PURPOSE: Alteration of p53 and telomerase activity may be responsible for gastric carcino- genesis. In this study, we tried to observe modulation of telomerase activity by wild type p53 in gastric cancer cell lines. MATERIALS AND METHODS: We used five gastric cancer cell lines (KATO-III, AGS, SNU-1, SNU-5, SNU-16). In order to find p53 mutation, we used western blot and PCR-SSCP. The TRAP-eze kit which supplied by Oncor (Gaithersburg, MD) was used to detect telomerase activity of the five gastric carcinoma cell lines. The wild type p53 gene was transfected by electroporation method. RESULTS: The expression of p53 protein was increased in four gastric carcinoma cell lines and one cell line (KATO-III) did not express. We found p53 point mutation in exon 5 and 8, and the p53 gene was deleted in KATO-III. The telomerase activity were observed in all five gastric carcinoma cell lines and there were no difference in telomere repeat length among five cell lines. After transfection with wild type p53, we could not find the change of telomerase activity in KATO-III. CONCLUSION: Although activation of telomerase activity and mutation of p53 gene may be needed in gastric carcinogenesis, the telomerase activity was not affected by restoration of p53 function in gastric carcinoma cell lines.
Blotting, Western ; Carcinogenesis ; Cell Line* ; Electroporation ; Exons ; Genes, p53* ; Point Mutation ; Stomach Neoplasms ; Telomerase* ; Telomere ; Transfection

Laryngeal granuloma is a localized inframmatory response to mucosal loss caused by endolaryngeal trauma. Endotracheal intubation is the most common cause of laryngeal granuloma. Mucosal loss is followed by ulceration and infection and then by an overproduction of reactive granuloma tissue. Granuloma formation is most frequent on the posterior one third of the vocal cord. The authors experienced two cases of laryngeal granuloma after endotracheal intubation for general anesthesia.

Vasopressor effects of epinephrine, norepinephrine, ephedrine, phenylephrine, methoxamine and of mephentermine were compared in resrpinized dogs with or without nitrous oxide-oxygen-halothane anesthesia. The results are as follows: (1) Epinephrine and norepinephrine were shown to have the most potent pressor effect in reserpinized and nitrous oxide-oxygen-halothane-anesthetized dogs. Phenylephrine, methoxamine, mephen-termine and ephedrine were less potent in decreasing order. (2) Decrease in mean arterial pressure was less marked in dogs reserpinized and anesthetized with nitrous oxide-oxygen-halothane than in reserpinized but unanesthetized dogs. (3) It revealed that nitrous oxide-oxygen-halothane anesthesia potentiated the vasopressor effects of the sympathomimetic amines studied. Nitrous oxide-oxygen-halothane anesthesia is implicated to exert an sympathomimetic effect.
Anesthesia* ; Animals ; Arterial Pressure ; Dogs* ; Ephedrine ; Epinephrine ; Mephentermine ; Methoxamine ; Norepinephrine ; Phenylephrine ; Sympathomimetics*

To determine the effects of hydrcxyethyl starch upon liver, kidney, serm electrolytes and particularly upon blood coagulation, 500 ml of 6% HES in saline solution was administered intravenously to 15 patients during elective minor surgery. In all cases weighted blood loss was less than 600 ml without replacement. The following laboratory tests were performed immediately before infusion and again 1 hour, 24 hours, 48 hours, and 1 week after the infusion: RBC, WBC, hemoglobin, hematocrit, ESR, platelet, bleeding time, coagulation time, prothrombin time, total protein, albumin, total bilirubin, direct bilirubin, SGOT, SGPT, alkaline phosphatase, BUN, sodium, potassium, and chloride. The results are as follows: 1) No anaphylactic shock or bleeding tendency characteristic of colloids was encountered. 2) No functional disturbance of liver or kidney directly attributable to HES was identified. 3) All laboratory parameters except WBC and ESR decreased after infusion. The decrease was, however, within the normal range and believed secondary to dilational effect of infusion. WBC increased somewhat, but returned to the preinfusion level in a week. 4) Exceptionally erythrocyte sedimentation rate increased notably during the 24 hour period following infusion. As with dextran, this was interpreted not due to direct effect of HES, but due to increased adsorption of fibrinogen, alpha-beta-gamma-glcbulin to red cell surface with changes in electric charge between red cells. 5) Clinical applicability, metabolic aspect, degree of subtitution of hydroxyethyl group and safety with multiple infusion of HES must be carefully determined.
Adsorption ; Alanine Transaminase ; Alkaline Phosphatase ; Anaphylaxis ; Aspartate Aminotransferases ; Bilirubin ; Bleeding Time ; Blood Coagulation ; Blood Platelets ; Blood Sedimentation ; Colloids ; Dextrans ; Electrolytes ; Fibrinogen ; Hematocrit ; Hemorrhage ; Humans ; Kidney ; Liver ; Potassium ; Prothrombin Time ; Reference Values ; Selective Estrogen Receptor Modulators ; Sodium ; Sodium Chloride ; Starch* ; Surgical Procedures, Minor

