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2. Abstracts

Author

Lacombe, P., Blaise, G., Plante, F., Hollmann, C., Penning, D. H., Patrick, J., Brien, J., Orser, B., Bertlik, M., Fedorko, L., O’Brodovich, H., Santos, A. C., Pedersen, H., Morishima, H. O., Finster, M., Arthur, G. R., Covino, B. G., Perreault, C., Albert, J. F., Couture, P., Meloche, R., Elliott, R. D., Stockwell, M., Roy, W. L., Lerman, J., McIntyre, B. G., Yee, D. A., Hunziker, P., Koch, J. P., Devitt, J. H., Daley, M. D., Colmenares, M. E., Norman, P. H., Sandler, A. N., Oyston, J. P., Knill, R. L., Skinner, M. I., Novick, T., Vandenberghe, H. M., Moote, C. A., Donati, François, Meistelman, Claude, Plaud, Benoit, Guay, J., Reinberg, C., Rivard, G. E., Poitras, B., Mathews, S., David, M., Dawe, G., Hall, R. I., Stringer D. G., Sandler A. N., Panos L., Lawson S., Einarson T. R., Badner N., Fiset, P., Balendran, P., Donati, F., Bevan, D. R., Hung, O. R., Varvel, J., Shafer, S., Stanski, D. R., Crawford, M. W., Carmichael, F. J., Orrego, H., Saldivia, V., Lerman, J., Ralley, F. E., Murkin, J. M., Hudson, R. J., Dunn, G., Perreault, L., Hardy, J. F., Donelly, M., Scott, W. A. C., Daly, D. S., McAllister, J. D., Sharpe, M. D., Manninen, P. H., Cuillerier, D. J., Gelb, A. W., Nantau, W. E., Leon, J. E., Bissonnette, B., Davies, K. R., Gelb, A., Boughner, D. R., Bisnaire, D., Shokeir, O., Code, W. E., Hertz, L., White, H. S., Hong, M., Milne, B., Loomis, C., Jhamandas, K., Lam A. M., Slee T., Hirst R., Cooper J. O., Pavlin E. G., Sundling N., Mutch, W. A. C., Ringaert, K., Ewart, F., White, I., Donen, N., Winn H. R., Grady M. S., Murkin, J. M., Farrar, J. K., McNeill, B., Lok, P., Nalder, B., Jivraj, K., Golar, S., Ford, G., Rosenal, T., Puchalski, S. A., Morison, D. H., Collins, R. M., Gascoyne, R. D., Taylor, R. H., Lerman, J., Gauthier R. A., Chung F., Dyck B., Romanelli J. R., Chapman K. R., Lavoie, J., Marcin, R., Tétrault, J. P., Murphy, I. L., Splinter, W. M., Segstro, R., Morley-Forster, P. K., Lu, G., Lessard, M. R., Trépanier, C. A., Brochu, J. G., Coté, J. J., Denault, P. H., Baribault, J. P., Gordon, A. R., O’Connor, J. P., Ramsay, J. G., Malcolm, I., Chang, P. C., Reynolds, F. B., Lang, S. A., Ha, H. C., Grant, R. P., Dolman, J. F., Harper, J. A., White, S. A., Parsons, D. G., Evans, K. G., Merrick, P., Trivedi, Narendra S., Halpern, Meyer, Robalino, Joffre, Shevde, Ketan, Wang, B. C., Hiller, J. M., Simon, E. J., Hillman, D. E., Li, D., Rosenberg, C., Turndorf, H., Penning, J. P., Nagasaka, Hiroshi, Yaksh, T. L., Forrest, J. B., Lam, L., Woo, J., Rifkind, A., Broadman, L., Hannallah, R., DeLeon, E., Reff, R., Tanaka, K., Watanabe, R., Harada, T., Dan, K., Aull, L., Woodward, E. R., Rout, R. W., Paulus, D. A., Reimer, E. J., Badner, N. H., Komar, W. E., Fancourt-Smith, P. F., McEwen, J. A., Warriner, C. B., Moore, R., Rosenblatt, M., Merai, B., Robalino, J., Shevde, K., Bryk, D., McCormack, J. P., Levine, M., Forster-Coull, J., Stasiuk, R. B. P., Jenkins, L. C., Chen, Kunzhou, Pan, Jianhui, Ji, Xuan, Vaidya, D., Tetzlaff, J. E., Baird, B. A., Yoon, H. J., Wood, G., Simpson, T., Pillow, K. J., Lampe, K. M., Hansen, L. M., Foldvari, M., Courtice, I. D., MacLeod, B. A., Panos L., Lawson S., Koren