No abstract available.
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We induced apoptosis in normal rats by intramuscular injection of 5-fluorouracil (5-FU) and immunohistochemically evaluated the thymus for the TdT-mediated dUTP biotin nick end labelling on the 1st, 3rd, 6th, 9th, 15th and 21st days following the bolus intramuscular injection. The injections of 5-FU induced a greater extent of apoptosis in the thymus. In the thymus, a mild increase in apoptosis was observed 24 hours after injection. The greatest number of apoptotic cells were seen at 72 hours. The size of the thymus decreased and the cortex thinned with hypocellularity. The injection of 5-FU caused massive cell loss in the thymus. Most apoptotic cells were scattered in the cortex and lower levels of apoptosis were also observed in the medulla. After 72 hours, the level of apoptosis returned to the control level. Considering the above results, we think that 5-FU induced toxicity may be related to 5-FU induced apoptosis in normal tissue, especially the thymus.
Animals ; Apoptosis* ; Biotin ; Fluorouracil* ; Injections, Intramuscular* ; Rats* ; Thymus Gland*

The study was undertaken to determine the most adequate tidal volume when used volume preset ventilator during anesthesia. The thirty patients were received controlled mechanical ventilation with constant inspiratory pressure of 10 cmH2O and respiratory frequency of 12/minute. The results were as follows: 1) The PH was 7.39±0.01 and it is within normal limit. 2) The PaCO2 was 34.0±0.6 mmHg and it is a slightly hyperventilatory state. 3) The PaO2 was 228.0±8.2 mmHg. 4) The Buffer base was 20.7±0.3 mEq/L and it is a slightly buffer base deficient state. From the above results. We concluded that if patients were fully relaxed during general anesthesia, it is desirable to maintain the inspiratory pressure of anesthetic mechanical ventilator to 10 cmH2O for adequate alveolar ventilation.
Anesthesia ; Anesthesia, General ; Humans ; Hydrogen-Ion Concentration ; Respiration, Artificial ; Tidal Volume ; Ventilation ; Ventilators, Mechanical*

This investigation was undertaken to determine whether venous blood, sampled under carefully controlled conditions, was an acceptable alternative to arterial blood for the measurement of arterial blood gas analysis. The arterial values for Pco2, pH, base excess and oxygen saturation were compared with the values of blood samples drawn simultaneously from the cephalic, external jugular and internal jugular vein during inhalation general anesthesia with 50% oxygen concentration in 25 cases. The results were as follows: 1) The blood gas analysis values of cephalic venous blood were closely comparable to those of arterial blood. There was no significant difference between the Pci2, pH and base excess of cephalic venous and arterial blood. 2) Although the oxygen partial pressure in cephalic venous blood was significantly less than that in arterial blood, the difference in oxygen saturation was small. 3) The blood gas analysis values of external jugular venous blood were between the cephalic venous blood and the internal jugular venous blood values. Those show that venous blood was arterialized and in general anesthesia, it's Pco2, pH and oxygen saturation will be near endough to those of the arterial blood. Although the oxygen partial pressure in venous blood was significantly less than that in arterial blood, the difference in oxygen saturation was small. Therefore arterialized venous blood from the cephalic vein may provide a reasonable estimate of presence or absence of hypoxia. in this study, we feel that the use of cephalic venous blood for Pco2, pH and oxygen saturation determination during general anesthesia is a reliable indirect method of arterial blood sampling.
Anesthesia, General ; Anoxia ; Blood Gas Analysis ; Hydrogen-Ion Concentration ; Inhalation ; Jugular Veins ; Oxygen* ; Partial Pressure ; Veins

We reviewed 7 cases of congenital mesoblastic nephroma (4 cases of classical mesoblastic nephroma (CMN) and 3 cases of atypical mesoblastic nephroma (AMN)) using immuno-histochemical and flow cytometric study. Results are as follows. 1) The mean tumor size was 5 (3 to 7cm)cm in CMN and 9 (7 to 10cm)cm in AMN. The AMN revealed hemorrhage and necrosis in two Of three cases. A case of AMN showed cystic change without hemorrhage and necrosis. Mitotic count ranged in 0~4/10HPF in CMN and 20-35/10HPF in AMN. 2) Immunohistochemistry for vimentin was all positive. Actin, desmin were weakly positive in CMN, but negative in AMN. The findings were consistent with myofibroblastic differentiation in CMN and AMN was considered to be the less differentiated form of CMN. 3) Flow cytometiic analysis showed diploidy in two of two CMNs and two of three AMNs. Only one AMN showed aneuploidy with DNA index of 1.41. %SG2M were 8.1 and 15.9 (mean 12.0) in CMN and 16.9, 32.9 and 19.3 (mean 22.9) in AMN, respectively. We concluded that AMN should be distinguished from CMN, clinicopathologically.

