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須見 洋行, 浜田 博喜, 吉田 悦男, 美原 恒
1988 年 19 巻 6 号 p.
545-557
発行日: 1988/12/01
公開日: 2010/08/05
ジャーナル
フリー
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牛山 茂, 郡山 たか子, 伊藤 福美, 浅井 史敏, 大島 武史, 松田 啓一
1988 年 19 巻 6 号 p.
558-565
発行日: 1988/12/01
公開日: 2010/08/05
ジャーナル
フリー
RS-5186, sodium 6-[2-[1-(1H)-imidazolyl] methyl-4, 5-dihydrobenzo[b]thiophene] carboxylate, potently inhibited platelet microsomal thromboxane (TX) synthetase with IC
50 values of 6nM for human and 13nM for rabbit microsomes, but had no effect on cyclooxygenase, PGI
2 synthetase, 5-lipoxygenase and phospholipase A
2 up to 300μM. When administered orally or intravenously to beagle dogs at 1mg/kg, RS-5186 suppressed the concentration of serum TXB
2 almost completely with sustained duration of action; the suppression during 0.5hr to 8hr after dosing was more than 90%, and was 70-80% even at 24hr. The suppression by RS-5186 was significantly stronger than that by OKY-046 and CV-4151 at all time points. Similar results were obtained with rats and rabbits. In experimental thrombosis induced by sodium arachidonate-injection in rabbits, pretreatment with RS-5186 (1mg/kg) completely protected against sudden death, preventing an increase in the plasma TXB
2 levels and thrombocytopenia. This protective effect extended over 8hr. Neither tachyphylaxis nor rebound phenomenon was observed in repeated administrations of RS-5186. All these results show that RS-5186 is a potent and highly selective TX synthetase inhibitor with a long duration of action, and suggest that the compound could be useful in diseases where TXA
2 production is involved.
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Ultrastructual and Optoelectronic Observations
C. Bourgain, R. H. Bourgain, R. Andries, Z. W. Xie
1988 年 19 巻 6 号 p.
566-577
発行日: 1988/12/01
公開日: 2010/08/05
ジャーナル
フリー
In this study electron microscopic and optoelectronic observations on arterial thrombi induced in the guinea pig by inflammatory inducing maneuvers such as electrical challenge, topical superfusion by PAF-acether or the combination of both are described. These maneuvers result within minutes in a well defined sequence of phenomena: the endothelial cells retract and develop blebs, platelets adhere onto the exposed intimal tissue, aggregate, degranulate and conflate into a thrombus. Recruitment of leukocytes occurs within 10 minutes and blood coagulation is triggered later on. Phagocytosis of platelets and fibrin by the invading cells is a constant finding but is insufficient to offset the propensity to vascular occlusion. The early platelet adhesion and aggregation as well as the recruitment of leukocytes is inhibited by specific PAF-acether antagonists, such as BN 52021 and 48740 RP. These observations indicate that arterial thrombosis induced by these techniques shares features pertaining to the inflammatory process.
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白井 馨, 豊田 武夫, 澤田 昌平, 小林 恭一郎, 高淵 洋影, 宇野 雅史, 辻 肇, 中川 雅夫
1988 年 19 巻 6 号 p.
578-585
発行日: 1988/12/01
公開日: 2010/08/05
ジャーナル
フリー
The regulatory mechanism of prostacyclin (PGI
2) generation and its enhancement by ouabain and monensin in cultured human vascular endothelial cells was investigated with references to the kinetics of Ca
++ and Na
+. Na
+-K
+ ATPase activity was assayed as ouabain-sensitive
86Rb uptake. Cytosolic free calcium ion concentration ([Ca
++]
i) was measured using fura-2. The kinetics of
45Ca of
22Na, and [Ca
++]
i preceded PGI
2 generation. Ouabain inhibited Na
+-K
+ ATPase activity (inhibition of
22Na release and
86Rb uptake) and increased
22Na uptake, while monensin enhanced
22Na uptake and Na
+-K
+ ATPase activity at 2.5min after starting incubation. Both of these reagents decreased
45Ca release and increased
45Ca uptake (inhibition of Na
+-Ca
++ exchange systems) at 2.5min. And all of these effects were attenuated at 10min. Ouabain and monensin increased [Ca
++]
i. Through these results it was concluded that the enhanced PGI
2 generation by ouabain or monensin was speculated to be brought about by the increased [Ca
++]
i and Ca
++ uptake which was based on the decreased Ca
++ release via the inhibition of Na
+-Ca
++ exchange systems, and that enhanced PGI
2 generation might be autoregulated by the attenuation of increased [Na
+]
i, which was derived from the attenuation of ouabain-induced inhibition of Na
+-K
+ ATPase activity, or from the enhancement of monensin-induced increase of its activity.