G., Volgyesi, G. A., Kolesar, R., Wolf, G. L., Sidebotham, G. W., Sprung, J., Gamulin, S., Bosnjak, Z. J., Kampine, J. P., Doyle, D. John, Harioka, T., Sone, T., Kakuyama, M., Miyake, C., Toda, H., Sosis, M., Oka, T., Ohwada, T., Kochi, A., Mizuguchi, T., Kay, J. C., Beauchamp, R. J., Mazer, C. D., Inada, E., Iwahashi, K., Aoki, K., Takanashi, S., Kohama, M., Aoki, Y., Poole, L., Murphy, J. T., Moffitt, E. A., Jolly, D., Finegan, B. A., Beach, J., Gulamhusein, S., Vincent, D., Sullivan, P. J., Martineau, R. J., Miller, D. R., Lewis, P., Staniland, J., Cuppage, A., Davies, J. M., Rose, D. K., Cohen, M. M., Rogers, K. H., Gellner, D., Duncan, P. G., Johnson, J. A., Cohen, J. A., Boisvenu, G., Haley, L. D., Parlow, J. L., Cervenko, F. W., Dillon, F., Harwood, T., Kolesar, R., Volgyesi, G., Reid, C. W., Samson, B., Beattie, W. S., Goldsmith, C. H., Sims, C. H., Welborn, L. G., Hannallah, R. S., Higgins, T., Fink, R., Luban, N., Murray, D. J., Forbes, R. B., Mehta, M., Dull, D. L., Horimoto, Y., Naide, M., Schaefer, J. D., Bonn, G. E., Rhine, E. J., MacNeill, H. B., Ménard, E. A., Roberts, D. J., Komocar, L., Kay, J., Chevrier, R., Marsh, B. J., Morton, N. S., White, M., Kenny, G. N. C., Yamashita, M., Tsuji, M., Malviya, S., Swartz, J., Brown, K. A., Holtby, H., Ein, S., Shandling, B., Smith, M. F., Beauprie, I. G., Clark, A. G., Keith, I. C., Spence, D., Ogata, Hiromaru, Midorikawa, Yukio, Doyle, D. John, Teves, Leonides Y., Jhawar, Balraj S., Kawamura, Takae, Wakusawa, Reiji, Hackmann, T., Steward, D. J., Maltby, J. R., Loken, R. G., Watson, N. C., Kubota, Tatsuya, Katano, Toshio, Yoshizawa, Mutsumi, Ohtake, Kazuei, Onodera, Fumio, Yoshitake, S., Matsumoto, S., Miyakawa, H., Takahashi, T., Kitano, T., Iwasaka, H., Hayano, Y., Noguchi, T., Taniguchi, K., Honda, N., Koyama, K., Takahashi, J., Ochiai, R., Takeda, J., Nagano, M., Rolbin, S., Hew, E., Morningstar, B., Mahesh, K., Yukioka, H., Fujimori, M., Siriwardhana, S. A., Kawas, A., Yates, S., Gulden, H., Upton, J. M., Giesecke, A. H., Suzuki, H., Maru, E., Fujita, M., Pagliarello, G., Simons, J., Irita, K., Shafiq, J., Tareen, F. M., Yoshitake, J., Suderman, V. S., Crosby, E. T., Mallon, J. S., Dunn, G. L., Hatano, Y., Nakamura, K., Nishiwada, M., Mori, Kenjiro, Pounder, D. R., Blackstock, D., Steward, D., Kumagai, M., Takinami, M., Tanaka, S., Shudo, Y., Amaki, Y., Kobayashi, K., Jansen, G. F. A., Kedaria, M., Zuurmond, W. W. A., Hartley, E., St. Louis, P., Rybczynski, J., McLeod, M. E., Byrick, R. J., Mullen, J. Brendan, Wong, P. Y., Wigglesworth, D., Kay, J. Colin, Swartz, J. S., Gold, M., Braude, B. M., Dolovich, J., Gilmour, R. F., Sutherland, L. R., O’Connor, G., Riding, K., Laird, B., Riou, S., Gross, Michael, Tang, T., Halpern, S. H., Roy, A. G., Côté, J. J., Lindblad, T., Buckley, D. N., Oxom, D. C., Whatley, G. S., Knox, J. W. D., Hooper, J. G. V., Dolman, J., Faneourt-Smith, P. F., Torsher, L., Gao, Yuhui, Chai, Xiaoqing, O’Leary, G., Qureshi, S. A., Laganiere, S., McGilveray, I., Boylan, J. F., Hassard, P., Teasdale, S. J., Kapnoudhis, P., Vaghadia, H., Turnbull, K. M., Villeneuve, E., Buluran, J., Amyot, Y., Tanguay, M., Pharm, B., Beique, G., Sidi, A., Rush, W., Clanachan, A. S., Duke, P. C., Leroux, M., Corne, R., Patton, N., Greenberg, D., Parrott, J., Desjardins, P., Merchant R. N., Brown W. F., Watson B. V., Burrows, F. A., Tatman, D. J., Starr, J. M., Symreng, T., Kall, R. I., Schweiger, I. M., Finlayson, D. C., Weisel, R. D., Ivanov, J., Mickle, D. A., Fuller, John, Lu, Grant, Dain, Steven, McLean, R. F., Noble, W. H., Kolton, M., Newfield, A. M., Lipton, J. M., Ide, T., Isono, S., Kochi, T., Izumi, Y., Erian, R. F., Stafford-Smith, M., Yamada, M., Johnson, D., Hurst, T., Mayers, I., Tsuda, Takako, Takeuchi, Mikio, Ishikawa, Kiyoshi, Ando, Hiroshi, Hanamura, Yasunori, Takasu, Hiroe, Hiyama, A., and Cardiac Anaesthesia Research Group

