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G Segoloni

Publications and source records attributed to G Segoloni.

86 records · Page 5Linked to original sources
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[Semeiotic significance of the clinical use of methods of determining serum immunocomplexes in human glomerulonephritis].

The application of tests for the determination of serum immune complexes in nephrology has supplied fresh pathogenetic and symptomatological information. An account is given of results obtained in primary and secondary glomerulonephritis using four methods; the solid-phase Clq test, the polyethylene glycol precipitation test, the immunofluorescence on polymorphonucleates tests, and the solid-phase conglutinins test (with anti-IgA antibodies). The results take on a symptomatological meaning in many classes of human glomerulonephritis, both in the differentiation of primary forms and those secondary to systemic diseases, and in prognosis. A critical review is made of the data obtained in a personal series in the light of a long-term follow-up. The limits and specificity of each test are also discussed.

Antigen-Antibody Complex↗
PubMedDate not supplied

Evidence for the involvement of the IgE-basophil-mastocyte system in human acute post-streptococcal glomerulonephritis.

Several findings reveal the involvement of the IgE-basophil-mastocyte-platelet-activating-factor (PAF) system in human acute post-streptococcal glomerulonephritis. In the acute phases of the disease there is a transient, marked reduction in the circulating metachromatically staining basophils, indicating an in vivo basophil degranulation. The blood reservoirs of PAF are depleted. The number of metachromatic mastocytes in renal biopsy samples was very low and morphological aspects of degranulation were present. In vitro, we demonstrated basophil degranulation and PAF release in presence of exogenous streptococcal Ags after recovery. These findings suggest that the IgE-basophil-mastocyte-PAF system may play a role in human pathology, as has been shown in immune complex (Ic) deposition in acute serum sickness in rabbits.

Acute Disease↗
PubMedDate not supplied

Immunological mechanisms of human platelet involvement.

Several immunological mechanisms of platelet involvement in inflammation are described. Basophils degranulate and release a platelet-activating factor (PAF) when challenged with anaphylotoxins, cationic proteins (CP) from polymorphonuclear cells (PMN) as well as with specific antigens from atopic patients. PAF is a newly-discovered mediator of anaphylaxis present in rabbit and human basophils. This factor is a small phospholipid, probably a lyso-1-phosphatidylcholine with a significant aggregating activity on rabbit and human platelets. PAF is released, together with a small amount of arachidonic acid, from basophils in the presence of anaphylotoxins, CP and specific antigens from atopic patients. The already well-known direct interaction between immune complexes (Ics) and human platelets is compared here with the mechanism of PAF-induced aggregation. It is shown that the latter process of aggregation differs from the former. Human platelet aggregation starts more rapidly in the presence of PAF than of Ics. PAF-induced aggregation is ADP-independent as it is not affected by ADP inhibitors. On the contrary, Ic-dependent aggregation is brought about by endogenous ADP release and therefore inhibited by ADP inhibitors. The interaction between Ics and platelets leads to the release of CP. The latter produce a cascade reaction involving basophils which degranulate and release PAF. A self-maintaining mechanism of tissue injury is thus triggered.

Adenosine Diphosphate↗