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91 results on '"Moorehead, R A"'

3. Irish society of gastroenterology: Proceedings of meeting held Friday 12th and Saturday 13th June, 1998

Author

Ryan, B. M., McKiernan, S., Keeling, P. W. N., Byrne, P. J., Quill, R., McCallion, K., Mitchell, R. M. S., Watson, R. G. P., Collins, J. S. A., Gardiner, K. R., Winter, D. C., O’Sullivan, G. C., Taylor, C. T., Fanning, N. F., Redmond, H. P., O’Donoghue, D. P., Baird, A. W., Harvey, B. J., Brannigan, A. E., O’Connell, P. R., Regan, M. C., Fitzpatrick, J. M., Watson, R. W. G., Lemass, H., Ryan, E., MacMathuna, P., Crowe, J., O’Keane, J. C., Goh, J., MacMathuna, P., Baird, A., Maher, L., Godson, C., Brady, H. R., Petasis, N. A., Fokin, V. V., O’Keane, J. C., Barry, M. K., Grant, D. C., Sheahan, K., O’Donoghue, D. P., Hyland, J. M. P., Sheehan, K. M., Sheahan, K., O’Donoghue, D. P., Fitzgerald, D. J., Murray, F. E., Heaney, A., Collins, J. S. A., Bamford, K. B., Watson, R. G. P., McFarland, R. J., Tham, T. C. K., McNamara, D., Franelli, S., Whelan, H., Hamilton, H., Beattie, S., O’Morain, C., Ryan, B. M., Keeling, P. W. N., Brennan, E. G., O’Hare, N., McDermott, R., Byrne, P. J., McDougall, N. I., Collins, J. S. A., Gieeson, C. M., Russell, S. E. H., Sloan, J. M., Morrisey, D., Murphy, L., Kiely, B., Fitzgerald, G., Daly, C., O’Sullivan, G., Shanahan, F., Collins, J. K., Marteau, P., Johnston, S. D., Watson, R. G. P., Coates, C., Feighery, C., O’Keeffe, J., Whelan, A., Lynch, S., Weir, D. G., Abuzakouk, M., Feighery, C., Barnes, L., O’Gorman, N., McKenna, M., Freaney, R., Young, M., Gaines, S., Brady, D., Drudy, D., O’Farrelly, C., Gilleece, A., Fenelon, L., McPartlin, J., Goh, J., MacMathuna, P., Baird, A., Godson, C., Brady, H. R., Petasis, N. A., Fokin, V. V., Hopkins, A. M., Myers, A., Moynagh, P., Baird, A. W., O’Donoghue, D. P., Kirby, J. M., Tham, T. C. K., Allen, M. J., Best, B., Calvert, H., Kirk, S., McKelvey, S. T. D., Moorehead, R. J., Varghese, J. C., Sookhai, S., Murray, F. E., Walsh, T., Osborne, H., Broe, P., Lee, M. J., Moriarty, D., Baird, A. W., Watson, R. W. G., Brannigan, A. E., Coffey, R., Murphy, E., Fitzpatrick, J. M., Shah, A. A., Murray, F. E., Murray, E., Thjodleifsson, B., Bjarnason, I., Fitzgerald, D. J., Sheehan, K. M., Murray, E., Shah, A. A., Murray, F. E., Thjodleifsson, B., Bjarnason, I., Fitzgerald, D. J., Montague, S., McNamara, D., Forkin, C., O’Morain, C., O’Toole, G. C., Grant, D. C., Barry, M. K., Sheahan, K., O’Donoghue, D. P., Hyland, J. M. P., Gallagher, C. M., Grant, D. C., Connell, P., Barry, M. K., Traynor, O., Hyland, J. M. P., Barry, M. K., Grant, D. C., Sheahan, K., O’Donoghue, D. P., Hyland, J. M. P., Ling, T. C., Johnston, B., Byrne, M. F., Farrell, M. A., Varghese, J. C., Lee, M. J., Murray, F. E., Goulding, C. A., Albloushi, S. S., O’Connell, P., Murray, F. E., Graham, L. E., Robinson, T. J., Graham, L. E., Robinson, T. J., Jabeen, T., Cannon, B., Jenkins, D., Whelton, M. J., Bohra, S., Cannon, B., Whelton, M. J., Keohane, C., Duggan, M., Bohra, S., Cannon, B., Whelton, M. J., Siddheshwar, R. K., Wilson, R. G., Hainsworth, P. J., Campbell, F. C., Kelly, S. B., Kirby, J. M., Tham, T. C. K., Best, B., Calvert, H., Moorehead, R. J., Kirk, S., Heaney, A., Collins, J. S. A., Watson, R. G. P., Heaney, A., Collins, J. S. A., Watson, R. G. P., Bamford, K. B., McFarland, R. J., Tham, T. C. K., Egan, B. M., Grant, D. C., Barry, M. K., Traynor, O., Hyland, J. M. P., Simutowe, C., McNamara, D. A., Collins, N., Walsh, T. N., Mukherjee, A., Scott, M., Pohl, C., Duggan, E., Wasi, M., Sarkar, A., Donnell, L. O., Eustace, P. W., Johnston, J. G., Waldron, R., Barrett, S., Ryan, E., MacMathuna, P., Crowe, J., Callagy, G., Keane, J. C. O., Coughlan, B., Crowe, J., Sheehan, J., Hickey, A., Carr, A., Kell, M. R., Lynch, M., Ryan, D., Winter, D. C., Rajpal, P., Kirwan, W. O., Redmond, H. P., Larkin, C. J., Sloan, J. M., Watson, R. G. P., Ardill, J. E. S., Collins, J. S. A., Buchanan, K. D., Lim, P. L., Gibbons, M., Crawford, E. J., Johnston, B. T., Mitchell, R. M. S., Watson, R. G. P., Gardiner, K. R., Collins, J. S. A., McCallion, K., Mitchell, R. M. S., Collins, J. S. A., Watson, R. G. P., McCallion, K., Gardiner, K. R., McCallion, K., Gardiner, K. R., Mitchell, R. M. S., Watson, R. G. P., Collins, J. S. A., Rodgers, C., Johnston, S., Watson, R. G. P., Crone, B. M., Love, A. H. G., Feighery, L., Feighery, C., Jackson, J., Abuzakouk, M., Lynch, S., Weir, D. G., Yassin, M. M. I., Harkin, D. W., Barros D’sa, A. A. B., Parks, T. G., Curry, M. P., Hegarty, J. E., Golden-Mason, L., O’Farrelly, C., Hannigan, E., and Parfrey, N.

Published
1998
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11. Irish society of gastroenterology: Proceedings of meeting held friday 20th and saturday 21st november 1998

