Decreased Expression of PTEN in Olfactory Bulb of Rat Pub after Naris Closure

PTEN (phosphatase and tensin homolog) is a dual specific phosphatase antagonizing phosphoinositide 3-kinase activity, and has first been cloned as a tumor suppressor for glioma. Although the role of PTEN as a tumor suppressor has been well studied, little is known about signaling mechanisms regulating expression and/or activity of PTEN in the central nervous system. In this study, we investigated whether PTEN expression is regulated by sensory deprivation. P5 rat pups were unilaterally naris-closed, and olfactory bulbs were immunohistochemically analyzed with PTEN antibody at the 7th day after naris closure. PTEN immunoreactivity was found to be down-regulated in both glomerular, external plexiform and subependymal cell layers, suggesting that odor deprivation signals down-regulate expression of PTEN in the olfactory bulb. To the best of our knowledge, this is the first report to suggest that PTEN expression is regulated by sensory deprivation signals in neonatal rats.

Curcumin Attenuates Glial Cell Activation But Cannot Suppress Hippocampal CA3 Neuronal Cell Death in i.c.v. Kanic Acid Injection Model

Kainic acid (KA) is a structural analogue of glutamate that interacts with specific presynaptic and postsynaptic receptors to potentiate the release and excitatory actions of glutamate. Systemic or intracerebroventricular (i.c.v.) administration of KA to experimental animals elicits multifocal seizures with a predominantly limbic localization, and results in neuronal death of cornu ammonia 1 (CA1), reactive gliosis and biochemical changes in the hippocampus and other limbic structures. Several lines of evidence suggest that reactive oxygen species (ROS) play a pivotal role in the pathogenesis of excitotoxic death by KA. Curcumin has been known to possess anti-oxidative and anti-inflammatory activities. In this study, the effects of curcumin on KA induced hippocampal cell death, reactive gliosis and biochemical changes in reactive glia were investigated by immunohistochemical methods. Our data demonstrated that curcumin attenuated KA-induced astroglial and microglial activation although it did not protect KA-induced hippocampal cell death.

Endomyocardial Fibrosis: A Case Report / 대한흉부외과학회지

Endomyocardial fibrosis(EMF) is an unusual type of cardiomyopathy characterized by a restriction to the ventricular filling and an obliteration of the inflow portion in the ventricular cavity by a fibrosis and often by a thrombus formation. The atrioventricular valve may be involved, resulting in an atrioventricular valvular regurgitation. The only known effective treatments are endomyocardiectomy and replacement of regurgitant AV valves. We report the experience of a case of EMF which required surgical management.

Expression of Bcl-2 Protein in Ischemia-Reperfused Myocardium of Rabbit / 대한흉부외과학회지

BACKGROUND: Myocardial cell death after myocardial infarction or reperfusion is classified into necrosis and apoptosis. Bcl-2 protein is a cytoplasmic protein, which inhibits apoptosis and is expressed in acute stage of myocardial infarction but not in normal heart. This study was performed to investigate whether Bcl-2 protein was expressed respectively to the reperfusion time. MATERIALS AND METHODS: Thirty nine New Zealand white rabbits weighing 1.5-4.8 kg (mean, 2.9kg) were alloted into 7 groups (n=5 in each group) which underwent left anterior descending coronary artery (LAD) occlusion for 30 minutes, followed by reperfusion. The animals were sacrificed at 1, 4, 8, 12, 24 hours, and 3, 7 days after occlusion. Ventricle was excised immediately after intervention. Tissues were fixed in 10% buffured formalin and embedded in paraffin. Bcl-2 protein was detected by immunohistochemical stain with using monoclonal antibody against Bcl-2 protein. RESULTS: The positive immunohistochemical reactivity for Bcl-2 protein was observed in 12, 24 hours, and 3 days reperfusion groups. Bcl-2 protein was detected in salvaged myocytes surrounding the infarcted area. CONCLUSIONS: Bcl-2 protein is expressed at the late acute stage of infarct. Therefore, the expression of Bcl-2 protein may not protect acute cell death, but may play a role in the prevention of late cell death after myocardial is chemia-reperfusion.

