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Dissertations / Theses on the topic 'Systemic lupus erythematosus'

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Published: 4 June 2021
Last updated: 1 August 2024

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1

Teh, Lee-Suan. "Neuropsychiatric systemic lupus erythematosus." Thesis, University of Aberdeen, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.240703.

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Neuropsychiatric (NP) symptoms are relatively common in patients with SLE. The diverse and dramatic clinical presentations, the unclear pathogenesis, the lack of diagnostic test/s and uncertainties about the optimal management are some problems facing a clinician. When serum anti P antibodies were claimed to be highly correlated to lupus psychosis, this needed confirmation. An ELISA for measuring anti P antibodies was developed and validated. The prevalence of anti P antibodies was determined in different patient groups in a large retrospective study. Although anti P antibodies were highly specific for SLE, there was no correlation between the presence of these antibodies and lupus psychosis or other NP symptoms. Two prospective studies were carried out to eliminate any bias in our retrospective study. In one, none of the patients developed psychosis and these antibodies were not found to be specific for lupus depression or anxiety. In the other, anti P antibodies were measured in Malaysian Chinese SLE patients. No correlation was found between these antibodies and NP-SLE but a high prevalence of these antibodies was demonstrated in this group. Genetic studies showed that there was an increase in HLA-Dr2w16X subtype allele in anti P-positive patients but this did not reach significance. The usefulness of measuring antineuronal antibodies in helping to diagnose NP-SLE was examined but these antibodies were not better indicators of NP-SLE. Although the clinical correlations of anti P antibodies remain controversial, anti P antibodies were found to selectively bind to neuroblastoma cell surfaces in vitro but the nature of the surface antigen was not determined. Finally, sera from patients with lupus psychosis were found to significantly influence the response of neuroblastoma cells to agonist-induced stimulation and if confirmed, would offer an explanation for the reversible changes in cell function associated with psychiatric lupus.
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2

Bernatsky, Sasha. "Malignancy in systemic lupus erythematosus." Thesis, McGill University, 2001. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=32761.

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Objectives. (1) To estimate cancer incidence in systemic lupus erythematosus (SLE) as compared to the general population. (2) To estimate the sensitivity and specificity of methods of cancer ascertainment. (3) To determine the prevalence of malignancy risk factors in SLE. Methods. (1) We determined the incidence of malignancy in the Montreal General Hospital (MGH) lupus cohort, through linkage with the Quebec tumor registry. Standardized incidence ratios (SIRS) were generated, using Quebec population rates. In addition, a meta-analysis was performed by pooling data from eight cohort studies of malignancy in SLE. (2) We administered a postal survey to cohort members to determine risk factors for cancer and self-report of cancer occurrence. For dead or lost-to-follow-up patients, data was abstracted from charts. We calculated the sensitivity and specificity of self-report and chart review for cancer ascertainment, compared to registry linkage results. (3) Using the data collected on self-report and chart review, we compared risk factor prevalence within the MGH cohort to that of the Quebec population. Results. (1) Observed cancers in our cohort were greater than what would be expected; for all cancers, the SIR was 1.8 (95% Confidence Interval 1.2--2.6). The meta-analysis SIR (for all malignancies) was 1.67 (1.42--1.94). Postal survey and chart review methods demonstrated high specificity. Sensitivity was imperfect, but did not greatly effect estimation of the SIR estimate. (2) Our lupus cohort had a distinct profile of risk factors for malignancy compared to the general population; differences included more prevalent nulliparity, obesity, and use of hormone replacement therapy. Conclusions. The risk of malignancy in SLE patients is increased. Risk factor profiles could influence the incidence of certain malignancies in SLE.
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3

Clarke, Alexander James. "Autophagy in Systemic Lupus Erythematosus." Thesis, King's College London (University of London), 2015. http://kclpure.kcl.ac.uk/portal/en/theses/autophagy-in-systemic-lupus-erythematosus(1e5a4a5e-99f7-456e-bcb4-634a4e3fd986).html.

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Autophagy has emerged as a critical homeostatic mechanism in lymphocytes, influencing proliferation and differentiation. I sought to explore the role of autophagy in the pathogenesis of human and murine lupus, a disease in which B cells are critical effectors of pathology. Autophagy was assessed using multiple techniques in NZB/W and control mice, and in patients with SLE compared to healthy controls. I evaluated the phenotype of the B cell compartment in Vav-Atg7-/- mice in vivo, and examined human and murine plasmablast formation following inhibition of autophagy. I found activation of autophagy in early developmental stages of B cell development in a lupus mouse model even before disease-onset, and which progressively increased with age. In human disease, again autophagy was activated compared with healthy controls, principally in naïve B cells. B cells isolated from Vav-Atg7-/- mice failed to effectively differentiate into plasma cells following stimulation in vitro. Similarly, human B cells stimulated in the presence of autophagy inhibition did not differentiate into plasmablasts. My data suggest activation of autophagy is a mechanism for survival of autoreactive B cells, and also demonstrate that it is required for plasmablast differentiation, processes that induce significant cellular stress. The implication of autophagy in two major pathogenic pathways in SLE suggests the potential to use inhibition of autophagy as a novel treatment target.
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4

Brown, Aaron Clifford. "Molecular and Phenotypic Characterization of the Y-Linked Autoimmune Accelerator (YAA)." Fogler Library, University of Maine, 2007. http://www.library.umaine.edu/theses/theses.asp?highlight=1&Cmd=abstract&ID=BMB2007-011.

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5

Wong, Kee-lam, and 黃基林. "Systemic lupus erythematosus in Hong Kong." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1990. http://hub.hku.hk/bib/B31981410.

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6

Peschken, Christine A. "Systemic lupus erythematosus in Manitoba Aboriginals." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape9/PQDD_0019/MQ55086.pdf.

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7

Svenungsson, Elisabet. "Cardiovascular disease in systemic lupus erythematosus /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-501-8.

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8

Russell, Andrew Ian. "Genetic predisposition to systemic lupus erythematosus." Thesis, Imperial College London, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.406513.

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9

Li, Hei Philip, and 李曦. "Subphenotype stratification in systemic lupus erythematosus." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hub.hku.hk/bib/B48334765.

