Biomedical subjects

I Bauer

Publications and source records attributed to I Bauer.

At least 73 records · Page 4Linked to original sources

PubMed1985

[Lymphocytic adenosine deaminase activity in children with acute and chronic respiratory tract diseases].

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Adenosine Deaminase↗

PubMed1982

Structure of nonintegrated, circular Herpesvirus saimiri and Herpesvirus ateles genomes in tumor cell lines and in vitro-transformed cells.

Nonintegrated, circular DNA molecules of Herpesvirus saimiri and Herpesvirus ateles were found in five lymphoid cell lines originating from tumor tissues or established by in vitro immortalization of T lymphocytes. The arrangement of unique (L) and repetitive (H) DNA sequences in circular viral genomes was analyzed by partial denaturation mapping followed by visualization with an electron microscope. Three types of circular viral DNA structures were found. (i) The virus-producing cell line RLC, which is derived from an H. ateles-induced rabbit lymphoma, contains circular viral genomes which consist of a single L-DNA and a single H-DNA region, both the same length as in virion DNA. (ii) The circular viral genomes of the nonproducer cell lines H1591 and A1601, in vitro transformed by H. saimiri and H. ateles, respectively, have deletions in the unique L-DNA region and larger H-DNA regions. Cell line A1601 lacks about 8% of virion L-DNA, and H1591 cells lack about 40% of viral L-DNA information. (iii) The nonproducing H. saimiri tumor cell lines 1670 and 70N2 harbor viral genomes with two L-DNA and two H-DNA regions, respectively. Both types of circular molecules have a long and a short L-segment. The sequence arrangements of circular DNA molecules from H. saimiri-transformed cell lines were compared with those of linear virion DNA by computer alignment of partial denaturation histograms. The L-DNA deletion in cell line H1591 was found to map in the right half of the virion DNA. Comparison of the denaturation patterns of both L regions of cell lines 1670 and 70N2 identified the short L regions as subsets of the long L regions. Thus, circular viral DNA molecules of all four nonproducer cell lines represent defective genomes.

Animals↗

PubMed1981

Episomal and nonepisomal herpesvirus DNA in lymphoid tumor cell lines.

Tumor cell lines derived from Herpesvirus saimiri (H. saimiri)- and Herpesvirus ateles (H. ateles)-induced lymphomas of New World primates and rabbits contain multiple copies of viral genomes. Partial denaturation mapping and blot hybridizations of episomal DNA from lymphoid tumor cell line No. 1670 showed that a 12.5md-fragment is missing which represents the EcoRI D- and H-fragments of virion L-DNA. However, the missing piece can be demonstrated in total cellular DNA by reassociation kinetics, possibly because it persists in integrated form. Both episomal and nonepisomal H-DNA are heavily methylated in a number of the lymphoid cell lines, and methylation may be reduced by conventional methylation inhibitors (S-adenosyl homocystein, SIBA) as well as by the tumor promoting phorbol ester TPA.

Animals↗

PubMed1981

[Adenosine deaminase activity and immune dysfunction (author's transl)].

Deficiency of adenosine deaminase (ADA) in lymphocytes seems to be responsible for severe combined immunodeficiency (SCID), a syndrome in early infancy untreated resulting in death. The highest amounts of ADA activity are found in lymphoid tissues. Considerable enzyme deficiency is associated with an inhibition of proliferation and differentiation, especially of the T lymphocytes, and gives rise primarily to disordered cellular immunity. The molecular mechanisms of the relationship between enzyme deficiency and immune dysfunction are widely unknown. Several possibilities are discussed. Deoxyadenosine and its nucleotides seem to be the toxic agents. The enzyme deficiency is thought to result from a mutation at the structural locus of ADA inherited in an autosomal recessive mode. In addition to transplantation of bone marrow, fetal liver, or thymus the "enzyme replacement" has been suggested for therapy of SCID in ADA deficiency, i.e. transfusion of irradiated erythrocytes with normal ADA activity.

Adenosine Deaminase↗

PubMed1980