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3. Royal Academy of Medicine in Ireland section of biological sciences Proceedings of Summer Meeting held at University of Ulster at Jordanstown, 22nd & 23rd June, 1990

Author

Allen, J. M., Shanab, A. A. Abu, Guthrie, D. J. S., Irvine, G. B., Walker, B., Bristow, H. E., Strain, J. J., Welch, R. W., Crotty, T. P., Kernan, R. P., Kearns, J. B., Hall, W. J., Cornell, D. P., Hall, W. J., O’Connell, D. P., Hooper, A. C. B., Doyle, J., O’Mahony, P., Murray, P., Farmer, M. F., Cresswell, M. J., Strain, J. J., Pórszász, J., Andrews, J. F., Kelly, M., Donne, B., Kelly, A., Szekely, M., Norris, L. A., Carroll, M. E., Bonnar, J., Sharma, S. C., Sheppard, B. L., Bonnar, J., Strain, J. J., Thompson, K. A., Shephard, R. A., Doran, M. A., Faulkner, A., Macartney, L. R., Keenan, M., Shields, T. D., Hannigan, B. M., Eason, S. J., Allen, J. M., Gillmore, W. S., Baxter, G. D., Bell, A. J., Allen, J. M., Ravey, J., McLoughlin, C. C., Mirakhur, R. K., Trimble, E. R., McCarthy, G. J., Carke, R. S. J., McCarthy, G., Mirakhur, R. K., McLoughlin, C. C., Elliott, P., McKinney, M. S., Clarke, R. S. J., Dundee, J. W., Yang, J., McMillan, C., McGeeney, K. F., Kelly, D., Fitzpatrick, J. M., McGuinness, N., Anwyl, R., Lee, T. C., Horner, E. B., Phillips, J. P., O’Brien, M., Lennon, G. M., Ryan, P. C., Gorey, T. F., Fitzpatrick, J. M., Hill, A. D. K., Folan-Curran, J., Richardson, S. A., Hannigan, B. M., McKenna, P. G., Cromie, E., Hannigan, B. M., Ranjbar, S., Briscoe, A., O’Neill, K. L., Bristow, H. E., Strain, J. J., Welch, R. W., McKenna, P. G., Tully, G. W., Grant, O., Daly, J. G., Russell, C. J., Tully, G. W., Stewart, A., Allen, J. D., Adgey, A. A. Jennifer, Nolan, P., McKeogh, D., Bradford, A., O’Regan, R. G., Nicholson, P., Hooper, A. C. B., Gaynor, S., Anwyl, R., Boyle, C., Shepard, B. L., Gleeson, N., Bonnar, J., Cahill, M., Murphy, E., McDonagh, P. D., White, M., Phelan, D., Murphy, N., McDonagh, P., Billet, J., Blunnie, W. P., Bradford, A., O’Regan, R. G., Pettersson, K., Dundee, J. W., Yang, J., McMillan, C., Wilson, N. E., Meert, T. F., Wubetu, Tayech, Meban, C., McGlone, E., Halliday, I., Blair, P., Rowlands, B. J., Tully, G. W., O’Neill, K. L., Bailie, K. E. M., Bridges, J. M., McKenna, P. G., Wilkinson, Y. A., Thompson, C. C. M., Amara, F. M., Ward, P. E., McKenna, P. G., Moore, G. W., Strain, J. J., Livingstone, M. B. E., Thumham, D. I., Nevin, G. B., Hannigan, B. M., McKenna, P. G., O’Neill, K. L., McKelvey, V. J., Monteverde, H., Logan, H., Abram, W. P., McKenna, P. G., Lennon, G. M., Nolan, C. P., Ryan, P. C., Sheehan, S. J., Gorey, T. F., Fitzpatrick, J. M., Heatley, M. K., Whiteside, C., Maxwell, P., Watt, P. C. H., Heatley, M. K., White, J., Whitside, C., Maxwell, P., Watt, P. C. H., O’Shea, Yvonne, and Dunne, Adrian

Published
1991
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4. Royal Academy of Medicine in Ireland Section of Biomedical Sciences: Proceedings of Summer Meeting held June 22nd–23rd, 1999

Author

Glasgow, P. D., Hill, I. D., Baxter, G. D., Allen, J. M., Cramp, A. F. L., Noble, J. G., Lowe, A. S., Walsh, D. M., Ryan, S., O’Regan, R. G., McNicholas, W. T., Nolan, P., Corkery, P. P., Leek, B. F., Carroll, O., O’Cuinn, G., Keane, F. M., Clarke, C. R., Robson, T., McKeown, S. R., Moore, S. D., Hirst, D., Sergeant, G. P., Hollywood, M. A., McHale, N. G., Thornbury, K. D., McCloskey, K. D., Magee, P. J., Barnett, C. R., Downes, C. S., Humphrey, R., McGuigan, A., Hutchinson, C., Hannigan, B. M., Saleshando, G., O’Connor, J. J., Curran, B. P., O’Neill, L. A. J., Kerrigan, S. W., Quinn, M., Fitzerald, D. J., Cox, D., Dunne, E. M., Herron, C. E., O’Loinsigh, E., Boland, G., O’Boyle, K. M., Cullen, V. C., Mackarel, A. J., O’Connor, C. M., Keenan, A. K., Cannon, D. M., McBean, G., Baird, A. W., Frizelle, H. P., Moriarty, D. C., McGuire, M., Bradford, A., Ryan, J. P., Quinn, T., Walker, M. D., Hirst, D. G., Hurley, D. A., McDonough, S. M., Moore, A., Lagan, K. M., Dusoir, A. E., Wilson, S., Sweeney, C., Curtis, T. M., Scholfield, C. N., O’Connor, S., Kilbride, E., McLoughlin, P., Gallagher, C. G., Harty, H. R., and Gormley, B. -A.

Published
1999
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5. Royal academy of medicine in Ireland section of biomedical sciences: Proceedings of meeting held Thursday & Friday 26th, 27th June, 1997 in University of Limerick

Author

MacDonncha, C., Watson, A. W. S., Jakeman, P. M., Welsh, L. J., McGrath, S., Watson, A. W. S., Ooi, H., Brady, H. R., O’Regan, R. G, McLoughlin, P., Cantillon, D., Bradford, A., Deacy, C., Garrett, M., Lowe, A. S., Baxter, G. D., Walker, M. D., Hirst, D. G., Kennovin, G. D., Leek, M., Watson, A. W. S., MacDonncha, C., Watson, A. W. S., Watson, A. W. S., Robinson, J., Hill, I. D., Baxter, G. D., Allen, J. M., Black, A. J., Baxter, G. D., Hughes, S., Bell, A. L., Orr, G., McDonagh, S., Baxter, G. D., Baker, R., Cadogan, E., Hopkins, N., O’Regan, R. G., McLoughlin, P., Lynch, F., O’Regan, R. G., McLoughlin, P., Nolan, Y. M., Connor, T. J., Kelly, J. P., Leonard, E., Shen, Y., Redmond, A. M., Kelly, J. P., Leonard, B. E., Connor, T. J., McNamara, M. G., Finn, D., Currid, A., O’Malley, M., Redmond, A. M., Kelly, J. P., Leonard, B. E., Healy, D. G., Kelly, J. P., Leonard, B. E., Walker, M. D., Lowe, A. S., Hirst, D. G., Kennovin, G. D., Leek, M., Cullen, V. C., Wilson, S., Love, G., Keenan, A. K., O’Hagan, B., Murray, D., Dooley, J. S. G., McKerr, G., Allen, J. M., Doyle, P., Healy, D. G., Kelly, J. P., Leonard, B. E., Hanna-Mitchell, A. T., Gebruers, E. M., Hill, I. D., Robinson, J., Baxter, G. D., Allen, J. M., Leonard, M., Ryan, M. P., Healy, E., Keane, T., Healy, E., Ryan, M. P., Egan, D., Dempsey, M., Healy, E., Ryan, M. P., Kelleher, S., Keenan, A. K., Esfandiary, H., Gilmore, W. S., Allen, J. M., Hannigan, B. M., Al-Assar, O., Robson, T., McKeown, S. R., and Hirst, D. G.

