BACKGROUND: The present study was carried out in association with neutrophilic respiratory burst in the lung in order to clarify the pathogenesis of acute respiratory distress syndrome(ARDS) following acute severe hemorrhage. Because oxidative stress has been suggested as one of the principal factors causing tissue injury, the role of free radicals from neutrophils was assessed in acute hemorrhage-induced lung injury. METHOD: In Sprague-Dawley rats, hemorrhagic shock was induced by withdrawing blood(20 ml/kg of B.W) for 5 min and the hypotensive state was sustained for 60 min. To determine the mechanism and role of oxidative stress associated with phospholipase A2(PLA2) by neutrophils, the level of lung leakage, pulmonary myeloperoxidase(MPO), and the pulmonary PLA2 were measured. In addition, the production of free radicals was assessed in isolated neutrophils by cytochemical electron microscopy in the lung. RESULTS: In hypotensive shock-induced acute lung injury, the pulmonary MPO, the level of lung leakage and the production of free radicals were higher. The inhibition of PLA2 with mepacrine decreased the pulmonary MPO, level of lung leakage and the production of free radicals from neutrophils. CONCLUSION: A. neutrophilic respiratory burst is responsible for the oxidative stress causing acute lung injury followed by acute, severe hemorrhage. PLA2 activation is the principal cause of this oxidative stress.
Acute Lung Injury* ; Free Radicals ; Hemorrhage ; Lung ; Lung Injury ; Microscopy, Electron ; Neutrophils* ; Oxidative Stress ; Phospholipases A2* ; Phospholipases* ; Quinacrine ; Rats, Sprague-Dawley ; Respiratory Burst* ; Shock, Hemorrhagic

Hypersensitivity myocarditis is an inflammatory disease of the myocardium usually related to drug allergy. The clinical manifestation may be nonspecific, and the diagnosis is seldom suspected or established during the life. So in most of the reported patients, the diagnosis was made at autopsy. Although, retrospectively, more than 90% of the patients described have had clinically recognizable cardiac involvement before death, tole clinical suspicion of hypersensitivity myocarditis is rare. The presence of nonspecific cardiac finding in a patient receiving any drug associated with hypersensitivity should alert the clinician to the possibility of drug related myocarditis. We experienced a case of hypersensitivity myocarditis accompanying allergic skin lesion in a 58 years old man with a history of taking cefadroxil. Fortunately, the outcome was favorable, therefore we do not have histologic confirmation of the diagnosis.
Autopsy ; Cefadroxil ; Diagnosis ; Drug Hypersensitivity ; Humans ; Hypersensitivity* ; Middle Aged ; Myocarditis ; Myocardium ; Retrospective Studies ; Skin

No abstract available.
Diaphragm* ; Ultrasonography*

BACKGROUND: Lung carcinogenesis is a multistage process involving alterations in multiple genes and diverse pathway. Mutational activation of oncogenes and inactivation of tumor suppressor genes, and subsequent increased genetic instability are the major genetic events. The p53 gene and FHIT gene as tumor suppressor genes contribute to the pathogenesis of lung cancer, evidenced by mutation, microsatellite instability(MI) and loss of heterozygosity(LOH). METHODS: We analysed genetic mutations of p53 and FHIT gene in 29 surgical specimens of nonsmall cell lung cancer using PCR-single strand conformation polymorphism, DNA sequencing and RT-PCR. MI and LOH were analyzed in loci of D3S1285, D9S171, and TP53. RESULTS: In 2 cases, point mutation of p53 gene was observed on exon 5. MI of 3 times and LOH of 14 times were observed in at least one locus. In terms of the location on microsatellite, D3S1285 as a marker of FHIT was observed in 5 cases out of 26 specimens;D9S171 as a marker of p16 in 5 out of 17;and TP53 as a marker of p53 in 7 out of 27. In view of histologic type, squamous cell carcinoma presented higher frequency of microsatellite alteration, compared to others. Mutation of FHIT gene was observed in 11 cases and 6 cases of those were point mutation as a silent substitution on exon 8. FHIT mRNA expression exhibited deletion on exon 6 to 9 in 4 cases among 15 specimens, presenting beta-actin normally. CONCLUSION: Our results show comparable frequency of genetic alteration in nonsmall cell lung cancer to previous studies of Western countries. Microsatellite analysis might have a role as a tumor marker especially in squamous cell carcinoma. Understanding molecular abnormalities involved in the pathogenesis could potentially lead to prevention, earlier diagnosis and the development of novel investigational approaches to the treatment of lung cancer.
Actins ; Carcinogenesis ; Carcinoma, Non-Small-Cell Lung* ; Carcinoma, Squamous Cell ; Diagnosis ; Exons ; Genes, p53 ; Genes, Tumor Suppressor* ; Loss of Heterozygosity ; Lung ; Lung Neoplasms ; Microsatellite Instability ; Microsatellite Repeats* ; Oncogenes ; Point Mutation ; RNA, Messenger ; Sequence Analysis, DNA

