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Dissertations / Theses on the topic 'Polyarthriris'

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Published: 4 June 2021
Last updated: 2 February 2022

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1

Rulli, Nestor Ezequiel, and na. "Ross River Virus Infection: Disease Mechanisms and Potential Treatment." University of Canberra. School of Health Sciences, 2007. http://erl.canberra.edu.au./public/adt-AUC20080227.091948.

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Ross River virus (RRV) is a mosquito-borne alphavirus and the aetiological agent of epidemic polyarthritis (EPA). Arthropod borne-Alphaviruses that are related to RRV, such as Chikungunya virus, Sindbis virus and Barmah Forest virus, are usually associated with epidemics of infectious arthritides in different parts of the world. In humans, RRV-induced disease symptoms include fever, rash, myalgia and pain and stiffness of the joints. Muscle and joint pain are the most debilitating symptoms in RRV patients and the best treatment available is non-steroidal anti-inflammatory drugs (NSAID). Previous studies in mice have demonstrated that RRV infection results in inflammation of skeletal muscle and joints and that macrophages play a primary role in disease. The present study was carried out to further elucidate the underlying mechanisms mediating RRV-induced muscle and joint pathology. Previous studies have reported that encephalitic alphaviruses trigger apoptosis of brain cells in mice and that blocking apoptosis reduces mortality rates. In the present study, the ability of RRV to induce muscle apoptosis was investigated in vitro, using a murine myoblast cell line (C1C12), and in vivo, using a mouse model of RRV disease. RRV-infected C1C12 myofibres displayed an array of morphological and biochemical makers of apoptosis. Apoptosis was also observed in the skeletal muscle of RRV-infected C57BL/6J mice. Blocking apoptosis by general caspase inhibition resulted in milder disease symptoms, reduced myofibre damage and decreased inflammation of muscle and joint tissues. The total number of cell infiltrates as well as the number of macrophages infiltrating muscle was significantly reduced by the treatment with a caspase inhibitor. The effects of RRV infection on the skeletal system were also investigated. Primary human osteoblast cells were infected with RRV and monitored for viral-induced cytopathic effect. Osteoblasts supported rapid virus growth and, by 48 hours after infection, succumbed to viral-induced necrosis. In addition, histological examination of bone tissue from RRV-infected C57BL/6J mice showed clear evidence of bone resorption. Tibias from infected mice showed an increased number of activated osteoclasts, a reduction in bone density and thinning of cortical bone. The expression of host factors involved in inflammatory responses and bone remodelling was studied in RRV-infected myofibres and osteoblast cell cultures and in the muscle and joint tissues from infected mice. RRV-infected muscle cells and tissue showed elevated mRNA levels for the chemokines CCL-2, CCL3, CCL5 and CXCL1, all of which are known to mediate the migration of monocytic cells. With the exception of CXCL1, these chemokines were also found to be up-regulated in RRV-infected osteoblast cultures and in joint tissues from infected mice. Muscle and joint tissue from infected mice also showed elevated mRNA levels for type I and type II interferons, TNF- and NOS2. In addition, joint tissues from infected animals contained high levels of IL-6 and IL-1, two cytokines known to mediate bone remodelling. Finally, the therapeutic potential of the drug bindarit was investigated using the mouse model of RRV disease. Bindarit is a known inhibitor of CCL-2 and TNF- and has been found to prevent protein denaturation. Treatment with bindarit resulted in mice developing milder disease symptoms, reduced muscle damage and decreased inflammation of muscle and joint tissues. In particular, bindarit significantly reduced macrophage infiltration into skeletal muscle tissue. This thesis has contributed to the understanding of RRV pathogenesis. It has identified novel mechanisms of RRV-induced muscle and bone pathology and provided further evidence that associate pro-inflammatory host factors to RRV disease. This work has also demonstrated that bindarit should be considered as a candidate for treating RRV disease in humans.
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2

Hass, Wolfgang. "Soziale Unterstützungsnetzwerke von Menschen mit chronischer Polyarthritis eine explorative, netzwerkanalytische Studie /." [S.l. : s.n.], 2002. http://deposit.ddb.de/cgi-bin/dokserv?idn=967083761.