Published
1998
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6. Royal Academy of Medicine in Ireland Section of Biomedical Sciences

Author

Ruddock, W., Burns, D. M., Brown, J. C. W., Allen, J. M., Hirst, D. G., Love, G. P., Keenan, A. K., Lally, C., Bird, A., Ryan, M. P., O’Connor, N., O’Boyle, K. M., McGeown, J. G., McCarron, J. G., Drummond, R. M., Fay, F. S., Connor, T. J., Kelly, J. P., Leonard, B. E., Gilmartin, L., O’Cuinn, G., MacDonncha, C., Watson, A. W. S., McGrath, S., Brady, K. J., McKillen, H-C., Taylor, C. W., Smith, S. K., Thornton, S., Martin, A. D., Bailie, J. R., McKeown, S. R., Higgins, C. A., Hatton, W. J., McKerr, G., Harvey, D., Carson, J., Hannigan, B. M., Morrow, D. M. P., McGlynn, H., Thompson, C. M. G., Higgins, C., Galligan, E. S., Murray, M. M., Leckey, J. L., Nevin, G. B., Soppitt, D. S., Esfandiary, M. H., Gilmore, W. S., Robson, T., Dineen, T., Greer, A., Houghton, J. A., O’Halloran, K. D., Bradford, A., McGuire, M., MacDermott, M., Coogan, A., O’Connor, J. J., Regan, C. S., Redmond, A. M., Harkin, A., Lowe, A. S., Baxter, G. D., Kennovin, G. D., Leek, M., Friery, O. P., Hejmadi, M. V., Patterson, L. H., Robinson, J., Hill, I., Kilbride, J., Cotton, K. D., Hollywood, M. A., McHale, N. G., Thornbury, K. D., Halligan, C. P., O’Connell, D. P., Harvey, B. J., Fanning, P., O’Farrell, A., Cantillon, D., Cryan, J. F., O’Leary, D., O’Malley, D. T., Nolan, A., Moran, A. P., Fitzgerald, K. A., O’Neill, L. A. J., McElligott, A., Baker, A. H., Joyce, K. M., Ruane, T., Hall, W. J., Markos, F., Carey, M. F., Galvin, C., Perl, E. R., Curran, A. K., Connolly, C., Abdullah, K., Docherty, J. R., Gavin, K. T., Browne, M., Frazer, C-A., Walsh, D. M., Atkinson, S., Brown, D., O’Connor, J. M., Wasson, G. R., Bonham, M. P., McKelvey-Martin, V. J., Strain, J. J., Downes, C. S., Dineen, T. M., Powell, R., Van Hemelrijk, B., Abujaffom, T. Mubarak, Caulfield, B., Garrett, M., Brennan, L., Griffin, M. J., McShane, A. J., Convery, P. N., Milligan, K. R., Quinn, P., Scott, K., Fee, J. P. H., Cashman, M., Dunne, A., Healy, E., Walsh, J., Watson, A. J., Walsh, D. M., Noble, G., Baxter, G. D., Allen, J. M., Campion, D. P., Leek, B. F., Ryan, J. P., Quinn, T., Dumbleton, M., Smith, K. M., McGrath, J. C., Macmillan, J. B., Doherty, L., Lynch, F., Sweeney, M., O’Regan, R. G., McLoughlin, P., Padua, R. A., Dudeney, S., O’Byrne, J., Moran, R., O’Kelly, K. U., McCormack, B. A. O., Lyons, C. G., Brady, C. L., Simms, C., Maher, S., Schreiber, B., Taylor, D., Carr, A. J., Higgins, B., Dempsey, G. J., Imam, S. Z., Harbinson, M., Adgey, A. A. J., Anderson, J., Aodha, S. Ní, Wilcox, D., Rice, J., Jenkinson, A., O’Rourke, K., O’Brien, T., Devitt, A., McCormack, D., Ikadi, Y., Quinlan, W., Noelke, L., McMahon, G. T., Mulville, J. P., Lee, T. C., Rizvi, A., Fitzpatrick, D., McCarthy, M. A., McGloughlin, T., Monaghan, J., Shine, J., Arendt, E., Lew, B., Lewis, J., Kelly, P. A., Lennon, A. B., Hill, R. G., Dunne, N. J., Thompson, C., Orr, J. F., Beverland, D. E., Prenderville, T., Prendergast, P. J., Huiskes, R., Søballe, K., Mukunda, M. C., Kelly, C. J., Cregg, N., Leahy, A., Dwyer, R., Watson, R. G. K., Bouchier-Hayes, D. J., O’Boyle, C. J., Murchan, P., Mitchell, C. J., Macfie, J., Delicata, R. J., Davies, E. V., Lloyds, D., Petitt, E. J., Carey, P. D., Buckley, D. J., Riordain, M. G. O., Barry, T., Gorey, T. F., Fitzpatrick, J. M., Rothwell, J., Flaherty, J., Wilson, G., Walsh, T. N., Hennessy, T. P. J., O’Donoghue, J., Panchal, J., Mehdi, S., O’Sullivan, S. T., O’Shaughnessy, M., O’Connor, T. P. F., Cox, M. A., Dingle, J. T., Flavin, B. M., Regan, M. C., and O’Connell, P. R.

Published
1997
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7. Royal academy of medicine in ireland section of biomedical sciences: Proceedings of summer meeting held june 1995

Author

Mescall, F. M., Kane, M. T., Keyes, W. M., Quinlan, L. R., Hynes, A. C., Kane, M. T., Jordan, F. M., Hynes, A. C., McGarvey, C., Kelly, J. P., O’Donnell, J. M., Kelliher, P., O’Donnell, J. M., Cotton, K. D., Hollywood, M. A., Thornbury, K. D., McHale, N. G., Curran, A. K., O’Halloran, K. D., Bradford, A., O’Rourke, M., Docherty, J. R., Brady, G., Lyall, P., Felle, P., Fanning, P., O’Boyle, K. M., Cummins, M., Naughton, Y., Ryan, M. P., Clarke, H., O’Connell, C., McNamara, B., Cuffe, J., O’Sullivan, G., Harvey, B., Urbach, V., Leguen, I., Butt, G., MacDonncha, C., Watson, A. W. S., Aherne, A. M., Vaughan, C. J., Murphy, M. B., O’Connell, D. P., Walsh, D. E., Harvey, B. J., Connor, T. J., Kelly, J. P., Leonard, B. E., Wrynn, A. S., Earley, B., Harkin, A. J., Cassidy, E. M., O’Connor, J. J., Brayden, D. J., Dunne, J. F., Baird, A. W., McCole, D. F., Newsholme, P. N., Love, G. P., Keenan, A. K., Doolan, C. M., Higgins, M. A., Higgins, T., Horwitz, E., Reidy, D., Redmond, A. M., McNamara, M. G., Maginn, M., Tamate, K., Charleton, M., Leavy, J., Nolan, A., Egan, D., Gosling, J. P., Fottrell, P. F., Kane, M., Murphy, N., Long, M., Fitzgerald, D., O’Fegan, P., O’Doherty, A., Forde, T., Molloy, G., Dawson, M. A., Maher, M., Houghton, J. A., Mccole, J. C., Moran, A. P., O/rsmalley, D. T., Helander, I. M., Lindner, B., Callaghan, G. A., Mcclorey, M. B., Hannigan, B. M., Gilmore, W. S., Allen, J. M., Whelton, H. J., Dowdall, D., Dawson, M., Smith, T., Whelton, H., O≿doherty, A., Mccusker, J., Joyce, K. M., Mlay, P., Leek, B. F., Clements, B. A., Grimes, F., Walsh, D. M., Baxter, G. D., Toussi, H., Lagan, K. M., and Ashford, R.

