Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Phosphodiesterase I (EC 3.1.4.1) activity was detected in normal human blood serum. The enzyme is stable at laboratory temperature for three days, but is inactivated at pH less than 7. The pH for optimum activity increases with the substrate concentration (under the conditions used, from pH 9.0 to 10.2) and, conversely, the Km increases with pH and buffer concentration. The enzyme is inhibited by ethylenediaminetetraacetate but not by phosphate (0.1 mol/liter). We developed a simple quantitative method for its determination, based on hydrolysis of the p-nitrophenyl ester of thymidine 5'-monophosphate and subsequent measurement of the liberated p-nitrophenol at 400 nm in NaOH (0.1 mol/liter). Normal values (mean +/- 2 SD) were determined to be 33 +/- 6.4 U/liter. Preliminary studies indicate that phosphodiesterase I activity is greater than normal in serum of patients with necrotic changes in the liver or kidney or in cases of breast cancer, but not in that of patients with myocardial infarction, bone cancer, lung cancer, or chronic liver cirrhosis.
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PMID:Determination of phosphodiesterase I activity in human blood serum. 16 91

Plasma and 24-hour urinary cyclic AMP and cyclic GMP levels were determined by saturation analysis in specimens from normal subjects and from 101 patients with tumours of the gastrointestinal tract, breast, lung, bladder or prostate, or with cirrhosis of the liver. Relative to 46 control subjects, plasma cyclic GMP concentrations were significantly elevated in seven patients with gastric tumours, 20 patients with cancer of the breast, six patients with lung cancer, and 12 patients with cirrhosis of the liver. Urinary cyclic GMP/creatinine ratios were significantly increased in cirrhotic patients and in the lung and oesophageal cancer groups. In no cancer group were increases in plasma or urine cyclic GMP levels sufficiently consistent to be of value in the diagnosis of human malignant disease. Changes in extracellular fluid cyclic nucleotide levels in the cirrhotic group were very similar to those that have been reported for primary hepatoma patients.
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PMID:Plasma and urine cyclic nucleotide levels in malignant disease and cirrhosis of the liver. 23 Feb 5

From 1951 to 1971 male doctors reduced their cigarette smoking more than did men in social classes I and II combined. In 1970-2, 665 male doctors died aged under 65. Had they shown the same improvements in cause-specific death rates over the 20 years as men in classes I and II, 699 deaths would have been expected. This "saving" of 34 deaths in the doctors comprised savings from coronary heart disease (83), stroke (16), and lung cancer (8) balanced by 60 "losses" from three stress-related causes--namely, accident, poisonings, etc (30); suicide (26); and cirrhosis of the liver (4)--plus 13 from other causes. As a relative reduction in mortality from heart disease in doctors (as compared with that in social classes I and II) also occurred during 1931-51--that is, before they began to give up smoking--some of the saving in heart-disease deaths in 1951-71 was probably not related to changes in smoking habits. The relative worsening in mortality from stress-related diseases may have been due partly to a possible adverse effect of giving up smoking if smoking had acted to reduce stress. From these findings, the benefits of giving up smoking may not be so great as has commonly been assumed.
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PMID:Has the mortality of male doctors improved with the reductions in their cigarette smoking? 53 59

An increased mortality from lung cancer, cardiovascular disease, haematolymphatic malignancy and cirrhosis of the liver has been reported among smelter workers and others exposed to arsenic. This study uses the case-referent (case-control) technique and is concerned with workers in a copper smelter in a complex work environment, characterised by the presence of trivalent arsenic in combination with sulphur dioxide and copper, and also with other agents. Lung cancer mortality was found to be increased about five-fold and cardiovascular disease about two-fold, showing a dose-response relationship to arsenic exposure. Mortality from malignant blood disease (leukaemia and myeloma) and cirrhosis of the liver was also slightly increased. This mortality pattern among the smelter workers is consistent with earlier reports. An increased mortality from cardiovascular disease in this type of industry is of particular interest as it has been reported only once before.
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PMID:Arsenic exposure and mortality: a case-referent study from a Swedish copper smelter. 62 94

