Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0032273 (pneumoconiosis)
1,578 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Since it is very rare that cardiac tamponade due to myocardial rupture caused by infective endocarditis, occurs we are reporting this case. A 62 year old man, who had underlying diseases of pneumoconiosis and hypertensive heart disease, visited Chikuho Rosai Hospital complaining of chest oppression and general fatigue on Feb. 7, 1987. He was diagnosed as having ischemic heart disease by electrocardiogram. Two days later, he suddenly had chills and a fever, and the laboratory data showed leukocytosis and a positive C-reactive protein (CRP). The echo cardiogram showed mitral regurgitation (MR) and aortic regurgitation (AR), but neither vegetation nor pericardial effusion was observed. On Feb. 16, he was admitted with shock, and he died the next day. The blood cultures grew gram-positive cocci, respectively. From the clinical symptoms, chest roentgenogram and electrocardiogram, we suspected a cardiac tamponade. On autopsy findings, though coronary arteries were intact, the aortic valves had severe valvular adhesions, calcifications and hypertrophies. The rupture hole was observed in the left ventricles, which was just under the aortic valve through the pericardiac space. It seemed that he died of a cardiac tamponade due to the outflow of blood from this hole. On histopathologic findings of the cardiac wall, gram-positive cocci and many of neutrophils were observed.
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PMID:[An autopsied case of infective endocarditis with cardiac tamponade due to myocardial rupture]. 207 73

The mortality experience of 5,406 men (cohort I) employed at one aluminum smelter on Jan. 1, 1950, and 485 men employed at a second plant (cohort II) on Jan. 1, 1951, is reported. For each man, the total number of years of exposure to tars, the number of years since first exposure to tars, and an index of exposure to tars expressed in tar-years were calculated. More than 99% of the men in the first cohort and 98% of the men in the second cohort were traced. Of the 1,539 men in cohort I who were deceased as of December 31, 1977, death certificates were obtained for 1,432 (93%). Of the 92 men in cohort II who were deceased as of December 31, 1977, death certificates were obtained for 80 (87%). The results showed that men in cohort I died of the following causes at approximately the same rate as or less frequently than men of similar age in the Province of Quebec: tuberculosis; circulatory disease; hypertensive heart disease; trauma; leukemia and aleukemia; and malignant neoplasms of the pancreas, genital organs, brain, intestine, and rectum and other abdominal areas. There were no deaths from pneumoconiosis or Alzheimer's disease. Although the observed and expected numbers of deaths in some of the cause-of-death categories were small, men in cohort I died of the following causes more frequently than did men of similar age in the Province of Quebec: respiratory disease; pneumonia and bronchitis; malignant neoplasms (all sites); malignant neoplasms of the stomach and esophagus, bladder, and lung; other malignant neoplasms; Hodgkin's disease; and other hypertensive disease. Mortality from malignant neoplasms of the bladder and lung was meaningfully related to numbers of tar-years and of years of exposure. Exposure-response relationships were less clear for malignant neoplasms of the esophagus and stomach and for other malignancies. Mortality from respiratory disease for men with 21 or more tar-years of exposure was approximately twice that of persons never exposed to tars. The apparent excess of other hypertensive disease was restricted to men never exposed to tars. Malignant neoplasm of the lung was the only cause of death in cohort II that was in excess of that expected at Quebec provincial rates.
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PMID:Mortality of aluminum reduction plant workers, 1950 through 1977. 406 80