No abstract available.
DNA* ; Humans* ; Polymerase Chain Reaction*

OBJECTIVE: Antidepressants Modulate Neuronal Plasticity. Tianeptine, An Atypical Antidepressant, Might Be Involved In The Restoration Of Neuronal Plasticity; It Primarily Enhances The Synaptic Reuptake Of Serotonin. Ncam140 Is Involved In Neuronal Development Processes, Synaptogenesis And Synaptic Plasticity. We Investigated The Effect Of Tianeptine On The Expression Of Ncam140 And Its Downstream Signaling Molecule In The Human Neuroblastoma Cell Line Sh-sy5y. METHODS: NCAM protein expression was measured in human neuroblastoma SH-SY5Y cells that were cultivated in serum-free media and treated with 0, 10, or 20 microM tianeptine for 6, 24, or 72 hours. NCAM140 expression in the tianeptine treatment group was confirmed by Western blot, and quantified through measurement of band intensity by absorbance. CREB and pCREB expression was identified after treatment with 20 microM tianeptine for 6, 24, and 72 hours by Western blot. RESULTS: Compared to cells treated for 6 hours, cells treated with 0 or 10 microM tianeptine for 72 hours showed a significant increase in NCAM140 expression and cells treated with 20 microM tianeptine showed a significant increase after 24 and 72 hours. The pCREB level in cells treated with 20 microM tianeptine increased in time-dependent manner. CONCLUSION: Our findings indicated that the tianeptine antidepressant effect may occur by induction of NCAM140 expression and CREB phosphorylation.
Antidepressive Agents ; Blotting, Western ; Cell Line ; Culture Media, Serum-Free ; Humans ; Neural Cell Adhesion Molecules ; Neuroblastoma ; Neuronal Plasticity ; Neurons ; Phosphorylation ; Plastics ; Serotonin

Endoscopic variceal ligation(EVL) is an accepted alternatives to endoscopic injection sclero- therapy(EIS) in many patients with bleeding esophageal varices. Esophageal hematoma is rare and an unusual complication after EVL or EIS. We present a patient with liver cirrhosis who developed an obstructive esophageal hematoma after EVL.
Esophageal and Gastric Varices ; Hematoma* ; Hemorrhage ; Humans ; Ligation* ; Liver Cirrhosis

PURPOSE: To evaluate the survival and prognostic factors in patients with stage III non-small cell lung cancer treated with curative radiotherapy alone or combined with chemotherapy. MATERIALS AND METHODS: A retrospective analysis was undertaken of 35 patients who had locally advanced non-small-cell lung cancer and t treated with curative radiotherapy in Department of Therapeutic Radiology, Kangdong Sacred Heart Hospital, from January 1991 through December 1993. According to AJCC staging, 15 patients were stage IIIA, and 20 were stage IIIB. Radotherapy was delivered with 1.8-2 Gy per fraction/day, 5 days per week using 6 MV X-ray, to a total dose ranging from 48.8 Gy to 66.6 Gy(median, 61.2 Gy) in 4 to 9 weeks. Ten patients received neoadjuvant or concurrent chemotherapy with FIP (5-FU, ifosfamide, and cisplatin) or FP(5-FU and cisplatin). RESULTS: For all patients, median survival was 6 months, 1-year and 2-year survival rates were 23.3% and 6.7%, respectively. The median survival was 8 months in stage IIIA and 5.5 months in stage IIIB. In patients treated with radiation therapy alone, median survival was 5 months and 1-year survival rate was 9%. In patients who received chemotherapy, median survival was 11 months and 1-year survival rate was 60%. The difference of survival between these two groups was statistically significant (p=0.03). Total radiation dose, degree of response, and post-treatment ECOG score were also significantly associated with survival. But it was not affected by age, sex, pretreatment ECOG score, presence or absence of weight loss, tumor location, pathologic type, N stage, and degree of response to treatment. CONCLUSION: Conventional radiotherapy alone is unlikely to achieve long term survival in patients with stage III NSCLC. Radiotherapy with altered fractionation schedule or multimodality treatment combined with surgery and/or chemotherapy should be considered if feasible.
Appointments and Schedules ; Carcinoma, Non-Small-Cell Lung* ; Drug Therapy ; Heart ; Humans ; Ifosfamide ; Lung Neoplasms ; Radiation Oncology ; Radiotherapy ; Retrospective Studies ; Survival Rate ; Weight Loss

