We report a case of left adrenal pheochromocytoma in 17-year-old girl, we observed all of vital sign were returned to normal in 19-th postoperative day
Adolescent ; Female ; Humans ; Pheochromocytoma* ; Vital Signs

PURPOSE: AP DNA endonuclease (APE), an enzyme responsible for the repair of damaged DNAs, is essential for the maintenance of genetic information of cells. Deficiency of APE in certain hereditary skin tumor and senescent cells has been implicated but the regulation of APE activity as well as the expression of APE gene in response to DNA damage has not been well documented. Genotoxic agents including ultimate carcinogens that can damage DNA were treated to cultured normal and transformed human cells and adaptive response of APE gene expression to these treatments was measured in order to evaluate the role of APE in chemical carcinogenesis. MATERIALS AND METHODS: Hydroxyl radical ('OH) generated from H2O2 (60 uM) through Fenton reaction, each 100 uM of N-nitrosomethylurea (NMU), 3-methyl-4-monomethyl- aminoazobenzene (3'-MeMAB) and N-acetoxy-2-acetaminofluorene (AAAF) were treated to umbilical cord blood cells (UCBC), HepG2 cells and HL-60 cells. APEX mRNA and APEX protein contents expressed in these cells exposed to each of these agents were measured by Northern blot hybridization and Western blot immunodetection analysis. The changes of APE activity in cells exposed to these genetoxic agents were measured. RESULTS: Treatment of H2O2 (60 uM) to UCBC, HepG2, and HL-60 cells increased APE activity significantly and pretreatment of a catalytic agent for OH, FeSO4 (60 pM) to the cells prior to H2O2 exposure did not further increase the APE activity in cells. Adaptive response to H2O2 in HL-60 cells increased in proportion to the concentration of H2O2 up to 60 pM. However, further increase in H2O2 concentration had no effect on the enzyme activity. Treatment of NMU (100 pM), 3-MeMAB (100 pM) and AAAF (100 pM) to these cells brought about a slight increase in the APE activity. APEX mRNA expression in UCBC and HepG2 cells exposed to H2O2, NMU, 3-MeMAB was markedly increased in APEX mRNA expression. APEX mRNA expression was also increased in HL-60 cells exposed to H2O2 (60 pM) and 3-MeMAB (100 uM) but NMU (100 pM) exposure to the cells resulted in a slight increase of it (Fig. 2). APEX protein expression was increased in all UCBC, HepG2 and HL-60 cells exposed to these genotoxic agents (Fig. 3). CONCLUSION: These results implicate that exposure of genotoxic agents to the cultured cells may cause DNA damage and lead to adaptive increase in APE activity as well as APE gene expression. It is probable that APE gene is transcriptionally regulated in response to the exposure of H2O2 or 3-MeMAB in cultured human cells as a consequence of activation of DNA repair system for the adaptation to the crisis.
Blotting, Northern ; Blotting, Western ; Carcinogenesis ; Carcinogens ; Cells, Cultured ; Deoxyribonuclease I* ; DNA Damage ; DNA Repair ; DNA* ; Fetal Blood ; Gene Expression ; Hep G2 Cells ; HL-60 Cells ; Hominidae ; Humans ; Hydroxyl Radical ; RNA, Messenger ; Skin

Phospholipase C (PLC) plays a pivotal role in transmembrane signal transduction pathway for cellular proliferation differentiation and growth. Thus far, there have been few reports in which PLC activity was investigated in human malignant neoplastic tissues. In the present study, we evaluated PLC activity in 23 human gastric cancer tissues and normal mucosal tissues to investigate whether alteration of PLC activity is associated with gastric cancer. The amount of [14C] diacylglycerol, one of the earliest products of inositol phospholipid hydrolysis by PLC, was measured by thin layer chromatography. Also, expression of PLC-gamma1, which is one of the most important PLC isozymes,was examined by immunohistochemistry using specific monoclonal antibody directed against PLC-gamma1. The results are summarized as follows. PLC activity in all 23 gastric cancer tissues (1.35+/-1.04 units/mg of protein) was significantly higher than normal mucosal tissues (0.28+/-0.21 units/mg of protein) (P<0.001). PLC activity in gastric cancer tissues was not correlated with histologic grade (P>0.05). PLC-gamma1 immunoreactivity was detected in all of 23 cases studied. The intensity and extent of PLC-gamma1 immunoreactivity was not correlated with PLC enzyme activity, although stronger intensity was demonstrated in malignant cells in comparison to normal gland epithelial cells. The present study provides the first evidence of significant elevation of PLC activity in human stomach cancer tissues. Our results strongly suggest that PLC might be involved in tumorigenesis and/or progression(uncontrolled continuous cycling of cells) of human gastric cancer. Further studies are needed to elucidate the role of elevated PLC activity in cancer tissues.
Humans ; Cell Transformation, Neoplastic ; Stomach Neoplasms