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小川 睦子, 今岡 真義, 置塩 達郎, 寺沢 敏夫
1988 年 19 巻 6 号 p.
586-592
発行日: 1988/12/01
公開日: 2010/08/05
ジャーナル
フリー
It is well known that α
2MG is an inhibitor of both thrombin and plasmin, but the interaction between α
2MG and activated factor X (Xa) has not been clarified. In the present study we investigated the inhibition of α
2MG on Xa.
α
2MG was incubated with
125I-Xa at 37°C for 15min. By gelfiltration of the incubation mixture on Sephadex G-200, the radio-activity of
125I was appeared with α
2MG in void volume.
The mixture of α
2MG with Xa was applied to a column of Sephadex G-200. The hydrolysed activity against S-2222 was observed in void volume, but the coagulation activity was not detected in this fraction. On the contrary, coagulation activity and hydrolysed activity against S-2222 were markedly reduced in albumin fraction.
Antithrombin III did not inhibit the hydrolysed activity of Xa after making the complex with α
2MG.
These results indicate that Xa makes a complex after binding to α
2MG, but its active site (s) is preserved.
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相馬 正幸, 前田 義久, 村上 昌弘, 田中 京子, 八木 登志員, 笠倉 新平, 島田 逸人, 高島 英世, 高田 明和, 高田 由美子
1988 年 19 巻 6 号 p.
593-599
発行日: 1988/12/01
公開日: 2010/08/05
ジャーナル
フリー
This study is desinged to investigate exercise-induced change of coagulation and fibrinolysis systems. The plasma levels of both the fibrinolytic factors including tissue type plasminogen activator (t-PA) antigen urokinase-type plasminogen activator (u-PA) antigen, plasminogen activator (PA) activity and plasmin-α
2 plasmin inhibitor (plm-α
2PI) complex, and the coagulation factors including factor VIII related antigen (VIII R: Ag), factor VIII activity (VIII: C) and protein C (PC) antigen were measured before exercise and immediately, 15min, 30 min and 60min after exercise on treadmill. The levels of VIII R: Ag and VIII: C rose slightly after exercise, but PC antigen did not change. The levels of t-PA antigen, PA activity and plm-α
2 PI complex elevated immediately after exercise and then decreased gradually. The levels of both t-PA antigen and PA activity returned to the control levels 60min after exercise. In contrast, the level of u-PA antigen was not affected by exercise. These data suggest that the exercise-induced elevation of plasma PA activity may be caused by t-PA but not by u-PA.
The degree of elevation of t-PA and PA activity in the plasma after exercise was lower in old aged group as comparied with that in young aged group.
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古井 宏彦, 山田 芳司, 古道 武夫, 鈴木 敏和, 横田 充弘, 山内 一信, 林 博史, 斎藤 英彦, 谷口 直樹, 大野 安男
1988 年 19 巻 6 号 p.
600-604
発行日: 1988/12/01
公開日: 2010/08/05
ジャーナル
フリー
The present study was designed to evaluate the effects of treadmill exercise (TME) on coagulo-fibrinolytic function. Near-maximal TME was performed according to the modified Bruce protocol for Japanese in 15 healthy men (22-45 years old; average, 34.8 years) and 16 male patients (36-61 years old; average, 45.6 years) with ischemic heart disease (IHD). Of the IHD patients, 8 had stable effort angina pectoris and 8 had a previous myocardial infarction without angina pectoris. Blood samples were obtained from the antecubital vein at rest and immediately after exercise. Measurements were made for levels of plasma protein C, tissue plasminogen activator (T-PA), fibrinopeptide A (FPA), fibrinopeptide Bβ
15-42 (FPBβ
15-42) and D-dimer.
