Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P00750 (PLA)
 16,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasminogen and tissue-type plasminogen activator bind to the platelet surface, and as a result, the catalytic efficiency of plasminogen activation is significantly enhanced. The plasmin that is generated on or near the platelet is known to affect a number of platelet surface events. For this reason, we examined the effect of plasmin on platelet-surface plasminogen activation and its determinants. Specifically, we measured the effects of plasmin treatment of platelets (1 caseinolytic unit/mL for 1 h at 37 degrees C) on plasminogen, tissue-type plasminogen activator, and plasmin binding to the unactivated and ADP-activated platelet surface; and on the kinetics of plasminogen activation on the platelet surface. Following plasmin treatment, the number of plasminogen binding sites on unactivated platelets increased by 78% (from 46,000 +/- 4000 to 88,000 +/- 9000 sites/platelet), while the number of tissue-type plasminogen activator sites did not change, and the number of diisopropyl fluorophosphate (DFP)-inactivated plasmin (DFP-plasmin) binding sites decreased by 31% (from 92,000 +/- 11,000 to 65,000 +/- 7000 sites/platelet); the dissociation constants (Kds) for each of these binding processes did not change significantly following treatment. On ADP-activated platelets, plasmin treatment increased the number of plasminogen binding sites by 41% (from 188,000 +/- 17,000 to 265,000 +/- 25,000 sites/platelet), decreased the number of plasmin binding sites by 28% (from 219,000 +/- 41,000 to 157,000 +/- 24,000 sites/platelet), and did not affect the number of tissue-type plasminogen activator sites; again, the Kds for each of these binding processes did not change significantly following treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Kinetics and mechanism of platelet-surface plasminogen activation by tissue-type plasminogen activator. 813 Feb 11

In our experience, severe pulmonary tuberculosis (PTB) is often complicated by deep venous thrombosis (DVT). Because of the association between inflammation and haemostatic changes that can result in a hypercoagulable state, we have prospectively examined such predisposing factors in representative patients. Sequential analyses in a control group with active PTB showed anaemia, thrombocytosis, elevations in plasma fibrinogen, fibrin(ogen) degradation products (FDP), tissue plasminogen activator (t-PA) and inhibitor (PAI-1) with depressed antithrombin III levels. Age, sex and disease matched individuals with venographically proven DVT had higher FDP (15.8 +/- 14.3 v 3.2 +/- 1.7 micrograms/ml:P < 0.01), t-PA (19.4 +/- 14.9 v 11.3 +/- 0.8 ng/ml:P < 0.01), and functional PAI-1 activity (11.6 +/- 6.3 v 4.2 +/- 4.1:P < 0.01) with lower platelet counts (347 +/- 110 v 563 +/- 230 x 10(9)/1:P < 0.01). Fibrinogen levels in all patients rose during the first 2 weeks of therapy and, together with related disturbances, corrected within 12 weeks. In conclusion, elevated plasma fibrinogen with impaired fibrinolysis coupled with a decrease in antithrombin III and reactive thrombocytosis would appear to favour the development of DVT in PTB.
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PMID:Acute-phase response and the hypercoagulable state in pulmonary tuberculosis. 870 31

Variations in erythrocyte glutathione peroxidase activity, serum concentrations of lipids and lipoproteins and in blood coagulation and fibrinolysis during the menstrual cycle were studied in healthy young women. Blood samples were drawn twice a week for 9 weeks. A group of males was used for estimation of the influence on the results of factors which were not related to the menstrual cycle. Variations during the menstrual cycle were demonstrated in several of the factors analysed. The activity of glutathione peroxidase was lowest at ovulation. The clotting activity of factor II+ VII+X and the concentration of fibrinogen were lowest during mid-cycle, and the number of platelets increased in the follicular phase (days 5-9). Statistically significant variations in the fibrinolytic factors analysed (tissue plasminogen activator (t-PA) and plasminogen activator inhibitor (PAI) were not observed during the menstrual cycle. The serum concentrations of cholesterol and LDL cholesterol were significantly higher at the start of the menstrual cycle (days 3-8) than later in the cycle (days 19-24). The concentration of HDL cholesterol was lowest in the late luteal phase (days 23-28).
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PMID:Variation in risk indicators of cardiovascular disease during the menstrual cycle: an investigation of within-subject variations in glutathione peroxidase, haemostatic variables, lipids and lipoproteins in healthy young women. 876 28

