Thèses sur le sujet « Pathophysiology »
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Farrán, Díaz-Cano Aina. « Pathophysiology of osteoarthritis ». Doctoral thesis, Universitat de Barcelona, 2017. http://hdl.handle.net/10803/456376.
Texte intégralL’artrosi (OA) és la malaltia articular més comuna i es caracteritza, principalment, per la destrucció del cartílag articular. El principal paper del cartílag articular és el de suportar les forces de tensió i compressió a les que es troba sotmès i que recau principalment en els seus components: el col·lagen i els proteoglicans. Durant el metabolisme normal del cartílag hi ha un equilibri entre la síntesi i degradació d’aquest components, però a l’artrosi, aquest equilibri es trenca i el metabolisme catabòlic supera l'anabòlic. Durant el desenvolupament de l'OA, els condròcits expressen la proteasa més involucrada en la degradació del cartílag, la MMP-13, que a diferència d’altres MMPs, en humans presenta 3 transcrits diferents. Malauradament, tot i la seva elevada prevalença, l'OA es troba orfe d’una bona tècnica diagnòstica, ja que actualment es realitza per mitjà de tècniques radiològiques que presenten l'inconvenient de que la malaltia només es reflecteix quan l’articulació es troba molt afectada. Actualment, els tractaments farmacològics més utilitzats són analgèsics, AINEs, i els nutracèutics, anomenats SYSADOA per les seves sigles en anglès (Symptomatic Slow Acting Drugs for Osteoarthritis) d’entre els que destaca el sulfat de glucosamina i el condroitin sulfat. Amb aquests antecedents previs, els objectius de la tesis són: 1. Demostrar la presència de 3 isoformes de MMP-13 en humans • Clonació (sistema Bac-to-bac) i purificació de les 3 isoformes en cèl·lules d’insecte (Sf9). • Producció d’anticossos policlonals específics de cada isoforma al Servei de Producció d’Anticossos de la UAB • Cerca de les isoformes en pacients artròsics per WB. • Comprovació de l’activitat de cada isoforma en front a diferents components matricials. 2. Estudiar l'efecte "in vivo" de la deleció del gen de l'Opticina en un model murí d'artrosi. • Confirmar l'expressió de l' OPTC al cartílag articular dels ratolins. • Induïr OA mitjançant el mètode de destabilització del menisc medial (DMM) a ratolins Optc-/- i Optc +/+ de 10 setmanes d'edat. • Analitzar l'efecte de la deficiència de l'OPTC al desenvolupament de l'OA, evaluant la degradació del cartílag i la hipertròfia de la membrana sinovial, deu setmanes després de l'inducció de l'OA per DMM. • Comparar l'expressió de marcadors pro-inflamatoris, catabòlics i anabòlics entre ratolins Optc-/- i Optc+/+. • Analitzar la producció al cartílag de differents SLRPs. • Analitzar l'organització i l'ultraestructura de les fibres de colàgen. 3. Estudiar l'efecte anti-angiogenic del condroitin sulfat en sinoviòcits sota condicions d'hipòxia i d'hipòxia més inflamació. • Mimetitzar condicions inflamatòries i d'hipòxia "in vitro" en sinoviòcits humans. • Estudiar l'expressió i la producció de mediadors angiogènics per sinoviòcits artròsics sota condicions d'hipòxia i inflamació. • Estudiar l'efecte del pretractament del CS en cultius de sinoviòcits humans artròsics • Estudiar l'interacció entre els sinoviòcits artròsics i les cèl·lules endotelials sota hipòxia i inflamació, amb o sense pretractament de CS. L'artrosi és una malaltia que engloba diferents fenotips, però tots comparteixen una sèrie de característiques com la degeneració del cartílag articular, inflamació de la membrana sinovial i esclerosi de l'ós subcondral. Aquestes característiques resulten en un conjunt de símptomes que impedeixen la correcte mobilitat del pacient i creen dolor que pot arribar a ser crònic. Alhora de desenvolupar noves eines de diagnòstic i prognòstic i eventualment avançar en el descobriment de tractaments exitosos, definir clarament els diferents fenotips de l'artrosi és de gran interès. En aquesta línia, els descobriments compresos en aquesta tesis revelen dues possibles maneres d'identificar subgrups de pacients. Per una part, com es descriu al capítol 1, la presència d'una nova isoforma de la colagenasa-3 podria utilitzar-se com a un indicador de diferencies en la degradació matricial del cartíleg humà articular. Per una altre banda, els resultats del capítol 2 suggereixen que la composició dels membres de la famíla de SLRP a la matriu extracel·lular del cartíleg podria aplicar-se com a una nova eina de classificació del prognòstic de la malaltia artròsic. Finalment, la controversia sobre l'eficàcia del tractament amb nutracèutics com el condroitin sulfat podria arribar a solucionar-se si es descobreixen noves eines per predir quins pacients poden respondre millor a un medicament donat. És important tenir en compte que s'ha de continuar investigant per entendre com integrar aquests resultats en un concepte final que pogués explicar l'heterogeneïtat dels pacients i les diferències en el prognòstic de l'artrosi.
