scholarly journals Total Complement Assay

2020 ◽  
Author(s):  
Keyword(s):  
Total Complement

Monkey Model for IgE-Mediated Otitis Media with Effusion

1983 ◽  
Vol 92 (6_suppl) ◽  
pp. 30-30
Author(s):  
R. A. Friedman ◽  
W. J. Doyle ◽  
J. Fagin ◽  
C. D. Bluestone ◽  
P. Fireman
Keyword(s):  
Otitis Media With Effusion ◽  
Challenge Test ◽  
Complement C3 ◽  
Monkey Model ◽  
Age Related ◽  
Additional Funding ◽  
Adults And Children ◽  
Total Complement ◽  
Invasive Techniques ◽  
Cellular Components

Allergic and other immune mechanisms have been suggested as important in the etiology and pathogenesis of OME, and both humoral and cellular components of the immune response have been identified in MEEs obtained from patients with OME. Yet, specific and direct documentation of an immune basis for OME has not been forthcoming. To establish a causal relationship between an immune hypersensitivity and middle ear pathophysiology, a provocative intranasal antigen challenge test has been designed using the nine-step inflation-deflation tympanometric test for ET dysfunction. These initial studies were undertaken by OMRC personnel in association with the allergy and immunology service. Subsequently, on the basis of the preliminary observations additional funding was obtained (NIAID AI 19262) to confirm and extend these studies to document antigen-induced ET dysfunction in allergic adults and children, and to establish a clinical relevance for antigen-induced ET dysfunction. Because questions concerning the etiology and pathogenesis required invasive techniques and are not suitable in humans, a monkey animal model has also been developed. Our future plans will be to further develop the monkey model of OME employing IgE and other immune reactions in monkeys with normal ET function, or with compromised, surgically created ET function. The experimental MEE will be assayed for immune components, including IgA and its secretory piece; IgG, IgM, and IgE, total complement; C3, C4, and cells including polymorphonuclear leukocytes, eosinophils, and lymphocytes (both T and B cells). Since OME is mainly a disease of the young child, it is essential that age-related differences be explored in each aspect of our experimental model. The reversal and prevention of ET dysfunction and/or OME with several drugs, including cromolyn, steroids, and antihistamines, will be studied in humans and in the monkey model.

Ultrastructure of the hepatopancreas of the Pacific white shrimp, Penaeus vannamei (Crustacea: Decapoda)

1988 ◽  
Vol 68 (2) ◽  
pp. 323-337 ◽  
Author(s):  
Thomas Caceci ◽  
Kay F. Neck ◽  
Donal D H. Lewis ◽  
Raymond F. Sis
Keyword(s):  
B Cells ◽  
Plasma Membranes ◽  
Ultrastructural Level ◽  
Pacific White Shrimp ◽  
White Shrimp ◽  
Penaeus Vannamei ◽  
Intact Cells ◽  
The Pacific ◽  
Total Complement ◽  
Electron Microscopes

Fourteen specimens of the hepatopancreas of the Pacific white shrimp, Penaeus vannamei, were prepared for examination with the transmission and scanning electron microscopes and with the light microscope. The histology and ultrastructure of this organ is similar to that seen in other Decapoda. At the ultrastructural level, it was observed that B-cells rupture at approximately the level of gap junctions located on the lateral plasma membranes of the cells, and discharge the contents of their large vacuoles into the intercellular space. This efflux of enzymatic material may be the mechanism by which cells are released from the wall of the tubule at the proximal end: the rupture and collapse of a B-cell may be analagous to the removal of the keystone which supports an arch. Deprived of support, and lacking structural adaptations for cohesion (there are no desmosomes or interdigitations in the epithelium) and with the intercellular material digested, the remaining intact cells collapse into the lumen of the tubule. The lysis of individual cells of all types - R-, F-, and B-cells - may contribute to the tubules’ total complement of digestive enzymes.

scholarly journals A Flow Cytometry-Based Assay for the Measurement of Total Complement Activity in the Serum and Clinical Practice

2022 ◽  
Vol 2022 ◽  
pp. 1-12
Author(s):  
Xuewei Ding ◽  
Shijun Li ◽  
Hui Liu
Keyword(s):  
Flow Cytometry ◽  
Nephrotic Syndrome ◽  
Linear Relationship ◽  
High Volume ◽  
Healthy Individuals ◽  
Serum Samples ◽  
Complement Activity ◽  
Significant Difference ◽  
Cell Groups ◽  
Total Complement

Objective. To develop a novel sensitive and accurate assay suitable for high-volume testing of the total complement activity in the serum for clinical laboratories. Methods. The total complement activity (TCA) to be measured was quantified by detecting the number of fragments produced by erythrocyte lysis and the erythrocyte fragmentation index (EFI), indicating TCA. EFI = M × M 2 / M 1 + M 2 , where M is the number of erythrocyte fragments (removed from the background), M 1 is the number of unagglutinated red cells, M 2 is the number of agglutinated red cell groups, and M 2 / M 1 + M 2 is the agglutination coefficient indicating the degree of erythrocyte agglutination. Mild changes in hemolysin and erythrocyte concentrations were made to optimize the testing conditions. The same serum samples were tested for 10 consecutive days to determine the stability of the experimental results. Serum EFI was detected in both nephrotic syndrome patients and healthy subjects. Results. There was a linear relationship between hemolysin and erythrocyte agglutination ( r = 0.999 , P < 0.001 ). A good linear relationship existed between EFI and TCA ( r = 0.991 , P < 0.001 ). The results were not affected by slight fluctuations in the concentrations of hemolysin or erythrocytes. The interbatch CV = 8.6 % of the test results showed good stability. There was a significant difference in the EFI between nephrotic syndrome patients and healthy individuals, P < 0.001 , and EFI was reduced in nephrotic syndrome patients compared to healthy individuals. Conclusion. The flow cytometry-based assay for TCA was sensitive and accurate and had potential value for clinical application.

