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4. Defining breeding objectives for sustainability in cattle: challenges and opportunities.

Author

Richardson, C. M., Crowley, J. J., and Amer, P. R.

Subjects
*CATTLE breeds, *CATTLE breeding, *SUSTAINABILITY, *SEMEN analysis, *CATTLE fertility, *CATTLE industry, DEVELOPING countries
Abstract

This paper reviews breeding objectives of the current global cattle industry and outlines existing challenges and opportunities for improving sustainability in the livestock sector through genetic selection. Cattle breeding programs have historically been focused on generating profit by selecting for high-producing animals and broadened to include traits related to health, reproduction, fertility, and efficiency. Now, cattle industries around the world are using genetics to reduce their environmental impacts and improve sustainability. Reducing emissions is vital to improve sustainability, and industry leaders have set emission goals to either reduce gross emissions, lower emissions intensity, or reach net-zero. However, additional traits should also be measured and compared in terms of their impact on the broader definition of sustainability. In addition to environmental impact, a sustainable breeding objective must consider profit, animal welfare, farmer wellbeing, and social responsibility. Traits to be considered include direct emissions (e.g. nitrogen and methane), production efficiency (e.g. feed efficiency, growth), closer to biology reproduction and fertility (e.g. oestrous strength and semen quality), health (e.g. calf and transition cow health) and welfare traits (e.g. polled). Many of these novel traits require labour-intensive or expensive phenotyping, resulting in small datasets and low reliability of estimated breeding values. Opportunities exist to overcome this limitation by utilising international collaboration to build large data bases, develop inexpensive and easy-to-measure proxy traits, and expand novel-phenotype reference populations by using female-driven reference populations and young stock and males. Non-economic values can be estimated that quantify the impact that a trait has on societal perspective (e.g. farmer preference) or the environmental impact (methane emissions), and combined with economic weights to calculate aggregate weights for each trait. While validation techniques are still uncertain, the United Nations Sustainable Development Goals may be applied to determine the improvement in sustainability due to genetic selection. This approach allows for various perspectives of sustainability, such as in the developed versus developing world, to be considered. The number and quality of relevant phenotypes are currently the main limiting factors. As confidence continues to grow in the opportunity to improve sustainability through genetic selection, substantial new investment will be required both in phenotyping activities, but also into novel breeding structures and scheme designs that can maximise the value and impact of these phenotypes. This paper reviews breeding objectives of the current cattle industry and outlines existing challenges and opportunities for improving sustainability in the livestock sector through genetic selection. As confidence continues to grow in the opportunity to improve sustainability through genetic selection, substantial new investment will be required both in phenotyping activities, but also into novel breeding structures and scheme designs that can maximise the value and impact of these phenotypes. [ABSTRACT FROM AUTHOR]

Published
2023
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5. Copy number variation in schizophrenia in Sweden

Author

Szatkiewicz, J P, O'Dushlaine, C, Chen, G, Chambert, K, Moran, J L, Neale, B M, Fromer, M, Ruderfer, D, Akterin, S, Bergen, S E, Kähler, A, Magnusson, P K E, Kim, Y, Crowley, J J, Rees, E, Kirov, G, O'Donovan, M C, Owen, M J, Walters, J, Scolnick, E, Sklar, P, Purcell, S, Hultman, C M, McCarroll, S A, and Sullivan, P F

Published
2014
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10. Irish cardiac society: Proceedings of annual general meeting held 1st November, 1997

