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650 results on '"Macdonald, Robert L."'

1. Learnings from curating a trustworthy, well-annotated, and useful dataset of disordered English speech

Author

Jiang, Pan-Pan, Tobin, Jimmy, Tomanek, Katrin, MacDonald, Robert L., Seaver, Katie, Cave, Richard, Ladewig, Marilyn, Heywood, Rus, and Green, Jordan R.

Subjects
Electrical Engineering and Systems Science - Audio and Speech Processing, Computer Science - Sound
Abstract

Project Euphonia, a Google initiative, is dedicated to improving automatic speech recognition (ASR) of disordered speech. A central objective of the project is to create a large, high-quality, and diverse speech corpus. This report describes the project's latest advancements in data collection and annotation methodologies, such as expanding speaker diversity in the database, adding human-reviewed transcript corrections and audio quality tags to 350K (of the 1.2M total) audio recordings, and amassing a comprehensive set of metadata (including more than 40 speech characteristic labels) for over 75\% of the speakers in the database. We report on the impact of transcript corrections on our machine-learning (ML) research, inter-rater variability of assessments of disordered speech patterns, and our rationale for gathering speech metadata. We also consider the limitations of using automated off-the-shelf annotation methods for assessing disordered speech., Comment: Interspeech 2024

Published
2024

2. Using Large Language Models to Accelerate Communication for Users with Severe Motor Impairments

Author

Cai, Shanqing, Venugopalan, Subhashini, Seaver, Katie, Xiao, Xiang, Tomanek, Katrin, Jalasutram, Sri, Morris, Meredith Ringel, Kane, Shaun, Narayanan, Ajit, MacDonald, Robert L., Kornman, Emily, Vance, Daniel, Casey, Blair, Gleason, Steve M., Nelson, Philip Q., and Brenner, Michael P.

Subjects
Computer Science - Human-Computer Interaction, Computer Science - Computation and Language
Abstract

Finding ways to accelerate text input for individuals with profound motor impairments has been a long-standing area of research. Closing the speed gap for augmentative and alternative communication (AAC) devices such as eye-tracking keyboards is important for improving the quality of life for such individuals. Recent advances in neural networks of natural language pose new opportunities for re-thinking strategies and user interfaces for enhanced text-entry for AAC users. In this paper, we present SpeakFaster, consisting of large language models (LLMs) and a co-designed user interface for text entry in a highly-abbreviated form, allowing saving 57% more motor actions than traditional predictive keyboards in offline simulation. A pilot study with 19 non-AAC participants typing on a mobile device by hand demonstrated gains in motor savings in line with the offline simulation, while introducing relatively small effects on overall typing speed. Lab and field testing on two eye-gaze typing users with amyotrophic lateral sclerosis (ALS) demonstrated text-entry rates 29-60% faster than traditional baselines, due to significant saving of expensive keystrokes achieved through phrase and word predictions from context-aware LLMs. These findings provide a strong foundation for further exploration of substantially-accelerated text communication for motor-impaired users and demonstrate a direction for applying LLMs to text-based user interfaces.

Published
2023

6. Alternatively Spliced Isoforms of TRIP8b Differentially Control h Channel Trafficking and Function

Author

Lewis, Alan S, Schwartz, Emily, Chan, C Savio, Noam, Yoav, Shin, Minyoung, Wadman, Wytse J, Surmeier, D James, Baram, Tallie Z, Macdonald, Robert L, and Chetkovich, Dane M

Subjects
Neurodegenerative, Brain Disorders, Neurosciences, Epilepsy, 1.1 Normal biological development and functioning, 2.1 Biological and endogenous factors, Aetiology, Underpinning research, Neurological, Alternative Splicing, Animals, Base Sequence, Brain, Cell Line, Cells, Cultured, Cyclic Nucleotide-Gated Cation Channels, Gene Knockdown Techniques, Hippocampus, Humans, Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels, Membrane Potentials, Membrane Proteins, Molecular Sequence Data, Neurons, Potassium Channels, Protein Isoforms, Rats, Rats, Sprague-Dawley, Medical and Health Sciences, Psychology and Cognitive Sciences, Neurology & Neurosurgery
Abstract

