No abstract available.
Factor V Deficiency* ; Factor V*

BACKGROUND: As one of the etiologies of acute respiratory distress syndrome (ARDS), sepsis is one of the morbid causes of this cryptogenic malady. Even though many documents on the role of endotoxin (ETX) in the pathogenesis of ARDS have been issued, still the underlying mechanism associated with oxidative stress and activation of PLA2 has been a controversy controversial . In the present study, the role of phospholipase A2 (PLA2) in the neutrophilic respiratory burst(,) which is presumed to cause acute lung injury during sepsis(,) was probed. METHOD: In glutathione (-)depleted Sprague-Dawley rats, lung leak, infiltration of neutrophils, PLA2 activity and lipid peroxidation in the lung were measured after intratracheal instillation of endotoxin intratracheally (delete). In addition, gamma glutamyl transferase (GGT) activity and the amount of pulmonary surfactant were measured. Morphologically, changes of the changes in ultrastructure and cytochemical demonstration of oxidants were presented to confirm the neutrophilic oxidative stress and to elucidate the effects of the activation of PLA2 activation on the (delete) oxidative stress. RESULTS: Instillation of ETX to glutathione (-) depleted rats intensified lung leak and lipid peroxidation when compared with non-glutathione depleted rats treated with the endotoxin. Moreover, oxidative stress was confirmed by the assay of GGT and malondialdehyde. Functionally, the depletion of glutathione altered the secretion of pulmonary surfactant from alveolar type II cells. Ultrastructurally and cytochemically, oxidative stress was also confirmed after treatment of with ETX and diethylmaleate (DEM). CONCLUSION: The endotoxin-induced acute lung injury was mediated by oxidative stress(,) which in turn was provoked by the neutrophilic respiratory burst. The activation of PLA2 in the lung seems to play the a pivotal role in the oxidative stress of the lung.
Acute Lung Injury ; Animals ; Glutathione* ; Lipid Peroxidation ; Lung* ; Malondialdehyde ; Neutrophils ; Oxidants ; Oxidative Stress* ; Phospholipases A2 ; Pulmonary Surfactants ; Rats* ; Rats, Sprague-Dawley ; Respiratory Burst ; Respiratory Distress Syndrome, Adult ; Sepsis ; Transferases

Autoimmune hemolytic anemia(AIHA) is characterized by the production of Coombs antibodies, which are responsible for the destruction of RBCs. The antibody specificity of warm A1HA(WAIHA) is very complex while all cells tested are usually reactive in routine test. Although some autoantibodies have broad specificity to the Rh system, apparent specificity for simple Rh antigen(D, C, E, c, e) is rare. A 63 year-old farmer was admitted at Inha University Hospital for evaluation of anemia. He had no history of blood transfusion. He presented overt anemia with decreased Hb (6.6g/dL) and increased reticulocyte count(18.5%, corrected reticulocyte count 8.4%). The direct antiglobulin test(DAT) was strongly positive for IgG and negative for C3d while indirect antiglobulin test(IAT) was weakly positive. Both two different antibody identification test kits identified this antibody as anti-e. His Rh phenotype was CDe. Although the eluted antibody from his own RBCs failed to show specificity against e but agglutinated all the reagent RBCs, we diagnosed this case as WAIHA induced by IgG anti-Rh(e) because his serum agglutinated all e-positive RBCs while it was non-reactive with e-negative RBC in the cross- matching test. Drugs(loxoprofen, cimetidine) couldn' t be ruled out as causative agent. (Korean J Blood Transfusion 10(1): 61-67, 1999)
Anemia ; Anemia, Hemolytic, Autoimmune* ; Antibodies ; Antibody Specificity ; Autoantibodies ; Blood Transfusion ; Humans ; Immunoglobulin G ; Middle Aged ; Phenotype ; Reticulocyte Count ; Reticulocytes ; Sensitivity and Specificity