A 6-year old boy was admitted with high fever and redness of the right eyelids and the surrounding area. He had previously suffered cerebral contusion, basal skull fracture and pneumocephalus following a traffic accident which required six months' hospitalization. Since then, and prior to admission, he had twice suffered probable bacterial meningitis and had been treated at an outstanding hospital. At the time of this admission, the patient again developed high fever, with redness of the right eyelid and surrounding area. His symptomatology suggested bacterial meningitis and cerebrospinal fluid culture revealed Streptococcus pneumoniae sensitive to penicillin. In accordance with the clinical course of meningitis and accompanying sinusitis, the appropriate antibiotic and its duration of usage were determined. Recurrent episodes of bacterial meningitis in this child raised the possibility of anatomical defect as an a contributory factor. Computerized tomographic(CT) cisternography suggested leakage of cerebrospinal fluid and revealed herniated frontal brain tissue protruding through a gap in the right frontal skull base, three dimensional CT(3-D CT) confirmed this defect, which was 3X4cm in size. After recovery from meningitis, surery to prevent recurrent meningitis, was performed. To locate pathologic areas, the subfrontal approach,involving bicoronal skin incision and bifrontal bone flap was used. Multiple fracture lines and a large bony defect on the orbital roof were observed, together with a dural defect, through which cerebromalatic tissue was herniated as encephalocele. Using lyophilized dura, the dural defect was made watertight; the bony defect was packed with autologous fats and covered with titanium mesh. The patient improved after surgery. Recurrent meningitis with anatomical pathologic focus after head trauma requires surgical intervention.
Accidents, Traffic ; Brain ; Cerebrospinal Fluid ; Child ; Contusions ; Craniocerebral Trauma ; Encephalocele ; Eyelids ; Fats ; Fever ; Hospitalization ; Humans ; Male ; Meningitis* ; Meningitis, Bacterial ; Orbit* ; Penicillins ; Pneumocephalus ; Sinusitis ; Skin ; Skull Base ; Skull Fractures* ; Skull* ; Streptococcus pneumoniae ; Titanium

BACKGROUND: Left ventricular dilatation after acute myocardial infarction is caused by infarct expansion and compensatory dilatation of noninfarct area. This study was done to investigate the contributory topographical change of left ventricle to left ventricular dilatation after acute myocardial infarction. METHODS: 24 first acute myocardial infarction was studied with 2-dimensional echocardiography serielly. First study was done at 7days and second study was done 9 months after an infarction attack. Left ventricular volume was measured by Simpson's method in end-diastolic frame and change of end diastolic left ventricular surface area was measured in apical 4 chamber view. Left ventricular surface area was devided by ischemic(noncontraction) and nonischemic(contracting) area by connecting central point of long axis of left ventricle and the junction of dyssynergic motion and normal motion point in outer rim of left ventricle in end diastolic frame of apical 4 chamber view. RESULTS: Mean left ventricular end-diastolic volume at entry was 114+/-23ml and increased to 121+/-27ml at 9 months after acute myocardial infarction in whole group(p=0.02). In a subgroup of anterior infarction, the left ventricular surface area was increaed in 9 cases with increared left ventricular volume(34.8+/-5.1cm2 to 36.4+/-4.1cm2, p=0.02) and ischemic surface area did not change in these group. In 7 patients without increase in left ventricular volume, the left ventricular surface area did not change and ischemic surface area decreased(9.4+/-4cm2 to 8+/-3.2cm2, p=0.03) at 9 months. CONCLUSION: Thus the increase in left ventricular end-diastolic volume between 13 days and 9 months after acute myocardial infarction is considered to be a consequence of noninfarct ventricular area dilatation.
Axis, Cervical Vertebra ; Dilatation ; Echocardiography ; Heart Ventricles ; Humans ; Infarction ; Myocardial Infarction* ; Stroke Volume ; Ventricular Remodeling*

BACKGROUND: Celiprolol is a new generation beta-adrenoreceptor blocking agent with intrinsic sympathomimetic activity characterized by selective blockade of beta1 receptors and partial agonist activity at beta2 receptors. This study was designed to investigate the antihypertensive efficacy and safety of celiprolol in patients with essential hypertension. METHODS: The study subjects consisted of 36 patients(mean age : 55 years, 11 males, 25 females). Celiprolol was administered orally in a aily dose of 200-800mg once or two divided dose for 10 weeks after the admimstration of placebo for 2 weeks. RESULTS: Blood pressure was significantly reduced from 171+/-19/106.8mmHg to 153+/-20/92+/-12mmHg(p<0.01) after 2 week of therapy and this effect was maintained throughout the study periods. The efficacy rates were total 94%(marked improve : 53%, moderate improve : 22%, mild improve : 19%). The cumulative efficacy rate was 72% at 200mg/day, 91% at 400mg/day, and 94% at 800mg/day. Heart rate did not change throughout 10 weeks. There were no significant change in hematologic and blood chemistry variables. During the period of medication, headache developed in 3 cases(8%) and each of dry cough, dyspnea, epigastric pain and diarrhea and facial flushing developed in 1 case(2.8%) but they were tolerable. CONCLUSIONS: This results suggest that celiprolol is effective and safe drug in the treament of patients with essential hypertension.
Blood Pressure ; Celiprolol* ; Chemistry ; Cough ; Diarrhea ; Dyspnea ; Flushing ; Headache ; Heart Rate ; Humans ; Hypertension* ; Male

