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Your search keyword '"Bateman, R.J."' showing total 17 results
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17 results on '"Bateman, R.J."'

1. Dominantly Inherited Alzheimer Network Trials Unit (DIAN-TU): Trial Satisfaction and Attitudes towards Future Clinical Trials

Author

Liu, H., primary, Li, J., additional, Ziegemeier, E., additional, Adams, S., additional, McDade, E., additional, Clifford, D.B., additional, Cao, Y., additional, Wang, G., additional, Li, Y., additional, Mills, S.L., additional, Santacruz, A.M., additional, Belyew, S., additional, Grill, J.D., additional, Snider, B.J., additional, Mummery, C.J., additional, Surti, G., additional, Hannequin, D., additional, Wallon, D., additional, Berman, S.B., additional, Jimenez-Velazquez, I.Z., additional, Roberson, E.D., additional, van Dyck, C.H., additional, Honig, L.S., additional, Sanchez-Valle, R., additional, Brooks, W.S., additional, Gauthier, S., additional, Galasko, D., additional, Masters, C.L., additional, Brosch, J., additional, Hsiung, G.-Y.R., additional, Jayadev, S., additional, Formaglio, M., additional, Masellis, M., additional, Clarnette, R., additional, Pariente, J., additional, Dubois, B., additional, Pasquier, F., additional, Bateman, R.J., additional, and Llibre-Guerra, J.J., additional

Published
2024
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2. Preclinical trials in autosomal dominant AD: Implementation of the DIAN-TU trial

Author

Mills, S.M., Mallmann, J., Santacruz, A.M., Fuqua, A., Carril, M., Aisen, P.S., Althage, M.C., Belyew, S., Benzinger, T.L., Brooks, W.S., Buckles, V.D., Cairns, N.J., Clifford, D., Danek, A., Fagan, A.M., Farlow, M., Fox, N., Ghetti, B., Goate, A.M., Heinrichs, D., Hornbeck, R., Jack, C., Jucker, M., Klunk, W.E., Marcus, D.S., Martins, R.N., Masters, C.M., Mayeux, R., McDade, E., Morris, J.C., Oliver, A., Ringman, J.M., Rossor, M.N., Salloway, S., Schofield, P.R., Snider, J., Snyder, P., Sperling, R.A., Stewart, C., Thomas, R.G., Xiong, C., and Bateman, R.J.

Published
2013
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3. Progressive White Matter Injury in Preclinical Dutch Cerebral Amyloid Angiopathy

Author

Shirzadi, Z., Yau, W.Y.W., Schultz, S.A., Schultz, A.P., Scott, M.R., Goubran, M., Mojiri-Forooshani, P., Joseph-Mathurin, N., Kantarci, K., Preboske, G., Wermer, M.J.H., Jack, C., Benzinger, T., Taddei, K., Sohrabi, H.R., Sperling, R.A., Johnson, K.A., Bateman, R.J., Martins, R.N., Greenberg, S.M., Chhatwal, J.P., and DIAN Investigators

Subjects
Cerebral Amyloid Angiopathy, Cross-Sectional Studies, Neurology, Humans, Hemorrhage, Neuroimaging, Neurology (clinical), Magnetic Resonance Imaging, White Matter, Cerebral Hemorrhage
Abstract

Autosomal-dominant, Dutch-type cerebral amyloid angiopathy (D-CAA) offers a unique opportunity to develop biomarkers for pre-symptomatic cerebral amyloid angiopathy (CAA). We hypothesized that neuroimaging measures of white matter injury would be present and progressive in D-CAA prior to hemorrhagic lesions or symptomatic hemorrhage. In a longitudinal cohort of D-CAA carriers and non-carriers, we observed divergence of white matter injury measures between D-CAA carriers and non-carriers prior to the appearance of cerebral microbleeds and14 years before the average age of first symptomatic hemorrhage. These results indicate that white matter disruption measures may be valuable cross-sectional and longitudinal biomarkers of D-CAA progression. ANN NEUROL 2022;92:358-363.

Published
2022

5. Blood Biomarkers from Research Use to Clinical Practice: What Must Be Done? A Report from the EU/US CTAD Task Force

Author

Angioni, D., primary, Delrieu, J., additional, Hansson, O., additional, Fillit, H., additional, Aisen, P., additional, Cummings, J., additional, Sims, J.R., additional, Braunstein, J.B., additional, Sabbagh, M., additional, Bittner, T., additional, Pontecorvo, M., additional, Bozeat, S., additional, Dage, J.L., additional, Largent, E., additional, Mattke, S., additional, Correa, O., additional, Gutierrez Robledo, L.M., additional, Baldivieso, V., additional, Willis, D.R., additional, Atri, A., additional, Bateman, R.J., additional, Ousset, P-J., additional, Vellas, B., additional, and Weiner, M., additional

Published
2022
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10. [Accepted Manuscript] Presymptomatic atrophy in autosomal dominant Alzheimer's disease: A serial MRI study

Author

Kinnunen, K.M., Cash, D.M., Poole, T., Frost, C., Benzinger, T.L.S., Ahsan, R.L., Leung, K.K., Cardoso, M.J., Modat, M., Malone, I.B., Morris, J.C., Bateman, R.J., Marcus, D.S., Goate, A., Salloway, S., Correia, S., Sperling, R.A., Chhatwal, J.P., Mayeux, R., Brickman, A.M., Martins, R.N., Farlow, M.R., Ghetti, B., Saykin, A.J., Jack, C.R. Jr, Schofield, P.R., McDade, E., Weiner, M.W., Ringman, J.M., Thompson, P.M., Masters, C.L., Rowe, C.C., Rossor, M.N., Ourselin, S., Fox, N.C., and Dominantly Inherited Alzheimer Network (DIAN), .