Stoodley, Marcus A. « Pathophysiology of Syringomyelia / ». Title page, contents and abstract only, 1996. http://web4.library.adelaide.edu.au/theses/09PH/09phs882.pdf.
Texte intégralRobinson, Monique Renee. « Cardiac pathophysiology of obesity ». Thesis, University of Oxford, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.414224.
Texte intégralPadera, Timothy P. (Timothy Patrick) 1975. « Lymphatic pathophysiology of tumors ». Thesis, Massachusetts Institute of Technology, 2003. http://hdl.handle.net/1721.1/29591.
Texte intégralIncludes bibliographical references (leaves 146-166).
Lymph node metastases have a negative impact on cancer survival, but the mechanisms for lymphatic metastasis are not well understood. The universal finding in solid tumors of an absence of functional lymphatic vessels seems paradoxical, as cancer cells do travel through lymphatics in order to disseminate. In order to address some of these issues, this thesis proposes two etiologies for the absence of functional lymphatic vessels in solid tumors. The first hypothesis addresses whether Vascular Endothelial Growth Factor-C (VEGF-C), a lymphangiogenic factor, was sufficient to induce lymphatic function in tumors. The overexpression of VEGF-C in tumors leads to an increase in lymph node metastasis as well as structures that positively stain for lymphatic markers, but does not induce functional lymphatics within the tumor. Thus VEGF-C is not sufficient to grow functional lymphatic vessels in tumors. The second hypothesis addresses whether mechanical forces generated by the proliferation of cancer cells in a confined space compress lymphatic vessels in tumors. The mechanical forces inside of the tumor were reduced by the selective killing of human cancer cells grown in mice by Diphtheria Toxin. Tumor cell death leads to an increase in the fraction of lymphatics with open lumen. In addition, lymphatic vessels with open lumen are surrounded by a lower cellular density than collapsed vessels. Thus, relieving solid stress allows lymphatic vessels to open. However, function was not restored in these vessels. This is presumably due to the inability of the lymphatic vessels to completely open along its entire length, leaving focal areas of lymphatic collapse. Compressive forces are common to all growing tumors, giving credence to the mechanical etiology of the absence of functional lymphatic vessels in tumors, regardless of tumor type or organ site.
(cont.) These findings lead to an interesting question: Does cancer treatment in humans relieve the mechanical compression allowing lymphatic and blood vessels to open? Furthermore, would the resumption of function of compressed blood and lymphatic vessels lead to a paradoxical increase in metastasis? These questions require further investigation.
by Timothy P. Padera.
Ph.D.
Fletcher, Jessica Louise. « Pathophysiology of canine fucosidosis ». Thesis, The University of Sydney, 2013. http://hdl.handle.net/2123/10420.
Texte intégralKirk, Calum Norman Robert. « Pathophysiology of anoctaminopathy (LGMD2L) ». Thesis, University of Newcastle upon Tyne, 2017. http://hdl.handle.net/10443/3861.
Texte intégralCheng, Allen Cheuk-Seng, et allencheng@ozemail com au. « MELIOIDOSIS : EPIDEMIOLOGY, PATHOPHYSIOLOGY AND MANAGEMENT ». Flinders University. Medicine, 2005. http://catalogue.flinders.edu.au./local/adt/public/adt-SFU20051121.141305.