Investigation in our laboratory has been undertaken to study the effect of ethanol on the triglyceride (TG) content in the liver, the free fatty acid (FFA) content in the serum and the glycogen in the liver of rats which were fed on various diets. Four hours after administration of a sing1e dose of glucose (5g/kg BW.) and ethanol (6g/kg BW.) by gavage tube to rats fed a norma1 diet for 20 days then fasted for 18 hours, TG content in the liver increased by 80%, 10% compared to the control. When a sing1e dose of equal amounts of both glucose and ethanol were administered to another group, TG content in the liver was 42% higher than the control. There was no great change in serum FFA content in the glucose treated group as compared with the control, however, there was an increment of serum FFA content in the ethanol treated group and in the group treated with both ethanol and glucose by 81% and 71% of the control, respectively. The results indicate that ethanol administration had an inhibitory effect on the TG accumulation in the liver of rats fed by glucose. There is a correlation between TG accumulation in the liver and FFA content in the serum, and it appears that the ethanol administration did not induce the TG accumulation in the liver but the increment of serum FFA content in rats is probably due to the increased fatty acid mobilization from adipose tissue. However, countercurrent results were observed in the glucose treated group as compared with the ethanol treated group suggesting that glucose administration does induce TG accumulation in the liver but does not increase the serum FFA content in rats. The increment of serum FFA content in rats. The increment of serum FFA content by ethanol treatment was not ameliorated by glucose administration. In the liver perfusion experiment with rats fed both ethanol and various other diets, the results of incorporation of ethanol-1-14C into the total lipid in the high carbohydrate, high fat, low carbohydrate and control diet group were 1925 +/- 257 (cpm/g liver), 1237 +/- 76, 1269 +/- 105, 2041 +/- 74, respective1y. The results indicate that amount of dietary carbohydrate and high fat had an effect on the total lipid accumulation derived from ethanol-1-14C molecule in the liver. Liver glycogen content in the control on rats, high fat, 1ow carbohydrate and high carbohydrate diets were 91.5 +/- 7.9(mg%), 93.0 +/- 1.8, 99.1 +/- 4.4, and 153.7 +/- 26.0, respectively. There were no great differences between each dietary group and the rest control group except in the case of the high carbohydrate group which was over 1.5 times greater than that of the control. The incorporation of labelled ethanol into liver glycogen in the control rats and those on high fatdiet, low carbohydrate diet and high carbohydrate diet were 525, 401, 351 and 806 cpm/g liver, respectively. The increased incorporation of ethanol-1-14C into liver glycogen in the high carbohydrate diet group is thought to be due to the increased gluconeogenesis from acetyl CoA derived from 14C from ethanol because rats were fasted for 18 hours before perfusion. It might be the result of increased gluconegenesis of acetyl CoA derived from ethanol-1-14C by spare action of high carbohydrate on acetyl CoA. During the liver perfusion, 14CO2 production from ethanol-1-14C was higher in the high fat diet and low carbohydrate diet groups than in the control group, however, no great difference was observed between the high carbohydrate and control groups. The higher production of 14CO2 from the single ethanol-1-14C dose in rats on the high fat diet and low carbohydrate diet groups than in the control group is probably due to the increased metabolism of ethanol through Kreb's cycle rather than the incorporation of it into the liver fat.
Animal ; Diet ; Ethanol/metabolism ; Ethanol/pharmacology* ; Fatty Acids, Nonesterified/blood ; Glucose/pharmacology ; In Vitro ; Liver/metabolism* ; Male ; Rats ; Triglycerides/metabolism*

