We studied effects of platelet lipoxygenase (LO) metabolites on 5-LO metabolism and degranulation of neutrophils by using 12-hydroperoxyeicosatetraenoic acid (12-HPETE) and 12-hydroxyeicosatetraenoic acid (12-HETE) which were prepared from human platelet lysate incubated with arachidonic acid (AA) in the presence of indomethacin.
When 5-LO products obtained from incubations of human neutrophils (3×10⁷ cells/ml) with platelet activating factor (PAF) and AA were analysed by reversed-phase high-performance liquid chromatography, the addition of platelets (15-30×10⁷ cells/ml) to the reaction mixture remarkably increased the synthesis of 5-LO products including leukotriene B₄, 5-HETE and 5S, 12S-diHETE. While the 5-LO metabolism of neutrophils was similarly stimulated by cyclo-oxygenase-inhibited platelets, the synthesis of 5-LO products was significantly (p<0.001) reduced when LO-deficient platelets from patients with myeloproliferative disorders were added to the incubation mixture instead of normal platelets. The addition of 12-HPETE activated the 5-LO metabolism of neutrophils incubated with PAF and AA, but 12-HETE did not have such stimulating effects at all.
Release of N-acetylglucosaminidase (NAGase) from cytochalasin B-treated neutrophils was estimated using p-nitrophenyl-2-acetamido-2-deoxy-β-D-glucopyranoside as a substrate. 12-HPETE induced not only the release of small amounts of NAGase, but also augmented the effects of N-formylmethionylleucylphenylalanine (FMLP) on the release reaction. Unlike the 5-LO metabolism, the release of NAGase from FMLP-stimulated neutrophils were increased by 12-HETE to some extent.
These findings suggest that platelet LO metabolites, especially 12-HPETE, modulate neutrophil functions in some pathological states including inflammation, thrombosis and hemorrhage.

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It is known that stimulation of platelets with physiological agents such as arachidonic acid (AA) induces rapid changes in membrane phospholipids via the activation of the phosphatidylinositol (PI) pathway. This study indicates the role of thromboxane (TX) A₂ in the changes in phospholipids in ³H-AA- or ³H-glycerol-labeled rabbit platelets using OKY-046, a specific TXA₂ synthetase inhibitor, and 9, 11-epithio-11, 12-methano-TXA₂ (STA₂).
Stimulation of platelets with 0.5mM AA induced breakdown of ³H-PI and formation of ³H-1, 2-diacylglycerol, ³H-phosphatidic acid (PA) and ³H-AA in platelets. OKY-046 (10^-6-10^-4M) dose-dependently inhibited these changes in phospholipids, especially PA formation, 3min after the addition of AA. Aspirin (10^-3M) also inhibited the changes in phospholipids. OKY-046 and aspirin also inhibited the changes after 5min induced by collagen (20μg/ml), however no effect was observed on the changes induced by 20μM ADP. On the other hand STA₂, a TXA₂ analogue, dose-dependently stimulated the formation of PA alone.
These results suggest that TXA₂ stimulates platelets through the activation of membrane phospholipid metabolism such as PA formation via the PI pathway.

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Danazol has been reported to be effective in patients with idiopathic thrombocytopenic purpura. Its mechanism, however, has not been clarified. We investigated the effects of danazol on megakaryocyte DNA content and and platelet size.
Megakaryocyte DNA content was measured by epifluorescent microfluorometer, using DAPI staining method. Mean platelet volume (MPV) and platelet counts were determined by E-4000 (Sysmex). Danazol was dissolved in sesame oil containing 10% ethanol (vehicle), and was injected subcutaneously into Hartley guinea pigs for 9 consecutive days. As control, only vehicle was injected for the same period.
Danazol-treated guinea pigs have more 32N and 64N megakaryocytes than only vehicle-treated guinea pigs (P<0.02). However, there was no difference in platelet counts and MPV between these two groups.
When anti-platelet serum (APS) was injected on day 8 intraperitoneally, more 32N and 64N megakaryocytes were observed in danazol-treated guinea pigs as compared with only vehicle-treated guinea pigs (P<0.01). Moreover, danazol-treated guinea pigs appeared to have larger platelets (P<0.01) and more platelet counts.
These findings suggest that danazol potentiates megakaryocyte endoreduplication accompanied by massive platelet formation.

