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Biomedical subjects

E Crawford

Publications and source records attributed to E Crawford.

11 recordsLinked to original sources
PubMed1990

Three genes under different developmental control encode elongation factor 1-alpha in Xenopus laevis.

We have cloned cDNAs encoding two variants of the elongation factor for protein synthesis in Xenopus laevis, called EF-1 alpha. One of these (42Sp50) is expressed exclusively in immature oocytes. It is one of two protein components of a 42S RNP particle that is very abundant in previtellogenic oocytes. The 42S RNP particle consists of various tRNAs, 5S RNA, 42Sp50 and a 5S RNA binding protein (42Sp43). A major function served by 42Sp50 appears to be the storage of tRNAs for later use in oogenesis and early embryogenesis. The second EF-1 alpha variant (EF-1 alpha O) is expressed mainly in oocytes but transiently in early embryogenesis as well. Its mRNA cannot be detected after neurulation in somatic cells. EF-1 alpha O is closely related to a third EF-1 alpha (EF-1 alpha S), discovered originally by Krieg et al. (1). EF-1 alpha S is expressed at low levels in oocytes but actively in somatic cells. The latter two proteins are very similar to known eukaryotic EF-1 alpha from other organisms and presumably function in their respective cell types to support protein synthesis.

Amino Acid Sequence↗
PubMed1987

Risk versus motivation: the emergency room treatment of attempted suicide.

This paper deals with patients who attempt suicide, focusing on their evaluation in the emergency room. It is suggested that as the actual risk of completed suicide in suicide attempters is low, the evaluating psychiatrist might preferentially focus on assessing the patient's motivation for self-destructive behaviour. Recent studies are reviewed which demonstrate a linkage between self-destructive acts and the status of relationships with significant others. An illustrative case history is presented.

Adult↗
PubMed1977

The repair of X-ray induced chromosomal damage in trisomy 2-and normal diploid lymphocytes.

The frequency of chromosomal aberrations produced by X-rays is greater in lymphocytes cultured from trisomy 21 patients (Down's syndrome) than from normal diploid donors. This increase, which can be detected by a micronucleus assay for chromosomal damage, was postulated by us to result from a defect in the rejoining system which repairs chromosomal breaks. The postulated defect would result in a longer rejoining time, therapy permitting more movement of broken ends and thus enhancing the frequency of exchanges. To test this possibility, the time required for the rejoining (repair) of chromosome breaks was measured in lymphocytes from five Down's syndrome (four trisomy 21 and one D/G translocation partial trisomy 21) donors, from a monosomy 21 donor, and from five diploid donors. The rejoining time was reduced in the Down's syndrome lymphocytes in comparison to the normal diploid and monosomy 21 lymphocytes. Thus the repair of chromosome breaks, far from being defective as evidenced by a longer rejoining time in Down's syndrome cells, occurred more rapidly than in normal cells. A mechanism is proposed by which reduced rejoining times would increase aberration frequencies as a consequence of competition between a (hypothetical) error-free repair system and the error-prone repair system that generates chromosomal aberrations. We suggest that the alteration in the rejoining of chromosomal aberrations may underlie the increased susceptibility of people with Down's syndrome to leukemia.

Cells, Cultured↗