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3

Pilhofer, Christoph. "Rückfussarthrodesen bei Polyarthritikern zwischen 1974 und 1997 an der I. Orthopädischen Klinik des BRK Rheuma-Zentrums Bad Abbach /." Aachen : Shaker, 2001. http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&doc_number=009328899&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA.

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4

Goodacre, John A. "Immunopathogenic mechanisms of chronic polyarthritis." Thesis, University of Newcastle Upon Tyne, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.241367.

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5

Denis, Pierre. "Les polyarthrites septiques." Clermont-Ferrand 1, 1988. http://www.theses.fr/1988CLF13005.

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6

Zeltner, Maria Cristina. "Individuell adaptierter Zahnbürstengriff für Patienten mit chronischer Polyarthritis /." [S.l : s.n.], 1987. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.

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7

Franklin, Jarrod Peter. "Epidemiology of cancer in patients with inflammatory polyarthritis." Thesis, University of Manchester, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.517729.

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8

FIELDS, PATRICK-PIERRE. "Correlations radio-serologiques des polyarthrites rhumatoides." Aix-Marseille 2, 1988. http://www.theses.fr/1988AIX20491.

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9

Connolly, Ashley Rex. "Cytokine gene expression in a rat model of polyarthritis /." Title page, contents and abstract only, 1998. http://web4.library.adelaide.edu.au/theses/09PH/09phc75238.pdf.

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10

Brasted, Melissa. "Effector CD4Ê T lymphocytes in the prodrome of polyarthritis /." Title page, abstract and table of contents only, 2001. http://web4.library.adelaide.edu.au/theses/09PH/09phb8239.pdf.

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Thesis (Ph.D.) -- University of Adelaide, Dept. of Molecular Biosciences, 2002.
"October 2001" Amendments (4 leaves) inserted inside back cover. Includes bibliographical references (leaves 215-266).
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11

Schwalbach, Bettina Spreng David. "Die rheumatoide Polyarthritis beim Hund ... Bettina Schwalbach, David Spreng." Bern, 1991. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.

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12

Rutherford, Sarah-Jayne. "Streptococcus dysgalactiae polyarthritis in lambs in England and Wales." Thesis, Royal Veterinary College (University of London), 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.572433.

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13

Trachsel, Madeleine. "Prävalenz der chronischen Polyarthritis in Azmoos und Analyse der diagnostischen Kriterien /." [S.l : s.n.], 1987. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.

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14

Matt, Peter. "Fc receptors and immunoglobulins in polyarthritis : A matter of function, supply and demand?" Doctoral thesis, Uppsala universitet, Institutionen för medicinska vetenskaper, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-301173.