Published
1996
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8. Royal academy of medicine in ireland section of biomedical sciences: Proceedings of winter meeting 1995

Author

Galligan, E., Al-Assar, O., McIntyre, I. A., McKeown, S. R., Hollywood, M. A., Thornbury, K. D., McHale, N. G., Keenan, A. K., Gierschik, P., Nelson, A. A., McKenna, P. G., Barnett, Y. A., Curran, A. K., O’Halloran, K. D., Bradford, A., O’Haloran, K. D., Curran, A. K., Bradford, A., Kent, A., Keenan, A. K., Redrobe, J. P., Kelly, J. P., Leonard, B. E., Chambers, P. L., Ryan, P. M., Kelly, J. P., Leonard, B. E., Chambers, P. L., Redmond, A. M., Kelly, J. P., Leonard, B. E., McNamara, M. G., Kelly, J. P., Leonard, B. E., McShane, A. J., Tobin, E., Smith, T., Fox, G. B., Kennedy, N., Regan, C. M., O’Farrell, F. J., Hannigan, B. M., Barnett, Y. A., Walsh, I. K., Johnston, S. R., McKelvey-Martin, V. J., McKeown, S. R., McAleer, J. J. A., O’Halloran, K. D., Curran, A. K., Bradford, A., Curran, A. K., O’Halloran, K. D., Bradford, A., O’Regan, R. G., Kelly, J. P., Leonard, B. E., Mullen, A. M., Earley, B., Leonard, B. E., O’Neill, J., O’Connor, J. J., Moynagh, P., O’Neill, L. A. J., Kelly, J. A., Keenan, A. K., McHale, N. G., Gierschik, P., Browne, I., Gavin, K., Docherty, J. R., Smith, K., Gavin, K., Docherty, J. R., Cawley, T., Docherty, J. R., Geraghty, J., Osborne, H., Hyland, P. L., McKinney, M. W., McKenna, P. G., Barnett, Y. A., McKeown, S. R., Hejmadi, M. V., McAleer, J. J. A., Patterson, L. H., Sweeney, M., McLoughlin, P., O’Donnell, M. D., McGeeney, K. F., and Cottell, D. C.

Published
1995
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9. Irish Association for Cancer Research: Proceedings of annual scientific meeting held at Kinsale on April 15–16th, 1994

Author

Lawler, M., Locasciulli, A., Bacigalupo, A., Humphries, P., Ljungman, P., McCann, S. R., Nolan, N., McDermott, E. W., Reynolds, J. R., McCann, A., Rafferty, R., Sweeney, P., Carney, D., O’Higgins, N. J., Duffy, M. J., Gardiner, C., Reen, D. J., O’Connell, M. A., Kelleher, D., Hall, N., O’Neill, L. A. J., Long, A., McCarthy, J. V., Fernandes, R. S., Cotter, T. G., Ryan, E., Kitching, A., MacMathuna, P., Mulligan, E., Merriman, R., Dervan, P., Kelly, P., Gorey, T. F., Lennon, J. R., Crowe, J., Bennett, M. A., Kay, E. W., Curran, B., O’Donoghue, D. P., Leader, M., Croke, D. T., O’Connor, J. M., McKelvey-Martin, V. J., McKenna, P. G., O’Riordan, J. M., Tobin, A., O’Mahoney, M., Keogh, F. M., O’Riordan, J., McNamara, C., McEneaney, P., Daly, P. A., Farrell, M., Young, S., Gibbons, D., McCarthy, P., Mulcahy, H., Parfrey, N. A., Sheahan, K., Lambkin, H., Mothersill, C., Chin, D., Sheehan, K., Kelehan, P., Parfrey, N., Morrin, M., Khan, F., Delaney, P., Rowan, D. M., Orminston, W. J., Donnellan, P. P., Khalid, A., Kerin, M., O’Hanlon, D. M., Kent, P., Given, H. F., Kennedy, S. M., McGeoch, G., Spurr, N. K., Barrett, J., O’Sullivan, G., Collins, J. K., Willcocks, T., Kennedy, S., Dolan, J., Gallagher, W., McDermott, E., O’Higgins, N., Hagan, R., McManus, R., Ormiston, W., Daly, P., Sheils, O., McDermott, M., O’Briain, D. S., Maher, D., Costello, P., Flanagan, F., Stack, J., Ennis, J., Grimes, H., Yanni, A., Harrison, M., Lowry, W. S., Russell, S. E. H., Atkinson, R. J., White, P., Hickey, I., Bell, D. W., Biggart, D., Doyle, J., Staunton, M. J., Gaffney, E. F., Dervan, P. A., McCabe, M. M., Fennelly, J. J., Carney, D. N., O’Reilly, M., McMahon, J. N., Moriarty, M., Hurson, B., O’Neill, A. J., Magee, H., O’Loughlin, J., Dervan, P. A., Cremin, P., Orminston, W., McCarthy, J., Redmond, P., Duggan, S., Rea, S., Bouchier-Hayes, D., O’Donnell, J., Duggan, C., Crown, J., Bermingham, D., Nugent, A., Fleming, C., Crosby, P., Wolff, S., McCarthy, D., Walsh, C. Barry, Cassidy, M., Husain, S., Kay, E., Thornhilll, M., Whelan, D., Barry, D., Turner, M., Prenderville, W., Murphy, F., Prendiville, W., Gibson, G., O’Grady, T., Carmody, M., Donohoe, J., Walshe, J., Murphy, G. M., O’Donoghue, J., Kerin, K., Ahern, S., Molloy, K., Goulden, N., Pamphilon, D. H., O’Connell, M., Power, C., Leroux, A., Perricaudet, M., Walls, D., Britton, F., Brennan, L., Barnett, Y. A., Madden, B., Wakelin, L. P. G., Loughrey, H. C., Corley, P., Redmond, H. P., Watson, R. W. G., Keogh, I., O’Hanlon, D., Walsh, S., Callaghan, J., McNamara, M., Benedict-Smith, A., Barnes, C., Neylon, D., Fenton, M., Searcey, M., Topham, C. M., Wakelin, L. G., Howarth, N. M., Purohit, A., Reed, M. J., Potter, B. V. L., Hatton, W. J., McKerr, G., Harvey, D., Carson, J., Hannigan, B. M., McCarthy, P. J., McClean, S., Hill, B. T., Costelloe, C., Denny, W. A., Fingleton, B., McDonnell, S., Butler, M., Corbally, N., Dervan, P. A., Stephens, J. F., Martin, G., McGirl, A., Lawlor, E., Gardiner, N., Lynch, S., Arce, M. de, O’Brien, F., Duggan, A., O’Herlihy, S., Shanahan, F., O’Keeffe, G., McCann, S., Sweeney, K., Neill, A. O., Pamphilon, D., Sheridan, M., Reid, I., Seymour, C. B., Walshe, T., Hennessy, T. P., O’Mahony, A., O’Connell’, J., Lawlor, C., Nolan, S., Morrisey, D., Pedlow, P. J., Walsh, M., Lowry, S. W., McAleer, J. J. A., McKeown, S. R., Afrasiabi, M., Lappin, T. R. J., Joiner, B., Hirst, K. V., Hirst, D. G., Sweeney, E., VanderSpek, J., Murphy, J., and Foss, F.

Published
1995
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10. Royal Academy of Medicine in Ireland Section of Biomedical Sciences Proceedings of Summer Meeting held 22nd & 23rd June, 1993

Author

Kent, A., Keenan, A. K., Herity, N. A., Allen, J. D., Silke, B., Adgey, A. A. J., O’Halloran, K. D., Curran, A. K., Bradford, A., Craig, J. A., Barlas, P., Baxter, G. D., Walsh, D. M., Allen, J. M., Logan, I. D., Wilkinson, Y. A., McKenna, P. G., Brayden, D. J., Dunne, J., Baird, A. W., Kelly, J. G., O’Connor, J. J., Rowan, M. J., Anwyl, R., Caldwell, M., Earley, B., Leonard, B. E., Wedlock, P. M., Shephard, R. A., Bracken, P. J., Fitzpatrick, J. M., O’Reilly, C., Quinn, E., Ryan, M. P., O’Neill, J., Kernan, R. P., Craven, C. D., Healy, E., Clarke, H., Nolan, C. A., O’Connell, C., Deegan, P. M., Abdelwahab, Y. H. A., Barnett, C. R., Flatt, P. R., MacSweeney, C., Kelly, J. P., Cawley, T., Geraghty, J., Osborne, H., Docherty, J. R., Nelson, A. A., McDowell, B. C., McCrory, M., Deasy, P. B., Finan, M. P., Klatt, P. R., Hornykiewytsch, Th., Campion, D. P., Leek, B. F., Sharma, S. C., Barry-Kinsella, C., Foran, K., Thomas, G., McKinney, M. W., O’Connor, J., McKelvey-Martin, V. J., Thompson, C. C. M., McCarthy, P. J., Hannigan, B. M., Thurnham, D. I., Chopra, M., Leake, D., Sheehy, P. J. A., Delanty, N., Murphy, N., Lawson, J. A., FitzGerald, G. A., Fitzgerald, D. J., Smyth, E. M., McCole, D., O’Neill, M., Canney, M., Turley, E., Strain, J. J., Gallagher, G. A., Shields, T. D., O’Kane, S., Eason, S. J., Gilmore, W. S., King, C. M., Hejmadi, M., McKeown, S. R., McAleer, J. J. A., Patterson, L. H., Gray, P. S. C., Lappin, T. R. J., Bridges, J. M., Richardson, S. -A. M., Murphy, P. G., Davidson, N., and Hooper, A. C. B.