Texte intégralBerg, Erika L. « Endocrinology of equine metabolic pathophysiology ». Diss., Columbia, Mo. : University of Missouri-Columbia, 2006. http://hdl.handle.net/10355/4472.
Texte intégralThe entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Title from title screen of research.pdf file (viewed on July 31, 2007) Includes bibliographical references.
Sethia, Krishna Kumar. « The pathophysiology of detrusor instability ». Thesis, University of Oxford, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.235958.
Texte intégralSteele, Ian Conrad. « Pathophysiology of chronic cardiac failure ». Thesis, Queen's University Belfast, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.337046.
Texte intégralOng, Patricia Mei Lin. « Pathophysiology of acute intermittent porphyria ». Thesis, University of Glasgow, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.318116.
Texte intégralRome, Susan Margaret. « On the pathophysiology of dystonia ». Thesis, University of Sheffield, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.369890.
Texte intégralRead, Simon James. « Free radical pathophysiology in migraine ». Thesis, University of Hertfordshire, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.391365.
Texte intégralYellon, Derek M. « The pathophysiology of myocardial protection ». Thesis, University of Bath, 1994. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.760654.
Texte intégralLoosemore, Michael. « The pathophysiology of boxing injuries ». Thesis, University of Bath, 2015. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.687310.
Texte intégralBorazjani, Ali. « Pathophysiology of Pelvic Organ Prolapse ». Cleveland State University / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=csu1432745397.
Texte intégralOwler, Brian Kenneth. « Pathophysiology of normal pressure hydrocephalus ». Thesis, The University of Sydney, 2004. http://hdl.handle.net/2123/685.
Texte intégralOwler, Brian Kenneth. « Pathophysiology of normal pressure hydrocephalus ». University of Sydney. Surgery, 2004. http://hdl.handle.net/2123/685.
Texte intégralSilva, José Pablo. « The pathophysiology of respiratory chain dysfunction / ». Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-234-9/.
Texte intégralMcMurdo, Lorraine. « Endothelin in cardiovascular physiology and pathophysiology ». Thesis, Queen Mary, University of London, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.321680.
Texte intégralMcKnight, John Alexander. « The pathophysiology of atrial natriuretic factor ». Thesis, Queen's University Belfast, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.335972.
Texte intégralBowers, Keith Cyril. « Pathophysiology of ATP in single cardiomyocytes ». Thesis, University of Liverpool, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.316576.
Texte intégralWallis, William Richard James. « The cellular pathophysiology of myocardial hypertrophy ». Thesis, King's College London (University of London), 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.265997.
Texte intégralParees, Moreno I. « Pathophysiology of functional (psychogenic) movement disorders ». Thesis, University College London (University of London), 2015. http://discovery.ucl.ac.uk/1466184/.
Texte intégralWashington, Georgita T. « Student Outcomes after Pathophysiology Course Revisions ». Digital Commons @ East Tennessee State University, 2020. https://dc.etsu.edu/etsu-works/7607.
Texte intégralRymut, Sharon Marie. « Microtubule Regulation in Cystic Fibrosis Pathophysiology ». Case Western Reserve University School of Graduate Studies / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=case1432730616.
Texte intégralSimpson, Kenneth J. « Studies on cytokines in liver pathophysiology ». Thesis, University of Edinburgh, 1997. http://hdl.handle.net/1842/21531.
Texte intégralBusbridge, Mark. « The physiology and pathophysiology of hepcidin ». Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/10743.
Texte intégralCheluvappa, Rajkumar. « Pathophysiology of Liver Sinusoidal Endothelial Cells ». Thesis, The University of Sydney, 2008. http://hdl.handle.net/2123/2802.
Texte intégralCheluvappa, Rajkumar. « Pathophysiology of Liver Sinusoidal Endothelial Cells ». University of Sydney, 2008. http://hdl.handle.net/2123/2802.
