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)

Twelve healthy young men followed a 10-d controlled diet that included 210 g of fatty fish d-1. The diet was repeated after 18 d, but with lean meat substituted for fish. Blood samples were collected for assessment of serum lipids and haemostatic variables in the plasma. Both experimental diets caused serum triglycerides and plasma factor VIIc to decline to the same extent. The meat diet was also associated with significant changes in plasma levels of tissue plasminogen activator (t-PA) antigen. PA inhibitor type I (PAI-1) antigen, PAI activity, and t-PA activity of the euglobulin fraction of plasma. The fish diet left these variables unchanged from initial values. Thus, in a paired comparison of the two diets, the fish diet was associated with higher levels of t-PA antigen (5.4 vs. 4.7 g ml-1), which is considered to be beneficial with regard to prevention of cardiovascular disease. However, the fish diet was concurrently associated with the putative unfavourable higher levels of PAI-1 antigen (3.0 vs. 1.2 ng ml-1) and PAI activity (6.1 vs. 3.2 IU ml-1), and lower t-PA activity (80 vs. 140 mIU ml-1). Thus it is unclear which of the two diets has the greatest potential in the prevention of cardiovascular disease.
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PMID:Effect of fish diet versus meat diet on blood lipids, coagulation and fibrinolysis in healthy young men. 190 69

New trends in tests for coagulation and fibrinolysis and advances in diagnosis for the hypercoagulable state and utilization of immunological techniques such as various polyclonal and monoclonal antibodies are reported. We discussed (1) the new markers for hypercoagulable states, (2) differential diagnosis of disseminated intravascular coagulation (DIC) and abnormalities of coagulation in liver cirrhosis (LC), and (3) new markers for fibrinolysis and vascular function. Thrombin-antithrombin III complex (TAT) levels were higher in thrombotic diseases than in healthy controls. Therefore, TAT should be a good marker for hypercoagulation as fibrinopeptide A (FPA) and soluble fibrin monomer complex (SFMC). Measurement of TAT, plasma-alpha 2 plasmin inhibitor complex (PIC), and D dimer were useful for differential diagnosis of DIC and liver cirrhosis. t-PA-PAI complex correlated well with t-PA, but not with fibrinolytic parameters such as PIC. The t-PA-PAI complex may be a good marker for the function of the vascular endothelium.
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PMID:[A new advance in theory of blood coagulation and fibrinolysis and its practical application]. 190 12

The content of PAI-I was measured in carcinoma tissues from the stomach and colorectum divided macroscopically into 3 portions: the central part of the carcinoma, the marginal part of the carcinoma containing some normal mucosa, and the normal mucosa. Among these tissues, the highest levels of PAI-I antigen were found in the central part of the carcinoma. On the other hand, no PAI-I antigen or activity was observed in the normal mucosae. The PAI-I produced in the stomach and colorectal carcinoma tissues showed a non-lytic zone with a molecular weight of 54 kDa by reverse fibrin autography, and this 54-kDa band reacted with anti-PAI-I IgG on an immunoblotted nitrocellulose membrane by the avidin-biotin complex method. The contents of PAI-2 in the carcinoma tissues were not significantly different from those in the normal mucosa of the stomach and colorectum. In both the stomach and colorectal carcinomas, the highest value of u-PA/total PA (sum of u-PA and t-PA) was observed in the central part of the carcinoma, followed by the marginal part of the carcinoma, and was lowest in the normal mucosa. We conclude that increased levels of PAI-I in malignant tissue of the stomach and colorectal tract may serve to modulate extra-cellular proteolysis by u-PA.
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PMID:Plasminogen activator inhibitor 1 in human carcinoma tissues. 190 4

