The glucose nonfermenting gram-negative bacilli encountered about 10% of all gram-negative bacilli isolated from clinical material. Therefore, a rapid and correct identification of glucose nonfermenting gram-negative bacilli is impotent for a better management of infectious disease. There are many conventional systems for the identification of glucose nonfermenting gram-negative bacilli but most of them have problems and difficulties. Commercial Kit Systems exist and they are too expensive for daily use in Korea because of high cost. Based on 12 selected tests we propose a new code system, MCRCODE-N for rapid and inexpensive identification of glucose nonfermenting gram-negative bacilli. The selective 12 tests are oxidase, glucose oxidation motihty, urease, DNase arginine dehydrolase, nitrate reduction, gelatin Liquefaction, esculin hydrolysis, mannitol oxidation, maltose oxidation, Lactose oxidation. The 12 tests are divided 4 group and then each group has 3 tests. The result of each group is expressed by the number as below. The positive test is given by specific number (1st test=1, 2nd test=2, 3rd test=4), while any negative result is 0. Each 3 numbers of one group are added and make number of 1 digit. Four digit number is referred to the code book of MCRCODE-N system or MCRCODE system using computer (Apple-II model) created by authors. This MCRCODE-N system is suitable ones for out use in Korea. We propose the MCRCODE-N system for clinical use.
Arginine ; Clinical Coding* ; Communicable Diseases ; Deoxyribonucleases ; Esculin ; Gelatin ; Glucose Oxidase ; Glucose* ; Hydrolysis ; Korea ; Lactose ; Maltose ; Mannitol ; Urease

Several immunosuppressive agents were used to prolong the survival of full-thickries skin homografts in albino rats. The grafts were squares in size of 2.0cm. The results were as follows. 1. The mean survival time of skin homografts in control group was 6.0 days. 2. Total body X-irradiation (500r) to the recipients 24 hours before grafting resulted in prolongation of survival of the grafts. (Mean, 12.5 days) 3. Administration of Imuran(azathioprine) to the recipients in a does of 5mg/kg/day for 7 days. before grafting resulted in prolongation of survival of the grafts. (Mean, 9. 6 days) 4. Spleneetomized homografted rats showed no prolongation of survival of the grafts. (Mean, 6.1days) 5. Administration of prednisolone to the recipients in a does of 2mg/kg/day for 7 days before grafting resulted in no prolongation of survival of the grafts. (Mean, 6.3 days) 6. Above results were discussed and compared with those of others.
Allografts* ; Animals ; Azathioprine* ; Immunosuppressive Agents* ; Prednisolone* ; Rats* ; Skin* ; Splenectomy* ; Survival Rate ; Transplants ; Whole-Body Irradiation*

PURPOSE: Endothelin-1(ET-1) is a potent vasoconstrictor peptide. It has potent contractile and proliferative effects on vascular smooth muscle cells. Congenital heart diseases are often accompanied by pulmonary hypertension, and the severity of pulmonary hypertension is important in the prognosis. The aim of this study was to elucidate changes of ET-1 after pulmonary venous stenosis in a dog model, and investigate the interaction between pulmonary venous pressure and ET-1. METHODS: Plasma ET-1 levels were measured by radioimmuno-assay at the thoracic aorta, left pulmonary artery and left pulmonary vein. Pressures were also monitored at the same sites. Immunohistochemical staining of ET-1 was performed in the lung tissue. RESULTS: Increased serum ET-1 levels were noted at 1 hour after left pulmonary vein stenosis in the left pulmonary vein and aorta, and at 2 days after stenosis in the left pulmonary artery. Left pulmonary venous pressure was significantly increased at 1 hour after pulmonary vein stenosis, and systolic pulmonary artery pressure at 2 days after stenosis. Increased expression of ET-1 was noted by immunohistochemical staining at the lung tissue at 7 days after stenosis of left pulmonary vein. CONCLUSION: Increased serum ET-1 level and expression of ET-1 in immunohistochemical staining at lung tissue were noted after stenosis of pulmonary vein. Serum ET-1 level would be useful in the diagnosis and prediction of pulmonary artery hypertension. (J Korean Pediatr Soc 2000;43:769 778)
Animals ; Aorta ; Aorta, Thoracic ; Constriction, Pathologic* ; Diagnosis ; Dogs ; Endothelin-1* ; Endothelins ; Heart Diseases ; Hypertension ; Hypertension, Pulmonary ; Lung ; Muscle, Smooth, Vascular ; Plasma ; Prognosis ; Pulmonary Artery ; Pulmonary Veins ; Venous Pressure

