Unresponsiveness of bone to PTH in aluminum-related renal osteodystrophy.
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Biomedical subjects
Publications and source records attributed to R Shoji.
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Induction of artificial fission of the inner cell mass in an in vitro embryonal culture system was attempted. Mouse blastocysts were collected from uteri on day 3 of gestation and exposed to vinblastine sulfate after removal of zona pellucida. Embryos in the control group had a single inner cell mass on the trophectoderm and developed to the postblastocyst stage. On the other hand, the inner cell masses of the embryos in experimental groups subdivided into two or more. The present results, therefore, revealed that the vinblastine treatment at the blastocyst stage induced fission of the inner cell mass in mouse embryos. Further studies are planned in improved culture conditions to determine whether each inner cell mass subdivision develops into independent embryos.
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In our search for a simplified in vitro test system to assess the teratogenic effects of physical factors, we studied the effects of total maternal body X-irradiation on aggregation patterns of enzymatically isolated fetal rat brain cells and on ultrastructural aggregate changes. The fetal brain cells were derived from day 14 gestation fetuses of pregnant Sprague-Dawley (CD strain) rats exposed to X-irradiation (25 - 200 R) one hour prior to sacrifice. Notable changes in the cell aggregates following X-irradiation included a reduction in cell aggregate size and an increase in number. The frequency of cell aggregates was higher in the treated than in the control group, and the mean diameter of cell aggregates was inversely related to increasing X-irradiation doses. Transmission electron microscopy revealed in isolated cells features of degenerative process which were similar to those found in intact fetal brain lesions caused by maternal X-irradiation. Furthermore, scanning electron microscopy revealed that inhibition of cell aggregation following X-irradiation could probably be attributed to inhibition of membrane filopodia development and a consequent failure fo cell aggregates to fuse into a greater cell aggregate mass. These results suggest that the membrane factors which influence cell aggregation may be a useful parameter to assess early effects of X-irradiation-induced brain deformity. Presently, the cell aggregation culture system is being further evaluated as a short term test system for environmental teratogens.
1. Rats were irradiated by 200 R of X ray on day 17 (the 18th day) of gestation through the body wall of the mother. When they underwent the following electrophysiological tests at the age of 3-4 mo, the somatosensory cortex showed a lack of layers II, III, IV, and Va, as described by previous investigators (3, 4). 2. Spike responses to quick whisker deflections were recorded from single cells in the somatosenory cortex of normal and prenatally X-irradiated rats. 3. In normal animals, single units often responded to several whiskers, but the magnitudes (response latency and firing probability) of the responses were graded around a whisker in the "center" of the field that gave rise to the strongest response. During electrode penetration perpendicular to the cortical surface, such a center remained unchanged or shifted to another whisker that was immediately adjacent. As for the large-sized, initially positive unitary spikes (typically 2 mV or higher) sampled in this study, no systematic change in the response latency, the size of receptive field, or response probability was detected during the penetration. 4. The above description holds also for the irradiated rats except that the response latency was prolonged when compared to the normal controls. 5. Cortical laminar analysis of field potentials revealed that while the earliest electric sink appeared in layer IV in the controls, that in the irradiated rats was observed in layer Vb. However, there was no difference in the latency of these potentials between the two groups, suggesting that vibrissal sensory signals reach the cortical level normally even in the irradiated rats. The prolonged latency of the irradiated cortical neuronal response could thus be ascribed to an abnormal intracortical delay, which was most likely associated with the failure of development of layer IV stellate cells in these preparations. 6. A possibility as to how the layer IV stellate cells are involved in input-output relationships in the normal somatosensory cortex is presented and discussed.