The studies showed that t-PA activity was elevated during the acute phase, remained elevated during the recovery stage and declined during the sequelar stage. Lowering of PAI activity was found during the acute phase, which was reversed during the recovery phase and remained significantly elevated during the sequelar stage compared with the controls (P less than 0.001), F test showed that both t-PA and PAI activities changed significantly during various stages (t-PA, P less than 0.01; PAI, P less than 0.001). Because of these changes, the ratio of PAI and t-PA fluctuated during different stages of the disease. This ratio decreased during the acute stage and came close to the normal levels during the recovery phase. The ratio, however, elevated abnormally during the sequelar stage, compared with healthy controls (P less than 0.05), In addition, the result of correlation test and linear regression analysis of serum t-PA and PAI activities in 54 cases showed a significant negative correlation (P less than 0.001) existed between t-PA and PAI activities. The balance of plasma t-PA and PAI activities have the function in maintaining the normal bloodstream in human body. In the process of disease, the abnormality of plasma t-PA and PAI activities may be the different pathological characteristics involved in this stagnation process. If coordinated with differentiation of syndrome in TCM, it may have the important significance to follow-up, and determine prognosis and early diagnosis for certain potential clinical stagnation of blood.
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PMID:[Plasma tissue-type plasminogen activator and plasminogen activator inhibitor activities and their ratio in patients with ischemic stroke associated with stagnation of blood during various stages]. 190 3

Tumour cells possess a cell surface protease referred to as guanidinobenzoatase (GB). The active centre of GB binds the fluorescent probe 9-amino acridine (9-AA) and this binding enables cells possessing active GB to be located by fluorescent microscopy. GB binding of 9-AA was inhibited by prior treatment of sections of tumour tissue with a specific polyclonal antibody recognising the tumour associated protease tissue plasminogen activator (t-PA). GB binding of 9-AA was also inhibited by prior treatment of sections of tumour tissues with PAI-I, a protein inhibitor of plasminogen activatory. We conclude from these studies and kinetic analyses that GB and t-PA are very similar both in structure and function.
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PMID:Evidence for the functional similarity between tumour cell surface guanidinobenzoatase and tissue type plasminogen activator. 190 3

Molecular forms of plasminogen activator inhibitor-1 (PAI-1) and tissue-type plasminogen activator (t-PA), identified by gel filtration and specific immunoassays, were studied in plasma from subjects with normal and elevated PAI-1 levels before and after in vitro or in vivo addition of t-PA. In normal plasma, PAI-1 occurs in three molecular forms, a Mr greater than 700 KDa inactive form of heterogeneous composition, an active 450 KDa form containing PAI-1/vitronectin complex and an inactive peak at Mr 50 KDa containing free PAI-1. Stimulation of platelets results in a significant increase of the 50 KDA form and a slight increase of the 450 KDa form. Patients with increased PAI activity levels have an increase of both the 450 KDa and the 50 KDa forms, whereas patients with thrombotic thrombocytopenic purpura have an increased 50 KDa form. In normal plasma, collected in the presence or absence of D-Phe-Pro-Arg-CH2Cl, t-PA occurs primarily as a Mr greater than 700 KDa form containing t-PA/PAI-1 complex. Addition of high concentrations of t-PA (70 ng/ml) to plasma in vitro or t-PA injection in vivo, results in t-PA inhibitor complexes, including t-PA/ alpha 2 antiplasmin. It is concluded that in subjects with increased PAI-1 levels in plasma, PAI-1 may occur as high molecular weight complexes with vitronectin of which 450 KDa was the most important part and as a 50 KDa inactive form; t-PA circulates primarily in complex with inhibitors. Thus, some of the molecular interactions between PAI-1, t-PA and vitronectin, previously demonstrated in purified systems in vitro, also occur in plasma.
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PMID:Molecular forms of plasminogen activator inhibitor-1 (PAI-1) and tissue-type plasminogen activator (t-PA) in human plasma. 190 71