Published
1990
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3. Abstracts

Author

Crosby, E. T., Halpern, S., Bill, K. M., Flynnn, R. J., Moore, J., Navaneelan, C., Cunningham, A., Yu, P. Y. H., Gamling, D. R., McMorland, G. H., Perreault, C., Guay, J., Gaudreault, P., Hollman, C., Meloche, R., Hackman, T., Sheps, S. B., Murray, W. B., Heiman, P. A., Slinger, P., Triolet, W., Jain, U., Rao, T. L. K., Dasari, M., Pifarre, R., Sullivan, H., Calandra, D., Friesen, R. M., Bjornson, J., Hatton, G., Parlow, J. L., Casey, W. F., Broadman, L. M., Rice, L. J., Dailey, M., Andrews, W. R., Stigi, S., Jendrek, V., Shevde, K., Withington, D. E., Saoud, A. Tazi, Ramsay, J. G., Bilodeau, J., Johnson, D., Mayers, I., Doran, R. J., Wong, P. Y., Mullen, Brendan J., Wigglesworth, D., Byrick, R. J., Kay, J. Colin, Stubbing, J. F., Sweeney, B. P., Dagher, E., Dumont, L., Lagace, G., Chartrand, C., Badner, N. H., Sandier, A. N., Leitch, L., Koren, G., Erian, R. F., Bunegin, L., Shulman, D. L., Burrows, F., O’Sullivan, K., Bouchier, D., Kashin, B. A., Wynands, J. E., Villeneuve, E., Blaise, G., Guerrard, M. J., Buluran, J., Effa, E., Vaghadia, H., Jenkins, L. C., Janisse, T., Scudamore, C. H., Patel, P. M., Mutch, W. A. C., Ruta, T. S., McNeill, B. R., Murkin, J. M., Gelb, A. W., Farrar, J. K., Johnson, G. D., Adams, M. A., Lillicrap, D. P., Lindblad, T., Beattie, W. S., Buckley, D. N., Forrest, J. B., Lessard, M. R., Trépanier, C. A., Baribault, J. P., Brochu, J. G., Brousseau, C. A., Cote, J. J., Denault, P., Whang, P., Moudgil, G. C., Daly, N., Morrison, D. H., Ogilvie, R., Man, J., Ehler, T., Leitch, L. F., Dupuis, J. Y., Martin, R., Tessonnier, J. M., Barry, A. W., Milne, B., Quintin, L., Gillon, J. Y., Pujol, J. F., DeMonte, F., Zhang, C., Hamilton, J. T., Zhou, Y., Plourde, G., Picton, T. W., Kellett, A., Pilato, M. A., Bissonnette, B., Lerman, J., Brown, K. A., Dundee, J. W., Sosis, M., Dillon, F., Stetson, J. B., Voorhees, W. D., Bourland, J. D., Geddes, L. A., Shoenlein, W. E., O’Leary, G., Teasdale, S., Knill, R. L., Rose, E. A., Berko, S. L., Smith, C. E., Sadler, J. M., Bevan, J. C., Donati, F., Bevan, D. R., Tellez, J., Turner, D., Kao, Y. J., Salidivia, V., Roldan, L., Orrego, H., Carmicheal, F. J., Kent, A. P., Parker, C. J. R., Hunter, J. M., Finley, G. A., Goresky, G. V., Klassen, K., McDiarmid, C., Shaffer, E., Vaughan, M., Randolph, J., Szalados, J. E., Lazzell, V. A., Creighton, R. E., Poon, A. O., Mclntyre, B., Douglas, M. J., Swenerton, J. E., Farquharson, D. F., Landry, D., Petit, F., Riegert, D., Koch, J. P., Maggisano, R., Devitt, J. H., Jense, H. G., Dubin, S. A., Silverstein, P. I., Rodriguez, N., Wakefield, M. L., Williams, R., Dubin, S., Smith, J. J., Hofmann, V. C., Jarvis, A. P., Forbes, R. B., Murray, D. J., Dillman, J. B., Dull, D. L., Cohen, M. M., Cameron, C. B., Johnston, R. G., Konopad, E., Jivraj, K., Hunt, D., Eastley, R., Strunin, L., Fairbrass, M. J., Laganiere, S., McGilvery, M., Foster, B., Young, P., Weisel, D., Parra, L., Suarez Isla, B. A., Lopez, J. R., Hall, R. I., Hawwa, R., Kashtan, H., Edelist, G., Mallon, J., Kapala, D., Dhamee, M. Saeed, Reynolds, A. C., Olund, T., Entress, J., Kalbfleisch, J., Bell, S. D., Goldberg, M. E., Bracey, B. J., Goldhill, D. R., Bennett, M. H., Emmott, R. S., Innis, R. F., Yate, P. M., Flynn, P. J., Gill, S. S., Saunders, P. R., Geisecke, A. H., Feldman, J. M., Banner, M. J., Siriwardhana, S. A., Kawas, A., Lipton, J. L., Giesecke, A. H., Doyle, D. J., Volgyesi, G. A., Hillier, S. C., Gallagher, J., Hargaden, K., Hamil, M., Cunningham, A. J., Scott, W. A. C., Sielecka, D., Illing, L. H., Jani, K., Scarr, M., Maltby, J. R., Roy, J., McNulty, S. E., Torjman, M., Carey, C., Bracey, B., Markham, K., Durcan, J., Blackstock, D., DaSilva, C. A., Demars, P. D., Montgomery, C. J., Steward, D. J., Sessler, D. I., Laflamme, P., McDevitt, S., Kamal, G. D., Symreng, T., Tatman, D. J., Durcharme, J., Varin, F., Besner, J. G., Dyck, J. B., Chung, F., Arellano, R., Lim, G., Bailey, D. G., Bayliff, C. D., Cunningham, D. G., Ewen, A., Sheppard, S. D., Mahoney, L. T., Bacon, G. S., Rice, L. R., Newman, K., Loe, W., Toth, M., Pilato, M., Classen, K., McDiamid, C., Burrows, F. A., Irish, C. L., Casey, W., Hauser, G. J., Chan, M. M., Midgley, F. M., Holbrook, P. R., Elliott, M. E., Man, W. K., Finegan, B. A., Clanachan, A. S., Hudson, R. J., Thomson, I. R., Burgess, P. M., Rosenbloom, M., Fisher, J. M., O’Connor, J. P., Ralley, F. E., Robbins, G. R., Moote, C. A., Manninen, P. H., English, M., Farmer, C., Scott, A., White, I. W. C., Biehl, D., Donen, N., Mansfield, J., Cohen, M., Wade, J. G., Woodward, C., Ducharme, J., Gerardi, A., Mijares, A., Code, W. E., Hertz, L., Chung, A., Meier, H. M. R., Lautenschlaeger, E., Seyone, C., Wassef, M. R., Devitt, F. H., Cheng, D. C. H., Dyck, B., Chan, V. W. S., Ferrante, F. M., Arthur, G. R., Rice, L., Annallah, R. H., Etches, R. C., Loulmet, D., Lacombe, P., Hollmann, C., Tanguay, M., Blaise, G. A., Lenis, S. G., Fear, D. W., Lang, S. A., Ha, H. C., Germain, H., Neion, A., Dorian, P., Salter, D., Pollick, C., Cervenko, F., Parlow, J., Pym, J., Nakatsu, K., Elliott, D., Miller, D. R., Martineau, R. J., Ewing, D., Martineau, R. J., Knox, J. W. D., Oxorn, D. C., O’Connor, J. P., Whalley, D. G., Rogers, K. H., Kay, J. C., Mazer, C. D., Belo, S. E., Hew-Wing, P., Hew, E., Tessonier, J. M., Thibault, G., Testaert, E., Chartrand, D., Cusson, J. R., Kuchel, O., Larochelle, P., and Couture, J.

Published
1989
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4. Nifedipine-alcohol interaction

Author

Qureshi, S., Laganiere, S., McGilveray, I.J., Lacasse, Y., and Caille, G.

Subjects
Nifedipine -- Adverse and side effects, Drug interactions -- Research
Published
1990

9. Proarrhythmia of a class Ic drug: suppression by combination with a drug prolonging repolarization in the dog late after infarction.

