The clinical studies were performen on 304 patients with heart disease who had been received corrective heart surgery at Kosin Medical Center from July, 1984 to December, 1991. The results were as follows: 1) Out of 304 patients, 162 cases (53.3%) were male and 142 cases (46.7%) were female and sex ratio was 1.15:1. 35 cases (11.5%) had clinical cyanosis and 269 cases (88.5%) had no evidence of cyanosis. 2) As age distribution of patients, under 2 years, 3~5 years, 6~10 years, 11~15 years, 16~18 years consist of 22.0%, 26.0%, 29.0%, 16.1% and 6.9%, respectively. 3) As disease distribution, out 304 patients, ventricular septal defect (57.9% of all) was the most common disease, and then atrial septal defect (13.2%), tetralogy of Fallot (11.2%), patent ductus arteriosus (9.9%) and pulmonic stenosis (5.3%), in their order. 4) As sex distribution of each disease, ventricular septal defect, atrial septal defect and tetralogy of Fallot were more common in male and patent ductus arteriosus and pulmonic stenosis were more common in female. 5) The most frequent cardiac anomaly associated with ventricular septal defect and atrial septal defect was pulmonic stenosis. In the case of subarterial ventricular septal defect, aortic insufficiency was associated in 13.3%. 6) Respiratory problems (11.3%), tricuspid regurgitation (9.5%), arrhythmia (6.2%) and congestive heart failure (5.8%) were the major complications after surgery. 7) Case fatality reat was 4.4%. Mortality rate in ventricular septal defect, tetralogy of Fallot and tricuspid atresia were 1.7%, 20.6% and 100%, respectively, Majority (75.0%) of expired patients were died within 24 hours after sugery and the cause of death was hypoxia due to low cardiac output syndrome.
Age Distribution ; Anoxia ; Arrhythmias, Cardiac ; Cardiac Output, Low ; Cause of Death ; Cyanosis ; Ductus Arteriosus, Patent ; Female ; Heart Diseases* ; Heart Failure ; Heart Septal Defects, Atrial ; Heart Septal Defects, Ventricular ; Heart* ; Humans ; Male ; Mortality ; Pulmonary Valve Stenosis ; Sex Distribution ; Sex Ratio ; Tetralogy of Fallot ; Thoracic Surgery ; Tricuspid Atresia ; Tricuspid Valve Insufficiency

All living organisms are destined to die. Cells, the core of those living creatures, move toward the irresistible direction of death. The question of how to die is critical and is very interesting. There are various types of death in life, including natural death, accidental death, questionable death, suicide, and homicide. The mechanisms and molecules involved in cell death also differ depending on the type of death. The dysenteric amoeba, E. histolytica, designated by the German zoologist Fritz Schaudinn in 1903, has the meaning of tissue lysis; i.e., tissue destroying, in its name. It was initially thought that the amoebae lyse tissue very quickly leading to cell death called necrosis. However, advances in measuring cell death have allowed us to more clearly investigate the various forms of cell death induced by amoeba. Increasing evidence has shown that E. histolytica can cause host cell death through induction of various intracellular signaling pathways. Understanding of the mechanisms and signaling molecules involved in host cell death induced by amoeba can provide new insights on the tissue pathology and parasitism in human amoebiasis. In this review, we emphasized on the signaling role of NADPH oxidases in reactive oxygen species (ROS)-dependent cell death by pathogenic E. histolytica.

No abstract available.
Cardiomyopathy, Dilated* ; Doxorubicin

The enteric protozoan parasite Entamoeba histolytica is the causative agent of human amebiasis. During infection, adherence of E. histolytica through Gal/GalNAc lectin on the surface of the amoeba can induce caspase-3-dependent or -independent host cell death. Phosphorylinositol 3-kinase (PI3K) and protein kinase C (PKC) in E. histolytica play an important function in the adhesion, killing, or phagocytosis of target cells. In this study, we examined the role of amoebic PI3K and PKC in amoeba-induced apoptotic cell death in Jurkat T cells. When Jurkat T cells were incubated with E. histolytica trophozoites, phosphatidylserine (PS) externalization and DNA fragmentation in Jurkat cells were markedly increased compared to those of cells incubated with medium alone. However, when amoebae were pretreated with a PI3K inhibitor, wortmannin before being incubated with E. histolytica, E. histolytica-induced PS externalization and DNA fragmentation in Jurkat cells were significantly reduced compared to results for amoebae pretreated with DMSO. In addition, pretreatment of amoebae with a PKC inhibitor, staurosporine strongly inhibited Jurkat T cell death. However, E. histolytica-induced cleavage of caspase-3, -6, and -7 were not inhibited by pretreatment of amoebae with wortmannin or staurosporin. In addition, we found that amoebic PI3K and PKC have an important role on amoeba adhesion to host compartment. These results suggest that amebic PI3K and PKC activation may play an important role in caspase-independent cell death in Entamoeba-induced apoptosis.
*Apoptosis ; Caspases/metabolism ; Entamoeba histolytica/*enzymology/*growth & development ; Humans ; Hydrolysis ; Jurkat Cells ; Phosphatidylinositol 3-Kinases/*metabolism ; Protein Kinase C/*metabolism ; T-Lymphocytes/*parasitology/*physiology

