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Your search keyword '"Byrne, Anne-Marie"' showing total 23 results
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23 results on '"Byrne, Anne-Marie"'

10. Education for juvenile offenders - process and experience in an Irish detention school

Author

Byrne, Anne Marie and Byrne, Anne Marie

Abstract

One of the little known areas relating to education in Ireland is the area of young offenders who are held in detention schools as a result of a criminal conviction. The rationale for this research is to bring focus onto a closed system of education, thereby giving representation to a marginalised sector of educationally disadvantaged children in Ireland. The issues that arise from the intersecting systems of criminalisation and of education are explored and discussed in terms o f inequality, education, and confinement and with reference to the international experience o f best practice. The theoretical framework for this thesis draws upon the theories of Michel Foucault and Pierre Bourdieu, particularly in relation to power, discipline, capitals and habitus. Their theorisation of these concepts provide useful lenses through which to examine the history of detention and schooling, the educational processes involved in detention schools, the educational experiences and the classed identities of the children incarcerated in them. Using mixed methods, which include classroom observations and semi-structured interviews, the research takes a phenomenological approach, giving voice to the boys who are held in detention schools. It examines how the educational process in a detention school operates in terms of curriculum, teaching methodologies and forms of assessment, to establish the ways in which the educational engagement of boys in detention schools shapes their future outlooks and life chances. Tensions between criminalisation o f young people, confinement, education rights and provision are made explicit. The phenomenon that most of the children in detention come from communities that are socio-economically under-resourced is explored. The findings reveal that the children in detention schools had low levels of educational engagement prior to detention mainly due to absenteeism and failing to make the transition from primary to second-level school. They shared low s

Published
2014

12. Mo1930 Beneficial Effect of Ursodeoxycholic Acid (UDCA) and Its Derivative UDCA-Cpa in Attenuation of Functional Impairment of Esophageal Mucosa in Rat Model of Barrett's Esophagus

Author

Majka, Jolanta, primary, Pabianczyk, Rafal, additional, Krzysiek-Maczka, Gracjana, additional, Ptak-Belowska, Agata, additional, Kwiecien, Slawomir, additional, Byrne, Anne-Marie, additional, Kelleher, Dermot P., additional, Gilmer, John, additional, and Brzozowski, Tomasz, additional

Published
2013
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22. Unconjugated secondary bile acids activate the unfolded protein response and induce golgi fragmentation via a src-kinase-dependant mechanism.

Author

Sharma R, Quilty F, Gilmer JF, Long A, and Byrne AM

Subjects
Bile Acids and Salts metabolism, Cell Line, Tumor, Endoplasmic Reticulum drug effects, Endoplasmic Reticulum metabolism, Endoplasmic Reticulum Chaperone BiP, Endoplasmic Reticulum Stress drug effects, Esophageal Mucosa metabolism, Humans, Models, Biological, Signal Transduction drug effects, Unfolded Protein Response genetics, eIF-2 Kinase metabolism, Bile Acids and Salts pharmacology, Golgi Apparatus drug effects, Golgi Apparatus metabolism, Unfolded Protein Response drug effects, src-Family Kinases metabolism
Abstract

Bile acids are components of gastro-duodenal refluxate and regarded as causative agents in oesophageal disease but the precise mechanisms are unknown. Here we demonstrate that a specific subset of physiological bile acids affect the protein secretory pathway by inducing ER stress, activating the Unfolded Protein Response (UPR) and causing disassembly of the Golgi apparatus in oesophageal cells. Deoxycholic acid (DCA), Chemodeoxycholic acid (CDCA) and Lithocholic acid (LCA) activated the PERK arm of the UPR, via phosphorylation of eIF2α and up-regulation of ATF3, CHOP and BiP/GRP78. UPR activation by these bile acids is mechanistically linked with Golgi fragmentation, as modulating the UPR using a PERK inhibitor (GSK2606414) or salubrinal attenuated bile acid-induced effects on Golgi structure. Furthermore we demonstrate that DCA, CDCA and LA activate Src kinase and that inhibition of this kinase attenuated both bile acid-induced BiP/GRP78 expression and Golgi fragmentation. This study highlights a novel mechanism whereby environmental factors (bile acids) impact important cellular processes regulating cell homeostasis, including the UPR and Golgi structure, which may contribute to cancer progression in the oesophagus.

Published
2017
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23. Ursodeoxycholic acid amides as novel glucocorticoid receptor modulators.

Author

Sharma R, Prichard D, Majer F, Byrne AM, Kelleher D, Long A, and Gilmer JF

Subjects
Amides pharmacology, Binding Sites, Binding, Competitive, Cell Line, Tumor, Dexamethasone metabolism, Dexamethasone pharmacology, Esophageal Neoplasms, Fluorescence Resonance Energy Transfer, Glucocorticoids metabolism, Glucocorticoids pharmacology, HEK293 Cells, Humans, Ligands, Models, Molecular, NF-kappa B metabolism, Protein Transport, Radioligand Assay, Receptors, Glucocorticoid agonists, Receptors, Glucocorticoid genetics, Response Elements, Structure-Activity Relationship, Transcriptional Activation, Tumor Necrosis Factor-alpha pharmacology, Ursodeoxycholic Acid pharmacology, Amides chemical synthesis, Receptors, Glucocorticoid metabolism, Ursodeoxycholic Acid analogs & derivatives, Ursodeoxycholic Acid chemical synthesis
Abstract

Ursodeoxycholic acid (UDCA) is used for the treatment of hepatic inflammatory diseases. Recent studies have shown that UDCA's biological effects are partly glucocorticoid receptor (GR) mediated. UDCA derivatives were synthesized and screened for ability to induce GR translocation in a high content analysis assay using the esophageal cancer SKGT-4 cell line. UDCA derivatives induced GR translocation in a time dependent manner with equal efficacy to that of dexamethasone (Dex) and with greatly increased potency relative to UDCA. The cyclopropylamide 1a suppressed TNF-α induced NF-κB activity and it induced GRE transactivation. 1a was unable to displace Dex from the GR ligand binding domain (LBD) in a competition experiment but was capable of coactivator recruitment in a time-resolved fluorescence energy transfer assay (TR-FRET). This represents a novel mechanism of action for a GR modulator. These derivatives could result in a new class of GR modulators.

Published
2011
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