It is known that antithrombin III is a potent vasodilator and plasmin is a vasoconstrictor, and some patients with a subarachnoid hemorrhage(SAH) develop clinical vasospasm and some patients do not. Under the hypothesis that the development of clinical vasospasm might depend on the difference of the blood level of antithrombin III in each patient with SAH and that the plasmin might have a role in the development of clinical vasospasm, we repeatedly checked the levels of blood antithombin III with a single radial immunodiffusion method and CSF fibrinogen degradation products(FDP : indirect indicator of plasmin activity) with a latex-test(Thrombo-Wellcotest(R)) during the period between 1-4, 5-11 and 12-24 days after a SAH in 29 patients. 10 patients with diseases except those with a SAH were selected as a control group. First, we analyzed the difference of the average of blood antithrombin III and CSF FDP between aneurysmal SAH patients and control patients and then, between patients with clinical vasospasm(8 cases) and patients without clinical vasospasm(21 cases). Secondly, we also analyzed the difference of these data between patients with clinical vasospasm and patients without clinical vasospasm according to the sampling day after a SAH. As a result, there was no statistical difference between the average blood level of antithrombin III in control and in SAH patients(29.06+/-3.04 vs. 25.61+/-6.95, respectively), and in patients with clinical vasospasm and in patients without clinical vasospasm(26.59+/-7.65 vs. 23.67+/-7.40, respectively). The average CSF levels of FDP is higher in SAH patients than in control patients(18.16+/-14.36 vs. 1.00+/-3.16, respectively : p<0.01). It is also higher in patients with clinical vasospasm than in patients without clinical vasospasm. However, there is no statistical significance(28.75+/-9.91 vs. 21.75+/-12.07, respectively : p>0.05). In the analysis of the average CSF levels of the FDP according to the sampling day after a SAH, even though the average levels is higher in patients with clinical vasospasm than in patients without clinical vasospasm(1-4 days : 31.43+/-14.64 vs. 27.33+/-16.24, 5-11 days : 23.75+/-17.68 vs. 18.10+/-16.32, 12-24 days : 32.50+/-13.89 vs. 18.82+/-16.54, respectively), a statistical significant difference was noticed only in levels which were checked between 12 and 24 days after a SAH(p<0.05). This study concludes that the blood level of antithrombin III shows no difference between the control and SAH patients, and patients with clinical vasospasm and patients without clinical vasospasm. Although it suggests a causal relationship between the FDP itself or plasmin in CSF and the development of clinical vasospasm, it does not justify any valid conclusion.
Aneurysm* ; Antithrombin III* ; Cerebrospinal Fluid* ; Fibrinogen ; Fibrinolysin ; Humans ; Immunodiffusion ; Subarachnoid Hemorrhage* ; Vasospasm, Intracranial

Disulfiram, tetraethylthiuram disulfide, has been used in the clinical treatment of alcoholism since 1948. Aside from the manifestations of a disulfiram-alcohol reaction, disulfiram causes direct toxic side effects including psychiatric, cardiovascular, hematologic and neurologic disorders. The most frequent neurologic side effects are drowsiness, apathy, headache, decreased sexual potency, neuropathy, and optic neuritis. We describe a 26-year-old man who insidiously developed a distal synunetric sensorimotor polyneuropathy after seven years of disulfiram ingestion confirmed by nerve biopsy. He showed nearly complete resolution after the disulfiram was stopped.
Adult ; Alcoholism ; Apathy ; Biopsy ; Disulfiram* ; Eating ; Headache ; Humans ; Nervous System Diseases ; Optic Neuritis ; Polyneuropathies ; Sleep Stages

No abstract available.