Author

Seifer, C., McNeill, B., O’Donnell, M., Daly, K., Kellett, J., McGee, H. M., Montogomery, A. J., O’Callaghan, D., Horgan, J. H., Mahon, N. G., Codd, M., Brennan, J., Egan, B., McCann, H. A., Sugrue, D. D., Menown, I. B. A., Patterson, R. S. H. W., McMechan, S. R., Hameed, S., Adgey, A. A. J., Baird, S. H., McBride, S. J., Trouton, T. G., Wilson, C., McRedmond, J. P., Fitzgerald, D. J., Crowley, J. J., Tanguay, J-F., Santos, R. M., Stack, R. S., Mahon, N. G., Keelan, P., McCann, H. A., Sugrue, D. D., McKenna, C. J., AuBuchon, R., Camrud, A. R., Holmes, D. R., Schwartz, R. S., McKenna, C. J., Camrud, A. R., Wolff, R., Edwards, W. D., Holmes, D. R., Schwartz, R. S., Hanratty, C., McAuley, D., Young, I., Murtagh, G., O’Keeffe, B., Richardson, G., Scott, M., Chew, E. W., Bailie, N. A., Graham, A. M. J., O’Kane, H., McKenna, C. J., Kwon, H. M., Ellis, L., Holmes, D. R., Virmani, R., Schwartz, R. S., Noelke, L., Wood, A. E., Javadpour, H., Veerasingham, D., Wood, A. E., O’Kane, D., Allen, J. D., Adgey, A. A. J., Hennessy, T., Johnson, P., Hildick-Smith, D., Winter, E., Shapiro, L., McKenna, C. J., Edwards, W. D., Lerman, A., Holmes, D. R., Schwartz, R. S., McGrath, L. T., Passmore, P., Silke, B., McAuley, D., Nugent, A. G., McGurk, C., Hanratty, C., Maguire, S., Johnston, G. D., McAuley, D., Nugent, A. G., McGurk, C., Hanratty, C., Maguire, S., Johnston, G. D., Lovell, S. L., McDowell, G., McEneany, D., Riley, M. S., Nicholls, D. P., Gilligan, D., Sargent, D., Dan, D., Gilligan, D., Elam, G., Rhee, B., Keane, D., Zhou, L., McGovern, B., Garan, H., Ruskin, J., O’Shea, J. C., Tan, H-C., Zidar, J. P., Stack, R. S., Crowley, J. J., O’Keeffe, D. B., Graffin, S., Fitzsimmons, D., Brown, S., Duff, D., Denham, B., Woods, F., Neligan, M., Oslizlok, P., Connolly, C. K., Danton, M. H. D., O’Kane, H., Danton, M., Gladstone, D. J., Craig, B., Mulholland, H. C., Casey, F., Chaudhuri, S., Hinchion, J., Wood, A. E., Hinchion, J., Wood, A. E., Menown, I. B. A., Patterson, R. H. S. W., MacKenzie, G., Adgey, A. A. J., Harbinson, M. T., Burgess, L. M., Moohan, V., McEneaney, D. J., Adgey, A. A. J., Menown, I. B. A., MacKenzie, G., Patterson, R. S. H. W., Adgey, A. A. J., Finnegan, O. C., Doherty, L., Silke, B., Riddell, J. G., Meleady, R., Daly, L., Graham, I., Quinn, M., Foley, B., Lee, J., Mulvihill, N., Crean, P., Walsh, M., O’Morain, C., Quinn, M., Crean, P., Foley, B., Walsh, M., Hynes, C., King, S. M., David, S., Newton, H., Maguire, M., Rafferty, F., Horgan, J. H., Sullivan, P. A., Murphy, D., Gallagher, S., Menown, I. B. A., Allen, J., Anderson, J. McC, Adgey, A. A. J., Dan, D., Hoag, J., Eckberg, D., Gilligan, D., Galvin, J., Garan, H., McGovern, B., Ruskin, J., Mahon, N. G., Diamond, P., Neilan, T., Keelan, E., H. A., McCarthy, C., Sugrue, D. D., Harbinson, M. T., Moohan, V. P., McEneaney, D. J., Burgess, L. M., Anderson, J. McC, Ayers, G. M., Adgey, A. A. J., Roberts, M., Burgess, L., Anderson, C., Wilson, C., Khan, M., Clements, I. P., Miller, W. L., Seifer, C., O’Donnell, M., McNeill, B., Daly, K., Turtle, F., McDowell, G., Long, H., McNair, W., Campbell, N. P. S., Mathew, T. P., Turtle, F., Smye, M., Nesbitt, G. S., Young, I. S., Adgey, A. A. J., Meleady, R., Mulcahy, D., Graham, I. M., Moore, D., Menown, I. B. A., McMechan, S. R., MacKenzie, G., Adgey, A. A. J., Diamond, P., Sugrue, D., Codd, M. B., Galvin, J., Zimmerman, P., Winget, J., Capeless, M., Galvin, J., Garan, H., McGovern, B., Ruskin, J., McKelvey, T. A., Danton, M. H. D., Sarsam, M. I. A., McEneaney, D., Roberts, M., Burgess, L., Anderson, C., Wilson, C., and Khan, M.

Published
1998
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18. Disease activity and treatment efficacy using patient-level Psoriasis Area and Severity Index scores from tildrakizumab phase 3 clinical trials

Author

Gordon, K. B., primary, Reich, K., additional, Crowley, J. J., additional, Korman, N. J., additional, Murphy, F. T., additional, Poulin, Y., additional, Spelman, L., additional, Yamauchi, P. S., additional, Mendelsohn, A. M., additional, Parno, J., additional, Rozzo, S. J., additional, and Ellis, C. N., additional

Published
2020
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20. Disease activity and treatment efficacy using patient-level Psoriasis Area and Severity Index scores from tildrakizumab phase 3 clinical trials.

Author

Gordon, K. B., Reich, K., Crowley, J. J., Korman, N. J., Murphy, F. T., Poulin, Y., Spelman, L., Yamauchi, P. S., Mendelsohn, A. M., Parno, J., Rozzo, S. J., and Ellis, C. N.