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Subsets of systemic lupus erythematosus (SLE) patients with distinct patterns of disease manifestations and autoantibody production have been reported, but seldom have these two phenomena been analysed together. Cluster analysis was performed on 1928 Chinese SLE patients based on autoantibody profile and the frequencies of various clinical manifestations were compared between each cluster. Separate association analyses between individual autoantibodies and clinical manifestations, as well as between clinical manifestations, were also performed. This study identifies three separate autoantibody clusters each with different clinical manifestations, and proposes that the phenomena of autoantibody clustering and clinical subsets may be inter-related. Patient clusters could also be stratified into a bipolar spectrum. On one end are patients with over-representation of anti-dsDNA and renal disorder; whilst on the other end are two distinct autoantibody clusters (anti-Sm/anti-RNP/aPL and aPL/anti-Ro/anti-La) with overlapping of other non-renal manifestations. Patient stratification could aid disease prediction and subsequent management. These findings may also elucidate disease pathogenesis and guide future study on potential common pathological processes within autoantibody clusters.
published_or_final_version
Paediatrics and Adolescent Medicine
Master
Master of Research in Medicine
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10

Courtney, Philip. "Leukocyte apoptosis in systemic lupus erythematosus." Thesis, Queen's University Belfast, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.326415.

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11

Chan, Madelynn Tsu-Li. "Serological biomarkers in systemic lupus erythematosus." Thesis, University of Bath, 2013. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.607470.

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Background: Systemic lupus erythematosus (SLE) is a multi-system autoimmune disease characterised by autoantibody production and variable clinical features, ranging from mild to severe disease. Patients with SLE are at increased risk of developing accelerated atherosclerosis. Biomarkers have potential utility in SLE as markers of disease or predictors of future clinical events and mortality. Objective The aim of this thesis was to identify serological biomarkers predictive for erosive arthritis (EA), cardiovascular events (CVEs), mortality and subclinical atherosclerosis in SLE. Methods: In chapters 2 to 4, study subjects were SLE patients from Bath. Anti-cyclic citrullinated peptide antibodies (ACPA) and HLA-DR and -DQ were studied for markers of EA, and anticardiolipin (aCL) and lipoprotein profiles for markers of CVEs and mortality. In chapters 5 and 6, study subjects were women with SLE from Manchester. B-mode ultrasound scans of subjects' carotid arteries were performed at baseline and follow-up time-points to detect atherosclerotic plaque. Baseline IgG and IgM antiphospholipid (aPL) antibodies and CV risk factors were studied for markers of subclinical atherosclerosis. Clinical data collected for all studies included SLE features and auto-antibody profiles. Results: ACPA was identified as a marker of a SLE phenotype with EA - "rhupus". Patients with major erosive arthritis were HLA-DQB1*0302 carriers. Increased aCL GPL levels and total cholesterol : high density lipoprotein-C (TC : HDL-C) ratio were markers for future CVEs, and increased TC : HDL ratio, aCL GPL and lipoprotein(a) concentrations were markers for increased mortality. Lower HDL-C concentrations and anti-annexin A5 (anti-AnxA5) GPL were markers of carotid plaque progression. Conclusion: This thesis identified new markers for EA, subclinical atherosclerosis and future CVE and mortality risk in SLE. Strategies to incorporate these new CV markers into clinical CV risk assessments may assist in distinguishing the subset of SLE patients most at risk of developing accelerated atherosclerosis.
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12

Niemela-Waller, Kirsi (Kirsi M. ). "Cognitive Dysfunction in Systemic Lupus Erythematosus." Thesis, University of North Texas, 1997. https://digital.library.unt.edu/ark:/67531/metadc278952/.

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The purpose of the study was to determine the point prevalence of cognitive dysfunction in patients with systemic lupus erythematosus (SLE) and to investigate its association with corticosteroids and depression. The severity of dysfunction and the pattern of cognitive changes were examined. This study hypothesized that cognitive dysfunction is common in SLE and many previous studies have underestimated its prevalence, partially due to using limited neuropsychological batteries and insensitive test instruments. It was further hypothesized that the pattern of cognitive changes in SLE patients will resemble that observed in subcortical dementias.
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13

Aronson, Ingrid. "The cytopenias in systemic lupus erythematosus." Master's thesis, University of Cape Town, 1989. http://hdl.handle.net/11427/26344.

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14

Scalzi, Lisabeth Victoria. "Subclinical Atherosclerosis in Systemic Lupus Erythematosus." Case Western Reserve University School of Graduate Studies / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=case1212695307.

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15

Lee, Loretta Lok-Yan. "Immune Profiling of Systemic Lupus Erythematosus." Thesis, The University of Sydney, 2015. http://hdl.handle.net/2123/14440.

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Studies in animal models and lupus patients suggest several mechanisms driving the loss of B cell regulation in Systemic Lupus Erythematosus (SLE). The first mechanism involves the overexpression of B cell activating factor and the second is driven by follicular T helper (Tfh) cells. Monocytes have been implicated in the pathogenesis of SLE through recognition of immune complexes containing TLR-binding self-antigens. The overall decrease of NK cells and increase of CD56briCD16- NK cells could further promote immune dysregulation in SLE. Our aim was to determine whether these abnormalities co-exist within each patient, or if human SLE can be subcategorised depending on the immune process driving the disease. We found that NK cells, CD4+ T cells and Tfh cells were decreased and lymphocytes, atypical memory B cells and CD56briCD16- NK cells were increased in SLE. Analysis with the complete data set showed no individual signatures of SLE but we could distinguish SLE patients from those without SLE based on the variables measured in the study. We developed models for predicting if an individual has SLE, if an SLE patient has renal involvement and predicting SLE Disease Activity Index, forming the basis for improved diagnosis and assessment of SLE in the future.
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16

Fan, Hiu-yi Rosie. "Cost of systemic lupus erythematosus in Hong Kong /." View the Table of Contents & Abstract, 2005. http://sunzi.lib.hku.hk/hkuto/record/B32020636.

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17

Rupanagudi, Khader Valli. "Immunoregulatory proteases in systemic lupus erythematosus and lupus nephritis." Diss., Ludwig-Maximilians-Universität München, 2013. http://nbn-resolving.de/urn:nbn:de:bvb:19-162652.

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18

Druley, Jennifer A. "Couples Coping with Wives' Systemic Lupus Erythematosus." Kent State University / OhioLINK, 1995. http://rave.ohiolink.edu/etdc/view?acc_num=kent1507726194610255.

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19

Strout, Stephen Lewis. "Association between systemic lupus erythematosus and periodontitis." [Gainesville, Fla.] : University of Florida, 2004. http://purl.fcla.edu/fcla/etd/UFE0004857.

