303 research outputs found

    ‘Born to Shop’: Malls, Dream-Worlds and Capitalism

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    It has been twenty years since the fall of the Berlin Wall, and a new generation, untouched by the previous communist regimes, has come to adulthood throughout the post-communist world. The Iulius Group’s logo – ‘Born to shop!’ – suggests that these are born shoppers: the capitalist babies of Central and Eastern Europe who are sustaining the largest growth in retail and shopping malls in Europe. With no living memory of shortages, queuing, or government restrictions, they know only the limit of their own – or their parents’ – pocket/credit. Their world could not be more different from the one that their parents and grandparents experienced: both the abundance of goods and services, as well as the opulent settings under which they are now sold, offer striking visual contrasts to the not-so-distant past. In addition, the very experience of consumption is directly connected to the way in which the current social fabric – and new social divisions within it – is interwoven with the physical and architectural changes taking place in the urban setting

    Global ethnic and geographic differences in the clinical presentations of anti-neutrophil cytoplasm antibody–associated vasculitis

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    © The Author 2017. Objectives. There are few data on clinical profiles of ANCA-associated vasculitis (AAV) in different ethnic populations. The aim of this study was to examine the differences in the ANCA type and clinical features of AAV between populations using the Diagnostic and Classification Criteria in Vasculitis Study (DCVAS) dataset. Methods. The DCVAS is an international, multicentre, observational study recruiting in 133 sites. Eight ethnic categories were analysed: Northern European, Caucasian American, Southern European, Middle Eastern/Turkish, Chinese, Japanese, Indian subcontinent and other. ANCA type was categorized as myeloperoxidase (MPO), PR3 and ANCA negative. Organ system involvement was recorded using a standard dataset. Differences were analysed by chi-squared tests using a Bonferroni correction and logistic regression (adjusting for age and sex). Northern European was the reference population. Results. Data from 1217 patients with AAV were available and the 967 (79.5%) patients recruited by rheumatology departments were analysed to reduce confounding by recruitment specialty. There were differences in ANCA type between ethnic categories (P < 0.001): MPO-ANCA was more common than PR3-ANCA in Japanese, Chinese and Southern Europeans; PR3-ANCA was more common in the other groups. Compared with Northern Europeans, Japanese had a nearly 60-fold increased chance of having MPO-ANCA (vs PR3-ANCA) [odds ratio (OR) 59.2 (95% CI 8.0, 440.7), P < 0.001] and Chinese had a nearly 7-times increased chance [OR 6.8 (95% CI 2.6, 17.8), P < 0.001]. Ophthalmologic and otorhinolaryngologic involvement were less common in Japanese and Chinese populations than Northern Europeans; otherwise, there were few differences in organ involvement between ethnic groups. Conclusion. This study confirms the previously observed differential occurrence of MPO-AAV and PR3- AAV between different ethnic groups

    Enhanced Formation and Disordered Regulation of NETs in Myeloperoxidase-ANCA-Associated Microscopic Polyangiitis.

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    Microscopic polyangiitis (MPA) is an ANCA-associated vasculitis that affects small vessels, especially renal glomeruli. We recently demonstrated that the abnormal formation and impaired degradation of neutrophil extracellular traps (NETs) may be crucially involved in the generation of myeloperoxidase (MPO)-ANCA and subsequent development of MPA. This study assessed the formation and regulation of NETs in patients with MPO-ANCA-associated MPA. Peripheral blood samples were obtained from 38 patients with MPO-ANCA-associated MPA, 23 patients with systemic lupus erythematosus (SLE), and 8 healthy controls. IgG eluted from MPO-ANCA-associated MPA sera demonstrated the highest ability to induce NETs, and this ability correlated with disease activity and paralleled ANCA affinity for MPO. Moreover, addition of recombinant human MPO to these IgG samples reduced NET induction. Additionally, MPO-ANCA-associated MPA sera exhibited lower rates of NET degradation that recovered partially upon depletion of IgG. The activity of DNase I, an important regulator of NETs, was also lower in MPO-ANCA-associated MPA and SLE sera. IgG depletion from MPO-ANCA-associated MPA sera partially restored the rate of NET degradation, and addition of DNase I synergistically enhanced this restoration. Addition of anti-MPO antibodies did not inhibit DNase I activity, and some MPO-ANCA-associated MPA sera contained anti-NET antibodies at levels not correlated with MPO-ANCA titers, suggesting the involvement of unidentified autoantibodies as well. The collective evidence suggests a vicious cycle involving MPO-ANCA and the regulation of NETs could be critically involved in the pathogenesis of MPO-ANCA-associated MPA

    Pathogenesis and therapeutic interventions for ANCA-associated vasculitis.