Author

Curry, M. P., Norris, S., Hegarty, J. E., Smith, F., Nolan, N., Golden-Mason, L., O’Farrelly, C., Walsh, K. M., Fletcher, A., MacSween, R. N. M., Morris, A. J., Bohan, A., Nolan, N., Hegarty, J. E., Ryan, E., Flanagan, A-M., Martinez-Dalmau, P., Crowe, J., O’Farrelly, C., Golden-Mason, L., Curry, M. P., Kelly, J., Traynor, O., Hegarty, J. E., Mathias, J., McCormick, P. A., McEntee, G., Hegarty, J., Traynor, O., Barrett, S., O’Keane, J. C., Crowe, J., Shah, A. A., Berry, M., Thjodleifsson, B., Bjarnason, I., Gudjohnsson, H., Oddson, E., Fitzgerald, D. J., Kay, E., Price, A., Murray, F. E., Carton, E., Mulligan, E. D., Caldwell, M. T. P., Rana, D., Ryan, B., Mahmud, N., Keeling, N., Tanner, W. A., Keane, F. B. V., McDonald, G., Reynolds, J. V., Mahmood, Z., Rathore, O., Ellis, I., Byrne, P., Mahmud, N., Keeling, P. W. N., Khan, I., McManus, K., Anikin, V., Mills, M., McGuigan, J., Taylor, C., Winter, D. C., O’Sullivan, G. C., Harvey, B. J., Bennett, M. W., O’Connell, J., O’Sullivan, G. C., Collins, J. K., Shanahan, F., Wieneke, P., O’Leary, C., Healy, M., O’Halloran, T., Barry, R., Cronin, C. C., O’Regan, P., Shanahan, F., Bennett, M. W., O’Connell, J., O’Sullivan, G. C., Collins, J. K., Shanahan, F., O’Grady, H., Grant, D., Sheahan, K., Hyland, J. M. P., O’Donoghue, D. P., Murphy, J., Lee, G., Madden, M., Kelly, J., Collins, J. K., Shanahan, P., Sullivan, G. O., Shima, H., Basisht, R., Ohshiro, K., Puri, P., Goh, J., MacMathuna, P., Baird, A., Godson, C., Brady, H. R., Petasis, N. A., Fokin, V. V., O’Keane, J. C., McCormack, G., McCormick, P. A., Hegarty, J. E., O’Donoghue, D. P., Hyland, J. M. P., Khosraviani, K., Weir, H. P., Williamson, K., Hamilton, P., Moorehead, R. J., Mcllmoyle, J., Watson, R. G. P., Collins, J. S. A., Tham, T. C. K., Doyle, R. M., Molony, C., Fitzpatrick, D., Coakley, D., Walsh, J. B., Kelleher, D., Devitt, E., Keane, C., Walsh, C., Bennett, M. W., O’Connell, J., O’Sullivan, G. C., Collins, J. K., Shanahan, F., Murray, K. P., Kaufman, H. S., Shin, J. H., Pitt, H. A., Johnston, S. D., Watson, R. G. P., McMillan, S. A., Larkin, C. J., Sloan, J. M., Watson, R. G. P., Ardill, J. E. S., Collins, J. S., Buchanan, K. D., Larkin, C. J., Curry, W. J., Watson, R. G. P., Johnston, C. F., Ardill, J. E. S., Buchanan, K. D., Larkin, C. J., Curry, W., Johnston, C., Sloan, J., Watson, R. G. P., Ardill, J., Collins, J. S., Buchanan, K. D., Larkin, C. J., Curry, W., Johnston, C., Sloan, J., Watson, R. G. P., Ardill, J., Collins, J. S., Buchanan, K. D., Larkin, C. J., Irvine, R., Gibson, L., Tham, T. C. K., Creedon, G., Mabruk, M., Leader, M., O’Grady, T., Murphy, M., Kay, E., Shah, A. A., Harhen, B., Fitzgerald, D. J., Murray, F. E., Hickey, A., Gannon, N., O’Boyle, C., Byrne, R., Smith, M., Murray, F., Byrne, M. F., Harhen, B., Fitzgerald, D. J., Murray, F. E., Quinlan, J., Delaney, C. P., O’Grady, H., Varadarajan, R., O’Donoghue, D. P., Hyland, J. M., MacEneaney, P. M., Skehan, S. J., Curry, M., Gibney, R. G., McCormick, P. A., Malone, D. E., Kealy, S., MacEneaney, P. M., Dodd, J., Murrary, R., Donoghue, D. P., Keating, D., Gibney, R. G., Malone, D. E., Hashim, Z., Donnellan, J., O’Connor, Y., Kearns, M., Stevens, F. M., Sookhai, S., Wang, J. H., Neary, P., McCourt, M., O’Connell, D., Redmond, H. P., Khosraviani, K., McAteer, E., Campbell, W. J., Mackle, E. J., Smyth, C., McKiernan, S., Lawlor, M., Pilkington, K., Hagan, R., Kelleher, D., Montague, S., Barry, R., Buckley, M., Morain, C. A. O., Connolly, C., Tierney, S., Gray, J., Lyons, N. D., Delaney, P. V., Grace, P. A., Nemeth, L., O’Briain, D. S., Puri, P., Carton, E., Mulligan, E. D., O’Toole, C., Roddy, D., Keeling, N., Griffin, M., McDonald, G., Hennessy, T. P. J., Reynolds, J. V., O’Keffe, C., O’Donoghue, D., Hegarty, J., McCormick, P. A., Murphy, E., Reynolds, J., Nolan, J. J., Goh, J., Barrett, S., McAndrew, M., Crowe, J., O’Keane, J. C., Clarke, G., Stewart, S., McKiernan, S., Cockram, A., O’Keane, J. C., Kelleher, D., Crowe, J., Coughlan, B., Sheehan, J., Hickey, A., Crowe, J., Lang, E. E., Caldwell, M. T. P., Tanner, W. A., McNamara, D., Hamilton, H., Beattie, S., Montague, S., O’Morain, C., Windle, H. J., Kelleher, D., Heaney, A., Collins, J. S. A., Tham, T. C. K., Chan, W. S., Mitchell, R. M. S., Collins, J. S. A., Watson, R. G. P., O’Leary, C., Wieneke, P., Feighery, L., Quane, K., Molloy, M., Shanahan, F., Feighery, C., Cronin, C. C., Golden-Mason, L., Curry, M. P., Traynor, O., McEntee, G., Kelly, J., Hegarty, J. E., Farrelly, C. O., Egan, B. M., Barry, M. K., Grant, D. C., O’Donoghue, D., Hegarty, J., Traynor, O., Hyland, J. M. P., Barry, P., Casey, P., Laffoy, M., Tracey, J., McCormick, P. A., Goode, T., O’Connell, J., Hopkins, A., Baird, A. W., O’Sullivan, G. C., Collins, J. K., Shanahan, F., O’Leary, C., Kingston, M., Blackwell, M., Wieneke, P., Cronin, C. C., O’Regan, P. F., Shanahan, F., Maher, L. J., Skelly, M. M., Godson, C., Brady, H. R., and Baird, A. W.

Published
1998
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12. Sylvester o’halloran surgical scientific meeting: Proceedings of meeting held 7th & 8th March 1997 in Charles parsons theatre, university of Limerick

Author

Fulton, G. J., Davies, M. G., O’Hagen, P., Rasheed, A., Kelly, C., Kay, E., Fitzgerald, S., Bouchier-Hayes, D., Leahy, A., Fennessy, F., Kelly, C., Fitzgerald, P., Bouchier-Hayes, D., Khosraviani, K., Weir, H. P., Williamson, K., Wilson, R., Moorehead, R. J., Rowlands, B. J., Morrissey, D., O’Connell, J., Lynch, D., O’Sullivan, C., Shanahan, F., Collins, J. K., Kelly, J. L., Soberg, C. C., Lyons, A., Mannick, J. A., Lederer, J. A., Chen, C., Kelly, C., Leahy, A., Bouchier-Hayes, D. J., Fitzsimons, H., O’Hanlon, D. M., Curran, C., Canney, M., Morris, S., Clinton, O., Given, H. F., Coveney, E., Lyerly, H. K., Murphy, F. L., Kelly, C. J., Osborne, D. H., Kelly, P., O’Riordan, D. S., Horgan, P. G., Keane, F. B. V., Tanner, W. A., Kilmartin, P., Delaney, C. P., Johnston, S. M., Fitzpatrick, J. M., Gorey, T. F., Mehigan, J., O/rsRiordan, M. G., Shines, N., Hill, A., Tanner, W. A., McDonnell, C. O., Coveney, E., Murphy, F., Javadpour, S. M., Alhadi, Y., Leahy, A., Waldron, R., Watson, R. G., Tarrant, A., Neelamekam, T. K., Mathias, J., Geoghegan, J., Boyle, T., Traynor, O., Hayes, S., O’Donovan, B., Ajmal, N., McCann, J., Corrigan, N. T., O’Riordan, M. G., Ross, P., O’Donohoe, M., Bresnihan, M., Feeley, T. M., Fiuza-Castineira, C., Coleman, D., Fisher, H., Butt, A., Ghumman, E., Grace, P., Burke, P., Johnston, S. M., Martin, S. A., Fox-Talbot, M. K., Lipsett, P. A., Lillemoe, K. D., Pitt, H. A., O’Keeffe, D. A., Hill, A. D. K., Sheahan, K., Ryan, F., Barton, D., Fitzgerald, R., McDermott, E. W., O’Higgins, N. J., Kavanagh, E., Kiely, P., O’Driscoll, D., Ramesh, M., Kirwan, W. O., Winter, D. C., Nally, K., O’Callaghan, J., Matthews, J. B., Harvey, B. J., O’Sullivan, G. C., Shanahan, F., Young, L. S., Regan, M. C., Sweeney, P., Bouchier-Hayes, D. M., Fitzpatrick, J. M., Dardis, R., Kelly, C., Broe, P., Bouchier-Hayes, D., O’Brien, M. G., Collins, J. K., Shanahan, F., O’Sullivan, G. C., Neary, P., Ridgeway, P., Condron, C., Wang, J. H., Redmond, H. P., Bouchier-Hayes, D., Redfern, D. R. M., Strachan, R. K. S., Hollingdale, J. M., Grace, P. A., Acheson, A., Graham, A., Weir, C., Lee, B., O’Donnell, C., Buckley, D., O’Donnell, J. A., Purcell, E., O’Donoghue, M., Sultan, S., Colgan, M., Molloy, M., Moore, D., Shanik, G., McCollum, P. T., Raza, Z., Naidu, S., Stonebridge, P. A., Colgan, M. P., Moore, D. J., Shanik, D. G., Dowdall, J., Hill, A. D. K., Williams, C., Shering, S. G., Duffy, G., McDermott, E. W., O’Higgins, N. J., Coveney, E., Greengrass, R., Iglehart, D., Little, G., Kim Lyerly, H., Fynes, M., Cahill, A., O’Herlihy, C., O’Connell, P. R., Ahmad, I., Etisham, M., Drumm, J., Flood, H., Mulhall, K., Murray, K., O’Rian, S., Garvey, N., Johnston, J., Waldron, R., McGreal, G. T., Kelly, J. L., O’Donnell, J. A., Kirwan, W. O., Brady, M. P., Duffy, M. M., Regan, M., Harrington, M. G., O’Connell, P. R., Fitzpatrick, J. M., Javadpour, M., Coveney, E., McDonnell, C., Watson, R. G., Eguare, E., Barry, M. C., Ghumman, E., Grace, P. A., O’Donovan, B., Hayes, S., Ajmal, N., McCann, J., O’Toole, G. C., O’Higgins, N., McDermott, E., Brady, C. M., Sultan, S. A., O’Donoghue, M. K., Molloy, M. P., Colgan, M. P., Moore, D. J., Shanik, G. D., McCollum, P. T., Holdsworth, R. J., Naidu, S., Raza, Z., Fehily, M., Hill, A. D. K., Doran, C., O’Riordan, M. G., O’Donoghue, M., Keane, F., Tanner, W. A., Rothwell, J. F., Staunton, M. J., O’Mahony, L., Gaffney, E. F., Mealy, K., Hennessy, T. P. J., Winter, D. C., O’Sullivan, G. C., Harvey, B. J., and Geibel, J.