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Thesis (M.S.)--University of Florida, 2004.
Typescript. Title from title page of source document. Document formatted into pages; contains 43 pages. Includes Vita. Includes bibliographical references.
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20

Casanova, Francesco. "maximal oxygen consumption in systemic lupus erythematosus." Thesis, Bangor University, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.531058.

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21

Mok, Chi-chiu, and 莫志超. "Gender, sex hormones and systemic lupus erythematosus." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2002. http://hub.hku.hk/bib/B29780147.

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22

Mak, Anselm, and 麥為憲. "Major organ damage in systemic lupus erythematosus." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B4765739X.

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Systemic lupus erythematosus (SLE) is an autoimmune disorder characterized by disease flares and damage accrual. The increased longevity allows SLE patients to accrue damage which has retarded their survival improvement since the 1980s. In the first study of this thesis, meta-analyses of observational studies revealed that renal and neuropsychiatric damage has been adversely affecting the survival of lupus patients in the past fifty years. While confirmatory studies are required, targeting at renal and neuropsychiatric involvement early might hopefully further improve the survival of SLE patients. As the survival of SLE patients improves, their psychosocial well-being becomes increasingly important. In the second study, anxiety symptoms were found to be significantly more frequent in lupus patients than those with other common inflammatory rheumatic conditions. Additionally, damage accrual and cumulative glucocorticoids accurately predicted anxiety in SLE patients. Related to neuropsychiatric damage, event-related functional brain imaging in the third study showed that new-onset SLE patients had poorer strategic planning skill that required compensatory cortical recruitment for executing comparable cognitive function as in healthy subjects. Even after sufficient control of SLE, they remained to demonstrate inferior strategic planning skill which necessitated compensatory recruitment of cortical areas to boost their executive function. These findings illustrated that cognitive dysfunction persists even after adequate control of SLE. Early recognition of the prognostically challenging renal, cardiovascular and musculoskeletal damage and their predictors is imperative. The fourth study revealed that failure to achieve complete renal remission 12 months after renal presentation predicted renal damage, irrespective of age and the choice of immunosuppressants. As to whether mycophenolate (MMF) or cyclophosphamide (CYC) is better; by meta-analysis, the fifth study concluded that MMF offers similar efficacy as CYC in inducing renal remission and preventing renal damage. As for the cardiovascular system, endothelial dysfunction exerts its impact very early during atherogenesis. As shown in the sixth study, SLE patients na?ve for cardiovascular disease had significantly poorer endothelial function than demographically and anthropometrically matched healthy controls. Higher serum high-sensitivity C-reactive protein level independently predicted poorer endothelial function in SLE patients. Osteoporotic fracture is a major lupus musculoskeletal damage which occurred in 9% of SLE patients as found in the seventh study. Increasing age and duration of corticosteroid use independently predicted osteoporotic fracture. While hormonal replacement therapy appeared fracture protective, its unfavorable long-term consequences limit its indication for fracture prevention. Mitigating fracture risk before fractures occur is the current management strategy. The eighth study found that the significantly higher FRAX? 10-year risk of major osteoporotic and hip fractures amongst SLE patients na?ve for clinical fracture compared with their demographically and anthropometrically matched healthy counterparts was driven by chronic glucocorticoid use and premature menopause. Modifiable factors including low hip bone mineral density (BMD), cumulative glucocorticoids and higher serum anti-dsDNA level independently predicted higher fracture risks. Finally, the relationship between lumbar bone loss and endothelial dysfunction was hitherto identified. Although potential drivers of this relationship remain to be identified, our findings serve to alert physicians to early atherosclerosis in lupus patients particularly in those with low lumbar BMD.
published_or_final_version
Medicine
Master
Doctor of Medicine
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23

Fraser, Louise. "Immunoglobulin light chains in Systemic Lupus Erythematosus." Thesis, King's College London (University of London), 2013. https://kclpure.kcl.ac.uk/portal/en/theses/immunoglobulin-light-chains-in-systemic-lupus-erythematosus(759b46c1-24bc-427d-8b25-8987eec6f61f).html.

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Systemic Lupus Erythematosus (SLE) is a chronic autoimmune disease of elusive origin and characterised by polyclonal B cell hyperactivity and the production of pathogenic antibodies targeting self DNA and nucleoproteins. Clinical manifestations of SLE are highly heterogeneous and include multisystem inflammation of connective tissue and vasculitis of the central nervous system (CNS). SLE is known to have genetic associations, and is widely acknowledged to involve a profound breakdown in immune tolerance. The aim of this project was to identify whether defects in early B cell development that affect the expressed repertoire of immunoglobulin light chains could be observed and to ask whether receptor editing contributes to disease pathogenesis. Chapter 3 describes a high-throughput sequencing analysis of the human immunoglobulin kappa light chain gene repertoire in healthy and SLE mature naive peripheral B cells. We observed that involvement of gene segments as the repertoire develops is equivalent in health and SLE and that a previously described bias towards usage of the gene segment IGKV4-1 in SLE is only observed in the expressed repertoire analysed. Chapter 4 describes an inefficient function of the kappa deleting element (KDE) in SLE, which manifests as reduced frequency of KDE rearrangement status in populations of CD19+ B cells and a failure to inactivate alleles of IGK allowing them to accumulate somatic hypermutations within non-productive IGK rearrangements. Chapter 5 identifies a potential biological outcome of a failure to inactivate rearranged alleles of IGK in SLE; cell surface expression of both kappa and lambda light chains were observed by flow cytometry analyses. Efforts to disprove this were unsuccessful anddetection of both light chain transcripts was confirmed through single cell PCR amplification of cDNA. The data in this thesis suggest that the failure of the KDE to inactivate alleles of IGK efficiently in SLE permits the expression of IGK light chains that have been selected against resulting in allelic inclusion. This mechanism may account for the broader and less stringently regulated antigen-binding B cell repertoire associated with SLE.
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24

Chen, Lingyan. "Genetics and epigenetics in systemic lupus erythematosus." Thesis, King's College London (University of London), 2018. https://kclpure.kcl.ac.uk/portal/en/theses/genetics-and-epigenetics-in-systemic-lupus-erythematosus(6257f5a2-eef5-4a55-9fb4-17bceed2c7d1).html.