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Factor VII antigen has been measured with the antibody neutralization assay according to Goodnight, until recent report of Fair in which a double-antibody equilibrium radio-immunoassay for factor VII antigen is employed. No quantitative precipitation arc of factor VII antigen in plasma has been reported because of its very low concentraiton.
In the present method developed by the authers, a clear precipitation arc of factor VII antigen appeared by immuno-electrophoresis using ¹²⁵I-labelled anti-factor VII antibody incorporated in the Laurell plate to enhance the sensitivity. A plasma sample was electrophoresed directly on 1% agarose containing 1% anti-human factor VII rabbit serum, 0.1% ¹²⁵I-labelled anti-human factor VII specific IgG and 0.5% polyethyleneglycol 6000, and after washing, autoradiographed at -70°C for 48hr. A distinct rocket was seen from 45μl of undiluted plasma to 16-fold diluted plasma. Of 5 cases with congential factor VII deficiency, 4 cases had no detectable factor VII antigen, one case had factor VII antigen. Factor VII antigen levels in 19 patients of liver disease varied from 9 to 125%, and the assayed values of factor VII antigen and activity correlated relatively well (r=0.96). In contrast, factor VII antigen levels in 20 patients treated with Warfarin varied from 16 to 100%, and the antigen levels were slightly higher than the activity.

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The purpose of this study is to evaluate the platelet function, blood coagulability and fibrinolytic activity in ischemic heart disease (IHD), lone atrial fibrillation (lone Af), diabetes mellitus (DM) and normal controls (Normal). Blood samples were obtained from the antecubital vein. Measurements were made for platelet counts in whole blood and platelet rich plasma (PRP), platelet sensitivity to ADP-aggregation and plasma concentrations of β-thromboglobulin (β-TG), fibrinogen (Fbg), antithrombin III (AT III), α2-plasmin inhibitor (α2-PI) and protein C.
Patients with DM showed a higher β-TG level than Normal (DM: 122.3±68.3ng/ml; Normal: 32.4±10.8ng/ml, p<0.001) although there were no significant differences in platelet counts and sensitivity to ADP-aggregation. Patients with IHD showed higher levels of α2-PI (IHD: 5.47±0.83mg/dl; Normal: 4.45±0.68mg/dl, p<0.01) and Fbg (IHD: 402.3±76.7mg/dl; Normal: 310.5±41.9mg/dl, p<0.001) compared with Normal. Lower levels of AT III were observed in lone Af and IHD than in Normal (lone Af: 24.1±4.0mg/dl, IHD: 25.3±3.3mg/dl, Normal: 27.5±3.6mg/dl; IHD vs Normal: p<0.05, lone Af vs Normal: p<0.01).
In conclusion, the hypercoagulable state observed in IHD, lone Af and DM may be related to a high incidence of thromboembolism in these diseases.

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Sudden death from cardiac rupture is a dramatic event after acute myocardial infarction (AMI), although such a complication is rare. Several authors have reported, however, an increasing incidence of this complication of AMI since thrombolytic and/or anticoagulant therapy has become more popular.
A 53-year-old male patient with hypertension and hyperlipidemia for 5 years and effort angina for a month developed a sudden severe retrosternal pain. ECG revealed ST elevation in _aV_L and V₁ to V₄. AMI was diagnosed and intracoronary thrombolysis (ICT) was performed 3.75 hours after the onset of the chest pain. A left ventriculogram showed dyskinetic and hypokinetic motion of the anterolateral and inferior walls, respectively. The ejection fraction was reduced to 37%. A left coronary arteriogram revealed 100% obstruction of the proximal portion of the left anterior descending artery which was recanalized with 99% remaining stenosis after administration of 960, 000IU of urokinase (UK). However re-obstruction developed and a total dose of 1, 440, 000IU of UK was given without success. Heparin was infused through a Swan-Ganz catheter at a rate of infusion was also given. His blood pressure remained high (150-170/90-100mmHg) and chest pain continued. The patient died of cardiac rupture 9 hours after ICT. Autopsy revealed a moderately hypertrophied heart (Wt=450g) and a wide area of hemorrhagic infarction in the anterolateral wall and interventricular septum. Cardiac rupture was noted in the anterior wall near the apex.
Fibrinolytic activity was measured soon and 8 hours after ICT and compared with that of 10 other cases in which an average dose of 984, 000 IU of UK was given in the same way (Figures 2-4). Markedly increased fibrinolytic activity was observed in this case.
Acute free wall rupture is one of the most dramatic and lethal complications of AMI because its repair is usually very difficult. Cardiac rupture after thrombolytic therapy is not uncommon. Hemorrhagic infarction is often reported after fibrinolytic therapy, and it seems very probable that this type of therapy causes hemorrhagic infarction, which is rare in patients who do not receive fibrinolytic therapy. Whether hemorrhagic infarction leads to cardiac rupture or not is still unknown. Datta et al, reported that intramural hemorrhage may be an important factor contributing to the rupture. The outcome in this case, also, indicates that intramural hemorrhage induced by extreme fibrinolytic activity may cause cardiac rupture, so great care must be taken when massive doses of UK, i. e, more than 1, 000, 000IU, are used.