Texte intégralOwing to its strategic position in the liver sinusoid, pathologic and morphologic alterations of the Liver Sinusoidal Endothelial Cell (LSEC) have far-reaching repercussions for the whole liver and systemic metabolism. LSECs are perforated with fenestrations, which are pores that facilitate the transfer of lipoproteins and macromolecules between blood and hepatocytes. Loss of LSEC porosity is termed defenestration, which can result from loss of fenestrations and/ or decreases in fenestration diameter. Gram negative bacterial endotoxin (Lipopolysaccharide, LPS) has marked effects on LSEC morphology, including induction LSEC defenestration. Sepsis is associated with hyperlipidemia, and proposed mechanisms include inhibition of tissue lipoprotein lipase and increased triglyceride production by the liver. The LSEC has an increasingly recognized role in hyperlipidemia. Conditions associated with reduced numbers of fenestrations such as ageing and bacterial infections are associated with impaired lipoprotein and chylomicron remnant uptake by the liver and consequent hyperlipidemia. Given the role of the LSEC in liver allograft rejection and hyperlipidemia, changes in the LSEC induced by LPS may have significant clinical implications. In this thesis, the following major hypotheses are explored: 1. The Pseudomonas aeruginosa toxin pyocyanin induces defenestration of the LSEC both in vitro and in vivo 2. The effects of pyocyanin on the LSEC are mediated by oxidative stress 3. Defenestration induced by old age and poloxamer 407 causes intrahepatocytic hypoxia and upregulation of hypoxia-related responses 4. Defenestration of the LSEC seen in old age can be exacerbated by diabetes mellitus and prevented or ameliorated by caloric restriction commencing early in life
Spratt, James Christopher Samuel. « Endothelin : cardiovascular pharmacology, physiology & ; pathophysiology ». Thesis, University of Edinburgh, 2003. http://hdl.handle.net/1842/23202.
Texte intégralKelly, Richard John. « The pathophysiology of paroxysmal nocturnal haemoglobinuria ». Thesis, University of Leeds, 2014. http://etheses.whiterose.ac.uk/6820/.
Texte intégralSulaiman, H. « Pathophysiology of post-operative peritoneal adhesions ». Thesis, University College London (University of London), 2007. http://discovery.ucl.ac.uk/1446209/.
Texte intégralTsang, Wing-ting Andrea, et 曾詠婷. « Investigating the potential significance of tau protein in corticosterone-induced depression and neurodegeneration : implication in Alzheimer's disease ». Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2014. http://hdl.handle.net/10722/208418.
Texte intégralpublished_or_final_version
Anatomy
Master
Master of Philosophy
Ráez, Bravo Arián. « Pathophysiology of sarcoptic mange in Iberian ibex ». Doctoral thesis, Universitat Autònoma de Barcelona, 2019. http://hdl.handle.net/10803/669361.
Texte intégralSarcoptic mange is a parasitic skin disease caused by the burrowing mite Sarcoptes scabiei. It affects mammals worldwide, including humans. Sarcoptic mange in wildlife is considered an emerging disease, and can cause severe population declines. Iberian ibex (Capra pyrenaica) is a medium-sized mountain ungulate endemic to the Iberian Peninsula. Since the end of the ‘80s, the Iberian Ibex populations of Southern and Eastern Spain have been affected by mange, suffering variables mortalities reported to reach up to 90%. Most of the studies on sarcoptic mange in Iberian ibex have focused on the epidemiology and the population consequences of the diseases, thus existing a lack of knowledge about the pathophysiology and pathogenesis of this disease in this species. The two first studies of this thesis analysed the acute phase proteins (APP) (Study I) and validated a test for the detection of immunoglobulins G (IgG) against S. scabiei (Study II) in free-ranging Iberian ibexes, both healthy and affected by sarcoptic mange. In the Study I, an increase of serum amyloid protein type A (SAA) and in lower magnitude of alpha-1 acid glicoprotein (AGP) concentrations was observed, in correlation with the extent of the skin lesions caused by sarcoptic mange. Conversely, haptoglobin (Hp) concentration was not different between the healthy and infested ibexes. Since there is not an effective laboratory diagnostic method, in the Study II three enzyme-linked immunosorbent assays were evaluated for IgG detection against S. scabiei in Iberian ibex, and one of the three showed high specificity and sensitivity by using the avidin-biotin system, which allowed it to be validated. The Studies III and IV were carried out on Iberian ibexes with different alleles of the DRB1 gen of the major