• Clinical and Experimental Reproductive Medicine
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• v.28 no.4
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• pp.301-305
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• 2001

Objective : To analyze the antithrombin II deficiency in patients with recurrent spontaneous abortion. Material and Method: The blood samples were tested by chromogenic assay to evaluate the activity of antithrombin III. Results: There was only one case of antithrombin III deficiency. This patient experienced one neonatal death after delivery and one FDIU (fetal death in utero). And also this patient showed a lupus anticoagulant and the prolongation of PTT. Conclusions: Women with recurrent miscarriage who have no obvious identified cause should consider hematologic screening. Antithrombin III deficiency could be a cause of recurrent spontaneous abortion. But the incidence is very rare in Korean patients.

• Environmental Mutagens and Carcinogens
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• v.22 no.1
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• pp.30-38
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• 2002

In view of the effect of antithrombin III on essential hypertension, we investigated the 5' untranslated exon 1 length (I/D) polymorphism and intron 5'-DdeI RFLP of the human antithrombin III gene in the Korean patients with essential hypertension. There were no significant differences in the allele, genotype and haplotype frequencies of these polymorphisms between normotensive and essential hypertensive subjects. The significant linkage disequilibrium was however, detected between I/D polymorphism and Dde I RFLP. The I/D polymorphism was also significantly associated with BMI, total cholesterol (TC) and HDL- cholesterol levels, while DdeI polymorphism with age and BMI. Therefore, our results suggest that the significant association between the genetic polymorphisms in the antithrombin III gene and variable cardiovascular risk factors may reflect the potential role of human antithrombin III gene in cardiovascular function.

• Tuberculosis and Respiratory Diseases
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• v.47 no.3
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• pp.394-399
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• 1999

We report a case of congenital and familial antithrombin III deficiency developing massive pulmonary thromboembolism. A 44-year-old man was admitted to our hospital because of sudden chest pain and severe dyspnea. Five years ago, he was operated due to a mesenteric vein thrombosis of unknown cause. On admission, radioisotopic venogram showed deep vein thrombosis and lung scintigram showed multiple segmental perfusion defects. His plasma antithrombin III level was 10.5 mg/dL which was less than 50% of normal and those of a son and two daughters were also decreased. After treatment with tissue plasminogen activator, heparin and coumadin, his symptom and lung scintigram were significantly improved. As far as we reviewed, there were very rare reports with congenital antithrombin III deficiency presenting as pulmonary thromboembolism in Korea.

• 대한예방의학회:학술대회논문집
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• 2002.05a
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• pp.93-93
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• 2002

• Clinical and Experimental Pediatrics
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• v.50 no.5
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• pp.443-448
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• 2007

Purpose : To evaluate the potential prognostic value of the antithrombin-III (AT-III) level in the children with acute lung injury (ALI), we analyzed several early predictive factors of death including AT-III level at the onset of ALI and compared the relative risk of them for mortality. Methods : Over a 18-month period, a total of 198 children were admitted to our pediatric intensive care unit and 21 mechanically ventilated patients met ALI criteria, as defined by American-European consensus conference, i.e., bilateral pulmonary infiltrates and $PaO_2/FiO_2$ lower than 300 without left atrial hypertension. Demographic variables, hemodynamic and respiratory parameters, underlying diseases, as well as Pediatric Risk of Mortality-III (PRISM-III) scores and Lung Injury Score (LIS) at admission were collected. AT-III levels were measured within 3 hours after admission. These variables were compared between survivors and non-survivors and entered into a multiple logistic regression analysis to evaluate their independent prognostic roles. Results : The overall mortality rate was 38.1% (8/21). Non-survivors showed lower age, lower lung compliance, higher PEEP, higher oxygenation index (OI), lower arterial pH, lower $PaO_2/FiO_2$, higher PRISM-III score and LIS, and lower AT-III level. PRISM-III score, LIS, OI and decreased AT-III level (less than 70%) were independently associated with a risk of death and the odds ratio of decreased AT-III level for mortality is 2.75 (95% confidence interval; 1.28-4.12) Conclusion : These results suggest that the decreased level of AT-III is an important prognostic factor in children with ALI and the replacement of AT-III may be considered as an early therapeutic trial.

• Korean Journal of Veterinary Service
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• v.18 no.2
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• pp.182-188
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• 1995

Hemodynamic values were assessed in cows with naturally mastatis. hemodynamic tests included WBC, RBC, PCV, Hemoglobin, Monocyte, Eosinophil, Neutrophil, Lymphocyte, and prothrombin time, activated partial thromboplastin time, thrombin time, fibrinogen, platelet, antithrombin-III, and plasminogen activities. Significant changes were observed in the mean values of most analytses : WBC, monocytes, eosinophil, neutrophil were increased and Iymphocyte were decreased. prothrombin time was increased： activated partial thromboplastin time, thrombin time. increased : activated partial thromboplastin time, thrombin time, fibrinogen concentration, plasminogen activity and platelet concentration were decreased : and RBC, PCV, hemoglobin and antithrombin-III activity were unchanged, compared with normal mean values. Thesse data indicated activation of hemodynamic mechanisms, initiated either directly by bacteria produced endotoxin of secondaly inflammatory mediators produced in response to caused bacteria and naturally acquired mastitis was very similar to the experimental endotoxin-induced mastitis.