Autoimmune hemolytic anemia (AIHA) is characterized by the production of Coombs' antibodies, which are responsible for the destruction of RBCs. The antibody specificity of warm AIHA (WAIHA) is very complex while all cells tested are usually reactive in routine test. Although some autoantibodies have broad specificity to the Rh system, apparent specificity for simple Rh antigen (D, C, E, c, e) is rare. A 63 year-old farmer was admitted at Inha University Hospital for evaluation of anemia. He had no history of blood transfusion. He presented overt anemia with decreased Hb (6.6g/dL) and increased reticulocyte count (18.5%, corrected reticulocyte count 8.4%). The direct antiglobulin test (DAT) was strongly positive for IgG and negative for C3d while indirect antiglobulin test (IAT) was weakly positive. Both two different antibody identification test kits identified this antibody as anti-e. His Rh phenotype was CDe. Although the eluted antibody from his own RBCs failed to show specificity against e but agglutinated all the reagent RBCs, we diagnosed this case as WAIHA induced by IgG anti-Rh(e) because his serum agglutinated all e-positive RBCs while it was non-reactive with e-negative RBC in the cross-matching test. Drugs (loxoprofen, cimetidine) couldn't be ruled out as causative agent.
Anemia ; Anemia, Hemolytic, Autoimmune* ; Antibodies ; Antibody Specificity ; Autoantibodies ; Blood Transfusion ; Coombs Test ; Humans ; Immunoglobulin G ; Middle Aged ; Phenotype ; Reticulocyte Count ; Sensitivity and Specificity

The present study evaluated the importance of ovarian functions and the renin-angiotensin system in the progression of the right ventricular (RV) hypertrophy. Female Sprague-Dawley rats were bilaterally ovariectomized (Ovx) and injected with monocrotaline (MCT, 60 mg/kg, sc). Four weeks after MCT-treatment, only the male and Ovx female rats showed marked RV hypertrophy. The hypertrophied RV of the male-MCT and Ovx-MCT rats exhibited remarkably elevated renin mRNA levels. Gene expression levels of angiotensinogen, TGF-beta1, and endothelin-1 in the hypertrophied RV also increased, but to the less degree than did the renin mRNA. To investigate beneficial effects of estrogen or enalapril on progression of the pulmonary hypertension and RV hypertrophy, histological changes of the lung and heart were examined. Sham-MCT female rats showed histological changes indicating pulmonary hypertension without RV hypertrophy. In contrast, Ovx-MCT rats showed marked RV hypertrophy with pathological changes, denoting severe pulmonary and myocardial injuries. Estrogen-or enalapril-treated Ovx-MCT rats did not show RV hypertrophy, and showed remarkably ameliorated ultrastructural changes in the lung and RV. These results from this rat model suggest that both estrogen and inhibition of the renin-angiotensin system have protective functions against the development of the pulmonary hypertension and cardiac remodeling.
Angiotensin-Converting Enzyme Inhibitors/pharmacology ; Angiotensinogen/biosynthesis ; Animals ; Body Weight/drug effects ; Densitometry ; Disease Progression ; Enalapril/*pharmacology ; Endothelin-1/biosynthesis ; Estrogens/*pharmacology ; Female ; Hypertrophy, Right Ventricular/chemically induced/*drug therapy ; Male ; Microscopy, Electron ; Monocrotaline/*pharmacology ; Ovariectomy ; RNA/metabolism ; RNA, Messenger/metabolism ; Rats ; Rats, Sprague-Dawley ; Renin/biosynthesis ; Reverse Transcriptase Polymerase Chain Reaction ; Sex Factors ; Support, Non-U.S. Gov't ; Transforming Growth Factor beta/biosynthesis ; Ventricular Remodeling