Published
1998
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13. Irish society of gastroenterology: Proceedings of meeting held in Craigavon on 28th and 29th May, 1993

Author

Gardiner, K. R., Barclay, G. R., McCaigue, M. D., Erwin, P. J., Halliday, M. I., Maxwell, R. J., Rowlands, B. J., Whiteside, M. C. R., Anderson, N., Wilson, R. H., Kee, F., Moorehead, R. J., H Russell, S. E., Clements, B., Hamilton, P., Cameron, S., Evoy, D. A., Regan, M., Attwood, S. E. A., Keeling, P. W. N., Stephens, R. B., Caldwell, M. T. P., Marks, P., Byrne, P. J., Walsh, T. N., Hennessy, T. P. J., O’Broin, E., Donohoe, J., Mealy, K., Kerin, M., Gillen, P., Tanner, W. A., Keane, F. B. V., O’Malley, K., Neligan, M., McEntee, G., Bouchier Hayes, D., Morrin, M., Kelly, M., Khan, F., Barrett, N., Williams, N., Delaney, P., Goggins, M. G., Mahmud, N., Hall, N., O’Connell, M., Weir, D. G., Kelleher, D., Thornton, G., O’Sullivan, M., O’Sullivan, G., Collins, J. K., Cahill, R. J., Beattie, S., Hamilton, H., O’Morain, C. A., Chua, A., Dinan, T. G., Noonan, N., Rovati, L. C., Keating, J., Somasundaram, S., Smithson, J., Menzies, I., Francis, N., Bjarnason, I., Gazzard, B. G., O’Donovan, D., Kelly, C., Bouchier-Hayes, D. M., Watson, W., Redmond, P., Burke, P., Bouchier-Hayes, D. J., O’Mahony, A. M., Erwin, P., McCaigue, M., Halliday, I., Rowlands, B., Golden, B., Loughnane, F., Brindley, N., Dudley, S., Drebin, J., Geraghty, J., Broe, P., Stinson, J., Feely, J., Fan, X. J., Fan, X. G., Caldwell, T. P., Evoy, D., Lawlor, P., Attwood, S. E., Gilvarry, J., O’Morain, C., Stafford Johnson, D. B., Keeling, F., Kent, P., Hennebry, T., Burke, J., Mooney, E., McMathuna, P., Crowe, J., Fitzpatrick, J. M., Gorey, T. F., Malone, F., Reynolds, J., Walsh, B., Ellias, Y., Traynor, O., Couse, N., Burke, G., Fallon, C., Kidney, D., Murray, E., Buckley, M., McCarthy, M., O’Donovan, N., Stack, W. A., Keely, S., O’Donoghue, D. P., Baird, A. W., Duggan, A., O’Brien, F., Abuzakouk, M., Feighery, C., Bergin, C., Casey, E., Weir, D., O’Farrelly, C., Mulcahy, H., Jeffers, M., O’Dowd, G., Stagg, M., Toner, M., Fenlon, H., Ashbury, K., O’ Brien, M., Ireland, A., and Morain, C. O.

Published
1993
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14. Irish society of gastroenterology: Proceedings of Winter Meeting held 4th/5th December 1992in Beaumont hospital, Dublin

Author

O’Sullivan, M., Thornton, G., O’Sullivan, G., O’Mahony, A. M., O’Connell, J., Hanvajanawong, C., Phelan, D., O’Sullivan, G. C., Collins, J. K., Bamford, K. B., Lutton, D. A., Collins, J. S. A., O’Loughlin, B., Johnston, B. T., McFarland, R. J., Love, A. H. G., Buchanan, K. D., Fillmore, D., Ardill, J. E. S., Clyne, M., Drumm, B., Cyne, M., Tham, T. C. K., McLaughlin, N., Hughes, D. F., Ferguson, M., Crosbie, J. J., Madden, M., Namnyak, S., O’Connor, F. A., Magbri, Awad El, Stevens, F. M., McCarthy, C. F., Lynch, M., O’Brien, M., Ryan, E., MacMathuna, P., Kelly, P., Lennon, J., Crowe, J., Mulvey, S., Maguire, C., Clarke, E., Cronin, K. J., Kent, P., Mooney, E., Corrigan, T., O’Connell, R., Fitzpatrick, J. M., Gorey, T. F., Prabhaker, M. C., Bannon, C. A., Delaney, C., Duggan, M., Gorey, T., Abuzakouk, M., Lynch, S., Casey, E., Weir, D., Feighery, C., O’Farrelly, C., Fan, X. J., Chua, A., Shahi, C. N., Kelleher, D., Keeling, P. W. N., Parks, R. W., Diamond, T., McCrory, D. C., Johnston, G. W., Clements, W. D. B., Ennis, M., Campbell, G. R., Halliday, M. I., Rowlands, B. J., Wilson, R. H., Williamson, K., McLoughlin, J., Moorehead, R. J., O’Connor, A. M., Johnston, C. F., Gillmore, D., Boreham, C., Caldwell, M. T. P., Jazrawi, S., Byrne, P. J., Walsh, T. N., Hennessy, T. P. J., Li, H., Kay, E. W., Mulcahy, H., Curran, B., O’Donoghue, D., Leader, M., Walsh, C. Barry, O’Sullivan, S. T., Reardon, C. M., Hardiman, C., O’Donnell, J. A., Kirwan, W. O., Brady, M. P., McGreal, G., Hehir, D. J., Brady, M. P., O’Donnell, J., Pender, S. M., Courtney, M. G., Fielding, J. F., Swan, N., Chong, A., Denesh, T. G., Coll, D., McElearney, C., Kay, E., Sant, S., Doyle, J. S., Buckley, M., Cahill, R. J., Beattie, S., Hamilton, H., O’Morain, C., O’Sullivan, K., Forde, A. M., Gilvarry, J., Jackson, J., Alvi, R., Leahy, A., Lynch, G., Lane, B., Browne, H. Y., Keeling, P., Stafford-Johnson, D., Kee, S., Carr, J., Ryan, M. J., Sheehan, S., Broe, P., Deasy, J., O’Donovan, D. A., Bouchier-Hayes, D. M., Kelly, C., Grace, P., Redmond, H. P, Burke, P., Bouchier-Hayes, D. J., O’Malley, K., Qureshi, A., Osborne, H., Monkhouse, W. S., Bouchier-Hayes, D., Goggin, M., Joyce, W. P., Traynor, O., Hyland, J., Beausang, E., Mealy, K., Prendergast, C., Joyce, L., McNicholas, M. M. J., Gibney, R. G., Dolan, J., MacErlean, D. P., Hyland, J. M., Fenlon, H. M., Mulcahy, H. E., Stack, W. A., Skelly, M. M., Hegarty, J. E., Stack, W., O’Donoghue, D. P., Norris, S. M., McNicholas, M., Murray, F. E., Williams, N., Burke, J., Lamort, W., Fitzpatrick, J., Afdhal, N., Gibney, R., McLoughlin, R. F., Mourad, F. H., O’Donnell, L. J. D., Dias, J., Ogutu, E., Farthing, M. J. G., Hoyle, C. H. V., Hill, A. D. K., Darzi, A., Carey, P. D., Menzies-Gow, N., Monson, J. R. T., Goggins, M. G., O’Broin, S., Kelleher, B., Scott, J. M., Weir, D. D., Watson, R. G. P., Goss, B., Angus, P. W., Duckham, N., Sewell, R. B., and Smallwood, R. A.