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Systemic lupus erythematosus (SLE) is a chronic inflammatory autoimmune disease associated with a wide range of clinical features involving different organs and the prognosis is also highly variable. It is a complex genetic trait in which more than 80 susceptibility loci show robust genetic association with disease risk. Firstly, I preformed eQTL mapping, incorporating co-localization analysis of GWAS in the functional immune cells, in order to identify likely causal genes. The results indicate that eQTLs present in a diverse set of immune cells, encompassing both the innate and adaptive immune responses for more than half of the loci. I then integrated genetics, epigenetics and gene expression to delineate the regulatory map of SLE risk loci across human cells and tissues. Using GARFIELD and GoShifter, I demonstrated that SLE genetic associations displayed a marked enrichment pattern for areas of open chromatin in blood, including B cells, T cells, monocytes, and NK cells. Moreover, I found that a large proportion (66%) of the SLE eQTLs showed to overlap with areas of open chromatin, denoting extensive local coordination of genetic influences on gene expression and epigenetics. SLE patients with renal involvement have more severe clinical outcomes and an increased mortality risk. By calculating the genetic risk score (GRS) using a list of SNPs that are reported to be significantly associated with SLE, I found a significant correlation between GRS and patients with renal involvement – the higher the GRS, the higher probability of getting renal disease. The GRS also correlated inversely with age of SLE onset. As part of the functional study of post-GWAS, I investigated the protein expression of selected SLE-susceptibility gene products, namely Ikaros family members and OX40L, in a range of immune cells, using multi-parameter flow cytometry. The results reveal some cellular specificity in gene expression in disease. In particular, IKZF3 expression on activated regulatory T cell subsets was decreased, while OX40L expression on B cell subsets was increased in SLE. In summary, I combined eQTLs and epigenomes to identify the functional tissues and causal genes. In addition, I measured the expression of OX40L and Ikraos family to help understand the cell effects at protein level. Finally, I found that the genetic risk factors that influence the severity of SLE are through a quantitative way but not qualitative way, suggesting that the GRS approach may become a useful factor in predicting outcome in this clinically heterogeneous disease.
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25

Vieson, Miranda Diane. "Selective HDAC6 Inhibition in Systemic Lupus Erythematosus." Diss., Virginia Tech, 2017. http://hdl.handle.net/10919/74872.

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Systemic lupus erythematosus (SLE) is a prototypic autoimmune disease characterized by abnormalities in multiple components of the immune system resulting in progressive damage to multiple organs. Current treatments for SLE are often intensive and result in side effects and the potential for continued flares and progression of disease. Histone deacetylase (HDAC) enzymes control multiple cellular functions by removing acetyl groups from lysine residues in various proteins. HDAC inhibitors have been investigated as a potential treatment for SLE with promising results, however selective HDAC6 inhibition (HDAC6i) has become a leading candidate for pharmacologic inhibition to reduce the potential for side effects. We hypothesize that HDAC6i will decrease SLE disease by targeting substrates of HDAC6 in multiple components of immunity and organ systems. NZB/W mice were treated with ACY-738 or ACY-1083, followed by evaluation of multiple disease parameters and mechanisms involved in disease pathogenesis within the kidney, bone marrow, and spleen. Within the kidney, HDAC6i decreased glomerular pathology scores, proteinuria, and IgG and C3 deposition. Within glomerular cells, HDAC6i increased alpha-tubulin acetylation and decreased nuclear NF-κB. Within the spleen, there was a dose-dependent decrease in the frequency of Th17 cells and a mild decrease in the frequency of Treg cells. Concurrently, there were decreased levels of IL-12/IL-23 and minimal decreases in TGF-β in the serum. Within the bone marrow, B cell development through Hardy fractions exhibited accelerated progression through later stages as NZB/W mice aged. This accelerated progression may allow B cells to bypass important regulatory checkpoints in maintaining immune tolerance and contribute to autoimmunity. Treatment with an HDAC6i corrected the aberrant B cell development in the bone marrow and RNAseq analysis unveiled six genes (Cebpb, Ccr9, Spib, Nfil3, Lgals1, and Pou2af1) that may play a role in the aforementioned abnormalities. Overall, these findings show that HDAC6i decreased disease in NZB/W mice by targeting multiple components of the immune response, including glomerular cells, T cell subsets in the spleen, and bone marrow B cells. In conclusion, selective HDAC6i is an excellent candidate for pharmacologic therapy for SLE because it targets multiple immune abnormalities involved in SLE pathogenesis while remaining selective and safe.
Ph. D.
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26

Ruth, Natasha M. "Childhood-Onset Systemic Lupus Erythematosus: Neurocognitive Function." Cincinnati, Ohio : University of Cincinnati, 2006. http://www.ohiolink.edu/etd/view.cgi?acc_num=ucin1148060762.

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Thesis (M.S.)--University of Cincinnati, 2006.
Advisor: Dr. Kim N. Dietrich. Title from electronic thesis title page (viewed June 3, 2009). Includes abstract. Keywords: Systemic Lupus Erythematosus; Neurocognitive Function; ANAM. Includes bibliographical references.
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27

Mok, Chi-chiu. "Gender, sex hormones and systemic lupus erythematosus /." Hong Kong : University of Hong Kong, 2002. http://sunzi.lib.hku.hk/hkuto/record.jsp?B25943479.

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28

Denton, Fiona. "Illness Self-Schema in Systemic Lupus Erythematosus." Thesis, The University of Sydney, 2003. http://hdl.handle.net/2123/596.