Entamoeba histolytica is a tissue-invasive protozoan parasite causing dysentery in humans. During infection of colonic tissues, amoebic trophozoites are able to kill host cells via apoptosis or necrosis, both of which trigger IL-8-mediated acute inflammatory responses. However, the signaling pathways involved in host cell death induced by E. histolytica have not yet been fully defined. In this study, we examined whether calpain plays a role in the cleavage of pro-survival transcription factors during cell death of colonic epithelial cells, induced by live E. histolytica trophozoites. Incubation with amoebic trophozoites induced activation of m-calpain in a time- and dose-dependent manner. Moreover, incubation with amoebae resulted in marked degradation of STAT proteins (STAT3 and STAT5) and NF-kappaB (p65) in Caco-2 cells. However, IkappaB, an inhibitor of NF-kappaB, was not cleaved in Caco-2 cells following adherence of E. histolytica. Entamoeba-induced cleavage of STAT proteins and NF-kappaB was partially inhibited by pretreatment of cells with a cell-permeable calpain inhibitor, calpeptin. In contrast, E. histolytica did not induce cleavage of caspase-3 in Caco-2 cells. Furthermore, pretreatment of Caco-2 cells with a calpain inhibitor, calpeptin (but not the pan-caspase inhibitor, z-VAD-fmk) or m-calpain siRNA partially reduced Entamoeba-induced DNA fragmentation in Caco-2 cells. These results suggest that calpain plays an important role in E. histolytica-induced degradation of NF-kappaB and STATs in colonic epithelial cells, which ultimately accelerates cell death.
Caco-2 Cells ; Calcium-Binding Proteins ; Calpain/genetics/metabolism ; Caspase 3/genetics/metabolism ; Caspases ; *Cell Death ; Colon/cytology ; Entamoeba histolytica/*physiology ; Epithelial Cells/cytology/parasitology ; Humans ; I-kappa B Proteins/metabolism ; Intestinal Mucosa/cytology ; NF-kappa B/genetics/*metabolism ; RNA Interference ; RNA, Small Interfering ; STAT3 Transcription Factor/genetics/*metabolism ; STAT5 Transcription Factor/genetics/*metabolism ; Signal Transduction

The pathogenic free-living amoeba Naegleria fowleri causes primary amoebic meningoencephalitis, a fatal infection, by penetrating the nasal mucosa and migrating to the brain via the olfactory nerves. N. fowleri can induce host cell death via lytic necrosis. Similar to phosphorylation, O-linked β-N-acetylglucosamine (O-GlcNAc) glycosylation (O-GlcNAcylation) is involved in various cell-signaling processes, including apoptosis and proliferation, with O-GlcNAc addition and removal regulated by O-GlcNAc transferase and O-GlcNAcase (OGA), respectively. However, the detailed mechanism of host cell death induced by N. fowleri is unknown. In this study, we investigated whether N. fowleri can induce the modulation of O-GlcNAcylated proteins during cell death in Jurkat T cells. Co-incubation with live N. fowleri trophozoites increased DNA fragmentation. In addition, incubation with N. fowleri induced a dramatic reduction in O-GlcNAcylated protein levels in 30 min. Moreover, pretreatment of Jurkat T cells with the OGA inhibitor PUGNAc prevented N. fowleri–induced O-deGlcNAcylation and DNA fragmentation. These results suggest that O-deGlcNAcylation is an important signaling process that occurs during Jurkat T cell death induced by N. fowleri.

