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Search Results: 1 - 10 of 17278 matches for " Andrew Filer "
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The relationship between the presence of anti-cyclic citrullinated peptide antibodies and clinical phenotype in very early rheumatoid arthritis
Mohammed Z Cader, Andrew D Filer, Christopher D Buckley, Karim Raza
BMC Musculoskeletal Disorders , 2010, DOI: 10.1186/1471-2474-11-187
Abstract: Patients were recruited from the Birmingham early inflammatory arthritis clinic. Participants were included in the current study if they presented within 3 months of symptom onset and fulfilled 1987 ACR criteria for RA at some point during an 18 month follow-up. Data were collected on demographic variables, joint symptoms and tender (n = 68) and swollen (n = 66) joint counts. CRP, ESR, rheumatoid factor and anti-CCP2 status were measured.92 patients were included (48 anti-CCP positive). The anti-CCP positive and negative groups were comparable in terms of demographic variables, inflammatory markers, joint counts and 1987 ACR classification criteria, except that more anti-CCP positive patients were rheumatoid factor positive (83.3% vs. 11.4%, p < 0.01). There was no significant difference in the pattern of joint involvement, except for an increased prevalence of knee joint swelling in anti-CCP positive patients (42.9% vs. 22.2%, p = 0.03).Patients with and without anti-CCP antibodies present in a similar way, even within three months of clinically apparent disease that eventually develops into RA.Rheumatoid arthritis (RA) is a chronic, inflammatory condition typically manifesting clinically as a symmetrical polyarthritis. Rheumatoid synovitis is characterised by complex leukocyte and cytokine networks. The persistence of inflammation is mediated, in part, by the stromal micro-environment, but the underlying causes remain unclear [1,2]. Over the last decade there has been particular interest in antibodies to citrullinated peptides and proteins as important aetiological and predictive factors in early RA [3-5]. Citrullination of proteins is a post-translational modification, which can occur as a normal part of cell apoptosis [6]. However, this process may induce antibody formation in susceptible individuals [7], which may predate clinical arthritis by several years [8]. Subsequent environmental triggers may enable anti-citrullinated protein/peptide antibodies to enter
Linking Power Doppler Ultrasound to the Presence of Th17 Cells in the Rheumatoid Arthritis Joint
Nicola J. Gullick,Hayley G. Evans,Leigh D. Church,David M. Jayaraj,Andrew Filer,Bruce W. Kirkham,Leonie S. Taams
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0012516
Abstract: Power Doppler ultrasound (PDUS) is increasingly used to assess synovitis in Rheumatoid Arthritis (RA). Prior studies have shown correlations between PDUS scores and vessel counts, but relationships with T cell immunopathology have not been described.
Monocytes/macrophages express chemokine receptor CCR9 in rheumatoid arthritis and CCL25 stimulates their differentiation
Caroline Schmutz, Alison Cartwright, Helen Williams, Oliver Haworth, John HH Williams, Andrew Filer, Mike Salmon, Christopher D Buckley, Jim Middleton
Arthritis Research & Therapy , 2010, DOI: 10.1186/ar3120
Abstract: CCR9 expression on PB monocytes/macrophages was analysed by flow cytometry and in synovium by immunofluorescence. Chemokine receptor CCR9 mRNA expression was examined in RA and non-RA synovium, monocytes/macrophages from PB and synovial fluid (SF) of RA patients and PB of healthy donors using the reverse transcription polymerase chain reaction (RT-PCR). Monocyte differentiation and chemotaxis to chemokine ligand 25 (CCL25)/TECK were used to study CCR9 function.CCR9 was expressed by PB monocytes/macrophages in RA and healthy donors, and increased in RA. In RA and non-RA synovia, CCR9 co-localised with cluster of differentiation 14+ (CD14+) and cluster of differentiation 68+ (CD68+) macrophages, and was more abundant in RA synovium. CCR9 mRNA was detected in the synovia of all RA patients and in some non-RA controls, and