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    Anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) affects systemic small vessels and is accompanied by the presence of ANCAs in the serum. This disease entity includes microscopic polyangiitis, granulomatosis with polyangiitis, eosinophilic granulomatosis with polyangiitis and drug-induced AAV. Similar to other autoimmune diseases, AAV develops in patients with a predisposing genetic background who have been exposed to causative environmental factors. The mechanism by which ANCAs cause vasculitis involves ANCA-mediated excessive activation of neutrophils that subsequently release inflammatory cytokines, reactive oxygen species and lytic enzymes. In addition, this excessive activation of neutrophils by ANCAs induces formation of neutrophil extracellular traps (NETs). Although NETs are essential elements in innate immunity, excessive NET formation is harmful to small vessels. Moreover, NETs are involved not only in ANCA-mediated vascular injury but also in the production of ANCAs themselves. Therefore, a vicious cycle of NET formation and ANCA production is considered to be involved in the pathogenesis of AAV. In addition to this role of NETs in AAV, some other important discoveries have been made in the past few years. Incorporating these new insights into our understanding of the pathogenesis of AAV is needed to fully understand and ultimately overcome this disease

    ANCA-negative pauci-immune crescentic glomerulonephritis

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    Crescentic glomerulonephritis is a severe form of glomerular injury that is characterized by disruption of the glomerular basement membrane, cellular proliferation within Bowman space, and (often) fibrinoid necrosis. Pauci-immune crescentic glomerulonephritis, so called because it involves little or no glomerular immunoglobulin deposition, is one of the most common causes of rapidly progressive glomerulonephritis. in the majority of patients, pauci-immune crescentic glomerulonephritis is a manifestation of antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis. However, some patients with pauci-immune crescentic glomerulonephritis lack ANCAs. This review compares the prevalence, clinical manifestations, histopathology, and outcomes of ANCA-negative pauci-immune crescentic glomerulonephritis with those of ANCA-positive disease. we also discuss the possible pathogenesis of ANCA-negative pauci-immune crescentic glomerulonephritis, paying particular attention to the mechanisms and role of neutrophil activation

    “SEGMENTATION OF ANTI NEUTROPHIL CYTOPLASMIC ANTIBODIES (ANCA) IMAGES BASED ON WATERSHED AND WAVELET”

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    Autoimmune disease is a type of disease where immune system unable to tell between the good side and bad side which lead to the misguided attack on the healthy cells and tissues. Autoimmune disease can be classified to more than 80 types depending on the affected area. The test also varies according to the suspected type of disease. Some examples of the test are Enzyme-Linked Immunosorbent Assay (ELISA) test, Indirect Immunofluorescence (IIF) test of Antinuclear Antibody (ANA) by using HeP-2 Cells and IIF test for Anti Neutrophil Cytoplasmic Antibodies (ANCA). However in this project, author only focus on the ANCA images with two major staining patterns which are P-ANCA and C-ANCA. Currently the positivity of the images depends solely on the experience of the physician which led to variety of result and lack of reliability. Besides the time to get the result is time consuming. Thus an automatic classification system has been developed to overcome the manual process. The vital process inside the automatic system is the segmentation part. Many researchers suggest different techniques of segmentation to segment the ANCA images before being further processed. In this research, author focus on Watershed technique to segment the ANCA images by implementing the algorithm in Matlab. Author use Wavelet transform to suppress noise to avoid from over segmentation of the ANCA images. Using Rand Index method, the result of segmentations is verified. Combination of Watershed and Wavelet transform gives a very promising result. Recommendation for future work is to explore on automatic determination of noise variance inside images

    Fatal cardiac small-vessel involvement in ANCA-associated vasculitis: an autopsy case report

