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Biomedical subjects

U K Abbott

Publications and source records attributed to U K Abbott.

At least 19 recordsLinked to original sources
PubMed1989

Distribution of extracellular matrix in the migratory pathway of avian primordial germ cells.

The appearance and distribution of extracellular matrix (ECM) was documented along the migratory route of chicken primordial germ cells (PGCs). The antimouse embryonal carcinoma cell antibody, EMA-1, was used to label PGCs (Urven et al.: Development 103:299-304, 1988). Antibodies against laminin, fibronectin, chondroitin sulfate proteoglycan and collagen type IV were used to label extracellular matrix components. When the PGCs emerged from the epiblast, all four ECM molecules were restricted principally to the basement membrane of the epiblast. Chondroitin sulfate was also located between hypoblast cells during this period. In late germinal crescent stages, when the PGCs entered the lumina of blood vessels, the same ECM molecules were more widespread in the mesoderm and in extracellular spaces. In addition, laminin and collagen type IV were identified on lateral surfaces of ectodermal cells at this stage. When the germ cells moved through the mesenchyme into the germinal ridge, the ECM molecules were found around mesenchymal cells, and, in the cases of laminin, fibronectin and collagen type IV, in the basement membranes of the germinal ridge epithelia. Because the appearance of these ECM components is temporally and spatially correlated with the movement of PGCs, we suggest that early PGC migration may depend on their timely appearance.

Animals↗
PubMed1988

Analysis of germ line development in the chick embryo using an anti-mouse EC cell antibody.

We have found that EMA-1, a monoclonal antibody originally raised against mouse embryonal carcinoma (Nulli SCC1) cells (Hahnel & Eddy, 1982), also labels chick primordial germ cells (PGCs). We have used this antibody in immunohistological studies to follow the development of PGCs in the chick embryo from the time of their initial appearance beneath the epiblast, through their migratory phase and subsequent colonization of the germinal epithelium. During hypoblast formation, individual EMA-1-labelled cells appeared to separate from the basal surface of the epiblast and enter the blastocoel, coincident with the appearance of morphologically identifiable PGCs in this same area. EMA-1 continued to label germ cells until the initiation of gametogenesis in each sex; specifically, labelling was absent by 7-8 days of incubation in females and started to decrease at 11 days of incubation in males. There was a recurrence of the epitope on oogonia at 15 days of incubation, but not on spermatogonia during the remainder of development through hatching. These observations are consistent with an epiblast origin for the avian germ line, and are strikingly similar to those reported for the early mouse embryo using the same antibody (Hahnel & Eddy, 1986).

Animals↗
PubMed1979

Adult and embryo responses to organophosphate pesticides: azodrin.

Azodrin was applied to adult embryo chickens, Chukar Partridge, and Bobwhite Quail. Chronic exposure of adult birds to Azodrin mixed in their feed indicated that no a priori predictions could be made about one species based on the results of another; each had a different no effect (MACT) level. The chickens were between 25 and 100 ppm, the Chukar Partridge 5 and 25 ppm, and the Bobwhite quail less than 1.25 ppm. The chicken adults were most resistant, and the quail were least resistant to chronic exposure to Azodrin. Yolk-injected Azodrin caused the embryos of all three species to develop abnormally. The chicken and Chukar embryos developed a generalized achondroplasia, the quail were amuscular, only. In general, the 3 day quail embryos were most resistant to injected Azodrin and the chicken embryo least resistant. The relationship between adult and embryo response was negative.

Animals↗
PubMed1978

Facial development in normal and mutant chick embryos. I. Scanning electron microscopy of primary palate formation.

Early facial development in normal chick embryos was studied by scanning electron microscopy, and compared to the abnormal facial development of a mutant in which primary palate formation does not occur, thus resulting in bilateral cleft lip. In both normal and "cleft primary palate" mutant embryos, subsequent to the appearance of the nasal placodes, the surrounding tissues elevate to give rise to the presumptive facial primordia. As the facial primordia grow forward, they gradually assume the configuration of a square which is most pronounced at five days development. In normal embryos, the square configuration is then lost as the facial primordia become aligned in preparation for primary palate formation. The primary palate is formed at six days development by fusion of the "free-ended" medial nasal processes with the combined lateral nasal and maxillary processes across the nasal grooves. Just prior to fusion, long, slender filaments extend from the apposing surfaces of the facial primordia in the regions of prefusion contact. It is speculated that these "prefusion filaments" may function in alignment or adhesion of the facial primordia. In "cleft primary palate" embryos, facial morphogenesis appears to arrest at five days development, so that the square configuration persists. The medial nasal processes never contact the lateral nasal and maxillary processes, but instead remain separated from them by wide nasal grooves. Furthermore, facial primordia of mutant embryos do not exhibit the "prefusion filaments" characteristic of normal embryos.

Animals↗
PubMed1977

Temporal, morphological, and genetic responses of avian embryos to Azodrin, an organophosphate insecticide.

The effect of Azodrin on avian development was studied using a bobwhite quail line and two chicken lines--a single comb White Leghorn (SCWL) and an Australorp line. The bobwhite quail embryos did not respond to injections of Azodrin until stages 22 to 23 (6 days of incubation); the SCWL embryos, not until stage 18 (3 days of incubation) with increasing susceptibility through stage 20. The threshold concentration, at stage 19, for the SCWL was 0.4 mg/kg, for the Australorp, less. Within one hour of treatment stage-20 embryo shape was altered. There was, however, no immediate response from embryos treated earlier. The effect appeared as a reduced growth rate in the cervical flexure, and may be mediated by interference with the normal energy balance. The response, once initiated, was continuous through 10 days of incubation.

Abnormalities, Drug-Induced↗
PubMed1977

Scoliosis in chickens.

Scoliosis developed in 55 per cent of sexually mature birds (68 per cent of male and 46 per cent of female birds) in a highly inbred line of chickens originally produced from white Leghorns. The curve could first be detected at five to six weeks of age and progressed until spontaneous fusion of the thoracic vertebrae occurred. Studies of these chickens indicated that abnormalities of growth and development of the spine are not the primary cause of the scoliosis. Preliminary studies of the paravertebral musculature also indicated that simple muscle imbalance is not responsible for the curve. Initial studies of collagen extracted from the scoliotic line of chickens showed it to be more soluble than similar collagen extracted from white Leghorn controls.

Animals↗
PubMed1975

Limb development in diplopodia4: a polydactylous mutation in the chicken.

In a study of the polydactylous mutation of the domestic chicken, diplopodia4, we have found that the genetic lesion affects primarily the mesoderm and only secondarily the ectoderm. The effect of this mutant mesenchyme on overlying ectodermal ridge, either mutant or normal, is to thicken the ridge preaxially, leading to increased outgrowth and preaxial polydactylism. A "zone of polarizing activity" in the normal limb-bud seems to have a role in the control of its anteroposterior polarity. We have examined diplopodia4 limb-buds for polarizing activity and found it to be normal in its activity and distribution. These results suggest that the supernumerary outgrowth in the mutant limbs result from increased ridge mainon of the polarizing zone.

Alleles↗