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Biomedical subjects

H Renner

Publications and source records attributed to H Renner.

At least 55 records · Page 3Linked to original sources
PubMed1983

[Reduction of the radiogenic tumor incidence by stimulation with lyophilized fetal cells. Experimentation on animals].

The effect of an immunization treatment with lyophilized xenogenic fetal cells was studied in 7 months old, female albino rats (strain Wistar). The tumor incidence was measured after a sublethal whole-body irradiation with 600 cGy. Furthermore, the spleen of the individual animals was histologically examined. 3,5 to 6 months after a whole-body irradiation with 600 cGy, the tumor incidence was 55%. The tumors found were tubular adenocarcinomas of the thyroid gland. A significant reduction of the tumor incidence can be achieved by an immunostimulation with xenogenic, lyophilized, fetal cells (connective tissue and bone marrow, respectively) administered twice, namely eight days before and four days after the whole-body irradiation. The tumor incidence measured after 3,5 months was 10% and 15%, respectively, and after 6 months 15% and 25%, respectively. No significant tumor protection is achieved, however, by a single stimulation before whole-body irradiation and by a stimulation performed one or two times after whole-body irradiation. Histologic examinations of the spleen show in the immunostimulized animals a strong regeneration of the immune system with a significantly increased number of follicles and a significant increase of lymphocytes in the red pulp. The authors stress the possible clinical importance for radio-oncology of an immunostimulation with lyophilized, xenogenic, fetal cells.

Adenocarcinoma↗
PubMed1982

The role of N-acetyl-neuraminic acid in the triggering of rat mast cells by polycationic molecules.

Three substances known to act on N-acetylneuraminic acid (NANA), were tested for their activity on rat peritoneal mast cells. Both neuraminidase, which splits off NANA, and the lectin from Cepaea nemoralis directed against NANA are histamine releasers. Periodate itself did not trigger the cells but inhibited the releasing action of other substances. The results provide further evidence for the role of NANA in the triggering of mast cells. A cytotoxic substance, benzyl-polyethylene imine, triggers mast cells without affecting NANA. In addition, the role of histamine-BSA conjugates as histamine releasers is described.

Agglutinins↗
PubMed1982

The effects of substance P on histamine and 5-hydroxytryptamine release in the rat.

1. Substance P (SP) induces histamine release from isolated rat peritoneal mast cells at concentrations of 0.1-10 muM.2. Inhibitors of glycolysis and oxidative phosphorylation prevent the release of histamine induced by SP.3. Cells heated to 47 degrees C for 20 min release histamine when treated with an agent causing cell lysis but fail to release in response to SP.4. SP does not release histamine by interacting with cell-bound IgE.5. Histamine release by SP is rapid, with more than 90% of the response occurring within 1 min of the addition of the peptide to mast cells at 37 degrees C.6. Substance P, unlike antigen-antibody or compound 48/80, does not show enhanced release of histamine when calcium (0.1-1 mM) is present in the extracellular medium but calcium increases the response to SP when the ion is added after the peptide. Extracellular calcium (0.1-1 mM), magnesium (1-10 mM) and cobalt (0.01-0.1 mM) all inhibit SP-induced histamine release when added before the peptide. Pre-treatment of the cells with EDTA (10 mM) and washing in calcium-free medium inhibits the histamine release induced by SP.7. Histamine release induced by SP was optimum at an extracellular pH of 7.2.8. A number of peptides structurally related to SP were examined for histamine-releasing activity. At the concentrations tested, the N-terminal dipeptides Lys-Pro and Arg-Pro, tuftsin, physalaemin, eledoisin, SP(3-11), SP(4-11) and [p-Glu(6), p-amino Phe(7)]-SP(6-11) were all found to be inactive. The relative activities of the other peptides were: [Formula: see text]9. Rat basophilic leukaemia cells (RBL-2H3) fail to respond to SP at concentrations which activate rat mast cells. Release of 5-hydroxytryptamine by immunological activation of RBL cells is not changed by the presence of SP.10. The mechanism of action of SP on mast cells and the nature of the SP receptor on mast cells is discussed in relation to SP receptors in other cell types.

Animals↗
PubMed1982

Mast cells and complement activating immune reactions.

A rosetting of isolated rat mast cells with complement coated zymosan does not induce a histamine release. However, this procedure potentiated the release induced by ATP. Treatment of rats with prednisolone diminishes the number of the rosette forming mast cells.

Animals↗
PubMed1982

Gastric cytoprotection by antacids and papaverine in rats.