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Fc receptors (FcR) and immunoglobulins (Ig) play important roles in the defence against pathogens. However, altered interactions of these may promote chronic inflammation in rheumatic diseases. An excess of Igs forming immune complexes (IC) could lead to continuous FcR activation and spreading of autoimmune inflammation to other tissues.This work focuses on the evaluation of the FcR status and function in the two most common polyarthritides - psoriatic arthritis (PsA) and rheumatoid arthritis (RA) – in relation to various Igs, joint and skin disease activity, and effect of anti-rheumatic treatment (determined by the EULAR response criteria for RA). Monocyte subpopulations (defined by surface CD14 and CD16 expressions) in patients and HC were also characterised, since different monocyte subsets may have opposing functions in inflammatory conditions. In addition, the effect and safety of long-term B-cell suppression in advanced RA was studied. In PsA, elevated serum levels of IgG1, 2, and 3 were noted while the early naïve RA patients - besides being positive for autoantibodies like IgMRF, IgARF, IgGRF, and ACPA IgG - were distinguished by high levels of IgG1 and IgG3. Monocytes of PsA and RA patients were heavily loaded with IgG and expressed more CD64 (i.e. the high affinity FcγR) than HC. An increase in CD64 turnover was specific for early RA, while a higher CD16a (i.e. a low affinity FcγR) turnover was seen in both RA and PsA compared with HC. The FcγR function was impaired in both polyarthritides compared to HC, but the RA monocytes were more affected of this than the PsA monocytes. RA non-responders had a much lower capacity of IC binding compared with RA good responders. Alterations of the FcR status and function reflected joint disease activity markers in both polyarthritides but not the skin disease activity in PsA. I therefore conclude that the observed FcR statuses in both diseases were specific for joint inflammation. In addition, RA patients with high levels and the occurrence of several simultaneously appearing RF isotypes presented a minor FcγR function, while patients experiencing a good treatment effect were more likely to show low levels of Igs. This suggests that RFs/IC in excess could be important promotors of the ongoing inflammation in RA. However, for ACPA IgG no associations with the rheumatoid monocytic FcR status/function were noted. CD16negative classical monocytes were elevated in early naïve RA, especially in the non-responders - while PsA patients showed an increase in CD16low expressing cells compared to HC. These observations indicate that different monocyte subpopulations could be important in the two polyarthritides. In a cohort of RA patients with advanced disease, long-term B-cell suppression resulted in conversion to RF negativity which indicated a good treatment response but not an increased risk of infection.  FcRs and Igs are important players that promote chronicity of inflammation in polyarthritis, especially in RA. An impaired FcγR function following an excess of Igs/IC reflects this state of the immune system. This work has identified an increased monocytic CD64 turnover as a RA specific feature. Future treatment options in RA might include supporting/normalizing the FcγR function. Today suppressing B-cell activity is an effective and relatively safe way to tackle the problem from the opposite side.
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15

Fuchs, Daniela. "TNF-alpha inhibierende Therapie bei Patienten mit florider chronischer Polyarthritis : Langzeitverlauf nach 10 Jahren /." Düsseldorf, 2008. http://opac.nebis.ch/cgi-bin/showAbstract.pl?sys=000278420.

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16

Tilger, Julius. "Über Polyarthritis rheumatica mit besonderer Berücksichtigung der Salicyl-Therapie UB Freiburg, Hs. 1415; Autograph /." Freiburg i. Br. : Univ.-Bibl, 2006. http://www.manuscripta-mediaevalia.de/hs/katalogseiten/HSK0547%5Fb247%5Fjpg.htm.

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17

Mirjafari, Hoda. "The prevalence and determinants of subclinical atherosclerosis in an early inflammatory polyarthritis inception cohort." Thesis, University of Manchester, 2011. https://www.research.manchester.ac.uk/portal/en/theses/the-prevalence-and-determinants-of-subclinical-atherosclerosis-in-an-early-inflammatory-polyarthritis-inception-cohort(071e4a81-5c0e-459a-8210-0c84b53f06a5).html.

