Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.21.73 (urokinase-type plasminogen activator)
 10,685 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasminogen activator (PA) activity of the gastric mucosa of liver cirrhotics was measured by use of Glt-Gly-Arg-MCA as the substrate. Gastroduodenal mucosal lesions were more frequently seen in cirrhotic patients with red spot of the gastric mucosa (RS (+) group) as compared to the cases without red spot (RS (-) group). RS (+) group had poor liver function as compared to RS (-) group. PA activity of the gastric mucosa in RS (+) group was higher than RS (-) and control groups. Furthermore, the elevated PA activity was highly associated with severe liver damage estimated by routine liver function test and Child's classification. Separately quantitative assay of PAs was performed by using Lysine-Sepharose 4B chromatography. Both the tissue type and urokinase type PA were higher in the RS (+) group than in control group. These results suggest that accelerated tissue fibrinolytic activity is one of the causative factors of gastric mucosal bleeding in cirrhotic patients with red spot.
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PMID:[Plasminogen activator activity and its separative measurement in the gastric mucosa of liver cirrhotics]. 192 Aug 98

Despite the limitations of individual ischemia models, experience with fibrinolytic agents suggests that 1) early intervention with rt-PA may result in rapid thrombolysis, functional recovery, and decreased mortality in small animal stroke thromboembolism models, 2) rt-PA has no general effect on clinical recovery following MCA occlusion and reperfusion in the nonhuman primate at dose rates capable of producing very high circulating rt-PA levels, while u-PA has an apparently salutary effect, and 3) intravenous infusion of rt-PA or u-PA early after ischemia/infarction in several model systems is not associated with significant intracerebral hemorrhage. The true clinical relevance of these general impressions must await the completion of human studies and studies in well-conceived models designed to define the vascular consequences to be expected from reperfusion achievable with thrombolytic agents.
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PMID:Relevance of focal cerebral ischemia models. Experience with fibrinolytic agents. 226 Jan 42

Fibromuscular dysplasia (FMD) is well known owing to the characteristic angiographical finding of a "string of beads" appearance, but intracranial involvement with this disease is extremely rare. Moreover, to our knowledge, only seven cases that had repeated angiograms disclosed progression of FMD lesion in the literature. Such cases of intracranial FMD which showed progression in the follow-up angiography are reported. Case 1: A 8-year-old boy was referred to our hospital because of aphasia and right hemiplegia following right hemiconvulsion. Left carotid angiography on the 7th day from the onset revealed a "string of beads" appearance involving the left middle cerebral artery from M1 to M2 portion. He was treated with low molecular dextran, urokinase and steroid. After these drugs were administered, his speech was normalized. A repeat left angiogram performed two months later disclosed definite increase in the degree of stenosis associated with FMD. Perivascular sympathectomy around common and internal carotid artery and superior cervical ganglionectomy on the left side carried out on the 70th day from the onset. Postoperative left carotid angiogram showed improvement of the stenosis markedly, and the motor disturbance was improved gradually. Case 2: A 34-year-old woman presented with head dullness and disorientation suddenly. Left carotid angiogram on the third day from the onset showed a "string of beads" appearance from C1 to M1 portion. Follow-up angiography three days later revealed some progression of the stenosis. Furthermore a repeat left angiogram disclosed occlusion of left internal carotid artery at the C2 portion. Left STA-MCA bypass surgery was performed on the 61st day from the onset.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Two cases of intracranial fibromuscular dysplasia whose repeated angiography disclosed progression of the lesion]. 332 87

An inactive form of human urinary kallikrein (inactive HUK) was highly purified from fresh urine collected from healthy men. Inactive HUK was separated from the active kallikrein (HUK) initially presents in the urine by affinity chromatography on a column of aprotinin immobilized on Sepharose 4B and further purified by gel filtration, ion-exchange chromatography and immunoaffinity chromatography on an anti-HUK antibody immobilized Sepharose 4B column. Inactive HUK was rapidly activated by a trace amount of trypsin. While, plasmin, urokinase, thrombin and chymotrypsin caused no activation of inactive HUK. The molecular weights of inactive HUK and HUK were estimated to be 4.8 X 10(4) and 4.5 X 10(4), respectively. The molecular weight of active HUK generated from inactive HUK by the action of trypsin (HUK'') was almost the same as that of HUK. The mobility of inactive HUK was slightly slower than that of HUK on both immunoelectrophoresis and polyacrylamide gel disc electrophoresis. On the other hand, the electrophoretic mobility of HUKK'' was almost the same as that of HUK. These two types of active HUK had no significant difference in the Km values for H-Pro-Phe-Arg-MCA hydrolysis and inhibition profiles by various protease inhibitors and anti-HUK antibody. Inactive HUK was unable to be measured by the direct radioimmunoassay (RIA) but HUK" generated by the action of trypsin could be measured by the RIA.
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PMID:An inactive form of kallikrein in human urine. 354 16