Published
1994
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12. Royal academy of medicine in ireland section of biological sciences: Proceedings of winter meeting held friday, 3rd January, 1992 in R.C.S.I.

Author

Bourke, W., O’Connor, C., Fitzgerald, M. X., McConnell, T. J., Kent, A., Redmond, E. M., Keenan, A. K., Smyth, E. M., Shanahan, R., O’Donnell, N., O’Connor, C. M., Kelly, V., Barry-Kinsella, C., Sharma, S. C., Cottrell, E., Harrison, R. F., Sheppard, B. L., Bonnar, J., McNally, O., Hannigan, B., Allen, J. M., Feely, J., Buggy, D., Barry, M., Keeling, P. W. N., Weir, D. G., Breathnach, A., Keogh, B., Cooke, T., Murphy, J., O’Sullivan, C., Walsh, M., Tyrrell, J., Bergin, C., Colgan, M., Moore, D., Shanik, D. G., Cooke, T., Southey, A., Costello, E., Jehn, B., Marti, R., Deane, R., Thornton, F., Jaggi, R., Martin, F., Armstrong, C., Mannion, D., Feely, T., Fitzpatrick, G., McCormack, P. M. E., O’Reilly, E., Walsh, J. B., Coakley, D., Stinson, J. C., Murphy, C. M., Andrews, J. F., Tomkin, G. H., Howe, J. P., Fogarty, D. J., Manahan-Vaughan, D., Rowan, M. J., Anwyl, R., Thornbury, K. D., Ward, S. M., Sanders, K. M., Murnin, M., Guthrie, D. J. S., Irvine, G. B., Doyle, E., Regan, C. M., Bannigan, J., Giles, J., Adebayo, G. I., Deasy, P. B., Omara, A. A. M., Lambert, M. B., Shields, T. D., O’Kane, S., Leckey, D., Gilmore, W. S., Hannigan, B. M., McKeogh, D., Bradford, A., O’Regan, R. G., Nolan, P., McEvoy, F., Edgell, T., Webbon, P., Creighton-Kempsford, L., Gaffney, P. J., O’Donnell, M. D., McGeeney, K. F., Breslin, E., Smith, K., Docherty, J. R., Adams, N., Ravey, J., Bell, A. J., Tong, K. K., Strain, J. J., Walsh, D. M., Baxter, G. D., Mokhtar, B., Victory, R., Bergin, D., Cooney, C., Staunton, M., Fitzgerald, J., Gardiner, J., Blunnie, W., Smith, J., Magee, O., Lowe, D., Robinson, R., Magner, J., Eustace, P., Martyn, C. J., Cooney, C. M., Adams, H., Lyons, J. B., Blunnie, W. P., and Moriarty, D. C.

Published
1992
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13. Royal academy of medicine in Ireland section of biological sciences: Proceedings of meeting held 19th & 20th June 1991, University College, Cork

Author

Jamison, J. P., McKinley, R. K., Sharma, S. C., Feely, J., Cooney, C. M., Lyons, J., Bourke, J. M., Gallagher, H., Blunnie, W. P., Moriarty, D. C., Sheppard, B. L., Bonnar, J., Gaffney, J., Creighton-Kempsford, L. J., Wheeler, S., Tarelli, E., McGuckin, C., Gilmore, W. S., Allen, J. M., McNally, O., Hannigan, B. M., McMillan, C. M., Moore, J., Dundee, J. W., Abram, W. P., Greally, M., Kelly, J., O’Donnell, J. M., Maclomhair, M., Lavelle, S. M., Deane, R., Giafri, S., Larkin, S., Tait, S., Ryan, F., Martin, F., Farrell, C. B., O’Boyle, K. M., Bradford, A., Savvas, A., Mantovani, P., Baird, A. W., Thombury, K. D., Ward, S. M., Dalziel, H. H., Westfall, D., Sanders, K. M., McHale, N. G., Conlon, D., Sunderland, S., Kane, Marion, Boland, M., Roche, J. F., Headon, D. R., Morgan, P. M., Kane, M. T., Nolan, S. B., Collins, J. K., O’Donoghue, M., O’Donoghue, E., O’Sullivan, G. C., Buggy, F., Ryan, M., Cook, T., Robinson, K., Graham, I., Younger, K., Cochrane, D. J., Adgey, A. A. J., Anderson, J., Allen, J. D., Manahan-Vaughan, D., Rowan, M. J., Anwyl, R., Gharbháin, F. Ó, Chambers, P. L., Smith, K., Connaughton, S., Docherty, J. R., Breslin, E., Teoh, T., Darling, M., Gebruers, E. M., Hall, W. J., Harris, A., Smith, J. J., Hynes, P. J., O’Sullivan, V. R., Fraher, J. P., Hughes, G. A., O’Mahony, A., and O’Sullivan, G.

Published
1992
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14. Irish association for cancer research: Proceedings of Annual Scientific Meeting, University College, Cork, 30th–31st March, 1990.

Author

Moriarty, M., Maher, M., Morton, G., Flavin, A., Mooney, E., Neilan, J., Nestor, P., Horgan, P. G., Kerin, M., Waldron, D., Gannon, F., Given, H., McCann, A. H., Dervan, P. A., Codd, M. B., Guillick, W. J., Carney, D. N., Horgan, P. G., O’Brien, D. P., Waldron, D. J., Mooney, E., McGuire, M., Given, H. F., Dolan, Jane, O’Hora, A., Droogan, Olivia, Curran, Bernadette, Henry, K., Leader, Mary, Meehan, S., Magee, H., Carney, D., Dervan, P., Lawler, M., McCann, S. R., Humphries, P., Barrett, J., O’Sullivan, G., Collins, J. K., Williams, N., Daly, J., Herlyn, M., Corbally, N., Sweeney, E., Dervan, P., Carney, D. N., Sheppard, M. N., Hamid, Q., Corrin, B., Weedle, Roisin M., Cotter, T. G., Wilkinson, Y. A., McKenna, P. G., Hahnvajanawong, C., O’Sullivan, G., McCarthy, M., Collins, J. K., Atkinson, R. J., Pedlow, P., McQuaid, S., Johnson, P., Stuart, J., O’Meara, A., Russell, S. E. H., White, P. M., Atkinson, R. J., Hickey, G. I., Pomeroy, M., Prosser, E., Barker, F., Casey, M., Carroll, K., O’Kennedy, R., Duffy, G., Fennelly, J. J., Duffy, M. J., Reilly, D., Fennelly, J. J., O’Higgins, N., Rochfort, H., O’Neal, K. L., Hoper, M., Odling-Smee, G. W., Abram, W. P., McKenna, P. G., Mooney, E., Brougham, C., Horgan, P., Waldron, D., O’Brien, D., Kerin, M., Heyden, D. R., Given, H. F., Lanigan, D., McLean, P., Murphy, D., Donovan, M. G., Curran, B., Leader, M., Martin, Angela, Clynes, M., Graham, D., Curran, B., McQuaid, S., Dorman, T., Breathnach, F., Fitzgerald, R. J., Leader, M., O’Meara, A., Lennon, S. V., Martin, S. J., Cotter, T. G., Ryan, L., Kilfeather, S. A., O’Malley, K., Nolan, K. B., Croke, D. T., Helene, C., Browne, P. V., Lawler, M., McCann, S. R., Clarke, E., McCann, S. R., Glynn, J., Cotter, K., Shine, M., Cotter, T., Sweeney, E., Dervan, P., Carney, D. N., McKelvey, V. J., Stefani, L. A. J., McKenna, P. G., Ranjbar, S., Cromie, E., Eason, S., Hannigan, B. M., Corbett, A., O’Sullivan, G., Collins, J. K., O’Brien, F., O’Sullivan, G., Collins, J. K., Carney, D. N., Grogan, L., Leonard, N., Morton, G., Flavin, A., Moriarty, M., Foley-Nolan, D., McCann, A., Carney, D. N., Fennelly, J. J., Jones, Mary, Garrett, C., Pomeroy, Maeve, Brennan, D. P., and Powell, D.