The causes of death among the dock-yard workers of Genoa from December 31, 1959 to January 1, 1970, have been investigated. These workers, mainly assigned to ship repair, refitting and construction, are exposed to several noxious substances, such as: asbestos, silica, paint solvents, welding smoke and volatile products of petroleum. Two different control groups were selected: the male population of Genoa and the staff of the San Martino Hospital in Genoa. Causes of death showing a significant increase were: gastric cancer (only in comparison with the hospital staff), cancer of colon excluding rectum, lung cancer, cancer of kidney, urinary bladder and other urinary organs, respiratory diseases, cirrhosis of the liver, cardiovascular diseases (only in comparison with the hospital staff).
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PMID:Mortality among dock-yard workers in Genoa, Italy. 87 25

In the contemporary United States, males have 60 percent higher mortality than females. In Part I, published in the previous issue, we showed that 40 percent of this sex differential in mortality is due to a twofold elevation of arteriosclerotic heart disease among men. Major causes of higher rates of arteriosclerotic heart disease in men include greater cigarette smoking among men; probably a greater prevalence of the competitive, aggressive Coronary Prone Behavior Pattern among men; and possibly a protective role of female hormones. In addition, men have higher death rates for lung cancer and emphysema, primarily because more men smoke cigarettes. In Part II we analyze the other major causes of men's higher death rates: accidents, suicide, and cirrhosis of the liver. Each of these is related to behaviors which are encouraged or accepted more in men than in women in our society--for example, using guns, being adventurous and acting unafraid, working at hazardous jobs and drinking alcohol. We conclude with suggestions for reducing male mortality; for example, by changing the social conditions which foster in men the behaviors that elevate their mortality.
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PMID:Why do women live longer than men? 101 15

A non-concurrent prospective study was made on deaths from cancer and other causes occurring among 2,675 male workers at a metal refinery from 1949 to 1971. The expected number of deaths computed by applying age- and cause-specific death rates of Japanese males to these workers was compared with the observed number of deaths. Among 839 copper smelters, significantly increased mortalities were noted for lung cancer (SMR = 1,189) and colon cancer, but nor for cancer of the stomach, liver (primary) and biliary passages, pancreas and skin or for leukemia, tuberculosis, cerebrovascular diseases, heart diseases and liver cirrhosis. A dose-response relationship was demonstrated between the mortality from lung cancer and the degree of exposure. A very high excess mortality from lung cancer (SMR = 2,500) was seen among copper smelters who were considered to have been most heavily exposed to arsenic or workers who had engaged in sintering and blast furnace operations for 15 years of more before 1949. The latent period of lung cancer was 37.6 years on average, and not related to level of exposure. Twenty-six of 29 deaths from lung cancer among copper smelters occurred after they had left the refinery. Other production workers and clerical workers showed no significant excess mortality from any kind of cancer.
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PMID:A cohort study on mortality from cancer and other causes among workers at a metal refinery. 125 55

This is the second update of a study of 3,444 taconite miners and millers who were first exposed to taconite, with associated exposures to silica and nonasbestiform amphiboles, in the period 1947 through 1958. Previous analyses of deaths through 1977, and again through 1983, showed no significant excess deaths from any specific causes. The present study continues the follow-up through 1988, adding 14,748 person-years of observation and 261 death certificates for analysis. The population, reduced to 3,431 because of the detection of 13 earlier duplications, has now been observed for 101,055 person-years, with 1,058 deaths and 1,039 death certificates. Death certificates were obtained for 98.2% of those known to be dead. The total number of deaths was significantly fewer than expected. Based on US rates, the standardized mortality ratio (SMR) was 83 (ie, 83% of expected). Based on Minnesota death rates, it was 91. With both US and Minnesota death rates, the SMRs for malignant neoplasms, cancer of the respiratory tract, cancer of the digestive system, heart disease, nonmalignant respiratory disease, and cirrhosis of the liver were all below 100. Slightly elevated SMRs were found for cancer of the colon, cancer of the kidney, and lymphopoietic cancer. These elevations were not statistically significant. Separate analyses were made of total deaths, lung cancer deaths, and kidney cancer deaths in men who had worked with taconite for time periods of less than 1 year, 1-5 years, 5-10 years, and over 10 years, during observation periods less than 10 years, 10-20 years, and over 20 years.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:An updated study of taconite miners and millers exposed to silica and non-asbestiform amphiboles. 133 7

