No abstract available.
Pulmonary Artery*

No abstract available.
Bronchi* ; Carcinoma, Mucoepidermoid*

No abstract available.
Chondrosarcoma* ; Sternum*

No abstract available.
Adenomatous Polyposis Coli* ; Carcinoid Tumor*

No abstract available.
Perfusion*

BACKGROUND: Although a laparoscopic cholecystectomy results in less pain than an open cholecystectomy, it is not a pain-free procedure. A controversy exists over the effectiveness and clinical value of intraperitoneal local anesthetics for treating pain after a laparoscopic cholecystectomy. We investigated the effects of intraperitoneal lidocaine on pain after a laparoscopic cholecystectomy. METHODS: Forty patients were randomly assigned to receive 200 ml saline containing 200 mg lidocaine or the same volume of saline instilled under the right hemidiaphragm and cholecystectomy site at the end of surgery. Intensity of abdominal and shoulder pain were assessed 0, 1, 6, 12, 24 and 48 hours after surgery and recorded on a visual analog scale (VAS) and verbal rating scale (VRS). RESULTS: The abdominal pain scores (VAS and VRS) were significantly lower in the lidocaine group than the control group at 0 - 24 hours after surgery (P < 0.05). The shoulder pain scores and incidence were significantly lower in the lidocaine group than the control group at 6 - 12 hours after surgery. In the lidocaine group, the incidence of epigastric and right flank pain were significantly lower than the control group. CONCLUSIONS: Intraperitoneal instillation of lidocaine significantly reduces shoulder and abdominal pain for 24 hours after a laparoscopic cholecystectomy.
Abdominal Pain ; Anesthetics, Local ; Cholecystectomy ; Cholecystectomy, Laparoscopic* ; Flank Pain ; Humans ; Incidence ; Lidocaine* ; Pain, Postoperative ; Shoulder Pain* ; Shoulder* ; Visual Analog Scale

No abstract available.
Adenoma*

PURPOSE: Bleeding from esophago-gastric varices needs urgent treatment. Esophageal varix bleeding usually was controlled by intervention, but rebleeding rate was high. Gastric varix bleeding is unable to be controlled by intervention. Recently, newly developed methods for varix bleeding controll have been used, but surgical intervention is still advocated. We report our experience with esophago-gastric devascularization for bleeding control in portal hypertension and its effectiveness. METHODS: This retrospective study was performed on 32 cases who underwent esophago-gastric devascularization in portal hypertension at Kyuung Hee University Hospital from Nov. 1990 to Feb. 2004. Author analyzed characteristics & patients, causes of portal hypertension, liver function reserve, operation methods, perioperative finding, complications and factors determining postoperative mortality. RESULTS: Sex ratios of male to female was 5.4:1. The ages were ranged from 25 to 70 years old with mean age of 50.5. Postoperative complication rate was 40.6% (13/32) and those were recovered by conservative management. There was one case of recurrent bleeding at 9months postperatively (3%). Mortality rate was 4% in Child-Pugh group A and B, and 57% in group C. The overall mortality rate was 15%. Preoperative hepatic reserve (P<0.05) & preoperative blood pressure (P<0.05) was a significant factors. A mean follow up period is 18.7 months. CONCLUSION: In our study, esophago-gastric devascularization in portal hypertension showed good results with 3% rebleeding rate and 85% overall survival rate. Esophago-gastric devascularization was effective method for esophago-gastric varix bleeding.
Aged ; Blood Pressure ; Esophageal and Gastric Varices ; Female ; Follow-Up Studies ; Hemorrhage ; Humans ; Hypertension, Portal* ; Liver ; Male ; Mortality ; Postoperative Complications ; Retrospective Studies ; Sex Ratio ; Survival Rate ; Varicose Veins

Tetrahydrobiopterin (BH4) deficiency is caused by mutations in genes encoding enzymes involved in the synthesis and regeneration of BH4. The condition is usually accompanied by hyperphenylalaninemia (HPA) and deficiency of neurotransmitter precursors L-dopa and 5-hydroxytryptophan. BH4 deficiency is much rarer than classical phenylketonuria. Dihydropteridine reductase (DHPR) deficiency, an autosomal recessive genetic disorder, is a cause of malignant hyperphenylalaninemia due to BH4 deficiency. When left untreated, DHPR deficiency leads to neurologic deterioration at the age of 4 or 5 months, including psychomotor retardation, tonicity disorders, drowsiness, irritability, abnormal movements, hyperthermia, hypersalivation, and difficulty swallowing. Treatment of DHPR deficiency should be initiated as early as possible with BH4 supplementation and replacement of the neurotransmitter precursors L-dopa and 5-hydroxytryptophan. We report the first case of DHPR deficiency in Korea, a child diagnosed at 9 years of age by genetic testing.
5-Hydroxytryptophan ; Biopterin ; Child ; Deglutition ; Dihydropteridine Reductase ; Dyskinesias ; Fever ; Genetic Testing ; Humans ; Korea ; Levodopa ; Neurotransmitter Agents ; Phenylketonurias ; Regeneration ; Sialorrhea ; Sleep Stages

Cortical spreading Depression(CSD) is a transient depression of neuronal activity that spreads across the cortical surface and is associated with profound changes in blood flow, extracellular ion concentration. Direct Current(DC) potentials and cell membrane potentials. One of the electrophysiological disturbance in the periinfarct surrounding is spontaneous occurrence of repeated CSD like DC shifts associated with increased energy demand. Due to restricted blood flow to the periinfarct border zone, elevated metabolic demand is potentially hazardous. So the authors designed this experiment to verify the correlation between periinfarct cortical spreading depression and ischemic volume following permanent middle cerebral artery(MCA) occlusion in rats. Sprague-Dawley rats(n=27) were anesthetized with 0.5~1% halothane, and artificially ventilated through a tracheal cannula. Arterial pressure, blood gases and body temperature were controlled. The middle cerebral artery(MCA) was occluded distally to the lenticulostriate branches. Measurements of CSD activity were made for 4 hours in each animal infarct volume was determined 6 hours later in 2,3,5-triphenyl tetrazolium chloride(TTC)- stained section. For 4 hours after MCA occlusion, the CSDs were found in all experimental animals with a range of 2~9 times. Those CSDs were of varying duration: "small"(1min) SDs and mean of total duration of SD was 10.5+/-10.3 min during 4 hours of MCA occlusion. Neuropathological evaluation of brain infarct in the rats, which had been allowed to survive for 6 hours after MCA occlusion showed a mean volume of 89.7+/-45.3 mm3. Serial observation of duration of CSD prologation of duration of CSD nor the frequency of CSD in the penumbral zone correlated with the volume of infarct.However total duration of CSD was slightly related with the infarct volume after 6 hours of the permanent MCA occlusion(r=0.414, p=0.0318) .
Animals ; Arterial Pressure ; Body Temperature ; Brain ; Catheters ; Cell Membrane ; Cortical Spreading Depression* ; Depression ; Gases ; Halothane ; Neurons ; Rats* ; Rats, Sprague-Dawley