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Homologous and cross-reactive precipitins in anti-pneumococcal sera raised in mules.

Serial bleedings were obtained from two mules during prolonged immunization, one with type XXV the other with type VIII pneumococcal vaccine. IgGa, IgGb, IgGc, IgB, IgG(T) and IgM present among purified Pn anti-XXV and Pn anti-VIII immunoglobulin isolated from various bleedings were identified by use of rabbit anti-equine heavy chain specific reagents. Radioimmunodiffusion with 14C-labelled type XXV pneumococcal capsular polysaccharide and horse and donkey reagents with species specificity directed against donkey or horse IgGa respectively, demonstrated both parental horse and donkey IgGa heavy chain isotypes among the anti-PnXXV antibodies of the interspecies hybrid. Qualtitative and quantitative examination of the cross-precipitation of mule anti-PnXXV sera with the capsular polysaccharides of pneumococcal types IV, X and XA, with birch sap, ketha gum, and with polysaccharides of E. coli, Klebsiella and Rhizobium was carried out and compared with data obtained with anti-PnXXV raised in a horse. Analysis of supernatants from the cross-reactions showed that distinct subfractions had reacted. indicating a marked heterogeneity of the antibodies.

Animals↗

Comparison of hemagglutination-inhibition, agar gel precipitin, and enzyme-linked immunosorbent assay for measuring antibodies against influenza viruses in chickens.

Individual variations in serological response to avian influenza virus infection were demonstrated after experimental infection of specific-pathogen-free chickens with H6N2 influenza virus. Homologous antibodies were detected from the 6th to the 157th day after infection using hemagglutination-inhibition or enzyme-linked immunosorbent assay and from the 11th to the 157th day by agar gel precipitation test.

Animals↗

[Extrinsic allergic alveolitis (extrinsic allergic broncho- alveolitis, pneumopathies with precipitins, hypersensitivity pneumopathies)].

The author does a general survey on this subject. Having evoked the EAA history, he describes the clinical syndrome with 3 forms (sharp to chronic). He relates in a first part, the main forms linked with rural occupation, from farmer's lung disease, the most frequent, to illnesses dues to cereals, woods exposition, then the one in touch with industry as coffee workers disease, and breeders of silkworms. At last, the ones in connection with urban activities as air-conditioner disease. These descriptions ended with EAA caused by a drug. Having evoked the complementary investigations necessary for diagnosis, he insists on the alveolitis washing and biochemicals studies. In conclusion, the author insists on the interest of steroids treatment in attacks.

Alveolitis, Extrinsic Allergic↗