Author

Duff, H J, Stemler, M, Thannhauser, T, Laganiere, S, Rude, E, and Lester, W

Abstract

Encainide treatment in patients after myocardial infarction is associated with increased risk of sudden cardiac death. This may relate to drug-induced changes in the electrophysiologic milieu, thus predisposing the patient to sustained ventricular tachyarrhythmias. The goals of this study were to first develop a model of class Ic-induced ventricular tachycardia (VT) and then to design treatments to oppose this prodysrhythmic activity. Dogs with time-dependent loss of inducible sustained VT in the antiarrhythmic drug-free state were studied late after infarction. These dogs received a series of three loading and maintenance infusions of O-demethyl encainide (ODME) to achieve concentrations of 60 +/- 31, 136 +/- 46 and 339 +/- 171 ng/ml. Drug maintenance continued until programmed stimulation induced monomorphic sustained VT. When ODME infusion allowed this induction, barium chloride infusions were added. ODME treatment allowed induction of monomorphic sustained VT in 9 of 10 dogs studied. Prodysrhythmic monomorphic VT was significantly related (P < .01) to prolongation of conduction velocity in the peri-infarct zone. ODME modestly increased ventricular refractoriness at some but not all peri-infarct sites. Infusion of barium chloride in the above nine dogs caused their hearts to return to the noninducible state. Prolongation of refractoriness in the peri-infarct zone was correlated to this suppression of prodysrhythmia. Prolongation of conduction velocity in the absence of substantial prolongation of refractoriness may underlie ODME-facilitated induction of monomorphic VT. Prolongation of refractoriness in the peri-infarct zone by combination treatment with barium chloride reversed prodysrhythmic VT in all of the dogs.

Published
1995

18. Deciphering Cognitive Impairments in Huntington's Disease: A Comparative Study of Stroop Test Variations.

Author

Sierra LA, Wynn A, Lanzaro E, Dzekon K, Russell A, Halko M, Claassen DO, Frank S, Considine CM, and Laganiere S

Subjects
Humans, Male, Female, Middle Aged, Adult, Aged, Eye Movements physiology, Huntington Disease physiopathology, Huntington Disease complications, Huntington Disease diagnosis, Cognitive Dysfunction physiopathology, Cognitive Dysfunction etiology, Cognitive Dysfunction diagnosis, Stroop Test
Abstract

Background: Huntington's disease (HD) is a neurodegenerative disorder marked by cognitive impairment, movement abnormalities, and behavioral disturbances. The Stroop Color Word Test (SCWT) is a widely used tool to detect cognitive decline in HD. Variations in SCWT formats-horizontal (original) and vertical (Golden)-may influence performance, given HD's impact on cognitive and oculomotor abilities., Objective: This study aimed to compare the effectiveness of the horizontal and Golden vertical SCWT formats in detecting cognitive decline in HD, and to determine how performance may have been influenced by eye movement abnormalities., Methods: Forty-five participants with genetically confirmed HD were recruited. Both SCWT formats were administered to each participant in a counterbalanced fashion. Individual performance of all three sections on each format was standardized across 2 different norms. Raw and normed scores on each variation were compared and correlated with eye movement ratings on the Unified Huntington's Disease Rating Scale., Results: The Golden variation elicited significantly slower responses, particularly in the Word Reading section, across two benchmark norms. Statistical analysis revealed significant performance differences between the two formats. Correlations between vertical eye movement ratings and performance on the Golden SCWT were highly significant, highlighting the impact of oculomotor coordination on cognitive assessments in HD., Conclusion: This study underscores the importance of considering test format in cognitive assessments for HD. The Golden vertical SCWT demonstrates increased sensitivity in detecting deficits in HD, possibly linked to vertical saccade abnormalities. These insights are important for improving the sensitivity of cognitive assessments and monitoring disease progression in HD research and clinical practice.

Published
2024
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19. LASSI-L detects early cognitive changes in pre-motor manifest Huntington's disease: a replication and validation study.

Author

Sierra LA, Hughes SB, Ullman CJ, Hall A, Pandeya SR, Schubert R, Frank SA, Halko MA, Corey-Bloom J, and Laganiere S

Abstract

Background and Objectives: Cognitive decline is an important early sign in pre-motor manifest Huntington's disease (preHD) and is characterized by deficits across multiple domains including executive function, psychomotor processing speed, and memory retrieval. Prior work suggested that the Loewenstein-Acevedo Scale for Semantic Interference and Learning (LASSI-L)-a verbal learning task that simultaneously targets these domains - could capture early cognitive changes in preHD. The current study aimed to replicate, validate and further analyze the LASSI-L in preHD using larger datasets., Methods: LASSI-L was administered to 50 participants (25 preHD and 25 Healthy Controls) matched for age, education, and sex in a longitudinal study of disease progression and compared to performance on MMSE, Trail A & B, SCWT, SDMT, Semantic Fluency (Animals), and CVLT-II. Performance was then compared to a separate age-education matched-cohort of 25 preHD participants. Receiver operating curve (ROC) and practice effects (12 month interval) were investigated. Group comparisons were repeated using a preHD subgroup restricted to participants predicted to be far from diagnosis (Far subgroup), based on CAG-Age-Product scaled (CAPs) score. Construct validity was assessed through correlations with previously established measures of subcortical atrophy., Results: PreHD performance on all sections of the LASSI-L was significantly different from controls. The proactive semantic interference section (PSI) was sensitive ( p  = 0.0001, d  = 1.548), similar across preHD datasets ( p  = 1.0), reliable on test-retest over 12 months (spearman rho = 0.88; p = <0.00001) and associated with an excellent area under ROC (AUROC) of 0.855. In the preHD Far subgroup comparison, PSI was the only cognitive assessment to survive FDR < 0.05 ( p  = 0.03). The number of intrusions on PSI was negatively correlated with caudate volume., Discussion: The LASSI-L is a sensitive, reliable, efficient tool for detecting cognitive decline in preHD. By using a unique verbal learning test paradigm that simultaneously targets executive function, processing speed and memory retrieval, the LASSI-L outperforms many other established tests and captures early signs of cognitive impairment. With further longitudinal validation, the LASSI-L could prove to be a useful biomarker for clinical research in preHD., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Sierra, Hughes, Ullman, Hall, Pandeya, Schubert, Frank, Halko, Corey-Bloom and Laganiere.)