• Proceedings of the PSK Conference
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• 2003.04a
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• pp.149.2-149.2
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• 2003

We have carried out a collaborative study to evaluate a candidate preparation of antithrombin III concentrate whether it is suitable to serve as a Korea National Biological Standard. Three National Control Laboratories and three manufacturers participated in this study. The potency of this candidate preparation was determined by using a heparin cofactor chromogenic method described in the Minimum Requirements for Biological Products and the European Phamacopoeia. (omitted)

• Journal of the Korean Society of Food Science and Nutrition
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• v.31 no.5
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• pp.917-923
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• 2002

Inhibitory mechanism of the anticoagulant polysaccharide purified from Codium fragile was investigated. The anticoagulant compounds (Cf-30-IV-4-ii, CF-30-IV) prolonged the clotting time at both activated partial thrombo-plastin time (aPTT) and thrombin time (TT). The Inhibition factor assay of instrinsic coagulation pathway in the blood showed that the anticoagulant polysaccharide (CF-30-IV-4-ii) inhibited other factors such as Ⅷ, Ⅸ, Ⅵ and Ⅷ of the coagulation cascade, which did not affect the lupus anticoagulant AB activity. In the thrombin inhibition pattern the CF-30-IV-4-ii did not directly influence the fibrine formation mediated by thrombin but af-fected the anticoagulant activity through the activation of antithrombin III. Base on these result, the anticoaglant polysaccharide (CF-30-IV-4-ii) was considered to inhibit serine pretense involved in the blood coagulation cascade through the enhancing antithrombin III activity. The residual effects of anticoagulant activity and antithrombosis were tested with ICR mice. The anticoagulant polysaccharide (CF-30-W) kept its anticoagulant activitv for 6 hrs with 100% survival at a dose of 150 mg/kg in the antithromboisis test. The anticoagulant effect of CF-30-RF in ex vivo was proportional to the concentration of intravenously injected dose up to 100 mg/kg.

• Korean Journal of Veterinary Research
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• v.35 no.3
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• pp.595-601
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• 1995

Hemodynamic values were assessed in the cows diseased with mastitis. Hemodynamic testes were performed for white blood cell(WBC), red blood cell(RBC), packed cell volume(PCV), hemoglobin concentration, monocyte, eosinophil, neutrophil, lymphocyte, prothrombin time, activated partial thromboplastin time, thrombin time, fibrinogen, platelet concentrations, antithrombin-III and plasminogen activities. Significant alterations were observed in the mean values of most analytes. The numbers of monocytes, eosinophil, and neutrophil, and prothrombin time were increased while the number of lymphocyte, activated partial thromboplastin time, thrombin time, fibrinogen concentration, plasminogen activity and platelet concentration were decreased. The number of RBC, PCV, hemoglobin and antithrombin-III activity were unchanged compared with normal mean values. These data indicated that activation of hemodynamic mechanisms was initiated either directly by the endotoxin-releasing or indirectly by the inflammatory mediators released by response to etiologic agents. We suspected that the changes of hemodynamic values in the cows diseased with mastitis were very similar to those of experimental endotoxin-induced mastitis.

• Biomedical Science Letters
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• v.3 no.2
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• pp.83-88
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• 1997

In septic patients, disseminated intravascula. coagulation (DIC) occurs frequently and is a pathologic condition associated with a variety of critical illness. DIC may complicate the already complex clinical situations and contribute to the high mortality. Nevertheless, its pathogenic mechanisms are not completely elucidated. Present study was prospectively designed to understand the pathogenetic mechanisms involved in the development of DIC. 15 rats were subjected to study and according to the aim, they were divided into three groups： group I, control (not treated-endotoxin, n=5)； group II (12 hours after endotoxin injection, n=5)； group III (24 hours after endotoxin injection, n=5). Experimental DIC was induced in rats by a bolus injection of endotoxin (1mg/kg, E. coli serotype 055:B5). Blood was collected by direct puncture of the heart. Platelet count, fibrinogen and plasminogen concentration, antithrombin III, D-dimer and complement components (C3 and C4) were measured in all subjects. In group II and III, there were apparent signs of DIC, including thrombocytopenia, decreased fibrinogen (but increase in group III), reduced C3 and antithrombin III, and elevated D-dimer. These data indicated that endotoxin might induce the activation of several pathways such as coagulation, fibrinolytic and complement cascade, causing DIC and subsequent multiple organ failures. Ultimately, the increased knowledge of the various pathogenetic mechanisms of coagulation activation and fibrinolysis in endotoxin-induced DIC may have prophylactic or therapeutic implications.