Published
1993
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15. Irish Society of Gastroenterology: Proceedings of meeting held November 1990

Author

Coleman, J., Hayes, D. Bouchier, Daw, M. A., O’More, R., Keane, C. T., O’Morain, C., Johnson G. W., Spencer E. F. A., Wilkinson A. J., Kennedy T. L., Collins, J. S. A., Bamford, K. B., Collins, B. J., Sloan, J. M., Moorehead, R. J., Love, A. H. G., McCarthy, C., Collins, R., Beattie, S., McDevitt, J., Feighery, C., O’Farrelly, C., Weir, D. G., Kelleher, D., Whelan, A., Williams, Y., Kellegher, D., Weir, D., Prabhakar, M. C., Daw, M., Keane, F., McDermott E. W. M., Duduric B., Brennan M. F., Gaffney, R., O’Leary, J., Doyle, T., Gaffney, A., Gough, D. B., Fearon, K. C. H., Winstanley, P., Carter, D. C., McAnena, O. J., Moore, F. A., Moore, E. E., Pogetti, R., Peterson, V. M., Abemathy, C. M., Parsons, P., Williams, N. N., Daly, J. M., Herlyn, M., Bouchier-Hayes, D., Course, N. F., Horgan, P. G., Fahy, A., Delaney, C., Fitzpatrick, J. M., Gorey, T. F., Jazrawl S., Walsh T. N., Byrne P. J., Lawlor P., Hennessy T. P. J., O’Sullivan, K. R., Mathias, P. M., McNicholas, M., Logan, M., Masterson, J., Gillen, P., Hyland, J., Beausang, E., Joyce, W. P., Williams, N., Maxwell, W., Reid, I., Sharpe, I., Geraghty, J. G., Tanner, W. A., Patchett, S., Mulcahy, H., Afdhal, N., O’Donoghue, D., Lohan, A., Darzi, A., Keane, F. B. V., Keeling, P. W. N., Gibney, R. C., Keane, R., Drumm, J., Egan, T. J., Delaney, P. V., O’Sullivan, G., Harte, P., Grace, P. A., Qureshi, A., Osbome, H., Bouchier-Hayes, D. J., Bamford, S. L., Geraghty, J., Keane, F. B., Coleman, J. E., Gleeson, A., Mealy, K., Barry, M., Traynor, O., Keating, J. J., Chua, A., Ah-Kion, S., McNulty, J., Heaney, L. G., Murphy, P., Connolly, J. H., Callender, M. E., MacMathuna, P., Farrant, M., Hourihane, D. O. B., Donaldson, P., Lombard, M., Westaby, D., Weir, D. G., Williams, Roger, Couse, N. F., Burke, J., Lennon, G., Delaneyc, C. P., O’Brien, S., O’Brien, A., Fitzgerald, M. X., Hegarty, J. E., Noonan, N., Healy, M., O’Moore, R., Corrigan, O. I., Keating, P. W. N., Li, H. U. I., Byrne, P. J., Lawlor, P., Stuart, R. C., Jazrawi, S., Walsh, T. N., Hennessy, T. P. J., Course, N. F., Wai, D., Jaeger, H., Jackson, A. M., Mitchell, C. J., MacFie, J., Delaney, C. P., McGeeney, K., Caldwell, M. T. P., O’Donoghue, D. P., Connolly J., Stuart R. C., Kay E., Gorey T., Keane R., McKiernan, P., Glasgow, J. F. T., Johnson, B. T., Ferguson, R., Davidson, I., Hurley, J., Keeling, P., Crowley, T., Long, A. A., O’Brien, D. P., Waldron, R. P., Shearer, M. J., Given, H. F., McEntee, G., Monson, J., Donohue, J., Nagomey, D., Trimble, K. C., Molloy, A. M., Scott, J. M., Kay, E., McKeever, J., and Hennessey, T. P. J.

Published
1993
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16. Irish society of gastroenterology: Proceedings Of Meeting Held

Author

Cotter, L. A., Healy, M., Buckley, M., O’Morain, C., Keane, C., O’Moore, R. R., Dickey, W., Roberts, G., Orr, G., Porter, K., McCrory, D., Halliday, M. I., Hoper, M., Crockard, A., Rowlands, B. J., Chua, A., Dinan, T., Dunbar, B., Weir, D. G., Keeling, P. W. N., Johnston, B. T., Collins, J. S. A., McFarland, R. J., Love, A. H. G., Darzi, A., Speakman, C. T. N., Spigelman, A., Henry, M. M., fnTanner, W. A., fnMcEntee, G. P., fnKeane, F. B., Tighe, O., Bennett, M., Mulcahy, H., Williams, N. N., Duignan, J. P., Bouchier-Hayes, D., O’Donoghue, D., Croke, D. T., Hill, A. D., Walsh, T. N., Hennessy, T. P. J., Goggin, M., Joyce, W. P., Prendergast, C., Gibney, E., Traynor, O. J., Hyland, J., O’Brien, S., Fitzgerald, M. X., Hegarty, J. E., Leahy, A., Grace, P., Qureshi, A., Leader, M., Broe, P., Eustace, S., Blake, N., McDevitt, J., Feighery, C. F., O’Farrelly, C., Kelleher, D., O’Connell, M. A., Stokes, M. A., Hill, G. L., Gaffney, P., O’Leary, J., Doyle, C., Hogan, J., Gaffney, Anne, Attwood, S. E. A., Murphy, P., Stephens, R. B., Wilson, R. H., Gilliland, R., Kee, F., Sloan, J. M., Moorehead, R. J., ’Suilleabhain, G., Horgan, A., Kirwan, W. O., Deans, G. T., Heatley, M., Williamson, K., Parks, T. G., Rowland, B. J., Spence, R. A. J., Mealy, K., Burke, P., Herlyn, M., Redmond, H. P., Clery, A. P., Deasy, J. M., Austin, O., Meenan, J., Canili, R. J., Mathias, P. M., Beattie, S., Hamilton, H., Geoghegan, J. G., Cheng, C. A., Lawson, D. C., Pappas, T. N., Collins, R., Beatie, S., Collins, J. K., O’Sullivan, G., Corbett, A., Clements, W. D. B., MacMathuna, P., Lombard, M., Gimson, A., Westaby, D., Williams, R., Duggan, M., Lennon, J., Crowe, J., Ritchie, A. J., Johnston, F., McGuigan, J., Gibbons, J. R. P., Buchanan, K. D., Gilvarry, J. M., Robinson, R., Fielding, J. F., Lawler, M., Humphries, P., Sheils, O., O’Briain, D. S., McCarthy, J., McDermott, M., Hourihane, D., Gallagher, H., Barry, M., Lennon, F., Hederman, W. P., O’Connell, P. R., Gorey, T. F., Fitzpatrick, J. M., Daly, J. M., Carthy, J. E., Redmond, H., Croake, D., Grace, P. A., Campbell, G., Maguire, O., Lynch, S., Atwood, J., Madrigal, L., Attwood, J., Murphy, A., Shovlin, P., Hegarty, J., Egleston, V., Mealy, K., MacErlean, D. P., Johnston, S., O’Malley, K., McEntee, G., Smyth, E., Moran, B., Plant, G., Rees, M., Brindley, N., Osborne, H., Lane, B., Lynch, G., Geraghty, J., Murphy, D., O’Brien, M., and Harte, P.

Published
1992
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22. Irish society of gastroenterology: Proceedings of winter meeting 1985 in gort muire conference centre, Ballinteer, Dublin on Friday 22nd and Saturday, 23rd November

Author

O’Byrne, P., Collins, P., Johnson, A., Ledwith, M., Lane, B., Bouchier-Hayes, D., MacMathuna, P., O’Reilly, T., Barry, M., Duanes-Laita, A., Feely, J., Keeling, P. W. N., Cotter, P., Burke, G., Waldron, R., Zinner, M. J., Jaffe, B. M., Givan, F., Keye, G., Byrne, P., O’Brien, M., O’Farrelly, Cliona, Stevens, F., McCarthy, C., Feighery, C., Weir, D. G., Hannigan, M. C., Stevens, F. M., McCarthy, C. F., Fottrell, P. F., O’Connor, M. P., Kennedy, N. P., Courtney, M. G., Kelleher, D., Weir, D. W., Senapati, A., Kitler, M. E., Thompson, R. P. H., O’Shea, B., Madigan, D., Keeling, P., Hennessy, T. P. J., Meenan, John J., Gaffney, Eoin F., Duigan, J. P., Johnson, A. H., Collins, P. B., Healy, M. V., Skehill, R., Grimes, H., O’Farrelly, C., Kelly, J., Rees, R., Hoey, H., Humphreys, H., Dooley, C., O’Leary, D., Bourke, S., McKenna, D., Power, B., Keane, C., Sweeney, E., O’Morain, C. A., Afdhal, N. H., McCormick, A., O’Donoghue, D. P., Quigley, E. M. M., Turnberg, L. A., Moorehead, R. J., Hoper, Margaret, McKelvey, S. T. D., Tobbia, I., Rafferty, R., Gillen, P., Stuart, R., Dawson, K., Collins, J. S. A., McKnigh, J. A., Pyper, P. C., Love, A. H. G., Dillon, M. E., O’Connor, E., Keeling, P. W. N., Broe, P. J., Harte, P. I., Keane, T., Garstin, W. I. H., Buchanan, K. D., Walsh, J. P., Bloomfield, F. J., Maxwell, W. J., Hogan, F. P., O’Malley, Vincent P., Postier, Russell G., Lombard, M., Craven, C., Spencer, S., Crowe, J., Quinn, Fergal, Templeton, John L., Tobin, M. V., Hughes, S., Gilmore, I T., Keane, R. M., Johnson, A. B., Duenas-Laita, A., Younger, K., O’Brien, T., Cotter, J., Cullinane, T., Whelton, M. J., Waldron, D., Bowes, K., Given, H. F., Gawley, W. F., Gorey, T. F., Osborne, D. H., Lane, B. E., Collins, P. G., Boston, V. E., and O’Mahony, C.