Electrophoretic analysis of plasminogen activators from pig heart, human uterus, human plasma and human melanoma cells was performed in SDS-polyacrylamide gradient slab gels containing plasminogen and casein. Direct visualization of activator activity bands in polyacrylamide gels was achieved after removal of SDS, incubation in buffer, and staining with Coomassie brilliant blue. Tissue activator extracted from pig hearts displayed a molecular weight of 72000 and migrated similarly to activator secreted by human melanoma cells and to one activator component present in extracts of human uterus. Immunoadsorption experiments with melanoma cell activator antiserum indicated that these 72-kDa activators are all related immunologically. Human uterus also contained a second activator component with a molecular weight 55000, which migrated similarly to a higher molecular weight component of urokinase and cross-reacted with urokinase antiserum. We conclude that the 72-kDa uterine activator component represents a tissue activator and the 55-kDa component represents a urokinase-like activator. A euglobulin solution from venous occlusion plasma displayed multiple bands of plasmin activity in the Mr range 85000-96000. Two activator components were also present, one of Mr 72000 and another of Mr 62000. The 72-kDa euglobulin activator was adsorbed by MCA antiserum, and we conclude that this component represents vascular activator. The 62000 activator also had weak plasminogen-independent caseinolytic activity and was not affected by either melanoma cell activator or urokinase antisera. Conclusions concerning its identity cannot be made at this time.
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PMID:Comparative electrophoretic analysis of human and porcine plasminogen activators in SDS-polyacrylamide gels containing plasminogen and casein. 634 80

Intra-carotid urokinase (UK) infusion in 20 patients with acute internal carotid artery (ICA) territorial ischemic stroke achieved immediate recanalization in 45% and the clinical outcome in patients with recanalization was superior to that of patients without recanalization. The procedure was most effective in patients with smaller arterial occlusions: 7 of 10 patients with MCA branch occlusions (M2 to M4) achieved recanalization compared to only 2 of 10 with distal ICA or M1 occlusions, which should be an important issue for the critical evaluation of the efficacy of thrombolytic therapy (TT). Hemorrhagic transformation was observed in 9 patients on CT scan; petechial hemorrhage in 5 and intraparenchymal hematoma formation in 4. Among 4 patients with hematoma formation, clinical deterioration was seen in 3 cases and the angiography at the immediate end of the UK infusion showed recanalization in only one patient. The average dose of UK in patients with parenchymal hematoma formation was higher than that of patients without hemorrhagic transformation (123.3 x 10(4) units vs 101 x 10(4) units). The administration of a large dose of UK, probably more than 100 x 10(4) units, and the absence of immediate recanalization seemed to increase the risk of parenchymal hematoma formation. Despite the effort of investigators, the in-hospital time delay for the TT was significant which was mainly related to the time consuming preparation for angiography especially during night. A more effective system for the earlier intervention of acute ischemic stroke needs to be developed.
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PMID:Intra-carotid thrombolytic therapy in acute ischemic stroke of carotid arterial territory. 800 97

A conjugate of annexin V and the B-chain of urokinase was prepared and its fibrinolytic properties were studied. First, a mutant of annexin V was constructed with an N-terminal extension of six amino acids (Met-Ala-Cys-Asp-His-Ser) and with Cys316 mutated to Ser; this molecule was expressed in Escherichia coli. The urokinase B-chain was prepared by limited reduction of the interchain disulfide bond between the A- and B-chains of urokinase. These two molecules were then then connected by a disulfide bond and purified to yield a 1:1 stoichiometric conjugate. The conjugate had the same catalytic activity as urokinase against a synthetic substrate, Glt-Gly-Arg-MCA, and a similar plasminogen activating activity. The conjugate showed the same binding affinity for phosphatidylserine-containing membranes as annexin V. The in vitro fibrinolytic activity of the conjugates on clots prepared from platelet-rich plasma was comparable to that of urokinase. However, the conjugate showed 3-4-fold stronger in vivo thrombolytic activity than urokinase in a rat pulmonary embolism model, while having essentially the same plasma clearance rate as urokinase or B-chain. These results show that annexin V is a useful agent for targeting plasminogen activators to phospholipid-containing thrombi.
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PMID:Preparation and characterization of a disulfide-linked bioconjugate of annexin V with the B-chain of urokinase: an improved fibrinolytic agent targeted to phospholipid-containing thrombi. 854 74