Published
2023
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20. Prevalence of neurocognitive disorder in Huntington's disease using the Enroll-HD dataset.

Author

Sierra LA, Ullman CJ, Baselga-Garriga C, Pandeya SR, Frank SA, and Laganiere S

Abstract

Background: Cognitive decline in Huntington's disease (HD) begins early in the disease course, however the reported prevalence and severity of cognitive impairment varies based on diagnostic approach. A Movement Disorders Society Task Force recently endorsed the use of standardized DSM-5-based criteria to diagnose neurocognitive disorder (NCD) in Huntington's disease., Objectives: To determine the prevalence and severity of cognitive impairment across different stages of HD by applying NCD criteria (mild and major) to participant data from the Enroll-HD database., Methods: Enroll-HD participants were triaged into either premanifest (preHD), manifest or control groups. PreHD was further dichotomized into preHD near or preHD far based on predicted time to diagnosis using the scaled CAG-age product score (CAPs). Embedded cognitive performance and functional independence measures were used to determine prevalence of NCD (mild and major) for all groups., Results: Prevalence of NCD-mild was 25.2%-38.4% for manifest HD, 22.8%-47.3% for preHD near, 11.5%-25.1% for preHD far, and 8.8%-19.1% for controls. Prevalence of NCD-major was 21.1%-57.7% for manifest HD, 0.5%-16.3% for preHD near, 0.0%-4.5% for preHD far, and 0.0%-3.0% for controls., Conclusion: The prevalence of NCD in HD is elevated in preHD and demonstrates a sharp rise prior to diagnosis. In manifest HD, the vast majority of participants meet criteria for NCD. These findings are important for optimizing clinical care and/or anticipating the need for supportive services., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Sierra, Ullman, Baselga-Garriga, Pandeya, Frank and Laganiere.)

Published
2023
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21. Using the LASSI-L to Detect Robust Interference Effects in Premanifest Huntington Disease.

Author

Sierra LA, Ullman CJ, Frank SA, and Laganiere S

Subjects
Humans, Longitudinal Studies, Memory, Learning, Neuropsychological Tests, Huntington Disease diagnosis, Cognitive Dysfunction diagnosis, Cognitive Dysfunction psychology
Abstract

Background: Diagnosis of manifest Huntington disease (HD) is based primarily on motor symptoms, but premanifest HD (preHD) is often associated with subtle cognitive decline. The Loewenstein-Acevedo Scales for Semantic Interference and Learning (LASSI-L) is a validated verbal learning test that can be used to detect early cognitive decline., Objective: To determine the utility of the LASSI-L for detecting early cognitive decline in individuals with preHD and to compare the results of the LASSI-L with those of commonly used neuropsychological tests in HD., Method: We administered the LASSI-L to 13 individuals with preHD and 13 healthy controls matched for age, sex, and education as part of a longitudinal study of disease progression. For comparison purposes, we administered the Mini-Mental State Examination; Stroop Color and Word Test; Symbol Digit Modalities Test; Trail-Making Test, Parts A and B; and category fluency (animals) task., Results: Five of the seven sections on the LASSI-L captured group differences: Proactive Semantic Interference (PSI; P < 0.001), Failure to Recover From PSI ( P = 0.038), Retroactive Semantic Interference (RSI; P = 0.013), Delayed Recall ( P < 0.001), and B1 Cued Recall Intrusions ( P = 0.036). Using a false discovery rate of <0.05, PSI, RSI, and Delayed Recall remained significant., Conclusion: The LASSI-L is a sensitive instrument for detecting early interference effects in individuals with preHD that outperforms commonly used neuropsychological tests. The LASSI-L could be a useful addition to clinical and research protocols involving individuals with preHD., Competing Interests: The authors declare no conflicts of interest., (Copyright © 2023 Wolters Kluwer Health, Inc. All rights reserved.)

Published
2023
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22. Finding the imposter: brain connectivity of lesions causing delusional misidentifications.

Author

Darby RR, Laganiere S, Pascual-Leone A, Prasad S, and Fox MD

Subjects
Aged, Aged, 80 and over, Brain diagnostic imaging, Female, Humans, Image Processing, Computer-Assisted, Magnetic Resonance Imaging, Male, Meta-Analysis as Topic, Motivation, Neuropsychological Tests, Psychiatric Status Rating Scales, Recognition, Psychology, Brain pathology, Brain Injuries complications, Brain Mapping, Schizophrenia, Paranoid diagnosis, Schizophrenia, Paranoid etiology
Abstract

SEE MCKAY AND FURL DOI101093/AWW323 FOR A SCIENTIFIC COMMENTARY ON THIS ARTICLE: Focal brain injury can sometimes lead to bizarre symptoms, such as the delusion that a family member has been replaced by an imposter (Capgras syndrome). How a single brain lesion could cause such a complex disorder is unclear, leading many to speculate that concurrent delirium, psychiatric disease, dementia, or a second lesion is required. Here we instead propose that Capgras and other delusional misidentification syndromes arise from single lesions at unique locations within the human brain connectome. This hypothesis is motivated by evidence that symptoms emerge from sites functionally connected to a lesion location, not just the lesion location itself. First, 17 cases of lesion-induced delusional misidentifications were identified and lesion locations were mapped to a common brain atlas. Second, lesion network mapping was used to identify brain regions functionally connected to the lesion locations. Third, regions involved in familiarity perception and belief evaluation, two processes thought to be abnormal in delusional misidentifications, were identified using meta-analyses of previous functional magnetic resonance imaging studies. We found that all 17 lesion locations were functionally connected to the left retrosplenial cortex, the region most activated in functional magnetic resonance imaging studies of familiarity. Similarly, 16 of 17 lesion locations were functionally connected to the right frontal cortex, the region most activated in functional magnetic resonance imaging studies of expectation violation, a component of belief evaluation. This connectivity pattern was highly specific for delusional misidentifications compared to four other lesion-induced neurological syndromes (P < 0.0001). Finally, 15 lesions causing other types of delusions were connected to expectation violation (P < 0.0001) but not familiarity regions, demonstrating specificity for delusion content. Our results provide potential neuroanatomical correlates for impaired familiarity perception and belief evaluation in patients with delusional misidentifications. More generally, we demonstrate a mechanism by which a single lesion can cause a complex neuropsychiatric syndrome based on that lesion's unique pattern of functional connectivity, without the need for pre-existing or hidden pathology., (© The Author (2016). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oup.com.)

