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I Byrne

Publications and source records attributed to I Byrne.

3 recordsLinked to original sources

Pupils' causal attributions for difficult classroom behaviour.

BACKGROUND: Studies of causal attributions within educational contexts have tended to concentrate on academic performance. There have been a smaller number of investigations of teachers' attributions for pupils' behaviour in school. AIMS: The present study examines the causal attribution made by pupils for difficult behaviour in classrooms. It reveals the structure of these attributions and serves as a comparison with the teacher studies. SAMPLE: The participants were 105 pupils (52 males and 53 females) in the first year of secondary schooling, all drawn from the same inner city school. METHOD: Four initial small group interviews were used to identify a wide range of factors that pupils viewed as being causes of difficult classroom behaviour in the 18 primary schools they had previously attended. A questionnaire was then constructed incorporating items from these discussions and administered to the whole of the year group of pupils, but omitting the participants in the initial group discussions. RESULTS: The results of a factor analysis indicated that pupils' attributions for misbehaviour at school were best represented by four factors: (1) 'fairness of teacher's actions', (2) 'pupil vulnerability', (3) 'adverse family circumstances' and (4) 'strictness of classroom regime'. While there were no gender differences, pupils saw the 'fairness of teacher's actions' and 'pupil vulnerability' as more significant contributors to pupil misbehaviour than either 'adverse family circumstances' or 'strictness of classroom regime'. CONCLUSION: The attributions by pupils for difficult classroom behaviour differ markedly from those obtained in studies of teachers. Policy and practice initiatives which do not attend to conflicting attributional styles are unlikely to succeed in improving levels of pupil behaviour in schools.

Child↗

Characterization of a vitamin D3-resistant MCF-7 cell line.

1,25-Dihydroxyvitamin D3 [1,25-(OH)2D3], the active metabolite of vitamin D3, is a potent inhibitor of breast cancer cell growth both in vivo and in vitro. We have previously demonstrated that 1,25-(OH)2D3 induces morphology (pyknotic nuclei, chromatin and cytoplasmic condensation, and nuclear matrix protein reorganization) consistent with the activation of apoptosis in MCF-7 cells. These morphological changes in 1,25-(OH)2D3-treated cells are associated with up-regulation of TRPM-2/clusterin and cathepsin B (genes associated with mammary gland apoptosis) and down-regulation of bcl-2, an antiapoptotic gene. Thus, the inhibitory effects of 1,25-(OH)2D3 on MCF-7 cell growth involve activation of apoptosis. To investigate the mechanisms by which vitamin D3 activates apoptosis, we have selected a vitamin D3-resistant variant (MCF-7D3Res cells) by continuous culture of MCF-7 cells in 100 nM 1,25-(OH)2D3. The MCF-7D3Res cells represent a stably selected phenotype that grows equally well with or without 100 nM 1,25-(OH)2D3. In contrast to the MCF-7 cells from which they were derived (MCF-7WT cells), MCF-7D3Res cells do not exhibit apoptotic morphology, DNA fragmentation, or up-regulation of apoptosis-related proteins after treatment with 1,25-(OH)2D3. MCF-7D3Res cells exhibit cross-resistance to several vitamin D3 analogs that are potent growth regulators of MCF-7WT cells. MCF-7WT and MCF-7D3Res cells exhibit comparable sensitivity to induction of apoptosis and up-regulation of clusterin in response to the antiestrogen 4-hydroxytamoxifen. MCF-7D3Res cells express comparable levels of the vitamin D receptor (VDR), as assessed by Western blotting or ligand binding, as MCF-7WT cells. In both sensitive and resistant cell lines, 1,25-(OH)2D3 up-regulates whereas 4-hydroxytamoxifen down-regulates VDR protein expression, indicating appropriate homologous and heterologous VDR regulation in MCF-7D3Ras cells. Gel shift analyses indicate that nuclear extracts from MCF-7WT and MCF-7D3Res cells bind equally well to the DR3 consensus vitamin D3 response element. These data suggest that MCF-7D3Res cells have a functional VDR that is uncoupled from a functional apoptotic pathway. MCF-7D3Res cells offer a unique model system for identification of the mechanisms by which vitamin D3 regulates the cell death pathway in breast cancer cells.

Apoptosis↗