Biotin-deficient rats were raised on a purified ration containing raw egg white plus avidin. Urea synthesis and excretion were compared between the biotin-deficient and the pair-fed control rats. 24hrurinary urea excretion and the specific activities of carbamylphosphate synthetase, ornithine transcarbamylase, and arginase in the liver mitochondria fraction were no different between these two groups. The net urea production in the liver slice and in the isolated perfused liver of the biotin-deficient rats was similar to that of the pair-fed control. Thus the conclusion must be that biotin is not in urea in mea biosynthesis in the rat.
Animal ; Avitaminosis/metabolism ; Biotin* ; Liver/metabolism* ; Rats ; Urea/biosynthesis* ; MH - ; Substances: ; Urea ; Biotin

The effect of alloxan-diabetic rat fed with normal, high fat, low protein and high protein diets on the rate of urea production and the activities of enzymes associated with the urea cycle (ornithine transcarbamoylase, E.C. 2.1.3.3, OTC; arginase, E.C. 3.5.5.1) have been studied in intact and isolated perfused liver. The amount of urea excretion was the highest in the high protein diet group. When each diet group was treated with alloxan, total urea excretion showed little differences between each diet group and its corresponding control group with the exception being in the normal diet group. However, the enzyme activity of OTC was increased significantly by alloxan treatment in low and high protein diet groups as compared to corresponding control groups. Similar results were obtained in arginase activity, although the magnitude of the change was less marked. In liver perfusion experiments on rats treated with alloxan, the amount of urea production and changes in OTC and arginase activity were very similar with those in the intact liver. These results suggest that alloxan treatment in normal diet group causes an increase in urea excretion both in intact and perfused liver regardless of changes in enzyme activities and total urea excretion, and enzyme activities are affected by changes in dietary components but the changes of enzyme activities may not correlate with total urea excretion.
Alloxan ; Animal ; Diabetes Mellitus, Experimental/metabolism* ; Dietary Fats/pharmacology* ; Dietary Proteins/pharmacology* ; In Vitro ; Liver/metabolism* ; Male ; Perfusion ; Rats ; Urea/metabolism* ; Urea/urine

The pharmacologic actions of ketamine in human volunteers were reported by Domino et al in 1965 and it was used in 130 patients by Corssen Domino in 1966. Chodoff and Stella were the first to investigate ketamines suitabilityas an in anesthetic in childbirth. Since then several authors reported that ketamine has several advantages over conventional anesthetics in obstetric anesthesia. Ketamine was used as the sole anesthetic agent for forceps delivery in 50 women who were selected randomly. Ketamine was administered intravenously just before delivery in doses of 30 to 60 mg and after delivery dosage was not limited, The following results were observed: 1) During delivery, a rapid and intense analgesic effect was sufficiently maintained with a small dose of ketamine. 2) With the use of ketarnine it is possible to shorten the second stage of labor with a short induction-delivery-interval because of the advantages of forceps delivery. 3) Ketamine could be used without intubation during with a short fasting time because protective laryngeal quate airway could be maintained. 4) Ketamine did not appear to induce an increase of Very. delivery even in patients and pharyngeal reflexes and an ade uterine bleeding during or after deli 5) The use of ketamine during delivery appeared to have almost no affect on the Apgar score. 6) The use of ketamine was accompanied by mild complications but they were not significant.
Anesthesia, Obstetrical* ; Anesthetics ; Apgar Score ; Fasting ; Female ; Gagging ; Healthy Volunteers ; Humans ; Intubation ; Ketamine* ; Parturition ; Pharmacologic Actions ; Surgical Instruments ; Uterine Hemorrhage

Ca45 resorption and incoporration into albino rat-bones in tissue culture was considered in studying the pathogenesis of osteoporosiscaused by cotinued administration of glucocorticoid, hydrocortisone succinate. 18-day old tibias were cultured in a chemically defined media, (BGJb). Hydrocotisone showed no effect on Ca45 resorption and little increase of Ca45 incorporation into bone. This may suggest that hydrocortisone produces osteoporosis not by direct effect but by secondary effects on calcium metabolism.
Animal ; Bone Development ; Bone and Bones/embryology ; Bone and Bones/metabolism* ; Calcification, Physiologic/drug effects ; Calcium/metabolism* ; Calcium Radioisotopes ; Hydrocortisone/adverse effects ; Hydrocortisone/pharmacology* ; Osteoporosis/chemically induced* ; Rats ; Tibia ; Tissue Culture

