No Abstract Available.
Hepacivirus* ; Hepatitis C* ; Hepatitis*

BACKGROUND: Ischemic preconditioning reduces the infarct size and the severity of arrhythmia in a post-ischemic reperfused heart although the detailed mechanism is unknown. In the ischemic heart, a large amount of catecholamine is released from the adrenergic nerve terminal and this aggravates cell destruction and arrhythmia. In this study, the possibility for ischemic preconditioning to inhibit the release of endogenous catecholamine from the ischemic heart was tested to investigate the probable cardioprotective mechanism of ischemic preconditioning. METHODS: In the isolated, Langendorff perfused rat hearts, we observed the protective effect of ischemic preconditioning against post-ischemic reperfusion injury, and measured the amount of catecholamine released into coronary effuent. In addition, we observed the effect of catecholamine depletion on reperfusion injury in non-preconditioned and preconditioned hearts. RESULTS: During the reperfusion(20min) after ischemia(30min), the cardiac function was markedly depressed with the development of severe contracture. In the heart preconditioned by three sequential episodes of 5min ischemia and 5min reperfusion, the reperfusion contracture decreased significantly and the cardiac function was almost recovered to normal after 20min reperfusion. The release of lactate dehydrogenase was also decreased in the preconditioned heart. The release of endogenous catecholamine was abruptly increased immediately after the reperfusion and the release was exponentially decreased throughout the reperfusion period. THe pattern of catecholamine release was much different from that of lactate dehydrogenase release. In the preconditioned heart, the release was significantly decreased to about half of that in non-preconditioned t\heart. Endogenous catecholamine depletion by reserpine treatment did not affect the post-ischemic functional recovery in both non-preconditioned and preconditioned hearts. CONCLUSION: It is suggested from these results that ischemic preconditioning inhibis the release of endogenous catecholamine during ischemic period, which may be partly related to cardioporotective effect of preconditioning in ischemic and reperfused heart.
Animals ; Arrhythmias, Cardiac ; Contracture ; Heart* ; Ischemia ; Ischemic Preconditioning* ; L-Lactate Dehydrogenase ; Rats* ; Reperfusion ; Reperfusion Injury ; Reserpine

Pulmonary artery sling is an uncommon and potentially lethal vascular anomaly that can produce airway obstruction. Despite the availibility of a corrective operation, the mortality rate remains very high due to the high incidence of associated obstructive anomalies of the tracheobronchial tree. We experienced a 70-day-old male infant who was admitted to our unit because of sudden dyspnea, cyanosis, coarse expiratory wheezing and inspiratory stridor. At first, he was treated with bronchodilator and steroid under the impression of infantile asthma, but the symptoms went on without interval change. We performed magnetic resonance imaging study followed esophagography and two dimensional echocardiography. Finally he was diagnosed as a vascular sling. We report this with a brief review and related literatures.
Airway Obstruction ; Asthma ; Cyanosis ; Dyspnea ; Echocardiography ; Humans ; Incidence ; Infant ; Magnetic Resonance Imaging ; Male ; Mortality ; Pulmonary Artery ; Respiratory Sounds

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

Eosinophilic gastroenteritis is a rare disorder of unknown etiology characterized by protein losing enteropathy, peripheral eosinophilia and iron deficiency anemia secondary to gastrointestinal blood loss. It is often accompanied by signs of systemic allergy. This case of a 26-month-old male patient who developed scrotal edema and diarrhea for a month had peripheral eosinophilia ranged from 24 to 32% of total leukocyte, iron deficiency anemia and hypoalbuminemia with slightly increased level of serum lgE. Biopsies of the stomach and duodenum demonstrated marked eosinophilic infiltration of the mucosa and lymphatic dilatation, which was consistent with eosinophilic gastroenteritis. We report a case of eosinophilic gastroenteritis with a brief review who was treated with corticosteroid alone and had marked symptomatic improvement.
Anemia, Iron-Deficiency ; Biopsy ; Child, Preschool ; Diarrhea ; Dilatation ; Duodenum ; Edema ; Eosinophilia ; Eosinophils* ; Gastroenteritis* ; Humans ; Hypersensitivity ; Hypoalbuminemia ; Leukocytes ; Male ; Mucous Membrane ; Protein-Losing Enteropathies ; Stomach

No abstract available.
Anticonvulsants* ; Carnitine* ; Liver*

Ovarian tumor in pregnancy is not rare and benign cystic teratoma is most common ovarian tumor in pregnancy. Most ovarian tumor in pregnancy is found at first and second trimester but sometimes found at third trimester and it is difficult to make a decision for management. Moreover physician should consider fetal age and mother's condition, and weigh outcome of operation for complicated ovarian tumor in pregnancy. Torsion of ovarian tumor is not an uncommon complication during first trimester of pregnancy and puerperium but rare occurs during the third trimester of pregnancy. We have experienced a case of torsion of benign cystic teratoma of ovary which occurred at 37 weeks gestation in a 25 year-old woman. So we report this case with a brief review of literature.
Adult ; Female ; Gestational Age ; Humans ; Impetigo* ; Ovary ; Postpartum Period ; Pregnancy Trimester, First ; Pregnancy Trimester, Second ; Pregnancy Trimester, Third ; Pregnancy* ; Teratoma

Colonic lesions by irritant laxative abuse are devided into melanosis coli, cathartic colon, soap or chemical colitis. Melanosis coli is the brownish or black discoloration of the colon because of the accumulation of lipofuscin pigment in macrophages located in lamina propria and associated with anthraquinone containing laxative abuse. The site of this lesion is more common in cecum and proximal colon, but whole colon can be involved. This lesion is occurred between 4 months and 13 months from initiation of drug medication, and the lesion is benign because the pigments disappear by withdrawning the laxatives. A number of cases were reported in our country, all of the cases were associated with prolonged administration of anthraquinone type laxatives. We presents two cases of melanosis eoli that had administrated aloe to treat the chronic constipation during long terms, and one case of melanosis coli that had not administrated laxatives or a specific drug with chronic constipation. All of three cases were confirmed by colonoscopy.
Aloe ; Cecum ; Colitis ; Colon ; Colonoscopy ; Constipation ; Laxatives ; Lipofuscin ; Macrophages ; Melanosis* ; Mucous Membrane ; Soaps

No abstract available.
Meningitis* ; Meningitis, Viral*

We report a patient with pachydermoperiostosis accompanied by hypertrophic gastritis. A 26-year-old man showed deep folds and furrows of the face and scalp, and terminal spade-like expansion of fingers and toes. Physical examination revealed no abnormalities except a grotesque appearance. Results of routine laboratory tests were unremarkable. Mild periosteal reactoins of both femurs and humeri were noted on long bone series, and hypertrophic gastritis on fibroscopic examination drew our attention. The relationship between pachydermoperiostosis and hypertrophic gastritis is uncertain. However it is probable that hypertrophic gastritis may be the endodermal counterpart of the ectodermal manifestations of pachydermoperiostosis.
Adult ; Ectoderm ; Endoderm ; Femur ; Fingers ; Gastritis, Hypertrophic* ; Humans ; Osteoarthropathy, Primary Hypertrophic* ; Physical Examination ; Scalp ; Toes