Pre-exercise levels of plasma T-PA and FPA were higher, and FPBβ
15-42 was lower in IHD patients than in healthy men. There were no significant changes observed in levels of plasma protein C, FPA, FPBβ
15-42 and D-dimer after TME in both groups. However, T-PA increased after exercise from 4.4ng/m
l to 4.8ng/m
l in IHD and from 2.6ng/m
l to 3.4ng/m
l in healthy men, the increase being greater in healthy men than in IHD.
In conclusion, moderate TME increases plasma T-PA levels without inducing abnormal intravascular coagulation in patients with IHD as well as in healthy controls.
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鈴木 節子, 金山 正明, 山中 學
1988 年 19 巻 6 号 p.
605-611
発行日: 1988/12/01
公開日: 2010/08/05
ジャーナル
フリー
The glycation of plasma fibrinogen (Fbg) in diabetic patients, an alteration in clotting and fibrinolytic activities of glycated Fbg and the effect of various drugs on glycation of Fbg were investigated. The amount of furosine, which was a specific product by hydrolysis of glycated lysine residue of Fbg were determined using HPLC in 92 diabetic patients and 90 age-matched normal subjects as a control. Also the cloting and fibrinolytic activity of the glycated Fbg separated by aminophenyl boronate chromatography and inhibitory effects of acetyl salicylic acid (ASA), ascrobic asid (ACA) and pyridoxal phosphate (PP) on the production of furosine by hydrolysis of Fbg or lysine were examined.
The amount of furosine in hydrolysate of plasma Fbg was significantly higher in diabetic patients than normal subjects (p<0.001).
There was no difference in the release of fibrinopeptide-A from glycated and non-glycated Fbgs by after an addition of thrombin.
The polymerization and cross linking of fibrin monomer, were however, accelerated in the glycated Fbg and the fibrinolysis by plasmin was delayed in fibrin formed from the glycated Fbg. The production of furosine by a hydrolysis of Fbg or lysine after an incubation with glucose was suppressed by an addition of ASA and ACA.
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田中 國義, 高尾 仁二, 矢田 公, 湯浅 浩, 草川 實, 出口 克巳
1988 年 19 巻 6 号 p.
612-620
発行日: 1988/12/01
公開日: 2010/08/05
ジャーナル
フリー
The purpose of this study was to evaluate the effects of gabexate mesilate (FOY
®) on coagulofibrinolytic system during cardiopulmonary bypass (CPB) in open heart surgery. Twenty-four patients were diveded into two groups: group A consisted of 13 patients administered only heparin (3mg/kg), and group B consisted of 11 patients administered FOY (40mg/kg/hr) in addition to heparin (3mg/kg). The following parameters were examined; fibrinopetide A (FPA), fibrinopeptide B β15-42 (FPB β15-42), tissue plasminogen activator antigen (t-PA; Ag), and contact factors (FXII, high molecular weight kininogen, prekallikrein). Fibrinolytic activity was also determined by the fibrin plate method. FPA increased significantly during CPB in group A, but it did not in group B. FPB β15-42 and t-PA; Ag increased druing CPB in both groups to the same degree. Cl-INA resistant fibrinolytic activity was similar in both groups, but fibrinolytic activity determined by kaolin activated euglobulin showed less change in group B. Factor XII decreased in group A, but they did not in group B. It's concluded that FOY suppresses the coagulation system and intrinsic fibrinolytic system probably by the effect on the contact factors.
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安倍 千之, 稲垣 稔, 上田 一博, 梶井 正, 塩川 優一, 白幡 聡, 永井 清保, 丸山 征郎, 藤巻 道男, 三間屋 純一, 山田 ...
1988 年 19 巻 6 号 p.
621-631
発行日: 1988/12/01
公開日: 2010/08/05
ジャーナル
フリー
Multi-center clinical traials of Neurotropin were carried out employing protocol made by the Committee of clinical studies on acquired immunodeficiency syndrome (AIDS). The patients, 29 hemophiliacs with human immunodeficiency virus (HIV) infection, consisting of 2 cases of AIDS, 11 of AIDS related complex (ARC) and 16 of asymptomatic carrier (AC), were studied in 9 institutes. Their ages ranged from 6 to 67 years (mean 23.4 years).
