41 research outputs found

    Chern-Simons Solitons, Toda Theories and the Chiral Model

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    The two-dimensional self-dual Chern--Simons equations are equivalent to the conditions for static, zero-energy solutions of the (2+1)(2+1)-dimensional gauged nonlinear Schr\"odinger equation with Chern--Simons matter-gauge dynamics. In this paper we classify all finite charge SU(N)SU(N) solutions by first transforming the self-dual Chern--Simons equations into the two-dimensional chiral model (or harmonic map) equations, and then using the Uhlenbeck--Wood classification of harmonic maps into the unitary groups. This construction also leads to a new relationship between the SU(N)SU(N) Toda and SU(N)SU(N) chiral model solutions

    Chern-Simons Solitons, Chiral Model, and (affine) Toda Model on Noncommutative Space

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    We consider the Dunne-Jackiw-Pi-Trugenberger model of a U(N) Chern-Simons gauge theory coupled to a nonrelativistic complex adjoint matter on noncommutative space. Soliton configurations of this model are related the solutions of the chiral model on noncommutative plane. A generalized Uhlenbeck's uniton method for the chiral model on noncommutative space provides explicit Chern-Simons solitons. Fundamental solitons in the U(1) gauge theory are shaped as rings of charge `n' and spin `n' where the Chern-Simons level `n' should be an integer upon quantization. Toda and Liouville models are generalized to noncommutative plane and the solutions are provided by the uniton method. We also define affine Toda and sine-Gordon models on noncommutative plane. Finally the first order moduli space dynamics of Chern-Simons solitons is shown to be trivial.Comment: latex, JHEP style, 23 pages, no figur

    Actualites vasculaires de la Pitie-Salpetriere Paris, 27 novembre 1997

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    Available from INIST (FR), Document Supply Service, under shelf-number : Y 31809 / INIST-CNRS - Institut de l'Information Scientifique et TechniqueSIGLEHopital de la Salpetriere, 75 - Paris (France)FRFranc

    Systemic Lupus Erythematosus

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    ‘We thought if it’s going to take two years then we need to start that now’: Age, infertility risk and the timing of pregnancy in older first-time mothers

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    Over the past few decades, the number of women having their first babies over the age of thirty-five in most developed societies has steadily increased. Concerns have been raised over this trend amidst warnings of both the increased risk of fertility problems and health risks to mother and child. Despite this, research into the timing of pregnancy in the context of decreasing fertility has been somewhat neglected, with research typically framed in biomedical rather than social terms. However, this area merits closer attention given the contradictory nature of societal messages that simultaneously encourage women to pursue careers and enhance lifestyle, whilst warning of ‘risks’ of infertility and problems in ‘delaying’ motherhood. This article is based on a small-scale qualitative study that uses data drawn from eleven in-depth interviews with ‘older mothers’ about their transition to motherhood. The data was thematically analysed. We found that the women drew upon risk discourses around decreasing fertility and advancing maternal age, and that these discourses impacted on their decisions about the timing of their pregnancies. Some mothers felt that they started trying to conceive at ‘non-ideal’ times, owing to expectations they held about decreasing fertility. We suggest that the impact of contradictory societal messages around the timing of motherhood need to be more clearly considered for their potential effects on the timing of pregnancy and note how this topic brings the personal, and, by implication, the societal, into conflict with the (narrated) biological

    Transfusion-associated TT virus co-infection in patients with hepatitis C virus is associated with type II mixed cryoglobulinemia but not with B-cell non-Hodgkin lymphoma

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    International audienceOBJECTIVE:To assess the prevalence of TT virus (TMV) infection in a series of patients with chronic hepatitis C virus (HCV) infection, with or without benign (mixed cryoglobulinemia) or malignant (B-cell non-Hodgkin lymphoma (B-NHL)) lymphoproliferative disease.METHODS:Sixty-six HCV patients were studied, including patients with mixed cryoglobulinemia (n=30), B-NHL (n=15), and no mixed cryoglobulinemia or B-NHL (n=21). All HCV patients had increased transaminase levels and were HCV RNA positive. Patients were considered to have mixed cryoglobulinemia if two successive determinations of their serum cryoglobulin level were above 0.05 g/L. Mixed cryoglobulinemia-negative patients never had mixed cryoglobulins in their serum on multiple determinations. Subjects without HCV infection included 79 patients with histologically proven B-NHL, and 50 healthy blood donors. Serum samples were analyzed for TTV DNA by nested polymerase chain reaction, with two couples of primers in different regions of the genome, in two independent laboratories.RESULTS:In the group of HCV-positive patients, TTV DNA was found in one of 15 (6.7%) patients with B-NHL, and in nine of 51 (17.6%, P = 0.43) of those without B-NHL. Among HCV-positive patients without B-NHL, TTV DNA was more frequently found in those with type II mixed cryoglobulinemia vasculitis than in those without it (six of 16 (37.5%) versus two of 21 (9.5%), P = 0.05). In subjects without HCV infection, TTV DNA was present in 10 of 79 (12.7%) patients with B-NHL and in seven of 50 (14.0%, P = 0.82) blood donors.CONCLUSION:In patients chronically infected with HCV, TTV co-infection: (1) is not associated with the presence of B-NHL; and (2) is more frequently found in patients presenting a type II mixed cryoglobulinemia vasculitis

    Rituximab associated vasculitis flare: incidence, predictors and outcome

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    International audienceTo report the incidence, predictor, and outcome of rituximab-associated autoimmune disease flare.METHODS: We conducted a retrospective study in a tertiary referral centre from 2005 to 2015. Disease flare was defined as the onset of a new organ involvement or worsening of autoimmune disease, within 4 weeks following rituximab.RESULTS: Among the 185 patients, we identified 7 (3.4%) disease flares. All were due to type II mixed cryoglobulinemia vasculitis. Vasculitis flare occurred after a median time of 8 [2; 16] days following rituximab infusion and included acute kidney insufficiency (n=7), purpura (n=7), gastrointestinal tract involvement (n=4), and myocarditis (n=1). Patients with rituximab-associated cryoglobulinemia vasculitis flare had more frequently renal involvement (p=0.008), B cell-lymphoproliferation (p=0.015), higher level of cryoglobulin (2.1 vs 0.4 g/l, p=0.004) and lower level of C4 level (0.02 vs 0.05, p=0.023) as compared to patients without flare after rituximab (n=43). Four patients (57%) died after a median time of 3.3 months. The 1-year survival rate was poorer in patients with vasculitis flare after rituximab as compared to their negative counterpart [43% (95% CI: 18-100) vs 97% (95% CI: 92-100), p<0.001]. Immunofluorescence analysis of kidney biopsy in patients with rituximab associated vasculitis worsening highlighted the presence of rituximab, IgM, and IgG1 positive staining of endomembranous deposits and thrombi within kidney lesions.CONCLUSION: Rituximab-associated involves cryoglobulinemia vasculitis and is associated with high mortality rate. We provided evidence that kidney lesions are due to immune complex deposition and to glomerular obstruction by cryoglobulinemia and rituximab
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