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Biomedical subjects

H Brunner

Publications and source records attributed to H Brunner.

At least 271 records · Page 15Linked to original sources
PubMed1977

Effect of A. laidlawii on murine and human lymphocyte cultures.

Heat-inactivated A. laidlawii (AL) was found to be a potent mitogen for mouse spleen cells. Spleen cells from homozygous nude mice and spleen cells treated with anti-theta serum and complement responded as well as their respective controls, indicating that AL represented a B-cell mitogen for mouse spleen cells. Spleen cells from LPS-unresponsive C3H/Hej mice responded well to AL. The peripheral blood leucocytes from unselected human donors were also stimulated by AL, which appeared to represent a T-cell mitogen for human leucocytes. However, the possibility that it acted as a specific antigen could not be excluded. Attention was drawn to the possibility that the presence of mycoplasma might considerably affect the results of tests where tissue-culture cells or derivatives thereof are added to leucocyte cultures.

Acholeplasma laidlawii↗
PubMed1976

[LDH isoenzymes and gastrin in achlorhydri (author's transl)].

Several haematological findings (especially the values of serum LDH and its isoenzymes) were compared with changes in the gastrin level in pernicious anaemia. While vitamin B12 substitution therapy led to normalization of the anaemia and of the enzyme levels, gastric atrophy and, hence, the elevation in serum gastrin levels remained unchanged. Determination of serum gastrin, therefore, provides a valuable tool for the verification of the diagnosis of pernicious anaemia in treated cases.

Achlorhydria↗
PubMed1976

Response of guinea pigs and hamsters to experimental infection with Mycoplasma pneumoniae.

In an effort to further delineate the mechanism of infection and pathogenicity of Mycoplasma pneumoniae infections, the hamster and guinea pigs were used as experimental models. These animals were chosen because of previous experience. The local antibody response in addition to organism growth patterns were examined in detail. Histological examination was carried out to determine the pathological lesions which occur. The significance of these findings is discussed.

Animals↗
PubMed1976

Complement-mediated killing of Acholeplasma laidlawii by antibodies to various membrane components.

Mycoplasmas are useful models for biochemical studies of the mechanism of complement-mediated killing by antibodies to various membrane components. The purpose of this study was to determine the membrane antigens involved in immune killing of Acholeplasma laidlawii. Antibodies to A. laidlawii membrane total lipids, glycolipids, and phospholipids could be induced in rabbits after injection of reaggregates of the purified lipids with Mycoplasma hominis protein as the carrier. Killing of A. laidlawii membrane lipids were less effective than anti-membrane protein antisera in killing the organisms. Of the antisera to lipid components of A. laidlawii membranes, antiserum to phospholipids showed a more pronounced killing effect than antiserum to glycolipids. The antibodies to A. laidlawii in the rabbit antisera belong predominantly to the immunoglobulin G class of immunoglobulins. Double-diffusion tests in agar indicated that two immunologically reactive proteins are located on the membrane surface.

Acholeplasma laidlawii↗
PubMed1976

Lysis of Acholeplasma laidlawii by antibodies and complement.

Membranes of Acholeplasma laidlawii were used to determine the membrane components involved in immune lysis and to eventually detect enzymatic changes in the membrane components during this reaction. In a previous publication we reported that A. laidlawii can be killed by antibody and complement and that antibodies to membrane proteins are by far more effective than antibodies to membrane lipids in the complement-dependent killing of this organism. In this report we demonstrate that membrane damage occurs after the combined action of antibody and complement. In addition, the cytoplasmic enzyme hexokinase is released during immune killing. As visualized by electron microscopy, the organisms lost their cytoplasm and were transformed into ghosts. In the majority of organisms, tears in the membrane could be seen. Ultrastructural lesions of about 8.0 to 10 nm in diameter were visible when the organisms were incubated with antiserum and complement. 14C-labeled fatty acids were incorporated during growth into A. laidlawii membrane lipids. After incubation of labeled organisms with antiserum and complement, release of radioactive material into the supernatant and changes in the lipid composition were not observeed. Enzymatic degradation of membrane lipids of A. laidlawii during immune lysis was not detected.

Acholeplasma↗
PubMed1976

Ultrastructural visualization of anionic sites on mycoplasma membranes by polycationic ferritin.

Anionic sites on mycoplasma membranes were visualized in the electron microscope by a polycationized ferritin derivative. The technique of thin sectioning was used. Staining prior to fixation led to clustering of ferritin granules on the mycoplasma cell surface. On glutaraldehyde-fixed Mycoplasma mycoides subsp. capri, M. gallisepticum, M. pneumoniae, and Acholeplasma laidlawii, the anionic sites were uniformly distributed over the entire membrane surface. M. hominis did not bind the polycationic ferritin label. Chemical and enzymatic treatments of the mycoplasmas indicated that the anionic sites may be lipid phosphate groups. Isolated M. mycoides subsp. capri membranes were labeled exclusively on only one membrane surface, presumably the outer one. Liposomes prepared from diphosphatidylglycerol and phosphatidylcholine were also labeled by the polycationic ferritin.

Acholeplasma laidlawii↗
PubMed1976

[Atypical pneumonia, etiology and possibilities for the diagnosis (author's transl)].

Beginning with the antimicrobial chemotherapy a decrease in the incidence of bacterial pneumonias is accompanied by a relative increase in the incidence of the so-called atypical pneumonia. This disease syndrome is predominantly caused by Mycoplasma pneumoniae, Chlamydia psittaci, Coxiella burneti and various viruses. In addition, bacteria which are usually involved in lobar pneumonia may occasionally cause atypical pneumonias. The present publication is concerned with the most frequently occurring causative agents of atypical pneumonia, the epidemiology of the disease and the possibilities for the diagnosis.

Adenoviridae Infections↗
PubMed1976

Gastric acid secretion, serum-gastrin levels and psychomotor function under the influence of placebo, insulin-hypoglycemia, and/or bromazepam.

Gastric acid output, blood-glucose, serum-gastrin and psychomotor-performance were measured in four healthy subjects one hour before and two hours after the intravenous injection of (a) 2ml saline, (b) 0.2 U/kg b.w. insulin, (c) 0.1 mg/kg b.w. bromazepam. Each subject underwent one experiment of each type. The study was layed out as a Latin-square and analysed accordingly. Gastric acid secretion was measured by means of intragastric titration and a telemetering capsule; blood-glucose and serum-gastrin levels as well as psychomotor performance as a measure of vigilance were determined in 15-minute-intervals. In the saline series (a), none of the four parameters showed any systematic variation. In series (b), a bimodal response of acid output to insulin, initial inhibition and subsequent stimulation was observed in all subjects. Serum-gastrin levels showed only a slight and transient increase in the first thirty minutes. Psychomotor performance decreased markedly with progressing hypoglycemia, and increased when glucose levels rose again. In the bromazepan series (c), acid output and psychomotor performance decreased and, after the first hour, increased almost parallely, while glucose and gastrin levels remained unchanged. In series (d), an additive effect of insulin and bromazepam occurred: acid output and psychomotor performance were lower than after insulin alone; peak acid secretion, maximal hypoglycemia and peak of serum-gastrin were shifted to the right. It is concluded that the lowered basal as well as insulin-stimulated acid secretion after bromazepam is due to the central effect of the drug, and that this effect is mediated to the gastric glands directly via autonomic nervous pathways without involving a release of endogenous gastrin.

Adult↗