monocytes/macrophages from PB and SF of RA and healthy controls. CCL25 was detected in RA and non-RA synovia where it co-localised with CD14+ and CD68+ cells. Tumour necrosis factor alpha (TNFα) increased CCR9 expression on human acute monocytic leukemia cell line THP-1 monocytic cells. CCL25 induced a stronger monocyte differentiation in RA compared to healthy donors. CCL25 induced significant chemotaxis of PB monocytes but not consistently among individuals.CCR9 expression by monocytes is increased in RA. CCL25 may be involved in the differentiation of monocytes to macrophages particularly in RA.Rheumatoid arthritis (RA) is a chronic inflammatory disease resulting in the accumulation of macrophages, T cells and B cells within the synovium. The accumulation of these cells is involved in the development of inflammation, joint destruction and pain [1]. Monocytes migrate from the blood across the walls of synovial blood vessels and differentiate into macrophages. The clinical importance of monocytes/macrophages is revealed by the correlation between their number, disease activity and radiographic progression [2-4] and by the beneficial effect of therapi
Hepatotoxicity associated with sulfasalazine in inflammatory arthritis: A case series from a local surveillance of serious adverse events
Paresh Jobanputra, Roshan Amarasena, Fiona Maggs, Dawn Homer, Simon Bowman, Elizabeth Rankin, Andrew Filer, Karim Raza, Ronald Jubb
BMC Musculoskeletal Disorders , 2008, DOI: 10.1186/1471-2474-9-48
Abstract: Serious ADR reports have been solicited from local clinicians by regular postcards over the past seven years. Patients', who had hepatotoxicity on sulfasalazine and met a definition of a serious ADR, were identified. Two clinicians reviewed structured case reports and assessed causality by consensus and by using a causality assessment instrument. The likely frequency of hepatotoxicity with sulfasalazine was estimated by making a series of conservative assumptions.Ten cases were identified: eight occurred during surveillance. Eight patients were hospitalised, two in hepatic failure – one died after a liver transplant. All but one event occurred within 6 weeks of treatment. Seven patients had a skin rash, three eosinophilia and one interstitial nephritis. Five patients were of Black British of African or Caribbean descent. Liver enzymes showed a hepatocellular pattern in four cases and a mixed pattern in six. Drug-related hepatotoxicity was judged probable or highly probable in 8 patients. The likely frequency of serious hepatotoxicity with sulfasalazine was estimated at 0.4% of treated patients.Serious hepatotoxicity associated with sulfasalazine appears to be under-appreciated and intensive monitoring and vigilance in the first 6 weeks of treatment is especially important.Spontaneous reporting systems for adverse drug reactions (ADRs), such as the yellow card system run by the Medicines and Healthcare products Regulatory Agency (MHRA) in the UK and the US Medwatch system, are handicapped by under-reporting and provide limited detail on individual cases. In an effort to learn more about ADRs associated with disease modifying anti-rheumatic drugs (DMARDs) we set up a local reporting system seven years ago[1] and reported preliminary findings in 2002 [2].Case reports of serious hepatotoxicity associated with sulfasalazine are common yet only 161 ADRs attributed to the liver and biliary system have been reported to the Medicines and Healthcare products Regulatory Agency
Roberto González Echevarría Amor y ley en Cervantes
Jorge Scherman Filer
Revista Chilena de Literatura , 2009,
Abstract:
Rheumatoid synovial fluid interleukin-17-producing CD4 T cells have abundant tumor necrosis factor-alpha co-expression, but little interleukin-22 and interleukin-23R expression
Leigh D Church, Andrew D Filer, Esther Hidalgo, Katherine A Howlett, Andrew MC Thomas, Stephen Rapecki, Dagmar Scheel-Toellner, Christopher D Buckley, Karim Raza
Arthritis Research & Therapy , 2010, DOI: 10.1186/ar3152