Subjects
sense organs, skin and connective tissue diseases
Abstract

Identifying at what point atrophy rates first change in Alzheimer's disease is important for informing design of presymptomatic trials. Serial T1-weighed magnetic resonance imaging scans of 94 participants (28 noncarriers, 66 carriers) from the Dominantly Inherited Alzheimer Network were used to measure brain, ventricular, and hippocampal atrophy rates. For each structure, nonlinear mixed-effects models estimated the change-points when atrophy rates deviate from normal and the rates of change before and after this point. Atrophy increased after the change-point, which occurred 1-1.5 years (assuming a single step change in atrophy rate) or 3-8 years (assuming gradual acceleration of atrophy) before expected symptom onset. At expected symptom onset, estimated atrophy rates were at least 3.6 times than those before the change-point. Atrophy rates are pathologically increased up to seven years before "expected onset". During this period, atrophy rates may be useful for inclusion and tracking of disease progression.

Published
2017

11. RFID enabled manufacturing: fundamentals, methodology and applications

Author

Lu, B.H., Bateman, R.J., and Cheng, K.

Subjects
Radio frequency identification (RFID) -- Usage, Manufacturing processes -- Case studies, Radio frequency identification, Manufacturing, Business
Abstract

Byline: B.H. Lu, R.J. Bateman, K. Cheng Manufacturing enterprises and their associated production activities are becoming increasingly information intensive but the information systems used often rely on data which is assumed rather than actual. RFID (Radio Frequency Identification) enabled manufacturing can bridge this gap between the physical flow of materials and the associated information flow. In this paper the fundamental issues, methodologies, applications and potential of RFID enabled manufacturing are reviewed, a simulated RFID machining process application case study is outlined, and finally a proposed methodology, framework and five-step deployment process aimed at developing a holistic approach to implementing RFID enabled manufacturing in manufacturing enterprises is detailed.

Published
2006

13. Erratum to “Preclinical trials in autosomal dominant AD: Implementation of the DIAN-TU trial” [Rev. Neurol. 169 (10) (2013) 737–743]

Author

Mills, S.M., primary, Mallmann, J., additional, Santacruz, A.M., additional, Fuqua, A., additional, Carril, M., additional, Aisen, P.S., additional, Althage, M.C., additional, Belyew, S., additional, Benzinger, T.L., additional, Brooks, W.S., additional, Buckles, V.D., additional, Cairns, N.J., additional, Clifford, D., additional, Danek, A., additional, Fagan, A.M., additional, Farlow, M., additional, Fox, N., additional, Ghetti, B., additional, Goate, A.M., additional, Heinrichs, D., additional, Hornbeck, R., additional, Jack, C., additional, Jucker, M., additional, Klunk, W.E., additional, Marcus, D.S., additional, Martins, R.N., additional, Masters, C.M., additional, Mayeux, R., additional, McDade, E., additional, Morris, J.C., additional, Oliver, A., additional, Ringman, J.M., additional, Rossor, M.N., additional, Salloway, S., additional, Schofield, P.R., additional, Snider, J., additional, Snyder, P., additional, Sperling, R.A., additional, Stewart, C., additional, Thomas, R.G., additional, Xiong, C., additional, and Bateman, R.J., additional

Published
2013
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17. α1-adrenergic receptors facilitate inhibitory neurotransmission to cardiac vagal neurons in the nucleus ambiguus

Author

Boychuk, C.R., Bateman, R.J., Philbin, K.E., and Mendelowitz, D.

Subjects
*ADRENERGIC receptors, *NEURAL transmission, *CELL nuclei, *PARASYMPATHETIC nervous system, *BRAIN stem, *NORADRENALINE, *TETRODOTOXIN, *EYE movements
Abstract

Abstract: The cholinergic cardiac vagal neurons (CVNs), located in the nucleus ambiguus, are the origin of cardioinhibitory parasympathetic activity. Catecholaminergic neurons in nearby regions of the brainstem, including the C1 and C2 cell groups, are thought to play a key role in both arousing from sleep and maintaining wakefulness. Because norepinephrine (NE) could play an important role in influencing the activity of CVNs, particularly in response to sleeping/waking and arousal states, the present study investigated the contribution of α1-adrenergic receptor activation to augment inhibitory and/or blunt excitatory neurotransmission to CVNs. To test the effects of α1-adrenergic receptor activation, CVNs were labeled in rats by retrograde tracing and synaptic events were recorded by whole cell voltage clamp techniques in vitro. Prazosin, an inverse agonist of α1-adrenergic receptor, significantly decreased the frequency of both GABAergic and glycinergic neurotransmission to CVNs. Activation of α1-adrenergic receptors by the α1-adrenergic receptor agonists NE or phenylephrine (PE) both significantly increased GABAergic and glycinergic inhibitory event frequency. This effect was prevented by the sodium channel blocker tetrodotoxin (TTX). Activation of α1-adrenergic receptors did not alter glutamatergic neurotransmission to CVNs. This study indicates that α1-adrenergic receptor activation in the brainstem can facilitate inhibitory GABAergic and glycinergic neurotransmission so as to reduce CVN activity; this synaptic modulation may play a role in the tachycardia seen during NE-dependent behavioral arousal. [Copyright &y& Elsevier]

Published
2011
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