We describe here the case of a 60 years man with POEMS syndrome associated with renal tumor and vascular lesions. The patient had osteosclerotic myeloma IgA-lambda, polyneuropathy, endocrinopathy and skin changes. In addition, he developed renal clear cell carcinoma and gangrena of lower limbs. The humoral study showed thrombocytosis, high levels of IL-1beta and IL-6 and of some coagulative/fibrinolytic and endothelial factors (von Willebrand factor, plasmin-antiplasmine complexes, plasminogen activator). We suggest the hypothesis that these factors are capable of determining some manifestations of POEMS syndrome.
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PMID:POEMS syndrome with vascular lesions and renal carcinoma - possible role of cytokines. 962 Aug 93

The authors describe the case of a 60-year-old man with POEMS syndrome associated with vascular lesions. The patient had osteosclerotic myeloma IgA (lambda), polyneuropathy, endocrinopathy, and skin changes. Subsequently, he developed gangrene of the lower limbs with no response to heparin therapy. The humoral study showed thrombocythemia, high levels of interleukin-1beta (IL-1beta) and IL-6 and of some coagulative/fibrinolytic and endothelial factors (von Willebrand factor, plasmin-antiplasmin complexes, plasminogen activator, and endothelial adhesion molecule ICAM-1). The authors suggest that these factors, induced by the increased levels of cytokines, could be responsible for microvascular damage, gangrene, and heparin resistance.
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PMID:POEMS syndrome with vascular lesions: a role for interleukin-1beta and interleukin-6 increase--a case report. 982 51

To clarify the possible role of persistent thrombocytosis after splenectomy as being a predisposing factor causing thromboembolism. Blood coagulation profiles were studied in 35 patients (20 M and 15 F, mean age 42 +/- 17.5) suffering from thrombocytosis (> 500,000/dl) who underwent splenectomy for non-malignant and non-traumatic diseases. Seventy healthy subjects acted as a control group. Tests were performed 6 months after the operation and for both groups (patients and controls) blood samples were collected for: platelets, fibrinogen, PT, APTT, AT III, plasminogen, F1 + 2, t-PA and DNA analysis for F V, F II and MTHFR. After one year all subjects were controlled for thrombocytosis, genomic abnormalities and venous thrombosis. All the analyses were performed according to the Statistical Package for Social Science. The significance of the differences in means was evaluated by non-parametric tests, differences with a P value < 0.05 being considered significant. Increased plasma levels of fibrinogen, D-dimer, F1 + 2 and PAI-1 were found in the patients compared with the control group. TPA was significantly lower in the patients than in the controls. At the one year follow-up, two patients with genetic polymorphism had suffered deep venous thrombosis. Our findings indicate that splenectomy contributes to abnormal platelet aggregation and endothelial cell activation with hypercoagulability.
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PMID:[Blood coagulation changes in patients with post-splenectomy persistent thrombocytosis]. 1158 73

Serial changes in coagulation and fibrinolysis studied among 42 patients admitted to hospital with a wide variety of injuries are reported. The first hours after trauma are dominated by an acceleration of fibrinolysis (clot lysis) and clotting time which are often followed by an abrupt rebound to prolonged fibrinolysis and normal clotting. Evidence is presented that acceleration of fibrinolysis is due to flooding of the circulation by plasminogen activator and that prolongation is probably due to an inhibitor. A prolonged prothrombin time, increased prothrombin consumption index, an acceleration of the heparin-retarded clotting time, and a fall in the platelet count are also frequent during the first hours after injury. There is evidence also of an early deficiency in factor V and the onset of a fall in factor VII and prothrombin. The following days are characterized by continued prolongation of fibrinolysis, a lengthening of clotting time, and an increased prothrombin consumption index suggestive of a defect in thrombo-plastin generation. Subsequent periods of prolonged fibrinolysis may develop. Prothrombin time often continues prolonged for one to three weeks and may vary phasically; plasma prothrombin and factor VII are reduced but there is now little change in factor V. The platelet count continues to fall for one to three days, then a thrombocytosis develops, often with abnormally high platelet levels, a week or so later. Plasma fibrinogen rises within 24 hours to reach a plateau maximum a few days later and levels remain high for prolonged periods in the severely injured. Various changes are related to or influenced by the severity of trauma. Mechanisms are discussed, including thrombosis in vivo, and reference is made to homeostatic significance and its possible breakdown.
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PMID:COAGULATION AND FIBRINOLYSIS IN INJURED PATIENTS. 1410 15