Neurotropin was administered intravenously and/or orally for 10.3 months in average. The results were as follows:
1. Global improvement rating: “Moderately improved or more” was observed in 18.2% (2/11) of ARC cases and 31.3% (5/16) of AC. “Slightly improved or more” was observed in 63.6% (7/11) of ARC cases and 43.8% (7/16) of AC, but not in AIDS cases.
2. The improvement ratings of clinical symptoms, immunological and hematological parameters were 46.2% (6/13), 20.7% (6/29) and 44.8% (13/29), respectively, of all cases. Of the clinical symptoms, generalized lymphadenopathy, diarrhea and fatigue were improved in 67% of AIDS and ARC cases.
After the treatment, the absolute number of OKT 4 positive lymphocytes and OKT 4/8 ratio had no significant changes comparing to the pretreatment values.
3. Platelet increased number significantly in 7 cases with thrombocytopenia both 3 and 6 months after the treatment with Neurotropin, and hemorrhagic tendency was also improved in 3 out of the 7 cases.
4. Twenty eight cases had no side effects by Neurotropin therapy. Only one of the ARC case had mild pruritus 3 months after the treatment.
These data revealed that Neurotropin had beneficial effects on hemophiliacs with HIV infection.
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西川 政勝, 駒田 文彦, 上村 泰弘, 和田 英夫, 出口 克己, 白川 茂
1988 年 19 巻 6 号 p.
632-635
発行日: 1988/12/01
公開日: 2010/08/05
ジャーナル
フリー
Polymyxin B (PMB), a cyclic polycationic peptide antibiotic, inhibited dose-dependently human platelet aggregation induced by a high level (45μg/m
l) of arachidonate (AA) or eicosadienoic acid (C20: 2), whereas this drug had no effect on a low level (0.45μg/m
l) of AA-induced platelet responses. Colistin (polymyxin E), a derivative of PMB, had no inhibitory effect on platelet aggregation induced by a high level of AA or C20: 2. When human platelets were stimulated with AA, phosphorylation of 40K and 20K proteins preceded the aggregation response and platelet response by AA correlated closely with the phosphorylation of these proteins. PMB (100μM) inhibited the phosphorylation of 40K and 20K proteins induced by 45μg/m
l AA, but not the phosphorylation event induced by 0.45μg/m
l AA. PMB also inhibited dose-dependently [Ca
2+]
i elevation in response to a high level (20μg/m
l) of AA, whereas PMB had no effect on a transient increase in [Ca
2+]
i induced by a low level (0.45μg/m
l) of AA. The present results indicate that PMB has no effect on protein phosphorylation systems in human platelets although the drug has been shown to inhibit protein kinase C
in vitro, and suggest that PMB selectively inhibit platelet aggregation induced by a high level of AA, possibly by interacting the lipid matrix of platelet membranes.
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出口 克巳, 岩崎 英二, 鈴木 彦次, 出口 晃, 森 美貴, 大久保 伊都子, 津田 雅之, 和田 英夫, 西川 勝政, 村嶋 正幸, ...
1988 年 19 巻 6 号 p.
636-639
発行日: 1988/12/01
公開日: 2010/08/05
ジャーナル
フリー
The effects of tissue-type plasminogen activator (t-PA) on platelet aggregation in platelet rich plasma (PRP) or washed platelets from healthy subjects were studied. Platelet aggregates induced by ADP in PRP dissociated immediately after the addition of t-PA (15×10
4IU/m
l). This disaggregation was dependent upon the concentration of t-PA (2-3O×10
4IU/m
l), time for the addition of it after ADP (30-180sec.), and the aggregation ability of platelet itself. Platelet aggregates in PRP, added α
2-plasmin inhibitor (final concentration: f. c.; 1IU/m
l) to, dissociated in response to t-PA but not to plasmin (f. c.; 1.5CU/m
l), although t-PA and plasmin induced the dissociation of them in PRP that α
2-PI was not added to. When t-PA or plasmin was added to washed platelet aggregates induced by ADP in the presence of fibrinogen with or without plasminogen, t-PA induced the dissociation of them and plasmin enhanced the extent of them.
These findings suggest that t-PA induced platelet disaggregation relates to the interaction among platelet, fibrinogen and t-PA, in addition to action of plasmin generated following plasminogen activation by t-PA on the platelet surface.
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内川 澄, 菅田 安男, 山口 敦美, 田上 憲次郎, 山崎 博男
1988 年 19 巻 6 号 p.