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We used W/W^v mice genetically deficient in mast cells to clarify whether mast-cell-derived heparin may play a role to inhibit thrombus formation in living body or not. After small veins in mesentery of W/W^v or congenic +/+ mice were streched on to an inverted microscope, a micropipette filled with varying concentrations of ADP was set close to the outside of a vein by using micromanipulator; thrombus formation was directly examined under the microscope. The concentration of ADP necessary for thrombus formation in veins of W/W^v mice was significantly lower than the concentration in veins of +/+ mice. Furthermore, the concentration of ADP necessary for aggregation of platelets in platelet-rich plasma (PRP) was significantly lower in W/W^v mice than +/+ mice. The higher sensitivity of PRP of W/W^v mice is not attributed to the platelets but to the plasma, since platelets of +/+ mice suspended in platelet-poor plasma (PPP) of W/W^v mice were more sensitive to ADP than platelets of W/W^v mice suspended in PPP of +/+ mice. The present results⁴ show that plasma of W/W^v mice may lack some inhibitory factor (s) or contain promoting factor (s) for platelet aggregation.

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Plasma levels of prothrombin, PIVKA-II, protein C (PC), PIVKA-PC, and urinary levels of γ-Carboxyglutamic acid (Gla) were measured in liver diseases.
Plasma samples for PIVKA-II and PIVKA-PC were obtained by ordinary absorption barium salfate. Concentrations of prothrombin and PIVKA-II were determined by Echis carinatus venom-chromogenic substrate (S-2238) method. Concentrations of PC and PIVKA-PC were determined by Laurell method. Concentration of urinary γ-Gla was determined using HPLC by Kuwada, et al.
Plasma samples were collected from 10 healthy adults, 8 patients with acute hepatitis, 11 patients with chronic hepatitis, 17 patients with liver cirrhosis, 8 patients with hepatoma and 9 patients with liver metastatic carcinomas.
The results obtained were as follows.
1) Concentrations of plasma prothrombin and PC were significantly decreased in liver diseases.
2) Concentration of urinary γ-Gla was decreased in most patients with hapatitis and liver cirrhosis, but γ-Gla levels were markedly increased in patients with decompensated liver cirrhosis, hepatic cancer.
3) Correlation between plasma prothrombin and urinary γ-Gla was significant in most patients with hepatitis and liver cirrhosis. In patients with decompensated liver cirrhosis, hepatic cancer, there were showed negative correlation between plasma prothrombin and urinary γ-Gla.
4) In the several cases with positive fibrin monomer, plasma levels of PIVKA-II and PIVKA-PC were increased.
These data suggest that patients with different types of liver disease have impared vitamin K-dependent carboxylase deficiency, but patients with severe liver disease e. g. decompensated liver cirrhosis, hepatic cancer have a increased levels of the urinary γ-Gla, PIVKA and fibrin monomer.

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Plasma levels of vitamin K-dependent coagulation factors (factors II, VII, IX and X) and protein C were measured in 100 specimens from patients on long-term warfarin therapy. Thrombotest values ranged from 7 to 50%. Both clotting activities and antigens of vitamin K-dependent coagulation factors decreased, depending on thrombotest values. The clotting activity levels of these factors were below their antigen levels, indicating the presence of circulating, inactive molecules ( PIVKAs). The activity to antigen ratios of these factors were correlated with thrombotest values, suggesting that the concentration of PIVKAs relative to normal molecules increases with increasing intensity of anticoagulation. Although protein C antigen was also decreased, the ratios of protein C antigen to factors II, VII, IX and X antigens remained constant, being independent of the intensity of warfarin therapy. These results indicate that long-term oral anticoagulant therapy results in the suppression of the synthesis of both vitamin K-dependent coagulation factors and protein C, and that the production of the coagulant and anticoagulant proteins is, on the whole, well-balanced. In addition, a considerable variation in the levels of protein C antigen was observed among individuals with a similar intensity of anticoagulation.