Essential thrombocythemia (ET) is one of the chronic myeloproliferative disorders which is characterized by megakaryocytic metaplasia. The most common complications of ET are thrombohemorrhagic events. The overall incidence of thrombosis is 70% and hemorrhagic events about 10-15%. We investigated 21 patients with ET. Median age was 51.0 (range 41-61 years). 29 healthy controls were similar in aspects of sex and age. Patients had examined whole blood count, blood smear, platelet counts, prothrombin time (PT), activated partial thromboplastin time (aPTT), euglobulin lysis time (ELT), fibrin degradation products (FDP), thrombin-antithrombin III complexes (TAT), plasmin-alpha2-antiplasmin complexes (PAP), antigen of tissue and urokinase plasimogen activators (t-PA:Ag, u-PA:Ag), antigen of tissue plasminogen activator inhibitor types 1 and 2 (PAI-1:Ag, PAI-2:Ag), fibrinogen, antitrombin (AT) and alpha2-antiplasmin (alpha2-AP) activity. TAT concentraction (26.83 ng/ml) was significantly higher in ET group than in controls (3.41 ng/ml). We also showed in patients with ET significantly prolonged aPTT (50.12 s) and elevated platelet count (859.5 G/l). Fibrinolytic parameters PAI-1:Ag (56.2 ng/ml) and PAP (662.5 ng/ml) were significantly higher in patients with ET. High TAT concentration means enhanced thrombinogenesis and prolonged aPTT-disturbances in coagulation activation process. A cause of increased plasminogenesis is increased concentration of PAP.
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PMID:[Haemostatic disturbances in essential thrombocythosis]. 1794 61

Warm water bathing is a popular recreational activity and is frequently used in rehabilitation medicine. Although well tolerated in most cases, there are reports indicating an increased risk of thrombotic events after hot tub bathing. The effects of a 45 min thermoneutral bath followed by a 50 min bath with increasing water temperature (maximum 41 degrees C) until reaching a body core temperature of 39 degrees C on factors of blood coagulation and fibrinolysis were studied in eight healthy male volunteers. Blood was obtained after a 45-min resting period as control and after the thermoneutral and hyperthermic bath as well as after another 45 min recovery period at the end of the study. Hyperthermic immersion (HI) lead to a shortening of activated partial thromboplastin time (aPTT) (P < 0.05). Fibrinogen concentration decreased immediately after HI (P < 0.05) but increased during recovery (P < 0.05). Plasminogen activator inhibitor (PAI) activity decreased during HI (P < 0.05), D-dimer concentration was not found to change. Thrombocyte count increased (P < 0.05) during HI. The increases in tissue-type plasminogen activator concentration as well as leucocyte count during HI were due to haemoconcentration. Prothrombin time, PAI-activity and granulocyte count decreased during thermoneutral immersion (P < 0.05). Warm water bathing leads to haemoconcentration and minimal activation of coagulation. The PAI-1 activity is decreased. A marked risk for thrombotic or bleeding complications during warm water bathing in healthy males could not be ascertained.
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PMID:Changes in the haemostatic system after thermoneutral and hyperthermic water immersion. 1804 35

Patients with inflammatory bowel disease are susceptible to microvascular thrombosis and thromboembolism. The increased incidence of thrombosis is accompanied by enhanced coagulation and abnormalities in platelet function. Clinical studies have revealed thrombocytosis, alterations in platelet activation, enhanced platelet-leukocyte interactions, and elevated plasma levels of prothrombotic cytokines. This study was directed toward determining whether the thrombocytosis, altered platelet functions, and enhanced platelet-leukocyte interactions observed in patients with inflammatory bowel disease can be recapitulated in the dextran sodium sulfate and T-cell transfer models of murine colonic inflammation. Flow cytometry was used to characterize platelet function in heparin-anticoagulated whole blood of control mice and in mice with colonic inflammation. Platelets were identified by characteristic light scattering and membrane expression of CD41. Thiazole orange labeling was used to differentiate between immature and mature platelets. Platelet activation was monitored using the expression of an activation epitope of GPIIb/IIIa integrin. The combination of CD41, CD45.2, Gr-1, F4/80, and isotype control antibodies was used to detect and quantify aggregates of leukocytes, neutrophils, and monocytes with platelets. Our results indicated that colonic inflammation is associated with thrombocytosis, leukocytosis, and the appearance of immature platelets. An increased number of circulating activated platelets was detected in colitic mice, along with the formation of aggregates of leukocytes (PLA), neutrophils (PNA), and monocytes (PMA) with platelets. Selectin blockade with fucoidin inhibited dextran sodium sulfate-induced PLA formation. The findings of this study indicate that many features of the altered platelet function detected in human inflammatory bowel disease can be reproduced in animal models of colonic inflammation.
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PMID:Platelet abnormalities during colonic inflammation. 2351 12


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