640-643
発行日: 1988/12/01
公開日: 2010/08/05
ジャーナル
フリー
The platelet thromboxane A
2 synthesizing activity in type II diabetes mellitus was studied by stimulating the washed platelets with either arachidonic acid or thrombin, and by measuring the amoutn of TBX
2 synthesized during the stimulation. In the poorly contolled diabetic state, the mean activity was elevated. The individual activities were not corelated to fasting plasma glucose (Fig. 1). By treating the diabetic state, the activities that were above the average before treatment tended to decrease, while the reverse was true for those that were below the average. The inverse correlation was noted fairly strongly between the pretreatment activities and their changes during treatment (Fig. 2). This finding indicated that the thromboxane A
2 synthesizing activity was under the negative feedback control mechanism, and the mechanism was operating probably at the level of cyclooxygenase, since the same correlations were noted on arachidonic acid as well as thrombin stimulation. The changes in the activities during treatment were not related to the changes in the mean platelet volume. In our study, the changes in activities were measured at near-normoglycemic state, which might resulted in observing the above-discribed control mechanism.
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伴野 雅洋, 上山 護, 浦山 功, 浅田 敏雄
1988 年 19 巻 6 号 p.
644-646
発行日: 1988/12/01
公開日: 2010/08/05
ジャーナル
フリー
Vitamin K brings calcium flux as well as γ-carboxylation in liver cells. Prothrombin in creased in the medium of the guinea pig liver cell culture along with the rise of intracellulr Ca
++ by vitamin K stimulation. This result indicates a secretion mechanism linked to some chemical stimulations. Pregnane-diol and oleic acid had no effect on the Ca
2++ flux but suppressed the prothrombin secretion induced by vitamin K stimulation, although the inhibition mechanism unknown.
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設楽 芳宏, 高橋 道, 佐藤 宏和, 久米 浩太, 成田 昌裕, 村田 誠, 真木 正博, 中尾 祐史, 名古屋 隆生, 才野 佑之
1988 年 19 巻 6 号 p.
647-650
発行日: 1988/12/01
公開日: 2010/08/05
ジャーナル
フリー
We reported a new placental protein having the anticoagulatnt activity in 1983.
This protein, placental coagulation inhibitor, later named Calphobindin (CPB), inhibited the coagulation cascade in which phospholipid and Ca
++ ions are involved.
The inhibitory mechanisms of CPB on blood coagulation are studied, and the results obtained are as follows.
(1) CPB bound to phospholipid in the presence of Ca
++ ions.
(2) CPB inhibited the factor X binding to phospholipid.
It is also possible that CPB interferes with another factors which bind to phospholipid, such as factor Xa and prothrombin.
These are the reasons why clotting system was inhibited by Calphobindin.
CPB concentrations in various fluid smples were measured by ELISA.
The concentrations of CPB in normal plasma {9.96±1.26ng/m
l (n=15)}, pregnant woman's plasma {6.78±0.55ng/m
l (n=15)}, pregnant women's urine {6.15±1.44ng/m
l (n=14)}, normal ascites {128.65±14.54ng/m
l (n=13)}, ascites in peritonitis carcinomatosa {599.23±185.07ng/m
l (n=13)}, amniotic fluid {180.9±97.7ng/m
l (n=43)}, and seminal fluid {4618.9±499.4ng/m
l (n=9)} were shown in parentheses.
The reason why CPB concentrations are high in malignant ascites and seminal fluid is not clear.
CPB has 40% homology in structure with lipocortin and also exists phospholipase A
2 inhibitor activity as in lipocortin.
Therefore, CPB may have complicated functions beside with anticoagulant activity.
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安達 知子, 矢谷 達樹, 渡辺 由佳里, 下島 千穂, 雨宮 照子, 岩下 光利, 中林 正雄, 武田 佳彦, 坂元 正一, 石井 秀美, ...
1988 年 19 巻 6 号 p.
651-653
発行日: 1988/12/01
公開日: 2010/08/05
ジャーナル
フリー
To evaluate the biochemical properties of placental thrombomodulin (TM) in normal pregnancy and toxemia of pregnancy, immunoreactive solubilized TM in 30, 000xg fraction which contained 80% of plasma membrane was measured by ELISA, and the biological activity of TM in 30, 000xg fraction was estimated by protein C activation method.