Subjects
CLINICAL trials, THERAPEUTICS, TREATMENT effectiveness, PSORIASIS, PSORIATIC arthritis, TRIAL practice
Abstract

It is unclear whether primary efficacy outcomes in plaque psoriasis clinical trials represent residual disease during treatment. To evaluate supplementing dichotomous efficacy with residual disease activity. This post hoc analysis used pooled, patient-level data after tildrakizumab 100 mg (N = 616) or placebo (N = 309) treatment from reSURFACE 1/2 (NCT01722331/NCT01729754) phase 3 clinical trials of patients with moderate to severe plaque psoriasis. Median baseline Psoriasis Area and Severity Index (PASI) was 17.9 for patients receiving tildrakizumab 100 mg. At Week 12, median PASI was 2.9, whereas dichotomous PASI 90 response rate was 36.9%, and absolute PASI <5.0, <3.0, and <1.0 were 64.0%, 50.8%, and 23.3%, respectively. At Week 28, median PASI was 1.7, whereas PASI 90 response rate was 51.9%, and absolute PASI <5.0, <3.0, and <1.0 were 75.3%, 62.8%, and 38.0%, respectively. Dermatology Life Quality Index and PASI scores were correlated through Week 28 (r = 0.51, p ≤.0001). Disease activity was more reliably estimated by PASI scores than percentage PASI improvement; this may partially explain efficacy disparities between clinical trials and practice. These results suggest supplementing dichotomous PASI improvement with PASI scores and consideration of patient treatment goals could facilitate clinical decisions. [ABSTRACT FROM AUTHOR]

Published
2022
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21. Irish cardiac society Proceedings of Annual General Meeting held 4th/5th November, 1994

Author

Oslizlok, P., Duff, D., Denham, B., Penny, W. J., Banning, A. P., Groves, P. H., Brewer, L., Lewis, M. J., Cheadle, H., Crawford, N., Kearney, P. P., Starkey, I. R., Fort, S., McMurray, J. V., Shaw, T. R., Sutherland, G. R., Hennessy, T., McCann, H., Sugrue, D., Foley, D. P., Melkert, R., Keane, D., Serruys, P. W., Vaughan, C. J., O’Connell, D. P., McDonald, D., Blake, S., Garadah, T., Mehana, N., King, G., Gearty, G., Crean, P., Walsh, M., Galvin, J., Codd, M. B., McCann, H. A., Sugrue, D. D., Gaylani, N. El, Weston, C., Thomas, A., Davies, L., Tovey, J., Musumeci, F., Singh, H. P., Hargrove, M., Fennell, W., Aherne, T., Crowley, J. J., Hassanein, H., Shapiro, L. M., McCrissican, D., Morton, P., O’Donnell, A. F., McBrinn, S., McCarthy, J., McCarthy, D., Neligan, M. C., McGovern, E., Herity, N. A., Allen, J. D., Silke, B., Adgey, A. A. J., Johnston, P. W., Anderson, J., McIlroy, R. L., Dunn, H. M., Nikookam, K., McNeill, A. J., Foley, P., Foley, D., de Jaegere, P., Serruys, P., O’Callaghan, D., Vela, J., Maguire, M., Horgan, J., Graham, A. N. J., Wilson, C. M., Hood, J. M., D’SA, A. A. B. Barros, Khan, M. M., McClements, B., Dalzell, G., Campbell, N. P. S., Webb, S. W., Shandall, A., Buchalter, M. B., Northbridge, D. B., McMurray, J., Dargie, H. J., Sullivan, P. A., McLoughlin, M., Varma, M. P. S., Charleton, P., Turkington, E., Rusk, R. A., Richardson, S. G., Hale, A., O’Shea, J. C., Murphy, M. B., Diamond, P., McAleer, B., Davies, S., Kinnaird, T., Duly, E., McKenna, C. J., Codd, M., McGee, H. M., Browne, C., Horgan, J. H., and The Council on Acute Coronary Care of the Irish Heart Foundation

Published
1995
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22. Irish Cardiac Society: Proceedings of the Annual General Meeting held November 1993

