23 research outputs found

    1989 as a mimetic revolution: Russia and the challenge of post-communism

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    Various terms have been used to describe the momentous events of 1989, including Jürgen Habermas’s ‘rectifying revolution,’ and my own notion of 1989 as a type of ‘anti-revolution’: repudiating not only what had come before, but also denying the political logic of communist power, as well as the emancipatory potential of revolutionary socialism in its entirety. In the event, while the negative agenda of 1989 has been fulfilled, it failed in the end to transcend the political logic of the systems that collapsed at that time. This paper explores the unfulfilled potential of 1989. Finally, 1989 became more of a counter- rather than an anti-revolution, replicating in an inverted form the practices of the mature state socialist regimes. The paucity of institutional and intellectual innovation arising from 1989 is striking. The dominant motif was ‘returnism,’ the attempt to join an established enterprise rather than transforming it. Thus, 1989 can be seen as mimetic revolution, in the sense that it emulated systems that were not organically developed in the societies in which they were implanted. For Eastern Europe ‘returning’ to Europe appeared natural, but for Russia the civilizational challenge of post-communism was of an entirely different order. There could be no return, and instead of a linear transition outlined by the classic transitological literature, Russia’s post-communism demonstrated that the history of others could not be mechanically transplanted from one society to another

    Antibodies to prothrombin

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    Binding of anticardiolipin antibodies to protein C via β2-glycoprotein I (β2-GPI): a possible mechanism in the inhibitory effect of antiphospholipid antibodies on the protein C system

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    It is known that antiphospholipid antibodies (aPL) hamper the anticoagulant activity of the protein C system, but the mechanism is still obscure. In this study, we demonstrate that anticardiolipin antibodies (not anti-protein C autoantibodies) can bind protein C via β2-GPI, which bears their binding epitope, in a fashion dependent on negatively charged phospholipids. We studied the binding of IgG from aPL to protein C in the presence of β2-GPI by ELISA (anti-‘protein C’ antibody ELISA), and compared their binding with those obtained in the absence of β2-GPI. In the anti-‘protein C’ antibody ELISA system, 47% of 78 aPL+ patients had a positive titre in the presence of cardiolipin (CL) and β2-GPI, but binding was not found in the absence of β2-GPI. Highly significant correlations were found between the titre of anti-‘protein C’ antibody in the presence of β2-GPI and that of anti-β2-GPI antibody (r = 0.802, P = 0.0001). We further analysed the interaction between protein C, phospholipids, β2-GPI and human aCL MoAbs established from patients with antiphospholipid syndrome. In a first set of experiments, the binding of β2-GPI to protein C and its phospholipid dependency were investigated. β2-GPI bound to protein C in the presence of CL or phosphatidylserine, but not in the presence of phosphatidylcholine or phosphatidylethanolamine. In a second group of experiments, the binding of three human monoclonal aCL recognizing the cryptic epitope of β2-GPI (virtually anti-β2-GPI antibodies) was evaluated in the presence of cardiolipin and β2-GPI. All three human monoclonal aCL bound to protein C in the presence of CL and β2-GPI, whereas they did not in the absence of either β2-GPI or CL. These data suggest that protein C could be a target of aCL by making a complex with CL and β2-GPI, leading to protein C dysfunction
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