Abstract: Flow cytometry was used to analyse the phenotype and cytokine production of mononuclear cells isolated from peripheral blood (PBMC) (n = 44), synovial fluid (SFMC) (n = 14) and synovium (SVMC) (n = 10) of RA patients and PBMC of healthy controls (n = 13).The frequency of IL-17-producing CD4 T cells was elevated in RA SFMC compared with RA PBMC (P = 0.04). However, the frequency of this population in RA SVMC was comparable to that in paired RA PBMC. The percentage of IL-17-producing CD4 T cells coexpressing tumor necrosis factor alpha (TNFα) was significantly increased in SFMC (P = 0.0068). The frequency of IFNγ-producing CD4 T cells was also significantly higher in SFMC than paired PBMC (P = 0.042). The majority of IL-17-producing CD4 T cells coexpressed IFNγ. IL-17-producing CD4 T cells in RA PBMC and SFMC exhibited very little IL-22 or IL-23R coexpression.These findings demonstrate a modest enrichment of IL-17-producing CD4 T cells in RA SFMC compared to PBMC. Th17 cells in SFMC produce more TNFα than their PBMC counterparts, but are not a significant source of IL-22 and do not express IL-23R. However, the percentage of CD4 T cells which produce IL-17 in the rheumatoid joint is low, suggesting that other cells may be alternative sources of IL-17 within the joints of RA patients.Rheumatoid arthritis (RA) is a systemic chronic inflammatory disorder associated with persistent and destructive synovitis leading to cartilage and bone erosion. The underlying cause of RA is unknown; however, the pathogenesis of RA is thought to be the result of complex cell to cell interactions between amongst others, T cells, macrophages and fibroblasts. In established disease, the preponderance of IFNγ-expressing and paucity of IL-4-expressing T cells, in situ and ex vivo, had until recently led to the description of RA as an immune mediated inflammatory disease associated with a predominantly T helper type-1 (Th1)-like cytokine profile [1-3].More recently, effector T cells (Th17 cells)
Differential expression, function and response to inflammatory stimuli of 11β-hydroxysteroid dehydrogenase type 1 in human fibroblasts: a mechanism for tissue-specific regulation of inflammation
Rowan S Hardy, Andrew Filer, Mark S Cooper, Greg Parsonage, Karim Raza, Debbie L Hardie, Elizabeth H Rabbitt, Paul M Stewart, Christopher D Buckley, Martin Hewison
Arthritis Research & Therapy , 2006, DOI: 10.1186/ar1993
Abstract: The profound effects of glucocorticoids on the immune system have underpinned their widespread use as therapeutic agents for inflammatory diseases [1]. In addition to their therapeutic effects during pathological persistent inflammation, glucocorticoids are also known to play a key role in physiological responses directed at resolving inflammation at both systemic and tissue-specific levels [2,3]. These effects are mediated at a molecular level by the nuclear glucocorticoid receptor (GR) [4], but recent studies have indicated that GR signalling is rheostatically regulated through tissue-specific metabolism of GR ligands. Specifically, the interconversion of active and inactive glucocorticoids is catalyzed by the enzyme 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1), which is located on the luminal surface of the endoplasmic reticulum [5,6]. The bidirectional nature of 11β-HSD1 means that it has capacity for both reductase (that is, conversion of inactive cortisone to active cortisol) and dehydrogenase (that is, cortisol to cortisone) metabolism. However, in most physiological settings the enzyme exhibits predominant reductase activity as a consequence of the coincident expression of hexose-6-phosphate dehydrogenase (H6PDH), which facilitates enhanced, localized concentration of the cofactor for 11β-HSD1, namely NADPH (nicotinamide adenine dinucleotide phosphate, reduced form), within the endoplasmic reticulum lumen [7].Expression of 11β-HSD1 occurs primarily in GR-rich tissues, where the enzyme acts to increase local levels of active glucocorticoids, thereby providing a system for autocrine induction of GR-mediated responses [5,6]. Prominent among these tissues is the liver, where glucocorticoids act as key metabolic regulators [8]. However, the enzyme is also abundantly expressed by cells such as adipocytes [9,10], osteoblasts [11], myocytes [12,13] and vascular cells [14], suggesting an additional role for 11β-HSD1 as a determinant of glucocorticoid responses