We report a case of pneumonia in 36 year-old male patient who presented acute respiratory failure and associated radiologic findings of bilateral ground-glass opacity with focal cystic changes, showing rapidly aggravating course and was diagnosed as concomitant Pneumocystis carinii and Cytomegalovirus pneumonia accompanied by acquired immunodeficiency syndrome through antemortem open lung biopsy.
Acquired Immunodeficiency Syndrome ; Biopsy ; Cytomegalovirus ; Humans ; Lung ; Male ; Pneumocystis carinii ; Pneumonia ; Respiratory Insufficiency*

Spontaneous regression is extremely rare in lung cancer and this in spite of its global high incidence. So far, less than 30 such cases have been reported in the literature. We report here on the case of a 68-year-old man who had the diagnosis of adenocarcinoma and in absence of any medical therapy, he had a partial spontaneous regression of tumor.
Adenocarcinoma ; Aged ; Carcinoma, Non-Small-Cell Lung ; Humans ; Incidence ; Lung Neoplasms

OBJECTIVES: Despite the advances in medical practice and technology, a steady increase in the incidence of sepsis has been reported and the mortality has been persistently high ranging from 20 to 50%, especially in medical intensive care unit. Therefore, objective assessment of severity of illness based on risk estimates derived from severity of illness score has been important. Thus this study was designed for identification of risk factors and comparison of severity of illness scores: Acute physiology and chronic health evaluation II(APACHE II), Acute physiology and chronic health evaluation III (APACHE III), Multiorgan failure scoring system(MOF), Simplified acute physiology score(SAPS), Septic severity score(SSS). METHODS: A retrospective clinical study was done on 97 patients with sepsis treated in medical intensive care unit, who had been admitted to Ewha Womans University Mokdong Hospital from September 1994 to May 1997. Multiple factors which may influence mortality and severity of illness score were evaluated by univariate and logistic regression analysis. RESULTS: 1) Of the 97 patients, 52 were male and 45 were female. The mean age was 62 years and the overall mortality was 59.8%. 2) On severity of illness, sepsis was 21cases, severe sepsis 36 and septic shock 40. On primary source of infection, pulmonary origin was 39cases, gastrointestinal origin 23 and urinary tract origin 13. The infection caused by documented organism was 53cases. 3) Based on the univariate analysis, age, sex, respiratory rate, number of organ failure, admission source, ventilatory support, hematocrit, WBC, prothrombin time, Na and K, pH, PaO2/FiO2, D(A-a)O2 and the following severity of illness scores :APACHE II, APACHE III, MOF, SAPS, and SSS for predicting mortality risk were all significant factors discriminating between survivors and nonsurvivors. 4) In distribution curve of APACHE II, APACHE III, MOF, SAPS, and SSS, the cut-off values in predictive risk of 50% were 21, 88, 4, 15, and 29. By logistic regression analysis after substituting their cut off value, APACHE II and APACHE III were significant independent predictors influencing survival with odd ratio 3.82 in APACHE II and 4.62 in APACHE III. In predictive risk of 50%, sensitivity was 55%, specificity 85%, accuracy 85% and relative risk 6.77 in APACHE II. And sensitivity was 47%, specificity 97%, accuracy 88% and relative risk 7.62 in APACHE III. CONCLUSION: APACHE II and APACHE III were significant predictor influencing mortality in sepsis patients treated in medical intensive care unit and APACHE III was superior to that of its predecessor. In near future, prospective and multicentral studies are required to confirm these results.
APACHE ; Female ; Hematocrit ; Humans ; Hydrogen-Ion Concentration ; Incidence ; Intensive Care Units* ; Critical Care* ; Logistic Models ; Male ; Mortality* ; Physiology ; Prothrombin Time ; Respiratory Rate ; Retrospective Studies ; Risk Factors* ; Sensitivity and Specificity ; Sepsis* ; Shock, Septic ; Survivors ; Urinary Tract

BACKGROUND: There have been many reports on the pathogenesis of sepsis-induced acute respiratory distress syndrome(ARDS) but, the precise mechanism has not been elucidated. This study examined the protective effect of an inhibition of platelet activating factor(PAF) remodeling and the adhesion molecule on the oxidative stress of the lungs in rats with an endotoxin induced acute lung injury(ALI). METHODS: ALI was induced in Sprague-Dawley rats by instilling an E-coli endotoxin into the trachea. Ketotifen and fucoidan were used respectively to inhibit PAF remodeling and adhesion molecule. The lung leak index, lung myeloperoxidase(MPO) activity, bronchoalveolar lavage(BAL) fluid neutrophil count and lyso PAF acetyltransferase activity(AT), were measured and an ultrastructural study and cytochemical electron microscopy were performed. RESULTS: The lung leak index, lung MPO activity, BAL fluid neutrophil count and lyso PAF AT activity was higher in the endotoxin-treated rats. In addition, severe destruction of the pulmonary architecture and increased hydrogen peroxide production were identified. These changes were reversed by ketotifen. However, fucoidan did not appear to have any protective effects. CONCLUSION: The inhibition of PAF remodeling appeared to be effective in decreasing the endotoxin-induced ALI. In addition, this effect might be derived from the inhibition of neutrophilic oxidative stress. However, the inhibition of the adhesion molecules by fucoidan appeared to be ineffective in decreasing the endotoxin-induced ALI.
Animals ; Blood Platelets ; Hydrogen Peroxide ; Ketotifen ; Lung* ; Microscopy, Electron ; Neutrophils ; Oxidative Stress* ; Rats* ; Rats, Sprague-Dawley ; Trachea