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Systemic lupus erythematosus (SLE) is a relatively rare autoimmune disease with no known aetiology or cure. In addition to numerous physical symptoms, those living with SLE have also been shown to experience significant emotional and psychosocial difficulties. There has been little psychological research into SLE despite the rapidly increasing interest in health psychology and quality of life issues over the last two decades. One such issue that has commanded particular attention is that of cognitive bias in individuals with chronic pain and/or chronic illness. Cognitive bias toward illness-related information is theorised to indicate the presence of an illness self-schema, and is a valuable tool of investigation as it permits access to a level of cognitive structure that is inaccessible via self-report instruments. The primary focus of the present study is to investigate recall bias for pain- and illness-related words in SLE patients. This bias is explored relative to the recall of neutral words and depression-related words, and also relative to the responses of rheumatoid arthritis (RA) patients and healthy controls. Two hypotheses are proposed: firstly, that bias is related to disease activity; and secondly, that bias is related to the combination of illness and depression. The findings provide support for the second hypothesis, with the additional caveat that the nature of the pain/illness stimuli used is important in determining the presence of cognitive bias. No recall bias for illness-related words as a whole was found in any of the groups, nor was there evidence of a recall bias in the SLE and RA patients when they were divided according to depression status. However, when the illness words were examined separately according to �sensory pain� and �disability-related� words, a clear bias for disability words was found in the depressed patient group. It is concluded that there is a relationship between depression in chronically ill individuals, and the way in which such individuals process disability-related words. In accordance with the schema-enmeshment model (Pincus & Morley, 2001), it is suggested that both a pain-schema and an illness-schema exist, and it is when these two schemas become enmeshed with the self-schema that depression occurs in chronic pain/chronically ill patients. The cognitive bias assessment paradigm adopted in this study-one that is typically used in similar investigations-is lengthy, requires sophisticated equipment and can be difficult to interpret on an individual level. The present study investigates the relationship between cognitive biases in SLE patients and a recently-developed task, PRISM, which appears to symbolise the enmeshment of illness-, pain- and self-schemas. Analyses confirmed that recall of negative illness words was the only independent predictor of PRISM scores. This suggests that PRISM, a quick and easy task to administer, may have considerable usefulness as a clinical tool to assess information relevant to the enmeshment of illness- and self-schema. A greater understanding of schema and the processing styles of chronically ill patients will allow for more effective psychological treatment such that quality of life can be improved.
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29

Denton, Fiona. "Illness Self-Schema in Systemic Lupus Erythematosus." University of Sydney. Psychology, 2003. http://hdl.handle.net/2123/596.

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Systemic lupus erythematosus (SLE) is a relatively rare autoimmune disease with no known aetiology or cure. In addition to numerous physical symptoms, those living with SLE have also been shown to experience significant emotional and psychosocial difficulties. There has been little psychological research into SLE despite the rapidly increasing interest in health psychology and quality of life issues over the last two decades. One such issue that has commanded particular attention is that of cognitive bias in individuals with chronic pain and/or chronic illness. Cognitive bias toward illness-related information is theorised to indicate the presence of an illness self-schema, and is a valuable tool of investigation as it permits access to a level of cognitive structure that is inaccessible via self-report instruments. The primary focus of the present study is to investigate recall bias for pain- and illness-related words in SLE patients. This bias is explored relative to the recall of neutral words and depression-related words, and also relative to the responses of rheumatoid arthritis (RA) patients and healthy controls. Two hypotheses are proposed: firstly, that bias is related to disease activity; and secondly, that bias is related to the combination of illness and depression. The findings provide support for the second hypothesis, with the additional caveat that the nature of the pain/illness stimuli used is important in determining the presence of cognitive bias. No recall bias for illness-related words as a whole was found in any of the groups, nor was there evidence of a recall bias in the SLE and RA patients when they were divided according to depression status. However, when the illness words were examined separately according to �sensory pain� and �disability-related� words, a clear bias for disability words was found in the depressed patient group. It is concluded that there is a relationship between depression in chronically ill individuals, and the way in which such individuals process disability-related words. In accordance with the schema-enmeshment model (Pincus & Morley, 2001), it is suggested that both a pain-schema and an illness-schema exist, and it is when these two schemas become enmeshed with the self-schema that depression occurs in chronic pain/chronically ill patients. The cognitive bias assessment paradigm adopted in this study-one that is typically used in similar investigations-is lengthy, requires sophisticated equipment and can be difficult to interpret on an individual level. The present study investigates the relationship between cognitive biases in SLE patients and a recently-developed task, PRISM, which appears to symbolise the enmeshment of illness-, pain- and self-schemas. Analyses confirmed that recall of negative illness words was the only independent predictor of PRISM scores. This suggests that PRISM, a quick and easy task to administer, may have considerable usefulness as a clinical tool to assess information relevant to the enmeshment of illness- and self-schema. A greater understanding of schema and the processing styles of chronically ill patients will allow for more effective psychological treatment such that quality of life can be improved.
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30

McKinney, Eoin Fergal. "Gene expression profiling in systemic vasculitis and systemic lupus erythematosus." Thesis, University of Cambridge, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609786.

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31

Liu, Tiefu. "The role of interleukin-12 in the pathogenesis of human systemic lupus erythematosus /." Hong Kong : University of Hong Kong, 1998. http://sunzi.lib.hku.hk/hkuto/record.jsp?B20381505.

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32

Barkhuizen, Andre. "Pulmonary hypertension in systematic lupus erythematosus." Thesis, University of Cape Town, 1994. http://hdl.handle.net/11427/25896.

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33

Tench, Colin Mark. "The study of fatigue in systemic lupus erythematosus." Thesis, Queen Mary, University of London, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.406905.

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34

Reefman, Esther. "Apoptotic cell clearance in Systemic Lupus Erythematosus (SLE)." [S.l. : [Groningen : s.n.] ; University Library Groningen] [Host], 2006. http://irs.ub.rug.nl/ppn/297988956.

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35

Fan, Hiu-yi Rosie, and 范曉怡. "Cost of systemic lupus erythematosus in Hong Kong." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B45012817.

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36

Leung, Wai-hin, and 梁瑋軒. "Neurogenesis in animal model of systemic lupus erythematosus." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/209497.

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Systemic Lupus Erythematosus (SLE) is an autoimmune disease which is characterized by high level of autoantibody detected in the body. This disease is female predominant with a male to female ratio 1: 9. SLE could cause damage to different organ systems and central nervous system is one of them. Patients diagnosed with SLE could suffer from psychiatric problems like cognitive dysfunction, depression and anxiety. Neurogenesis refers to the process by which new neurons are generated. Although it has been widely reported that neurogenesis could be enhanced under pathological conditions such as stroke, Huntington’s disease and epilepsy, study focusing on the relationship between neurogenesis and SLE remains limited. In the present study, by using NZB/W F1 mice as the animal model of SLE, we could demonstrate that there was dramatic increase of neuronal precursor cells at the corpus callosum after the onset of SLE symptoms. Meanwhile, as IBA-1 positive cells and GFAP positive cells also increased significantly there, this suggested inflammation has taken place. I hypothesized there were upregulation of immunological factors after the onset of SLE symptoms and those factors were responsible for the neurogenesis. In my in vitro study, cytokine- interferon gamma (IFN gamma) has been shown to promote neuronal progenitor cells (NPCs) to differentiate into neuronal linage but it did not obviously affect the cell proliferation and migration. For the other cytokine and chemokines, including interleukin-10 (IL-10), interleukin-8 (IL-8), macrophage-derived chemokine (MDC), stromal cell-derived factor 1 alpha (SDF-1alpha) and thymus and activation regulated chemokine (TARC), all of them had no effect on NPC proliferation and differentiation. As far as we know, this is the first study to report SLE could enhance neurogenesis. Concerning the role of inflammation and IFN gamma on the neurogenesis in our case, it should be worth for further investigation, which will benefit future development of novel treatment targeting psychiatric symptoms in SLE.
published_or_final_version
Anatomy
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Master of Philosophy
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37

Zandi, Michael Surena. "Biomarkers and immunotherapy of neuropsychiatric systemic lupus erythematosus." Thesis, University of Cambridge, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.608051.