Benign hemangioma of the mediastinum is rare. This slowly growing tumor is described as well circumscribed, cystic, hemorrhagic tumor. Histologically it can be differentiated into capillary or cavernous form. We present a case of mediastinal hemangioma. A 20-year-old-man was presented with a slowly growing posterior mediastinal mass of 6 years duration, 8x6 cm in size. The mass was relatively well defined but focally invasive. Microscopically, it was differentiated into vessels of capillary, cavernous, and venous patterns. A solid cellular proliferation with inconspicuous capillary lumens was focally seen. The stroma between variable-sized vessels showed marked myxoid change associated with some smooth muscle bundles and adipose tissue. Ultrastructurally, areas of solid cellular proliferation showed formation of lumens. These lumens were lined by active endothelial cells showing plasmalemmal vesicles and Weibel-Palade bodies on the abluminal surface.
Adipose Tissue ; Capillaries ; Cell Proliferation ; Endothelial Cells ; Hemangioma* ; Mediastinum ; Muscle, Smooth ; Weibel-Palade Bodies

MAGE (melanoma antigen gene) is a tumor specific shared antigen, presented by HLA class I molecules, which is recognized by cytotoxic T lymphocytes. MAGE proteins are expressed in malignant tumor cells, in contrast to no expression in normal or benign tissues except for testis and placenta. MAGE might be a potential target for immunotherapy of malignant tumors. However, its biological aspects associated with cell cycle are not yet described. The flow cytometry is a useful tool for objective and quantitative analyses of heterogenous tumor cell population. To understand the status of MAGE related to cell cycle and its relationship with p53 as the G1 checkpoint regulator, p21, and PCNA as a proliferative index, we investigated expression of MAGE-3 protein, mutant p53, p21, and PCNA by flow cytometry and immunohistochemical stain. In addition, double stains for MAGE-3/p53, p53/PCNA, and p53/p21 were analysed with bivariate flow cytometry. DNA histograms using MAGE-3/PI (DNA) and p53/PI (DNA) were also analysed. The cell line (PNUH- 12) used for this study originated from a hypopharyngeal squamous cell carcinoma, which has point mutation (exon 7, C-->G) of p53. The expression rate of MAGE-3 was 83%, PCNA 85%, and p53 81%. No expression for p21 was identified. MAGE-3 was expressed in cytoplasm, while both PCNA and p53 were expressed in nuclei of tumor cells. With bivariate analyses, coexpression rates of MAGE-3/p53 and p53/PCNA were 0.96 and 0.97, respectively. Both MAGE-3 and p53 showed constantly high level throughout the cell cycle. These results suggest that expression of MAGE-3 and mutant p53 is not dependent on the cell cycle. p21 seems to be inactivated.
Carcinoma, Squamous Cell* ; Cell Cycle ; Cell Line* ; Coloring Agents ; Cytoplasm ; DNA ; Flow Cytometry* ; Immunotherapy ; Mutant Proteins ; Placenta ; Point Mutation ; Proliferating Cell Nuclear Antigen* ; T-Lymphocytes, Cytotoxic ; Testis