A historical prospective cohort study of 6630 drivers from the Canton of Geneva was carried out to evaluate mortality and incidence of cancer in this occupation. The study population was all men (of all vocations) who held in 1949 a special licence for driving lorries, taxis, buses, or coaches and all new licence holders in the period 1949-61. Men born before 1900 and those with only an ordinary driving licence were excluded. According to the occupation registered on their licence, the 6630 drivers were distributed into three groups: (1) professional drivers (n = 1726), (2) non-professional drivers "more exposed" to exhaust gas and fumes (this group included occupations such as vehicle mechanic, policeman, road sweeper; n = 712), and (3) non-professional drivers "less exposed," composed of all other occupations (n = 4192). The cohort was followed up from 1949 to December 1986 and the trace of 197 men (3%) was lost. Compared with the general population of the Canton of Geneva, professional drivers experienced significant excess risks, taking into account 15 years of latency, for all causes of death (standardised mortality ratio (SMR) 115, 90% confidence interval (90% CI) 107-123) and for all malignant neoplasms (SMR 125, 90% CI 112-140; standardised incidence ratio (SIR) 128, 90% CI 115-142). Cause specific analysis showed significant excesses for lung cancer (SMR 150, 90% CI 123-181; SIR 161, 90% CI 129-198), oesophageal cancer (SMR 183, 90% CI 108-291), stomach cancer (SMR 179, 90% CI 117-263; SIR233, 90% CI 156-336), rectal cancer (SMR 258, 90% CIU 162-392; SIR 200, 90% CI 127-300), and cirrhosis of the liver (SMR 145, 90% CI 104-198). Risk of lung cancer increased significantly with time from first exposure. Among non-professional drivers no significant excess risk was found except for lung cancer mortality among the "less exposed" group (SMR 121, 90% CI 103-140), and for incidence of lung cancer among the "more exposed" group (SIR 161, 90% CI 111-227). The possible casual relation between exposure to engine exhaust emissions and the increased risk for lung cancer and for cancer of the gastrointestinal tract found among professional drivers is discussed.
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PMID:Increased risk for lung cancer and for cancer of the gastrointestinal tract among Geneva professional drivers. 137 39

Eastern Austrian regional mortality patterns of oral cancer (oral cavity, pharynx and larynx) and oesophageal, lung and urinary bladder cancer were compared to smoker rates and to liver cirrhosis mortality by type of residence: Vienna (1.7 x 10(6) inhabitants), middle towns (50,000-100,000 and 10,000-50,000 inhabitants), small towns (2000-10,000 inhabitants) and rural areas categorized by agrarian quota less than or equal to 10%, 10%-20% and greater than 20%. The study area (Vienna, Lower Austria and Burgenland) covers 23,600 km2 with 3.23 x 10(6) inhabitants. In men, liver cirrhosis correlated negatively with smoker rates (r = 0.74, P = 0.1). Deaths from oral cancer and oesophageal cancer correlated significantly with deaths from liver cirrhosis (r = 0.81, P = 0.03; r = 0.78, P = 0.04, respectively) but not with smoker rates; lung cancer and bladder cancer correlated significantly with smoker rates (r = 0.91, P = 0.01; r0.83, P = 0.04, respectively), but not with liver cirrhosis. In women, similar urban-rural gradients for all parameters resulted in a positive correlation between liver cirrhosis and smoker rates (r = 0.59, P = 0.22) and a significant correlation of lung cancer with liver cirrhosis (r = 0.75, P = 0.05). Oral cancer correlated significantly with liver cirrhosis (r = 0.83, P = 0.02), but not with smoker rates; lung cancer correlated more significantly with smoker rates (r = 0.92, P = 0.01) than with liver cirrhosis; bladder cancer correlated positively with smoker rates (r = 0.70, P = 0.12). Geographical distribution of oral and oesophageal cancer in Eastern Austria seems thus to be highly subject to the prevalence of heavy drinking. Sociocultural influences upon the occurrence of these cancers seem to be mediated through drinking habits rather than through smoking habits alone.
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PMID:Tobacco-related cancer in relation to prevalence of drinking and smoking in eastern Austria. 151 83


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