Urokinase-type (u-PA) and tissue-type plasminogen activator antigen (t-PA) as well as plasminogen activator-inhibitor activity were determined in seminal plasma and lysates of the respective spermatozoas in 67 ejaculate of males in infertile marriage without genito urinary pathology. U-PA was determined by a competition RIA, t-PA by an ELISA and PAI by a spectrophotometric assay. 15 patients showed normozoospermia, 11 azoospermia and 41 oligoasthenoteratozoospermia (OAT-syndrome). In lysates of spermatozoas, significantly higher levels of both plasminogenactivators and PAI were found in patients with OAT syndrome as compared to those exhibiting normozoospermia. Whereas PAI was absent in the seminal plasma of normozoospermic ejaculate, patients with azoospermia (180 +/- 13 mU/ml.) and OAT-syndrome (60 +/- 5 mU/ml.) showed high PAI levels. The similarly high values of t-PA (190.8-227.8 ng./ml.) and u-PA (19.4-32 ng./ml.) in the same compartment confirm their predominantly prostatic origin and seem to have no influence on the quality of the ejaculate.
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PMID:Fibrinolytic parameters in spermatozoas and seminal plasma. 190 31

We evaluated a new enzyme immunoassay for determination of t-PA-PAI-1 complex (PAI-C) and studied the clinical utility of measuring PAI-C. This assay was performed by the capture/tag antibody technique using polystylene beads, in which the beads were coated with monoclonal antibody against PAI-1 and anti-t-PA polyclonal antibody was tagged (TDC-88, TEIJIN-LIMITED, Japan). The assay gave an excellent sensitivity with a detection limit of 0.1 ng/ml, and we were able to detect a trace amount of PAI-C in normal plasma. PAI-C in 6 volunteers showed significant daytime fluctuations. The normal value of PAI-C in plasma was below 13.8 ng/ml (n = 40). PAI-C levels in patients with accelerated fibrinolysis (n = 31) ranged from 2.9 to 66.4 ng/ml and 15 of them were outside the normal range. However, all of patients with DIC (n = 10) showed abnormally high PAI-C levels. In patients with accelerated fibrinolysis, PAI-C values correlated with t-PA antigen (r = 0.838), PAI-1 antigen (r = 0.519), ATIII activity (r = -0.669) (p less than 0.01) and D dimer levels (r = 0.391, p less than 0.05). However, PAI-C values did not correlate with plasminogen and alpha 2PI activity, alpha 2PI-plasmin complex or the FDP-E level in these patients. Our data suggests that PAI-C may be a new molecular marker that reflects t-PA release from endothelial cells and a useful indicator to study hypercoagulable states.
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PMID:[Evaluation of a new enzyme immunoassay method for determination of t-PA-PAI-1 complex]. 190 14

The influence of the TXA2-synthetase inhibitor OKY-046 (Xanbon) on haematological findings for the coagulation-fibrinolysis system and platelet aggregation was investigated in patients with subarachnoid bleeding during or after the administration. Changes in alpha 2-PI activity and the levels of fibrinogen, t-PA and PAI antigen were observed. Especially, PAI activity and PAI antigen were found to be significantly increased as compared with levels before the administration. On the other hand, the platelet aggregation induced by various agents and the activity of AT-III were not greatly altered after the administration of OKY-046.
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PMID:Changes in parameters of the coagulation-fibrinolysis system and platelet function after OKY-046 administration to patients with ruptured aneurysm of the cerebral artery. 190 91

Severe lower limb ischemia in patients with acute arterial occlusion was associated with a significant increase in systemic fibrinolytic activity. Plasmatic level of t-PA activity was twice the normal value at the peak of ischemia. This level declined gradually within no less than 40 hours after reperfusion procedure or limb amputation had reverted the ischemic state. In spite of major tissue damage and surgical trauma, plasmatic PAI activity stayed within normal range, and did not increase within the first 24 hours postoperatively. These findings strongly suggest that acute ischemia initiates systemic induction of excessive and continuous release of t-PA, which outweighs any anticipated increase in PAI activity.
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PMID:Changes in plasmatic tissue-type plasminogen activator and plasminogen activator inhibitor activity during acute arterial occlusion associated with severe ischemia. 191 Feb 11


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