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38

Quinlan, C. T. "Cardiovascular morbidity in juvenile-onset systemic lupus erythematosus." Thesis, University College London (University of London), 2015. http://discovery.ucl.ac.uk/1466735/.

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Cardiovascular disease (CVD) is a leading cause of mortality in adults with systemic lupus erythematosus (SLE). As children with conditions such as chronic kidney disease have been shown to have a risk of CVD similar to their adult counterparts, clinicians have become concerned that paediatric patients with SLE are at increased risk of CVD. The aim of this project was to examine the vascular phenotype of a British paediatric population with SLE and gain mechanistic insights into this process. Structural changes in vessels were measured using carotid intima media thickness (cIMT) and function was assessed using pulse wave velocity (PWV). These findings were compared with clinical information, traditional cardiovascular risk factors, disease activity, medications and adipokine activity. 45 children were recruited to the study and compared to historical controls previously studied in our centre. Children with SLE had higher cIMT than controls (0.45 V 0.37mm, p<0.0001) but no difference in PWV (5.27 v 5.34m/s, p=0.77). The increase in cIMT is most marked in patients with hypertension, those on higher doses of prednisolone and those of Afro-Caribbean descent. No significant association was found between increased cIMT and biopsy-proven nephritis, disease activity, age, family history of CVD or physical activity score. Patients with JSLE had increased serum leptin levels (15.5 V 7.56ng/ml, p=0.024). There were slightly higher adiponectin levels in patients than controls (14.2 V 12.4ug/L, p=0.49). Patients with proteinuria had higher leptin (35.5 V 18.8ng/ml) and adiponectin (21.9 V 10.5ug/ml, p=0.03) levels, and cIMT increased with leptin and adiponectin levels. This cohort of children with JSLE show structural changes in their vessels indicative of early CVD but with adaptive changes resulting in normal functional scans. In contrast to adult data this group displays an early increase in serum adiponectin suggesting a possible early protective mechanism, which may be overwhelmed in later disease.
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39

Watson, Louise. "Renal biomarkers in juvenile-onset systemic lupus erythematosus." Thesis, University of Liverpool, 2012. http://livrepository.liverpool.ac.uk/10293/.

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Background: Juvenile-onset Systemic Lupus Erythematosus (JSLE) is a rare, but severe, autoimmune condition with lupus nephritis (LN) occurring in up to 80% of patients and predisposing to an increased mortality. Aims/Objectives: As part of the UK JSLE Cohort Study this study aimed to identify whether standard and/or novel biomarkers are useful for monitoring LN and to assess whether novel urine biomarkers are released from the podocyte (kidney epithelial cell). Method/Results: A prospective translational study encompassing a clinical cross sectional biomarker analysis, a longitudinal observational biomarker study and scientific laboratory investigation. The study had full ethical approval. Cross sectional investigation identified whether (a) urine biomarkers (monocyte chemoattractant protein-1, MCP1; alpha-1-acid glycoprotein, AGP; interferon producing protein-10, IP10; neutrophil gelatinase associated lipocalin, NGAL) or (b) plasma biomarkers (interferon-gamma, IFN-γ; IP10; tumour necrosis factor alpha, TNF-α; interleukin 6, IL6; IL1β; MCP1; IL13; vascular endothelial growth factor, VEGF) are increased in JSLE patients with active renal disease. JSLE patients (n=60) and healthy controls (n=23) were recruited. Of JSLE patients, 45 were female (75%) and aged 14.7 (12.2-16.1) years. All had ≥ 4 ACR SLE classification criteria (median 5, range 4-9). Urinary MCP1 concentration increased in patients with JSLE active renal disease compared to JSLE non-active renal disease (582 (251-2100) pg/mgCr; 207 (121-280) pg/mgCr; p=0.018) and healthy controls (117 (68-193) pg/mgCr; p=0.005), AGP concentration also increased (JSLE active renal disease: 1517 (753-2389) ng/mgCr; JSLE non-active renal disease: 485 (212-967) ng/mgCr; p=0.027; healthy controls 313 (108-729) ng/mgCr; p=0.013). On cross sectional testing IP10 and NGAL showed no significant difference. Plasma analysis demonstrated increased IL-13 and a trend toward increased IFN-γ, TNF-α, IL-6 and VEGF in patients with JSLE active renal disease (n=12). For prospective longitudinal analysis, JSLE samples were collected at clinical reviews and standard/novel biomarkers assessed against disease activity. The longitudinal JSLE cohort (n=64), seen at 3 (IQR: 2-5) clinical reviews over 364 (182-532) days were aged 14.1 (11.8-15.8) years and 80% female. Active renal episodes had increased concentration of; MCP-1, NGAL, ESR, anti-double stranded DNA, urine albumin:creatinine ratio (UACR), creatinine, and reduced complement 3 (C3), C4 and lymphocytes. On multivariate analysis, MCP-1 and C3 were independent variables (p<0.001) of active renal disease. MCP-1 was an excellent predictor of improved renal disease (AUC: 0.81; p=0.013; specificity 71%, sensitivity 70%); NGAL was a good predictor of worsened activity (AUC 0.76; p=0.04; specificity 60%, sensitivity 61%). An in vitro model was developed using a human podocyte cell line. Podocytes were cultured in macrophage media (activated with IFN-γ or inactive), and subsequently TNF-α, and protein/gene biomarker, TNF-α receptor (TNFR) podocyte expression quantified. Podocyte MCP-1 gene expression increased when exposed to active macrophage media (8.87x10-3+1.3x10-3) compared to inactive media (1.29x10-3+0.9x10-3; p<0.01), as did protein analysis. Podocyte NGAL expression was not directly related to macrophage exposure. The podocyte adopted a pro-inflammatory TNFR2 predominance when exposed to active macrophages. Conclusion Novel biomarkers perform well for monitoring and predicting JSLE associated renal disease. The podocyte up regulates MCP-1 and adopts a pro-inflammatory TNFR2 pathway; the podocyte may be responsible for urinary MCP-1. Further studies are required to determine NGAL signalling. Impact: Increased local, national and international awareness of lupus nephritis. Advancing biomarkers from planning/discovery to prospective validation. Understanding biomarker regulation using in vitro techniques may explain their renal specificity. Biomarker commercialization would truly improve the renal management of JSLE patients.
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40

Chiewchengchol, Direkrit. "Neutrophil function in juvenile systemic lupus erythematosus (JSLE)." Thesis, University of Liverpool, 2013. http://livrepository.liverpool.ac.uk/14115/.