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    An 80-year-old Japanese man, who had fever and generalized fatigue not improved by antibiotics, was admitted to our hospital. Laboratory data indicative of renal dysfunction and antineutrophil cytoplasmic antibody (ANCA) in the serum led to the consideration of ANCA-associated vasculitis as a differential diagnosis. However, before the diagnostic confirmation, he was found dead on the bed. Autopsy revealed necrotizing crescentic glomerulonephritis in the kidneys. In addition, necrotizing granulomatous vasculitis with infiltration of multinucleated giant cells and neutrophils but not eosinophils was present in multiple organs. The direct cause of death was presumed as cardiac arrest by lethal arrhythmia because vasculitic lesions were distributed widely in the cardiac walls, acute congestion was observed in the systemic organs, and other causes of death were ruled out. This report presents the unusual manifestation of cardiac small-vessel involvement in ANCA-associated vasculitis related to sudden death

    New advances in the pathogenesis of ANCA-associated vasculitides

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    Anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitides (AAV) are a group of autoimmune disorders including Wegener granulomatosis (WG), microscopic polyangiitis (MPA), Churg-Strauss syndrome (CSS) and renal-limited vasculitis (RLV). This paper reviews updated information on the pathogenesis of AAV Additional clinical evidence for a pathogenic role of ANCA comes from the observation that patients with severe acute renal failure treated with plasma exchange had a lower risk for progression to end-stage renal disease than patients who received intravenous methylprednisolone therapy, both in addition to standard treatment. Recent data also suggest that antibodies to complementary proteinase-3 (cPR3), probably cross-reacting with plasminogen, may induce PR3-ANCA. Furthermore, a new ANCA, directed against human lysosome membrane protein-2 (LAMP-2), concurrent with PR3-ANCA or MPO-ANCA, was described as a sensitive and specific marker for renal AAV In vitro, ANCA can further activate printed neutrophils to release reactive oxygen species and lytic enzymes, and, in conjunction with neutrophils, damage and lyse endothelial cells. In vivo, tran, fer of splenocytes from myeloperoxidase-deficient mice immunized with mouse myeloperoxidase into wild-type mice resulted in pauci-immune systemic vasculitis. A similar experiment in PR3-deficient mice did not cause significant vasculitic lesions. In the anti-MPO induced vasculitis mouse model, a critical role of complement activation was suggested. The anti- LAMP-2 antibody can also induce pauci-immune necrotizing crescentic glomerulonephritis in rats. Rats developed both cross-reactive antibodies to LAMP-2 and crescentic glomerulonephritis when immunized with FimH, an adhesin from Gram-negative bacteria which has strong homology with human LAMP-2. Together, clinical, in vitro and in vivo data support a pathogenic role for ANCA in AAV, although this role is more evident for myeloperoxidase-ANCA than for PR3-ANCA. The role of anti- LAMP-2 requires further studies

    Pharmaceutical immunoglobulins reduce neutrophil extracellular trap formation and ameliorate the development of MPO-ANCA-associated vasculitis

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    Objectives: Intravenous immunoglobulin (IVIG) therapy is effective against some autoimmune diseases. Although its efficacy on peripheral neuropathy due to eosinophilic granulomatosis with polyangiitis-one of myeloperoxidase-antineutrophil cytoplasmic antibody (MPO-ANCA)-associated vasculitis (MPO-AAV)-has been established, that on other MPO-AAV remains undetermined. We examined the effects of pharmaceutical immunoglobulins on the formation of neutrophil extracellular traps (NETs) related to MPO-ANCA production and the development of MPO-AAV. Methods: Peripheral blood neutrophils from healthy volunteers were pretreated with 5 mg/ml human sulfo-immunoglobulins (IVIG-S) and then exposed to 100 nM phorbol myristate acetate (PMA). Thereafter, neutrophils were stained with SYTOX Green and then subjected to flow cytometry. Next, Wistar-Kyoto rats were given oral administration of 10 mg/kg/day propylthiouracil for 28 days and intraperitoneal (i.p.) injection of 1 µg PMA on days 0 and 7. These rats were divided into two groups: Group 1 with i.p. injection of 400 mg/kg IVIG-S on days 8-12 and Group 2 with i.p. injection of vehicle similarly. ANCA titers were chronologically determined by indirect immunofluorescence. On day 28, all rats were killed to examine NET formation in the peritoneum and the development of AAV. Results: IVIG-S significantly inhibited NET formation induced by PMA in vitro. NET amounts in the peritoneum in Group 1 were significantly smaller than in Group 2, and ANCA titers in Group 1 were significantly lower than in Group 2. The degree of pulmonary hemorrhage in Group 1 was also smaller than in Group 2. Conclusion: Pharmaceutical immunoglobulins reduce NET formation and ameliorate the development of MPO-AAV
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