Prostaglandin E2 (PGE2) prevented hemorrhagic ulceration of rat stomach mucosa induced by various procedures when given orally at a non-antisecretory dose. This effect of PGE2 is called gastric cytoprotection. We used absolute ethanol, 0.6 N hydrochloric acid and 0.2 N sodium hydroxide as damaging agents. Ranitidine at an antisecretory dose did not exhibit any cytoprotective effect. However, the poorly absorbable antacids, magnesium hydroxide plus aluminium hydroxide and aluminium phosphate inhibited the development of hemorrhagic lesions significantly. A similar protective effect was seen after intragastric administration of papaverine, which is known to stimulate endogenous prostaglandin synthesis. However, the question as to whether or not stimulation of endogenous prostaglandin synthesis is the mode of action of the cytoprotective effect of papaverine and poorly absorbable antacids, cannot yet be answered.

Aluminum Compounds↗
PubMed1982

Identification of two granulocyte/macrophage colony-stimulating factors from porcine leukocyte cultures.

Granulocyte/macrophage colony-stimulating factors (CSF) were found in large-scale serum-free cultures of porcine blood leukocytes. The factors were concentrated from the conditioned culture medium of Concanavalin A-stimulated leukocytes using ammonium sulfate salting-out fractionation. The protein precipitate at 45-90% salt saturation contained two CSF types upon gel filtration on Sephadex G-100: One type was found to be active on mouse, but not on human bone marrow stem cells and had an apparent molecular mass of 85 000-100 000 Da; the other of about 40 000-45 000 Da stimulated both mouse and human bone marrow stem cells.

Animals↗
PubMed1981

Histamine release from rat mast cells induced by protamine sulfate and polyethylene imine.

The protamine sulfate-induced release of histamine from mast cells in a non-cytotoxic reaction, similar to the 48/80-induced secretion. Polyethylene imine was found to be a less potent releaser. It is a cytotoxic substance without specificity for mast cells and acts on membranes generally. Although the two agents are related concerning their molecular weight and polybasicity, their mode of action on mast cells is clearly different.

Animals↗
PubMed1981

[Malignant tumors of the upper urinary passages (author's transl)].

Malignant tumors of the upper urinary passages are more frequent than one had formerly thought. Eleven case reports are presented in order to explain X-ray and differential diagnosis. The treatment consists in surgical nephrourethrectomy with lymphadenectomy. There are only few reports about indication and value of radiotherapy. A postoperative irradiation of the primary tumor region and the lymphatic outflow region is recommended for the stages B, C and D (without remote metastases). The suggested target volumes and doses are described.

Aged↗
PubMed1980

[Mode of action of protamine sulfate on histamine secretion in the rat mast cells].

Protamine sulfate, known for a long time as a histamine releaser, was labeled with a fluorescent dye (FITC). This conjugate was shown to stain selectively the mast cell fraction of rat peritoneal cells. Within a few seconds, the protamine was found inside the cells. Although the cells had lost their histamine completely, no granules were found outside the cells. In the electron microscope, the protamine treated mast cells showed a loss of the electron density of their granules, a vacuolization, and other signs of histamine release. Evidence for a direct connection between the vacuoles and the extracellular fluid was gained by incubating mast cells in FITC-labeled human serum albumin followed by the addition of unlabeled protamine. After washing, the fluorescence was found to be located inside the cells, demonstrating an influx of the FITC-HSA under the influence of protamine. The protamine-induced release reaction is increased after addition of Ca2+, reduced by lowering the temperature, addition of 2-deoxyglucose, or cytochalasin B. Disodium cromoglycate also diminished the histamine release in a dose dependent manner. Protamine did not induce a loss of lactate dehydrogenase from the mast cells. The release reaction is mediated by the cell membrane, as shown by the releasing activity of insolubilized protamine. We conclude that the protamine-induced release is a non-cytotoxic reaction, fulfilling some criteria of the anaphylactic histamine release.

Animals↗
PubMed1978

[Receptors for complement on rat mast cells and release of histamine].

Using rat complement-treated zymosan particles a rosetting of purified rat peritoneal mast cells could be demonstrated. The question was investigated whether the binding of activated complement could be a trigger of histamine release. Varying the degree of complement label on the zymosan particles, the time and temperature of incubation and the dependence on Ca2+ ions, we could not induce a release of histamine in any case. The addition of labeled zymosan increased slightly the mediator release induced by ATP. The immunologic significance of the complement receptors on mast cells is still unclear.

Animals↗