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The role of the Asian summer monsoon on the interannual variability of the global climate system particularly relevant to the ENSO time scales is discussed, by examining the statistical and dynamical links between the Asian summer monsoon, the atmosphere/ocean system in the tropics and the westerly flow regimes in the extratropics.The Asian monsoon, the ocean and the atmosphere in the tropical Pacific are tightly linked together as one climate system, named here as the MAOS (Monsoon and the Coupled Atmosphere/Ocean System). The MAOS prominently shows the biennial oscillatory nature which tends to have anomalous states starting in the northern summer monsoon season and persisting for about one year (Yasunari, 1990a(Yasunari, : 1991.The anomalous state of the MAOS produces the anomalous atmospheric circulation over the subtropics and the extratropics of the north Pacific during summer through the early winter, through the modulation of the subtropical high and the stationary Rossby wave propagation mechanism. In the mid winter, this anomalous circulation over the north Pacific is evolved to the hemispheric winter anomalous circulation with wavenumber-one and/or-two structure.The anomalous circulation over Eurasia associated with this hemispheric anomalous flow regime seems to provide a favorable condition for the extensive (or diminished) snow cover area over central Asia, which in turn is responsible for the reversed anomalous state of the next Asian summer monsoon and the MAOS. That is, the biennial nature of the climate system in the northern hemisphere may be due, at least partly, to this two-way interactions between the tropics and the extratropics. In these processes, the Asian monsoon plays a key role as a transmitter of climate signals between the tropics and the extratropics through the land/atmosphere/ocean interaction in the seasonal cycle.In addition, it is strongly suggested that the North Atlantic Oscillation (NAO), in reality, plays a crucial role in the timing of the occurrence of the ENSO event, by stochastically amplifying or damping the biennial oscillation of this coupled climate system. That is, the more or less irregular ENSO cycle may result from this interaction between the MAOS and the NAO, where the former seems to have the nature of an almost-intransitive climate system, while the latter seems to represent the more chaotic nature of the westerly flow regime.

Circulating thrombomodulin is a novel endothelial cell marker, which may reflect the endothelial injury. Plasma levels of thrombomodulin were quantitated by an enzyme-linked immunosorbent assay (ELISA) in patients with hematological malignancies, liver disease, diabetes mellitus, collagen disease, thrombotic disease, and disseminated intravascular coagulation (DIC), and the thrombomodulin values were compared with those of von Willebrand factor antigen (vWf:Ag) and tissue-type plasminogen activator (t-PA) which are released from stimulated or damaged endothelial cells. The mean plasma concentrations of thrombomodulin in these disease states were elevated as compared with healthy subjects. A relatively high mean thrombomodulin level was observed in DIC, liver disease, and collagen disease. Abnormally high thrombomodulin values (greater than normal mean value + 3 SD) were found in 32.3% of patients with hematological malignancies, 57.7% of patients with liver disease, 39.3% of patients with diabetes mellitus, 30.0% of patients with collagen disease, 23.1% of patients with thrombotic disease, and 69.0% of patients with DIC. Plasma concentrations of both vWf:Ag and t-PA were also elevated in these patients. On the whole, the plasma thrombomodulin concentration was positively correlated with vWf:Ag (r = 0.441, P less than 0.001) and t-PA (r = 0.398, P less than 0.001). These findings indicate that the elevation of plasma thrombomodulin is frequently seen in a variety of diseases and circulating thrombomodulin is possibly useful for evaluating the endothelial damage in selected disease states.

Recently it has been shown that tissue factor (TF), an important trigger for initiating blood coagulation, is present in the circulating plasma. In order to assess the clinical implications of TF in plasma, plasma concentration of TF was quantitated in 65 patients with disseminated intravascular coagulation (DIC). The mean concentration of plasma TF was elevated in patients with DIC at presentation as compared with healthy subjects (446 +/- SD 536 pg/ml vs. 138 +/- 51 pg/ml, P < 0.001). Abnormally high levels were found only in 46.2% of the patients, predominantly in patients with non-hematological solid tumors and acute leukemia. Plasma TF did not correlate with hemostatic markers of DIC such as thrombin-antithrombin III complex, prothrombin fragment 1 + 2, plasma-alpha 2-plasmin inhibitor complex, FDP, D-dimer, or fibrinogen. Serial determinations of plasma TF demonstrated that plasma TF changes roughly in parallel with the course of DIC in most patients with elevated TF at presentation of DIC. These findings suggest that plasma TF is potentially valuable for monitoring the progress of DIC in a limited population of patients.

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