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

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

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

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

OBJECTIVE: Dysfunction of neural plasticity in the brain is known to alter neural networks, resulting in depression. To understand how fluoxetine regulates molecules involved in neural plasticity, the expression levels of NCAM, NCAM140, CREB and pCREB, in rat C6 glioma cells after fluoxetine treatment were examined. METHODS: C6 cells were cultured after 20 min or after 6, 24 or 72 h treatments with 10 microM fluoxetine. Immunocytochemistry was used to determine the effect of fluoxetine on the expression of NCAM. Western blot analysis was used to measure the expression levels of NCAM140 and CREB and the induction of pCREB after fluoxetine treatment. RESULTS: NCAM expression following 72-h fluoxetine treatment was significantly increased around cell membranes compared to control cells. Cells treated with fluoxetine for 6 and 72 h showed a significant increase in NCAM140 expression compared to cells treated for 20 min. The level of pCREB in the cells treated with fluoxetine for 72 h not only increased more than 60%, but was also significantly different when compared with the other treatment times. The 72-h fluoxetine treatment led to the increase of NCAM140 and the phosphorylation of CREB in C6 cells. CONCLUSION: Our findings indicate that fluoxetine treatment regulates neuronal plasticity and neurite outgrowth by phosphorylating and activating CREB via the NCAM140 homophilic interaction-induced activation of the Ras-MAPK pathway.
Animals ; Blotting, Western ; Brain ; Cell Membrane ; Depression ; Fluoxetine ; Glioma ; Immunohistochemistry ; Neural Cell Adhesion Molecules ; Neurites ; Neuronal Plasticity ; Phosphorylation ; Plastics ; Rats

BACKGROUND: It is known that there is a pronounced circardian periodicity for the time of onset of acute myocardial infarction(AMI), with prominent increase in incidence of onset in the morning hours. However, the characteristic circardian variability in AMI is blunted in patients receiving beta-blockers or aspirin therapy before their presentation with AMI. These findings are attributed to the increase in platelet aggregability, blood coagulability, and plasma catecholamine that change coronary tone and myocardial oxygen demand. We hypothesize that, in addition to above physiologic and biochemical parameters, morphologic patterns of the coronary artery lesions are related to the development of circardian variation in AMI. METHOD: Subjects were 160 patients with AMI(male 92, female 68, mean age 56.9 +/-10.5 years old). Patients were classified by the time of onset of typical chest pain(AMI) by 6-hour interval from mid-night. Circardian variability of onset of AMI was compared with clinical findings and coronary angiographic findings. RESULTS: Incidence of onset of AMI was most frequent in the morning hours(6AM-noon,42.5%). There was no difference in degree of stenosis, lesion length, incidence of intraluminal thrombus, among 3 subgroups of AMI according to time of attack. Morning hour group had more frequent ulceration of coronary lesion than that of other groups(22.4% vs. 5.4%, p<0.01), and less frequent calcified lesion than that of other groups(3.0% vs 5.4%, p<0.05). Normal or minimal coronary artery lesion, that is Iess than 25% stenosis, was more frequent in the morning hour group comparing to that of other groups(11.9% vs. 9.78%). Eccentric stenosis(15.7% vs, 11,1%) and diffuse irregular lesion(25.5% vs. 16.7%) tended to be more frequent in the morning hour group. There were no differences in sex, age, incidence of hypertension, cigarette smoking, diabetes, degree of alcohol ingestion, ejection fraction, maximal CK value, preinfarction angina duration, past history of MI, and in incidence of arrhythmia. CONCLUSIONS: There were more ulcerative coronary atherosclerotic lesions, but fewer calcified coronary lesions in the morning group than in afternoon and night group. These findings indicate that morphology of coronary artery lesions may play a role in causing circardian variation in AMI.
Angina, Unstable ; Arrhythmias, Cardiac ; Aspirin ; Blood Platelets ; Constriction, Pathologic ; Coronary Vessels* ; Eating ; Female ; Humans ; Hypertension ; Incidence ; Myocardial Infarction* ; Oxygen ; Periodicity ; Plasma ; Smoking ; Thorax ; Thrombosis ; Ulcer

