No abstract available.
Leukemia*

BACKGROUND: This study examined the efficacy of patient-controlled epidural analgesia (PCEA) for post-cesarean section pain control and compared the suitability of four different volumes of continuous background infusion (CBI). METHODS: Sixty patients were received 0.125% bupivacaine with 5 g/ml fentanyl by PCEA (2 ml of demand dose and 10 minutes of lockout interval) and CBI. Experimental groups were divided four groups according to the volumes of CBI; 1 ml/hr, 2 ml.hr, 3 ml/hr and 4 ml/hr of CBI during 48 hours postoperatively. RESULTS: Total amount of fentanyl and bupivacaine consumption was significantly higher in 1ml/hr of CBI group than 2 ml/hr of CBI group during first 24 hours, and in 4 ml/hr of CBI group than 1 ml/hr and 3 ml/hr of CBI group during second 24 hours. CBI/maximum hourly demand dose was 15~23%. There is no significant difference between the groups in pain score, side effects and patient's satisfaction. CONCLUSIONS: This study suggests that two or three ml/hr of CBI can provide the most effective postoperative analgesia and the optimal ratio of CBI/maximum hourly demand dose is about 20%.
Analgesia ; Analgesia, Epidural* ; Bupivacaine ; Fentanyl ; Humans

Arrhythmogenic right ventricular dysplasia is a rare heart muscle disorder of unknown cause that primarily involves the right ventricle. It is characterized pathologically by fibrofatty replacement of the right ventricular myocardium. Clinical manifestations include structural and functional abnormalities of the right ventricle, electrocardiographic depolarization/repolarization changes, and presentation with sudden death or ventricular arrhythmias of right ventricular origin. It is one of the important causes of the ventricular arrhythmia or sudden death among apparently healthy young people. We report a case of arrhythmogenic right ventricular dysplasia with the review of the literature.
Arrhythmias, Cardiac ; Arrhythmogenic Right Ventricular Dysplasia* ; Death, Sudden ; Electrocardiography ; Heart Ventricles ; Myocardium

No abstract available.
Osteogenesis Imperfecta* ; Osteogenesis*

No abstract available.
Child* ; Humans ; Lung*

No abstract available.
Hyperthyroidism*

A 25-year-old woman with focal seizure, intermittent morning headache and vomiting for 2 years showed microcytic hypochromic anemia on peripheral blood smear and a 6x7.5cm sized intracranial mass with cystic and solid portions at the right temporoparietal convexity on brain CT and MRI which was hypervascular on cerebral angiography. Histopathologic findings on light microscopy suggested chordoma, but it was confirmed as a chordold meningioma by immunohistochemical study. The present case suggests that the diagnosis of chordold meningioma shoud be considered in a juvenile or young adult who is presented with an extra-axial mass with typical location of meningiomas, findings of chordomas on light microscopy, and clinical findings of Castleman syndrome.
Adult ; Anemia, Hypochromic ; Brain ; Cerebral Angiography ; Chordoma ; Diagnosis ; Female ; Headache ; Humans ; Magnetic Resonance Imaging ; Meningioma* ; Microscopy ; Seizures ; Vomiting ; Young Adult

No abstract available.
Depression*

No abstract available.
Hand*

BACKGROUND: Cardiac hypertrophy is an adaptive mechanisms in response to an increased cardiac work load. Alterations in gene expression play an important role in this adaptive process. Recent investigations have indicated that the alpha-1 adrenergic stimulation in vitro induces hypertrophic change of neonatal cardiomyocytes. The signalling mechanisms of this alpha-1 agonist induced cardiomyocyte hypertrophy are largely unknown. however, recent evidence favors an effector pathway that involves phospholipase C(PLC) mediated hydrolysis of phosphatidylinositol 4,50 bisphosphate. It should be recognized that the demonstration of enhanced phosphoinositol turnover in the presence of alpha-1 adrenergic agonist in vitro does not necessarily imply that a similar response is operative in vivo. Furthermore, the role of subtypes of phospholipase C in this system should be determined. In this context, we produced in vivo cardiac hypertrophy by repeated injection of alpha-1 adrenergic agonist, phenylephrine, and tried to evaluate any change of phospholipase C subtypes by immunohistochemistry and immunoblotting technique and also measured the phosphatidylinositol hydrolyzing activity of the enzyme. METHOD: To produce cardiac hypertrophy, we injected phenylephrine 12mg/kg i.p. to the 28 female S-D rats weighing 150-250g daily for 5 days. This measures produced 22% increase of heart weight/body weight ratio. After 5 days. rats were sacrificed and hearts were rapid excised and freezed for next procedure. The immunohistochemical stainings of myocardium were carried out using monoclonal antibodies against PLC-beta1,-gamma1,-delta1 with Avidine-Biotin Complex method. Immunoblotting was done with monoclonal anti-PLC-gamma1 antibody after immnoprecipitation. The activity of PLC-gamma1 was determined in the assay mixture containing [3H] phosphatidylinositol of 20,000 cpm. The reaction was performed by incubating with resuspended immunoprecipttol of 20,000 cpm. The reaction was performed by incubating with resuspended immunoprecipitate for 10 min and supernatant was collected for -scintillation counting. RESULTS: Immunohistochemical staining demonstrated increased staining of PLC-gamma1 in the phenylephrine induced hypertrophied heart as compared with normal control heart. PLC-beta1 and-o1 did not showed any change. Elghteen out of 20 hypertrophied cardiac tissue(90%) demonstrated increased expression of the PLC-gamma1 compared with control heart tissue in immunoblotting. [3H] PI hydrolyzing activity of PLC-gamma1 in the immunoprecipitates of the hypertrophied hearts(4650+/-614 cpm) were increased consistently in 6 samples as compared with control normal hearts (2387+/-651 cpm). CONCLUSION: In the present experiments we demonstrated that Phospholipase C-gamma1 was overexpressed compared with control normal heart of rat by immunohistochemistry and immunoblotting technique and showed that the activity of this isoenzyme was elevated. Our findings of increased PLC-gamma1 expression in the alpha1-adrenergic agonist induced cardiac hypertrophy tissue suggest that the phosphatidylinositol signalling pathway is important in the genesis of cardiac hypertrophy and the isoenzyme of PLC-gamma1 may play a central role in this mechanism.
Adrenergic Agonists ; Animals ; Antibodies, Monoclonal ; Cardiomegaly* ; Female ; Gene Expression ; Heart ; Humans ; Hydrolysis ; Hypertrophy ; Immunoblotting ; Immunohistochemistry ; Myocardium ; Myocytes, Cardiac ; Phenylephrine* ; Phosphatidylinositols ; Phospholipases* ; Rats* ; Signal Transduction ; Type C Phospholipases