Published
1991
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17. Changes in health in England, with analysis by English regions and areas of deprivation, 1990-2013 : A systematic analysis for the Global Burden of Disease Study 2013

Author

Newton, J. N., Briggs, A. D. M., Murray, C. J. L., Dicker, D., Foreman, K. J., Wang, H., Naghavi, M., Forouzanfar, M. H., Ohno, S. L., Barber, R. M., Vos, T., Stanaway, J. D., Schmidt, J. C., Hughes, A. J., Fay, D. F. J., Ecob, R., Gresser, C., McKee, M., Rutter, H., Abubakar, I., Ali, R., Anderson, H. R., Banerjee, A., Bennett, D. A., Bernabé, E., Bhui, K. S., Biryukov, S. M., Bourne, R. R., Brayne, C. E. G., Bruce, N. G., Brugha, T. S., Burch, M., Capewell, S., Casey, D., Chowdhury, R., Coates, M. M., Cooper, C., Critchley, J. A., Dargan, P. I., Dherani, M. K., Elliott, P., Ezzati, M., Fenton, K. A., Fraser, M. S., Fürst, T., Greaves, F., Green, M. A., Gunnell, D. J., Hannigan, B. M., Hay, R. J., Hay, S. I., Hemingway, H., Larson, H. J., Looker, K. J., Lunevicius, R., Lyons, R. A., Marcenes, W., Mason-Jones, A. J., Matthews, F. E., Moller, H., Murdoch, M. E., Newton, C. R., Pearce, N., Piel, F. B., Pope, D., Rahimi, K., Rodriguez, Alina, Scarborough, P., Schumacher, A. E., Shiue, I., Smeeth, L., Tedstone, A., Valabhji, J., Williams, H. C., Wolfe, C. D. A., Woolf, A. D., Davis, A. C. J., Newton, J. N., Briggs, A. D. M., Murray, C. J. L., Dicker, D., Foreman, K. J., Wang, H., Naghavi, M., Forouzanfar, M. H., Ohno, S. L., Barber, R. M., Vos, T., Stanaway, J. D., Schmidt, J. C., Hughes, A. J., Fay, D. F. J., Ecob, R., Gresser, C., McKee, M., Rutter, H., Abubakar, I., Ali, R., Anderson, H. R., Banerjee, A., Bennett, D. A., Bernabé, E., Bhui, K. S., Biryukov, S. M., Bourne, R. R., Brayne, C. E. G., Bruce, N. G., Brugha, T. S., Burch, M., Capewell, S., Casey, D., Chowdhury, R., Coates, M. M., Cooper, C., Critchley, J. A., Dargan, P. I., Dherani, M. K., Elliott, P., Ezzati, M., Fenton, K. A., Fraser, M. S., Fürst, T., Greaves, F., Green, M. A., Gunnell, D. J., Hannigan, B. M., Hay, R. J., Hay, S. I., Hemingway, H., Larson, H. J., Looker, K. J., Lunevicius, R., Lyons, R. A., Marcenes, W., Mason-Jones, A. J., Matthews, F. E., Moller, H., Murdoch, M. E., Newton, C. R., Pearce, N., Piel, F. B., Pope, D., Rahimi, K., Rodriguez, Alina, Scarborough, P., Schumacher, A. E., Shiue, I., Smeeth, L., Tedstone, A., Valabhji, J., Williams, H. C., Wolfe, C. D. A., Woolf, A. D., and Davis, A. C. J.

Abstract

Background In the Global Burden of Disease Study 2013 (GBD 2013), knowledge about health and its determinants has been integrated into a comparable framework to inform health policy. Outputs of this analysis are relevant to current policy questions in England and elsewhere, particularly on health inequalities. We use GBD 2013 data on mortality and causes of death, and disease and injury incidence and prevalence to analyse the burden of disease and injury in England as a whole, in English regions, and within each English region by deprivation quintile. We also assess disease and injury burden in England attributable to potentially preventable risk factors. England and the English regions are compared with the remaining constituent countries of the UK and with comparable countries in the European Union (EU) and beyond. Methods We extracted data from the GBD 2013 to compare mortality, causes of death, years of life lost (YLLs), years lived with a disability (YLDs), and disability-adjusted life-years (DALYs) in England, the UK, and 18 other countries (the first 15 EU members [apart from the UK] and Australia, Canada, Norway, and the USA [EU15+]). We extended elements of the analysis to English regions, and subregional areas defined by deprivation quintile (deprivation areas). We used data split by the nine English regions (corresponding to the European boundaries of the Nomenclature for Territorial Statistics level 1 [NUTS 1] regions), and by quintile groups within each English region according to deprivation, thereby making 45 regional deprivation areas. Deprivation quintiles were defined by area of residence ranked at national level by Index of Multiple Deprivation score, 2010. Burden due to various risk factors is described for England using new GBD methodology to estimate independent and overlapping attributable risk for five tiers of behavioural, metabolic, and environmental risk factors. We present results for 306 causes and 2337 sequelae, and 79 risks or risk clu, Export Date: 21 December 2015 CODEN: LANCA Correspondence Address: Newton, J.N.; Public Health England, Wellington HouseUnited Kingdom; email: john.newton@phe.gov.uk References: Murray C.J.L., Richards M.A., Newton J.N., UK health performance: Findings of the Global Burden of Disease Study 2010 (2013) Lancet, 381, pp. 997-1020; Greer S.L., Devolution and divergence in UK health policies (2008) BMJ, 337, p. a2616; England N.H.S., (2014) Five Year Forward View, , http://www.england.nhs.uk/ourwork/futurenhs/, (accessed Aug 24, 2015); Naghavi M., Wang H., Lozano R., Global, regional and national levels of age-specific mortality and 240 causes of death, 1990-2013: A systematic analysis for the Global Burden of Disease Study 2013 (2015) Lancet, 385, pp. 117-171; Global, regional, and national incidence, prevalence, and years lived with disabilities for 301 acute and chronic diseases and injuries for 188 countries, 1990-2013: A systematic analysis for the Global Burden of Disease Study 2013 (2015) Lancet, 386, pp. 743-800; Global, regional, and national comparative risk assessment of 76 behavioural, environmental, occupational, and metabolic risks or clusters of risks in 188 countries 1990-2013: A systematic analysis for the Global Burden of Disease study 2013 (2015) Lancet, , http://dx.doi.org/10.1016/S0140-6736(15)00128-2, published online Sept 11; Global, regional, and national disability-adjusted life years (DALYs) for 306 diseases and injuries and healthy life expectancy (HALE) for 188 countries, 1990-2013: Quantifying the epidemiological transition (2015) Lancet, , http://dx.doi.org/10.1016/S0140-6736(15)61340-X, published online Aug 27; Vos T., Flaxman A.D., Naghavi M., Years lived with disability (YLDs) for 1160 sequelae of 289 diseases and injuries 1990-2010: A systematic analysis for the Global Burden of Disease Study 2010 (2012) Lancet, 380, pp. 2163-2196; Murray C.J.L., Ezzati M., Flaxman A.D., GBD 2010: Design, definitions, and metrics (2012) Lancet, 380, p

Published
2015
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23. Vitamins C and E: acute interactive effects on biomarkers of antioxidant defence and oxidative stress.

Author

Choi SW, Benzie IF, Collins AR, Hannigan BM, and Strain JJ

Subjects
Adult, Antioxidants, Biomarkers blood, Cross-Over Studies, DNA Damage, Double-Blind Method, Drug Interactions, Female, Humans, Male, Middle Aged, Oxidative Stress, Placebos, Ascorbic Acid blood, Ascorbic Acid pharmacology, Vitamin E pharmacology, alpha-Tocopherol blood
Abstract

Oxidative stress is implicated in the aetiology of many diseases; however, most supplementation trials with antioxidant micronutrients have not shown expected beneficial effects. This randomized, double-blinded, placebo-controlled study evaluated acute effects (at 90, 180min and 24h [fasting] post-ingestion) of single doses of Vitamins C (500mg) and E (400IU), alone and in combination, on biomarkers of plasma antioxidant status, lipid peroxidation and lymphocyte DNA damage in 12 healthy, consenting volunteers. Plasma ascorbic acid increased significantly (P < 0.01) within 2h of ingestion of Vitamin C, and alpha-tocopherol was significantly (P < 0.01) higher at 24h post-ingestion Vitamin E. The pattern of response was not significantly different whether Vitamin C (or Vitamin E) was taken alone or in combination, indicating no augmentation of response to one by co-ingestion of the other vitamin. No significant changes were seen in plasma FRAP in the group overall (although increases (P < 0.05) were seen at 90 and 180min post-ingestion in women after Vitamin C ingestion) or in MDA across treatments, and no evidence of increased DNA damage, or of DNA protection, was seen at any time point after Vitamin C and/or E ingestion. In conclusion, the data from this first controlled study of acute effects of single doses of Vitamin C and/or E show no evidence of either a protective or deleterious effect on DNA damage, resistance of DNA to oxidant challenge, or lipid peroxidation. No evidence of a synergistic or cooperative interaction between Vitamins C and E was seen, but further study is needed to determine possible interactive effects in a staggered supplementation cycle, and study of subjects under increased oxidative stress or with marginal antioxidant status would be useful. It would be of interest also to study the effects of these vitamins ingested with, or in, whole food, to determine if they are directly protective at doses above the minimum required to prevent deficiency, if combinations with other food components are needed for effective protection, or if Vitamins C and E are largely surrogate biomarkers of a 'healthy' diet, but are not the key protective agents.