Published
1986
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23. Irish Society of Gastroenterology Winter Meeting 1986 held in Belfast City Hospital on Friday, 21st November and Saturday, 22nd November, 1986

Author

Keating, J. J., Mahapatra, D. N., Stevens, F. M., Connolly, C. E., McNicholl, B., McCarthy, C. F., O’Connor, B. J., Lennon, J. R., Crowe, J., Ramgh, Bashir, Bourke, M., O’Reilly, T., MacMathuna, P., Keeling, P. W. N., Feely, J., O’Connor, M. P., Kelleher, D., Skuce, A., Buckley, T., Cafferky, M. T., Weir, D. G., O’Connor, P., Kennedy, N., Courtney, G., O’Connell, P. R., Pemberton, J. R., Kelly, R. A., O’Connor, M., Drumm, J., Hogan, J., Keohane, Catherine, Kirwan, W. O., Nee, J. M., Jaffe, B. M., Pollock, T. W., Horgan, P. G., O’Sulivan, F., Nunes, D., McCann, S., Keeling, N., Gillen, P., Healy, M., Keeling, P., Byrne, P. J., O’Moore, R. R., Hennessy, T. P. J., Gaffney, Peter, McCormick, P. A., Afdhal, N., Hegarty, J. E., McKenna, D., Humphreys, H., Bourke, S., Dooley, C., Keane, C., Sweeney, E., O’Morain, C. A., Donovan, I. A., Lasarides, P., Burkitt, D., Doricott, N. J., Temple, J. G., Alexander-Williams, J., Collins, P. G., Kehely, A., Moorehead, R. J., Mills, J. O. ML, Wilson, H. K., McKelvey, S. T. D., McCall, Therest, O’Brien, P. A., O’Mahony, S., O’Sullivan, J., MacFeely, L., Whelton, M. J., Toner, M., Condell, D. O., O’Brian, D. S., Wilson, B. G., Spence, R. A. J., Anderson, J. R., McDonald, G. S. A., Freyne, P., O’Rourke, S., Duignan, J. P., Bouchier-Hayes, D., Johnson, A. H., Collins, P. B., Kennedy, M. John, Daly, Peter A., O’Brien, A. A. J., Lawlor, Emer, Tanner, W. A., Conway, V., Farrell, R., Templeton, J. L., Harvey, C. F., Hanna, W. A., Parks, T. G., Feeley, T. M., Gill, K., Barry, M., Tobi, M. V., and Gilmore, I. T.

Published
1987
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24. Irish Society of Gastroenterology Proceedings of the Summer Meeting of the Irish Society of Gastroenterology, held in Universitly College, Cork on Friday 6th and Saturday 7th June, 1986

Author

Moorehead, R. J., Donaldson, John, McKelvey, S. T. D., Drumm, J., Harding, L. K., Clarke, E. A., Alexander-Williams, J., Donovan, I. A., Lorigan, G., Butler, F., Broe, P. J., O’Hara, Martin J., McCormick, P. Aidan, Molloy, Aishling, McGrath, Derek, O’Donoghue, Diarmuid P., Farrell, T., O’Donoghue, D., Daly, L., Masterson, J. B., Breen, E. G., Coughlan, J., Connolly, C. E., Stevens, F. M., McCarthy, C. F., Tobin, M. V., Fiskan, R. A., Dissory, R. T., Gilmore, I. T., McCormick, Deirdre, Cullen, Alan, McCormick, P. Aidan, Towers, Robert P., Keane, R. M., Coleman, J. E., Clery, A. P., Keane, T., Dillon, B., Afdhal, N. H., McCormick, C. J., Stevens, F. M., Connolly, C. E., McCarthy, C. F., Hitchcock, H., Waldron, David J., Fitzgerald, Raymond J., Quigley, E. M. M., Hall, L., Turnberg, L. A., Brennan, F. N., Buchanan, K. D., Afdhal, N. H., Duffy, M. J., Thornton, A., O’Sullivan, F., O’Donoghue, D. P., Mullen, P., O’Connor, B., Lombard, M., Coakley, J. B., Crowe, J., Lennon, J. R., Keeling, P., Hennessy, T. P. J., Gleeson, D., Quereshi, Y., Murphy, G. M., Dowling, R. H., O’Connor, H. J., Dixon, M. F., Wyatt, J. I., Axon, A. T. R., Gillen, P., Keeling, P., Byrne, P. J., West, A. B., Hennessy, T. P. J., Walsh, T. N., O’Higgins, N., Quigley, E. M. M., Turnberg, L. A., O’Hara, Martin J., McCormick, P. Aidan, McGowan, Katherine, Miller, Joan C., Masterson, James, O’Donoghue, Diarmuid P., Courtney, M. G., McPartlin, J. M., Scott, J. M., Weir, D. G., Wilson, B. G., Howe, J. P., Parks, T. G., McCormick, P. A., Ramsay, N., Afdhal, N., Tubridy, P., Shattock, A. G., Hillery, I., O’Donoghue, D. P., Collins, J. S. A., Knill-Jones, R. P., Crean, G. P., Love, A. H. G., Quigley, E. M. M., Hole, D. J., Gillis, C. R., Watkinson, G., Moore, Helena, Moylan, H. E., Fottrell, P. F., Stevens, F. M., Brady, H. R., Godson, C., Ryan, M. P., Bourke, S., FitzGerald, M. X., McCormick, P. A., O’Farrelly, C., Graeme-Cook, F., Finch, A., Feighery, C., Weir, D. G., O’Donoghue, D. P., FitzGerald, M. X., Maxwell, W. J., Walsh, J. P., Hogan, F. P., Kennedy, N. P., Keeling, P. W. N., Sheil, O., Barniville, H., and Fitzgerald, O.

Published
1987
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25. Re-Staging Following Long-Course Chemoradiotherapy For Rectal Cancer: Does It Influence Management?

Author

McBrearty, A., McCallion, K., Moorehead, R. J., McAllister, I., Mulholland, K., Gilliland, R., and Campbell, W. J.

Abstract

Background: In patients with locally advanced or low rectal cancers, long-course chemoradiotherapy (LCCRT) is recommended prior to surgical management.1 The need for restaging afterwards has been questioned as it may be difficult to interpret imaging due to local tissue effects of chemoradiotherapy. The pupose of this study was to determine if restaging affected the management of patients receiving long-course chemoradiotherapy for rectal cancer. Methods: A retrospective review of patients with rectal cancer discussed at the South Eastern Health and Social Care Trust Lower Gastrointestinal Multi-Disciplinary Team Meeting (LGIMDT) in 2013 who had received long-course chemoradiotherapy was performed. Patients were identified from the Trust Audit Department, LGIMDT notes and patient records. Imaging results and outcomes from meetings were obtained through the Northern Ireland Picture Archiving and Communications System® (NIPACS) and Electronic Care Record® (ECR). Data including patient demographics, initial radiological staging and LGIMDT discussion, restaging modality and result, outcome from post-treatment LGIMDT discussion and recorded changes in management plans were documented using a proforma. Results: Seventy-one patients with rectal cancer were identified as having LCCRT in 2013 (M:F 36:35; age range 31 - 85 years). Fifty-nine patients were restaged following long-course treatment with computed tomography (CT) and magnetic resonance imaging (MRI). Twelve patients did not undergo restaging. Data was not available for 6 patients, one patient underwent emergency surgery, two patients were not fit for treatment, one failed to attend for restaging and two patients died prior to completion of treatment. Of the 59 patients restaged, 19 patients (32%) had their management plan altered from that which had been proposed at the initial LGIMDT discussion. The most common change in plan was not to operate. Ten patients had a complete clinical and radiological response to treatment and have undergone intensive follow-up. Nine patients had disease progression, with 3 requiring palliative surgery and 6 referred for palliative care. Conclusion: Of those patients who were restaged, 32% had their management plan altered from that recorded at the initial LGIMDT discussion. Seventeen per cent of patients in this group had a complete clinical and radiological response to treatment. Fifteen percent demonstrated disease progression. We recommend, therefore, that patients with rectal cancer be restaged with CT and MRI following long-course chemoradiotherapy as surgery may be avoided in up to 27% of cases. [ABSTRACT FROM AUTHOR]

Published
2016

26. Osteopontin regulates proliferation, apoptosis, and migration of murine claudin-low mammary tumor cells.

Author

Saleh, S., Thompson, D. E., McConkey, J., Murray, P., and Moorehead, R. A.

