We analyzed soluble vascular adhesion molecules (sVCAM-l), reactive oxygen metabolites (ROMs) level, total antioxidant status (TAS) and telediastolic left ventricular volume (TLVV) in patients with myocardial infarction undergoing reperfusion therapy and treated with antioxidant vitamins (AT) or placebo (P) before and for 1 month after reperfusion. After reperfusion, sVCAM-l serum concentration, reactive oxygen metabolites level, and TLVV were significantly higher in patients treated with placebo than in those treated with antioxidant vitamins, while TAS was significantly higher in patients treated with antioxidant supplementation. We observed that 48 hours after reperfusion sVCAM-l (P) vs sVCAM -l(AT) was 2.03±O.5 vs 1.63±O.7 ug/ml with p

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Neurological paraneoplastic syndromes are a rare group of disorders that occur in 1-2% of people with malignancy. They are usually caused by an immune response, triggered by and directed against a tumour, that cross-reacts with protein expressed by the peripheral or central nervous system. Any part of the nervous system can be affected and patients often develop severe and permanent disability. Diagnosis can be difficult as in two-thirds of patients the neurological problems appear up to 5 years before the tumour manifests. However, certain of these syndromes are often associated with specific serum autoantibodies that can be useful both in diagnosis of the neurological syndrome and in focusing the search for a particular tumour. Thus, these antibodies can allow earlier identification and treatment of cancer and, potentially, a reduction in morbidity and mortality. It was only in the 1980s that the first anti-neuronal autoantibodies were characterized and their associations with clinical syndromes and tumours defined. Further antibodies have been isolated over the past 20 years and novel pathogenic mechanisms for several syndromes have been recognized. For example, voltage-gate ion channels seem to be a common target for autoantibodies involved in peripheral nerve diseases such as the Lambert-Eaton myasthenic syndrome and neuromyotonia (Isaacs' syndrome). However, the place of most paraneoplastic antibodies in the pathogenesis of central syndromes is yet to be fully elucidated.

Antithrombin-III exerts antiinflammatory effects via ligation of heparan sulfate proteoglycans. Here we show in vitro that recombinant human antithrombin-III attenuates CDllb/CD18 expression ofaetivated neutrophils and monocytes in whole blood ex vivo. As leukocyte integrin expression is triggered by extracorporeal circulation, this observation may be of relevance for pharmacological treatment during cardiopulmonary bypass.Cardiac surgery involving cardiopulmonary bypass leads to fulminant activation of the hemostatic-inflammatory system (1). Transgenic recombinant human antithrombin III (rhAT-III) is in phase III clinical trials in the US and Europe as an anticoagulant and antiinflammatory agent in patients undergoing elective cardiac surgery with cardiopulmonary bypass (2).AT-III supplementation to maintain normal physiologic concentrations during cardiopulmonary bypass does not alter significantly thrombin generation, fibrinolytic activity, or blood loss in adults undergoing cardiac surgery (3). However, treatment with AT-III concentrate of heparin resistance, which is frequently associated with cardiopulmonary bypass due to aquired AT-III deficiency, is more effective and faster for obtaining adequate anticoagulation than using additional heparin (4, 5). Effects of AT-III supplementation on the inflammatory response during cardiac surgery are less well investigated.Cardiopulmonary bypass is associated with extensive granulocyte and monocyte activation including the release of pro-and antiinflammatory cytokines and up-regulation ofadhesion molecules including CD 11blCD 18 which is responsible for firm leukocyte adhesion to platelets and fibrinogen (6-7). Blood contact with artificial surfaces decreases the ability of platelets, leukocytes and their aggregates to pass through organ capillaries, and neutrophil sequestration has been implicated in the inflammatory response associated with cardiopulmonary bypass (8). In the presence of plasma and platelets, aggregation of normal white blood cells after stimulation with lectin is inhibited by AT-III (9). Here we show that rhAT-III reduces CD 11blCD 18 expression of neutrophils and monocytes. MATERIALS AND METHODSVenous blood from healthy adult donors was collected intosterile bloodcollection tubesanticoagulated with EDTA. Blood samples were incubated with 1 UI mL of rhAT-III (Genzyme Transgenics, Boston, MA) or vehicle at 37°C for 20 min. After the end of the incubation period, blood cells were washed and resuspendedin phosphate-bufferedsaline. All samples wereimmediately processed forstimulationandstaining procedures.