The levels of TM antigen per mg protein significantly increased during normal pregnancy, and the highest level was detected at 27-31 weeks of gestation. There was no significant difference in the levels of TM antigen between normal pregnancy and toxemia.
The Kd of thrombin for TM was 1.10-2.62nM and showed no significant difference in normal pregnancy and toxemia, and Vmax of thrombin-TM complex for protein C activation also showed no significant difference in normal pregnancy and toxemia.
These data suggest that placental TM has no difference between biochemical properties of normal pregnancy and those of toxemia. Moreover, it is suggested that the increase of TM antigen in normal placenta along with gestational age may be essential to maintain the normal coagulation and fibrinolysis systems in placental circulation in late pregnancy.
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In-111血小板シンチグラフィー, FPA, FDP-Eを中心に
首藤 裕, 長田 鉄也, 清水 隆, 小西 正樹, 山口 寛, 石丸 新, 古川 欽一, 藤巻 道男
1988 年 19 巻 6 号 p.
654-657
発行日: 1988/12/01
公開日: 2010/08/05
ジャーナル
フリー
We evaluated the examinations to predict intra-aneurysmal thrombus-formation by the estimation of FPA and FDP-E in blood, and scintigraphy by In-111-loaded platelets (platelets scintigraphy) in 11 patients.
The FDP-E value was 682.7±761.97ng/m
l (Mean±SD), and seems to reflect the quantity of intra-aneurysmal thrombus. Especially, all 4 cases with FDP-E higher than 500ng/m
l had massive intra-aneurysmal thrombus by CT scan.
The FPA valuue was 33.0±63.25ng/m
l (Mean±SD), and seemed to indicate thrombogenicity. All 5 cases with FPA values higher than 5.0ng/m
l showed strong radioactivity at the same site of intra-aneurysmal thrombus shown by platelets scientigraphy.
Both acute dissecting aneurysm cases showed high FPA values (238ng/m
l and 5.9ng/m
l), while all 3 chronic cases showed normal FPA values (less than 2.0ng/m
l).
In the case of acute dissecting aneurysm with FPA value of 23.8ng/m
l, platele scintigraphy showed strong radioactivity in the false luemn. Moreover, the false lumen was occluded by thrombus after 6 months later, and FPA decreased to 0.6ng/m
l. This case shows that platlet scintigraphy is valuable for the diangosis of the site of active thrombus in aortic aneurysm.
These results suggests that it is possible to predict intra-aneurysmal thrombus formation by measuring FPA and FDP-E and In-111 loaded platelet scintigraphy.
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1988 年 19 巻 6 号 p.
657a
発行日: 1988年
公開日: 2010/08/05
ジャーナル
フリー
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1988 年 19 巻 6 号 p.
657b
発行日: 1988年
公開日: 2010/08/05
ジャーナル
フリー
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今井 英雄, 大柴 進, 高尾 恭一, 澤井 洋子, 今井 重之, 関 泰一郎, 有賀 豊彦
1988 年 19 巻 6 号 p.
658-661
発行日: 1988/12/01
公開日: 2010/08/05
ジャーナル
フリー
The plasminogen activator released from primary cultured rat hepatocyte has been recognized to be identical with a biliary plasminogen activator, Bilokinase (BK) in terms of its enzymatic properties (Blood & Vessel 16, 449, 1985).
In the present investigation, we attempted to find out cell lines derived from human liver which produce and release plasminogen activator, and to elucidate the enzymatic properties of these particular plasminogen activator.
The following results were obtained;
1) HuL-1 cell line (derived from fetal liver) was observed not to secrete plasminogen activator (PA). PLC cell line (derived from hepatocellula carcinoma) and KN 73 (derived from hepatitis) were observed to produce a trace amount of PA.
2) HuH-7 cell line (derived from hepatocellular carcinoma) and KN 7-7 cell line (derived from hepatitis) were observed to produce high active PA releasable into culture medium.
3) The molecular weights of two kinds of PA of HuH-7 were 72, 000 and 50, 000, and the molecular weight of single PA of KN 7-7 was 50, 000.
