S Kleindienst | PubMed Health

PubMed1986

A computer program for comparative analysis of nucleic acid sequences.

The programs offer the possibility of comparing pairs of homologous sequences in order to find out percentage of homology, number of identical and deviating nucleotides, of transitions and transversions and, derived from these, KNUC-values according to Kimura (1) and the corresponding standard error sigmaK. The sequences can be printed in pairs underneath each other, homologies are indicated by asterisks between the identical nucleotides. Out of a set of homologous sequences stored on a disk any number of sequences can be compared in pairs in this way, and a matrix containing either the percentage of homology values, the number of deviating nucleotides or the KNUC-values together with the corresponding standard errors can be sent to screen, printer or disk. A program will be available soon which creates a dendrogram representing the similarity between the sequences by use of an average linkage clustering method deduced from this matrix. The programs are written for Apple II computers using UCSD-PASCAL and for Sirius I/Victor 9000 computers using TURBO-PASCAL.

Base Sequence↗

PubMed1986

Impaired humoral immune response in complement C3-deficient guinea pigs: absence of secondary antibody response.

A recently described genetically controlled C3 deficiency (C3D) in guinea pigs (GP) provided a unique model for studying the role of C3 in the afferent limb of the humoral immune response in a direct manner. These C3D animals, which have only 5-7% of normal serum C3 level, were immunized with the bacteriophage phi chi 174, a T cell-dependent antigen, followed by a booster injection after 4 weeks (1.5 X 10(9) plaque-forming units/kg). The formation of IgM and IgG antibody in the course of the primary and secondary response was determined and compared with a control group of inbred strain 2 GP. The C3D animals showed a markedly diminished antibody response to this antigen. Amplification of the antibody titer as well as regular isotype switching from IgM to IgG was absent in the secondary response. Increasing the amount of antigen to a high dose (1 X 10(10) plaque-forming units/kg) led to a normalization of the antibody response. The impairment in antibody formation resembles closely the impaired antibody response in C4-deficient or C2-deficient GP, which both have a block in activation of C3 via the classical pathway. However, in contrast to C4D GP or C2D GP the C3D GP do not exhibit serological characteristics of immune complex disease. They have normal levels of total serum IgM, of IgM anti-2,4-dinitrophenyl antibodies and of IgM rheumatoid factors.

Animals↗