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E Mollenhauer

Publications and source records attributed to E Mollenhauer.

12 recordsLinked to original sources
PubMed1984

Population and formal genetics of the human C81(alpha-gamma) polymorphism.

One hundred and ninety-six unrelated healthy individuals and 30 families with 75 offspring have been studied for the C81(alpha-gamma) polymorphism. The following allele frequencies were calculated: C81*A = 0.5536; C81*B = 0.4286; C81*A1 = 0.0178. Observed and expected phenotype frequencies were in a good agreement according to the Hardy Weinberg law. No exceptions from the mode of inheritance were found. In family W the segregation of the rare allele C81*A1 could be followed. Comparing the results of this study with previous data from Boston and Oslo, a combined technology including C8-dependent lysis and C8 structural variation is suggested for future investigations.

Alleles↗
PubMed1984

Genetics of human C4 polymorphism: detection and segregation of rare and duplicated haplotypes.

Applying a combined technology for the detection of allotypic variation of the fourth component of human complement (C4), including immunofixation with anti-C4 and C4-dependent lysis after agarose electrophoresis, sodium dodecyl sulfate-polyacrylamide gel electrophoresis of C4 to separate the C4A and B alpha-chains, and the determination of Rodgers (Rg) and Chido (Ch) determinants of C4 in serum and at the blotted C4 alpha-chains, we detected rare human C4 allotypes and studied the genetic linkage. Partial inhibitors (p.i.) of anti-Rg and anti-Ch sera were found; the C4A51 allotype characterized as Rg p.i. and the C4A1 and C4B51 allotypes as Ch p.i. were genetically inherited. The C4A1 allotype has a unique Rg- Ch+ C4A alpha-chain. Duplicated C4A loci, A*3, A*2, and A*5, A*2 were both associated with a C4BQO and the HLA haplotype A3-Cw4-Bw35-DR1. These additions to the already known extensive C4 polymorphism may help to sort out their significance for the biological functions of human C4.

Complement C4↗
PubMed1984

Partial C4 deficiency in subacute sclerosing panencephalitis.

In an immunogenetic study, 23 subacute sclerosing panencephalitis (SSPE) patients and their families were studied for the HLA region markers HLA-A, B, C, DR, BF, C2, C4A, C4B, GLO I, and PGM3. In addition, C3, C4, and factor B serum levels were determined. A highly significant association of C4A QO with SSPE was found. Furthermore, two rare haplotypes, C4A QOB QO, two C4ACh+ allotypes, and four Ch partial inhibitors were detected, which possibly impair the function of the C4 molecules. HLA-DR5 was increased. In addition, a number of rare HLA-A, C, B, DR haplotypes were observed. It is postulated that rare C4 molecular deficiency might be a predisposing factor in the pathogenesis of SSPE.

Complement C4↗
PubMed1984

An international reference typing for Ch and Rg determinants on rare human C4 allotypes.

Red cells, serum and plasma samples of 20 individuals, selected for their C4 allotypes, were distributed from Bonn to five laboratories, for investigation of their Chido (Ch) and Rodgers (Rg) determinants. One anti-Ch (M.H.) and one anti-Rg(Prest.) were distributed, but the individual laboratories also used their own reagents and their own typing methods. There was general agreement in interpretation of the majority of samples. Partial inhibition for Ch and Rg was detected. Two samples gave anomalous results; one sample with C4 A1,3 BQO, QO had Ch determinants on the red cells and in plasma (partial inhibition), and another sample with C4 A3,4 B5, QO apparently lacked Ch determinants on the red cells and in plasma. Heterogeneity of anti-Ch and anti-Rg was suggested in testing red cells, perhaps, reflecting a quantitative effect. This heterogeneity was confirmed by inhibition studies. The capacity of some reagents to detect partial inhibition probably reflects qualitative as well as quantitative differences.

Alleles↗
PubMed1984

Rodgers (Rg) and Chido (Ch) determinants on human C4: characterization of two C4 B5 subtypes, one of which contains Rg and Ch determinants.

The genetically determined polymorphism of the fourth component of human complement was further extended with the aid of a panel of human allo-anti-C4 sera, anti-Rodgers and anti-Chido. These antisera were found previously to react with the alpha-chains of the C4 molecules controlled by the C4A and C4B loci, respectively. We analyzed a number of new and rare C4 allotypes, and found that they generally followed the expected pattern. Some interesting exceptions, however, were found. The alpha-chain of the allotype C4A1 was found to react with anti-Chido, unlike all other C4A allotypes. Also the C4B5 allotype could be subdivided into two subtypes on the basis of their reaction with anti-Rodgers. They were tentatively named B5Rg+ and B5Rg-. Moreover, the B5Rg+ subtype reacted not only with anti-Rodgers but also with some anti-Chido sera, indicating for the first time that Chido and Rodgers determinants are present on the same allotype.

Antigen-Antibody Reactions↗
PubMed1983

Pigeon breeder's lung: association with HLA-DR 3.

52 symptomatic (SPB) and 64 asymptomatic (APB) pigeon breeders were investigated for the HLA-A, -B, -C, -DR; C2, C3, C4 and Bf systems, and C3, C4 and factor B serum concentrations. HLA-DR3 and Bf S frequencies were significantly higher in the SPB than the APB group. Mean factor B concentrations were lower in the SPB than in the APB group. A positive two-way association between HLA-DR3 and the disease was found. It is concluded that a gene or genes responsible for type III and IV allergic reactions leading to the disease is associated with HLA-DR3. The increase of Bf S allotype and low mean factor B concentrations, however, can be explained by the strong linkage disequilibrium between BfS and HLA-DR3.

Alveolitis, Extrinsic Allergic↗
PubMed1982

A molecular basis for the two locus model of human complement component C4.

The major histocompatibility complex(MHC)-linked fourth component of complement (C4) shows a high degree of polymorphism in several animal species. In man C4 polymorphism was detected by distinct charge differences of the variants. O'Neill et al. showed that this C4 polymorphism was controlled by two closely linked genetic loci, F (C4A) and S (C4B) and these results were extended by Awdeh et al. with an improved typing method. Biochemical analysis of human C4 has revealed that it consists of three polypeptide chains, alpha, beta and gamma. In all reports so far on the molecular analysis of human C4, no molecular weight differences between the A and B locus-encoded molecules have been noticed. Here we demonstrate that the C4A and C4B locus-encoded alpha-chains have a molecular weight (MW) of 96,000 and 94,000, respectively, presenting for the first time a molecular basis for the difference between all C4A and C4B variants tested. Even rare variants that are difficult to allocate to the A or B locus on the basis of charge differences could be identified as C4A or C4B variants in this way, thereby providing new insights into the relationships between the C4A and C4B loci.

Complement C4↗
PubMed1979

[C6-polymorphism of the sixth component of complement: application to paternity cases (author's transl)].

The results of a study of the polymorphism of the sixth component of human complement by means of isoelectric focusing in polyacrylamide gels with subsequent C-dependent lysis in an agarose overlay containing C6 deficient rabbit serum are reported. The allele frequencies obtained (C6A = 0.613, C6B = 0.379, C6R = 0.008) are in good agreement with those previously published. The mode of inheritance in 47 families with 173 offspring as well as 26 mother-child combinations is in agreement with a formal genetical model: "C6A, C6B, C6A1 and C6B1 at an autosomal locus". The inclusion of this system into a blood group expertise in Germany can be recommended.

Adult↗