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Biomedical subjects

E Frindel

Publications and source records attributed to E Frindel.

At least 91 records · Page 5Linked to original sources

Abscopal effect of irradiation on haemopoietic stem cells of shielded bone marrow--role of migration.

Immediately after partial-body irradiation, the number of colony-forming units (CFU) of the protected marrow decreases. This decrease seems to be dose-dependent and cannot be completely explained by migration for the following reasons: there is no evidence of CFU entry to irradiated territories and the number of circulating CFU does not increase. A more plausible explanation for the phenomena is an accelerated differentiation during the first 15 min after irradiation. The migration of CFU to the spleen is observed between 15 min and 3 hours after irradiation, after which it ceases. The absence of migration 3 hours after irradiation may be due to one of the two possibilities: (1) a depletion of the mobile pool of CFU if one admits that such a pool is responsible for migration in the organism; (2) a depletion of a temporarily increased stimulus due to irradiation.

Animals↗

Study of an inhibiting factor of epidermal proliferation in plucked skin and various tumours of mice.

The aim of our research was to investigate, by autoradiographic methods, the presence of an inhibitory factor (IF) in normal skin, in plucked skin and in five experimental skin tumors of the mouse, capable of inhibiting epidermal proliferation. The experimental model used was that of Bullough & Laurence (1960), i.e. a wound in the ear of a mouse. After tritiated thymidine administration the measurement of the labelling index confirmed the existence of an inhibitory substance in normal skin. The plucked skin had no inhibitory effect when it was taken 24 h after plucking, but after 4 days its effect had returned to normal. The skin tumours, whether epithelial or mesenchymal, showed the same inhibitory effect as normal skin whereas a non-cutaneous tumour tested had no inhibitory effect.

Animals↗

A technique for determining the proportion of the clonogenic cells in S phase in ENT6 cell cultures and tumors.

The survival of cultured EMT6 cells was examined after treatment with hydroxyurea (HU) or high specific activity tritiated thymidine (3H-TdR). The concentrations of the agents, duration of exposure to the agents, and post-exposure treatment of the cultures were found to influence the cell survival; the effects of these factors are reported. Conditions were defined under which the proportions of cells killed by HU and by 3H-TdR were the same and were also the same as the proportion of labeled cells seen on autoradiographs of cultures labeled with small doses of 3H-TdR. Under these conditions, either 3H-TdR or HU could be used to determine the proportion of the clonogenic cells in S phase. Single cell suspensions prepared from solid EMT6 tumors were treated in vitro with HU or 3H-TdR, using the conditions found optimal for each agent with cultured cells. The proportion of the tumor cells killed by treatment with HU in vitro was the same as the proportion killed by HU in vivo and as the proportion labeled by 3H-TdR in vivo, and incubation of tumor cell suspensions with HU in vitro appeared to provide a valid measurement of the proportion of clonogeneic tumor cells in S phase. Incubation of tumor cell suspensions with 3H-TdR in vitro proved difficult to perform and the results were relatively unreliable because of severe problems with reutilization of 3H-TdR during the incubation for colony formation.

Animals↗

Thymus dependency of bone marrow stem cell proliferation in response to certain antigens.

The activity of mouse bone marrow CFU's following systemic injection of antigen has been investigated. In normal mice quiescent CFU's may be triggered into cycle after antigenic challenge. Prior adult thymectomy prevents stimulation of CFU if thymus-dependent antigens are injected but not when thymus-independent antigens or non-specific stimuli are used. Similar results were obtained in congenitally athymic mice. This seems to indicate an independent pathway for CFU triggering for each cell lineage and for T and B cells.

Animals↗