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It has been demonstrated that myeloma immunoglobulin has an inhibitory effect of fibrin formation. However, the exact mechanism of this anticoagulant activity has been subject to controversy. In this study a hypothesis was tested whether this phenomenon would originate from binding of immunoglobulin with fibrinogen. Blood was obtained from 7 patients with IgG myeloma, 7 with RA, 3 with SLE, 8 with hepatic desease, 6 with cancer and 9 with other different diseases.
The similar abnormal coagulabilities as well known in fibrinogen from myeloma patients were also observed in the fibrinogen from all those patients with immunoglobulin in high concentration.
Partial purified fibrinogen taken from some of the patient's plasma prepared by (NH₄)₂SO₄ were electrophoresed on 8M Urea-SDS-PAGE and showed another peculiar band different from α, β, γ-chains of normal fibrinogen in the higher molecular weight region. Rocket immunoelectrophoresis containing 1% anti Ig (A+G+M) antibody clearly observed the presence of immunoglobulin in the same partial purified fibrinogen. But the additional observation with intermediate gel containing 1.25% anti fibrinogen antibody did not go so far as to decide that this immunoglobulin was binding with fibrinogen. Yet the two dimensional immunoelectrophoresis using SDS-agarose gel gave very different patterns from the normal plasma fibrinogen as to the plasma fibrinogen from the patients with the above diseases. Further study is sure to demonstrate the presence of fibrinogen-immunoglobulin complex in the hyperimmunoglobulinemia patients.

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Diabetes mellitus is one of the common diseases which often involve thrombi formation in major and microcirculation. Although these thrombi might be caused by a hypercoagulable and hypofibrinolytic state in this disease, precise mechanism is not get clearly understood.
In this study, we measured Fibrinopeptide A (FPA) and Fibrinopeptide B_β15-42 using radioimmunoassay in patients with diabetes mellitus. In the plasma of diabetic patients, FPA and FPB_β15-42 were elevated, although fibrinogen, FDP, α₂-PI and ATIII levels remained the same. Fasting blood sugar levels did not correlate to plasma FPA and FPB_β15-42. Fibrinogen levels in patients with diabetic nephropathy (Group I) were statistically higher than those in patients without nephropathy (Group II). Urinary FPA, FPB_β15-42 and FDP levels in group I were higher than those in group II. Urinary FPA had an inverse relationship to 24 hours creatinine clearance. After administration of heparin to patients with high urinary FPA and FDP excretion, we observed a remarkable reduction of urinary FPA and FDP levels but no changes in urinary protein, plasma FPA and serum FDP. These data suggest that (1) blood sugar per se does not cause activation of the coagulation system, (2) intrarenal coagulation is involved in group I, but not in group II, (3) the measurement of urinary FPA can be a potential value in determining intrarenal coagulation in patients with diabetic nephropathy.

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A proform of urinary plasminogen activator (Pro-PA) was obtained from culture medium of human kidney cells, purified to a single band on SDS-PAGE and used for the experimental studies. Pro-PA was converted to active PA, urokinase (UK) by plasmin. The CD showed significant difference between Pro-PA and plasmin-treated Pro-PA, indicating conformational change upon the cleavage of Pro-PA by plasmin. The affinity of Pro-PA for fibrin was much higher than that of UK. High concentration of UK promoted clot lysis promptly, but Pro-PA induced clot lysis progressively. In the experimental system, where fibrin and fibrinogen co-exist, 200IU/ml of Pro-PA or UK lyzed clot in similar degree, but fibrinogenolysis by UK was two times larger than that of Pro-PA. 100IU/ml of Pro-PA lyzed clot almost completely with only 6% fibrinogenolysis. However, 100IU/ml of UK brought 12% clot lysis with 12% fibrinogenolysis. Systemic activation of fibrinogenolysis in UK infusion was observed by the consumption of α₂-plasmin inhibitor as well as plasminogen. However, Pro-PA did not induce systemic activation of fibrinolysis. In the presence of tissue-plasminogen activator in thrombus, the thrombolytic effect of Pro-PA was argued. The results obtained indicate that Pro-PA is much more efficient thrombolytic agent.