Hyperpolarization-activated cyclic nucleotide-gated (HCN) channels (h channels) are the molecular basis for the current, I(h), which contributes crucially to intrinsic neuronal excitability. The subcellular localization and biophysical properties of h channels govern their function, but the mechanisms controlling these characteristics, and especially the potential role of auxiliary subunits or other binding proteins, remain unclear. We focused on TRIP8b, an h channel-interacting protein that colocalizes with HCN1 in cortical and hippocampal pyramidal neuron dendrites, and found that it exists in multiple alternative splice variants with distinct effects on h channel trafficking and function. The developmentally regulated splice variants of TRIP8b all shared dual, C terminus-located interaction sites with HCN1. When coexpressed with HCN1 in heterologous cells individual TRIP8b isoforms similarly modulated gating of I(h), causing a hyperpolarizing shift in voltage dependence of channel activation, but differentially upregulated or downregulated I(h) current density and HCN1 surface expression. In hippocampal neurons, coexpression of TRIP8b isoforms with HCN1 produced isoform-specific changes of HCN1 localization. Interestingly, the TRIP8b isoforms most abundant in the brain are those predicted to enhance h channel surface expression. Indeed, shRNA knockdown of TRIP8b in hippocampal neurons significantly reduced native I(h). Thus, although TRIP8b exists in multiple splice isoforms, our data suggest that the predominant role of this protein in brain is to promote h channel surface expression and enhance I(h). Because I(h) expression is altered in models of several diseases, including temporal lobe epilepsy, TRIP8b may play a role in both normal neuronal function and in aberrant neuronal excitability associated with neurological disease.

Published
2009

8. Reduced Sodium Channel Density, Altered Voltage Dependence of Inactivation, and Increased Susceptibility to Seizures in Mice Lacking Sodium Channel β2-Subunits

Author

Chen, Chunling, Bharucha, Vandana, Chen, Yuan, Westenbroek, Ruth E., Brown, Angus, Malhotra, Jyoti Dhar, Jones, Dorothy, Avery, Christy, Gillespie, Patrick J., Kazen-Gillespie, Kristin A., Kazarinova-Noyes, Katie, Shrager, Peter, Saunders, Thomas L., Macdonald, Robert L., Ransom, Bruce R., Scheuer, Todd, Catterall, William A., and Isom, Lori L.

Published
2002

10. GABRG2 Variants Associated with Febrile Seizures

Author

Hernandez, Ciria C., primary, Shen, Yanwen, additional, Hu, Ningning, additional, Shen, Wangzhen, additional, Narayanan, Vinodh, additional, Ramsey, Keri, additional, He, Wen, additional, Zou, Liping, additional, and Macdonald, Robert L., additional

Published
2023
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13. Personalized structural biology reveals the molecular mechanisms underlying heterogeneous epileptic phenotypes caused by de novo KCNC2 variants

Author

Mukherjee, Souhrid, primary, Cassini, Thomas A., additional, Hu, Ningning, additional, Yang, Tao, additional, Li, Bian, additional, Shen, Wangzhen, additional, Moth, Christopher W., additional, Rinker, David C., additional, Sheehan, Jonathan H., additional, Cogan, Joy D., additional, Newman, John H., additional, Hamid, Rizwan, additional, Macdonald, Robert L., additional, Roden, Dan M., additional, Meiler, Jens, additional, Kuenze, Georg, additional, Phillips, John A., additional, and Capra, John A., additional

Published
2022
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17. De novo GABRG2 mutations associated with epileptic encephalopathies

Author

Shen, Dingding, Hernandez, Ciria C., Shen, Wangzhen, Hu, Ningning, Poduri, Annapurna, Shiedley, Beth, Rotenberg, Alex, Datta, Alexandre N., Leiz, Steffen, Patzer, Steffi, Boor, Rainer, Ramsey, Kerri, Goldberg, Ethan, Helbig, Ingo, Ortiz-Gonzalez, Xilma R., Lemke, Johannes R., Marsh, Eric D., and Macdonald, Robert L.

Published
2017
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18. Heterozygous GABAA receptor β3 subunit N110D knock‐in mice have epileptic spasms.

Author

Qu, Shimian, Jackson, Laurel G., Zhou, Chengwen, Shen, DingDing, Shen, Wangzhen, Nwosu, Gerald, Howe, Rachel, Catron, Mackenzie A., Flamm, Carson, Biven, Marshall, Kang, Jing‐Qiong, and Macdonald, Robert L.