We reported a rare case of Moyamoya disease in the aged associated with cerebral embolism. A 76-year-old female was brought into our hospital by ambulance 30 min after an attack of fainting. She had no past history of cerebrovascular disease. On admission her consciousness level was JCS 3-IA and she showed Rt. hemiparesis ECG exhibited Af tachycardia. No abnormal region was recognized on brain CT. Emergency cerebral angiograms (AG) disclosed that unexpectedly she had Moyamoya disease. Stenotic or occluded lesions were seen from bilateral IC terminal portions to MCA and ACA, and basal moyamoya vessels were visualized. Transdural anastomosis was poor and posterior circulation was the main source of collateral flow. Mode of onset and neurological signs suggested that the cause of the attack was Lt. MCA occlusion at its sphenoidal portion by cardiogenic embolism. Superselective endovascular fibrinolysis was carried out by the use of urokinase and low molecular weight Dextran and Lt. MCA was able to be recanalized. She was recovered without neurological deficit. Lt. STA-MCA anastomosis and encephalo-myosynangiosis was performed in the chronic stage because stenosis had remained in Lt. MCA and hypo-perfusion in bilateral frontal lobes was presented on SPECT. Post-operative AG demonstrated that Lt. MCA was occluded but Lt. frontal lobe was supplied with plenty of blood flow from Lt. STA. During the next day morning, she had another attack of fainting and showed moderate consciousness disturbance and motor aphasia. No abnormal change was noticed on brain CT. Emergency AG revealed that Lt. STA had become stuffed up with embolic and bypass flow had disappeared. Superselective endovascular fibrinolysis was able to recanalize the blood flow imperfectly, but mild motor apasia remained due to Lt. frontal infarction.
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PMID:[A case of moyamoya disease in the aged associated with cerebral embolism]. 855 66

Comparative studies of membrane-associated, intracellular and secreted activities of serine (uPA, kallikrein-like proteinase) and metalloproteinases (type I and IV collagenases) were carried out on rat embryo fibroblasts, sequentially immortalized and transformed by two different genes. Using this experimental model it was shown that (1) activity of uPA was expressed at the stage of immortalization solely; (2) intracellular and secreted activity of type I and IV collagenases decreased during process of transformation, (3) kallikrein-like proteinase activity was not revealed either in the primary or in transformed cells, (4) Z-Phe-Arg-MCA hydrolysis was the result of the action of cysteine proteinases alone; the increase in this activity was correlated with the stages of oncogenic transformation of fibroblasts.
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PMID:Plasminogen activators, kallikrein-like proteinase and type I and type IV collagenases at various stages of oncogenic transformation. 879 90

To clarify the pathophysiological role of cathepsins in rheumatoid arthritis (RA), we investigated whether cathepsin B or cathepsin L was increased in synovial fluid (SF) of RA joints, and whether the cathepsin isolated from SF of RA patients activated pro-urokinase or not. Thus, we estimated the content of cathepsins in SF of RA patients by measuring their activities by fluorospectrometry, using Z-Phe-Arg-MCA as the substrate. Cathepsin activity was approximately 4-fold higher in the SF of RA patients than in those of patients with osteoarthritis. Cathepsin B and cathepsin L were separated by cation-exchange column chromatography. As a result, a large peak corresponding to cathepsin B and a very small peak corresponding to cathepsin L were detected. Biochemical sequential fractionation of the cathepsin purified from the SF showed that the large peak was mainly composed of cathepsin B. This purified enzyme induced conversion of pro-urokinase to urokinase, and the Km for pro-urokinase was approximately 8.27 microM. These findings indicated that an imbalance between cathepsin B and its inhibitors occurred due to increased concentrations of active cathepsin B in RA articular lesions, and that cathepsin B might be related to the degradation of cartilage in RA by activating the fibrinolytic cascade.
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PMID:Cathepsins B and L in synovial fluids from patients with rheumatoid arthritis and the effect of cathepsin B on the activation of pro-urokinase. 1074 Sep 81


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