Talc pleurodesis is a safe and effective treatment for a recurrent malignant pleural effusion. However, acute hypoxemia, pulmonary edema or acute respiratory failure can develop in a small number of patients. We report 2 patients who developed fatal hypoxemia after talc pleurodesis which was necessary the control recurrent pleural effusion. The first case was an 18-year old male diagnosed with Ewing's sarcoma with bilateral lung metastases and pleural effusion. The performance status was ECOG (Eastern Cooperative Foncology Group) grade 3. Fever along with hypoxemia and leukocytosis developed 10 hours after the second talc pleurodesis on the right side for an uncontrolled pleural effusion, The patient died from respiratory failure after 13 days. The second case was a 66-year old female diagnosed with non-small cell lung cancer with a bone metastasis. Two weeks after systemic chemotherapy, she complained of dyspnea, and a pleural effusion was observed on the right side. Her performance status was ECOG grade 3. Talc pleurodesis was performed for recurrent pleural effusion, but hypoxemia developed 6 days after pleurodesis and she died from respiratory failure 10 days after pleurodesis. In conclusion, talc pleurodesis should be performed very carefully in patients with a poor performance status, in cases with repeated pleurodesis, bilateral pleural effusion, recent chemotherapy, radiotherapy and when there are parenchymal metastatic lesions present.
Adolescent ; Aged ; Anoxia* ; Carcinoma, Non-Small-Cell Lung ; Drug Therapy ; Dyspnea ; Female ; Fever ; Humans ; Leukocytosis ; Lung ; Male ; Neoplasm Metastasis ; Pleural Effusion ; Pleural Effusion, Malignant* ; Pleurodesis* ; Pulmonary Edema ; Radiotherapy ; Respiratory Insufficiency ; Sarcoma, Ewing ; Talc*

Apolipoprotein (apo) E deficient mouse can produce reproducible fixed stenotic primary atherosclerotic lesion, which reveals failure to remodel of vascular lumen, in the ascending aorta, external carotid, common carotid, iliac, femoral and popliteal arteries. To evaluate the effect of drugs in regarding to both prevention of primary atherosclerotic lesion and vascular remodeling, a systematic analysis of distribution of atherosclerotic lesions was undertaken in chow-fed, 9-momth-old apo E deficient mice, which was administrated drugs including asprin, methotrexate, probucol, sulodexide, diltiazem, cilazapril, trimetazidine, molsidomine, pentoxiphylline and Ginexin (R) for 7 month from 3 month-old. On gross and microscopic examination, formation of primary atheroscleotic lesions could be delated and/or prevented patially by effets of these drugs. On morphometric examination, failure to remodel forming vascular stenosis could not be seen, though relatively mild atherosclerotic lesion occured at vascular tree. These data suggest that the stenotic process in advanced atherosclerotic vessels can be delayed and/or prevented by several drugs including methotrexate, probucol, sulodexide, diltiazem, cilazapril, trimetazidine, molsidomine, pentoxiphylline and Ginexin (R) in vivo state.
Animals ; Aorta ; Apolipoproteins ; Apolipoproteins E* ; Atherosclerosis ; Cilazapril ; Constriction, Pathologic ; Diltiazem ; Humans ; Infant ; Methotrexate ; Mice ; Mice, Knockout* ; Molsidomine ; Popliteal Artery ; Primary Prevention ; Probucol ; Trimetazidine

Mannose-binding lectin (MBL) plays an important role in immune defense. This study was undertaken to investigate the association between hepatitis B virus infection and polymorphisms of MBL gene. We assessed the single nucleotide polymorphism at codon 54 in exon 1 of MBL in patients with hepatitis B virus infection and HBsAg negative controls in Korean population. A total of 498 enrolled subjects was classified into four groups. Group 1; Clearance, Group 2; Inactive healthy carrier, Group 3; Chronic hepatitis, Group 4; Liver cirrhosis. MBL gene polymorphisms at codon 54 led to three genotypes (G/G, G/A, A/A). When we divided subjects into clearance group (group 1) and persistence group (group 2-4), G/G genotype and A-allele carrier were observed in 55.6% and 44.4% in clearance group, 64.8% and 35.2% in persistence group (p=0.081), respectively. When hepatitis B virus persistent cases were divided into inactive healthy carrier (group 2) and disease progression group (group 3 and 4), MBL gene polymorphisms at codon 54 were not related to disease progression (p=0.166). MBL gene polymorphism at codon 54 was not associated with the clearance of hepatitis B virus infection nor progression of disease in chronic hepatitis B virus infection.
Adult ; Alleles ; Codon ; Disease Progression ; Female ; Fibrosis ; Genotype ; Hepatitis ; Hepatitis B/*genetics/*metabolism ; Hepatitis B virus/*metabolism ; Heterozygote ; Humans ; Korea ; *Lectins ; Male ; Mannose-Binding Lectin/*chemistry/*genetics ; Middle Aged ; *Polymorphism, Genetic ; Polymorphism, Single Nucleotide ; Research Support, Non-U.S. Gov't