An Experience of Cox-maze III Procedure for Chronic Atrial Fibrillation / 대한흉부외과학회지

During the past several years, the maze operation has become the most effective method of treatment for chronic atrial fibrillation. When the maze procedure is done concomittantly with other cardiac operations, surgeons, in their initial experiences, may be concerned about the additional operative risks and uncertainty of the results. We performed the Cox-maze III procedure in six cases of chronic atrial fibrillation associated with mitral, mitral & aortic, or coronary arterial disease. Maze III procedure was done with open mitral commissurotomy (3 cases), mitral valve replacement (1 case), aortic and mitral valve replacement (1 case), and two-vessel coronary bypass graft (1 case). In spite of rather prolonged aortic cross clamp time, cardiac recovery was uneventful in all cases. No cases required reexploration for postoperative bleeding. All patients showed regular sinus rhythms immediate or between 2 and 20 days postoperateratively. Transient postoperative supraventricular arrhythmarias were easily controlled by various antiarrhythmic agents. In follow up evaluations, all cases showed regular sinus rhythm on ECG and the right and left atrial transport function was confirmed by Doppler echocardiography in all except one. Though our experience was limited in case number, the Cox-maze III procedure was effective in controlling the chronic atrial fibrillation without serious additional operative risks.

Apoptosis in Ischemia-Reperfused Myocardium of Rabbit

BACKGROUND: Apoptosis, as opposed to necrosis, is a active and regulated mode of cell death. Persistent myocardial ischemia results in necrosis. The most effective method to limit ischemic myocardial injury is reperfusion, however, reperfusion itself may be associated with tissue injury. The pathophysiologic findings of myocardial ischemia-reperfusion are well known. However, involvement of apoptosis, as a form of tissue damage, has not neen well defined. Recently apoptosis has been suggested as a specific feature of myocardial reperfusion injury leading to late cell death. This study was performed to investigate whether reperfusion induces apoptosis irrespective of reperfusion time, and the pattern of distribution and the extent of apoptosis in rabbit myocardium. METHOD: New Zealand white rabbits weighing 1.8-2.9kg underwent 20 or 30 minutes left anterior descending(LAD) or left circumflex coronary artery occlusion followed by reperfusion for 30 minutes(n=1), 1 hour(n=1), 3 hours (n=2), and 4 hours (n=3). Ventricles were excised immediately after intervention. Tissues were fixed in 10% buffered formalin and embedded in paraffin. Apoptosis was examined by hematoxylin and eoisin(H & E) staining, in situ nick end labeling, and transmission electron microscopy. Number of apoptotic cells was evaluated semiquantitatively on H & E stained section. Myocardial tissues of ischemia only(LAD occlusion for 30 minutes, n=2) and normal rabbits(n=2) were also examined. RESULTS: Evidence of apoptosis was detected in every ischemia-reperfused myocardium irrespective of reperfusion time of 30 minutes to 4 hours. Apoptotic cells were found in the non-necrotic myocardium near necrotic areas and in islets of the non-necrotic myocarium inside necrotic areas. In the areas where apoptotic cells were distributed, the average number of apoptotic cells ranged from 1.0(30 minutes and 1 hour reperfused myocardium) to 1.1(3 hours and 4 hours reperfused myocardium) per high power field(X400)(the proportion ; less than 1% of cardiomyocytes at specific time point of reperfusion). Apoptotic cells were not detected in ischemia only and normal myocardium. CONCLUSION: These fingings suggest that apoptosis is involved as a form of cell death and it may contribute to cardiomyocyte loss not to a large extent in ischemia-reperfusion injury of rabbit myocardium.

Effect of Superoxide Dismutase on Apoptosis in Ischemia-Reperfused Myocardium of Rabbit

