No abstract available.
Humans ; Infant*

PURPOSE: The enhanced cytotoxic effect of combined treatement of hyperthermia and chemotherapy by increasing intracellular acidify with HMA was investigated. MATERIALS AND METHODS: Fsall tumor cells were injected on the hindlegs of female C3H mice. When the tumor volume reached about 200mm3 , experiments were performed on the groups classified as follows : Group I : Control Group II : Melphalan alone (2.5 mg/kg, 5 mg/kg, 10 mg/kg, 15 mg/kg). Group III : Heat alone (42.5degree C for 1 hour) Group IV : Melphalan + Heat (42.5degree C for 1 hour) Group V : HMA(10 mg/kg) + Melphalan (5.0 mg/kg) + Heat (42.5degree C for 1 hour) Each group included 8-12 mice on each experiment. HMA (3-amino-6-chloro-5(1-homopiperidyl)-N-(diaminomethylene)-c-pyrazinecarboxamide), an analog of amiloride which increases intracellular pH(pHi) was dissolved in dimethyl sulfoxide(DMS) and injected into the tumor-bearing mice through the tail vein. 10mg/kg of HMA and each dose of melphalan were injected into peritoneum of the tumor-bearing mice 30 minutes before heating. Tumor growth delay was calculated when the tumor vlme reached at 1500mm3 . Excision assay was performed on each group and repeated 2-4 times. RESULTS: Tumor growth delay of each experimental groups at 1500 mm3 were 9, 10, 13 and 19 days respectively. In vivo-in vitro excision assay using Fsall tumor cells, the cytotoxicity of each experimental groups was 1.2 X 107 , 1 X 107 , 6 X 106 , 1.7 X 106 and 1 X 105 clonogenic cells/gm respectively. When HMA was added to the combined treatment of heat and chemotherapy, the tumor growth ws delayed more than combined treatment without HMA i.e., 6 days tumor growth delay at 1500 mm3 of tumor volume. CONCLUSION: he combined effect of cytotoxicity by heat and chemotherapy can be much more enhanced by HMA.
Amiloride ; Animals ; Drug Therapy* ; Female ; Fever* ; Heating ; Hot Temperature ; Humans ; Hydrogen-Ion Concentration* ; Melphalan ; Mice ; Mice, Inbred C3H ; Peritoneum ; Tumor Burden ; Veins

No abstract available.
Lung Neoplasms* ; Lung*

No abstract available.
Coronary Artery Bypass* ; Saphenous Vein*

No abstract available.
Pulmonary Aspergillosis*

No abstract available.
Decompression* ; Head* ; Osteonecrosis*

In the figure 3, designation of severity of bronchopulmonary dysplasia (BPD) was misprinted. Open bars (white) represent severe BPD, not mild BPD. Closed bars (Black) represent mild BPD, not severe BPD. Gray bars in the middle represent moderate BPD without change.

Systemic lupus erythematosus (SLE) is a multisystemic disease that can involve the gastrointestinal tract, liver, and biliary system. Symptomatic pancreatic involvement, however, has rarely been reported. It may be part of the primary disease process, such as vasculitic or autoimmune etiology, or associated with drug therapy, in particular corticosteroid. We report here a lupus patient who developed severe pancreatitis within 30 hours of initiation of corticosteroid therapy; we also discuss the relation between pancreatitis and systemic lupus erythematosus.
Biliary Tract ; Drug Therapy ; Gastrointestinal Tract ; Humans ; Liver ; Lupus Erythematosus, Systemic* ; Pancreatitis*