Published
2017
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23. Network localization of hemichorea-hemiballismus.

Author

Laganiere S, Boes AD, and Fox MD

Subjects
Adult, Aged, Aged, 80 and over, Case-Control Studies, Chorea diagnostic imaging, Chorea physiopathology, Connectome, Dyskinesias diagnostic imaging, Dyskinesias physiopathology, Female, Functional Laterality, Humans, Magnetic Resonance Imaging, Male, Middle Aged, Neural Pathways diagnostic imaging, Neural Pathways physiopathology, Reproducibility of Results, Rest, Sensitivity and Specificity, Stroke diagnostic imaging, Stroke physiopathology, Young Adult, Brain diagnostic imaging, Brain physiopathology, Chorea etiology, Dyskinesias etiology, Stroke complications
Abstract

Objective: To determine whether neuroanatomically heterogeneous strokes causing hemichorea-hemiballismus localize to a common functional network., Methods: We identified 29 cases of lesion-induced hemichorea-hemiballismus from the literature and mapped each lesion volume onto a reference brain. Using a recently validated technique termed lesion network mapping, we tested whether these lesions belonged to the same functional network. To accomplish this, the network of brain regions functionally connected to each lesion was identified using a connectome dataset from healthy participants. Network maps were overlapped to identify any region functionally connected to our set of lesions. Specificity was evaluated using a case-control design; control cohorts included a group of similar lesions randomized to different brain locations and a second group of lesions causing a separate movement disorder, asterixis. Reproducibility was evaluated using an independent cohort of 10 additional hemichorea-hemiballismus cases., Results: Lesions showed heterogeneity in anatomical location, consistent with prior reports. However, at least 90% of these lesions showed network overlap in the posterolateral putamen. This result was specific to lesions causing hemichorea-hemiballismus and reproducible in an independent cohort. The putaminal overlap site was itself connected to a broader motor network that predicted the distribution of lesions causing hemichorea-hemiballismus., Conclusions: Strokes causing hemichorea-hemiballismus, while anatomically heterogeneous, localize to a common functional network. Specifically, lesions occur in regions functionally connected to the posterolateral putamen, a region previously implicated in hyperkinetic movement disorders. Lesion network mapping may be useful in identifying the neuroanatomical substrates of heterogeneous lesion-based disorders., (© 2016 American Academy of Neurology.)

Published
2016
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24. Noninvasive Brain Stimulation in Pediatric Attention-Deficit Hyperactivity Disorder (ADHD): A Review.

Author

Rubio B, Boes AD, Laganiere S, Rotenberg A, Jeurissen D, and Pascual-Leone A

Subjects
Humans, Pediatrics, Attention Deficit Disorder with Hyperactivity therapy, Brain physiology, Transcranial Direct Current Stimulation methods, Transcranial Magnetic Stimulation methods
Abstract

Attention-deficit hyperactivity disorder (ADHD) is one of the most prevalent neurodevelopmental disorders in the pediatric population. The clinical management of ADHD is currently limited by a lack of reliable diagnostic biomarkers and inadequate therapy for a minority of patients who do not respond to standard pharmacotherapy. There is optimism that noninvasive brain stimulation may help to address these limitations. Transcranial magnetic stimulation and transcranial direct current stimulation are 2 methods of noninvasive brain stimulation that modulate cortical excitability and brain network activity. Transcranial magnetic stimulation can be used diagnostically to probe cortical neurophysiology, whereas daily use of repetitive transcranial magnetic stimulation or transcranial direct current stimulation can induce long-lasting and potentially therapeutic changes in targeted networks. In this review, we highlight research showing the potential diagnostic and therapeutic applications of transcranial magnetic stimulation and transcranial direct current stimulation in pediatric ADHD. We also discuss the safety and ethics of using these tools in the pediatric population., (© The Author(s) 2015.)

Published
2016
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25. Cytoplasmic targeting of mutant poly(A)-binding protein nuclear 1 suppresses protein aggregation and toxicity in oculopharyngeal muscular dystrophy.

Author

Abu-Baker A, Laganiere S, Fan X, Laganiere J, Brais B, and Rouleau GA

Subjects
Amino Acid Sequence, Blotting, Western, Cell Survival, Cytoplasm metabolism, Enzyme-Linked Immunosorbent Assay, HeLa Cells, Humans, Immunohistochemistry, Inclusion Bodies chemistry, Inclusion Bodies genetics, L-Lactate Dehydrogenase analysis, L-Lactate Dehydrogenase metabolism, Microscopy, Fluorescence, Molecular Sequence Data, Mutagenesis, Site-Directed, Poly(A)-Binding Protein I chemistry, Protein Structure, Tertiary, Inclusion Bodies metabolism, Muscular Dystrophy, Oculopharyngeal metabolism, Mutation, Poly(A)-Binding Protein I genetics, Poly(A)-Binding Protein I metabolism
Abstract

Oculopharyngeal muscular dystrophy (OPMD) is an adult-onset disorder characterized by progressive eyelid drooping, swallowing difficulties and proximal limb weakness. The autosomal dominant form of this disease is caused by a polyalanine expansion from 10 to 12-17 residues, located at the N-terminus of the poly(A)-binding protein nuclear 1 (PABPN1). A distinct pathological hallmark of OPMD is the presence of filamentous intranuclear aggregates in patients' skeletal muscle cells. Wildtype PABPN1 protein is expressed ubiquitously and was shown to be mostly concentrated in discrete nuclear domains called 'speckles'. Using an established cell- culture model, we show that most mutant PABPN1- positive (alanine expanded form) intranuclear aggregates are structures distinct from intranuclear speckles. In contrast, the promyelocytic leukaemia protein, a major component of nuclear bodies, strongly colocalized to intranuclear aggregates of mutant PABPN1. Wildtype PABPN1 can freely shuttle between the nucleus and cytoplasm. We determined whether the nuclear environment is necessary for mutant PABPN1 inclusion formation and cellular toxicity. This was achieved by inactivating the mutant PABPN1 nuclear localization signal and by generating full-length mutant PABPN1 fused to a strong nuclear export sequence. A green fluorescence protein tag inserted at the N-terminus of both wildtype PABPN1 (ala10) and mutant PABPN1 (ala17) proteins allowed us to visualize their subcellular localization. Targeting mutant PABPN1 to the cytoplasm resulted in a significant suppression of both intranuclear aggregates formation and cellular toxicity, two histological consequences of OPMD. Our results indicate that the nuclear localization of mutant PABPN1 is crucial to OPMD pathogenesis.