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Objectives: This project aimed to investigate the abnormal neutrophil functions in terms of cell survival, phagocytosis, ROS production and chemotaxis in JSLE patients. Furthermore, factors that could affect normal neutrophil functions (such as patient sera, recombinant human cytokines and commonly-used medications) were investigated. Methods: Neutrophils and sera were isolated from whole blood of JSLE patients, healthy juvenile controls and healthy adult controls. Neutrophils from healthy adult controls were incubated with 10% serum from either JSLE patients or juvenile controls. Different recombinant cytokines or hydroxychloroquine were added in 10% human AB serum to neutrophils from healthy adult controls. Neutrophil apoptosis was measured using flow cytometry using annexin V-FITC and propidium iodide. The expression of proteins (Mcl-1, caspases 3,7,8 and 9) was measured by Western blotting. Phagocytosis and ROS production from neutrophils incubated with S. aureus opsonised with JSLE serum were quantified. Levels of cytokines in JSLE serum were measured using a Luminex assay and effects of GM-CSF and TNF-α on neutrophil apoptosis induced by JSLE serum were measured. JSLE neutrophil apoptosis was measured and Mcl-1 mRNA expression from JSLE neutrophils was quantified using real-time PCR. Phagocytosis, ROS production and neutrophil chemotaxis by JSLE neutrophils were investigated. Lastly, the effects of hydroxychloroquine on neutrophil functions were explored. Results: The results showed that neutrophils incubated with inactive and active JSLE sera had significantly increased apoptosis at 6 h compared to control sera. Cleaved (active) forms of caspases 3,7,8 were identified in neutrophils incubated with inactive and active JSLE sera (that showed high rates of apoptosis) compared to control sera. Decreased bacterial opsonisation leading to defective phagocytosis and ROS production was observed in neutrophils incubated with S. aureus opsonised with JSLE serum. Serum analysis showed IL-8 levels in active JSLE patients were significantly increased. GM-CSF was the most potent cytokine in delaying apoptosis and significantly saved neutrophil apoptosis induced by JSLE serum. Low concentrations of TNF-α significantly protected neutrophils against apoptosis by down-regulating several genes and proteins involved in death receptor signaling pathway (e.g. TNFR, FADD, TRADD, caspases 8 and 10). No significant differences were detected in apoptosis, phagocytosis, ROS production and chemotaxis of neutrophils isolated from JSLE patients compared to healthy juvenile controls, and healthy adult neutrophils treated with hydroxychloroquine compared to untreated cells. Conclusions: This study demonstrated that JSLE serum played an important role in regulating the functions of JSLE neutrophils. Factor(s) in JSLE serum induced neutrophil apoptosis and caused decreased bacterial opsonisation, leading to defective neutrophil phagocytosis and ROS production. Increased IL-8 levels could be used as an indicator of disease activity. GM-CSF was the most protective cytokine and overcame the pro-apoptotic effects of JSLE serum; thus, GM-CSF could potentially be used as an alternative treatment in JSLE patients. Effects of TNF-α are probably tissue-specific and the clinical application of TNF blockers in JSLE patients needs to be carefully considered. The functions of JSLE neutrophils were unimpaired and hydroxychloroquine showed no effects on neutrophil functions.
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41

Hunnankul, Saowalak. "Analysis of antibody data in systemic lupus erythematosus." Thesis, London School of Hygiene and Tropical Medicine (University of London), 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.536668.

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42

Lynch, Kimberly Vandermark. "Narratives of Men Living with Systemic Lupus Erythematosus." ScholarWorks, 2017. https://scholarworks.waldenu.edu/dissertations/3704.

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While systemic lupus erythematosus (SLE) has been traditionally viewed as a woman's disease, SLE impacts men as well. Although most research on SLE has concentrated on how it affected women, little is known about how it impacts men. The purpose of this phenomenological study was to examine how men who live with SLE perceive its psychological impact. Using the lens of the biopsychological theory, common themes were examined pertaining to how men with SLE perceive the impact that SLE has on their cognitive and emotional functioning. Data were collected via interviews with 9 men with SLE, and the data were analyzed using thematic analysis to determine common themes. The following common themes emerged: reflections on life before SLE, changes in interpersonal relationships, changes in intimate relationships, changes in self-concept, and changes in perspective about living with lupus. These themes suggest that, in order to improve the quality of life for patients living with SLE, it is not enough to address the physical symptoms; it is necessary to address the cognitive and emotional impacts of the disease process as well. Implications for positive social change of this research study include providing a greater level of understanding of the psychological impact of SLE on men as a resource for professional therapists and psychologists who are trying to find information that would be beneficial for their male SLE clients. Additional potential implications for positive social change include providing information for families and caregivers of those men with SLE, and how the disease impacts them from a psychological standpoint.
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43

Lövgren, Tanja. "Endogenous type I interferon inducers in systemic autoimmune diseases /." Uppsala : Acta Universitatis Upsaliensis, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-7181.

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44

Mu, Qinghui. "The role of gut microbiota in systemic lupus erythematosus." Diss., Virginia Tech, 2018. http://hdl.handle.net/10919/82856.