BACKGROUND: Leptin gene is known to be related to obesity in human and animals and complete genetic defect of the gene in ob/ob mouse has been identified. Therefore, ob/ob mouse is widely used as an animal model for the study of etiology and therapy of obesity. The main biological function of leptin was thought to involve in the regulation of food intake and weight gain, however, the regulatory mechanisms by which leptin functions in the weight reduction and lowering the blood glucose level are uncertain. In the present study, retroviral-mediated leptin gene transduction into ob/ob mouse was attempted for the correction of biochemical parameters of obesity. METHODS: Leptin cDNA was inserted into pLXSN retroviral vector (pLXSN-lep) and recombinant leptin expressing retrovirus particles (3 X10 CFU/mL) were produced in psi2 ecotropic packaging cells and subsequent transfection into PA317 amphotropic packaging cells. The leptin expressing recombinant viruses (LER) were transduced into NIH3T3 mouse fibroblasts and insertion of leptin cDNA into chromosomal DNA of PA317 and MH3T3 mouse fibroblasts was confirmed by Southern blot hybridizations. Leptin mRNA and its protein expressed in the cells were identified by Northern blot hybridization and Western blot immunodetection method, respectively. LER were injected I. P. into ob/ob mice, and body weight, food intake, serum leptin level and blood glucose level were measured. RESULTS: Expression of leptin was identified in PA317 and NIH3T3 mouse fibroblasts transduced with LER. Leptin content in sera of mice transfused with LER was drastically increased after 1 week and decreased to the almost basal level at 3 weeks after the transfusion. The body weight as well as food intake of ob/ob mouse transduced by LER decreased for the first 3 weeks and slightly increased thereafter. The reduction of both body weight and food intake in ob/ob mice transduced with LER was observed with the concomitant increase of serum leptin level, indicating that retroviral-mediated transduction of leptin gene in ob/ob mouse in vivo produced a biologically active leptin protein and released it into blood circulation. CONCLUSION: A transient expression of leptin cDNA in ob/ob mice by a retroviral-mediated transduction was performed and further studies are required for long term expression of the gene in vivo.
Animals ; Blood Circulation ; Blood Glucose ; Blotting, Northern ; Blotting, Southern ; Blotting, Western ; Body Weight ; DNA ; DNA, Complementary ; Eating ; Fibroblasts ; Humans ; Leptin* ; Mice ; Mice, Obese* ; Models, Animal ; Obesity ; Product Packaging ; Retroviridae ; RNA, Messenger ; Transfection ; Weight Gain ; Weight Loss ; Zidovudine*

C-fos protein is a gene regulatory third messenger involved in long-term responses of cells to various stimuli. Kainic acid(KA), a powerful excitatory analogue, induces seizures and damages the hippocampus and other limbic regions in rats. KA treatment induces c-fos protein production in the hippocampus. This study was undertaken to investigate the expression of c-fos protein in the hippocampus according to seizure stage induced by systemic injection of KA. Twenty-three adult male Sprague-Dawley rats experienced convulsions by a single intraperitoneal injection of convulsive dose (20-40 mg/Kg) of KA. Seven control rats received normal saline. Animals were sacrificed 3 hr after KA treatment. The expression of c-fos protein was tested in the hippocampus by immunohistochemical staining using polyclonal anti-Fos. Most of the rats exhibited limbic motor epileptic activity. C-fos protein immunoreactivity increased in the CA1, CA3 and dentate gyrus at stage 1-2, and not only in the CA1, CA3 and dentate gyrus but also in the CA4 at stage 3-4. At stage 5, c-fos protein immunoreactivity increased in all areas of the hippocampus. C-fos protein immunoreactivity increased progressively with increasing severity of convulsions. These results show that KA produces limbic motor seizure associated with a rise in the c-fos protein in the hippocampus, and that the expression of c-fos protein may has some relevance to the progressive and permanent brain changes occurring during epilepsy.
Adult ; Animals ; Brain ; Dentate Gyrus ; Epilepsy ; Genes, vif ; Hippocampus* ; Humans ; Injections, Intraperitoneal ; Male ; Rats* ; Rats, Sprague-Dawley ; Seizures*