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Physiochemical character was investigated of plasminogen and its fragments obtained by elastase digestion. Plasminogen fragments were obtained by treatment of human plasminogen by elastase, and purified by gel filtration, affinity chromatography on lysine-Sepharose and column chromatography on DEAE-cellulose. Plasminogen fragments obtained above were specified as four variants (FIT-C₁, C₂, D and E₁) containing the Kringle 1-3 region, two variants (FII-E₂ and F) containing the Kringle 1-4 region, a variant (FIJI-B) containing the Kringle 4 only, and mini-plasminogen (FIT-A) containing the Kringle 5 region and light chain. CD analysis of these fragments revealed that fragments containing the Kringle 1-3 or 1-4 showed a positive band at 228nm, which disappeared by the reduction of fragments by 2-mercaptoethanol. The fragment including Kringle 1-4 had the highest affinity to fibrin among other fragments of plasminogen. These results suggest that a special domain is required to express fibrin affinity, which may locate possibly in Kringle 1-4.

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When Clu-plasminogen (pig) was incubated with various units of plasmin for 60min and 120min at 37°C in the presence or absence of fibrin, Glu-plg was hardly converted to modified (Lys) pig by up to 0.1cu/ml plasmin in the absence of fibrin. On the other hand, Glu-pig was significantly converted to Lys-plg by plasmin in the presence of fibrin. Increase in the amounts of plasmin used resulted in more conversion of Glu-plg to Lys-plg in the presence of fibrin. When human plasma or clotted plasma was activated by urokinase (UK), Glu-plg was activated better to plasmin by UK in the presence of clot. The presence of fibrin resulted in faster conversion of Glu-plg to Lys-plg by plasmin in both purified and plasma systems.

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A hitherto unknown synergism exerted by vitamin A (retinol, retinal, retinoic acid) and vitamin C (L-ascorbic acid) was discovered using endothelial cells. Vitamin A alone stimulated the extracellular and intracellular activities of plasminogen activator up to 8- and 4-fold from control values, respectively. Vitamin C alone enhanced the extracellular and intracellular activities up to approximately 1.5-fold. It was, however, demonstrated that their effects on extracellular activity were synergistic: simultaneous administration of these two vitamins enhanced the extracellular activity up to a 20- to 50-fold. Increase of plasminogen activator activity induced with these vitamins was inhibited by a protein synthesis inhibitor, cycloheximide.

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Recently, thrombotic diseases such as myocardial infarction and cerebral infarction are increasing. In order to prevent thrombotic diseases, it is important to clarify the mechanism of thrombus formation. It is accepted that activated platelets and fibrin networks (transformed from fibrinogen) are indispensable to thrombus formation. However there are many unknown problems about contractile proteins in activated platelets. In the present study, changes of myosin structure and localization was investigated during clot retraction by immuno-electron microscopy, using specific rabbit antibodies against human platelet myosin heavy chain and Protein-A gold complex.
The results were as follows; 1) in non-activated platelets, no filamentous structure was found and gold particles were diffusely deposited in the cytoplasm. 2) in activated platelets (retracted platelets), thick filaments were found in the center of the cytoplasm and gold particles were selectively were deposited on the thick filaments. 3) consequently, it was demonstrated that the thick filaments in activated platelets were myosin polymers.
In conclusion, the polymerization of myosin was found in the center of activated platelets.

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A technique of Western blotting using peroxidase conjugated actin was was developed.
After SDS gel electrophoresis of supernatant of platelet homogenate, the proteins were transferred on nitrocellulose membrane and then incubated with peroxidase conjugated actin in the presence of 1mM C_aCl₂. The membrane was washed 3 times with 1mM C_aCl₂ containing buffer and then air dryed. The bands which interacted with peroxidase conjugated actin were detected by using 4-chloro 1-naphthol as a colouring substrate. The bands of the proteins having molecular weights about 2.2×10⁴, 5.1×10⁴, 6.4×10⁴, 7.0×10⁴, 7.8×10⁴, 9.2×10⁴, were detected on the nitrocellulose membrane.
Among them, the bands of 4.9×10⁴, 3.8×10⁴, 3.3×10⁴, 5.1×10⁴, 7.0×10⁴, 7.8×10⁴, 9.2×10⁴ were also recognized on the Coomasie stained SDS gel of the samples which were obtained by actin Sepharose affinity chromatography of platelet homogenate. These were thought to be the proteins that interact with actin of platelets.