Subjects
OSTEOPONTIN, APOPTOSIS, MOUSE leukemia, CELL migration, CLAUDINS, PROTEIN metabolism, ANIMAL experimentation, BREAST tumors, CELL lines, CELL physiology, CELL motility, GENETIC techniques, MEMBRANE proteins, MICE, PROTEINS, RESEARCH funding, OLIGONUCLEOTIDE arrays, GENE expression profiling
Abstract

Background: Osteopontin is a secreted phosphoglycoprotein that is expressed by a number of normal cells as well as a variety of tumor cells. With respect to breast cancer, osteopontin has been implicated in regulating tumor cell proliferation and migration/metastasis and may serve as a prognostic indicator. However it remains unclear whether osteopontin has the same impact in all breast cancer subtypes and in particular, osteopontin's effects in claudin-low breast cancer are poorly understood.Methods: cDNA microarrays and qRT-PCR were used to evaluate osteopontin expression in mammary tumors from MTB-IGFIR transgenic mice and cell lines derived from these tumors. siRNA was then used to determine the impact of osteopontin knockdown on proliferation, apoptosis and migration in vitro in two murine claudin-low cell lines as well as identify the receptor mediating osteopontin's physiologic effects.Results: Osteopontin was expressed at high levels in mammary tumors derived from MTB-IGFIR transgenic mice compared to normal mammary tissue. Evaluation of cell lines derived from different mammary tumors revealed that mammary tumor cells with claudin-low characteristic expressed high levels of osteopontin whereas mammary tumor cells with mixed luminal and basal-like features expressed lower levels of osteopontin. Reduction of osteopontin levels using siRNA significantly reduced proliferation and migration while increasing apoptosis in the claudin-low cell lines. Osteopontin's effect appear to be mediated through a receptor containing ITGAV and not through CD44.Conclusions: Our data suggests that mammary tumors with a mixed luminal/basal-like phenotype express high levels of osteopontin however this osteopontin appears to be largely produced by non-tumor cells in the tumor microenvironment. In contrast tumor cells with claudin-low characteristics express high levels of osteopontin and a reduction of osteopontin in these cells impaired proliferation, survival and migration. [ABSTRACT FROM AUTHOR]

Published
2016
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27. Extracellular Matrix Proteins and Tumor Angiogenesis.

Author

Campbell, N. E., Kellenberger, L., Greenaway, J., Moorehead, R. A., Linnerth-Petrik, N. M., and Petrik, J.

Subjects
TUMOR growth, CELL compartmentation, EXTRACELLULAR matrix proteins, CARCINOGENESIS, REGULATION of neovascularization, BLOOD vessels
Abstract

Tumor development is a complex process that relies on interaction and communication between a number of cellular compartments. Much of the mass of a solid tumor is comprised of the stroma which is richly invested with extracellular matrix. Within this matrix are a host of matricellular proteins that regulate the expression and function of amyriad of proteins that regulate tumorigenic processes. One of the processes that is vital to tumor growth and progression is angiogenesis, or the formation of new blood vessels from preexisting vasculature.Within the extracellular matrix are structural proteins, a host of proteases, and resident pro- and antiangiogenic factors that control tumor angiogenesis in a tightly regulated fashion. This paper discusses the role that the extracellular matrix and ECM proteins play in the regulation of tumor angiogenesis. [ABSTRACT FROM AUTHOR]

Published
2010
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28. The Role of Dysregulated Glucose Metabolism in Epithelial Ovarian Cancer.

Author

Kellenberger, L. D., Bruin, J. E., Greenaway, J., Campbell, N. E., Moorehead, R. A., Holloway, A. C., and Petrik, J.

Subjects
GLUCOSE synthesis, CARCINOMA, OVARIAN cancer, OBESITY in women, DIABETES in women, BLOOD sugar
Abstract

Epithelial ovarian cancer (EOC) is the most lethal gynecologic cancer and also one of the most poorly understood. Other health issues that are affecting women with increasing frequency are obesity and diabetes, which are associated with dysglycemia and increased blood glucose. The Warburg Effect describes the ability of fast-growing cancer cells to preferentially metabolize glucose via anaerobic glycolysis rather than oxidative phosphorylation. Recent epidemiological studies have suggested a role for hyperglycemia in the pathogenesis of a number of cancers. If hyperglycemia contributes to tumour growth and progression, then it is intuitive that antihyperglycemic drugs may also have an important antitumour role. Preliminary reports suggest that these drugs not only reduce available plasma glucose, but also have direct effects on cancer cell viability through modification of molecular energy-sensing pathways. This review investigates the effect that hyperglycemia may have on EOC and the potential of antihyperglycemic drugs as therapeutic adjuncts. [ABSTRACT FROM AUTHOR]

Published
2010
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29. Inhibition of mammary epithelial apoptosis and sustained phosphorylation of Akt/PKB in MMTV-IGF-II transgenic mice.

Author

Moorehead, R A, Fata, J E, Johnson, M B, and Khokha, R

Subjects
*INSULIN-like growth factor-binding proteins, *APOPTOSIS
Abstract

IGF-II is a growth factor implicated in human cancers and animal tumor models. While the mitogenic properties of IGF-II are well documented, its ability to suppress apoptosis in vivo has never been proven. We generated independent MMTVIGF-II transgenic mice to examine the control of epithelial apoptosis at the morphological, cellular and molecular levels during the physiological event of postlactation mammary involution. Transgenic IGF-II expression was achieved in mammary epithelium and increased IGF-II bioactivity was confirmed by phosphorylation of the insulin receptor substrate-1, a signaling molecule downstream of the type I IGF receptor. IGF-II overexpression induced a delay in mammary involution, as evident by increased mammary gland to body weight ratios and persistence of both functionally intact Iobulo-alveoli and mammary epithelial cellularity. The delayed mammary involution resulted from a significant reduction in mammary epithelial apoptosis, and not from increased epithelial proliferation. Recombinant IGF-II pellets implanted into involuting mammary glands of wild-type mice provided further evidence that IGF-II protein inhibited local epithelial apoptosis. At the molecular level, phosphorylated Akt/PKB, but not Erk1 or Erk2, persisted in IGF-II overexpressors and temporally correlated with reduced epithelial apoptosis. Levels of the phosphatase PTEN were unaltered in the transgenic tissue suggesting that the maintenance of Akt/PKB phosphorylation resulted from sustained phosphorylation rather than altered dephosphorylation of PIP-3. [ABSTRACT FROM AUTHOR]

Published
2001
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31. Does preoperative computed tomography scanning aid assessment of oesophageal carcinoma?

Author

Kirk, S. J., Moorehead, R. J., McIlrath, E., Gibbons, J. P., and Spence, R. A.

Abstract

In this study 50 patients (36 male, 14 female) with oesophageal carcinoma have been examined preoperatively by computed tomography. Three parameters were assessed, nodal involvement, invasion of adjacent organs, and metastatic disease. For all patients the computed tomography findings were correlated with the subsequent surgical and pathological findings. Sensitivity for both invasion and node involvement is low (36% to 67%). Specificity however, is high (85% to 95%). Computed tomography is therefore relatively reliable when it predicts a 'negative result' for either invasion or node involvement. However, its predictive value for a positive result is not as reliable. [ABSTRACT FROM PUBLISHER]

Published
1990

35. Relationship between duodenal bile acids and colorectal neoplasia.

Author

Moorehead, R J, Campbell, G R, Donaldson, J D, and McKelvey, S T

Abstract

To investigate a possible relationship between bile acids and colorectal neoplasia duodenal bile acids were analysed in 50 patients with colorectal adenomas and 14 with carcinoma. Using gas liquid and high performance liquid chromatography a small, but significant increase in the proportion of chenodeoxycholic acid was found in the bile of adenoma patients compared with controls (mean % +/- SD 31.0 +/- 10.8, 26.4 +/- 8.3, p = 0.01). The difference in the proportions of chenodeoxycholic acid correlated with increasing malignant potential of the adenomas as determined by increasing size, histological type, degree of dysplasia and number present. In carcinoma patients an increase in the proportion of chenodeoxycholic acid was also observed compared with controls (mean % +/- SD, 47.2 +/- 9.6, 28.0 +/- 4.5, p less than 0.01). The proportions of other bile acids in those with adenoma or carcinoma were normal. [ABSTRACT FROM PUBLISHER]

Published
1987

36. THE MOBILE PHONE AS A TOOL IN THE ASSESSMENT OF NONSPECIFIC ABDOMINAL PAIN.

Author

McBrearty, A., Porter, D., and Moorehead, R. J.

Abstract

The article describes cases of 100 emergency admissions for abdominal pain. Of these, 13 female patients less than 35 years who are actively using mobile phones during consultant-led ward rounds were likely to have been found without underlying pathological cause for their non-specific abdominal pain (NSAP) and did not require surgical intervention. It also discusses clinical diagnosis' 68%-92% predictive yield with no significant improvement using additional diagnostic tools like laparoscopy.

Published
2014

42. cAMP response element-binding protein is expressed at high levels in human ovarian adenocarcinoma and regulates ovarian tumor cell proliferation.

