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Biomedical subjects

M Heger

Publications and source records attributed to M Heger.

27 records · Page 2Linked to original sources
PubMed1994

Seasonal occupational asthma in an agricultural products merchant--a case report.

A 52-year-old agricultural products merchant reported mild occupational asthma and rhinitis throughout the year, with severe asthma from February to May. He had been exposed to various substances, particularly grain, insecticides, fungicides, and fertilizers over 35 years. We identified a castor-bean-containing fertilizer as the cause of the disease by skin prick test and bronchial provocation test. Specific IgE against castor bean was detected by enzyme allergosorbent test, and proteins with mol. mass of less than 14.4 kDa and masses of 15.5, 29.5, and 30.5 kDa were identified as allergens by Western blot analysis. The seasonal character of symptoms could be explained by a more frequent use of the fertilizer during spring. Six months after avoidance of the allergen, the patient reported chronic bronchitis without asthma. Occupational allergy to castor bean should be considered in subjects with seasonal asthma and exposure to "natural" fertilizers.

Asthma↗
PubMed1988

Investigations on metabolism and carcinogenicity of 1,1,2-trichloroethane.

Two groups of male and female Sprague-Dawley rats (50 animals/group per sex) were treated with either 15.37 or 46.77 mumole of 1,1,2-TCE in DMSO/rat for 2 years. The animals were treated once a week by s.c. injection of test compound in the skin of neck. Two groups of controls received either DMSO or no treatment at all. The incidence of benign mesenchymal and epithelial tumors was not significant when compared with either DMSO-treated or untreated controls. The animals treated with 46.77 mumole 1,1,2-TCE significantly developed sarcomas when compared with the untreated controls. In a further experiment, either 40 mumole or 160 mumole 1,1,2-TCE was injected into male Wistar rats and the metabolites, TdGA and HEMA, were determined in 24-h urine samples. Comparative studies were carried out giving equimolar amounts of chloroethanol and 2-chloroacetaldehyde diethyl acetal. Analysis of the metabolites showed that no detectable HEMA was excreted in urine after treatment of rats with 1,1,2-TCE or chloroethanol. TdGA was excreted in urine much more among chloroacetaldehyde-treated animals than among 1,1,2-TCE- or chloroethanol-treated rats.

Acetaldehyde↗
PubMed1986

Investigations on metabolism, genotoxic effects and carcinogenicity of 2,2'-dichlorodiethylether.

Either 40 mumole or 160 mumole 2,2'-DDE was injected into male Wistar rats and the metabolites, TdGA and HEMA, were determined in the 24-h urine specimens. Comparative investigations were carried out giving equimolar amounts of chloroethanol and 2-chloroacetaldehyde diethyl acetal. In a further step, inhalation experiments were performed to determine urinary excretion of the two metabolites after an 8-h exposure of male Wistar rats to 10, 50, 100, and 500 ppm 2,2'-DDE and to 50, 200, und 1,000 ppm vinyl chloride. A long-term study was conducted to investigate the possible carcinogenicity of 2,2'-DDE in male and female Sprague-Dawley rats following s.c. injections of 4.36 mumole and 13.1 mumole 2,2'-DDE in DMSO per week. The evaluation of tumor development in treated groups and controls were based on macroscopic inspection and histological examinations of the suspect organs and tissues. Analysis of the metabolites showed that HEMA excretion was much lower than the excretion of TdGA following the uptake of 2,2'-DDE, 2-chloroethanol and 2-chloroacetaldehyde diethyl acetal. Contrary to these, vinyl chloride uptake resulted in a higher urinary excretion of HEMA than TdGA. There was no appreciable increase in the number of tumors detected in 2,2'-DDE-treated animals when compared with untreated or DMSO-treated groups. Since irradiation of 2,2'-DDE with UV did not elevate mutagenic activity of the compound against Salmonella typhimurium TA100, the high mutagenicity of the compound found in a desiccator cannot be due to the liberation of mutagenic compounds produced under the influence of UV light.

Acetaldehyde↗
PubMed1984

Urinary excretion of frameshift mutagens in rats caused by passive smoking.

Several male Wistar rats were individually placed in a chamber resembling a room provided with minimal air flow. They were exposed separately to the main- and sidestream smoke of a commercial brand of cigarettes smoked by a smoking machine. Exposure to both sidestream and mainstream smoke of at least two cigarettes resulted in significant excretions of frameshift mutagens in urine within 24 h, detected by the bacterial microtiter fluctuation test with Salmonella typhimurium TA1538. Doubling exposure to the mainstream smoke resulted in similar quantitative mutagenic activities. Doubling exposure to the sidestream smoke resulted in reduced water intake by the animals and thus toxic effects of the urine concentrates on the test bacteria.

Air↗
PubMed1982

[Investigations on the correlation between vinyl chloride (VCM)-uptake and excretion of its metabolites by 15 VCM-exposed workers. II. Measurements of the urinary excretion of the vcm-metabolite thiodiglycolic acid ].

Fifteen workers employed in a PVC producing plant were investigated concerning their individual vinyl chloride (VCM) exposure and the urinary excretion of the VCM metabolite thiodiglycolic acid (TdGA). The urine concentrations found were in the range 0.94-20.4 microgram/ml. These could be compared with exposure data calculated from VCM air analyses performed by personal air sampling and corrected with respect to the exposure times of the workers. The amounts of TdGA excreted within 24 h were correlated with the effective VCM body concentrations calculated from the exposure data as mean values for 12 h periods (Spearman coefficient P=alpha less than 0.005). This correlation resembles a function of the Michaelis-Menten type. It could be shown that during short exposure periods of less than 5 min, the metabolite formation in relation to the exposure data was lower than during longer periods of exposure although, as would be expected, there were some fluctuations of the exposure level. Therefore, the VCM body concentrations could not normally reach steady state values.

Environmental Exposure↗
PubMed1979

Afferent connections of the laterodorsal thalamic nucleus in the rat.

The laterodorsal thalamic afferent connections have been studied by means of the retrograde transport of horseradish peroxidase (HRP). The following new sources of projections to the laterodorsal thalamic nucleus (LD) were observed: the zona incerta, the lateral dorsal tegmental nucleus (bilaterally), the lateral hypothalamus and the precentral agranular cortex.

Afferent Pathways↗