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Biomedical subjects

C A Finn

Publications and source records attributed to C A Finn.

At least 37 records · Page 2Linked to original sources
PubMed1986

Control of leucocyte infiltration into the decidualized mouse uterus.

Ovariectomized mice were treated with oestrogen and progesterone on a schedule to mimic early pregnancy. Decidualization was induced with oil and uteri were examined at various times after the last progesterone injection. The first morphological change detected in the uterus of decidualized mice following withdrawal of progesterone was infiltration of leucocytes into the stroma. This preceded overt tissue breakdown and extravasation of blood cells, and did not occur following withdrawal of progesterone without decidualization. It is suggested either that there is a release of a chemoattractant from decidual cells before any morphological changes are apparent or that the signal for attracting the leucocytes is released at the time of decidual induction, but that their migration is suppressed by progesterone.

Animals↗
PubMed1984

Vascular and cellular changes in the decidualized endometrium of the ovariectomized mouse following cessation of hormone treatment: a possible model for menstruation.

Ovariectomized mice were prepared for decidualization with oestrogen and progesterone and arachis oil injected into the uterine lumen. Hormone injections were then stopped and uteri examined at intervals between 31 and 84 h after the last progesterone injection. At 31 and 35 h the stroma showed a normal decidual reaction. Between 45 and 79 h the stroma underwent a series of changes which started with the congestion of dilated blood vessels with swollen erythrocytes followed by breakdown of the vessel walls and extravasation of blood. At the same time the decidual cells showed typical apoptotic changes and there was invasion by leucocytes. An outer ring of stroma did not take part in the degenerative process and eventually a central core of blood cells and degenerating decidual cells became detached and was shed into the lumen. Animals treated in exactly the same way but with the omission of the decidual stimulus did not show such changes in the stroma. It is suggested that the changes in the endometrium resemble those of menstruation and support the suggestion that for menstruation to occur the stroma must be differentiated for implantation. This occurs during the cycle in women but does not occur in non-primates unless a decidual stimulus is applied to the uterus.

Animals↗
PubMed1981

Hormonal control of cell death in the luminal epithelium of the mouse uterus.

An attempt has been made to assess quantitatively the extent of cell death in the uterine epithelium after oestrogen treatment. [3H]Thymidine was injected into ovariectomized mice at an interval after oestrogen treatment when many of the luminal epithelial cells were in the S phase of mitosis. Uptake of [3H]thymidine was confirmed by autoradiography of sections of uterus and scintillation counting of trichloracetic acid-insoluble fraction of whole uterine horns. Radioactivity declined after the cessation of oestrogen treatment but remained high if treatment was continued. The decline appears to be correlated with the cell death previously demonstrated in histological sections of uteri under similar conditions.

Animals↗
PubMed1979

Varying effects of an IUD on decidualization in mice.

Chronically implanted IUDs consisting of silk suture threads induced decidualization in regions of the uterus remote from the suture site in ovariectomized mice treated with a regimen of progesterone and oestrogen which sensitizes the uterus to a decidual stimulus. In these conditions the IUDs did not inhibit decidualization induced by instilled oil, although they did so in pregnant animals of the same strain. Varying the dose of progesterone and oestrogen did not produce conditions in which IUD's inhibited oil-induced decidualization in ovariectomized mice and progesterone treatment did not prevent IUDs inhibiting decidualization in pregnant animals. However, when ovariectomized mice, sensitized as before, were primed repeatedly with oestrogen to simulate continuing oestrous cycles after IUD insertion, the IUD's inhibited oil-induced decidualization. This involved the premature loss of instilled oil from the uterine lumen and was associated with heavy infiltration of leucocytes into the luminal epithelium. Numbers of leucocytes free in the uterine lumen did not appear to be critical. It appears that contact between the oil and the luminal epithelial surface must be sustained for some length of time to induce a decidual reaction; brief contact is not sufficient to trigger the response.

Animals↗
PubMed1978

Effects of an intra-uterine device on uterine cell division and epithelial morphology in ovariectomized mice treated with oestrogen and progesterone.

Silk threads placed in the uteri of ovariectomized mice increased cell proliferation in all tissues including regions of the uterus remote from the site of insertion. Many of the effects resembled those produced by oestrogens. An intra-uterine device (IUD) increased luminal and glandular mitosis and produced various degrees of luminal epithelial hyperplasia in untreated animals. In progesterone-treated mice bearing IUD's, luminal and stromal mitosis was increased. Epithelial morphology was not affected or luminal mitosis inhibited in oestrogen-treated animals with IUD's, but stromal and glandular mitosis was increased. After combined treatment with progesterone and oestrogen, stromal mitosis was suppressed at the contact site but was increased elsewhere. Both oestrogen and progesterone suppressed the luminal leucocytosis induced by the IUD. Despite this, the IUD prevented complete progestational differentiation of the luminal epithelium and closure of the lumen. The degree to which IUD-induced abnormalities were observed depended on the hormonal status of the animal at the time of sampling.

Animals↗
PubMed1978

Effects of a long-acting progestin on reproductive function in female mice.

The duration of activity of a long-acting progestin, medroxyprogesterone acetate, was compared using three tests for progestational activity: the induction of stromal mitosis in the endometrium, implantation of blastocysts and inhibition of ovulation. The duration of activity was similar in each test and was longer when higher doses were given.

Animals↗
PubMed1975

Changes in the endometrium of mice after the induction of implantation by actinomycin D.

Actinomycin D can induce a small number of implantations in pregnant mice undergoing progestin-induced delayed implantation following ovariectomy. However, the response of the uterus to the blastocyst is considerably retarded compared with the response observed when implantation is precipitated by oestradiol. With the electron microscope the attachment reaction between the trophoblast and uterine epithelium is evident about 48 h after administration of the drug. However, the differentiation of the luminal surface of the epithelial cells in areas of uterus distant from a blastocyst (2nd stage of closure), which normally accompanies implantation, and can be induced by oestradiol in progesterone-treated animals, is not seen. Thus actinomycin D, although allowing implantation to proceed, does not completely mimic the actions oestradiol on the progesterone-treated uterus.

Animals↗
PubMed1975

The development of embryos in the uteri of mice treated with actinomycin D before implantation.

This investigation follows the development of embryos in the uteri of mice in which the differentiation of the implantation chamber has been retarded by the administration of actinomycin D before implantation. For the first 48 h after the induction of implantation both embryonic and extra-embryonic parts of the blastocyst develop, but after 72 h the embryonic parts cease to grow and die. The giant cells and other extra-embryonic tissues, on the other hand, continue to develop for a much longer period, up to 288 h. It is suggested that the actinomycin D, by delaying the formation of the implantation chamber in the endometrium, interferes with the formation of a proper functional connection between the trophoblast and endometrium with the result that the embryo receives insufficient nutrition for its development.

Animals↗