Author

O’Callaghan, D., Horgan, J. H., Kellett, J., Graham, J., Deb, B., Caldwell, M. T. P., O'Callaghan, P., Byrne, P. J., Hennessy, T. P. J., Crean, P., Walsh, M., Gearty, G., Boyle, D. McC, Higginson, J. D. S., Salathia, K., Chandler, R., Shah, P., Lavin, F., Daly, K., Steele, I. C., Nugent, A. M., Vallely, S. R., Campbell, N. P. S., Nicholls, D. P., Coghlan, J. G., Flitter, W. D., Daly, R., Wright, G. D., Ilsley, C. D., Slate, T., Foley, D. P., Melkert, R., Keane, D., Serruys, P. W., Foley, J. B., Sridhar, K., Brown, R. I. G., Penn, I. M., Umans, V. A., de Jaegere, P., Galvin, J., Codd, M., Hennessy, A., Leavey, S., Keelan, E., McCarthy, C., Sugrue, D., Craig, B. G., Mulholland, H. C., Kearney, P., Erbel, R., Koch, L., Ge, J., Görge, G., Meyer, J., Anderson, D., Marrinan, M., Sulke, N., Cooke, R., Jackson, G., Sowton, E., McEneaney, D. J., Anderson, J., Adgey, A. A. J., Marks, P., Walsh, T. N., Leavey, Crowley, J. J., Kenny, A., Dardas, P., Shapiro, L. M., Delanty, N., Moran, N., Catella, F., FitzGerald, G. A., Fitzgerald, D. J., Umans, V., Moore, D., Weston, A., Hughes, M., Maurer, B., Cleland, J., McGee, H. M., Graham, I., Cullen, C., Dempsey, G., Wright, G., Martin, L., MacKenzie, G., Adgey, J., Lawson, J. A., Herity, N. A., Allen, J. D., Silke, B., Northridge, D. B., Jackson, N. C., Metcalfe, M. J., Dargie, H. J., Gates, A. R. C., Huang, C. L. H., Gresham, A., Carpenter, T. A., Hall, L. D., Johnston, P. W., Jossinet, J., Imam, Z., Sheahan, R., Newman, D., Dorian, P., Meleady, R., Tan, K. S., O’Brien, C., Graham, I. H., Maderna, P., Fitzgerald, D., O'Callaghan, D. M., Rafferty, S. M., Canton, M. C., Connolly, B. F., Buchalter, M. B., Shandall, A., Rees, A., Rajan, L., Sheehan, R., Ghaisas, N., and Geraty, G.

Published
1994
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23. Inaugural national scientific medical meeting

Author

Walsh, P. Noonan, Conliffe, C., Abdulkadir, A. S., Kelehan, P., Conroy, R., Foley, M., Lenehan, P., Murphy, J. F., Stronge, J., Cantwell, B., Wright, C., Millward, M., Carpenter, M., Lennard, T., Wilson, R., Home, C., Corbett, A. R., O’Sullivan, G., Collins, J. K., Doran, M., McDermott, E. W. M., Mercer, P., Smyth, P., O’Higgins, N. J., Duffy, M. J., Reilly, D., McDermott, E., Faul, C., Fennelly, J. J., O’Higgins, N., Lowry, S., Russell, H., Atkinson, R., Hickey, I., O’Brien, F., O’Mahony, A., O’Donoghue, M., Pomeroy, M., Prosser, E. S., Barker, F., Casey, M., Carroll, K., Davis, M., Duffy, G., O’Kennedy, R., Smyth, P. P. A., O’Carroll, D., Hetherton, A. M., Coveney, E., McAlister, V., Murray, M. J., Brayden, D. J., O’Hora, A., Street, J., O’Leary, J., Pollock, A. M., Crowley, M., Healy, I., Murphy, J., Landers, R., Burke, L., O’Brien, D., Annis, P., Hogan, J., Kealy, W., Lewis, F. A., Doyle, C. T., Callaghan, M., Whelan, A., Feighery, C., Bresnihan, B., Kelleher, D., Reams, G., Murphy, A., Hall, N., Casey, E. B., Mulherin, D., Doherty, E., Yanni, G., Wallace, E., Jackson, J., Bennett, M., Tighe, O., Mulcahy, H., O’Donoghue, D., Croke, D. T., Cahill, R. J., Beattie, S., Hamilton, H., O’Morain, C., Corridan, B., Collins, R. A., O’Morain, C. A., Fitzgerald, E., Gilvarry, J. M., Leader, M., Fielding, J. F., Johnson, B. T., Lewis, S. A., Love, A. H. G., Johnston, B. T., Collins, J. S. A., McFarland, R. J., Johnston, P. W., Collins, B. J., Kilgallen, C. M., Murphy, G. M., Markey, G. M., McCormack, J. A., Curry, R. C., Morris, T. C. M., Alexander, H. D., Edgar, S., Treacy, M., O’Connell, M. A., Weir, D. G., Sheehan, J., O’Loughlin, G., Traynor, O., Walsh, N., Xia, H. X., Daw, M. A., Keane, C. T., Dupont, C., Gibson, G., McGinnity, E., Walshe, J., Carmody, M., Donohoe, J., McGrath, P., O’Moore, R., Kieran, E., Rogers, S., McKenna, K. E., Walsh, M., Bingham, E. A., Hughes, A. E., Nevin, N. C., Todd, D. J., Stanford, C. F., Callender, M. E., Burrows, D., Paige, D. G., Allen, G. E., O’Brien, D. P., Gough, D. B., Phelan, C., Given, H. F., Kamal, S. Zia, Kehoe, S., Coldicott, S., Luesley, D., Ward, K., MacDonnell, H. F., Mullins, S., Gordon, I., Norris, L. A., Devitt, M., Bonnar, J., Sharma, S. C., Sheppard, B. L., Fitzsimons, R., Kingston, S., Garvey, M., Hoey, H. M. C. V., Glasgow, J. F. T., Moore, R., Robinson, P. H., Murphy, E., Murphy, J. F. A., Wood, A. E., Sweeney, P., Neligan, M., MacLeod, D., Cunnane, G., Kelly, P., Corcoran, P., Clancy, L., Drury, R. M., Drury, M. I., Powell, D., Firth, R. G. R., Jones, T., Ferris, B. F., O’Flynn, W., O’Donnell, J., Kingston, S. M., Cunningham, F., Hinds, G. M. E., McCluskey, D. R., Howell, F., O’Mahony, M., Devlin, J., O’Reilly, O., Buttanshaw, C., Jennings, S., Keane, E. R., Foley-Nolan, C., Ryan, F. M., Taylor, M., Lyons, R. A., O’Kelly, F., Mason, J., Carroll, D., Doherty, K., Flynn, M., O’Dwyer, R., Gilmartin, J. J., McCarthy, C. F., Armstrong, C., Mannion, D., Feely, T., Fitzpatrick, G., Cooney, C. M., Aleong, J. Chin, Rooney, R., Lyons, J., Phelan, D. M., Joshi, G. P., McCarroll, S. M., Blunnie, W. P., O’Brien, T. M., Moriarty, D. C., Brangan, J., Kelly, C. P., Kenny, P., Gallagher, H., McGovern, E., Luke, D., Lowe, D., Rice, T., Phelan, D., Lyons, J. B., Lyons, F. M., McCoy, D. M., McGinley, J., Hurley, J., McDonagh, P., Crowley, J. J., Donnelly, S. M., Tobin, M., Fitzgerald, O., Maurer, B. J., Quigley, P. J., King, G., Duly, E. B., Trinick, T. R., Boyle, D., Wisdom, G. B., Geoghegan, F., Collins, P. B., Goss, C., Younger, K., Mathias, P., Graham, I., MacGowan, S. W., Sidhu, P., McEneaney, D. J., Cochrane, D. J., Adgey, A. A. J., Anderson, J. M., Moriarty, J., Fahy, C., Lavender, A., Lynch, L., McGovern, C., Nugent, A. M., Neely, D., Young, I., McDowell, I., O’Kane, M., Nicholls, D. P., McEneaney, D., Nichols, D. P., Campbell, N. P. S., Campbell, G. C., Halliday, M. I., O’Donnell, A. F., Lonergan, M., Ahearne, T., O’Neill, J., Keaveny, T. V., Ramsbottom, D., Boucher-Hayes, D., Sheahan, R., Garadaha, M. T., Kidney, D., Freyne, P., Gearty, G., Crean, P., Singh, H. P., Hargrove, M., Subareddy, K., Hurley, J. P., O’Rourke, W., O’Connor, C., FitzGerald, M. X., McDonnell, T. J., Chan, R., Stinson, J., Hemeryck, L., Feely, J., Chopra, M. P., Sivner, A., Sadiq, S. M., Abernathy, E., Plant, L., Bredin, C. P., Hickey, P., Slevin, G., McCrory, K., Long, M., Conlon, P., Walker, F., Fitzgerald, P., O’Neill, S. J., O’Connor, C. M., Quigley, C., Donnelly, S., Southey, A., Healy, E., Mulcahy, F., Lyons, D. J., Keating, J., O’Mahony, C., Roy, D., Shattock, A. G., Hillary, I. B., Waiz, A., Hossain, R., Chakraborthy, B., Clancy, L. P., O’Reilly, L., Byrne, C., Costello, E., O’Shaughnessy, E., Cryan, B., Farrell, J., Walshe, J. J., Mellotte, G. J., Ho, C. A., Morgan, S. H., Bending, M. R., and Bonner, J.

