Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.4.21.5 (thrombin)
33,306 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To study the existence of platelet activation before the onset of cerebral infarction, the ultrastructural features of platelets (7-day survival) and coagulation-fibrinolytic markers (70-100-min life span) were measured 2-12 h (acute phase), 7 days (subacute phase) and 6 months (chronic phase) after onset in 18 patients with cerebral infarction. Seven patients with atherosclerosis but without cerebral infarction and eight healthy subjects were studied as controls. Ultrastructural study included folds, pseudopods, vacuoles and centralization in addition to immunochemical staining such as platelet peroxidase and fibrinogen. Furthermore, beta-thromboglobulin, platelet factor-4, thrombin antithrombin complex and alpha(2)-plasmin inhibitor plasmin complex were examined as coagulation-fibrinolytic markers. Ultrastructural study of circulating platelets demonstrated no difference between acute and chronic phases and little difference between cerebral infarction and atherosclerosis, although plasma coagulation-fibrinolytic markers showed an increase in cerebral infarction at the acute phase but no difference among the chronic phase of cerebral infarction, atherosclerosis and normal healthy subjects. It is considered that shape change in circulating platelets was caused by pre-existed atherosclerosis rather than the thrombotic event itself though coagulation-fibrinolytic markers were derived from the thrombotic event.
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PMID:Possible existence of platelet activation before the onset of cerebral infarction. 1105 16

Oral thrombin inhibitors are under development as potential drugs for prophylaxis and treatment of thrombotic events. The effect of pretreatment with two direct thrombin inhibitors, melagatran and inogatran, was evaluated in a rat model of cerebral infarction. Ischaemic stroke was induced by photochemical reaction after an injection of Rose Bengal and focused posterior and to the right of the intersection of the coronal and sagittal sutures on the intact calvarium. A single oral dose of melagatran (30 micromol/kg) significantly reduced the volume of the cortical infarct by 53% (P<.05) compared with control. In addition, following intravenous inogatran (6 micromol/kg) or oral inogatran (100 micromol/kg), the volume of the cortical infarct decreased by 83% and 19%, respectively, compared with control. This study showed that experimental focal ischaemic infarction, elicited by photochemically induced endothelial cell damage, can be significantly reduced with melagatran and inogatran, direct thrombin inhibitors.
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PMID:The effects of oral and intravenous direct thrombin inhibitors on the size of photochemically induced cortical infarction in rats. 1132 5

Large left atrium (LA) and LA appendage (LAA) dysfunction are known to relate to cardiogenic thromboembolism, so the present study investigated the relation of the atrial fibrillatory wave (F wave) amplitude to hemostatic markers and LAA function. Transthoracic and transesophageal echocardiographic studies were performed in 82 consecutive patients with chronic, nonrheumatic atrial fibrillation (AF). Patients were divided into 2 groups according to F wave amplitude in lead V1 on the 12-lead ECG: coarse AF (the greatest amplitude of F wave > or =1 mm, n=44) and fine AF (<1 mm, n=38). Plasma levels of thrombin-antithrombin III complex, D-dimer, platelet factor 4 and beta-thromboglobulin were determined. Compared with patients with coarse AF, those with fine AF had lower LAA peak flow velocity (p<0.05) and higher prevalence of embolic cerebral infarction (50% vs 27%, p<0.05). Platelet activity did not differ between the 2 groups; however, plasma levels of thrombin-antithrombin III complex and D-dimer were significantly higher in patients with fine AF than in those with coarse AF (p<0.05). Multiple logistic regression analysis showed that fine AF was independently associated with cerebral embolism. Therefore, the presence of fine F wave in V1 would be a useful marker of LAA dysfunction and hypercoagulability, and indicate a risk for cerebral embolism in patients with chronic, nonrheumatic AF.
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PMID:Relation of fibrillatory wave amplitude with hemostatic abnormality and left atrial appendage dysfunction in patients with chronic nonrheumatic atrial fibrillation. 1134 39

