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Biomedical subjects

I Gray

Publications and source records attributed to I Gray.

58 records · Page 4Linked to original sources
PubMedDate not supplied

Cadmium inhibition of RNA metabolism in murine lymphocytes.

Cadmium, as Cd2+, has become an environmental pollutant of significant proportions. We and others have reported that cadmium in in vitro culture can alter several metabolic parameters including the synthesis of RNA. In the present study, a detailed examination of the mechanism of inhibition was undertaken. Cadmium, at 30 microM, decreased cellular uptake of uridine as well as incorporation into RNA up to 60 microM. Above this concentration, uridine incorporation fell to zero while that associated with the lymphocytes remained at a significantly higher value. LPS caused an increase in the fraction of the precursor incorporated into RNA. In the presence of cadmium, the fraction incorporated by non-stimulated cells fell continually while in the stimulated cells, the fraction had increased at 10 microM above which it dropped until at the highest concentration it was as for the unstimulated lymphocytes. It was found that up to 30 microM the ability of LPS to stimulate the lymphocytes in the presence of cadmium was enhanced while above that concentration it decreased so that at 70 microM no stimulation occurred. Cadmium also inhibited the formation of phosphorylated intermediates from uridine with UTP the most affected and the unstimulated lymphocytes the more sensitive. From the study of the intermediate steps it was found that RNA synthesis was directly inhibited and the most sensitive of the several inhibitory points.

Animals↗
PubMedDate not supplied

Bilateral optic nerve hypoplasia associated with cerebral atrophy.

We present a series of 12 consecutive cases of optic nerve hypoplasia. Eight of these were unassociated with significant CNS malformations; of these, two had tomographic evidence of cerebral atrophy. This represents the first adequately documented cases of isolated cerebral atrophy associated with optic nerve hypoplasia. We discuss the increasing prevalence and marked variability of optic nerve hypoplasia, note the lack of clear distinction between primary failure of differentiation and secondary degeneration of optic pathways, and mention the inadequacy of the classic explanation of primary failure of ganglion cell development as the cause of hypoplastic nerves. The cause of cerebral atrophy are mentioned, and we hypothesize that the wide range of CNS insults resulting in atrophy may be responsible for a correspondingly wide range of abnormalities of the optic nerves. We speculate that cerebral atrophy may result in an inadequate cortical mass for induction of normal optic nerve growth, possibly by decreased retrograde axoplasmic flow and insufficient nerve growth factor. We encourage a complete neurologic evaluation, including CAT scan of the brain, in children with optic nerve hypoplasia.

Adolescent↗
PubMedDate not supplied

Mobius syndrome and limb abnormalities.

Most ophthalmologists are aware of the cranial nerve dysfunctions that have been associated with the facial diplegias of Mobius syndrome. However, many are not aware of the combined limb deficiencies and cranial nerve dysfunctions. Limb malformations have been associated with a spectrum of oral facial anomalies consisting of micrognathia, hypoglossia, microstomia, hypodontia, oral bands, and dysarthria. It has been suggested that the differences which exists between these entities may in fact represent a common etiology. The variability may be related to an intrauterine insult at slightly different times. The oral-facial anomalies associated with absence of limbs or of limb anomalies suggests a correlation between the limbs and the first visceral arch possibly within the second month of gestation.

Abnormalities, Multiple↗