Published
1993
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25. Irish cardiac society: Proceedings of annual general meeting held in galway, 8th & 9th november 1991

Author

Crowley, J. J., Naughton, M. A., King, G., Maurer, J., Quigley, P. J., McNeill, A. J., Fioretti, P. M., Salustri, A., Pozzolu, M. M. A., Broekema, C. C., Elsaid, E. M., Roelandt, J. R., Garadaha, M. T., Algazzar, A. H., Dayem, H., Crean, P., Cairn, H. A. M., Blanchard, D. G., Rivera, I., Peterson, K. L., Buchbinder, M., Dittrick, H., MacGowan, G. A., Herlihy, M., O’Brien, E., Horgan, J. H., Purvis, J. A., Roberts, M. J. D., Cave, M., Webb, S. W., Campbell, N. P. S., Patterson, G. C., Wilson, C. M., Khan, M. M., Adgey, A. A. J., McClements, D. M., Cochrane, D., Jauch, W., Scriven, A. J., Cobbe, S. M., Jauch, W., Sheehan, R., McAdam, B., Foley, D., Kinsella, A., Walsh, N., White, U., Gearty, G., Walsh, M., Rush, R., Cooper, A., Crowe, P., Young, I. S., Trimble, E. R., Adgey, A. A. J., Jauch, W., Sheehan, R., McAdam, B., Sheehan, R., Kinsella, A., Walsh, N., White, U., Gearty, G., Walsh, M., King., G., Elgaylani, N., Hamilton, D., Gearty, G., Walsh, M., McAleer, B., Ruane, B., Dalton, G., Varma, M. P. S., Sheahan, R., Freyne, P. J., Kidney, D. D., Gearty, G. F., Ryan, M., Cooke, T., Robinson, K., Younger, K., Feely, J., Graham, I., Hurley, J., McDonagh, P. M., White, M., Phelan, D., Luke, D., McGovem, E., Clements, B., Ruane, B., Dalton, G., Varma, M. P. S., Lonergan, M., Daly, L., Wood, A. E., Craig, B., Mulholland, D., Gladstone, D., O’Kane, H., Cleland, J., Rajan, L., Murphy, S., Fielding, J., Smith, E., Pahy, G., Deb, B., Graham, I., Campbell, N. P. S., Elliott, J., Maguire, C., Wilson, M., McEneaney, D., Adgey, J., Anderson, J., Foley, D., Sheahan, R., Gibney, M., Primrose, E. D., Savage, J. M., Cran, G. W., Mulholland, H., Thomas, P. J., Donnelly, M. D. I., Kenny, R. A., Traynor, G., Burges, L., Wilson, C., Gladstone, D. J., Walsh, K., Sreeram, N. S., Franks, R., Arnold, R., Gaylani, N. EL, White, U., McAdam, B., Gearty, G., Walsh, M., Jaison, T. N., Daly, L., McGovern, E., O’Sullivan, J., Wren, C., Bain, H. H., Hunter, S., O’Donnell, A. F., Lonergan, M., McGovern, E., Jayakrishnan, A. G., Desai, J., and Forsyth, A. T.

Published
1992
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28. Altered Brain Structure in Infants with Turner Syndrome

Author

Davenport, M L, primary, Cornea, E, additional, Xia, K, additional, Crowley, J J, additional, Halvorsen, M W, additional, Goldman, B D, additional, Reinhartsen, D, additional, DeRamus, M, additional, Pretzel, R, additional, Styner, M, additional, Gilmore, J H, additional, Hooper, S R, additional, and Knickmeyer, R C, additional

Published
2019
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29. Irish cardiac society

Author

Seifer, C., McNeill, B., OʼDonnell, M., Daly, K., Kellett, J., McGee, H. M., Montogomery, A. J., OʼCallaghan, D., Horgan, J. H., Mahon, N. G., Codd, M., Brennan, J., Egan, B., McCann, H. A., Sugrue, D. D., Menown, I. B. A., Patterson, R. S. H. W., McMechan, S. R., Hameed, S., Adgey, A. A. J., Baird, S. H., McBride, S. J., Trouton, T. G., Wilson, C., McRedmond, J. P., Fitzgerald, D. J., Crowley, J. J., Tanguay, J F., Santos, R. M., Stack, R. S., Keelan, P., McKenna, C. J., AuBuchon, R., Camrud, A. R., Holmes, D. R., Schwartz, R. S., Wolff, R., Edwards, W. D., Hanratty, C., McAuley, D., Young, I., Murtagh, G., OʼKeeffe, B., Richardson, G., Scott, M., Chew, E. W., Bailie, N. A., Graham, A. M. J., OʼKane, H., Kwon, H. M., Ellis, L., Virmani, R., Noelke, L., Wood, A. E., Javadpour, H., Veerasingham, D., OʼKane, D., Allen, J. D., Hennessy, T., Johnson, P., Hildick-Smith, D., Winter, E., Shapiro, L., Lerman, A., McGrath, L. T., Passmore, P., Silke, B., Nugent, A. G., McGurk, C., Maguire, S., Johnston, G. D., Lovell, S. L., McDowell, G., McEneany, D., Riley, M. S., Nicholls, D. P., Gilligan, D., Sargent, D., Dan, D., Elam, G., Rhee, B., Keane, D., Zhou, L., McGovern, B., Garan, H., Ruskin, J., OʼShea, J. C., Tan, H C., Zidar, J. P., OʼKeeffe, D. B., Graffin, S., Fitzsimmons, D., Brown, S., Duff, D., Denham, B., Woods, F., Neligan, M., Oslizlok, P., Connolly, C. K., Danton, M. H. D., Danton, M., Gladstone, D. J., Craig, B., Mulholland, H. C., Casey, F., Chaudhuri, S., Hinchion, J., Patterson, R. H. S. W., MacKenzie, G., Harbinson, M. T., Burgess, L. M., Moohan, V., McEneaney, D. J., Finnegan, O. C., Doherty, L., Riddell, J. G., Meleady, R., Daly, L., Graham, I., Quinn, M., Foley, B., Lee, J., Mulvihill, N., Walsh, M., OʼMorain, C., Crean, P., Hynes, C., King, S. M., David, S., Newton, H., Maguire, M., Rafferty, F., Sullivan, P. A., Murphy, D., Gallagher, S., Allen, J., Anderson, McC J., Hoag, J., Eckberg, D., Galvin, J., Diamond, P., Neilan, T., Keelan, E., A., H., McCarthy, C., Moohan, V. P., Ayers, G. M., Roberts, M., Burgess, L., Anderson, C., Khan, M., Clements, I. P., Miller, W. L., Turtle, F., Long, H., McNair, W., Campbell, N. P. S., Mathew, T. P., Smye, M., Nesbitt, G. S., Young, I. S., Mulcahy, D., Graham, I. M., Moore, D., Sugrue, D., Codd, M. B., Zimmerman, P., Winget, J., Capeless, M., McKelvey, T. A., Sarsam, M. I. A., and McEneaney, D.