BACKGROUND: Although there have been many studies on the risk factors for coronary artery disease, the etiology and risk factor of coronary artery spasm has not yet been determined. The objective of this study was to examine the risk factors for coronary vasospasm through a comparison of patients with angiographically determined vasospastic angina and patients without vasospasm and normal coronary artery. METHODS: Intracoronary injection of acetylcholine in order (20microg, 50microg, 100microg) were administered to all patients (Total 81:34 males, 47 females : mean age 50 years) who had a history of chest pain with normal or near normal coronary arteriographic fingings. After documentation of vasospasm in major epicardial coronary arteries by acetylcholine (Ach)-provocated dcoronary angiography, various risk factors (smoking, hypertension, diabetes, drinking and hyperlipidemia) were compared between patients with vasospasm and patients without vaspasm. RESULTS: 24 patients showed significant luminal narrowing (> or =75%)(Vasospasm group) and 57 patients showed no significant change (Control). Vasospasm group were suffered from typical chest pain in 92% of patients but control complained typical chest pain in 51% of subjects. The sites of vasoconstriction induced by Ach were LAD (11 cases), LCX (4 cases), RCA (11 cases) and vasoconstriction occurred 2 vessels (LAD and LCx) at the same time in two cases. The amount of Ach to provocate vasoconstriction was 20~50microg (90%) and there were no difference between left and right coronary arteries. The ratio of smoker was more frequent in the vasospasm group than control (58.3% vs 30.4%, p=0.046). But total cholesterol, low density lipoprotein, high density lipoprotein, triglycerides, apolipoprotein A, apolipoprotein B, lipoprotein (a), diabetes and body mass index, drinking were not statistically significant between two groups. CONCLUSION: Smoking appears to be a major risk factor for vasospastic angina by endotheilal dysfunction without significant coronary artery narrowing. But other fisk for coronary artery disease may not contribute to coronary vasospasm.
Acetylcholine* ; Angiography ; Apolipoproteins ; Body Mass Index ; Chest Pain ; Cholesterol ; Coronary Artery Disease ; Coronary Vasospasm ; Coronary Vessels* ; Drinking ; Female ; Humans ; Hypertension ; Lipoprotein(a) ; Lipoproteins ; Male ; Phenobarbital ; Risk Factors* ; Smoke ; Smoking ; Spasm* ; Triglycerides ; Vasoconstriction

No abstract available.
Coronary Occlusion* ; Echocardiography* ; Perfusion*

BACKGROUND: QT dispersion(QTD=QTmax-QTmin) on the 12 lead ECG has been known to reflect regional variation of ventricular repolarization, and thus a marker of an increased risk of arrhythmia events. Late potential(LP) on signal averagina ECG(SAECG) is independent risk factor of ventricular arrhythmia following acute myocardial infaction(AMI). However, the relation between LP and QTD as indicator of electrophysiologic instability in AMI remains to be determined. METHOD: To determine whether there is a difference in QTD between in parients with AMI during acute phase and in normal control and whether thrombolytic therapy is assiciated with a reduction in QTD, and to determine the relationship between change of QTD and late potential on SAECG, we studied 71 patient with AMI(male 54, female 14, mean age 57yrs) and 23 controls(malw 17, female 6, mean age 58yrs). QT interval was measured on a standard 12 lead ECG in patients with AMI on admission, 2 hours after urokinase IV and 10-14 days post-AMI, and QT dispersion was calculated by difference of maximal and minimal corrected QT interval(QTmax-QTmin). A signal averaged ECG was recorded in 36 patients before discharge and coronary angiogeaphy(CAG) was performed in all patients 10-14 days post-AMI. RESULT: QTD is significantly increased in AMI compared to control(78.7+/-39.5ms vs. 24.6+/-22.3ms, P < 0.01). In patients who received thrombolytic therapy with urokinase, QTD is decreased from 75.0+/-34.4ms to 53.9+/-36.0ms(P < 0.01), whereas there is no significant change in patients who did not received thrombolytic therapy(84.8+/-47.6ms vs. 78.9+/-36.2ms, NS). There in no difference in QTD between patients with positive LP(68.4+/-23.6ms) and those with negative LP(77.8+/-32.1ms) on admission, those with positive LP(66.6+/-27.6ms) and those with negative LP(56.0+/-26.4ms) after 10-14days post-AMI. But magnitude of change of 10-14 days post-AMI QTD in patients with negative LP is larger than those with positive LP(-21.7+/-33.4ms vs. -1.8+/-15.2ms, P=0.06). CONCLUSION: QTD in acute phase of AMI is significantly reduced by the thrombolytic therapy. Patients with negative late potential tent to have greater QTD reduction within 14 days after AMI. These finding suggest that QT dispersion in patients with AMI can be reduced by early recanalization and its reduction is associated with the presence of late potential.
Arrhythmias, Cardiac ; Electrocardiography ; Female ; Humans ; Myocardial Infarction* ; Risk Factors ; Thrombolytic Therapy ; Urokinase-Type Plasminogen Activator