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Biomedical subjects

W Piotrowski

Publications and source records attributed to W Piotrowski.

At least 55 records · Page 3Linked to original sources
PubMed1985

On the actions of substance P, somatostatin, and vasoactive intestinal polypeptide on rat peritoneal mast cells and in human skin.

Substance P (SP), somatostatin (Som), and vasoactive intestinal polypeptide (VIP) induced a concentration-dependent release of histamine from isolated rat peritoneal mast cells. The release of histamine induced by these neuropeptides was inhibited by preincubation of the cells with the SP analogue [D-Pro4,D-Trp7,9,10]-SP4-11 (SP-A) (10 microM), and also by benzalkonium chloride (10 microM). In addition, SP-A inhibited histamine release induced by compound 48/80, whilst that induced by goat anti-(rat-IgE) was unaffected. In human skin, intradermal injection of SP, Som, or VIP produced flare and wheal responses. The flares to all three peptides were inhibited by preinjection of the skin with SP-A (25 pmol), whilst the wheal responses were unaffected. It is concluded that the receptors mediating histamine release and the flare response are similar, and that SP, Som, and VIP are acting at a similar receptor to produce these effects. It is probable that this receptor is also the site of action of compound 48/80.

Animals↗
PubMed1985

The ability of thapsigargin and thapsigargicin to activate cells involved in the inflammatory response.

The ability of thapsigargin and thapsigargicin to activate mast cells and leukocytes has been investigated. The thapsigargin-induced histamine release from rat peritoneal mast cells was found to be dependent on the concentration of thapsigargin, the purity of the mast cell preparations, and the number of mast cells in suspension. Thapsigargin induced histamine release from human basophil leukocytes. Thapsigargin induced beta-glucuronidase and lysozyme release from human neutrophil leukocytes. Thapsigargin caused a release of histamine from mesentery, lung, and heart mast cells of the rat, but only to a minor extent from the corresponding guinea-pig cells. Thapsigargicin induced histamine release from mesentery, lung, and heart mast cells of the rat at concentrations from 0.1 microM but provoked only a release from the corresponding guinea-pig cells in the concentration-range 0.16 to 1.6 microM. Thapsigargin increased the cytoplasmic free calcium level in intact human blood platelets at concentrations from 3.0 nM.

Adult↗
PubMed1984

[Brain injuries in skiers].

During the last skiing season (November 1981 to March 1982), 33 patients were treated for craniocerebral injuries caused by skiing accidents. Based on the classification made by Tönnis und Loew, 11 patients had grade I, 11 patients grade II and 11 patients grade III (including 3 open craniocerebral injuries). Four patients underwent operation for intracranial hematoma. Out of 33 patients 79% recovered completely. One patient has a permanent neurologic defect, two patients have an apallic syndrome and four died.

Adolescent↗
PubMed1984

The substance P receptor on rat mast cells and in human skin.

(D-Pro4 D- Trp7 ,9,10)SP4-11 (SPA) has been shown to be a competitive antagonist of the histamine releasing action of substance P in rat peritoneal mast cells. Antagonist activity of SPA is expressed in the concentration range 1 to 10 microM, but at higher concentrations SPA releases histamine. SPA inhibits the flare response induced by substance P in human skin but is without effect on the wheal response. Up to 12.5 pmol SPA produces neither wheal nor flare response by itself. The structurally related peptide, kassinin , does not cause histamine release from rat mast cells at concentrations up to 10 microM whereas the methyl ester of substance P was found to 1.6 times more active than substance P in this respect. The findings are discussed in terms of the classification of substance P receptors and the mechanism of wheal and flare in human skin.

Adult↗
PubMed1982

Natural antibodies to cell-surface antigens of human astrocytoma.

Sera of 200 non-transfused healthy male blood donors were tested for antibody reactivity to cell-surface antigens of cultured astrocytoma cells. Positive reactions were observed only rarely by protein-A assay (PA), in about half the cases by immune adherence assay (IA) and in nearly all cases by anti-C3 mixed hemadsorption assay (C3-MHA). In general, titers were low and only seven sera showed reactivity at 1:1,000. Serum 537 showed the strongest reaction. The anti-astrocytoma reactivity in this serum was due to an IgG antibody. Extensive absorption analysis with a panel of cell lines and fresh cells of both benign and malignant origin, as well al fetal cells, revealed that this serum detected an antigen that was present on most neural-crest-derived tumors (astrocytomas, melanomas and neuroblastomas), on very few other malignant tumors and on fetal brain. The antigen detected by serum 537 shows close relationship to the astrocytoma antigen AJ which had been defined by the serum of a patient with astrocytoma. Both antigens appear to be differentiation antigens present predominantly on non-epithelial neoplasms. The antigen detected by serum 537 is heat-stable and pronase-resistant. The sera of two other healthy donors apparently had a similar specificity, whereas the four other high-titered sera and all other sera detected class-III antigens which were non-specific and not tumor-restricted.

Absorption↗
PubMed1982

Interaction of neurotensin with the substance P receptor mediating histamine release from rat mast cells and the flare in human skin.

1 Substance P induced histamine release from rat peritoneal mast cells in a dose-dependent manner over the concentration range 1 to 10 microM. 2 At concentrations in the range 2.5 to 1 0 microM, neurotensin produced only about 5% release of histamine, which was substantially less than the maximum effect obtained with substance P. 3 Neurotensin, 2.5 to 10 microM produced graded inhibition of histamine release induced by substance P. The inhibitory effect of neurotensin was not seen when histamine release was induced by an antigen-antibody effect of neurotensin was not seen when histamine release was induced by an antigen-antibody reaction or by the ionophore, A 23187. Some evidence was obtained to suggest that compound 48/80 may interact with the same receptor as substance P and neurotensin. 4 [D-Arg8]neurotensin, [D-Arg9]neurotensin, xenopsin and the C-terminal octapeptide of substance P (SP4-11) all inhibited histamine release by substance P, but physalaemin did not. 5 Neurotensin inhibited the wheal and flare reactions induced by substance P in human skin. 6 [D-Trp7,9]substance P released histamine from rat mast cells and was about 12 times more potent than substance P itself. [D-Trp7,9]SP1-11 also produced wheal and flare responses in human skin, being 1.8 times more potent than substance P in the production of flare.

Adult↗
PubMed1975

Long-term results of Gasserian ganglion electrocoagulation.

This report is a follow-up study of 315 patients under 46 years old who suffered from trigeminal neuralgia and were treated by electrocoagulation of the Gasserian ganglion. The average foll-up period was 12.7 years, the maximum 33 years. Eighty percent had a return of pain, but 96.7% ultimately attained freedom from pain after repeat electrocoagulation.

Adolescent↗