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Introduction: Patients with inflammatory polyarthritis (IP) have an excess risk of cardiovascular (CVD) mortality due to accelerated atherosclerosis. Markers identifying individuals with subclinical atherosclerosis as measured by carotid intima-medial thickness (cIMT) and plaque may allow for attenuation of CVD risk. The objective of this study was to identify associated risk markers for atheromatous plaque and cIMT in an incident cohort of patients with early IP and to assess the risk markers associated with progression of cIMT and plaque after 2 years of follow-up.Methods: From 2004 to 2008 consecutive patients with early IP (≥2 joints swollen for ≥4 weeks) aged 18-65 years, who were within 24 months of symptom onset (±6 months) were recruited as part of a primary-care-based inception cohort. Apparently healthy controls were recruited on a frequency matched 'buddy' pair system. Patients underwent joint and blood pressure examination. Patients and controls underwent BMI measurement and their medication was recorded. Patients' blood was taken for measurement of rheumatoid factor, anti-citrullinated protein antibody, C reactive protein, glucose, lipids (LDL, HDL, triglycerides, paroxonase 1, apolipoprotein A1 and B) and markers of vascular damage (E-selectin, VCAM) and adipocytokines (leptin and adiponectin). Patients and controls underwent B mode Doppler ultrasound examination of the carotid arteries to assess for cIMT and the presence of plaque. In univariate analyses we identified factors that were associated with cIMT and plaque presence after age and gender adjustment. An additive stepwise multivariable logistic regression model was created to investigate the independence of any associations.Results: The 329 IP subjects had a median (IQR) age of 51 (42-58) years and 96 (29%) were male. IP subjects were more likely to be smokers, have a family history of CVD, have diabetes, higher BP and be overweight than their apparently healthy counterparts. IP subjects with plaque at baseline often did not have prior CVD. Subjects with IP had a 2.87 fold higher plaque frequency at the baseline but a similar median cIMT relative to the controls. Traditional CVD risk markers such as age, systolic BP and LDL were associated with cIMT and plaque at baseline. Adiponectin levels were negatively associated with cIMT and positively associated with plaque. IP subjects had a significant increase in their cIMT in the first 2 years of follow-up. The rate of progression of cIMT was 1.5-2.2 fold greater in IP than reported in the general population. Novel risk factors added to the model above and beyond traditional risk factors in predicting atherosclerosis. Steroid exposure at 2 years was associated with atherosclerosis progression.Conclusion: Markers known to be associated with atherosclerosis in the general population are associated with cIMT and plaque presence in early IP prior to established inflammatory disease and therapy. While cIMT in subjects and controls was the same at baseline there was an accelerated rate of progression of cIMT in IP subjects relative to that reported in the general population.
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18

Wegert, Stefanie [Verfasser], and Carsten [Akademischer Betreuer] Spitzer. "Chronische Polyarthritis und frühkindliche Traumatisierungen : eine klinische Fall-Kontroll-Studie / Stefanie Wegert. Betreuer: Carsten Spitzer." Hamburg : Staats- und Universitätsbibliothek Hamburg, 2014. http://d-nb.info/1046940120/34.

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19

Ramjeet, Janet. "The role of coping strategies in psychological adjustment of patients with recent onset inflammatory polyarthritis." Thesis, University of East Anglia, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.426813.

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20

Perler, Martin. "Chronische Polyarthritis: Assoziation mit HLS-DRB1-Allelen und deren Nutzen als prädiktive Marker für den Krankheitsverlauf /." Bern : [s.n.], 1995. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.

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21

Harrison, Mark James. "An evaluation of a health status measure and two health utility measures in patients with inflammatory polyarthritis." Thesis, University of Manchester, 2008. http://www.manchester.ac.uk/escholar/uk-ac-man-scw:77828.

