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Biomedical subjects

M Buchner

Publications and source records attributed to M Buchner.

4 recordsLinked to original sources

[Anti-oxidative therapy of pancreatitis--an 18-month interim evaluation].

99 patients affected with acute pancreatitis of different genesis were treated in hospital (necrotizing n = 38, mild form n = 61) from May 1990 to November 1991. Nearly 80% of these illnesses were ethanol-induced, 12% were of biliary origin. 90 patients were submitted to an adjuvant antioxidant therapy with selenium and D-alpha-tocopherol (necrotizing form n = 29, mild form n = 61). The average lethality rate of 34% (1982-1989) fell to 1.1% (1 female patient with biliarily induced pancreatitis). No lethal courses were observed in alcohol-induced, idiopathic, post-traumatic, and post-operative forms. Clinical courses proceeded more easily under adjuvant antioxidant therapy, surgical treatment was not necessary. A treatment at reasonable costs can be made in all general internal wards.

Acute Disease

[Acute pancreatitis--a free radical disease. Decrease in fatality with sodium selenite (Na2SeO3) therapy].

Malonic dialdehyde as an indirect marker of the lipid peroxidation was found increased in the acute pancreatitis compared with persons of the same age and sex. Its concentrations inversely correlated to those of the serum calcium during the course of the disease and additionally they proved to be indicator of the prognosis. Postulating that the acute pancreatitis must be a "free radical disease", in a randomized clinical study the adjuvant therapy of the acute necrotizing pancreatitis (n = 8) with sodium selenite was carried out in a daily dose of 500 micrograms. The lethality of the control group was 89% (8 out of altogether 9 patients), no patient died in the therapy group. By the selenium therapy within 24 hours a normalization of the serum calcium and a decrease of the increased MDA-values could be achieved. It was concluded that by selenium increased activities of the phospholipid-hydroperoxide-glutathione peroxidase were induced, by means of which a peroxidation protection of membrane fatty acids, an inhibition of the activity of phospholipase A2 and an interruption of the arachidonic acid cascade must have been reached.

Acute Disease

[Distribution of aflatoxin M1 in whey and curd during cheese processing (author's transl)].

In model experiments on the distribution of aflatoxin M1 in whey and curd, the influence of the different processing steps was investigated. Taking the same weight ratio between whey and curd, the following results were obtained: a) The aflatoxin M1-distribution in whey and curd was not changed with increasing amounts of rennet, thus decreasing the renneting time at constant renneting temperatures. b) With increasing renneting temperatures, however, the toxin's percentage in the curd decreased at constant amounts of rennet, whereas the whey's content remained stable. For the commonly used temperature variations between 28 and 35 degrees C, the toxin content of the cheese varied in the range of about 12%. c) Processing of curd by acidification with different organic acids at constant temperatures did not show any change in the aflatoxin M1 distribution as compared to rennet coagulation. d) Curd processing by means of starter cultures led to a decrease in the aflatoxin M1 in curd only at higher temperatures; the toxin's percentage in whey remained practically the same. e) Washing of the curd with the 2 1/2 volumes of water decreased the aflatoxin M1 content of cheese by 22%.

Aflatoxins