The anti-phospholipid syndrome (APS) is characterized by thrombosis and the presence of anti-phospholipid antibodies (aPL). Tissue factor (TF), the major initiator of the coagulation system, is induced on monocytes by aPL in vitro, explaining, in part, the pathophysiology in this syndrome. However, little is known regarding the nature of the aPL-induced signal transduction pathways leading to TF expression. In this study, we investigated aPL-inducible genes in PBMC using cDNA array system and real-time PCR. Our results indicated that the mitogen-activated protein kinase (MAPK) pathway was related to TF expression when PBMCs were treated, in the presence of beta(2)Glycoprotein I (beta(2)GPI), with human monoclonal anti-beta(2)GPI antibodies [beta(2)GPI-dependent anti-cardiolipin antibodies (aCL/beta(2)GPI)]. Western blotting studies using monocyte cell line (RAW264.7) demonstrated that p38 MAPK protein was phosphorylated with nuclear factor kappaB (NF-kappaB) activation by monoclonal aCL/beta(2)GPI treatment, and that SB203580, a specific p38 MAPK inhibitor, decreased the aCL/beta(2)GPI-induced TF mRNA expression. The p38 MAPK phosphorylation, NF-kappaB translocation and TF mRNA expression triggered by aCL/beta(2)GPI were abolished in the absence of beta(2)GPI. These results demonstrated that the p38 MAPK signaling pathway plays an important role in aPL-induced TF expression on monocytes and suggest that the p38 MAPK may be a possible therapeutic target to modify a pro-thrombotic state in patients with APS.

The presence of anti-PS/PT greatly correlated with increased thrombin generation in APS patients. The in vitro effects of monoclonal antibody 231D on thrombin generation are "biaxial" according to the FVa/FXa balance. These data may serve as a clue to understanding the LAC paradox and the thrombogenic properties of anti-PS/PT.

MRI findings correlated with CNS manifestations in SLE. Where there is a high suspicion of CNS involvement, the combination of MRI and SPECT may be useful in predicting CNS manifestations after starting steroid therapy.

The ignition behavior of a newly developed biomass briquette, Bio-coke (BIC), is investigated. The fuel has unique features such as economical advantages for its versatility of biomass resources, high volumetric calorific value because of its high density (1300 kg/m 3 ; twice or more than that of ordinary wood pellets) and high mechanical strength. The ignition characteristics of cylindrical BIC blocks (48 mm in diameter and 85 mm in length), important when using the fuel in actual combustion furnaces, are investigated in high temperature air flows (473-873 K, 550-750 NL/min.). In the experiments, preheated air is blown onto the bottom surface of BIC cylinders and the ignition behavior of the bottom surface is observed monitoring the surface temperature as well as the time dependent mass loss rates. The results show two ignition modes; (1) solid surface ignition preceding gas-phase ignition in high air temperature conditions (T≥598K), and (2) gas-phase ignition accompanied by simultaneous surface ignition occurring at relatively low air temperature conditions. The appearance of each mode depends on the preheated air supply condition in terms of the air temperature, flow velocity, and moisture content of the fuel. The rate of evolution of volatile gases is closely correlated with the temperature distribution inside the BIC briquette which depends on the heating rate, implying that variations in the temperature distribution inside the fuel could be one reason for the appearance of the observed ignition modes. It is suggested that the temperature distribution inside the fuel has to be taken into account in the control of the ignition behavior of BIC briquettes.

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