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Background: The ability to measure health and the value of improving or declining health is crucial to the evaluation of health care interventions. Many generic and disease specific health status measures exist for use in patients with rheumatoid arthritis (RA). The Overall Status in Rheumatoid Arthritis (OSRA) measure is a new and simple measure with early evidence of construct validity. Generic health profiles with attached utility weights such as the EuroQol EQ-5D and the SF-6D (calculated from the Medical Outcome Study 36-item short-form health survey) allow the quantification of a patient's health relative to perfect health and death, and can be used to estimate quality adjusted life years (QALYs). The EQ-5D is extensively used in RA, but has potential limitations. The SF-6D appears to have potential, but needs further evaluation. The aim of this thesis was to assess the validity and responsiveness of the EQ5D, SF-6D and OSRA in UK RA patients, and compare the performance and implications of the use of the EQ-5D and SF-6D.Methods and subjects: Patient data were obtained from three sources; the Steroids in Very Early Arthritis (STIVEA) (n=256) and British Rheumatoid arthritis Outcome Study Group (BROSG) (n=466) randomised controlled trials, and the British Society for Rheumatology Biologics Register (BSRBR) (n=129). The data used included lifestyle and demographic factors, disease activity (DAS28), functional disability (HAQ), X-rays to assess erosive damage, the EQ-5D and the SF-6D. The OSRA was collected only in the BROSG trial. Visual analogue scales (VAS) of pain and fatigue were collected in BROSG and STIVEA. Construct validity was tested by correlating the EQ-5D, SF-6D and OSRA with a range of outcome measures for RA. Responsiveness to change was assessed using minimum important differences (MID), effect size (ES) and standardised response means (SRM), and compared using ratios. EQ-5D profiles placing arthritis patients in utility states 'worse than death' (negative scores) were described and assessed using linear and logistic regression. The implications of using the EQ-5D and SF-6D in economic evaluation were compared by cost-effectiveness analyses of the BROSG trial. Results: The correlation of the EQ-5D and SF-6D was moderate to high (0.67). Both measures had moderate to high correlations with disease activity, physical function, joint damage and fatigue. The OSRA Activity (OSRA-A) and Damage (OSRA-D) correlated strongly with measures of related aspects of disease. The EQ-5D, SF-6D and OSRA discriminated between known differences in health status across groups defined by social deprivation and disease activity. The EQ-5D MID was 0.04 for improvement and 0.10 for deterioration. The SF-6D MID was 0.04 in both directions. The SF-6D was more responsive to improvement (EQ-5D: SF-6D ES ratio 0.78-0.88) and the EQ-5D more responsive to deterioration (ES ratio 1.14) in health. The OSRA-A was the most sensitive disease specific measure in the BROSG trial, and the OSRA-D was more responsive than the HAQ. The factors associated with being in a 'worse than death' health state were male gender, the HAQ, SF-36 mental composite scale, pain VAS, and erythrocyte sedimentation rate (a marker of inflammation). Pain was the predominant factor and was scored at the most extreme level in every worse than death profile. The cost-effectiveness analyses (BROSG trial), found net quality adjusted life years (QALYs) were greater for the EQ-5D (0.07) than the SF-6D (0.05), but had higher variance than the SF-6D. Conclusions: The EQ-5D and SF-6D appear valid and responsive to changes in health in RA, but measure subtly different aspects of health. There are issues with both measures, and cost-effectiveness conclusions of a study could differ according to which measure was used. The EQ-5D may be more likely to demonstrate that an intervention is cost effective than the SF-6D, due to its larger mean change in response to change in health status. The OSRA is valid for use in RA and its responsiveness suggests potential for inclusion in clinical trials.
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22

Lariviere, William R. "The role of the hypothalamic-pituitary-adrenal axis in the susceptibility to adjuvant-induced polyarthritis in the rat /." Thesis, McGill University, 2000. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=36631.

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The hypothalamic-pituitary-adrenal (HPA) axis, a system activated by stress, is traditionally considered to affect the susceptibility to chronic pain via effects on peripheral processes. This study investigates whether the HPA axis contributes to the development of chronic pain in an animal model via direct effects on central pain mechanisms.
First, correlations between pain processes and the susceptibility to chronic pain in an animal model that is correlated with HPA-axis function were examined. The results show that, in the Fischer rat, the amount of pain suppression observed during the formalin interphase depression is negatively correlated with susceptibility to polyarthritis. Since the formalin interphase depression mechanisms are within the central nervous system, the results suggest a role for central pain mechanisms in the development of polyarthritis.
Hypophysectomy inhibits the development of adjuvant-induced arthritis. To test whether hypophysectomy inhibits adjuvant-induced polyarthritis via central pain mechanisms, the analgesic effect of hypophysectomy was examined in the formalin test. The results show that hypophysectomy specifically prolongs the formalin interphase depression, further supporting that the underlying central pain suppression mechanisms are associated with resistance to adjuvant-induced polyarthritis.
Corticotropin-releasing factor (CRF) was then investigated as a possible underlying mechanism of the effects of hypophysectomy. Peripheral injection of CRF into inflamed tissue affects pain mechanisms unrelated to the susceptibility to adjuvant-induced polyarthritis. However, central and intravenous administration of CRF preferentially affect the formalin interphase depression mechanisms. The observed dose-response relationships indicate that these effects are due to direct actions of CRF within the central nervous system.
In conclusion, the results strongly suggest that the HPA axis modulates the susceptibility to adjuvant-induced polyarthritis via direct effects on supraspinal pain suppression mechanisms. Thus, the HPA axis may contribute to the development of chronic pain syndromes associated with HPA-axis abnormalities, such as rheumatoid arthritis and fibromyalgia, via effects on pain mechanisms within the central nervous system.
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Larivière, William R. "The role of the hypothalamic-pituitary-adrenal axis in the susceptibility to adjuvant-induced polyarthritis in the rat." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp03/NQ64597.pdf.

