Natural killer cell activity in mouse aggregation chimeras.
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Aging↗
Biomedical subjects
L Elbling
Publications and source records attributed to L Elbling.
Lewis lung tumor system as a model for studying the immune function in syngeneic in equillibrium allogeneic chimeras.
Lewis lung tumor (LLT) passaged in F1 hybrids of the original C57B1/6 strain, where it arose spontaneously, is rejected by allogeneic SWA (Swiss albino) mice. However, aggregation chimeras derived from these SWA mice and the F1 hybrids of C57B1/6 developed an increased growth of primary tumor and reduced number of metastases when compared with the F1 hybrids. In the present study LLT passaged in C57B1/6 mice is not rejected by SWA mice. It is demonstrated that in aggregation chimeras now derived from two strains both taking the tumor, primary tumor growth was enhanced and the number of metastases reduced as in the former experiment. The tendency of reactions of lymphatic orgains in chimeras to tumor burden was comparable with the SWA and F1 hybrid (C57B1/6 multiplied by SWA and SWA multiplied by C57B1/6) recipients' response. Furthermore, chimeras had the highest spleen enlargement. Possible alternations in immune functions of chimeras due to their differing genotype combination are discussed in the LLT model.
Animals↗
[Mosaic (Chimeric) animals: their experimental production and application (author's transl)].
A method introduced by Tarkowski permits the aggregation (mosaic-like fusion) of mammalian eggs in the early stages of division. In this paper, a modification of the Tarkowski method designed to create multiparental (mostly quadriparental) chimeric mice is discussed. The method described is simple, more practical and time-saving. The problems in analysing clonal processes of development in mammals and the mechanisms connected with sex differentiation and tumour development are discussed.
Animals↗
Enhanced tumor growth in chimeric mice.
Chimeras were produced by aggregation of B6D2F1 and SWA early embryos. Lewis lung tumor, syngeneic in B6D2F1, was used to study tumor growth and metastases in these chimeras. Enhanced tumor growth, low metastases rate and pronounced enlarged spleen could be observed in SWA equilibrium B6D2F1 chimeras 21 days after inoculation of tumor cells. Increased activity of suppressor T-cells which might be due to permanent allogeneic stimulation in chimeras is discussed as one of the possible mechanisms.
Animals↗
Malformations induced by hormones in mice and their transmission to the offspring.
A fore foot defect occurring after gonadotropin stimulated ovulation in the offspring of Swiss albino mice is described as an abnormality which is transmitted to the offspring of several inbred generations. This malformation is a combination of postaxial oligodactylism and polydactylism, in literature so far not described previously. The defect originally observed after hormone treatment (postaxial oligodactylism) occurred most frequently. With others it has been considered whether the defect of the foot, which is in all probability subject to polygenic control, manifests itself as a result of selective factors during embryogenesis. A possible mutagenic effect of the sex hormones on the germ cells is also under consideration. This view is supported by clinical observations.
Abnormalities, Drug-Induced↗
Congenital malformations in mice after gonadotropin-induced ovulation.
Virgin mice were treated with gonadotropic hormones in order to induce superovulation; at term the embryos were removed by cesarean section. This treatment induced malformations (mainly forelimb defects and to a smaller extent central nervous system anomalies) as well as an altered sex ratio in the offspring. Both phenomena were statistically significant. These hormone-induced effects on the progeny were significantly dependent on both the dosage of hormones and the time (season) of administration. Because the time of administration (before mating) of gonadotropic hormones does not coincide with the critical period during embryogenic development for the teratogenic induction of malformations in the limbs and in the central nervous system (ca. 8th-12th day of gestation), the investigated defects are interpreted as of mutagenic origin.
Abnormalities, Drug-Induced↗
Does gonadotrophin-induced ovulation in mice cause malformations in the offspring?
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Abnormalities, Drug-Induced↗
A method for analysing sister-chromatid exchange in mouse preimplantation embryos.
Analysis of sister-chromatid exchange (SCE) has been shown to be a sensitive and reproducible method for detecting the action of mutagens and carcinogens. We have succeeded in establishing a reliable technique which allows to perform SCE in preimplantation embryos in order to make the pre-uterine stages of development accessible to routine detection of DNA damage. Using the mouse strain and technique described, approximately 30-40% of mice will mate successfully after synchronization and spontaneous ovulation. From 3 pregnant females, about 30 four- to eight-cell embryos will be obtained, representing one experimental group providing approximately 50-80 two-S-phase labelled metaphases with a SCE frequency baseline below 6 exchanges.
Animals↗