Published
2005
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26. Transgenic expression of an expanded (GCG)13 repeat PABPN1 leads to weakness and coordination defects in mice.

Author

Dion P, Shanmugam V, Gaspar C, Messaed C, Meijer I, Toulouse A, Laganiere J, Roussel J, Rochefort D, Laganiere S, Allen C, Karpati G, Bouchard JP, Brais B, and Rouleau GA

Subjects
Animals, Humans, Mice, Mice, Inbred C57BL, Mice, Transgenic, Peptides genetics, Peptides physiology, Poly(A)-Binding Protein I physiology, Ataxia genetics, Ataxia metabolism, Muscle Weakness genetics, Muscle Weakness metabolism, Poly(A)-Binding Protein I biosynthesis, Poly(A)-Binding Protein I genetics, Trinucleotide Repeat Expansion genetics
Abstract

Oculopharyngeal muscular dystrophy (OPMD) is a late-onset disorder caused by a (GCG)n trinucleotide repeat expansion in the poly(A) binding protein nuclear-1 (PABPN1) gene, which in turn leads to an expanded polyalanine tract in the protein. We generated transgenic mice expressing either the wild type or the expanded form of human PABPN1, and transgenic animals with the expanded form showed clear signs of abnormal limb clasping, muscle weakness, coordination deficits, and peripheral nerves alterations. Analysis of mitotic and postmitotic tissues in those transgenic animals revealed ubiquitinated PABPN1-positive intranuclear inclusions (INIs) in neuronal cells. This latter observation led us to test and confirm the presence of similar INIs in postmortem brain sections from an OPMD patient. Our results indicate that expanded PABPN1, presumably via the toxic effects of its polyalanine tract, can lead to inclusion formation and neurodegeneration in both the mouse and the human.

Published
2005
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27. Study on the lipid composition of aging Fischer-344 rat lymphoid cells: effect of long-term calorie restriction.

Author

Laganiere S and Fernandes G

Subjects
Animals, Cell Division, Concanavalin A pharmacology, Fatty Acids metabolism, Glutathione metabolism, Linoleic Acid, Linoleic Acids metabolism, Male, Rats, Rats, Inbred F344, Spleen cytology, Thymus Gland cytology, Aging metabolism, Energy Intake, Lipid Metabolism, Lymphocytes metabolism
Abstract

Long-term calorie restriction (LCR) is widely known to increase the survival rate of laboratory rodents and appears to retard the aging and senescence process. The present study was undertaken in Fischer-344 male rats maintained on ad libitum (AL) or LCR (40% less food intake than AL starting at 6 weeks of age). Age-associated changes in the proliferative response of lymphoid cells to mitogenic stimuli were studied in relation to alterations in the fatty acid composition of adherent and non-adherent-enriched subpopulations of spleen cells. Increases in spleen cell long-chain highly unsaturated fatty acids (20:4, 22:4 and 22:5) were accompanied by decreases in linoleic acid (18:2) in aging AL-fed rats. However, LCR stabilized levels of 18:2 and prevented the rise in highly unsaturated fatty acids. In addition, LCR markedly modulated the fatty acid profiles of thymocytes and bone marrow cells. A 70% decline in concanavalin A (Con A) stimulated [3H]thymidine uptake of spleen cells from AL animals was normalized by LCR. Splenic reduced glutathione (GSH), a potential modulator of the mitogenic response, was unaffected by age and nutritional regimen. Thus, normalization of lymphoid cell fatty acid composition by LCR parallels the preservation of mitogenic responsiveness to Con A.

Published
1991
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28. Intranasal nifedipine for post-bypass hypertension--hemodynamics and pharmacokinetics.

Author

O'Leary G, Qureshi SA, Laganiere S, McGilveray I, Boylan JF, Hassard P, and Teasdale SJ

Subjects
Administration, Intranasal, Blood Pressure drug effects, Dose-Response Relationship, Drug, Humans, Hypertension blood, Nifedipine pharmacokinetics, Postoperative Complications blood, Randomized Controlled Trials as Topic, Coronary Artery Bypass, Hemodynamics drug effects, Hypertension drug therapy, Nifedipine administration & dosage, Postoperative Complications drug therapy
Published
1990

29. Studies on membrane lipid peroxidation in omega-3 fatty acid-fed autoimmune mice: effect of vitamin E supplementation.

Author

Laganiere S, Yu BP, and Fernandes G

Subjects
Animals, Corn Oil pharmacology, Fish Oils pharmacology, Male, Mice, Mice, Inbred NZB, Microsomes, Liver ultrastructure, Mitochondria, Liver ultrastructure, Tocopherols, Vitamin E administration & dosage, Vitamin E analogs & derivatives, Vitamin E metabolism, Autoimmunity, Dietary Fats pharmacology, Fatty Acids, Omega-3 pharmacology, Intracellular Membranes metabolism, Lipid Peroxidation drug effects, Vitamin E pharmacology, alpha-Tocopherol analogs & derivatives
Abstract

Enzyme-dependent and non-enzymatic in vitro lipid peroxidation was studied in autoimmune prone B/W mice fed diets containing high levels of dietary corn oil (CO) or menhaden fish oil (FO) as lipid source since weaning. Lipid analysis revealed that FO-fed mouse liver mitochondrial and microsomal membrane fractions incorporated 20:5 omega 3 and 22:6 omega 3 in replacement of 18:2 omega 6 and 20:4 omega 6 found in corn oil (CO) fed control animals reflecting the composition of the dietary oils. Lower concentrations of vitamin E were found in the FO-fed mouse membranes and serum than those of CO-fed mice when diets were supplemented with a standard 75 I.U. alpha-tocopheryl acetate/kg diet. The rate and extent of membrane lipid peroxidation was greatly increased in FO-fed, vitamin-E-depleted membranes. Full repletion of membrane vitamin E levels by supplementation with 500 I.U./kg of FO diet for 30 days significantly decreased lipid peroxidation and showed that in FO-fed mice, membrane peroxidation is inversely proportional to vitamin E content. However, due to a lower ratio of vitamin E and highly unsaturated fatty acids, FO-fed mouse membranes were more sensitive to pro-oxidant stimulus than were those from CO-fed mice. These findings illustrate the action of vitamin E against membrane lipid peroxidation and stress the importance of adequate supplementation of antioxidant with high omega-3 fatty acids intake.