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24

Leybrand, Sabine. "Molekular-zytogenetische Charakterisierung komplexer, struktureller Chromosomenaberrationen bei einer Patientin mit schwerer mentaler Retardierung, chronischer Polyarthritis und physischen Dysmorphien." [S.l. : s.n.], 2009. http://nbn-resolving.de/urn:nbn:de:bsz:289-vts-66722.

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Paravert, Sylvain. "Caractéristiques cliniques, biologiques et immunologiques de deux groupes de polyarthrites rhumatoi͏̈des à forme lytique et non lytique." Montpellier 1, 1990. http://www.theses.fr/1990MON11233.

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Berthelot, Jean-Marie. "Discussion nosologique de quatre cas de polyarthrites sero-negatives destructrices a predominance proximale chez des hommes de moins de cinquante ans." Nantes, 1990. http://www.theses.fr/1990NANT029M.

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Ghiringhelli, Charles-Benoît Pourel Jacques. "Polyarthrites, hépatites granulomateuses et miliaires pulmonaires : complications dysimmunitaires ou septiques de l'immunothérapie endovésicale par BCG dans les cancers superficiels de la vessie." [S.l] : [s.n], 2003. http://www.scd.uhp-nancy.fr/docnum/SCDMED_T_2003_GHIRINGHELLI_CHARLES_BENOIT.pdf.

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Almohmedhusain, Awal. "Lipid associated biomarkers in patients with systemic lupus erythematosus and rheumatoid arthritis." Thesis, University of Manchester, 2013. https://www.research.manchester.ac.uk/portal/en/theses/lipid-associated-biomarkers-in-patients-withsystemic-lupus-erythematosus-andrheumatoid-arthritis(e62f01eb-debe-4510-9489-13f05249dbc1).html.

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Patients with chronic inflammatory conditions such as systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA) experience premature cardiovascular mortality and morbidity compared with the general population. The increased risk of cardiovascular disease (CVD) may in part, result from an interaction between traditional and non-traditional risk factors, modulated by chronic inflammation. The aim of this project was to look at lipid associated biomarkers in patients with SLE/RA and the association between these markers and cardiovascular disease outcomes. We also aimed to study the effect of inflammation reduction on vascular biomarkers. In the first study we examined 168 SLE patients median (IQR) age was 53 (46-61) years and median disease duration 13 (7, 23) years and 56 healthy controls median age 50 (39-60) years. We demonstrated elevated level of oxidised-LDLin SLE patients compared with healthy controls (76 (57, 99) U/l vs 56 (42, 88)U/l P= 0.02). We further explored the association between oxidant stress and premature atherosclerosis as measured by carotid intima media thickness (cIMT) and plaque. In addition to age and systolic blood pressure, oxidised-LDL and urinary 8-isoprostane were significantly and independently associated with cIMTin SLE patients _ coefficient 95%CI [0.00007 (5.29−6, 0.0001) and 0.003 (0.0008,0.004)], respectively. In healthy controls, age was the only independent variable. In the Norfolk Arthritis Register, 1266 patients with early inflammatory polyarthritis (IP) were studied. A linear regression analysis revealed a significant negative association between CRP and lipid profile namely TC, LDL, TG and ApoA-1. During a median (IQR) follow up = 5.5 (3.7-7.7) years 100 (7%) patients died (all causes) of which 33% (33) deaths were attributed to CVD. Forward stepwise regression analysis demonstrated that a low total cholesterol was independently associated with all cause mortality HR (95%CI) 0.75 (0.61, 0.91) and CVD mortality HR (95%CI) 0.49 (0.29, 0.85). In a small cohort 27 SLE patients and 15 healthy controls. We measured endothelial function using flow mediated dilatation of the brachial artery. At baseline we found a significant increase in TG level [1.36 (0.9, 1.87) mmol/l vs0.88 (0.64, 1) mmol/l P= 0.009] and a significant impaired endothelial function in SLE patients compared to the healthy controls [2.86 (0.6, 5.3) vs 6.81 (3.46,8.57), P= 0.03]. After treatment, there was a trend towards reduced TG level and improved endothelial function. Oxidised-LDL did not change significantly. In conclusion, oxidant stress is increased in SLE patients and relates to some measures of subclinical atherosclerosis. Control of inflammation may not be sufficient to completely control this in routine practice. In early RA, active inflammationmay mask any tendency to hyperlipidemia in this population. Low total cholesterol may be the best biomarker of the overall metabolic and inflammatory status of the patients as well as indicating a group with increased risk of future mortality.
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Vernhes, Jean-Philippe. "Traitement des polyarthrites rhumatoi͏̈des sévères et des vascularites associées, par le Chlorambucil à faible dose initiale (4mg/jour en moyenne) : étude rétrospective d'une population de 28 patients." Bordeaux 2, 1994. http://www.theses.fr/1994BOR23077.