Published
2004
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24. Age-related differences in parameters of feline immune status.

Author

Campbell DJ, Rawlings JM, Koelsch S, Wallace J, Strain JJ, and Hannigan BM

Subjects
Age Factors, Animals, Apolipoproteins blood, Apolipoproteins immunology, Cats blood, Colorimetry veterinary, Complement System Proteins immunology, Enzyme-Linked Immunosorbent Assay veterinary, Female, Flow Cytometry veterinary, Haptoglobins immunology, Immunodiffusion veterinary, Immunoglobulins blood, Immunoglobulins immunology, Leukocyte Count veterinary, Lymphocyte Subsets immunology, Male, Serum Amyloid A Protein immunology, Statistics, Nonparametric, Cats immunology
Abstract

In order to assess age-related differences in feline immune status, 101 domestic short haired cats were assigned to two groups, adult (2-5 years, n=50) and senior (10-14 years, n=51). Analyses of leucocyte populations, lymphocyte subsets, complement activity, serum immunoglobulins and acute-phase proteins were undertaken and revealed significant differences between the two groups. The senior group had significantly lower WBC, lymphocyte and eosinophil counts than the adult group. Neutrophil, monocyte and basophil counts did not differ between the groups. Flow cytometry analysis, in combination with differential WBC data, revealed that the absolute values (cells/l) of T-cells, B-cells and natural killer (NK) cells were significantly lower in the older animals. While serum immunoglobulins IgA and IgM were higher in the senior group when compared with the adult group, no significant differences were observed in complement activity or in serum acute-phase proteins. Our findings suggest that age-related changes to parameters of immune status in the feline model are likely to follow a similar pattern to those observed in other long-lived mammalian species.

Published
2004
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25. Insulin-like growth factor-I (IGF-I) and its association with lymphocyte homeostasis in the ageing cat.

Author

Campbell DJ, Rawlings JM, Heaton PR, Blount DG, Pritchard DI, Strain JJ, and Hannigan BM

Subjects
Animals, Apoptosis drug effects, Cats, Cell Proliferation drug effects, Cells, Cultured, Deoxyribose pharmacology, Flow Cytometry methods, Homeostasis physiology, Insulin-Like Growth Factor I pharmacology, Lymphocyte Subsets, Lymphocytes drug effects, Oxidative Stress, Recombinant Proteins pharmacology, Aging physiology, Insulin-Like Growth Factor I metabolism, Lymphocytes physiology
Abstract

Ageing affects feline lymphocyte homeostasis in a similar pattern to that observed in other long-lived mammalian species, contributing to increased levels of morbidity and mortality in the ageing cat. Insulin-like growth factor-I (IGF-I) is now recognised as an important endocrine regulator of immunity and has been shown to decline with age in humans and rodent species. Analysis of plasma IGF-I in adult and senior cats confirmed that the older cats had significantly lower circulating levels of IGF-I. In order to determine whether an association existed between lymphocyte subpopulations and IGF-I levels in the cat, each parameter was measured and subjected to regression analysis. A highly significant association was found in vivo between plasma IGF-I and CD4(+) T-cell values in the senior group, but no such association was observed in the adult group. In order that this relationship could be examined further, in vitro studies were undertaken to investigate the effects of physiologically relevant concentrations of recombinant human IGF-I (rhIGF-l) on peripheral blood lymphocyte (PBL) cultures from adult and senior cats. While rhlGF-I induced low-level thymidine incorporation in the lymphocytes isolated from the senior group, it did not enhance the proliferative response to T-cell mitogens, Con A and PHA in either group, nor did it rescue cells from oxidatively induced apoptosis. Furthermore, the proliferative response of PBL from seniors did not attain the magnitude of that from the adults at any concentration of rhIGF-l. We propose that the observed association is not a direct effect of IGF-I on PBL, but may be mediated through an effect of IGF-I on the thymus.

Published
2004
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26. Vitamin C decreases intracellular calcium level in human lymphoid cells.

Author

Oztürk G, Mulholland CW, and Hannigan BM

Subjects
Calcimycin pharmacology, Cell Line, Transformed, Humans, Intracellular Fluid metabolism, Ionophores pharmacology, Antioxidants pharmacology, Ascorbic Acid pharmacology, Calcium antagonists & inhibitors, Calcium metabolism, Intracellular Fluid drug effects, Lymphocytes drug effects, Lymphocytes metabolism
Abstract

Human lymphocytes have low levels of many antioxidant enzymes however they are know to concentrate vitamin C. Cell injury, including oxidative stress effects, is associated with calcium influx so the influence of vitamin C on the maintenance of calcium levels in leukocytes was studied. Incubation of Molt-3 human lymphoblastoid cells with physiologically relevant concentrations of vitamin C and the calcium ionophore A23187 reversed the calcium influx and increased nuclear protein level associated with the ionophore alone. It is concluded that intracellular vitamin C can inhibit calcium influx into leukocytes so helping to minimise cell damage.

Published
2001

27. The effect of vitamin C or vitamin E supplementation on basal and H2O2-induced DNA damage in human lymphocytes.

Author

Brennan LA, Morris GM, Wasson GR, Hannigan BM, and Barnett YA

Subjects
Adult, Antioxidants pharmacology, Ascorbic Acid blood, Catalase metabolism, Female, Glutathione Peroxidase metabolism, Humans, Hydrogen Peroxide toxicity, Male, Superoxide Dismutase metabolism, Vitamin E blood, Ascorbic Acid pharmacology, DNA Damage physiology, Dietary Supplements, Lymphocytes drug effects, Vitamin E pharmacology
Abstract

There is a wealth of epidemiological information on antioxidants and their possible prevention of disease progression but very little of the research on antioxidants has involved intervention studies. In this study, the potential protective effect of vitamin C or E supplementation in vivo against endogenous and H2O2-induced DNA damage levels in lymphocytes was assessed. The supplementation involved fourteen healthy male and female non-smokers mean age 25-53 (SD 1.82) years, who were asked to supplement an otherwise unchanged diet with 1000 mg vitamin C daily for 42 d or 800 mg vitamin E daily for 42 d. DNA damage in H2O2-treated peripheral blood lymphocytes (PBL) and untreated PBL before and after supplementation, and during a 6-week washout period was assessed using an ELISA. At each sampling time-point, the red cell concentrate activities of superoxide dismutase, catalase and glutathione peroxidase were also determined. Supplementation with vitamin C or vitamin E decreased significantly H2O2-induced DNA damage in PBL, but had no effect on endogenous levels of DNA damage. The activities of the antioxidant enzymes superoxide dismutase and glutathione peroxidase were suppressed during the supplementation period. These supplementation regimens may be used to limit the possible adverse effects of reactive oxygen species (including those produced during the course of an immune response) on lymphocytes in vivo, and so help to maintain their functional capacity.

Published
2000
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28. Radioadaptation in Indian muntjac fibroblast cells induced by low intensity laser irradiation.