CYTOTAXONOMY OF BOMBYLIIDAE (DIPTERA)

1973 ◽  
Vol 15 (1) ◽  
pp. 21-37 ◽  
Author(s):  
J. W. Boyes ◽  
G. E. Shewell
Keyword(s):  
Sex Chromosomes ◽  
Chromosome Numbers ◽  
Total Complement ◽  
Variable Group

The karyotypes of 34 species of Bombyliidae are described, some in greater detail than others. It is suggested that two subfamilies, the Bombyliinae (for Homoeophthalmae) and Anthracinae (for Tomophthalmae) be recognized. In the Bombyliinae, one species has 2n = 8, one 2n = 10, three 2n = 12 and one 2n = 14. In the Anthracinae, two species have 2n = 10, four 2n = 12, six 2n = 14, three 2n = 16 and thirteen 2n = 18. Seventeen complements of Bombyliinae averaged 41.4 μ in total complement length (TCL) and thirtyeight of Anthracinae averaged 46.6 μ; so the 55 complements of the Bombyliidae averaged 44.9 μ in TCL, the complements with lower chromosome numbers averaging less than those with higher numbers. Thus Bombyliinae species have lower chromosome numbers and shorter complements than Anthracinae species which tend to have longer metacentric sex chromosomes. Thus both morphologically and karyotypically the Bombyliinae appear to be more advanced whereas the Anthracinae are a more primitive but highly variable group of species.

Computer-Assisted Kinetic Assay for Quantification of Total Complement Activity

1991 ◽  
Vol 8 (2) ◽  
pp. 92-103 ◽  
Author(s):  
M. Abbal ◽  
J. Tkaczuk ◽  
C. Praud ◽  
F. Msayeh ◽  
E. Ohayon
Keyword(s):  
Computer Assisted ◽  
Kinetic Assay ◽  
Complement Activity ◽  
Total Complement

scholarly journals Clinical and Genetic Spectrum of a Large Cohort With Total and Sub-total Complement Deficiencies

2019 ◽  
Vol 10 ◽  
Author(s):  
Carine El Sissy ◽  
Jérémie Rosain ◽  
Paula Vieira-Martins ◽  
Pauline Bordereau ◽  
Aurélia Gruber ◽  
...  
Keyword(s):  
Large Cohort ◽  
Total Complement

Effect of protein malnutrition and tumor growth on serum total complement, C3, and IgG levels during E. coli infection in the rat

1982 ◽  
Vol 2 (3) ◽  
pp. 277-287
Author(s):  
S. Lanza-Jacoby ◽  
J. Skibber ◽  
E. Miller ◽  
J. Kerr ◽  
S.M. Weiss ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Protein Malnutrition ◽  
Complement C3 ◽  
E Coli ◽  
Total Complement

scholarly journals Activation of the classical pathway of complement by Hageman factor fragment.

1981 ◽  
Vol 153 (3) ◽  
pp. 665-676 ◽  
Author(s):  
B Ghebrehiwet ◽  
M Silverberg ◽  
A P Kaplan
Keyword(s):  
Normal Serum ◽  
Classical Pathway ◽  
Hageman Factor ◽  
Concomitant Reduction ◽  
Dose Dependent Fashion ◽  
Total Complement ◽  
Trimolecular Complex ◽  
Comparable Activity ◽  
The Individual ◽  
Antigen Antibody

A fragment of activated Hageman factor (HFf) has been demonstrated to activate the classical pathway of complement in a manner that is analogous to complement activation by antigen-antibody complexes or aggregated IgG. Thus C1, C4, C2, C3, and C5 were found to be depleted on addition of HFf to serum. The reduction of serum hemolytic activity was maximal upon addition of 5 micrograms HFf and an incubation time of 60 min at 37 degrees C. Consumption of the total complement activity and of the individual components proceeded in a dose-dependent fashion. No comparable activity was observed when equimolar concentrations of either the native Hageman factor (HF) or two-chain activated form of Hageman factor (HFa) were incubated with serum. Further, the ability of HFf to convert serum C3 and C4 was similar to that of aggregated IgG as assessed by immunoelectrophoresis. This function of HFf appeared to be independent of plasminogen (or plasmin) since plasminogen-free serum was indistinguishable from normal serum. Radial double immunodiffusion experiments using antiserum to C1q, C1r, and C1s on HFf-treated serum demonstrated the dissociation of the C1 trimolecular complex, with concomitant reduction of C1r antigenicity that is indicative of C1 activation. Thus, HFf appears to lead to C1 activation upon incubation with serum or when incubated with partially purified C1. This may represent a control link between activation of the intrinsic coagulation-kinin pathway and the initiation of the classical complement cascade.

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