about
Treatment of MRL/lpr mice, a genetic autoimmune model, with the Ras inhibitor, farnesylthiosalicylate (FTS)Hyperactivity in a mouse model of the antiphospholipid syndrome.Inhibition of ras by farnesylthiosalicylate significantly reduces the levels of autoantibodies in two animal models of the antiphospholipid syndrome.Immunoglobulin-mediated neuro-cognitive impairment: new data and a comprehensive review.16/6-idiotype expressing antibodies induce brain inflammation and cognitive impairment in mice: the mosaic of central nervous system involvement in lupus.Coagulopathy triggered autoimmunity: experimental antiphospholipid syndrome in factor V Leiden mice.CNS dysfunction in the antiphospholipid syndrome.Significant changes in the levels of secreted cytokines in brains of experimental antiphospholipid syndrome miceThe strategies used for treatment of experimental autoimmune neuritis (EAN): a beneficial effect of glatiramer acetate administered intraperitoneally.The role of apolipoprotein E polymorphisms in levodopa-induced dyskinesia.Quantitative detection of thrombin activity in an ischemic stroke model.The pathogenesis of neural injury in animal models of the antiphospholipid syndrome.Immunization with hepatitis B vaccine accelerates SLE-like disease in a murine model.Altered receptor binding densities in experimental antiphospholipid syndrome despite only moderately enhanced autoantibody levels and absence of behavioral features.Anti-P ribosomal antibodies induce defect in smell capability in a model of CNS -SLE (depression).Inhibition of Ras attenuates the course of experimental autoimmune neuritis.Interaction of inflammation, thrombosis, aspirin and enoxaparin in CNS experimental antiphospholipid syndrome.Minimal Traumatic Brain Injury in Mice: Protease-Activated Receptor 1 and Thrombin-Related Changes.IgG accumulates in inhibitory hippocampal neurons of experimental antiphospholipid syndrome.Antibody-specific behavioral effects: intracerebroventricular injection of antiphospholipid antibodies induces hyperactive behavior while anti-ribosomal-P antibodies induces depression and smell deficits in mice.Calpastatin levels affect calpain activation and calpain proteolytic activity in APP transgenic mouse model of Alzheimer's disease.Passive transfer of narcolepsy: anti-TRIB2 autoantibody positive patient IgG causes hypothalamic orexin neuron loss and sleep attacks in mice.Hyperactivity induced by antiphospholipid syndrome serum.Induction of autoimmune depression in mice by anti-ribosomal P antibodies via the limbic system.Neurological impairment in experimental antiphospholipid syndrome is associated with increased ligand binding to hippocampal and cortical serotonergic 5-HT1A receptors.Genetic and immunological factors interact in a mouse model of CNS antiphospholipid syndrome.Mice with experimental antiphospholipid syndrome display hippocampal dysfunction and a reduction of dendritic complexity in hippocampal CA1 neurones.Antiphospholipid syndrome induction exacerbates a transgenic Alzheimer disease model on a female background.Treatment for experimental autoimmune neuritis with clodronate (Bonefos).Behavioral and cognitive deficits occur only after prolonged exposure of mice to antiphospholipid antibodies.In vitro effects of antiphospholipid syndrome-IgG fractions and human monoclonal antiphospholipid IgG antibody on human umbilical vein endothelial cells and monocytes.
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Aviva Katzav
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Aviva Katzav
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Aviva Katzav
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Aviva Katzav
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Aviva Katzav
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Aviva Katzav
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Aviva Katzav
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Aviva Katzav
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Aviva Katzav
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Aviva Katzav
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Aviva Katzav
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Aviva Katzav
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Aviva Katzav
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Aviva Katzav
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Aviva Katzav
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Aviva Katzav
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Aviva Katzav
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Aviva Katzav
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Aviva Katzav
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Aviva Katzav
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Aviva Katzav
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Aviva Katzav
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P106
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P569
1972-01-01T00:00:00Z
P7859
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