peripheral and axial forms. The typical spondyloarthritis-attended enthesites’ localizations are: the site of Achilles tendon and plantar aponeurosis’ attachment to the calcaneus, the lateral condyle of the humerus, the

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Dissertationen zum Thema "Bones Pathophysiology"

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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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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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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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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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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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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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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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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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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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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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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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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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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Bücher zum Thema "Bones Pathophysiology"

Medicine, Conference on Skeletal Biology and. Skeletal biology and medicine. Boston, Mass: Published by Blackwell Pub. on behalf of the New York Academy of Sciences, 2007.

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NATO Advanced Study Institute on Advances in Bone Regulatory Factors: Morphology, Biochemistry, Physiology, and Pharmacology (1989 Erice, Italy). Bone regulatory factors: Morphology, biochemistry, physiology, and pharmacology. New York: Plenum Press, 1990.

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Jacques, Arlet, and Mazières B, eds. Bone circulation and bone necrosis: Proceedings of the IVth International Symposium on Bone Circulation, Toulouse (France), 17th-19th September 1987. Berlin: Springer-Verlag, 1990.

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Mone, Zaidi, New York Academy of Sciences, and Mount Sinai School of Medicine, eds. Skeletal biology and medicine. Boston, Mass: Blackwell Pub., on behalf of the New York Academy of Sciences, 2007.

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Conference on Skeletal Biology and Medicine (4th 2011 New York, N.Y.). Skeletal biology and medicine II: Bone and cartilage homeostasis and bone disease. Edited by Zaidi Mone. Boston, Mass: Published by Blackwell Pub. on behalf of the New York Academy of Sciences, 2011.

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Behari, Jitendra. Biophysical bone behavior. Singapore: John Wiley, 2009.

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Mone, Zaidi, and New York Academy of Sciences, eds. Skeletal biology and medicine. Boston, Mass: Published by Blackwell Pub. on behalf of the New York Academy of Sciences, 2010.

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Linda-Joy, Lee, and Vleeming Andry, eds. The pelvic girdle: An integration of clinical expertise and research. 4th ed. Edinburgh: Elsevier/Churchill Livingstone, 2011.

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Lundon, Katie. Orthopedic rehabilitation science: Principles for clinical management of nonmineralized connective tissue. Amsterdam: Butterworth-Heinemann, 2003.

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Buchteile zum Thema "Bones Pathophysiology"

Mori, Satoshi. "Bone Microdamage and Its Repair: Pathophysiology of Bone Fatigue." In Mechanical Loading of Bones and Joints, 139–45. Tokyo: Springer Japan, 1999. http://dx.doi.org/10.1007/978-4-431-65892-4_14.

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Roodman, G. David. "Pathophysiology of Bone Metastases." In Bone Metastases, 31–50. Dordrecht: Springer Netherlands, 2009. http://dx.doi.org/10.1007/978-1-4020-9819-2_2.

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Chirgwin, John M., and G. David Roodman. "Pathophysiology of Bone Metastases." In Bone Metastases, 3–17. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-7569-5_1.

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Van der Wall, Hans, Barry Elison, Clayton Frater, Warwick Bruce, and Stephen Clarke. "Pathophysiology of Bone Metastases." In Radionuclide and Hybrid Bone Imaging, 59–84. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-02400-9_3.

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Kerschan-Schindl, Katharina, Ursula Föger-Samwald, and Peter Pietschmann. "Pathophysiology of Bone Fragility." In Principles of Bone and Joint Research, 83–97. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-58955-8_6.

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Bartl, Reiner, and Christoph Bartl. "Classifying Bone Disorders According to Pathophysiology." In Bone Disorders, 55–59. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-29182-6_9.

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Caniggia, Angelo. "Pathophysiology of Bone Formation and Resorption." In Bone Regulatory Factors, 235–52. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4757-1508-8_14.

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Jones, John Paul. "Pathophysiology of Osteonecrosis." In Bone Circulation and Vascularization in Normal and Pathological Conditions, 249–61. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-2838-8_28.

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Pietschmann, P., R. Gruber, and M. Peterlik. "Pathophysiology and Aging of Bone." In Radiology of Osteoporosis, 3–24. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-662-05235-8_1.

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Thürlimann, Beat. "Physiology and Pathophysiology of Bone." In Recent Results in Cancer Research, 1–20. Berlin, Heidelberg: Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-642-59845-6_1.

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Konferenzberichte zum Thema "Bones Pathophysiology"

Hedrich, Christian. "SP0187 PATHOPHYSIOLOGY AND THERAPEUTIC CONSEQUENCES AUTO-INFLAMMATORY BONE DISORDERS." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.8494.

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Slichter, Sherrill J. "PATHOPHYSIOLOGY OF THROMBOCYTOPENIA AND RESULTANT CLINICAL INDICATIONS FOR PLATELET TRANSFUSION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643996.

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Careful evaluation of platelet survival data in normal individuals and patients with thrombocytopeniasecondary to marrow aplasia has demonstrated that platelets are lost from circulation by two mechanisms a fixed fraction of platelets, amounting to approxi mately 7,100 platelets/ul/day, are lost randomly while the remaining platelets are removed by senescent mechanisms. At platelet counts of <100,000/ul, platelet survival becomes progressively shorter as the fixed platelet loss becomes a proportionately greater fraction of the circulating platelets. Thus, there is a direct relationship betw

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de la Puente, Pilar, Rebecca Gilson, Barbara Muz, Feda Azab, Justin King, Samuel Achilefu, Ravi Vij, and Abdel Kareem Azab. "Abstract 5356: 3D tissue-engineered bone marrow niche as novel method to study pathophysiology and drug resistance in multiple myeloma." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-5356.

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Berichte der Organisationen zum Thema "Bones Pathophysiology"

Zhang, Jiwang. The Role of Necroptosis in the Pathophysiology of Bone Marrow Failure. Fort Belvoir, VA: Defense Technical Information Center, March 2014. http://dx.doi.org/10.21236/ada604192.

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