Biomedical subjects

A J Copp

Publications and source records attributed to A J Copp.

79 records · Page 5Linked to original sources

PubMed1979

Interaction between inner cell mass and trophectoderm of the mouse blastocyst. II. The fate of the polar trophectoderm.

Selective labelling of polar trophectoderm cells in early mouse blastocysts has allowed the fate of polar cells to be followed during in vitro and in vivo blastocyst development. Results show that there is cell movement from polar to mural regions as blastocysts grow. This indicates that trophectoderm cells directly opposite the inner cell mass are the oldest mural cells. However, after implantation polar cells invaginate into the blastocoelic cavity and contribute to the extra-embryonic ectoderm. It is suggested that the morphogenetic changes occurring in the mouse embryo at implantation result from the maintenance of a balance between (a) regional differences in rates of cellular proliferation, and (b) mechanical constraints on the direction in which growth can occur.

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PubMed1978

Effect of implantation delay on transfer of rat embryos to mice.

Rat and mouse blastocysts were transferred to the uteri of ovariectomized mice, maintained by progesterone for a few days and induced to implant by oestradiol administration. Mouse implantation sites contained normal embryos; all rat embryos were retarded, although some had developed to the egg-cylinder stage.

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PubMed1978

Interaction between inner cell mass and trophectoderm of the mouse blastocyst. I. A study of cellular proliferation.

Increase in cell number has been compared with mitotic activity in the polar and mural trophectoderm and in the inner cell mass (ICM) of mouse blastocysts. The results indicate that whereas ICM cells divide at a rate which is compatible with the rate of increase of ICM cell number, polar trophectoderm cells divide faster and mural trophectoderm cells slower than can account for their own rates of cell number increase. It is suggested that the ICM induces a high rate of proliferation in the polar trophectoderm and that there is a resulting cell shift from polar to mural regions during blastocyst development. Mural trophectoderm cells close to the ICM divide faster than those farther away, indicating that cells may retain a 'memory' of ICM contact for some time after leaving the ICM. There is considerable cell death in the blastocyst, but this is restricted to a short period of time coincident with the appearance of primitive endoderm.

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PubMedDate not supplied

Role of the polar trophectoderm in determining the pattern of early post-implantation morphogenesis in mammals: evidence from development of the short-tailed field vole, Microtus agrestis.

The peri-implantational embryogenesis in the field vole, Microtus agrestis, is described. Implantation is interstitial, as it is in the mouse, but egg cylinder formation occurs by invagination of the blastocyst's embryonic pole and not (as in the mouse) by formation of a multilayered extra-embryonic ectoderm. This difference can be attributed to loss in the field vole of the central portion of the polar trophectoderm at the time of blastocyst attachment. In comparing early postimplantation development of mammalian species, three morphogenetic variables should be considered: (i) continued proliferation of polar trophectoderm; (ii) mechanical constraints on the direction of its growth; (iii) variations in the degree to which polar trophectoderm is maintained intact after implantation.

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PubMedDate not supplied

The development of field vole (Microtus agrestis) and mouse blastocysts in vitro: a study of trophoblast cell migration.

Outgrowth of field vole blastocysts and their constituent tissues in vitro results in the appearance of trophoblast giant cell monolayers plus migratory cells of two types. The large migratory cells, which are never seen in mouse outgrowths, resemble trophoblast giant cells in morphology and DNA content. They probably correspond to giant cells which have been observed to migrate throughout the endometrium of vole implantation sites in vivo. It is suggested that their appearance in vitro may depend upon an interaction between the trophectoderm and inner cell mass (ICM) of the blastocyst. Small migratory cells also emerge from vole explants and are occasionally seen in mouse outgrowths. They are probably of ICM origin, and in some cases have given rise to long-term vole cell lines.

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PubMedDate not supplied

Covergowns and the control of operating room contamination.

This study assessed the effectiveness of cotton/polyester covergowns in protecting scrubsuits against bacterial contamination when operating room (OR) personnel are outside the clean environment of the operating suite. Rodac impression plates were used to measure bacterial contamination. The subjects were nurses working a normal daily OR routine. Bacterial colony counts on the right shoulder decreased when covergowns were worn over scrubsuits during the lunch period outside the OR and when fresh scrubsuits were put on following the lunch period. Colony counts rose over the lunch period when scrubsuits were worn unprotected outside the OR and when scrubsuits were removed before and put on again following lunch. Left thigh samples showed no significant effects of experimental treatments and yielded a mean colony count 2.8 times higher than right shoulder samples. Fifty-three percent of subjects were positive for Staphylococcus aureus and 16% yielded positive plates on 3 or more study days. The incidence of S. aureus contamination was affected by experimental treatments in a way similar to overall bacterial contamination. The results indicated that wearing covergowns protects against above-waist bacterial contamination of scrubsuits.

Adult↗

PubMedDate not supplied

Birth defects: from molecules to mechanisms.

Birth defects remain a major clinical problem and, although much progress has been made in prenatal diagnosis, few measures are available for primary prevention. This is due, in large part, to our rudimentary understanding of the embryonic mechanisms of birth defects. Until recently it was customary to concentrate on defining teratogenic factors that may be active in humans. Now, with the rapid expansion in molecular biological technology, it has become possible to identify and isolate the genes that determine heritable predisposition to birth defects. The most productive strategy appears to be the genetic analysis of animal, principally mouse, models in which particular classes of birth defects develop owing to known genetic mutations. Gene targeting techniques allow mutations to be induced in previously cloned genes, permitting their potential as birth defect-inducing genes to be evaluated. Gene cloning alone, however, cannot reveal the entire pathogenetic sequence for any birth defect, since the most downstream events can be elucidated only by experimental embryological analysis. Culture methods are now available in which intact mouse and rat embryos undergo normal development for limited periods in vitro. Studies of this type have revealed several steps in the embryonic development of genetically determined spina bifida. The combination of gene centered and embryo centred research promises to advance our understanding of the pathogenesis of major birth defects.

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