PURPOSE: MAGE (melanoma antigen gene) is a tumor associated antigen, presented by HLA class I molecules, which is recognized by cytotoxic T lymphocytes. The expression of MAGE proteins are confined to malignant tumor tissues, except for the normal testis and placental tissues. Therefore, MAGE may be a potential target for immunotherapy of malignant tumors. However, biological aspects associated with the cell cycle are not yet described. MATERIALS AND METHODS: The material used for this study was a novel human squamous cell carcinoma cell line (PNUH-12) from the hypopharynx, which had one point mutation of 78th base, C to G, in exon 7 of p53 gene. To understand the role of MAGE in relation to cell cycle and its relationship with p53 as the Gl checkpoint regulator, the expressions of MAGE-3 protein and mvtant p53 (Mtp53) were accessed by flow cytometry and immunohistochemistry. Double stains for MAGE-3/Mtp53 was analyzed with bivariate flow cytometry. DNA histograms using MAGE-3/PI (DNA) and Mtp53/PI (DNA) were also analyzed. RESULTS: The expression rate of MAGE-3 and Mtp53 were 83% and 85%, respectively. MAGE-3 was expressed in cytoplasm, while M:p53 were expressed in the nuclei of the tumor cells on the immunohistochemical sections. With bivariate analyses, coexpression rate of MAGE-3/Mtp53 was 0.96, and MAGE-3 and Mtp53 constantly showed high levels throughout the cell cycle except Go. CONCLUSIONS: These results mean that (I) MAGE-3 might have yet unknown relationship with mutant p53, (2) expressions of MAGE-3 and Mtp53 are not dependent on the cell cycle in PNUH-12 hypopharyngeal squamous carcinoma cell line, and suggest that MAGE-3 might have a role as important as p53 during the development of malignant tumors.
Carcinoma, Squamous Cell ; Cell Cycle* ; Cell Line ; Coloring Agents ; Cytoplasm ; DNA ; Exons ; Flow Cytometry* ; Genes, p53 ; Humans ; Hypopharynx ; Immunohistochemistry ; Immunotherapy ; Point Mutation ; T-Lymphocytes, Cytotoxic ; Testis

Malignant fibrous histiocytoma (MFH) of the liver is uncommon, representing less than 1% of the primary malignant lesions of the liver. We report primary MFH of the liver in a 59-year-old woman. The tumor, measuring 9.0 9.0 6.0 cm, was located in the left lobe of the liver. It showed multiple areas of hemorrhage and necrosis. Microscopically, the tumor consisted of plump spindle cells haphazardly arranged in short fascicle and focal storiform pattern. Multiple bizarre giant cells were also noted. Immunohistochemically, many of the tumor cells were positive for vimentin and alpha1-antitrypsin but negative for epithelial markers. Ultrastructurally, the tumor cells showed fibroblastic and histiocytic features.
Female ; Fibroblasts ; Giant Cells ; Hemorrhage ; Histiocytoma, Malignant Fibrous* ; Humans ; Liver* ; Microscopy, Electron ; Middle Aged ; Necrosis ; Vimentin

Glycogen storage diseases(GSD) are inherited disorders affecting glycogen metabolism and type I GSD is due to the absence or deficiency of glucose-6-phosphatase(G6Pase) enzyme in the liver, kidney, and intestinal mucosa. The defect leads to inadequate hepatic conversion of G6P to glucose and thus make affected individuals susceptible to fasting hypoglycemia, and the accumulation of glycogen occurs in the liver and other organs. Type Ia is the most common form of GSD and clinically growth retardation may manifest of GSD itself rather than growth hormone deficiency(GHD), but we experienced a case of type I GSD with GHD in a 14-year-o1d male. The height was 125 cm, compatible with 50 th percentile of height of 8 years of age. He has doll-like face with fat cheek, relatively thin extremities, and metabolic acidosis, hyperuricemia, hypoglycemia, hyperlipidemia. GH stimulation test with clonidine and L-dopa revealed that the patient had decreased GH secretion. After laboratory work up including liver biopsy, he was diagnosed as type I GSD. Hypoglycemia was managed with frequent feeding with high starch diet(uncooked cornstarch). Metabolic acidosis and hyperuricemia were treated with sodium bicarbonate, allopurinol and probenecid. The patient is being followed at out-patient clinic with clinical improvement after of diet therapy and GH administration.
Acidosis ; Allopurinol ; Biopsy ; Cheek ; Clonidine ; Diet Therapy ; Extremities ; Glucose ; Glycogen Storage Disease* ; Glycogen* ; Growth Hormone* ; Humans ; Hyperlipidemias ; Hyperuricemia ; Hypoglycemia ; Intestinal Mucosa ; Kidney ; Levodopa ; Liver ; Male ; Metabolism ; Outpatients ; Probenecid ; Sodium Bicarbonate ; Starch