Author

Joyce KM, Downes CS, and Hannigan BM

Subjects
Animals, Cell Cycle radiation effects, Cell Survival radiation effects, Cells, Cultured, Chromosome Aberrations, Comet Assay, DNA Damage, Dose-Response Relationship, Radiation, Fibroblasts radiation effects, Lasers, Okadaic Acid pharmacology, Radiation Tolerance drug effects, Deer physiology, Radiation Tolerance physiology
Abstract

Earlier reports have indicated that an adaptive, protective response to ionizing radiation is inducible by pre-treatment with low intensity laser irradiation (LILI). We have investigated the potential of LILI to induce an adaptive response against the damaging effects of ionizing radiation in Indian muntjac fibroblasts. LILI at 660, but not 820 nm, at 11.5 and 23.0 J/cm2, induced an apparent adaptive response in the form of a reduction in the frequency of radiation-induced chromosome aberrations, but not in cell survival. There was also a trend towards a reduction in the level of single-stranded and double-stranded DNA breaks induced by ionizing radiation when cells were preconditioned with LILI. However, this did not contribute to the reduced chromosome aberration frequency. Further analysis revealed that the reduced aberration frequency was caused by a laser-induced extension of G2 delay. The adaptive response was therefore the result of cell cycle modulation by LILI, at a wavelength where there is no known DNA damaging effect to induce the checkpoint mechanisms that are normally responsible for altering cell cycle progression.

Published
1999
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29. Cell-cycle delay is induced in cells of a U937 promonocytic cell line by low-intensity light irradiation at 660 nm.

Author

Joyce KM, Downes CS, and Hannigan BM

Subjects
Calcium metabolism, Cell Division radiation effects, DNA Damage, DNA, Neoplasm radiation effects, Flow Cytometry, G2 Phase, Humans, Hydrogen-Ion Concentration, Light, Mitosis, S Phase, U937 Cells, Cell Cycle radiation effects
Abstract

Visible-light irradiation (VLI) at 660 nm and 11.5 J/cm2 inhibits proliferation of cells of the U937 promonocytic cell line, as monitored by autoradiographical analysis. The S-phase cell population is reduced at 6 h post-radiation treatment. Flow cytometric analysis confirms this, and also shows that light irradiation of cells induces a statistically significant increase in G2/M cells at 6 h post-radiation treatment. It has been postulated that VLI at 660 nm can alter cell-cycle progression by affecting intracellular concentrations of ions, in particular pH and calcium. However, no significant effects of light irradiation on these intracellular ions have been observed. These effects of VLI are not a consequence of radiation-induced DNA strand breaks, therefore events other than direct DNA damage are involved. These findings demonstrate a direct photobiological effect of VLI at 660 nm on the cell cycle, and indicate a previously unsuspected mechanism for the induction of cell-cycle delay that is neither a result of changes in the concentration of intracellular ions nor initiated by DNA strand breaks.

Published
1999
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32. Macrophages and apoptotic cells in human colorectal tumours.

Author

Higgins CA, Hatton WJ, McKerr G, Harvey D, Carson J, and Hannigan BM

Subjects
Cell Count, Humans, Apoptosis, Colorectal Neoplasms pathology, Macrophages pathology
Abstract

The numerical relationship between tumour associated macrophages (TAM) and apoptotic cells in 12 human colorectal tumours was evaluated. TAM were labelled immunohistochemically and apoptotic cells were visualized by counterstaining with haematoxylin and eosin (H&E). The stereological techniques, Cavalieri's estimator of volume and the Disector were used to estimate both tumour volume and numerical density of both cell types. The occurrence of TAM per unit volume of tissue increased with increasing tumour volume to a maximum in a tumour of 110.5 cm3, after which numbers declined. Levels of apoptosis also increased with tumour volume though more erratically than levels of TAM and declined for tumour volumes greater than 80 cm3. This is the first report of an attempt to assess the relationship between apoptotic cells and TAM in human tumours.

Published
1996
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34. The effect of antioxidant supplementation on the oxidant-induced stress response in human lymphocytes.

Author

Brennan LA, Hannigan BM, and Barnett YA

Subjects
Administration, Oral, Ascorbic Acid administration & dosage, Cells, Cultured, DNA drug effects, Female, Humans, Lymphocytes drug effects, Lymphocytes pathology, Male, Placebos, Reference Values, Vitamin E administration & dosage, Antioxidants pharmacology, Ascorbic Acid pharmacology, DNA Damage, DNA, Single-Stranded drug effects, Hydrogen Peroxide toxicity, Lymphocytes physiology, Oxidative Stress, Vitamin E pharmacology
Published
1996
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35. The effects of copper deficiency on human lymphoid and myeloid cells: an in vitro model.

Author

Tong KK, Hannigan BM, McKerr G, and Strain JJ

Subjects
Calcium analysis, Cell Division, Copper analysis, Electron Transport Complex IV metabolism, HL-60 Cells physiology, Humans, Superoxide Dismutase metabolism, T-Lymphocytes chemistry, T-Lymphocytes ultrastructure, B-Lymphocytes physiology, Copper deficiency, T-Lymphocytes physiology
Abstract

Cu has long been known to influence immune responses. An in vitro model system was established in which human myeloid (HL-60), B-lymphoid (Raji) and T-lymphoid (Molt-3) cell lines could be grown in culture media of varying Cu levels. Initially Cu was removed from the medium by dialysis of fetal calf serum against a metal-ion chelator, minor depletion of other trace metals being obviated by repletion with appropriate metal salts. The growth rate of HL-60 was significantly (P < 0.05) inhibited by 72 h Cu depletion. Molt-3 cells required a longer period, up to 144 h, in Cu-depleted medium before growth was impaired. Raji-cell growth was not affected. These results confirmed clinical observations that T-cell functions were more sensitive to Cu deprivation than B cells. Analysis of intracellular metal levels in Molt-3 cells showed that Cu levels had been significantly lowered (P < 0.05) although Ca2+ levels were raised. Intracellular activity of the antioxidant enzyme superoxide dismutase (EC 1.15.1.1) was significantly impaired (P < 0.05) in Molt-3 cells grown in Cu-depleted medium. Activity of the mitochondrial enzyme cytochrome c oxidase (EC 1.9.3.1) was also significantly impaired (P < 0.05) by Cu depletion. Each of these findings indicates an increase in the potential for cellular damage by reduced antioxidant activity, impairment of normal mitochondrial activity and excessive Ca2+ influx. A major consequence of the type of damage occurring under these circumstances is membrane disruption. This was confirmed by scanning electron microscopy of Molt-3 cells grown under varying Cu levels.

Published
1996
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36. Reactive oxygen species inducible by low-intensity laser irradiation alter DNA synthesis in the haemopoietic cell line U937.

Author

Callaghan GA, Riordan C, Gilmore WS, McIntyre IA, Allen JM, and Hannigan BM

Subjects
Catalase pharmacology, Cell Line, DNA biosynthesis, Hydrogen Peroxide, Thymidine metabolism, DNA radiation effects, Hematopoietic Stem Cells radiation effects, Lasers, Reactive Oxygen Species physiology
Abstract

Background and Objective: The purpose of this study was to evaluate the possible role of reactive oxygen species (ROS) in mediating previously recorded alterations in DNA synthesis, inducible by low-intensity laser irradiation (LILI), in the haemopoietic cell line U937., Study Design/materials and Methods: The ability of LILI (660 nm, 12 mW, 5 kHz) to induce ROS from U937 cells was assessed spectrophotometrically at energy densities (E.D.) from 1.0 to 11.5 J/cm2. In order to assess whether laser-induced ROS could alter cellular proliferation DNA synthesis was measured post-irradiation, by the incorporation of tritiated thymidine (3H-TdR) into the cells in both the presence and absence of the antioxidant catalase (CAT)., Results: Detectable ROS were produced post-irradiation only from the differentiated form of the cell line. Analysis by Student's t-test for unrelated groups showed a significant difference, at E.D.s 2.9 and 8.6 J/cm2, in the extent of DNA synthesis occurring in cells irradiated in the presence of CAT or in its absence., Conclusion: These findings demonstrate that laser-inducible ROS can mediate laser's effects on this cell line.

Published
1996
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37. Oxidant-induced stress response in lymphoid cells.

Author

Barnett YA, Brennan LA, O'Farrell F, and Hannigan BM

Subjects
Cell Division drug effects, Cell Survival drug effects, Cells, Cultured, DNA Damage drug effects, Humans, Hydrogen Peroxide pharmacology, Lymphocytes metabolism, Oxidants pharmacology, Oxidative Stress drug effects
Abstract

The stress response to reactive oxygen species is an important defence system which can reduce their potential to induce biomolecule damage. In this investigation the effect of exposing Molt-3 lymphoblastoid cells or peripheral blood lymphocytes to a non-toxic dose of hydrogen peroxide (10 microM) was studied. Cellular response to a subsequent high dose of hydrogen peroxide (100-200 microM) was assessed by measurement of growth, viability, proliferation and DNA damage (lymphocytes only) and intracellular activities of the enzymes, superoxide dismutase, glutathione peroxidase and catalase (Molt-3 only). The results indicate that pretreatment of lymphocytes with 10 microM hydrogen peroxide can elicit a response which is protective against DNA damage normally inducible in these cells by subsequent exposure to toxic doses of hydrogen peroxide. It appears from the results with Molt-3 cells that altered activities of glutathione peroxidase may contribute to this enhanced resistance to hydrogen peroxide.