Published
1990
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30. Effect of chronic food restriction in aging rats. II. Liver cytosolic antioxidants and related enzymes.

Author

Laganiere S and Yu BP

Subjects
Analysis of Variance, Animals, Catalase metabolism, Cytosol enzymology, Diet, Glutathione Transferase metabolism, Liver enzymology, Male, Rats, Rats, Inbred F344, Aging metabolism, Antioxidants metabolism, Cytosol metabolism, Food Deprivation physiology, Liver metabolism
Abstract

The cytosolic status during aging of several antioxidants and enzymatic activities which protect the cell from oxidative damage was explored in the liver of ad libitum-fed and food restricted rats. Restricting calories effectively prevented the age-related decrease in cellular glutathione that occurs in ad libitum-fed rats. Although glutathione reductase exhibited little change with age in ad libitum-fed rats, dietary restriction resulted in greater activity of this enzyme than that of ad libitum-fed animals. Glutathione S-transferase activity of ad libitum-fed rats decreased significantly with age in ad libitum-fed rats but not in food restricted rats. The glutathione peroxidase activity which increased until 12 months in the ad libitum-fed rats declined by 24 months; there was little change with adult age in this enzymatic activity in food restricted rats. Catalase activity declined steadily from 3-24 months in the ad libitum-fed rats, and food restriction prevented this age-related decline. The significance of antioxidants and the related protective enzymes is discussed relative to membrane alterations and the anti-oxidative action of food restriction in relation to age-related degenerative damages.

Published
1989
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31. Effect of chronic food restriction in aging rats. I. Liver subcellular membranes.

Author

Laganiere S and Yu BP

Subjects
Age Factors, Animals, Body Weight, Cell Membrane metabolism, Cell Membrane ultrastructure, Fatty Acids, Unsaturated analysis, Lipids analysis, Liver metabolism, Male, Rats, Rats, Inbred F344, Vitamin E analysis, Aging physiology, Food Deprivation physiology, Liver ultrastructure
Abstract

To assess which membrane properties are modulated by the action of food restriction, characteristics of liver membrane structures of ad libitum-fed and food restricted Fischer 344 rats were analyzed over a wide age range. The results show that the yields of mitochondrial and microsomal membranes decreased in ad libitum-fed rats, but this age-related loss did not occur in food restricted rats until 30 months. Changes in membrane fatty acid composition which occurred with age were substantially modified by food restriction. Linoleic acid content progressively decreased in the membranes of ad libitum-fed rats with a concomitant increase of docosapentaenoic acid while an opposite pattern of change occurred in food restricted rats. Furthermore, food restriction maintained a low docosahexaenoic acid level in microsomes at all ages studied. While serum tocopherol increased markedly with age, there was little change in membrane tocopherol content in ad libitum-fed rats.

Published
1989
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32. Anti-lipoperoxidation action of food restriction.

Author

Laganiere S and Yu BP

Subjects
Aging, Animals, Kinetics, Male, Malondialdehyde metabolism, Rats, Rats, Inbred F344, Submitochondrial Particles metabolism, Diet, Reducing, Intracellular Membranes metabolism, Lipid Peroxides metabolism, Liver growth & development, Microsomes, Liver metabolism, Mitochondria, Liver metabolism
Abstract

Chronic food restriction inhibited the age-related increase of malondialdehyde production and lipid hydroperoxides in liver mitochondrial and microsomal membranes of ad libitum fed Fischer 344 rats. The anti-lipoperoxidation action of food restriction could not be attributable to the changes in membrane lipid content nor vitamin E status. Restricting calories modified membrane fatty acid composition by increasing linoleic acid and decreasing docosapentaenoic acid content in both membranes. The significance of the fatty acid modification was discussed in terms of anti-lipoperoxidation and membrane fluidity.

Published
1987
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34. Chemical aspects of propranolol metabolism. Synthesis and identification of 3-(4-hydroxy-1-naphthoxy)propane-1,2-diol as a metabolite of propranolol in the dog, in man and in the rat liver 9000g supernatant fraction.

Author

Gupte SM, Bartels MJ, Kerr BM, Laganiere S, Silber BM, and Nelson WL

Subjects
Aged, Animals, Dogs, Gas Chromatography-Mass Spectrometry, Humans, In Vitro Techniques, Male, Propranolol chemical synthesis, Propranolol isolation & purification, Rats, Rats, Inbred Strains, Liver metabolism, Propranolol analogs & derivatives, Propranolol metabolism
Abstract

4-Hydroxypropranolol glycol (2), a suspected metabolite of propranolol was synthesized from 4-allyloxy-1-naphthaldehyde (4). Osmium tetroxide oxidation of 4 afforded a glycol (5) and subsequent Baeyer-Villiger rearrangement afforded 2. Its presence as a biliary metabolite in a dog maintained on a constant infusion of pseudoracemic propranolol (made up of equal molar 2S-propranolol-3',3'-d2 and 2R-propranolol-d0) into the portal vein was confirmed based on GC-MS data of the TFA and TMS derivatives of the standard and biliary metabolites. Greater amounts of 2 arose from 2R-propranolol than from 2S-propranolol (1.5:1). Similarly, 2 was formed as a urinary metabolite in one subject maintained on oral propranolol, 80 mg every 6 hours. Compound 2 was also formed when propranolol and propranolol glycol were incubated in the presence of the rat liver 9000g supernatant fraction. In addition to 2, an isomeric ring-hydroxylated propranolol glycol, perhaps 7-hydroxypropranolol glycol, was formed when propranolol glycol was the substrate.

Published
1983

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