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30

CARON, LAVIOLETTE XAVIER. "Etude de l'association dysthyroidies auto-immunes - maladies systemiques : analyse de cent cas (40 polyarthrites rhumatoides, 38 lupus erythemateux dissemines, 12 sclerodermies et 10 syndromes de gougerot-sjogren) et revue de la litterature." Reims, 1990. http://www.theses.fr/1990REIMM081.

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Brasted, Melissa. "Effector CD4Ê T lymphocytes in the prodrome of polyarthritis." 2001. http://web4.library.adelaide.edu.au/theses/09PH/09phb8239.pdf.

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32

Haß, Wolfgang [Verfasser]. "Soziale Unterstützungsnetzwerke von Menschen mit chronischer Polyarthritis : eine explorative, netzwerkanalytische Studie / vorgelegt von Wolfgang Haß." 2002. http://d-nb.info/967083761/34.

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33

Küttner, Tina [Verfasser]. "Entwicklung klinischer Behandlungspfade in der Rheumatologie : Möglichkeiten und Grenzen am Beispiel der chronischen Polyarthritis / vorgelegt von Tina Küttner." 2009. http://d-nb.info/995379084/34.

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34

Lemburg, Anna Katharina [Verfasser]. "Histologische und immunhistologische Untersuchungen an der Synovialmembran von Hunden mit spontanem vorderen Kreuzbandriß oder Polyarthritis / vorgelegt von Anna Katharina Lemburg." 2001. http://d-nb.info/963600648/34.

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35

Leybrand, Sabine [Verfasser]. "Molekular-zytogenetische Charakterisierung komplexer, struktureller Chromosomenaberrationen bei einer Patientin mit schwerer mentaler Retardierung, chronischer Polyarthritis und physischen Dysmorphien / vorgelegt von Sabine Leybrand." 2008. http://d-nb.info/1000829138/34.

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36

Farmer, Elizabeth A. "Lymphocyte-synovial microvascular endothelial cell interactions in experimental polyarthritis : a microassay for screening monoclonal antibodies that block adhesion / by Elizabeth-Anne Louise Farmer." 2004. http://hdl.handle.net/2440/22118.

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Abstract:
Bibliography: leaves 250-284.
xviii, 284 leaves : ill., plates (some col.) ; 30 cm.
Title page, contents and abstract only. The complete thesis in print form is available from the University Library.
Thesis (Ph.D.)--University of Adelaide, School of Molecular and Biomedical Science, Discipline of Microbiology and Immunology, 2004
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37

Moheb, Afshin [Verfasser]. "Auswirkungen einer Ganzkörperkältetherapie von -80°C, 2 min. auf T-Lymphozytenpopulation im peripheren Blut bei der rheumatoiden Arthritis (chronischen Polyarthritis) / vorgelegt von Moheb, Afshin." 2006. http://d-nb.info/990441245/34.

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