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Biomedical subjects

R A Pedersen

Publications and source records attributed to R A Pedersen.

106 records · Page 6Linked to original sources
PubMed1976

Ultrastructural observations of lethal yellow (Ay/Ay) mouse embryos.

Ay/Ay embroys were identified by the presence of large exluded blastomeres (Pedersen, 1974) and examined cytologically and ultrastructurally. Cell organelles, inclusions and junctions in the excluded blastomeres were compared with those of non-excluded cells of Ay/Ay embryos and control embryos. Excluded blastomeres always had the fine structural characteristics of earlier developmental stages and may have arrested at the 4- to 8-cell stage of slightly later. Interior cells (inner cell mass) were observed in all mutant blastocysts. Non-excluded cells of Ay/Ay embryos were normal until degenerative changes appear in the late blastocyst stage. The mode of action of the +Ay gene was not determined, but evidence from this study and others indicate that the effects of +Ay gene action occur over a wide range of time in early cleavage and implantation.

Alleles↗
PubMed1975

In vitro development of t6/t6 embryos.

Embryos from matings in which approximately a third of the zygotes were expected to be t6/t6, a condition known to be lethal at the egg cylinder stage in vivo, were compared to normal control embryos during post-implantation culture. The percentage success of trophoblast outgrowths was the same in both groups while the experimental group showed a 25% deficiency of embryos with inner cell masses. Those experimental embryos which did have inner cell masses developed comparably to the control group and both groups showed roughly similar numbers of morphologically abnormal egg cylinders. Autoradiography disclosed no deficiency in 3H-thymidine and 3H-uridine labeling in disorganized egg cylinder embryos.

Animals↗
PubMedDate not supplied

Midgestational exposure of pregnant BALB/c mice to magnetic resonance imaging conditions.

The potential for producing reproductive toxicity or teratogenesis in mice by exposure to magnetic resonance imaging (MRI) conditions was evaluated by means of reproduction studies and the homeotic shift test. Embryos from pregnant BALB/c mice were exposed in vivo for 16 hours beginning on gestation day 8.75 to MRI conditions of modest field strength (static field, 0.35 tesla (T); pulsed gradients, 2.3 X 10(-4) T/cm for 2.5 to 10 msec; and radio frequency, 15 MHz at an average of 61.2 mW). Unexposed, sham-exposed (both MRI and X-ray) and X-irradiated (0.5 Gy) animals were the control groups. Neither placental resorptions nor stillbirths were increased by MRI. Fetal weight at birth and crown-rump length were proportional; however, crown-rump length was significantly less (p less than 0.001) in the MRI-exposed fetuses (respective mean values for MRI-exposed fetuses were 21.8 +/- 0.2 mm compared to 22.4 +/- 0.1 for sham-exposed fetuses). Both crown-rump length and fetal weight were significantly reduced after X-irradiation. The percentage of homeotic skeletal shifts was scored for each of eight anatomic sites. Only X-radiation produced significant increases in skeletal shifts. Prolonged midgestational exposure of mice to MRI conditions currently used for human clinical imaging, therefore, failed to reveal overt embryotoxicity (resorptions, stillbirths) or teratogenicity (homeotic shifts), consistent with the non-ionizing properties of MR. However, the slight but significant reduction in fetal crown-rump length after prolonged exposure justifies further study of higher MRI energy levels and consideration of other endpoints for establishing with greater confidence the safety of MRI during pregnancy.

Animals↗
PubMedDate not supplied

Interspecies approaches for the analysis of parental imprinting during mouse development.

Genomic imprinting results in the functional specialization of the maternal and paternal genomes during development whereby offspring inherit only one active copy of a gene. Although the reason for its evolutionary genesis remains speculative, the consequences of genomic imprinting are evidenced by the failure of parthenogenetic and androgenetic development in mammals, and parental-specific effects in the etiology of a number of human diseases. While the precise molecular mechanism of imprinting is unknown, evidence suggests that the specialization of the parental genomes is established during gametogenesis when the parental genomes are epigenetically modified to reflect the parent of origin. To examine the epigenetic modification of specific imprinted genes and subsequent differential expression, an assay is required that can distinguish between the maternal and paternal alleles and their respective transcripts. During the past 5 years several strategies have been used to identify imprinted genes, ranging from the fortuitous disruption of specific parental alleles to subtraction hybridization between cDNAs from normal and parthenogenetic embryos. To study the developmental regulation of these imprinted genes during mammalian development, we describe a relatively simple interspecies "mRNA phenotyping" approach applicable to the analysis of allele-specific expression as well as the identification of candidate imprinted genes.

Animals↗
PubMedDate not supplied

Abnormalities of gaze in cerebrovascular disease.

Disorders of ocular motility may occur after injury at several levels of the neuraxis. Unilateral supranuclear disorders of gaze tend to be transient; bilateral disorders more enduring. Nuclear disorders of gaze also tend to be enduring and are frequently present in association with long tract signs and cranial nerve palsies on opposite sides of the body. Nystagmus is a reliable sign of posterior fossa or peripheral eight nerve pathology. Familiarity with these concepts may help the clinician answer questions regarding localization and prognosis.

Cerebrovascular Disorders↗
PubMedDate not supplied

Mouse embryonic stem (ES) cell lines established from neuronal cell-derived cloned blastocysts.

We have established mouse embryonic stem (ES) cell lines from blastocysts derived by transfer of nuclei of fetal neuronal cells. These neuronal cell-derived embryonic cell lines had properties that characterize them as ES cells, including typical cell markers and alkaline phosphatase activity. Moreover, the cells had a normal karyotype and were pluripotent, as they were capable of differentiating into all three germ layers. Although they were derived from neuronal donor nuclei, the cells no longer expressed neuronal markers; however, they were capable of differentiating into cells with neuronal characteristics. These results suggest that the clone-derived cells have fully acquired an ES cell character. Thus, ES cells can be derived from embryos resulting from nuclear transfer, which results in reprogramming of the genetic information and acquisition of pluripotency. ES cells established from somatic cell-derived blastocysts could be useful not only as research tools for studying reprogramming but also as models for cell-based transplantation therapy.

Alkaline Phosphatase↗