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Biomedical subjects

W Stenzel

Publications and source records attributed to W Stenzel.

34 records · Page 2Linked to original sources
PubMed1975

[Pathogenicity factors of gramnegative enteropathogenic bacteria and pathogenesis of intestinal diseases (author's transl)].

Enterotoxins as produced by the majority of enteropathogenic bacteria play a central role in the pathogenesis of cholera and E. coli enteritis but are obviously of little significance as to the development of Salmonella enteritis and dysentery. Pathology of Salmonella enteritis and dysentery results from multiplication of bacteria within the bowel wall and from the damage of tissue caused thereby. The lipopolysaccharides (endotoxins) of invasive enteropathogenic bacteria do not possess the character of a primary pathogenicity factor but operate as a protective agent versus bactericidal mechanisms of the macroorganism and probably also as an agent toxic for the tissue.

Animals↗
PubMed1975

[The cathode bound group antigen of dysentery-provoking escherichieae (author's transl)].

Antigens from disrupted cells of dysentery-provoking and of non-enteropathogenic Escherichieae were submitted to immunoelectrophoresis on cellulose acetate stripes at pH 8.0. Among 6 immune sera produced for this purpose by immunizing rabbits against desintegrated dysentery bacteria, only one contained a precipitine reacting with an antigen similar to the "generic antigen" of BELAYA. This - at pH 8.0 - cathode-bound group antigen (KGA) could not only be found in virulent but also in 5 attenuated cultures and in 5 from 6 avirulent strains of several dysentery types. Only the - apathogenic - type culture 1111/55 of dysentery-provoking E. coli O 136 showed no KGA-reaction. Some sources of methodical errors responsible for false outcomes of immunopherogrammes have been discussed.

Antigens, Bacterial↗
PubMedDate not supplied

Vitamin E alters alveolar type II cell phospholipid synthesis in oxygen and air.

Newborn rats were injected with vitamin E or placebo daily until 6 days after birth. The effect of vitamin E pretreatment on in vitro surfactant phospholipid synthesis was examined in isolated type II cells exposed to oxygen or air form 24 h in vitro. Type II cells were also isolated from untreated 6-day-old rats and cultured for 24 h in oxygen or air with control medium or vitamin E supplemented medium. These cells were used to examine the effect of vitamin E exposure in vitro on type II cell phospholipid synthesis and ultrastructure. Phosphatidylcholine (PC) synthesis was reduced in cells cultured in oxygen as compared with air. This decrease was not prevented by in vivo pretreatment or in vitro supplementation with vitamin E. Vitamin E pretreatment increased the ratio of disaturated PC to total PC and increased phosphatidylglycerol synthesis. The volume density of lamellar bodies in type II cells was increased in cells maintained in oxygen. Vitamin E did not affect the volume density of lamellar bodies. We conclude that in vitro hyperoxia inhibits alveolar type II cell phosphatidylcholine synthesis without decreasing lamellar body volume density and that supplemental vitamin E does not prevent hyperoxia-induced decrease in phosphatidylcholine synthesis.

Air↗