Biomedical subjects

Peter E Bryant

Publications and source records attributed to Peter E Bryant.

3 recordsLinked to original sources

PubMed2005

Object-centred spatial reference in 4-month-old infants.

An appreciation of object-centred spatial relations involves representing a 'within-object' spatial relation across changes in the object orientation. This representational ability is important in adult object recognition [Biederman, I. (1987). Recognition-by-components: A theory of human image understanding. Psychological Review, 94, 115-147; Marr, D., & Nishihara, H. K. (1978). Representation and recognition of the spatial organisation of three-dimensional structure. Proceedings of the Royal Society of London, Series B (Biological Sciences), 200, 269-294; Tarr, M. J., & Pinker, S. (1990). When does human object recognition use a viewer-centred reference frame? Psychological Science, 1, 253-256] and is also thought to be a fundamental component of the mature object concept [Piaget, J. (1954). The Construction of Reality in the Child. Routledge & Kegan-Paul: London, UK. (Originally published in French in 1937)]. An experiment is reported in which eighteen 4-month-old infants were familiarised to a specific spatial relation within an object, across six different orientations of the object. On subsequent test trials the object was presented to the infants in an entirely novel orientation. Between successive test trials the within-object spatial relation was alternated between novel and familiar. The infants demonstrated significant sensitivity of their looking to both the novelty of the stimuli and the order in which novel and familiar stimuli were presented. It is concluded that by 4 months of age infants are able to form object-centred spatial frames of reference. These findings are discussed in the light of our current understanding of the development of object representation during infancy.

Attention↗

PubMed2004

Repair and chromosomal damage.

Chromosomal aberrations in somatic cells link DNA damage with radiation-induced cell killing and individual susceptibility to oncogenesis, and are also potential markers of cancer susceptibility. While there is general acceptance that the DNA double-strand break (DSB) is the principal initiating lesion the complexity of the relationship between the induced frequency and the rates of repair and misjoining of DSB, and the production of chromosome and chromatid aberrations has led to much controversy. The principal models of chromosome aberrations are: the classical 'breakage-and-reunion' or 'breakage-first' model of Sax [Genetics 25 (1940) 41-68], the 'mis-recombination' model of Chadwick and Leenhouts [Mutat Res 404 (1998) 113-117] and the 'transcription-based' model of Radford [Int J Radiat Biol 78 (2002) 1081-1093]. Chromatid aberrations have also been variously interpreted on the 'breakage-first model', Revell's 'exchange' model [Proc R Soc B 150 (1959) 563-589] and the 'signal' model [Int J Radiat Biol 73 (1998) 243-251]. Recent evidence argues strongly for different mechanisms for chromosome (formed in G1 or Go) and chromatid (formed in G2) aberrations, i.e. there is little or no correspondence in the relative frequencies between chromosome and chromatid aberrations. The balance of evidence indicates that chromosome aberrations may be formed by a breakage-first type mechanism. Elevated frequencies of chromosomal aberrations occur to various extents in cell lines mutated in genes involved in both non-homologous DSB end-joining and homologous recombinational rejoining of DSB. Chromatid breaks, seem to be formed by a more complex mechanism since there is a lack of correspondence between the rates of DSB rejoining and chromatid break 'disappearance' (assumed by some to represent DSB repair). Thus, a model based on the dissociation of DSB rejoining from chromatid break rejoining is required to explain these data. A substantial proportion (approximately 20%) of both spontaneous and induced chromatid breaks visibly involve inter-chromatid rearrangements (determined using harlequin staining of chromatids). It is postulated that the remaining proportion may also involve rearrangements, but within a single chromatid (i.e. intra-chromatid rearrangements). Disappearance of chromatid breaks with time is postulated to result from the completion of rearrangements, i.e. rather than simply from repair of DSB.

Cells, Cultured↗

PubMed2003

Induction of chromatid breaks by carbon K-shell ultrasoft X rays.

Chromatid breaks have previously been shown to be induced in G2-phase cells after exposure to ionizing radiation (X and gamma rays) as a linear function of dose, consistent with a single-event mechanism. DNA double-strand breaks (DSBs) are thought to be the initiating lesion, and experiments with a genetically engineered cell line containing a single DSB site also indicate that a single DSB is sufficient to induce a chromatid break. Although the precise mechanism of conversion of an isolated DSB into a chromatid break is not yet understood, it is known that a proportion of chromatid breaks result from rearrangements between sister chromatids. Here we report further evidence for the single-event hypothesis for the formation of chromatid breaks. The evidence derives from experiments in which chromatid breaks have been induced by exposure of Chinese hamster cells to ultrasoft carbon K-shell X rays. Since the energy of carbon K-shell X rays is not sufficient for the secondary electrons to span more than one DNA double helix, we conclude that single traversals, and hence single (complex) DSBs, are responsible for the formation of chromatid breaks. We find that, as for 60Co gamma rays, around 10% of the carbon K-shell X-ray-induced chromatid breaks have associated color switches at breakpoints, indicating that they arise through sister chromatid rearrangements.

Animals↗