Published
1998
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32. A total-population multigenerational family clustering study of autoimmune diseases in obsessive-compulsive disorder and Tourette's/chronic tic disorders

Author

Mataix-Cols, D., Frans, E., Pérez-Vigil, A., Kuja-Halkola, R., Gromark, C., Isomura, K., Fernández de la Cruz, L., Serlachius, E., Leckman, J. F., Crowley, J. J., Rück, C., Almqvist, C., Lichtenstein, P., Larsson, Henrik, Mataix-Cols, D., Frans, E., Pérez-Vigil, A., Kuja-Halkola, R., Gromark, C., Isomura, K., Fernández de la Cruz, L., Serlachius, E., Leckman, J. F., Crowley, J. J., Rück, C., Almqvist, C., Lichtenstein, P., and Larsson, Henrik

Abstract

The association between obsessive-compulsive disorder (OCD) and Tourette's/chronic tic disorders (TD/CTD) with autoimmune diseases (ADs) is uncertain. In this nationwide study, we sought to clarify the patterns of comorbidity and familial clustering of a broad range of ADs in individuals with OCD, individuals with TD/CTD and their biological relatives. From a birth cohort of 7 465 455 individuals born in Sweden between 1940 and 2007, we identified 30 082 OCD and 7279 TD/CTD cases in the National Patient Register and followed them up to 31 December 2013. The risk of 40 ADs was evaluated in individuals with OCD, individuals with TD/CTD and their first- (siblings, mothers, fathers), second- (half siblings) and third-degree (cousins) relatives, compared with population controls. Individuals with OCD and TD/CTD had increased comorbidity with any AD (43% and 36%, respectively) and many individual ADs. The risk of any AD and several individual ADs was consistently higher among first-degree relatives than among second- and third-degree relatives of OCD and TD/CTD probands. The risk of ADs was very similar in mothers, fathers and siblings of OCD probands, whereas it tended to be higher in mothers and fathers of TD/CTD probands (compared with siblings). The results suggest a familial link between ADs in general (that is, not limited to Streptococcus-related conditions) and both OCD and TD/CTD. Additional mother-specific factors, such as the placental transmission of antibodies, cannot be fully ruled out, particularly in TD/CTD., Funding Agencies:Tourette Association of AmericaAlicia Koplowitz FoundationNIMH R01MH105500 R01MH110427Swedish Research Council through the SIMSAM (Swedish Initiative for Research on Microdata in the Social And Medical Sciences) 340-2013-5867

Published
2018
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41. A total-population multigenerational family clustering study of autoimmune diseases in obsessive–compulsive disorder and Tourette’s/chronic tic disorders

Author

Mataix-Cols, D, primary, Frans, E, additional, Pérez-Vigil, A, additional, Kuja-Halkola, R, additional, Gromark, C, additional, Isomura, K, additional, Fernández de la Cruz, L, additional, Serlachius, E, additional, Leckman, J F, additional, Crowley, J J, additional, Rück, C, additional, Almqvist, C, additional, Lichtenstein, P, additional, and Larsson, H, additional

Published
2017
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45. International Genetic Evaluations for Feed intake in Dairy Cattle

Author

Berry, Dognah, Coffey, Mike, Pryce, Jennie E, de Haas, Yvette, Løvendahl, Peter, Krattenmacher, Nina, Crowley, J J, Wang, Zhiquan, Spurlock, Diane, Macdonald, K, Veerkamp, Roel F, and Weigel, K

Subjects
dry matter intake, dairy, genetic evaluations
Abstract

Feed represents a large proportion of the variable costs in dairy production systems. The omission of feed intake measures explicitly from national dairy cow breeding objectives is predominantly due to a lack of information on which to make selection decisions. Individual cow feed intake data are available in different countries, mostly from research or nucleus herds. None of these datasets are sufficiently large enough on their own to generate accurate genetic evaluations. Here we collate data from ten populations in nine countries. A total of 224,174 test-day records from parity one to five animals, as well as 1,784 records from growing heifers were available. Random regression models fitted to lactating cow test-day records were used to predict feed intake at 70 days post calving. Heritability estimates of predicted cow feed intake 70-days post-calving was 0.34 across the entire dataset and varied, within population, from 0.08 to 0.52. Repeatability of feed intake across lactations was 0.66. Heritability of feed intake in growing heifers was 0.20 to 0.34. The genetic correlation between feed intake in lactating cows and heifers was 0.67. A combined pedigree and genomic relationship matrix was used to improve linkages between populations for the estimation of genetic correlations between countries categorized as North America, Grazing, Other low input, and High input EU. Genetic correlation estimates between populations varied from 0.14 to 0.84 but was stronger (0.76 to 0.84) between the populations representative of high input production systems

Published
2013

48. Behavioral metabolomics analysis identifies novel neurochemical signatures in methamphetamine sensitization: Methamphetamine sensitization metabolomics

Author

Adkins, D. E., Vann, R. E., Sullivan, P. F., Crowley, J. J., Clark, S. L., van den Oord, E. J. C. G., and Batman, A. M.