BACKGROUND: It is known that there is a pronounced circardian periodicity for the time of onset of acute myocardial infarction(AMI), with prominent increase in incidence of onset in the morning hours. However, the characteristic circardian variability in AMI is blunted in patients receiving beta-blockers or aspirin therapy before their presentation with AMI. These findings are attributed to the increase in platelet aggregability, blood coagulability, and plasma catecholamine that change coronary tone and myocardial oxygen demand. We hypothesize that, in addition to above physiologic and biochemical parameters, morphologic patterns of the coronary artery lesions are related to the development of circardian variation in AMI. METHOD: Subjects were 160 patients with AMI(male 92, female 68, mean age 56.9 +/-10.5 years old). Patients were classified by the time of onset of typical chest pain(AMI) by 6-hour interval from mid-night. Circardian variability of onset of AMI was compared with clinical findings and coronary angiographic findings. RESULTS: Incidence of onset of AMI was most frequent in the morning hours(6AM-noon,42.5%). There was no difference in degree of stenosis, lesion length, incidence of intraluminal thrombus, among 3 subgroups of AMI according to time of attack. Morning hour group had more frequent ulceration of coronary lesion than that of other groups(22.4% vs. 5.4%, p<0.01), and less frequent calcified lesion than that of other groups(3.0% vs 5.4%, p<0.05). Normal or minimal coronary artery lesion, that is Iess than 25% stenosis, was more frequent in the morning hour group comparing to that of other groups(11.9% vs. 9.78%). Eccentric stenosis(15.7% vs, 11,1%) and diffuse irregular lesion(25.5% vs. 16.7%) tended to be more frequent in the morning hour group. There were no differences in sex, age, incidence of hypertension, cigarette smoking, diabetes, degree of alcohol ingestion, ejection fraction, maximal CK value, preinfarction angina duration, past history of MI, and in incidence of arrhythmia. CONCLUSIONS: There were more ulcerative coronary atherosclerotic lesions, but fewer calcified coronary lesions in the morning group than in afternoon and night group. These findings indicate that morphology of coronary artery lesions may play a role in causing circardian variation in AMI.
Angina, Unstable ; Arrhythmias, Cardiac ; Aspirin ; Blood Platelets ; Constriction, Pathologic ; Coronary Vessels* ; Eating ; Female ; Humans ; Hypertension ; Incidence ; Myocardial Infarction* ; Oxygen ; Periodicity ; Plasma ; Smoking ; Thorax ; Thrombosis ; Ulcer

BACKGROUND: A group of patients with chest pain and normal coronary angiograms without spasm of epicardial artery is known to have decreased coronary flow reserve in response to vasodilatory stimuli, but the mechanisms responsible for the impairment of vasodilatory reserve are undefined. The purpose of this study was to determine whether dysfunction of coronary microvascular endothelium contributes to the reduced vasodilatory responses in patients with chest pain and normal coronary angiograms. METHODS: Twenty patients, 12(group A) with and 8(group B) without ST depression on exercise ECG or 24 hours ambulatory ECG. with chest pain and normal coronary angiograms and no spasm of epicardial coronary artery. were studied. As the endothelium-independent vasodilator, acetylcholine at doses of 20microg, 50microg and 100microg, and as the endothelium-independent vasodilator, nitroglycerin 200microg were infused into left coronary artery. The functional response of coronary vasomotion was studied with atrial pacing. By themodilution pacing catheter. great cardiac vein flow(GCVF) was measured. The changes in the diameter of proximal and distal of left anterior descending artery were analyzed. RESULTS: Intracoronary acetylcholine increased GCVF by 12.3% with 20microg(NS),by 38.9% with 50microg(p<0.05) and by 14.8% with 100microg(NS). The changes in GCVF with 20microg and 50microg dose of acetylcholine were positively related with those with atrial pacing(r=0.59 and r=0.62, respectively), but not at dose of 100microg(r=0.12). Thus, patients with diminished flow response with atrial pacing had reduced endothelium-dependent dilation with low dose acetylcholine. Also changes in GCVF with atrial pacing and acetylcholine were smaller in the patients of group A than group B. However, the changes in GCVF to nitroglycerin was not related with the changes with acetylcholine and did not differ between A and B group, indicating this vasodilatory response was not associated with the endothelium-independent vasodilation. Acetylcholine caused similar degree of change in diameter at proximal and distal epicardial artery in two groups and their changes were not related with changed in GCVF with acetylcholine, suggesting the changes in GCVF with acetylcholine were mainly influenced by the changes at the level of microvasculature. CONCLUSION: In patients with chest pain and normal coronary angiograms without spasm of epicardial artery, reduced vasodilatory response with atrial pacing was associated with the impairment of endothelium-dependent dilation at the level of coronary microvasculature, suggesting the endothelial dysfunction of coronary microvessels is one of the causes of inducible myocardial ischemia.
Acetylcholine ; Arteries ; Catheters ; Chest Pain* ; Coronary Vessels ; Depression ; Electrocardiography ; Endothelium ; Humans ; Microvessels* ; Myocardial Ischemia ; Nitroglycerin ; Spasm ; Thorax* ; Vasodilation ; Veins