In order to understand the pathogenetic mechanism of adult respiratory distress syndrome (ARDS), the role of phospholipase A2 (PLA2) in association with oxidative stress was investigated in rats. Interleukin-1alpha (IL-1, 50 mug/rat) was used to induce acute lung injury by neutrophilic respiratory burst. Five hours after IL-1 insufflation into trachea, microvascular integrity was disrupted, and protein leakage into the alveolar lumen was followed. An infiltration of neutrophils was clearly observed after IL-1 treatment. It was the origin of the generation of oxygen radicals causing oxidative stress in the lung. IL-1 increased tumor necrosis factor (TNF) and cytokine-induced neutrophil chemoattractant (CINC) in the bronchoalveolar lavage fluid, but mepacrine, a PLA2 inhibitor, did not change the levels of these cytokines. Although IL-1 increased PLA2 activity time-dependently, mepacrine inhibited the activity almost completely. Activation of PLA2 elevated leukotriene C4 and B4 (LTC4 and LTB4), and 6-keto-prostaglandin F2alpha (6-keto-PGF2alpha) was consumed completely by respiratory burst induced by IL-1. Mepacrine did not alter these changes in the contents of lipid mediators. To estimate the functional changes of alveolar barrier during the oxidative stress, quantitative changes of pulmonary surfactant, activity of gamma glutamyltransferase (GGT), and ultrastructural changes were examined. IL-1 increased the level of phospholipid in the bronchoalveolar lavage (BAL) fluid, which seemed to be caused by abnormal, pathological release of lamellar bodies into the alveolar lumen. Mepacrine recovered the amount of surfactant up to control level. IL-1 decreased GGT activity, while mepacrine restored it. In ultrastructural study, when treated with IL-1, marked necroses of endothelial cells and type II pneumocytes were observed, while mepacrine inhibited these pathological changes. In histochemical electron microscopy, increased generation of oxidants was identified around neutrophils and in the cytoplasm of type II pneumocytes. Mepacrine reduced the generation of oxidants in the tissue produced by neutrophilic respiratory burst. In immunoelectron microscopic study, PLA2 was identified in the cytoplasm of the type II pneumocytes after IL-1 treatment, but mepacrine diminished PLA2 particles in the cytoplasm of the type II pneumocyte. Based on these experimental results, it is suggested that PLA2 plays a pivotal role in inducing acute lung injury mediated by IL-1 through the oxidative stress by neutrophils. By causing endothelial damage, functional changes of pulmonary surfactant and alveolar type I pneumocyte, oxidative stress disrupts microvascular integrity and alveolar barrier.
Acute Lung Injury ; Animals ; Bronchoalveolar Lavage ; Bronchoalveolar Lavage Fluid ; Cytokines ; Cytoplasm ; Endothelial Cells ; gamma-Glutamyltransferase ; Insufflation ; Interleukin-1 ; Interleukin-1alpha* ; Leukotriene C4 ; Lung Injury* ; Lung* ; Microscopy, Electron ; Necrosis ; Neutrophils ; Oxidants ; Oxidative Stress ; Phospholipases A2 ; Pneumocytes ; Pulmonary Surfactants ; Quinacrine ; Rats ; Reactive Oxygen Species ; Respiratory Burst ; Respiratory Distress Syndrome, Adult ; Trachea ; Tumor Necrosis Factor-alpha

To estimate the incidence rate of coronary heart disease in Korea, of all residents of the Taegu city aged 25 or above, those who had an acute MI or fatal coronary event between 1 July 1996 and 30 June 1997 were registered. Seven hundreds and eight patients were registered during the study period(685 were identified at hospital and 23 were autopsy cases). Age-standardized annual incidence rate of men in city area was 93 per 100,000(95% CI; 61-142) and 33(95% CI; 16-67) in women(100 in men and 20 in women aged 35-64). The incidence was rapidly increased after age 40 in men, however, in women after age 60. Twenty-eight-days case fatality rate was 45% in men and 47% in women. However, in the age group of 45-59 case fatality rate in women was two times higher than that in men. In conclusion, crude annual incidence rate of CHD in city area was 73 per 100,000 in men and 33 in women. The age-standardized annual incidence of CHD in men(93 per 100,000) was 3.2 times higher than that in women (33 per 100,000) in Korea.
Autopsy ; Coronary Disease* ; Daegu ; Female ; Humans ; Incidence* ; Korea ; Male ; Mortality