BACKGROUND: Hemorrhagic shock and trauma are two of the most common causes of acute lung injury. The activation of cyclooxygenase is one of the important causes of acute lung injury. This study investigated the effect of aspirin, a well-known cyclooxygenase inhibitor, on severe hemorrhage-induced acute lung injury in rats. METHODS: The hemorrhagic shock was induced by withdrawing blood; 20ml/kg of B.W., through the femoral artery in 5 min. The mean arterial pressure was recorded through the femoral artery on a polygraph. RESULTS: In the present investigation, the lung tissue myeloperoxidase activity, protein contents and leukocyte counts, in bronchoalveolar lavage fluid, increased significantly 2 and 24 h after the hemorrhage induction. Although the decreased mean arterial pressure spontaneously recovered, acute lung injury occurred after severe hemorrhage. These changes were effectively prevented by a single intravenous injection of aspirin (10 mg/kg of B.W.) 30 min before the hemorrhage. CONCLUSION: These results suggest that severe hemorrhage-induced acute lung injury is mediated, in part, by the activation of cyclooxygenase. Furthermore, pretreatment of aspirin in acute lung injury-prone patients, or prophylactic treatment of aspirin to the patients with precipitating conditions, could be helpful in the prevention of acute lung injury.
Acute Lung Injury* ; Animals ; Arterial Pressure ; Aspirin* ; Bronchoalveolar Lavage Fluid ; Femoral Artery ; Hemorrhage* ; Humans ; Injections, Intravenous ; Leukocyte Count ; Lung ; Peroxidase ; Prostaglandin-Endoperoxide Synthases ; Rats* ; Shock, Hemorrhagic

In order to review the epidemiological data of cardiovascular diseases, statistical observation was made on the 7,271 patients with cardiovascular diseases who were treated in the Department of Internal Medicine, Han-Yang University Hospital during the 10 year period from May 1972 to December 1981. A. General Findings (1) Cardiovascular disease was seen in 18.6% out of a total 39,004 medical inpatients treated during this 10 year time span. (2) Incidences of cardiovascular disease seemed to increase in frequency in consecutive years, especially incidence of coronary heart disease and arrhythmia. (3) Incidence of cardiovascular disease occurred most frequently to patients in their fifth decade, and next most frequently to those in their sixth and fourth decade, in that order. (4) The overall ratio of male to female incidence of cardiovascular disease was 1:1. B. Specific Epidemiology (1) Hypertension was the most common form of cardiovascular problem, accounting for 52.9% of patients with cardiovascular disease and 9.9% of the total medical in-patients population. Incidence of hypertension occured most frequently in the fifth decade of life. It occured next most in the sixth and fourth decades, in that order. The male to female ratio of incidence of hypertension was 1:1. Patients with malignant hypertension made up 5.9% all hypertension patients. (2) Patients with rheumatic heart disease made up 6% of those patients with cardiovascular diseases. Male to female ratio of incidence of rheumatic heart disease was 1:2.4. The most common form of this disease was mitral valvular disease, but isolated aortic valvular disease proved to be rather uncommon in this study in Korea. (3) Coronary heart disease made up 15.5 % of all incidence of cardiovascular diseases. It occured most frequently to patients in their fifth and sixth decades, and in a male to female ratio of 1.5 to 1. (4) Congenital heart disease made of 0.9% of the total incidence of cardiovascular diseases with ventricular septal defect as the most common form of this disease. (5) The remaining forms of cardiovascular diseases diagnosed during the time span of this study were arrhythmia 16.8%, cor pulmonale 1.4%, cardiomyopathy 1.3%, peripheral vascular disease 1.0%, pericarditis 1.0%, thyrotoxic heart disease 0.8%, endocarditis 0.5%, postpartum cardiomyopathy 0.3%, myxedematous heart disease 0.1%, and miscellaneous heart ailments 1.5%.
Arrhythmias, Cardiac ; Cardiomyopathies ; Cardiovascular Diseases* ; Coronary Disease ; Endocarditis ; Epidemiology ; Female ; Heart ; Heart Defects, Congenital ; Heart Diseases ; Heart Septal Defects, Ventricular ; Humans ; Hypertension ; Hypertension, Malignant ; Incidence ; Inpatients ; Internal Medicine ; Korea* ; Male ; Pericarditis ; Peripheral Vascular Diseases ; Postpartum Period ; Pulmonary Heart Disease ; Rheumatic Heart Disease