OBJECTIVE: To assess the clinical effect of bucillamine in rheumatoid arthritis (RA), we performed an open clinical trial for 3 months. METHODS: 10 out of 12 patients completed bucillamine trial(200mg/day) for their initial treatment against arthritis, and 9 out of 11 patients with refractory RA completed the bucillamine trial. Disease activity was assessed by the duration of morning stiffness(MS), visual analogue pain scale(VAPS), functional capacity(FC), tender joint counts(TJC), swollen joint counts(SJC), ESR, and CRP every month. Adverse effects were monitored monthly. RESULTS: At the end of trial, all parameters were decreased in the initial treatment group except of CRP. No parameters were decreased in the refractory group. Gastrointestinal disturbance was the most commmon adverse effect. Skin rash, stomatitis, proteiuria and elevated hepatic enzyme were minor adverse effects. CONCLUSION: Bucillamine was effective in the initial treatment of rheumatoid arthritis, but not effective in the patients with refractory rheumatoid arthritis. Bucillamine is relatively safe in the treatment of rheumatoid arthritis in both groups.
Arthritis ; Arthritis, Rheumatoid* ; Exanthema ; Humans ; Joints ; Stomatitis

BACKGROUND: The Histidine-Tryptophan-Ketoglutarate (HTK) solution has been shown to provide the excellent myocardial protection as a cardioplegia. The HTK solution has relatively low potassium as an arresting agent of myocardium, and low sodium content, and high concentration of histidine biological buffer which confer a buffering capacity superior to that of blood. Since HTK solution has an excellent myocardial protective ability, it is reported to protect myocardium from ischemia for a considerable time (120 minutes) with the single infusion of HTK solution as a cardioplegia. The purpose of this study is to evaluate the cardioprotective effect of HTK solution on myocardium when the ischemia is exceeding 120 minutes at two different temperature (10 to 12degrees C, 22 to 24degrees C) using the Langendorff apparatus. MATERIAL AND METHOD: Hearts from Sprague-Dawley rat, weighing 300 to 340 g, were perfused with Krebs-Henseleit solution at a perfusion pressure of 100 cm H2O. After the stabilization, the heart rate, left ventricular developed pressure (LVDP), and coronary flow were measured. Single dose of HTK solution was infused into the ascending aorta of isolated rat heart and hearts were preserved at four different conditions. In group 1 (n=10), hearts were preserved at deep hypothermia (10~12degrees C) for 2 hours, in group 2 (n=10), hearts were preserved at moderate hypothermia (22~24degrees C) for 2 hours, in group 3 (n=10), hearts were preserved at deep hypothermia for 3 hours, and in group 4 (n=10), hearts were preserved at moderate hypothermia for 3 hours. After the completion of the preservation, the heart rate, left ventricular developed pressure, and coronary flow were measured at 15 minutes, 30 minutes, and 45 minutes after the initiation of reperfusion to assess the cardiac function. Biopsies were also done and mitochondrial scores were counted in two cases of each group for ultrastructural assessment. RESULT: The present study showed that the change of heart rate was not different between group 1 and group 2, and group 1 and group 3. The heart rate was significantly decreased at 15 minutes in group 4 compared to that of group 1 (p<0.05 by ANCOVA). The heart rate was recovered at 30 minutes and 45 minutes in group 4 with no significant difference compared to that of group 1. The decrease of LVDP was significant at 15 minutes, 30 minutes and 45 minutes in group 4 compared to that of group 1 (p<0.001 by ANCOVA). Coronary flow was significantly decreased at 15 minutes, 30 minutes, and 45 minutes in group 4 compared to that of group 1 (p<0.001 by ANCOVA). In ultrastructural assessment, the mean myocardial mitochondrial scores in group 1, group 2, group 3, and group 4 were 1.02+/-0.29, 1.52+/-0.26, 1.56+/-0.45, 2.22+/-0.44 respectively. CONCLUSION: The HTK solution provided excellent myocardial protection regardless of myocardial temperature for 2 hours. But, when ischemic time exceeded 2 hours, the myocardial hemodynamic function and ultrastructural changes were significantly deteriorated at moderate hypotherma (22~24degrees C). This indicates that it is recommended to decrease myocardial temperature when myocardial ischemic time exceeds 2 hours with single infusion of HTK solution as a cardioplegia.
Animals ; Aorta ; Biopsy ; Cardioplegic Solutions ; Heart Arrest, Induced ; Heart Rate ; Heart* ; Hemodynamics ; Histidine ; Hypothermia ; Ischemia ; Myocardium ; Organ Preservation ; Perfusion ; Potassium ; Rats* ; Rats, Sprague-Dawley ; Reperfusion ; Sodium