Spontaneous echo contrast in the descending aorta (DA-SEC) was examined as a possible risk factor for cerebral thromboembolism. In 19 patients (10 males, 9 females) in the chronic stage of cerebral infarction, abnormal findings by transesophageal echocardiography, flow dynamics of the common carotid artery (CCA), and hemostatic factors including blood coagulation and fibrinolysis were investigated. In nine patients, DA-SEC was detected, and SEC in left atrium (LA-SEC) was detected in nine patients. The DA-SEC positive group showed decreased blood-flow velocity (BFV) in bilateral CCA, high levels of thrombin-antithrombin III complex (TAT) and prothrombin fragment 1.2 (F1+2), a decrease in platelet count and a slight increase in D-dimer, which means an activated state of thrombin generation and resulting fibrinolysis, compared to the DA-SEC negative group. On the other hand, the LA-SEC positive group showed normal BFV in CCA and only a slight increase in D-dimer. We conclude that the condition producing DA-SEC is a stronger risk factor for cerebral infarction than that producing LA-SEC.
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PMID:Spontaneous echo contrast in descending aorta correlates with low blood-flow velocity in carotid arteries and hemostatic abnormalities. 1171 27

The activity of thrombinogenesis process is shown by thrombin restrain reaction by its physiological inhibitor antithrombin III, as a result of which biologically nonactive thrombinantithrombin III complexes (TAT) are created. The aim of the study was to evaluate TAT complexes in the blood of ischaemic stroke patients. 25 persons with ischaemic stroke and 15 controls took part in the examination. Taking into consideration brain CT outcomes 2 groups of patients were selected: with ischaemic stroke of small and great extent. The patients were also divided into a group of patients with less severe and with more severe ischaemic stroke, and into a group of patients with ischaemic stroke with and without accompanying atrial fibrillation. TAT complexes were determined with an enzyme-linked immunosorbent assay method on days 1st, 5th, and 12th after ischaemic stroke onset. TAT complexes were significantly higher in patients with cerebral infarction than in controls, significantly higher in patients with ischaemic stroke of great extent compared to patients with ischaemic stroke of small extent, and significantly higher in patients with more severe cerebral infarction than in patients with less severe cerebral infarction. In patients with cerebral infarction and atrial fibrillation TAT complexes were significantly higher only on the 1st day of the disease compared to patients with cerebral infarction without atrial fibrillation. Our investigations confirm intense activity of thrombinogenesis process in ischaemic stroke patients.
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PMID:[Thrombogenesis in patients with ischemic stroke]. 1187 92

The improvement of decreased cerebral blood flow using thrombolytic agents, anti-thrombin drugs, and antiplatelet drugs has been essential for acute ischemic stroke. Edaravone, a free radical scavenger, has been commercially available as a novel neuroprotective agent for ischemic stroke in Japan from 2001. The appearance of a neuroprotective agent implies that therapeutic strategy can be expanded through a combination with thrombolysis. In the previous development, several cases have reported that neuroprotective compounds failed in clinical trials. However, recent studies have clarified that the cerebral ischemia induced the neuronal cell death by mediating multiple mechanisms with necrosis and/or apoptosis. The cytotoxicity derived from the NO/peroxynitrite/free radical generating system, one of intracellular Ca2+ signaling, is a typical event in ischemic injury, which is protected by edaravone. Furthermore, it is suggested that suppression of excessively activated voltage-dependent Na+ and Ca2+ channels is effective as a strategy for neuroprotection, since abnormal excitatory stimuli in the neuronal network result in the cerebral infarction. The development of several compounds having different mechanisms of action for acute stroke is in progress. It is therefore prospected that the various novel neuroprotective agents will be provided for assuring the option of therapeutic strategy, since the reinforcement of medical stroke care including diagnosis contributes to the prolongation of the therapeutic time window.
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PMID:[Current state on development of neuroprotective agents for cerebral ischemia]. 1218 23