It has been emphasized that continuous monitorings of arterial pressure, central venous pressure, electrocardiogram, blood gas analysis, serum electrolytes, body temperature, hematacrit and urinary output are mandatory for the anesthetic management of pheochromocytoma. In addition, it is necessary for the anesthetists to understand pharmacologic effects of drugs which influence the peripheral vascular tone and cardiac excitability. We experienced recently anesthetic management of two cases of pheochromocytoma; one raised problems of ventricular arrhythmias and hypertension that aggravated nature of arrhythrmias by increasing blood pressure and responded favorably to treatment with propranolol and trimetaphan. Tumor of this case originated from abdominal aortic wall. The other was managed by injection of d-tubocurarine which induced narrowing of pulse pressure by depletion of increasing systolic pressure and accompanied tachycardia without cardiac decompensation. We have reported proper anesthetic managements of two cases of pheochromocytoma with N2O O2-halothane anesthesia and reviewed literatures in discussion.
Anesthesia ; Arrhythmias, Cardiac ; Arterial Pressure ; Blood Gas Analysis ; Blood Pressure ; Body Temperature ; Central Venous Pressure ; Electrocardiography ; Electrolytes ; Hypertension ; Pheochromocytoma* ; Propranolol ; Tachycardia ; Trimethaphan ; Tubocurarine

d-tubocurarine is one of the non-depolarizing muscle relaxants which is most commonly used in clinical situations d-Tc is used as a selective muscle relaxant in hypertensive patients or patients for renal transplantation. The most common side effect of d-Tc is a dose-related fall in arterial pressure. Although the cause of the hypotension is still controversial, the two mechanism most frequently suggested are ganglionic block and histamine release. d-Tc is an active ganglionic blocking agent. Howver, because its potency at the neuromuscular junction is greater than at the ganglia, there is some doubt that a clinical concentration of d-Tc is sufficient to cause hypotension. histamine release may play a role in this blood pressure reduction. Indeed, decrease in blood pressure produced by d-Tc have been shown to be less when the muscle relaxant was preceded by and antihistamine. The amount of histamine release substance depends on plasma levels of the drug achieved and thus on the rapidity of intravenous administration of that drug. If d-Tc produces histamine release, then slow intravenous injection would be associated with minimal histamine release and a resulting attenuation of the typical blood pressure reduction that follows' this drugs injection. Therefore, we measured changes in mean arterial pressure(MAP) and heart rate in patients anesthetized with nitrous oxide-halothane during and after the intravenous injection of d-Tc at varying rates of administration. The results are as follows: 1) Group 1: Maximum reduction in MAP were present 3 minutes following d-Tc injection over 1 second (81+/- 3 torr). Comparative with control group (99+/-6 torr), significant reduction was revealed(18.1%). 2) Group 2: Decrease in MAP 3 minutes after administration of d-Tc over 90 seconds(11.1%) were intermediate between the other injection rates. 3) Group 2: Decrease in MAP 3 minutes after d-Tc administration was significantly less in patients receiving the drug over 180 seconds(5.1%). Heart rate did not change significantly after d-Tc injection regardless of the rate of administration.
Administration, Intravenous ; Arterial Pressure ; Blood Pressure* ; Ganglia ; Ganglion Cysts ; Heart Rate ; Histamine Release ; Humans ; Hypotension ; Injections, Intravenous ; Kidney Transplantation ; Neuromuscular Junction ; Neuromuscular Nondepolarizing Agents ; Plasma ; Tubocurarine*