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Antigen-antibody complexes or aggregated-IgG caused human platelet aggregation and release reaction. Although presence of Fe receptor on the platelet surface is obvious so far, the entity of Fc receptor has not been elucidated. We have tried to isolate Fc receptor using photosensitive heterobifunctional cross-linking reagents. Human platelets were obtained from PRP through an albumin cushion and a Sepharose 2B column. ¹²⁵I-platelet and methyl azidobenzoimidate-coupled IgG (MABI-IgG) were brought to bind each other, and then excess molecules of MABI-IgG were washed away gently at 4°C. These processes were carried out in a dark room. The platelets which bound with MABI-IgG at the sites of Fc receptor were then exposed to UV light, thereby platelet and IgG were cross-linked covalently.
Comparing the compositions of ¹²⁵I-labeled proteins between IgG-crosslinked and non-cross-linked platelets, after these platelets were solubilized with SDS and urea, the cross-linked platelets showed, in SDS-PAGE, an appearance of giant molecules which barely entered the gel, and also showed disappearance of a protein having molecular weight of 255K. This protein was, therefore, assumed to be an Fc receptor. Taking the molecular size and its rate of iodination (Ca. 13%) into consideration, the receptor protein is localized inside of the membrane, representing a subtle expression on the surface.

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The effect of daily oral administration of 250mg aspirin and 200mg ticlopidine on platelet functions was evaluated in 50 patients with thrombophilia. Platelet aggregation was significantly inhibited (60-80% of control) after administration of aspirin for 5 years and of ticlopidine for 1 year. The second purpose of our study was to observe the changes of platelet aggregation, levels of plasma malondialdehyde (MDA), plasma thromboxane B₂ (TXB₂) and plasma β-thromboglobuline (β-TG) after medication off. In the cases of aspirin administration, platelet aggregation with all aggregation inducing agents increased significantly after medication off. In ticlopidine administration, platelet aggregation with only 5.0μM ADP increased significantly after medication off. Levels of TXB₂ β-TG and MDA showed no significant change after medication off. In conclusion, it is very important therapy for the thromophilic patients.

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Anti-platelet and anti-atherogenic properties of eicosapentaenoic acid (EPA) are being focused. We have reported that platelet aggregation is depressed after intravenous infusion of emulsion of fish oil containing 30% EPA. We, then, manufactured an emulsion of 1, 2, 3-trieicosapentaenoylglycerol (EPA-TG). 90% of fatty acids in EPA-TG were EPA. We examined influences of two intravenous injections of the EPA-TG emulsion on platelet aggregation, serum lipids and liver function in rabbits. Platelet aggregation induced by ADP (5μM) and collagen (10μg/ml) was depressed significantly after injections. No significant changes in serum lipids and liver function were observed after injections. Our results suggest that in those patients, who can not eat anything, such as postoperative patients, EPA-TG emulsion may inhibit the initiation and progression of thrombosis.

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It has been suspected that granulocyte elastase is released into the plasma of the patients in some pathologic states and digests various coagulation factors. The enzyme, however, bound to plasma inhibitors so rapidly that the activity was not assayed directly, although the enzyme-inhibitor complex was reported in immunological studies.
This paper deals with the activities of elastase-like proteinase ( ELP) and chymotrypsin-like proteinase (CLP) in neutrophils and plasma of patients with leukemia. The results obtained are summarized as follows.
(1) In the average value, ELP values per neutrophils in CML and AML were almost similar to that in normal control, but standard deviation in CML and AML was larger than that of the control.
(2) Amidolytic activities of ELP (Suc-Ala-Tyr-Leu-Val-pNA) and CLP (Suc-Tyr-Leu-Phe-pNA) per blood (3ml) did not varied in normal control and AML, but those in CML increased in proportion to neutrophil numbers.
(3) There was a high correlation between the amidolysis by ELP and fibrinolysis per neutrophils, but little correlation between amidolysis by CLP and fibrinolysis per neutrophils.
(4) In the plasma of patients with CML (including crisis cases), ELP was detected in high ratio, although any treatment was not thought to induce the increase.

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