A 52-year-old previously healthy woman was admitted to our hospital for status epilepticus in November 1999. She had not taken oral contraceptives. After treatment with intravenous diazepam and phenytoin, she did not develop seizures anymore. When she became alert, there was a mild left hemiparesis. Lumbar puncture showed an opening pressure of 145 mm H2O, and the cerebrospinal fluid was acellular. Cranial MR imaging demonstrated thrombosis of the superior sagittal sinus and fresh infarction in the right frontal lobe. Plasma fibrinogen, fibrin degradation product, and prothrombin fragment 1 + 2 levels were elevated. Proteins S and C activities and anti-thrombin III levels were within the normal range. Lupus anticoagulant and anti-cardiolipin antibody were negative. She was treated with continuous heparin infusion for ten days and with oral warfarin thereafter. Six months after the first admission, platelet count became more than 400 x 10(3)/microliter. In July 2002, she developed slowly progressive monoplegia of the left arm. Cranial MR imaging demonstrated patent superior sagittal sinus, fresh infarction in the right parietal lobe, and old small infarction in the right corona radiata. The patient was maintained on warfarin and 100 mg of aspirin thereafter. In September 2002, platelet count was 737 x 10(3)/microliter. Bone marrow examination showed increased megakaryopoiesis with normal erythroid and myeloid series and no chromosomal aberrations. Serum C-reactive protein and iron levels were in the normal range. An abdominal ultrasound demonstrated mild splenomegaly. Thus, we made a diagnosis of essential thrombocythemia (ET). ET causes thrombotic events in the course of the disease at a rate of 7% per year. Cerebral infarction is not uncommon, but occurrence of cerebral sinus thrombosis has been rarely reported. Recently, several cases have been reported in which cerebral infarction was the first manifestation of ET even with platelet counts lower than 600 x 10(3)/microliter. To our knowledge, there have been no reported cases of ET presenting with cerebral venous sinus thrombosis. Platelet count should be monitored in the patients with venous sinus thrombosis of undetermined etiology.
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PMID:[Superior sagittal sinus thrombosis as first manifestation of essential thrombocythemia]. 1519 36

We recently reported that the serum level of macrophage colony-stimulating factor (M-CSF) was elevated in patients with cerebral infarction. In the present study, we measured serum M-CSF level, as well as coagulo-fibrinolytic markers and general laboratory tests in adult healthy subjects of various ages, and investigated the relationship between age and M-CSF level. M-CSF in aged subjects (>or=65 years of age) was significantly higher than that in the younger subjects (<65 years of age), and a significant positive correlation between age and M-CSF was found. Significant positive correlations between M-CSF, and plasma levels of thrombomodulin (TM), von Willebrand factor antigen (vWF), thrombin-antithrombin III complex (TAT), prothrombin fragment 1+2 (F1+2), d-dimer products cross-linked fibrin degradation products (d-dimer) and plasmin-antiplasmin complex (PAP) were also found. Among the general laboratory tests, there was only a significant correlation between M-CSF and serum creatinine; however, no significant correlation was found between M-CSF and other tests including blood cell counts. From these results, age-related elevation of serum M-CSF level was confirmed, and was suggested not to indicate the alteration of hemopoietic condition in aged subjects but to be related to thrombotic state or systemic damaged blood vessel in the apparently healthy aged people.
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PMID:Age related elevation of serum macrophage colony stimulating factor (M-CSF) level. 1537 73

We report two cases of Duchenne muscular dystrophy (DMD) complicated with dilated cardiomyopathy (DCM), who were affected with cerebral infarction. Case 1 suddenly developed dysarthria and right facial weakness at age 21. Cranial CT study disclosed a low density area in the left basal ganglia and internal capsule. Case 2 had a history of transient ischemic attack (TIA) at age 21. Five months after the TIA, he developed right hemiplegia and dysarthria, and a low density area in the corona radiate in left cerebral hemisphere was observed in cranial CT. These two cases showed the radiographic cardiomegaly with cardio thoracic ratio (CTR) of 72.8% and 66.6%, the decreased echocardiographic left ventricular ejection fraction below 20%, and the elevated titer of thrombin-anti-thrombin III complex (TAT) and D-dimer. The autopsy of Case 2 at age 26 disclosed the remarkable degeneration and fibrosis of myocardium and old ischemic lesion in the left cerebral frontal cortex. Despite the negative finding of the emboli in the left heart, cardiogenic cerebral infarction secondary to DCM was strongly suspected in both cases.
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PMID:[Two cases of Duchenne muscular dystrophy complicated with dilated cardiomyopathy and cerebral infarction]. 1662 52

Cerebral infarction is a common cause of seizures in neonates with a prevalence of I in 4000 live births. We report two neonates with different presentations due to cerebral infarction and discuss their etiological and neuroradiological findings in this case report. The initial signs were cyanosis and convulsion. In case 1, tonic convulsion, eye deviation, while case 2 had additionally poor sucking and dehydration as a risk factor. Their evaluation for hereditary causes of thrombosis was unremarkable. With these 2 cases, it is emphasized that neonatal cerebal infarction may be a cause of neonatal convulsion. Hence, neonates with cerebral infarction should be evaluated for hereditary conditions like protein C and S deficiency, anti-thrombin III deficiency, Factor V leiden mutation, prothrombin gene mutation and homocystinuria.
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PMID:Cerebral infarctions manifesting as neonatal seizure. 1790 13


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