In order to comparatively evaluate the effects of cyclopropane and fluothane upon mean arterial pressure. cardiac output and splanchnic blood flow during hemorrhagic shock a Iaboratory investigation was conducted in the following three successive phases in two groups: Group I (cyclopropane):1l. Observation 60 minutes following Nembutal I .V. injection 2. Observation 30 minutes following acute hemorrhage 3. Observation 30 minutes following cyclopropane anesthesia Group II (fluothane): 1. Observation 60 minutes following Nembutal I .V. injection 2. Observation 30 minutes following acute hemorrhage 3. Observation 30 minutes following fluothane anesthesia Nine mongrel dogs weighing 11.2±1. 2kg composed each group. Immediately following induction of anesthesia with intravenous pentobarbital (Nembutal), all dogs were endotracheally intubated with the aid of intravenous succinylcholine chloride. Spontaneous respiration was allowed during pentobarbital anesthesia, but ventilation was controlled with Ohio Anesthesia Ventilator during cyclopropane or fluothane anesthesia. In order to insure the adepuacy of ventilation, arterial blood samples were drawn at appropriate intervals for analysis of pH and Pco2 by Beckman Blood Gas Measurement System. Ventilation was adjusted so that the pH and Pco were maintained in the range of 7.30~7.35 and 30~35 mmHg. A heating pad was used to maintain the esophageal temperature at the normal leveal (±0.5 ℃). The internal carotid artery and femoral vein were cannulated. Carotid arterial pressure was measured by sensing with a Statham transducer. Lead II of the electrocardiograph and arterial presaure were continuously monitored end recorded on the Beckman RM 4-Channel Monitor/Recorder. The abdomen was opened and the portal vein and common hepatic artery were cannulated with IVM FT-P Blood Flow Transducer and the blood flow was recorded on EMF-120 Electromagnetic Blood Flowmeter. Bleeding amounted to approximately 2per cent of the body weight. Cardiac output was measured by the direct Fick method. Cyclopropane was administered in the concentration of 10 per cent(100cc/min cyclopropane-900cc/min oxygen) and fluothane-was administered in 1 per cent concentration from Mark II Fluotec vaporizer. Both anesthetics were delivered in semiclosed circle carbon dioxide absorption system. The results are summarized in Tables 1~2. In brief both cyclopropane and fluothane caused a further reduction in splanchnic blood flow by 14 per cent and 21 per cent respectively during hemorrhagic hypotension. Mean arterial pressure rose 24 per cent and cardiac output increased 17 per cent by cyclopropane, whereas mean arterial pressure fell 25 per eent and cardiac output decreased 24 per eent by fluothane. Furthermore, five out of nine dogs inhaled fluothane did not survive despite retransfusion after the experiment. All changes were conaistent and atatistically significant (P<0. 001). The reults suggest that for patients with hypovolemie hypotension without blood replacement cyclo- propane would be the inhalation anesthetic of choice, fluothane might be detrimental in such circum-stances, and that the choice of fluothane ahould be reserved for normovolemic vasnconatrictive states.
Abdomen ; Absorption ; Anesthesia* ; Anesthetics ; Animals ; Arterial Pressure ; Body Weight ; Carbon Dioxide ; Cardiac Output ; Carotid Artery, Internal ; Dogs* ; Electrocardiography ; Femoral Vein ; Flowmeters ; Halothane* ; Heating ; Hemorrhage ; Hepatic Artery ; Hot Temperature ; Humans ; Hydrogen-Ion Concentration ; Hypotension ; Inhalation ; Magnets ; Methods ; Nebulizers and Vaporizers ; Ohio ; Pentobarbital ; Portal Vein ; Propane ; Respiration ; Shock* ; Shock, Hemorrhagic ; Succinylcholine ; Transducers ; Ventilation ; Ventilators, Mechanical

A total of 4757 apparently healthy aged persons over 65 years of age was surveyed for geriatric hypertension. A single blood pressure measurement was taken in the sitting position. Mean systolic blood pressure rose significantly with age in female but didn't in male and mean diastolic blood pressure didn't change with age in both sex. The prevalence of pure systolic hypertension, i.e., a systolic blood pressure greater than or equal to 160 mmhg and a diastolic blood pressure less than 95mmhg, increased with age. The prevalence was slighty lower for female than it was for male, being 7.0% for female and 8.0% for male. The prevalence of classical hypertension-defined as diastolic blood pressure greater than or equal to 95mmhg - was 42.7% for female and 48.2% for male and it rose with age in female. The prevalence of both pure systolic and classical hypertension was 49.7% for female and 56.1% for male.
Blood Pressure ; Epidemiologic Studies* ; Female ; Humans ; Hypertension* ; Korea* ; Male ; Prevalence

A patient who had been admitted to the B.N.U.H. with coma and respiratory arrest from possible acute alcohol intoxication, has been treated with intensive care and discharged without any complication. It should be emphasized that a patient with respiratory arrest even due to unknown etiology must have continued intensive care, without giving up the patient.
Coma ; Humans ; Critical Care ; Resuscitation*

A patient who had been admitted to the B.N.U.H. with coma and respiratory arrest from possible acute alcohol intoxication, has been treated with intensive care and discharged without any complication. It should be emphasized that a patient with respiratory arrest even due to unknown etiology must have continued intensive care, without giving up the patient.
Coma ; Humans ; Critical Care ; Resuscitation*