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Biomedical subjects

K E Lovering

Publications and source records attributed to K E Lovering.

10 recordsLinked to original sources
PubMed1991

Restriction of the participation of copper in radical-generating systems by zinc.

Zinc was able to reduce the availability of copper for several radical-generating reactions: lucigenin-amplified chemiluminescence due to copper and hydrogen peroxide: copper-dependent ascorbate oxidation and its concomitant oxygen consumption: and copper-dependent benzoate hydroxylation. This was the case both in the presence of bovine serum albumin (when most zinc was protein-bound) and in its absence (when zinc was 'available'). Competition between zinc and copper for binding to the fluorophore calcein was also examined, and this allowed assessment of copper availability in several circumstances. Competition between copper and zinc for binding to biological components seems to be a rather general phenomenon, and thus zinc is commonly a protective entity, restricting free radical generation.

Binding Sites↗
PubMed1987

Isolation of the CD7 gene from the DNA of transfected L cells.

Using DNA from L cells which expressed high levels of the CD7 (Leu-9 or HuLy-m2) antigen obtained after two cycles of transfection, a genomic library was constructed in the lambda phage Charon 4A. Recombinant clones containing the gene coding for this antigen were identified by first screening the library with both the HSV-tk gene and a probe detecting the human repetitive (Alu) sequences. DNA from 10 tk+ and 12 Alu+ recombinant clones was used to transfect L cells which were analyzed for the cell-surface expression of CD7 either early (48-72 h posttransfection) or later when hypoxanthine aminopterin thymidine-resistant colonies were obtained. Transfection with either Alu+ or tk+ recombinant phages led to transient early expression of CD7, and stable CD7+ transfectants were also established. Thus the CD7 gene has been isolated in a number of clones in association with either the Alu repetitive sequence or with the HSV-tk gene; the insert size in one of the genomic clones was 13.5 kb.

Animals↗
PubMed1987

Gene transfection of the HuLy-m2 (Leu-9) antigen into mouse L cells.

Human DNA was transfected into mouse L cells and tk+ HuLy-m2+ (= CD7+) transfectants isolated after growth in hypoxanthine, aminopterin, thymidine medium and repeated cloning. After several cycles of transfection, greater than 90% of HuLy-m2+ L cells could be detected, by rosetting and by cytofluorography, which showed the transfectants to have a density of CD7 two to five times that found on peripheral blood lymphocytes. Despite this, the 37 kd CD7+ dimer could only be identified with difficulty using cell-surface radioiodination and sodium dodecyl sulfate-polyacrylamide gel electrophoresis techniques. An antiserum was produced (C3H anti-HuLy-m2+ L cells) which, after absorption, was shown to react with HuLy-m2+ antigens present on human thymocytes and lymphocytes and on CD7+ transfected L cells.

Animals↗
PubMed1984

A monoclonal antibody detecting a new human T cell antigen, HuLy-m2.

HuLy-m2 is a new T cell antigen detected by a monoclonal antibody. The antibody (anti-HuLy-m2) reacts with 85% of human T cells, 20% B cells, and 50% null cells in peripheral blood. The antibody is cytotoxic, binds protein A, and is of the IgG2a subclass. HuLy-m2 antigen consists of a glycoprotein dimer Mr 37,000 subunit structure, in which sialic acid and carbohydrate play some role in antigenicity. Capping studies showed the HuLy-m2 antigen to be distinct from the previously described OKT-3, 4, 8, HuLy-m1 (OKT11), and HuLy-m3 antigens.

Animals↗
PubMed1980

Trypsin fails as Australian snake bite cure.

Trypsin has been claimed a new and effective treatment for venomous snake bite. We found that significant inactivation of snake venom lethal potency occurred in vitro when trypsin was incubated with venom and subsequently injected into mice. Premixing of tiger snake venom (TSV) and trypsin just before injection did not significantly increase the survival rate of mice over that of controls injected with TSV alone. Trypsin injected 10 to 30 minutes after TSV injection did not increase the survival rate of mice compared with controls. Specific antivenom was effective as an antidote when there was a 10 minute delay after venom injection. There was varying susceptibility of different venoms to trypsin inactivation in vivo.

Animals↗