Author

Linnerth NM, Greenaway JB, Petrik JJ, and Moorehead RA

Subjects
Adenocarcinoma genetics, Animals, Cell Line, Tumor, Cell Proliferation, Cyclic AMP Response Element-Binding Protein genetics, Disease Models, Animal, Down-Regulation, Female, Gene Expression Regulation, Neoplastic, Humans, Mice, Neoplasm Staging, Ovarian Neoplasms genetics, Phosphorylation, Tissue Array Analysis, Adenocarcinoma metabolism, Adenocarcinoma pathology, Cyclic AMP Response Element-Binding Protein metabolism, Ovarian Neoplasms metabolism, Ovarian Neoplasms pathology
Abstract

Approximately 90% of human ovarian tumors result from transformation of ovarian surface epithelial cells. It has been hypothesized that repeated destruction of the epithelial cells during ovulation, followed by proliferation and migration of epithelial cells to restore the ovarian surface, renders these cells susceptible to mutagenic events. One of the proteins found to promote ovarian surface epithelial cell survival and proliferation was the transcription factor, cAMP response element-binding protein (CREB). Thus, the objective of this study was to determine whether CREB was also highly expressed in tumor cells originating from the ovarian epithelium. Using an ovarian cancer tissue array, it was observed that approximately 54% of the epithelial-derived human ovarian tumors displayed moderate or high levels of CREB immunostaining, while none of the normal ovarian samples did. Comparison of CREB levels in a human ovarian tumor cell line to those of a normal ovarian epithelial cell line revealed elevated levels of CREB and phosphorylated CREB in the ovarian tumor cells. To determine whether CREB regulated proliferation and/or apoptosis in the ovarian tumor cell line, CREB expression was suppressed using RNA interference. Decreased CREB expression significantly reduced ovarian tumor cell proliferation, while there was no effect on apoptosis in these cells. Finally, we showed that CREB is highly expressed in an in vivo murine model of ovarian tumorigenesis. Therefore, CREB is frequently overexpressed in ovarian cancer where it appears to promote cell proliferation.

Published
2008
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43. Accelerated apoptosis in the Timp-3-deficient mammary gland.

Author

Fata JE, Leco KJ, Voura EB, Yu HY, Waterhouse P, Murphy G, Moorehead RA, and Khokha R

Subjects
Adipose Tissue anatomy & histology, Animals, Culture Techniques, Enzyme Activation, Epithelial Cells cytology, Epithelial Cells metabolism, Female, Fibronectins metabolism, Lactation physiology, Mammary Glands, Animal physiology, Matrix Metalloproteinase 2 metabolism, Mice, Mice, Knockout, Pregnancy, Tissue Inhibitor of Metalloproteinase-3 genetics, Apoptosis physiology, Mammary Glands, Animal cytology, Mammary Glands, Animal metabolism, Tissue Inhibitor of Metalloproteinase-3 deficiency, Tissue Inhibitor of Metalloproteinase-3 physiology
Abstract

The proapoptotic proteinase inhibitor TIMP-3 is the only molecule of this family thought to influence cell death. We examined epithelial apoptosis in TIMP-3-deficient mice during mammary gland involution. Lactation was not affected by the absence of TIMP-3, but glandular function, as measured by gland-to-body weight ratio and production of beta-casein, was suppressed earlier during post-lactational involution than in controls. Histological examination revealed accelerated lumen collapse, alveolar-epithelial loss, and adipose reconstitution in Timp-3(-/-) females. Epithelial apoptosis peaked on the first day of involution in Timp-3-null glands but at day 3 in wild-type littermates. Unscheduled activation of gelatinase-A was evident by zymography and correlated with earlier fragmentation of fibronectin in Timp-3(-/-) mammary. To obtain independent evidence of the proapoptotic effects of TIMP-3 deficiency, we introduced recombinant TIMP-3-releasing pellets into regressing Timp-3(-/-) mammary tissue and showed that this treatment rescued lumen collapse and epithelial apoptosis. Ex vivo, involuting Timp-3(-/-) mammary tissue demonstrated accelerated epithelial apoptosis that could be reduced by metalloproteinase inhibition. The physiological relevance of TIMP-3 became apparent as Timp-3(-/-) dams failed to reestablish lactation after brief cessation of suckling. Thus, TIMP-3 is a critical epithelial survival factor during mammary gland involution.

Published
2001
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44. The osteoclast differentiation factor osteoprotegerin-ligand is essential for mammary gland development.

Author

Fata JE, Kong YY, Li J, Sasaki T, Irie-Sasaki J, Moorehead RA, Elliott R, Scully S, Voura EB, Lacey DL, Boyle WJ, Khokha R, and Penninger JM

Subjects
Animals, Bone Remodeling drug effects, Bone Remodeling physiology, Carrier Proteins genetics, Cell Division physiology, Cell Survival physiology, Epithelial Cells cytology, Epithelial Cells metabolism, Epithelial Cells transplantation, Female, Glycoproteins genetics, Glycoproteins metabolism, Gonadal Steroid Hormones metabolism, Gonadal Steroid Hormones pharmacology, Mammary Glands, Animal cytology, Mammary Glands, Animal drug effects, Membrane Glycoproteins genetics, Mice, Mice, Knockout, Osteoporosis etiology, Osteoporosis physiopathology, Osteoprotegerin, Phenotype, Phosphorylation, Pregnancy metabolism, Protein Serine-Threonine Kinases genetics, Protein Serine-Threonine Kinases metabolism, Proto-Oncogene Proteins c-akt, RANK Ligand, Receptor Activator of Nuclear Factor-kappa B, Receptors, Cytoplasmic and Nuclear genetics, Receptors, Cytoplasmic and Nuclear metabolism, Receptors, Tumor Necrosis Factor, Carrier Proteins metabolism, Mammary Glands, Animal growth & development, Mammary Glands, Animal metabolism, Membrane Glycoproteins metabolism, Proto-Oncogene Proteins
Abstract

Osteoprotegerin-ligand (OPGL) is a key osteoclast differentiation/activation factor essential for bone remodeling. We report that mice lacking OPGL or its receptor RANK fail to form lobulo-alveolar mammary structures during pregnancy, resulting in death of newborns. Transplantation and OPGL-rescue experiments in opgl-/- and rank-/- pregnant females showed that OPGL acts directly on RANK-expressing mammary epithelial cells. The effects of OPGL are autonomous to epithelial cells. The mammary gland defect in female opgl-/- mice is characterized by enhanced apoptosis and failures in proliferation and PKB activation in lobulo-alveolar buds that can be reversed by recombinant OPGL treatment. These data provide a novel paradigm in mammary gland development and an evolutionary rationale for hormonal regulation and gender bias of osteoporosis in females.

Published
2000
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45. Influence of the proto-oncogene c-fos on cisplatin sensitivity.

Author

Moorehead RA and Singh G

Subjects
Animals, Cell Line, Cell Survival drug effects, Drug Interactions, Drug Resistance, Neoplasm, Female, Fibroblasts drug effects, Fibroblasts metabolism, Gene Expression, Humans, Oligonucleotides, Antisense pharmacology, Ovarian Neoplasms, Proto-Oncogene Mas, Proto-Oncogene Proteins c-fos genetics, Proto-Oncogene Proteins c-fos physiology, Rats, Tumor Cells, Cultured, Antineoplastic Agents pharmacology, Cisplatin pharmacology, Genes, fos
Abstract

Cisplatin resistance has been associated with overexpression of the c-fos gene in a human ovarian carcinoma cell line. To determine whether the correlation between c-fos overexpression and cisplatin resistance was limited to this cell line or was a more generalized phenomenon, we investigated cisplatin sensitivity in rat fibroblast cells that overexpressed the c-fos gene. The cisplatin Ic50 values for two different c-fos transfectants, CMVc-fos and L1-3c-fos, were 7.6 +/- 0.8 and 5.6 +/- 1.0 microM, respectively, whereas the cisplatin Ic50 value for the parental line, 208F, was 2.4 +/- 0.1 microM. This represented a 3.2- and 2.3-fold resistance to cisplatin for CMVc-fos and L1-3c-fos cells, respectively. The correlation between c-fos expression and cisplatin resistance also was examined in a human ovarian carcinoma cell line, 2008, and its cisplatin-resistant variant, C13*. Expression of c-fos was elevated slightly at both the mRNA and protein levels in the C13* cells compared with 2008 cells, and c-Fos protein levels were induced in C13* cells following cisplatin treatment. In addition, it was observed that C13* cells were significantly more sensitive than 2008 cells to a c-fos antisense oligonucleotide. The Ic50 values for the c-fos antisense oligonucleotide were 19.9 +/- 5.0 pmol for C13* cells and 58.1 +/- 6.0 pmol for 2008 cells (P = 0.0012). Furthermore, combinations of c-fos antisense and cisplatin reduced the amount of cisplatin required to kill 50% of the C13* cells, although the interaction was not synergistic. These results suggest that expression of the c-fos gene can influence cisplatin sensitivity, and that c-fos antisense oligonucleotide based therapy may be effective at killing parental and cisplatin-resistant ovarian carcinoma cells, either alone or in combination with cisplatin.