BACKGROUND AND PURPOSE: Although thrombolytic strategies with streptokinase(STK) and tissue-type plasminogen activator(t-PA) in the treatment of acute myocardial infarction(AMI) have been studied in large-scale clinical trials in the western countries, such large-scale studies with urokinase(UK) are scanty. Even though UK is most commonly used thrombolytic agent for the treatment of AMI in Korea, there is no consensus on the dosage and the way of administration of UK in patients with AMI. Accordingly, a prospective clinical study was performed to evaluate the effects of thrombolytic strategies of intravenous double bolus method and standard double-infusion method with different dosage of UK in the treatment of AMI. SUBJECTS AND METHODS: Ninety there patients with AMI(male 75, female 18, age 57.5+/-10.8 years) were studied. The patients were divided into 3 groups according to dosage of UK and method of administration. Group I : 19 patients who received 1.5 million U of UK IV bolus, followed by 1.5 million U IV infusion for an hour(High Dose Group). Group II : 34 patients received 20,000U/kg body weight of UK IV bolus, followed by 20,000U/kg IV infusion for an hour(Double Dose Group). Group III : 40 patients received 1.5 million U of UK IV bolus and followed by 20,000U/kg IV bolus in 30 minutes with total dose of no more than 3 million U(Double Bolus Group). Coronary angiography(CAG) and left ventriculography(LVG) were performed 90 minutes after the administration of UK and post-AMI 7-10 days to investigate the patency of infarct-related artery(IRA) and LV function. Patency of IRA was graded according to the extent of flow of IRA. TIMI grade 0-1 was regarded as occluded, and grade 2-3 flow as patent. LV ejection fraction(EF) by echocardiography was measured on day 1, day 7-10 and 1 month after AMI. Indirect clinical parameters of thrombolysis were evaluated and were compared with CAG findings. RESULTS: 1) The 90 minutes IRA patency in Group III(Double bolus ; 79.0%) was higher than that in Group 1, but showed no statistically significant difference(High dose ; 61.5%, p=0.790). The 90 minutes IRA patency in Group III showed borderline significance with Group II(Double dose ; 57.1%, p=0.057). TIMI flow III in Group III(60.6%) was significantly higher than that in Group II(53.6%, p=0.0468) but showed no statistically significant difference with Group I(61.5%, p=0.158). 2) The EF by LVG were 49.1% in Group I, 41.7% in Group II and 49.2% in Group III. The difference in EF between Group I and Group III vs Group II was significant(p=0.008 in Group I, p=0.014 in Group III vs Group II). 3) Fatal bleeding complications(1 intracranial hemorrhage and 1 gastric ulcer bleeding) developed in Group II (Double dose). 4) Pain to door time, pain to needle time and door to needle time tended to be shorter in open(TIMI flow II-III) IRA group than in closed IRA group. 5) Initial EF were similar between open IRA group and closed IRA group(46.1% and 42.1% ; p=NS). The EF of open IRA group measured by LVG on initail coronary angiography(41.8% in closed IRA vs 48.0%, in open IRA, p=0.03) and by 2D-Echo on 7-10 day(41.7% in closed IRA vs 51.0% in open IRA, p=0.004) were better than those of closed IRA group. 6) Indirect clinical indices of reperfusion such as mean CPK peak, time to CPK peak significantly lower in open IRA group than in closed IRA group. 7) Fatal bleeding complications(1 intacranial hemorrhage and 1 gastric ulcer bleeding) developed in closed IRA group. CONCLUSION: The findings we observed in this trial showed that earlier initiation and more rapid infusion of UK were associated with more increased 90min patency of infarct-related artery and more improved LV function without any obviously increased bleeding complications or other serious life-threatening complications than conventional UK therapy. Specifically, double bolus IV injection of UK(1.5 million U bolus followed by 20,000 U/Kg bolus in 30min)was more effective method of thrombolysis than conventional method for achieving optimal reperfusion in AMI patients. Also, IRA patency at 90 minutes after the initiation of thrombolysis was important in preserving global LV function in early recovery phase of AMI. Further trials may be needed to determine more effective thrombolysis with UK in AMI.
Arteries ; Body Weight ; Consensus ; Echocardiography ; Female ; Hemorrhage ; Humans ; Intracranial Hemorrhages ; Korea ; Myocardial Infarction* ; Needles ; Plasminogen ; Prospective Studies ; Reperfusion ; Stomach Ulcer ; Urokinase-Type Plasminogen Activator*