4) The affinity to fibrin of PA of HuH-7 as well as that KN 7-7 were extremely higy. The affinity to lysine of PA of HuH-7 and KN 7-7 were similarly very high. The activity of these PA on fibrinolysis was not inhibited by UK anti-body, but was inhibited by t-PA anti-body. The above properties of PA of HuH-7 and KN 7-7 were so called melanoma t-PA type characteristic.
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岡田 忠, 山之内 博明, 中島 昭, 塩野 裕之, 酒井 淳一, 真田 進, 若松 伸治, 中村 吉宏, 椙江 勇
1988 年 19 巻 6 号 p.
662-664
発行日: 1988/12/01
公開日: 2010/08/05
ジャーナル
フリー
Mast cells are known to be involved in hyper-sensitivity reactions such as asthma and allergic rhinitis, and may probably participate in fibrinolysis at the site of acute inflammation. Rat mast cells were purified with a modified coil planet centrifuge at an average purity of 97%. In electron microscopy, mast cells were tightly packed with dense granules, and microvilli and cytoplasmic folds were well preserved, suggesting that the separation caused little damages to the cells. Sensitized cells responded well to the antigenic stimuli and released about 60% of histamine. Mast cell lysate showed remarkable fibrinolytic activity when measured with fibrin plates (BfP, BSP) and also showed chymotrypsin -like amydolytic activity, for it released substantial amount of chromophore from S-2586, S-2288, S-2444 and S-2251, S-2238 as well.
Fractions showing fibrinolytic activity were separated with AGI-X2, DEAE Sephadex A-25 ion -exchange column, followed by heparin Sepharose CL6B affinity column chromatography according to the method reported by Schwartz, L. B. et al.
Some of the characteristics of the enzyme are discussed in comparison with the tryptase from human lung mast cells and chymase from rat peritoneal mast cells.
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佐藤 典宏, 桜間 照喜, 家子 正裕, 半田 洋, 藤間 祐紀, 藤江 禎二, 佐藤 雅寛男, 安河内 太郎, 中川 昌一
1988 年 19 巻 6 号 p.
665-667
発行日: 1988/12/01
公開日: 2010/08/05
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フリー
Our studies focused on the necessity of the immediate acidification for measuring the biological activity of tissue-plasminogen activator (t-PA) in the blood samples. The following results were obtained: 1. Biological Activity (BA) and immunological activity (IA) of t-PA increased after venous occlusion. However, the BA of t-PA was considerly lower in plasma than in the blood samples immediately acidified after venous puncture. 2. BA of t-PA in the blood decreased rapidly after sampling without acidification. 3. PAI activity in plasma correlated inversely to the specific activity of t-PA released venous occlustion.
In conclusion, when measuring the t-PA activity in the blood, immediate acidification is necessary to prevent its inactivation probably by PAT co-existing in the plasma.
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須見 洋行, 浜田 博喜, 吉田 悦男, 津島 弘文, 丸山 真杉, 美原 恒
1988 年 19 巻 6 号 p.
668-671
発行日: 1988/12/01
公開日: 2010/08/05
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フリー
The NH
2-terminal amino acid sequences (H
2N-Ala
1-Met
36) of highly purified urinary trypsin inhibitor (UTI) and plasma UTI related acid-stable trypsin inhibitor (ASTI) were found to be completely identical. Neither of the inhibitors was not completely inactivated even under acidic conditions with 70% HCOOH at 60°C for 17hr. In particularly, a much higher stability of antiplasmin activity was confirmed in contrast to the antitrypsin activity which gradually decreased.
The reagent 1, 2-cyclohexanedione was used to modify the guanidino group of Arg residues in the UTI molecule. This resulted in complete disappearance of both activities, possibly indicating that UTI and related inhibitors belong to the “Arg-type inhibitor” previously defined by Laskowsky and Sealock. On the other hand, for modification of the ε-amino group of Lys residue in the UTI molecule, 2, 4, 6-trinitrobenzenesulfonic acid was used. The resultant trinitrophenyl derivative of the inhibitor (TNP-UTI) was found to demonstrate approximately 50 times stronger antiplasmin fibrinolysis than the intact inhibitor. Almost no change in antitrypsin or antichymotrypsin activity occurred as a result of the inhibitor modification. The modified inhibitor was also shown to be a potent inhibitor of non-plasmin mediated fibrinolysis with human leukocyte protease.
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