[Epidemiologic properties of myocardial infarct under 40 years of age].
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Biomedical subjects
Publications and source records attributed to L Keller.
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Elastase-type activity and elastase inhibitory capacity were determined in the sera of 130 atherosclerotic patients, suffering from ischemic vascular disease (IVD) localized at various sites, and of 60 control subjects. The concentrations of serum lipoprotein constituents (triglycerides, total cholesterol, HDL cholesterol, apo-A, apo-B) have also been investigated. HDL cholesterol and apo-A levels were decreased at every site on IVD. Plasma HDL concentration in men was lower than that in women. There was a sex-related difference in the elastase-type activity of the sera: within every atherosclerotic group, elastase-type activity in women was significantly higher than in men. Elastase-type activity did not appear to vary with age and did not show any correlation with the concentration of serum lipoprotein constituents. Pancreatic elastase inhibitory capacity of sera was significantly elevated in the sera of atherosclerotic patients. There was a significant negative correlation between the inhibitory capacity and the HDL cholesterol and apo-A content of sera, respectively. Inhibitory capacity did not show sex-, or age-related variation. There was a significant positive correlation between elastase-type activity and elastase inhibitory capacity measured in control sera. In the sera of atherosclerotic patients this correlation could not be established.
The anthropogenic contribution to the global cadmium flux exceeds natural sources by a factor of three. The most important pathway is the atmosphere; therefore, high cadmium concentrations can be found even in remote areas. On a local level, the increase in cadmium consumption can be observed in increasing concentrations in the soil, plants, and food. The question arises as to what extent the soil-plant-man-waste-soil cycle can be loaded with cadmium in order to function without negative impact on the environment. In Switzerland, 120 tons (t) of cadmium are consumed per year. Of this amount, 25 t end up in municipal solid waste, 3 t in wastewater, and 19 t in precipitation and dry fallout. As a consequence of today's waste management practice (75% incineration, 20% sanitary landfill, 5% composting; 75% of all sewage is purified), the annual input to the soil is 40 t: 18 t concentrated in landfills, 19 t dissipated via the atmosphere, and 3 t directly spread via sewage sludge, compost, and fertilizer on agricultural land. If even distribution were possible, the cadmium content of the soil would theoretically double in 150 years. The accumulation in the soil will increase the cadmium content of plants grown on such a soil. According to a simple model, the level of 3 ppm cadmium in soils should not be surpassed. At such concentrations, plants are likely to contain greater than 0.4 mg Cd/kg, a concentration which can cause toxic effects in long-term experiments. The safe level in food might be even lower. In reality, cadmium is not evenly distributed over Switzerland. According to today's practice, it must be assumed that in only 14 years the use of compost will have enriched soils to such an extent that its cadmium content will prohibit the production of food for human consumption. For sewage sludge, this timespan is 130 years. If heavy metal limits in food are to be observed, the input of such metals to the soil has to be limited. In a steady state, the cadmium input to the soil should be equal to its output via plants, leachate, and erosion. This implies that today's dissipative use of cadmium must be stopped.
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A female infant was born with generalized blue-gray discoloration of the skin. Light microscopy demonstrated the diffuse distribution of dihydroxyphenylalanine-positive, dermal melanocytes. Electron microscopy confirmed the identification of the pigment-bearing cells as melanocytes and demonstrated individual melanocytes to be invested with a filamentous extracellular sheath. To our knowledge, comparable, generalized, dermal melanocytosis has not previously been reported in a newborn.
An examination of the skin in a nine day old infant revealed multiple cherry-red superficial hemangiomas, which progressively increased in size and number. At the age of three weeks these skin lesions involved the scalp, trunk, extremities, palms, soles, and buccal mucous membranes. In addition, similar lesions of the liver and gastrointestinal tract were found. Steroids and irradiation were tried with limited success. Finally, hepatic artery ligation was successful in eliminating the heart failure.
Insulin self-inhibition is still a controversial subject. The majority of data is in favour of an inhibition; however, whether this mechanism is of physiologic relevance in the regulation of insulin secretion is open to discussion. We examined the effect of exogenous insulin on beta cell secretion in 16 volunteers, including 3 who were overweight. Blood glucose (BG) was clamped by means of the dextrose infusion unit of the artificial beta cell, and the secretion of the pancreatic beta cell was monitored by immunomeasureable C-peptide (IMCP) before, during, and after infusion of insulin. The subjects were divided into 3 experimental groups. The inhibition of the basal insulin secretion was examined in group I by clamping BG at the fasting level. The inhibition of the glucose-stimulated insulin secretion was examined in group II by clamping BG at a raised level. The stimulation of insulin secretion by glucose during insulin infusion was examined in group III by stepwise BG rises from the fasting level. An inhibition of the basal insulin secretion was observed in all volunteers examined according to the protocol for group I (n = 9, including 3 overweight volunteers). The lowest insulin infusion rate applied was 1.75 U/h. An inhibition occurred at this low infusion rate corresponding to 44 mu U immunomeasurable insulin (IMI) per ml of serum. However the inhibition was impaired in the overweight participants, who, in addition, were the only ones showing a rebound rise of IMCP after stopping the insulin infusion. An inhibiting effect of exogenous insulin appeared as likely in only 1 of 5 participants examined according to the protocol for group II. Sudden rises of BG abolished the inhibition, while a total or partial inhibition was found at a constantly raised BG level in both participants examined according to protocol III. We conclude that exogenous insulin inhibits beta cell secretion, depending on the BG level, the mode of glucose stimulation, and the time relation between glucose and insulin application. Physiologically occuring IMI levels in peripheral serum were sufficient to cause an inhibition. A disturbance of the negative feedback inhibition of insulin should be discussed as a pathogenetic factor of adipositas.
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