In 2007, seven detector dogs were produced by somatic cell nuclear transfer using one nuclear donor dog, then trained and certified as excellent detector dogs, similar to their donor. In 2011, we crossed a cloned male and normal female by natural breeding and produced ten offspring. In this study, we investigated the puppies' temperaments, which we later compared with those of the cloned parent male. The results show that the cloned male had normal reproductive abilities and produced healthy offspring. All puppies completed narcotic detector dog training with a success rate for selection of 60%. Although the litter of cloned males was small in this study, a cloned male dog bred by natural mating produced puppies that later successfully completed the training course for drug detection. In conclusion, cloning an elite dog with superior genetic factors and breeding of the cloned dog was found to be a useful method to efficiently procure detector dogs.
Animals ; Breeding ; Clone Cells* ; Cloning, Organism ; Dogs* ; Female ; Humans ; Male* ; Methods ; Parents ; Temperament ; Tissue Donors

BACKGROUND: Brief episodic ischemias prior to subsequent prolonged ischemia limit infarct size and attenuate the reperfusion arrythmia. But the effect of ischemic preconditioning on post-ischemic myocardial dysfunction, coronary flow and nitric oxide (NO) remains unclear. METHODS: To investigate the effect of ischemic preconditioning on myocardial function and coronary flow during reperfusion after 15 minutes of global myocardial ischemia, 30 isolated hearts of Sprague-Dowley rats were perfused under constant pressure. Two episodes of three minutes global ischemia followed by 12 minutes of reflow were employed to precondition the hearts. The hearts were randomized to one of three groups : group I had no preconditioning, group II had preconditioning, group III had preconditioning as well as L-arginine pretreatment. Left ventricular developed pressure (LVDP), LV dp/dt, perfused coronary flow, concentration of NO and heart rate were continuously measured. RESULTS: In preconditioning groups (Group II, Group III), LVDP decreased during reflow and was lower than that of the control group. LV dp/dt decreased after reflow and gradually recovered with time but recovered was less in preconditioning groups. Coronary flow increased in the first few minutes after reflow in all groups, but decreased gradually. The decrease of coronary flow was greater in preconditioning groups. NO increased during the first 10 minutes after reflow and then decreased. In preconditioning groups, NO tends to be lower than that in the non-preconditioning group. CONCLUSION: Ischemic preconditioning was not beneficial to post-ischemic myocardial dysfunction, coronary flow and NO concentration in the flow. Cummulative effect of stunning due to repetitive ischemia for preconditioning may be an explanation for worse post-ischemic myocardial dysfunction and coronary flow in preconditioning groups.
Animals ; Arginine ; Arrhythmias, Cardiac ; Heart Rate ; Heart* ; Ischemia ; Ischemic Preconditioning* ; Myocardial Ischemia ; Myocardial Stunning ; Nitric Oxide ; Rats* ; Reperfusion

BACKGROUND: Brief episodic ischemias prior to subsequent prolonged ischemia limit infarct size and attenuate the reperfusion arrythmia. But the effect of ischemic preconditioning on post-ischemic myocardial dysfunction, coronary flow and nitric oxide (NO) remains unclear. METHODS: To investigate the effect of ischemic preconditioning on myocardial function and coronary flow during reperfusion after 15 minutes of global myocardial ischemia, 30 isolated hearts of Sprague-Dowley rats were perfused under constant pressure. Two episodes of three minutes global ischemia followed by 12 minutes of reflow were employed to precondition the hearts. The hearts were randomized to one of three groups : group I had no preconditioning, group II had preconditioning, group III had preconditioning as well as L-arginine pretreatment. Left ventricular developed pressure (LVDP), LV dp/dt, perfused coronary flow, concentration of NO and heart rate were continuously measured. RESULTS: In preconditioning groups (Group II, Group III), LVDP decreased during reflow and was lower than that of the control group. LV dp/dt decreased after reflow and gradually recovered with time but recovered was less in preconditioning groups. Coronary flow increased in the first few minutes after reflow in all groups, but decreased gradually. The decrease of coronary flow was greater in preconditioning groups. NO increased during the first 10 minutes after reflow and then decreased. In preconditioning groups, NO tends to be lower than that in the non-preconditioning group. CONCLUSION: Ischemic preconditioning was not beneficial to post-ischemic myocardial dysfunction, coronary flow and NO concentration in the flow. Cummulative effect of stunning due to repetitive ischemia for preconditioning may be an explanation for worse post-ischemic myocardial dysfunction and coronary flow in preconditioning groups.
Animals ; Arginine ; Arrhythmias, Cardiac ; Heart Rate ; Heart* ; Ischemia ; Ischemic Preconditioning* ; Myocardial Ischemia ; Myocardial Stunning ; Nitric Oxide ; Rats* ; Reperfusion