Prolonged, granulocyte–macrophage colony-stimulating factor-dependent, neutrophil survival following rheumatoid synovial fibroblast activation by IL-17 and TNFalpha
Greg Parsonage, Andrew Filer, Magdalena Bik, Debbie Hardie, Sian Lax, Katherine Howlett, Leigh D Church, Karim Raza, See-Heng Wong, Emily Trebilcock, Dagmar Scheel-Toellner, Mike Salmon, Janet M Lord, Christopher D Buckley
Arthritis Research & Therapy , 2008, DOI: 10.1186/ar2406
Abstract: IL-17-expressing cells in the rheumatoid synovium, and IL-17-expressing cells in the peripheral blood, and synovial fluid were examined by confocal microscopy and flow cytometry, respectively. Peripheral blood neutrophils were cocultured either with rheumatoid arthritis synovial fibroblasts (RASF) or with conditioned medium from RASF that had been pre-exposed to recombinant human IL-17, TNFα or a combination of the two cytokines. Neutrophils were harvested and stained with the vital mitochondrial dye 3,3'-dihexyloxacarbocyanine iodide before being enumerated by flow cytometry.TH17-expressing CD4+ cells were found to accumulate within rheumatoid synovial tissue and in rheumatoid arthritis synovial fluid. RASF treated with IL-17 and TNFα (RASFIL-17/TNF) effectively doubled the functional lifespan of neutrophils in coculture. This was entirely due to soluble factors secreted from the fibroblasts. Specific depletion of granulocyte–macrophage colony-stimulating factor from RASFIL-17/TNF-conditioned medium demonstrated that this cytokine accounted for approximately one-half of the neutrophil survival activity. Inhibition of phosphatidylinositol-3-kinase and NF-κB pathways showed a requirement for both signalling pathways in RASFIL-17/TNF-mediated neutrophil rescue.The increased number of neutrophils with an extended lifespan found in the rheumatoid synovial microenvironment is partly accounted for by IL-17 and TNFα activation of synovial fibroblasts. TH17-expressing T cells within the rheumatoid synovium are likely to contribute significantly to this effect.In established rheumatoid arthritis (RA), highly differentiated CD4+ T lymphocytes persist within synovial tissue, and are prevented from undergoing apoptosis by high local concentrations of type I interferons [1]. Simplistically, the preponderance of IFNγ-expressing T cells and the paucity of IL-4-expressing T cells, in situ and ex vivo, has led to the description of RA as an immune-mediated inflammatory disease that
Los retos de la genealogía de la memoria en la narrativa finisecular judío-chilena
Cánovas Emhart,Rodrigo; Scherman Filer,Jorge;
Acta literaria , 2007, DOI: 10.4067/S0717-68482007000100002
Abstract: in this paper we analyze three novels of chilean-jewish writers, who dealt with the tradition of this millenary people: donde mejor canta un pájaro (alejandro jodorowsky); por el ojo de la cerradura (jorge scherman filer); and las jaulas invisibles (ana vásquez-bronfman). these novels have been composed from the figure of the genealogical tree, based on parodical, allegorical and grotesque discourses, and the humorous irony so familiar among hebrews.
Voces femeninas en Chile: miradas sobre el ser mosaico
Cánovas Emhart,Rodrigo; Scherman Filer,Jorge;
Estudios filológicos , 2008, DOI: 10.4067/S0071-17132008000100002
Abstract: in this paper we analyze the books of four female chilean-jewish writers, in which very different views on what it means to be hebrew are observed: para siempre en mi memoria (sonia guralnik); sagrada memoria: reminiscencias de una ni?a judía en chile y always from somewhere else: a memoir of my jewish chilean father (marjorie agosín); poste restante (cynthia rimsky); and escenario de guerra (andrea jeftanovic). these texts have been written from the following spaces: the ghetto, the genealogical tree and the wandering jew, the circular journey between hebrew and chilean origins and the family and world tragedies associated with the war conflicts of the twentieth century.
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