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Systemic lupus erythematosus (SLE) is a multi-system autoimmune disease with no known cure. Despite years of study, the etiology of SLE is still unclear. Both genetic and environmental factors have been implicated in the disease mechanisms. Gut microbiota as an environmental factor and the immune system interact to maintain tissue homeostasis, but whether this interaction is involved in the pathogenesis of SLE is unclear. In a classical model of lupus nephritis, MRL/lpr, we found decrease of Lactobacillales but increase of Lachnospiraceae in the gut microbiota. Increasing Lactobacillales in the gut by suppling a mixture of 5 Lactobacillus strains improved renal function of these mice and prolonged their survival. Further studies revealed that MRL/lpr mice possessed a "leaky" gut, which was reversed by increased Lactobacillus colonization. Inside the kidney, oral Lactobacillus treatment also skewed the Treg-Th17 balance towards a Treg phenotype. To remove Lachnospiraceae that was higher in lupus-prone mice than controls, we administered vancomycin orally to MRL/lpr mice after disease onset from 9 to 15 weeks of age. Vancomycin functions by removing Gram-positive bacteria such as Lachnospiraceae but sparing Lactobacillus spp. The treatment during active lupus reshaped the gut microbiota and significantly ameliorated systemic autoimmunity and kidney histopathology at 15 weeks of age. However, when vancomycin treatment was initiated from a very early age, the beneficial effect was not observed. Strikingly, mice given vancomycin only at the young age exhibited an even worse disease outcome. Indeed, regulatory B (Breg) cells were found to be reduced after the vancomycin treatment at young age. Importantly, adoptive transfer of Breg cells at 6-7 weeks of age rescued the beneficial effect, which indicates that Breg cells, inducible by vancomycin-sensitive gut microbiota, plays an important role in suppressing lupus disease initiation and progression. Finally, we demonstrated that bacterial DNA from the gut microbiota might be the inducer of Breg cells, as bacterial DNA administration at young age reproduced the beneficial effect seen in the Breg adoptive transfer experiment. Future studies are required to examine the clinical efficacy of targeting gut microbiota as a novel treatment against SLE.
Ph. D.
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45

Leung, Wai-nor. "Stress and coping of patients with systemic lupus erythematosus /." Hong Kong : University of Hong Kong, 1994. http://sunzi.lib.hku.hk/hkuto/record.jsp?B13991279.

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46

Johanneson, Bo. "Genetic Mapping of Susceptibility Genes for Systemic Lupus Erythematosus." Doctoral thesis, Uppsala University, Department of Genetics and Pathology, 2002. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-2950.

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Systemic lupus erythematosus (SLE) is a complex autoimmune disease with unknown etiology. The aim of this thesis was to identify susceptibility regions through genetic mapping, using model-based linkage analysis on nuclear and extended SLE multicase families.

In the first paper we performed a genome scan on 19 genetically homogenous Icelandic and Swedish families. One region at 2q37 was identified with a significant linkage with contribution from both populations (Z=4.24). Five other regions 2q11, 4p13, 9p22, 9p13 and 9q13 showed suggestive linkage (Z>2.0).

In the second paper, 87 families from 10 different countries were analysed only for chromosome 1. One region at 1q31 showed significant linkage (Z=3.79) with contribution from families from all populations, including Mexicans and Europeans. Four other regions 1p36, 1p21, 1q23, and 1q25, showed levels of suggestive linkage. Linkage for most regions was highly dependent on what population was used, which indicated strong genetic heterogeneity in the genetic susceptibility for SLE.

In the two last papers, we used the positional candidate gene strategy, in order to investigate candidate genes in two regions linked to SLE. For the Bcl-2 gene (at 18q21) we could not detect any association with SLE using three different markers. However, when we investigated the tightly linked low-affinity family of FcγR genes (at 1q23), we could find association for two risk alleles in the FcγRIIA and FcγRIIIA genes. The risk alleles were transmitted to SLE patients on one specific haplotype and therefore are not independent risk alleles.

The results show that model-based linkage analysis is a strong approach in the search for susceptibility genes behind complex diseases like SLE.

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47

Båve, Ullvi. "Mechanisms of Interferon-α Induction in Systemic Lupus Erythematosus." Doctoral thesis, Uppsala University, Department of Medical Sciences, 2003. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-3436.

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Patients with systemic lupus erythematosus (SLE) have an activated type I interferon (IFN) system with an ongoing IFN-α synthesis. This may be caused by circulating immune complexes, consisting of anti-DNA antibodies (Abs) and DNA, with IFN-α inducing capacity. Produced IFN-α may be crucial in the pathogenesis, because this cytokine can break tolerance and promote autoimmunity.

In the present thesis, possible mechanisms of the IFN-α production in SLE were studied. To investigate whether IFN-α inducing material could be derived from apoptotic cells, IgG from SLE patients (SLE-IgG) were combined with apoptotic cells. This combination induced high IFN-α production in normal peripheral blood mononuclear cells (PBMC). The IFN-α induction was associated to presence of anti-RNP Abs, but not to anti-dsDNA Abs, indicating that two inducers could be active in SLE, one containing DNA and the other RNA.

Apoptotic cells and SLE-IgG exclusively activated the natural interferon producing cells (NIPC) and the IFN-α response was enhanced by type I IFN and inhibited by IL-10 and TNF-α. The IFN-α induction was dependent on FcγRII, because blocking this receptor reduced IFN-α production and NIPC were found to express FcγRIIa.

To further elucidate the role of different autoantibodies in the IFN-α induction, sera from patients with Sjögren´s syndrome (SS), containing autoantibodies to RNA binding proteins (SSA, SSB, RNP and/or Sm) were investigated. The combination of SS or SLE sera and apoptotic or necrotic cell material induced high IFN-α production in PBMC. RNA, but not DNA, was required for IFN-α induction, indicating that RNA and Abs to RNA-binding proteins form potent IFN-α inducing complexes.

The findings in this thesis can explain central mechanisms for the activation of NIPC in SLE, and perhaps also other autoimmune diseases. This activation is mediated by interferogenic immune complexes, and modulating the NIPC activation may be a novel therapeutic approach in SLE.

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48

Shek, Ka-wai. "DNASE2, CR2, TYK2 genes polymorphisms in systemic lupus erythematosus /." View the Table of Contents & Abstract, 2007. http://sunzi.lib.hku.hk/hkuto/record/B38278765.

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49

葉偉基 and Wai-kee Eddie Ip. "Mannose-binding lectin and systemic lupus erythematosus: molecular studies." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1998. http://hub.hku.hk/bib/B31220952.

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50

Lee, Fung-shan, and 李鳳珊. "Body and self in women with systemic Lupus Erythematosus." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2000. http://hub.hku.hk/bib/B31250865.

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