Calcium ions have long been recognized as necessary for clot formation. It was 1972 that γ-carboxyglutamic acid (Gla) was discovered in bovine prothrombin. In two decades, the relationship of the Gla residues in vitamin K-dependent clotting factors and calcium binding properties has been extensively studied by many investigators. Recent advances in molecular biology and crystallographic study brought us to construct the experiments for understanding the role of the individual Gla residues in their calcium ion-dependent functions. In this report, the very recent studies about the Gla-dependent and independent calcium binding properties of vitamin K-dependent clotting factors were reviewed.

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Determination was made of serum soluble interleukin-2 receptor (sIL-2R), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) levels, and plasma D-dimer, plasmin-α 2 plasmin inhibitor (PIC) and thrombin-antithrombin III complex (TAT) levels in patients with aortic aneurysm for clarification of the functions of cytokines in the pathogenesis of atherosclerosis.
Mean sIL-2R and IL-6 values in the patients were 1158.61±778.53 U/ml and 12.80±13.90 pg/ml respectively, these being significantly higher (p<0.01) than in the aged controls (488.22±164.25 U/ml and 3.04±0.21pg/ml). TNF-α was essentially the same in the patients and aged controls. Mean plasma D-dimer, PIC and TAT in the patients were 1197.59±1342.11 ng/ml, 2.34±2.41μg/ml, 25.20±17.08 ng/ml, respectively, significantly exceeding the values for the aged controls (103.71±44.47 ng/ml, 0.72±0.27μg/ml and 2.52±1.21ng/ml respectively).
Many more patients (6/6) with higher IL-6 than those (6/11) with lower IL-6 had higher D-dimer (χ2=3.8, p<0.05) and far more patients (9/10) with higher sIL-2R than those (3/8) with lower sIL-2R had higher D-dimer (χ2=5.5, p=0.04).Significant correlation was noted between IL-6 and sIL-2R levels (r=0.76, n=17) in the patients. No correlatinship could be found between TNF-α and IL-6, sIL-2R.It thus follows that sIL-2R and IL-6 in patients should be determined to clarify the pathogenesis of atherosclerosis.

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Polyether urethane nylon (PEUN) is one of in vivo thromboresistant polymers. In this work, compatibility of human vascular endothelial cells (HUVEC) with PEUN was studied in vitro mainly in the absence and presence of thrombin-treated fibrinogen (f). In the initial attachment, a number of HUVEC in a round shape were observed to be attached on PEUN, while slightly less HUVEC, plated on f-coated PEUN, were attached and spread much better than on PEUN. The presence of both tetrapeptides, RGDS and RGES, respectively, specific and nonspecific to cell adhesion decreased the number of HUVEC attached on PEUN, which implies the nonspecific binding, ie, not in a binding mechanism between receptors and ligands for cell adhesion.
The incorporation of thymidine by HUVEC and LDH activity of HUVEC component were extremely lowered after a longer term-culture on PEUN than two days. At that time the number of HUVEC attached somehow decreased, which indicates possibly the damage and death of HUVEC plated on PEUN. Taking into consideration the high affinity of PEUN surface to albumin, vascular endothelial cells should be prolonged to adhere and grow on a direct PEUN surface. Thus, cells adhesive proteins should improve the above-written inferior compatibility between PEUN and vascular endothelial cells.

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Zimmerman et al reported that normal plasma vWF contains proteolytic fragments of 225, 189, 176, and 140 kDa with anti-vWF monoclonal antibodies in the presence of protease inhibitors and partial cleavage of the plasma vWF subunit is a normal event. Now we report here the analysis of normal plasma vWF with home-made polyclonal anti-reduced vWF antibody by using a small amount of normal plasma itself. With this reference, the vWF fragments with mobility corresponding to 240, 216 (220, 210), 194, 164, and 144 kDa were detected. Also by means of employing anti-reduced SP III and SP II antibody, we suggested that the 164 kDa fragment is located close to the carboxy terminal and the 194 and 144 kDa fragments are located close to the amino terminal. Furthermore, the vWF fragments showed no difference in mobility with or without protease inhibitor. In vivo proteolytic degradation of vWF occurring normally was also shown by our technique.

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