Published
1995

38. Diet and immune function.

Author

Hannigan BM

Subjects
Aging immunology, Avitaminosis immunology, Diet, Dietary Fats immunology, Humans, Infections immunology, Trace Elements deficiency, Immunity physiology, Nutritional Physiological Phenomena physiology
Abstract

Adequate human nutrition is essential to maintain all normal physiological functions including defence of the self. Controversy exists about the precise constituents of diets optimal for all stages in the human life-span. Dietary composition may also need to be altered under such stressful conditions as infection or recovery from major surgery. Understanding how specific nutrients can alter immune responses may add to the quality of human lives by minimising the impact of disease morbidity and mortality. Dietary modification also offers hope of new therapeutic regimens for human diseases.

Published
1994

39. Thymidine kinases: the enzymes and their clinical usefulness.

Author

Hannigan BM, Barnett YA, Armstrong DB, McKelvey-Martin VJ, and McKenna PG

Subjects
Antiviral Agents pharmacology, Herpesviridae drug effects, Humans, Neoplasms enzymology, Retroviridae drug effects, Thymidine Kinase genetics, Virus Diseases enzymology, Thymidine Kinase analysis
Abstract

Thymidine kinases (TK) convert thymidine, or deoxythymidine (dT) to the respective monophosphate. TK occurs in many different procaryotic and eucaryotic species and different TK isoenzymes are found within the same eucaryotic cell. One isoenzyme (foetal, cytoplasmic, TK1) is associated with cell division while the other (adult, mitochondrial, TK2) is cell cycle independent. The relative isoenzyme activities in a tissue thus reflect the fraction of proliferating cells. The gene encoding TK1 has been cloned for many species and regulation of its expression is known to be complex. Increases in TK activity appear to correlate with the presence of human neoplasia and disease progression and regression have been reported to correlate with TK levels in many cancer types. TK estimations in human lymphoproliferative diseases have implicated this enzyme as an early marker of maldifferentiation. TK levels may also be increased in non-dividing mammalian cells infected with RNA or DNA viruses. Some virus encoded TK has been shown to differ biochemically, immunologically and in substrate specificity from the corresponding TK isoenzymes in target host cells thus facilitating the development of specific antiviral therapeutics. Further, TK1 in leukemic cells may differ biochemically from normal cellular TK1 such that tumor-specific TK may provide a target for tumor detection and therapy. TK quantitation has conventionally been performed in assays of enzyme activity using radiolabeled (3H or 125I) nucleoside substrates. The development of TK1-specific, non-radioisotope based immunoassays and the measurement of TK mRNA in tumour tissue using TK (DNA or RNA) probes may prove sufficiently valuable to be incorporated into the routine clinical management of human cancer.

Published
1993
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40. Tumour cell inhibition of macrophage cytokine activity.

Author

Hannigan BM, McNally OR, Kirrane O, and Eason SJ

Subjects
Animals, Female, Macrophage Activation, Macrophages enzymology, Mice, Mice, Inbred BALB C, Protein Kinase C metabolism, Interleukin-1 antagonists & inhibitors, Interleukin-6 antagonists & inhibitors, Macrophages immunology, Tumor Cells, Cultured immunology, Tumor Necrosis Factor-alpha antagonists & inhibitors
Abstract

Macrophages elaborate both effector and regulatory immune functions. It was hypothesised that tumours can exert a local alteration of macrophage function. Murine peritoneal macrophage-derived cytokines were assayed in the presence and absence of cells, cytosol fractions or conditioned media (TCCM) from established murine tumour lines. Interleukin-1 beta, interleukin-6 and tumour necrosis factor-alpha activities were significantly inhibited by tumour cells or their products, as were the corresponding recombinant human cytokines. Intracellular protein kinase C activation was also measured and was significantly inhibited by murine TCCM, thus suggesting one possible site of inhibitor action. Data analyses indicate that the inhibitory factor(s) is probably not an already well-characterised macrophage inhibitor.

Published
1992
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41. DNA damage in mammalian cell lines with different antioxidant levels and DNA repair capacities.

Author

Hannigan BM, Richardson SA, and McKenna PG

Subjects
Animals, Cell Division, Lymphoma, Mice, Thymidine metabolism, Tumor Cells, Cultured, X-Rays, Antioxidants metabolism, Catalase metabolism, DNA Damage, DNA Repair, Glutathione Peroxidase metabolism, Superoxide Dismutase metabolism
Abstract

A wide range of DNA damage is known to be caused by reactive oxygen species (ROS). Defence against the effects of such damage include damage prevention (e.g. antioxidant activity) and the removal of damaged moieties from DNA (DNA repair). Radiation (X-ray) sensitive murine lymphoma (LY) cells were seen to be more susceptible to ROS-induced damage than were radiation resistant cells. This difference was unlikely to be due to the marginally decreased DNA excision repair capacity of the sensitive cells. Radiation sensitive cells did, however, have lower endogenous antioxidant enzyme levels. Thus, the importance of assessing all levels of a cell's response to ROS, in determining the major factors leading to increased mutagen sensitivity, is emphasised.

Published
1992
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42. Recombinant human granulocyte colony stimulating factor (rhG-CSF) and superoxide production in a haematopoietic cell line.

Author

Gilmore WS, Hannigan BM, Easton SJ, McGuckin CP, and Nelson AA

Subjects
Cell Line, Humans, Monocytes cytology, Monocytes drug effects, Recombinant Proteins pharmacology, Superoxide Dismutase metabolism, Tetradecanoylphorbol Acetate pharmacology, Granulocyte Colony-Stimulating Factor pharmacology, Monocytes physiology, Superoxides metabolism
Published
1991
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44. Selective inhibition of thymidine kinase isoenzymes by (E)-5-(2-bromovinyl)-2-deoxyuridine.

Author

Armstrong B, Modjtahedi H, O'Neill KL, Hannigan BM, and McKenna PG

Subjects
Animals, Breast Neoplasms enzymology, Bromodeoxyuridine pharmacology, Humans, Isoenzymes blood, Leukemia enzymology, Leukocytes, Mononuclear enzymology, Thymidine Kinase blood, Bromodeoxyuridine analogs & derivatives, Isoenzymes antagonists & inhibitors, Thymidine Kinase antagonists & inhibitors
Published
1990
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46. DNA single-strand breaks induced by activated macrophages.

Author

Ranjbar S and Hannigan BM

Subjects
Animals, DNA Damage, DNA, Single-Stranded drug effects, Female, In Vitro Techniques, Macrophages drug effects, Macrophages metabolism, Mice, Superoxide Dismutase metabolism, Superoxide Dismutase pharmacology, Superoxides metabolism, DNA, Single-Stranded metabolism, Macrophage Activation physiology
Published
1990
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49. Thymidine kinase activities in mononuclear leukocytes and serum from breast cancer patients.

Author

McKenna PG, O'Neill KL, Abram WP, and Hannigan BM

Subjects
Adult, Aged, Aging blood, Breast Neoplasms pathology, Female, Humans, Isoenzymes blood, Male, Middle Aged, Neoplasm Staging, Sex Factors, Breast Neoplasms enzymology, Leukocytes, Mononuclear enzymology, Thymidine Kinase blood
Abstract

Levels of the nucleotide pathway enzyme thymidine kinase (TK) were assayed in the mononuclear leukocytes and serum of 70 female patients with breast cancer and 98 male and 77 female non-cancer hospital patients. The total TK levels in both mononuclear leukocytes and serum from patients with breast cancer were significantly higher than in controls. The serum TK levels showed a significant correlation with cancer stage. No such correlation was observed with mononuclear leukocyte TK levels. Serum TK from 20 patients with breast cancer and 19 control patients was further assayed to ascertain the relative contributions of the thymidine kinase isozymes TK1 and TK2 to total TK levels. The increase in serum TK from breast cancer patients appears to be due to an increase in both TK1 and TK2 levels.

Published
1988
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