We aimed to compare the immune response induced by natural infection with 2009 pandemic influenza A/H1N1 (pH1N1) virus and by monovalent pH1N1 vaccination in children and adolescents. This cross-sectional clinical study was conducted at 3 hospitals in Korea from February to May 2010. A total of 266 healthy subjects aged from 6 months to 18 yr were tested for the presence of the antibody against pH1N1 using hemagglutination inhibition (HI) test. Information about pH1N1 vaccination and laboratory-confirmed pH1N1 infection history was obtained. The overall rate of HI titers of > or = 1:40 against pH1N1 was 38.7%, and the geometric mean titer (GMT) was 20.5. Immunogenicity of pH1N1 vaccination only was reflected by a 41.1% of seroprotection rate and a GMT of 22.5. Immunogenicity of natural infection only was reflected by a 61.0% of seroprotection rate and a GMT of 40.0. GMT was significantly higher in the subjects of natural infection group than in the subjects of pH1N1 vaccination group (P < 0.001). The immune responses induced by natural pH1N1 infection exceed those induced by pH1N1 vaccinations.
Adolescent ; Antibodies, Neutralizing/blood ; Antibody Formation ; Child ; Child, Preschool ; Cross-Sectional Studies ; Hemagglutination Inhibition Tests ; Humans ; Infant ; Influenza A Virus, H1N1 Subtype/*immunology/metabolism ; Influenza, Human/epidemiology/*immunology/prevention & control ; Pandemics ; Vaccination

Perirenal hematoma after a renal biopsy is a common complication that usually resolves spontaneously, but this rarely requires transfusions or surgical/radiological intervention. We report here on a case of a renal perforating artery that was mistaken for renal arterial bleeding in a 53-year-old woman who was complicated with perirenal hematoma after undergoing a percutaneous renal biopsy. On the color and pulsed wave Doppler ultrasonography, linear blood flow was seen in the perirenal hematoma, which extended perpendicularly from the renal parenchyma into the perirenal space, and this linear blood flow exhibited an arterial pulse wave. On CT angiography, the renal perforating artery was demonstrated as a curvilinear vessel coursing tangentially to the renal margin and we decided that it was a pseudolesion caused by the renal perforating artery. A renal perforating artery may be mistaken for renal arterial bleeding after a percutaneous renal biopsy. A renal perforating artery and arterial bleeding can be differentiated by the location and shape seen on a color Doppler examination and the pulse waves characteristics.
Angiography ; Arteries ; Biopsy ; Female ; Glycosaminoglycans ; Hematoma ; Hemorrhage ; Humans ; Middle Aged ; Ultrasonography, Doppler ; Ultrasonography, Doppler, Color

Objectives: The objective of this study was to determine the effect of atrial fibrillation (AF) on the risk of dementia in the Korean elderly. Methods: A 10-year retrospective cohort study was conducted using the National Health Insurance Service-Senior Cohort database. We excluded those who were under 65 years of age as of January 2006 (n=46 113), those who were diagnosed with dementia between 2002 and 2005 (n=9086), and those with a history of stroke prior to AF diagnosis (n=8392). We used a Cox proportional hazards model with a time-varying covariate to determine whether AF is associated with the risk of dementia after adjusting for potential confounders. Results: In univariable Cox regression, the hazard ratio (HR) of dementia according to AF status was 1.28 (95% confidence interval [CI], 1.23 to 1.33). After adjusting for potential confounders, AF was found to increase the risk of dementia (HR, 1.12; 95% CI, 1.07 to 1.17), Alzheimer dementia (HR, 1.12; 95% CI, 1.07 to 1.17), and vascular dementia (HR, 1.10; 95% CI, 1.03 to 1.18). In patients diagnosed with AF, the incidence of dementia was lower (HR, 0.50; 95% CI, 0.47 to 0.52) in patients who were treated with oral anticoagulants. Conclusions Investigating the potential risk factors of dementia in an aged society is important. We found a slightly higher risk of dementia in those with AF than in those without AF, and we therefore concluded that AF is a potential risk factor for dementia.

We report a case of gastric inflammatory myofibroblastic tumor in a 25-month-old boy. The condition is very rare and is of unknown pathogenesis. Because it is large and invades adjacent organs, imaging procedure do not provide easy differentiation between an inflammatory myofibroblastic tumor and malignacy, and it should thus be included in the differential diagnosis of an infiltrative upper abdominal mass occurring in children.
Child ; Child, Preschool ; Diagnosis, Differential ; Granuloma, Plasma Cell ; Humans ; Male ; Myofibroblasts*