BACKGROUND: A group of patients with chest pain and normal coronary angiograms without spasm of epicardial artery is known to have decreased coronary flow reserve in response to vasodilatory stimuli, but the mechanisms responsible for the impairment of vasodilatory reserve are undefined. The purpose of this study was to determine whether dysfunction of coronary microvascular endothelium contributes to the reduced vasodilatory responses in patients with chest pain and normal coronary angiograms. METHODS: Twenty patients, 12(group A) with and 8(group B) without ST depression on exercise ECG or 24 hours ambulatory ECG. with chest pain and normal coronary angiograms and no spasm of epicardial coronary artery. were studied. As the endothelium-independent vasodilator, acetylcholine at doses of 20microg, 50microg and 100microg, and as the endothelium-independent vasodilator, nitroglycerin 200microg were infused into left coronary artery. The functional response of coronary vasomotion was studied with atrial pacing. By themodilution pacing catheter. great cardiac vein flow(GCVF) was measured. The changes in the diameter of proximal and distal of left anterior descending artery were analyzed. RESULTS: Intracoronary acetylcholine increased GCVF by 12.3% with 20microg(NS),by 38.9% with 50microg(p<0.05) and by 14.8% with 100microg(NS). The changes in GCVF with 20microg and 50microg dose of acetylcholine were positively related with those with atrial pacing(r=0.59 and r=0.62, respectively), but not at dose of 100microg(r=0.12). Thus, patients with diminished flow response with atrial pacing had reduced endothelium-dependent dilation with low dose acetylcholine. Also changes in GCVF with atrial pacing and acetylcholine were smaller in the patients of group A than group B. However, the changes in GCVF to nitroglycerin was not related with the changes with acetylcholine and did not differ between A and B group, indicating this vasodilatory response was not associated with the endothelium-independent vasodilation. Acetylcholine caused similar degree of change in diameter at proximal and distal epicardial artery in two groups and their changes were not related with changed in GCVF with acetylcholine, suggesting the changes in GCVF with acetylcholine were mainly influenced by the changes at the level of microvasculature. CONCLUSION: In patients with chest pain and normal coronary angiograms without spasm of epicardial artery, reduced vasodilatory response with atrial pacing was associated with the impairment of endothelium-dependent dilation at the level of coronary microvasculature, suggesting the endothelial dysfunction of coronary microvessels is one of the causes of inducible myocardial ischemia.
Acetylcholine ; Arteries ; Catheters ; Chest Pain* ; Coronary Vessels ; Depression ; Electrocardiography ; Endothelium ; Humans ; Microvessels* ; Myocardial Ischemia ; Nitroglycerin ; Spasm ; Thorax* ; Vasodilation ; Veins