• Tuberculosis and Respiratory Diseases
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• v.47 no.1
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• pp.103-110
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• 1999

A thromboembolic event in patients later given a diagnosis of cancer is the result rather than the cause of the cancer. The risk of hidden cancer is significantly higher for patients with recurrent idiopathic thromboembolism compared to those with secondary deep vein thrombosis. Microemboli from hepatic or adrenal metastases and large-sized emboli from the great veins invaded by the tumor are the sources of tumor embolization The intraarterial tumor emboli less likely invade the arterial wall. Thrombus formation and organization may be capable of destroying tumor cells within pulmorlary blood vessels. Therefore, all tumor emboli are not true metastases. The treatment of deep vein thrombosis and pulmonary embolism in patients with cancer consists of anticoagulation with heparin and warfarin, venacaval filters, appropriate anti-neoplastic agents, and surgical methods(embolectomy, thromboendarterectomy). However, considerable literatures suggest that oral anticoagulant such as warfarin is ineffective in the treatment of those. We report a case of primary unknown squamous cell carcinoma incidentally found in the thrombus after pulmonary embolectomy.

• Tuberculosis and Respiratory Diseases
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• v.68 no.2
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• pp.62-66
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• 2010

Background: Extracorporeal membrane oxygenation (ECMO) during severe acute respiratory failure helps to recover the pulmonary function. This study evaluated our experience with veno-venous ECMO in adult patients with acute respiratory failure. Methods: From January 2007 to July 2009, ECMO was used on 54 patients. Of these 54 patients, 7 were placed on veno-venous ECMO for acute respiratory failure. The indications of ECMO were based on the lung dysfunction measured as a $PaO_2/FiO_2$ ratio <100 mm Hg on $FiO_2$ of 1.0, or an arterial blood gas pH <7.25 due to hypercapnia despite the optimal treatment. $EBS^{(R)}$, $Bio-pump^{(R)}$, and Centrifugal Rotaflow $pump^{(R)}$ were used and all cannulations were performed percutaneously via both femoral veins. When the lung function was improved, an attempt was made to wean on ECMO at moderate ventilator settings followed by decannulation. Results: Five of the 7 patients were male and the mean age was $46.3{\pm}18.3$. The causes of acute respiratory failure were 3 cases of pneumonia, 2 near-drownings, 1 pulmonary hemorrhage due to acute hepatic failure and 1 mercury vapor poisoning. The mean support time of ECMO was $17.3{\pm}13.7$ days. Of the 7 patients implanted with ECMO, 5 patients (71%) were weaned off ECMO and 3 patients (43%) survived to hospital discharge after a mean 89.6 hospital days. Conclusion: The early use of ECMO for acute respiratory failure in adults due to any cause is a good therapeutic option for those unresponsive to the optimal conventional treatments.

• The Korean Journal of Zoology
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• v.16 no.2
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• pp.79-96
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• 1973

In order to elucidate the effects of copper on Corassius carassius, the following were studied: 1) lactate dehydrogenase isozyme patterns by cellulose acetate electrophoresis, 2) LDH activity and copper effect on LDH enzyme system y spectrophotometry, 3) esterase isozyme patterns by agar thin layer electrophoresis, 4) hemoglobin patterns by starch gel electrophoresis, and 5) histological study. 1. There were two bands of LDH isozymes (LDH-3 and LDH-5) in the gill, three bands (LDH-2, LDH-4, and LDH-5) in the liver, and two bands (LDH-3 and LDH-4) in the muscle of the normal fish. The LDH-1 bond was not found in the above three tissues. When the fish were exposed to copper, LDH-3 appeared in the liver, LDH-5 in the muscle, but no new LDH band appeared in the gill. 2. The sepcific activities of the LDH were lowest in the gill and highest in the muscle of the normal fish, and they were gradually decreassed in the gill and highest in the muscle of the normal fish, and they were gradually decreased in the liver and mucle except in the gill from 1-day to 10-day exposure to copper. It indicates that LDH activities in the liver and muscle of the fish were inhibited by copper. 3. Through in vitro experiment, it is clear that the decrease of the LDH activities of the liver and muscle of the fish exposed to copper is mainly caused by the inhibition on the M-LDH in the fish. 4. The numbers of the esterase isozyme bands of the gill, liver, muscle, blood, brain, and kidney of the normal fish were 3, 6, 2, 2, 2, and 2 respectively, and these numbers were the same as those exposed to copper. The relative mobilities of the esterase bands in the gill, liver, blood, and kidney of the exposed group were different from those of the control. 5. There was one hemoglobin band on the anode in the normal fish. It seems that the nobility of hemoglobin band of the fish exposed to copper was slightly faster than that of the normal fish. 6. The normal gill lamellae of the fish consisted of centrally located pillar cells and a number of mucus cells. When the fish were exposed to copper, the epithelial layer was divorced first, disintegrated, and then destroyed completely. 7. The liver of the normal fish had prominent central veins, cords of hepatic cells, and sinusoids. When the fish were exposed to copper, numerous droplets of fat appeared in the cells around the central vein of the liver. It is assumed that the fatty droplets were accumulated by the lesion due to fatty metamorphosis of the liver caused by copper. 8. There was no histological difference between the muscle of the normal fish and that of the fish exposed to copper. 9. In the normal fish, the tubules of the kidney were surrounded by hemopoetic tissues. However, the kidney tissue of the fish exposed to copper received some damage on the proximal tubules. Since the tubule cells were reduced in height, the lumens of the tubules were enlarged. Consequently many proximal tubules exhibited some pink-stained granular casts and various stages of degeneration.