BACKGROUND: Recently involvenment of apoptosis, or programmed cell death, has been suggested in myocardial reperfusion injury. Free radicals are one of the inducers of apoptosis, and superoxide dismutase(SOD), a oxygen free radical scavenger, inhibits apoptotic cell death of neurons. Reperfusion of ischemic myocardium results in a burst of oxygen free radical production, however, it has not been defined that oxygen free radicals mediate apoptosis in myocardial reperfusion injury. This study was undertaken to investigate the role of oxygen free radicals by examining the inhibition of apoptosis by SOD. METHOD: New Zealand white rabbits (n=16) weighing 1.8-20kg underwent 30 minutes of left anterior descending coronary artery occlusion followed by reperfusion for 1 or 4 hours. In control group, bovine serum albumin(5mg/kg) was administered continuously via the left atrial appendage starting 10 minutes before reperfusion and ending simultaneously with reperfusion for 1 hour(n=4) or 4 hours(n=4). In SOD group, bovine erythrocyte SOD(15,000u/kg) was administered starting 10 minutes before reprefusion and ending simultaneously with reperfusion for 1 hour(n=5) or 4 hours(n=3). Ventricles were excised immediately after intervention. Tissues were fixed in 10% buffered formalin and 2.5% glutaraldehyde. Apoptosis was examined by hematoxylin and eosin(H&E) staining, in situ nick end labeling, and transmission electron microscopy. Number of apoptotic cells was evaluated semi-quantitatively on H&E stained section. RESULTS: Evidence of apoptosis was detected in every ischmia-reperfused myocardium, and apoptotic cells were found in the non-necrotic myocardium near areas of contraction band necrosis. In control group, the average number of apoptotic cells was 1.7(range 1.5-2.0)for 1 hour reperfused myocardium and 1.4(range 0.3-2.5) for 4 hours reperfused myocardium per high power field(x400). In SOD group, the average number of apoptotic cells was 0.2(range 0.2 -0.3) for 1 hour reperfused myocardium and 0.3(range 0.2-0.4) for 4 hours reperfused myocardium. There was a significant difference in the number of apoptotic cells between conrol and SOD groups (as a whole group 1.5 +/- 0.2 vs 0.3 +/- 0.1,p<0.01). CONCLUSION: SOD partially, however, singificantly inhibits apoptosis, which suggests that oxygen free radicals may induce apoptosis in ischemia-reperfused myocardium of rabbit.

Increased Expression of Phospholipase C-gamma1 in Phenylephrine Induced Cardiac Hypertrophy of Rats

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.

Management of post-pneumonectomy empyema / 대한흉부외과학회지

No abstract available.

Surgical experience of Takayasu'arteritis / 대한흉부외과학회지

No abstract available.

Risk factors of recurrent spontaneous pneumothorax / 대한흉부외과학회지

No abstract available.

A Case of Dissection in Marfan Syndrome with Ascending Aortic Aneurysm / 영남의대학술지

The Marfan syndrome is a generalized connective tissue disease involving eye, musculoskeletal system, cardiovascular system, and inherited autosomal dominant with various expression type. The cardiovascular complications such as aortic aneurysm, aortic dissection, aortic regurgitation, mitral regurgitation and aortic dissection which usually occurs in previously normal sized aorta are poor prognostic factors. However, the aortic dissection which developed in patient with Marfan syndrome and aortic aneurysm was rare. We experienced one case of dissecting aneurysm in patient diagnosed as previous aortic aneurysm, aortic regurgitation, and Marfan syndrome, receiving successful operation.

Clinical Study of 459 Cases Cardiovascular Surgery / 영남의대학술지

Between April, 1984 and September 1988, 459 patients underwent cardiovascular surgery at the Yeungnam University Hospital. Of these, 355 cases were open heart surgeries and 104 cases were non-open heart surgeries. There were 237 patients of acyanotic congenital cardiac anomalies, 40 patients of cyanotic congenital cardiac anomalies, and 85 patients of acquired heart diseases. The sex ratio of cardiovascular diseases was represented as 1:1.3 in male and female. The age distribution was ranged from 1 day to 65 years old. The common congenital cardiovascular anomalies were ventricular septal defect (38.7%), patent ductus arteriosus (25.5%), atrial septal defect (20.7%), Tetralogy of Fallot (8.3%), and pulmonary stenosis (2.4%) in order of frequency. Among 87 acquired cardiovascular diseases, 81 patients underwent operation for cardiac valvular lesions, 51 patients had mitral valve replacement and 13 patients had aortic valve replacement and 17 patients had double valve replacement. The overall mortality of cardiovascular surgery was 3.3% and mortality of open heart surgery was 3.9%.

Effects of Dimethyl Sulfoxide on the Differentiation of Myocardial and Endothelial Cells / 영남의대학술지

To elucidate the effects of dimethyl sulfoxide on of myocardial and endothelial cells in culture, the cells were exposed to 10% dimethyl sulfoxide in culture medium for 1 hour at 48 hours after cell isolation. The general morphology and the cytochemical reaction of marker enzymes for mitochondria and Golgi complexes were investigated. The results were summarized as follows 1. DMSO induced elongation and narrowing of the cells and increase of mitochondrial reaction in myocardial cells. 2. DMSO induced destruction and disruption of myofibrils in myocardial cells resulting in increase of contractile activities. 3. In the endothelial cells, DMSO suppressed proliferative activities but thiamine pyrophosphatase reactions were enhanced indicating increase of Golgi complex activity. 4. DMSO seemed to hamper with the adhesiveness and motility of the endothelial cells causing the decrease of the number of cells in vitro.