Published
2000
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46. Timp-1 is important for epithelial proliferation and branching morphogenesis during mouse mammary development.

Author

Fata JE, Leco KJ, Moorehead RA, Martin DC, and Khokha R

Subjects
Animals, Epithelial Cells cytology, Female, Gene Expression Regulation, Developmental physiology, Immunohistochemistry, Mammary Glands, Animal physiology, Mice, Morphogenesis, RNA, Messenger analysis, Epithelial Cells physiology, Mammary Glands, Animal embryology, Tissue Inhibitor of Metalloproteinase-1 physiology
Abstract

The dynamic process of mammary ductal morphogenesis depends on regulated epithelial proliferation and extracellular matrix (ECM) turnover. Epithelial cell-matrix contact closely dictates epithelial proliferation, differentiation, and survival. Despite the fact that tissue inhibitors of metalloproteinases (Timps) regulate ECM turnover, their function in mammary morphogenesis is unknown. We have delineated the spatiotemporal expression of all Timps (Timp-1 to Timp-4) during discrete phases of murine mammary development. Timp mRNAs were abundant in mammary tissue, each displaying differential expression patterns with predominant localization in luminal epithelial cells. Timp-1 mRNA was unique in that its expression was limited to the stage at which epithelial proliferation was high. To assess whether Timp-1 promotes or inhibits epithelial cell proliferation we manipulated mammary Timp-1 levels, genetically and biochemically. Down-regulation of epithelial-derived Timp-1 in transgenic mice, by mouse mammary tumor virus promoter-directed Timp-1 antisense RNA expression, led to augmented ductal expansion and increased number of ducts (P < 0.004). In these transgenics the integrity of basement membrane surrounding epithelial ducts, as visualized by laminin-specific immunostaining, was breached. In contrast to these mice, ductal expansion was markedly attenuated in the proximity of implanted recombinant Timp-1-releasing pellets (rTIMP-1), without an increase in basement membrane deposition around migrating terminal end buds. Epithelial proliferation and apoptosis were measured to determine the basis of altered ductal expansion. Luminal epithelial proliferation was increased by 55% (P < 0.02) in Timp-1-reduced transgenic mammary tissue and, conversely, decreased by 38% (P < 0.02) in terminal end buds by implanted rTIMP-1. Epithelial apoptosis was minimal and remained unaffected by Timp-1 manipulations. We conclude that Timps have an integral function in mammary morphogenesis and that Timp-1 regulates mammary epithelial proliferation in vivo, at least in part by maintaining basement membrane integrity., (Copyright 1999 Academic Press.)

Published
1999
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47. Mitochondrial membrane potential regulation is independent of c-fos expression.

Author

Moorehead RA and Singh G

Subjects
Animals, Cell Line, Female, Humans, Membrane Potentials, Ovarian Neoplasms physiopathology, Rats, Rhodamine 123 metabolism, Mitochondria physiology, Proto-Oncogene Proteins c-fos physiology
Abstract

Tumour cells contain mitochondria with elevated membrane potentials compared with normal cells, and thus this feature provides a selective target for destroying tumour cells. To improve mitochondrial-based therapies, a better understanding of the factors involved in regulating mitochondria are required. Since v-fos overexpression has been shown to elevate mitochondrial membrane potentials in rat fibroblasts, we investigated whether the human homologue, c-fos, was also capable of regulating the mitochondrial membrane potential in cells. Rat fibroblasts transfected with the c-fos gene did not accumulate more rhodamine 123 (Rh123) nor did they retain this Rh123 for extended periods of time compared with their parental line. Moreover, there was no difference in survival following dequalinium chloride (Deca) treatment between transfectants and controls. Similarly, reduction of c-fos expression in rat fibroblasts did not significantly alter their mitochondrial membrane potential. In addition, human ovarian carcinoma cells, which overexpress the c-fos gene, did not accumulate more Rh123 nor were they hypersensitive to Deca compared with their parental line. In another human ovarian carcinoma cell line, selection of variants with lower mitochondrial membrane potential did not alter c-fos mRNA or protein levels. These data suggest that alterations in c-fos expression do not regulate the magnitude of the mitochondrial membrane potential.

Published
1999

48. Nucleotide excision repair in the human ovarian carcinoma cell line (2008) and its cisplatin-resistant variant (C13*).

Author

Moorehead RA, Armstrong SG, Rainbow AJ, and Singh G

Subjects
Adenoviridae drug effects, Adenoviridae genetics, Aphidicolin toxicity, Carcinoma pathology, Cell Survival drug effects, DNA Adducts metabolism, DNA Polymerase II metabolism, DNA, Viral drug effects, Drug Synergism, Enzyme Inhibitors toxicity, Female, Humans, Tumor Cells, Cultured drug effects, Antineoplastic Agents toxicity, Cisplatin toxicity, DNA Damage drug effects, DNA Repair, Ovarian Neoplasms pathology
Abstract

Repair of cisplatin-damaged DNA was investigated in a human ovarian carcinoma cell line (2008) and its cisplatin-resistant variant (C13*) using a host-cell reactivation (HCR) assay. The HCR of cisplatin-damaged adenovirus (Ad) was not significantly different in C13* cells compared to 2008 cells. The cisplatin concentrations required to reduce the amount of viral DNA replicated to 50% were 0.12 +/- 0.02 microM and 0.10 +/- 0.01 microM after 48 h of repair in 2008 and C13* cells respectively. Similarly, the cisplatin concentration required to reduce the expression of a reporter gene inserted in the viral DNA was not significantly altered in C13* cells compared to the parental line (IC50 values were 0.28 +/- 0.04 microM in 2008 cells and 0.17 +/- 0.06 microM in C13* cells after 48 h of repair). Pretreatment of the cells with cisplatin, immediately prior to Ad infection, did not significantly alter the HCR of cisplatin-damaged Ad in either cell type. In addition, a cisplatin-sensitive variant derived from the C13* cells, namely the RH4 cells, did not differ significantly from either the 2008 or C13* cells in their ability to reactivate cisplatin-damaged Ad. Furthermore, a component of the nucleotide excision repair (NER) pathway, DNA polymerase alpha, was investigated using the competitive inhibitor aphidicolin. The combination of cisplatin and aphidicolin resulted in similar synergistic growth inhibition in both the 2008 and C13* cells providing additional support to the HCR results which suggest that enhanced NER is not responsible for the cisplatin resistance in C13* cells.

Published
1996
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49. Cross-resistance to cisplatin in cells resistant to photofrin-mediated photodynamic therapy.

Author

Moorehead RA, Armstrong SG, Wilson BC, and Singh G

Subjects
ATP Binding Cassette Transporter, Subfamily B, Member 1, Animals, CHO Cells, Carrier Proteins analysis, Cell Survival, Cisplatin analysis, Cisplatin pharmacology, Cricetinae, DNA analysis, Drug Resistance, Fibrosarcoma chemistry, Fibrosarcoma drug therapy, Fibrosarcoma ultrastructure, Glutathione analysis, Membrane Glycoproteins analysis, Membrane Potentials, Neoplasms, Radiation-Induced chemistry, Neoplasms, Radiation-Induced drug therapy, Neoplasms, Radiation-Induced ultrastructure, Porphyrins, Rhodamine 123, Rhodamines metabolism, Tumor Cells, Cultured, Cisplatin metabolism, DNA Adducts, Fibrosarcoma metabolism, Mitochondria ultrastructure, Neoplasms, Radiation-Induced metabolism, Photochemotherapy
Abstract

This study shows that a Photofrin-induced photodynamic therapy-resistant variant (RIF-8A) of a radiation-induced fibrosarcoma-1 cell line (RIF-1) is cross-resistant to cis-diamminedichloroplatinum(II) (cisplatin). This is the first study to show cross-resistance to cisplatin in photodynamic therapy-resistant variants in vitro. Resistance does not appear to be the result of elevated glutathione levels since neither the resistant variant (RIF-8A) nor the parental line (RIF-1) varied in total glutathione levels. However, cisplatin-DNA adduct levels differed significantly between the two cell types. Immediately following a 1-h exposure to cisplatin (50 microM), RIF-1 cells contained 44.6 +/- 2.0 (SEM) pg platinum/micrograms DNA while RIF-8A cells contained 24.8 +/- 6.3 pg platinum/micrograms DNA. In addition, the resistant variant had decreased plasma and mitochondrial membrane potentials. The plasma and mitochondrial membranes of the resistant variant accumulated 3- and 3.6-fold less rhodamine 123, respectively. The difference in rhodamine 123 accumulation could not be attributed to elevated P-glycoprotein expression because both the parental line and the variant contained similar amounts of P-glycoprotein. In conclusion, alterations in the plasma and/or mitochondrial membrane potentials may provide cells with a survival advantage when challenged with either photodynamic therapy or cisplatin in vitro. This appears to be a novel mechanism of resistance.

Published
1994

50. Ulster benefits from experience.

Author

Moorehead RA

Subjects
Facility Design and Construction, Health Facilities, Hospital Design and Construction, Northern Ireland
Published
1971

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