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Organizations could deliver training programmes for their managers aimed at enhancing the use of fair procedures in allocating outcomes and developing their autonomy-supportive behaviours to improve nurses' work satisfaction, organizational identification and job performance.

The pathogenesis of thrombosis in heparin-induced thrombocytopenia (HIT) was studied by investigating whether antibodies to heparin-platelet factor 4 (H-PF4) induced tissue factor (TF) synthesis by monocytes. Plasma from 5 patients with HIT containing IgG to H-PF4 was incubated with peripheral blood mononuclear cells without or with purified PF4 and heparin. Significant TF-dependent procoagulant activity (PCA) expressed by monocytes, measured with a factor Xabased chromogenic assay, was induced after incubation of each HIT plasma sample. This monocyte PCA required the presence of PF4 and was inhibited by high concentrations of heparin. Furthermore, purified HIT IgG added to whole blood with PF4 and heparin also provoked significant synthesis of TF mRNA by monocytes, demonstrated by RT-PCR, and this effect was not observed with normal IgG. These findings strongly support the hypothesis that antibodies to PF4 developed in HIT trigger the production of tissue factor by monocytes, and this effect could account in vivo for hypercoagulability and thrombotic complications in affected patients. IntroductionHeparin-induced thrombocytopenia (HIT) is a common complication of unfractionated heparin (UFH) therapy, often associated with arterial or venous thrombosis. 1 Such thrombocytopenia results from platelet activation caused by antibodies specific for complexes composed of heparin and platelet factor 4 (FP4). [2][3][4][5] The platelet activation involves the binding of HIT IgG to specific Fc receptors (Fc␥RIIA), 6 partly explaining why HIT differs from most other types of drug-induced immune thrombocytopenia, which are mainly complicated by hemorrhage.The most frequent manifestation in HIT is thrombosis, sometimes associated with disseminated intravascular coagulation, and one of the mechanisms proposed to explain the hypercoagulability in HIT is the production of phospholipid platelet microparticles after platelet activation. 7 However, HIT antibodies might also bind to endothelial cells and trigger the synthesis of tissue factor (TF), 4,8,9 a transmembrane glycoprotein that initiates the coagulation pathway. 10,11 TF can be produced by monocytes when activated by lipopolysaccharides, cytokines, or immune complexes, 12 and it can be triggered in the presence of activated platelets. 13 We therefore investigated whether antibodies to PF4 developed in patients with HIT to induce the synthesis of TF by human monocytes. Study design Plasma and purification of immunoglobulin GPlasma from 5 patients with definite HIT complicated by venous (n ϭ 5) and arterial (n ϭ 1) thromboses was studied. Every sample contained significant levels of antibodies to H-PF4 complexes (mean A 492 , 1.7; range, 1.0-2.1) (Asserachrom HPIA, Stago; Asnières, France) 14 able to induce heparin-dependent platelet activation in serotonin release assay (SRA). 15 Normal human plasma without antibodies to H-PF4 complexes (mean A 492 Ͻ 0.2) was collected from 5 healthy volunteers not receiving heparin. All samples were heated at 56°C for 1 hour, centrifuged ...