histocompatibility complex (MHC) class II, experimentally infested with S. scabiei. Although all the infested ibexes developed lesions compatible with sarcoptic mange, the clinical evolution varied from extensive lesions affecting most of the body surface to mild lesions and clinical recovering of the disease (Study III). However, such clinical differences seemed unrelated to MHC differences. The severely affected ibexes showed anaemia, possibly related to the inflammation caused by the mite, as well as neutrophilia and lymphopenia, probably due to secondary infections favoured by sarcoptic mange. Immunoglobulin G concentration also increased in agreement with the severity of the lesions. Finally, the Study IV addressed the genomic response of Iberian ibexes to the experimental infestation with S. scabiei. The severely affected Iberian ibexes showed an increase in the gene expression of pathways related to immunity and inflammation, agreeing with the exacerbated and non-effective generalized immune response induced by the mite and the response to secondary infections. Moreover, the Iberian ibexes that recovered showed an increase in the local skin expression of genes related with antigen presentation and T-lymphocytes activation. To summarize, sarcoptic mange induces both systemic and local changes in the Iberian Ibex, causing an increase in APP and antibodies, as well as haematological and local and systemic gene expression disorders. Although the causes of the differences found in the clinical evolution have not been completely elucidated, local skin cellular immunity may be key in controlling the infestation. Immunoglobulin G detection by ELISA can be a useful and effective diagnostic tool for sarcoptic mange in Iberian Ibex, while APP are a prognostic indicator.
Forcada, Yaiza. « Genetics and pathophysiology of feline diabetus mellitus ». Thesis, Royal Veterinary College (University of London), 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.701655.
Texte intégralAlix, James John Philip. « The physiology and pathophysiology of central axons ». Thesis, University of Leicester, 2006. http://hdl.handle.net/2381/29957.
Texte intégralByrne, Philip John. « Pathophysiology of bacterial gill disease in trout ». Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2002. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/NQ65820.pdf.
Texte intégralPrunell, dos Santos Giselle F. « Pathophysiology of subarachnoid hemorrhage in the rat / ». Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-610-3/.
Texte intégralCalming, Ulrika. « Langerhans cell histiocytosis : detection, monitoring and pathophysiology / ». Stockholm, 2002. http://diss.kib.ki.se/2002/91-7349-180-2.
Texte intégralLomas, David Arthur. « The molecular pathophysiology of alphaâ†1-antitrypsin ». Thesis, University of Cambridge, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.308299.
Texte intégralCalder, James David Forbes. « The anatomical extent and pathophysiology of osteonecrosis ». Thesis, Imperial College London, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.368712.
Texte intégralWilliamson, G. « Studies in the Pathophysiology of Childhood Asthma ». Thesis, Queen's University Belfast, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.527903.
Texte intégralAbuderman, Abdulwahab Ali. « Pathophysiology of Helicobacter-induced gastric precancerous changes ». Thesis, University of Liverpool, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.539509.
Texte intégralMaile, Charlotte Amy. « Pathophysiology of equine type1 polysaccharide storage myopathy ». Thesis, Royal Veterinary College (University of London), 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.618291.
Texte intégralDoherty, G. M. « Studies on the pathophysiology of childhood wheeze ». Thesis, Queen's University Belfast, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.431605.
Texte intégralHunt, Judith Mary. « The pathophysiology of equine post-operative ileus ». Thesis, Royal Veterinary College (University of London), 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.309273.
Texte intégralBendall, Jennifer Kate. « Physiology and pathophysiology of cardiac NADPH oxidase ». Thesis, King's College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.289766.
Texte intégralMoyes, Lisa Helen. « Studies of the pathophysiology of Barrett's oesophagus ». Thesis, University of Glasgow, 2013. http://theses.gla.ac.uk/4741/.
Texte intégralHall, Judith. « Physiology and pathophysiology of vitamin D metabolism ». Thesis, University of Newcastle upon Tyne, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.377459.
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