BACKGROUND: Intracellular calcium overload is a common final feature of the ischemic-reperfused heart and mediates the genesis of irreversible cell damage. Reactive oxygen medabolites have been known to play and important role as toxic mediators in myocardial injuries resulting from ischemia and reperfusion. In order to investigate the mechanism of intracellular calcium accumulation in the ischemic-reperfused myocardium, the present study observed the possible contribution of the reactive oxygen metabolite to the calcium transport of cardiac mitochondria. METHODS: Mitochondrial were isolated from rabbit hearts. The effects of a reactive oxygen metabolite, H2O2 on calcium uptake and release, redox states of endogenous pyridine nucleotides and glutathiones of mitochondria respiring with succinate were observed. Calcium uptake and release were monitored by dual-wave length spectrophotometer using a calcium indicator, arsenaze III. Contents and redox states of pyridine nucleotides and glutathiones were measured by enzymatic methods using spectrofluorometer and HPLC. RESULTS: Hydrogen peroxide(10-500microM) promoted calcium release dose-dependently from CA++-preloaded mitochondria, but did not affect the mitochondrial calcium uptake. The H2O2-induced calcium release was accompanied by simultaneous oxidation of the pyridine nucleotides and decrease in the content of the reduced form of glutathione(GSH). When mitochondria were treated with BCNU(N,N=bis(2-chloroethyl)-N-nitrosourea) to inhibit glutathione reductase and so as to reduce the GSH content, there were no increase in calcium release from the mitochondria. These results may indicate that H2O2 increases the permeability of cardiac mitochondrial membrane to calcium in association with the changes in redox state of endogenous pyridine nucleotides, but not with that of glutathiones. CONCLUSION: It is suggested that the reactive oxygen metabolites induce the release of calcium from mitochondria by altering the redox state of pyridine nucleotides, and it may partly be involved in the elevation of cytosolic calcium concentration in the ischemic-reperfused myocardial cells.
Calcium* ; Chromatography, High Pressure Liquid ; Cytosol ; Glutathione Reductase ; Heart ; Hydrogen ; Ischemia ; Mitochondria* ; Mitochondrial Membranes ; Myocardium ; Nucleotides ; Oxidation-Reduction ; Oxygen* ; Permeability ; Reperfusion ; Succinic Acid

No abstract available.
Prostate* ; Prostatic Neoplasms*

Under the extreme change of the environment, animals react physiologically to adapt to the stress and secrete catecholamines. Cold exposure is a kind of the environmental stress. Author tried to determine the amount of catecholamines in rat urine as a parameter of physiological response to cold stress. Urinary catecholamine was measured by using HPLC with fluorescence detector, coation exchange column prepacked with Bio-Rex 70 and ammonium pentaborate as catecholamine eluent. The amount of dopamine in normal state rat urine was 42.0 ng, but under the low temperature of 5 degrees C, the dopamine amount was increased to 221.25 ng/5 ml. Above findings are suggesting that catecholamine secretion, especially dopamine, increase in the stressful condition such as cold exposure.
Ammonium Compounds ; Animals ; Catecholamines ; Chromatography, High Pressure Liquid ; Dopamine ; Fluorescence ; Rats*

BACKGROUND: It has been found that sterss challenge with heat shock produces the acquisition of cellular resistance to ischemin injury in the hearts, which is associated with stress protein induction. The conventional heat shock(42degrees C of rectal temperature for 15min, anesthetized animal), however, is strong enough to endanger the animal life and then not suitable for practiocal application in human. The present study was performedd in an attempt to search the safely applicabel stress modalities to acquire the myocardial tolerance to ischemia-reperfusion in jury. METHODS: Male, Sprague-Ddawley rats(200-250g) were exposed to various stressful conditions, such as heat stimulation(environmental temperature of 42degrees C for 30min, live animal), swimming(20min), immobilization(60min), treadmill exercise(20M/min, 30min) and hyperbaric oxygenation(3atm, 60min) given once a day for 5 days. Twenty-four hours after the last application the hearts were isolated and perfused with oxygenated Krebs-Henseleit buffer solution by Langendorff method. Ischemia-reperfusion injury was produced by 20 min-global ischemia followed by 30 min-reperfusion. Cardiac mechanical function, lactate dehydrogenase release, the induction of stree proteins were assayed and compared dbetween the stressed dand the control animals. RESULTS: Upon reperfusion after ischemia the recovery of cardiac function was significantly improved in the stressed animals. The percentile recovery at 30min of reperfusion was in a range from 55.3%(swimming) to 89.3%(treadmill exercise), which was significantly higher than that of the control hearts(38%). The functional recovery of the conventional heat shocked heart was 57.7%. In stressed animals, lactate dehydrogenase release, which indicates myocardial cell injury, was significantly reduced by 20 to 30% compared to that for the control. The expression of an inducible form of 70 series stress protein, SP72, which was assayed by immunoblotting method, was markedly increased by heat stimulation while the other stress modalities failed to increase, it. There were no appreciable inductions of SP73(constitutive form) and GRR78 in the stressed animals. CONCLUSION: These results suggest that the cardiac protection from the ischemia-reperfusion injury could be induced by the repetitive non-fatal stress stimulations and that SP70 family proteins may be partly involved in the cardioprotective effect produced by heat stimulation, but not play the essential roles in anti-ischemic effects produced by other stress modalities.
Animals ; Heart* ; Hot Temperature ; Humans ; Immunoblotting ; Ischemia ; L-Lactate Dehydrogenase ; Male ; Oxygen ; Rats* ; Reperfusion ; Reperfusion Injury ; Shock

No abstract available.
Hypersensitivity* ; Meperidine* ; Skin*

No abstract available.
Voice*

No abstract available.
Biopsy* ; Lung Diseases* ; Lung*