Abstract

Behavioral sensitization has been widely studied in animal models and is theorized to reflect neural modifications associated with human psychostimulant addiction. While the mesolimbic dopaminergic pathway is known to play a role, the neurochemical mechanisms underlying behavioral sensitization remain incompletely understood. In the present study, we conducted the first metabolomics analysis to globally characterize neurochemical differences associated with behavioral sensitization. Methamphetamine-induced sensitization measures were generated by statistically modeling longitudinal activity data for eight inbred strains of mice. Subsequent to behavioral testing, nontargeted liquid and gas chromatography-mass spectrometry profiling was performed on 48 brain samples, yielding 301 metabolite levels per sample after quality control. Association testing between metabolite levels and three primary dimensions of behavioral sensitization (total distance, stereotypy and margin time) showed four robust, significant associations at a stringent metabolome-wide significance threshold (false discovery rate < 0.05). Results implicated homocarnosine, a dipeptide of GABA and histidine, in total distance sensitization, GABA metabolite 4-guanidinobutanoate and pantothenate in stereotypy sensitization, and myo-inositol in margin time sensitization. Secondary analyses indicated that these associations were independent of concurrent methamphetamine levels and, with the exception of the myo-inositol association, suggest a mechanism whereby strain-based genetic variation produces specific baseline neurochemical differences that substantially influence the magnitude of MA-induced sensitization. These findings demonstrate the utility of mouse metabolomics for identifying novel biomarkers, and developing more comprehensive neurochemical models, of psychostimulant sensitization.

Published
2013
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49. Antipsychotic-induced vacuous chewing movements and extrapyramidal side effects are highly heritable in mice

Author

Bogue, M A, Pratt, A L, Moy, S S, Quackenbush, C R, Adkins, D E, Wilhelmsen, K C, Sullivan, P F, van den Oord, E J, McLeod, H L, Cooper, T B, and Crowley, J J

Abstract

Pharmacogenomics is yet to fulfill its promise of manifestly altering clinical medicine. As one example, a predictive test for tardive dyskinesia (an adverse drug reaction consequent to antipsychotic exposure) could greatly improve the clinical treatment of schizophrenia but human studies are equivocal. A complementary approach is the mouse-then-human design in which a valid mouse model is used to identify susceptibility loci which are subsequently tested in human samples. We used inbred mouse strains from the Mouse Phenome Project to estimate the heritability of haloperidol-induced activity and orofacial phenotypes. 159 mice from 27 inbred strains were chronically treated with haloperidol (3 mg/kg/day via subdermal slow-release pellets) and monitored for the development of vacuous chewing movements (VCMs, the mouse analog of TD) and other movement phenotypes derived from open field activity and the inclined screen test. The test battery was assessed at 0, 30, 60, 90, and 120 days in relation to haloperidol exposure. As expected, haloperidol caused marked changes in VCMs, activity in the open field, and EPS. Unexpectedly, factor analysis demonstrated that these measures were imprecise assessments of a latent construct rather than discrete constructs. The heritability of a composite phenotype was ~0.9 after incorporation of the longitudinal nature of the design. Murine VCMs are a face valid animal model of antipsychotic-induced TD and heritability estimates from this study support the feasibility of mapping of susceptibility loci for VCMs.

Published
2012
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50. Comparative genomic evidence for the involvement of schizophrenia risk genes in antipsychotic effects

Author

Kim, Y, Giusti-Rodriguez, P, Crowley, J J, Bryois, J, Nonneman, R J, Ryan, A K, Quackenbush, C R, Iglesias-Ussel, M D, Lee, P H, Sun, W, de Villena, F P-M, and Sullivan, P F

Abstract

Genome-wide association studies (GWAS) for schizophrenia have identified over 100 loci encoding >500 genes. It is unclear whether any of these genes, other than dopamine receptor D2, are immediately relevant to antipsychotic effects or represent novel antipsychotic targets. We applied an in vivo molecular approach to this question by performing RNA sequencing of brain tissue from mice chronically treated with the antipsychotic haloperidol or vehicle. We observed significant enrichments of haloperidol-regulated genes in schizophrenia GWAS loci and in schizophrenia-associated biological pathways. Our findings provide empirical support for overlap between genetic variation underlying the pathophysiology of schizophrenia and the molecular effects of a prototypical antipsychotic.

Published
2018
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