Subjects
THALAMOCORTICAL system, SPASMS, LENNOX-Gastaut syndrome, INFANTILE spasms, EPILEPSY, PEOPLE with epilepsy, PYRAMIDAL neurons, SOMATOSENSORY cortex
Abstract

Objective: Infantile spasms is an epileptic encephalopathy of childhood, and its pathophysiology is largely unknown. We generated a heterozygous knock‐in mouse with the human infantile spasms‐associated de novo mutation GABRB3 (c.A328G, p.N110D) to investigate its molecular mechanisms and to establish the Gabrb3+/N110D knock‐in mouse as a model of infantile spasms syndrome. Methods: We used electroencephalography (EEG) and video monitoring to characterize seizure types, and a suite of behavioral tests to identify neurological and behavioral impairment in Gabrb3+/N110D knock‐in mice. Miniature inhibitory postsynaptic currents (mIPSCs) were recorded from layer V/VI pyramidal neurons in somatosensory cortex, and extracellular multi‐unit recordings from the ventral basal nucleus of the thalamus in a horizontal thalamocortical slice were used to assess spontaneous thalamocortical oscillations. Results: The infantile spasms–associated human de novo mutation GABRB3 (c.A328G, p.N110D) caused epileptic spasms early in development and multiple seizure types in adult Gabrb3+/N110D knock‐in mice. Signs of neurological impairment, anxiety, hyperactivity, social impairment, and deficits in spatial learning and memory were also observed. Gabrb3+/N110D mice had reduced cortical mIPSCs and increased duration of spontaneous oscillatory firing in the somatosensory thalamocortical circuit. Significance: The Gabrb3+/N110D knock‐in mouse has epileptic spasms, seizures, and other neurological impairments that are consistent with infantile spasms syndrome in patients. Multiple seizure types and abnormal behaviors indicative of neurological impairment both early and late in development suggest that Gabrb3+/N110D mice can be used to study the pathophysiology of infantile spasms. Reduced cortical inhibition and increased duration of thalamocortical oscillatory firing suggest perturbations in thalamocortical circuits. [ABSTRACT FROM AUTHOR]

Published
2023
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33. Automatic Speech Recognition of Disordered Speech: Personalized Models Outperforming Human Listeners on Short Phrases

Author

Green, Jordan R., primary, MacDonald, Robert L., additional, Jiang, Pan-Pan, additional, Cattiau, Julie, additional, Heywood, Rus, additional, Cave, Richard, additional, Seaver, Katie, additional, Ladewig, Marilyn A., additional, Tobin, Jimmy, additional, Brenner, Michael P., additional, Nelson, Philip C., additional, and Tomanek, Katrin, additional

Published
2021
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34. Disordered Speech Data Collection: Lessons Learned at 1 Million Utterances from Project Euphonia

Author

MacDonald, Robert L., primary, Jiang, Pan-Pan, additional, Cattiau, Julie, additional, Heywood, Rus, additional, Cave, Richard, additional, Seaver, Katie, additional, Ladewig, Marilyn A., additional, Tobin, Jimmy, additional, Brenner, Michael P., additional, Nelson, Philip C., additional, Green, Jordan R., additional, and Tomanek, Katrin, additional

Published
2021
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37. Hyperglycosylation and reduced GABA currents of mutated GABRB3 polypeptide in remitting childhood absence epilepsy

Author

Tanaka, MiyabI, Olsen, Richard W., Medina, Marco, Duron, Reyna M., Castro-Ortega, Ramon, Martinez-Juarez, Iris E., Pascual-Castroviejo, Machado-Salas, Jesus, Silva, Rene, Bailey, Julia N., Dongsheng Bai, Ochoa, Adriana, Jara-Prado, Aurelio, Pineda, Gregorio, Macdonald, Robert L, and Delgado-Escueta, Antonio V.

Subjects
Gene mutations -- Research, Epilepsy in children -- Research, Biological sciences
Abstract

A study was conducted to screen mutations in the [GABA.sub.A] receptor (GABAR) [beta]3 subunit gene (GABRB3) in 48 probands and families with remitting childhood absence epilepsy (CAE). The functional analysis of human GABAR transiently expressed in HEK293T cells with the use of rapid agonist application showed that each amino acid transversion in the [beta]3-v2 subunit (P11S, S15F, G32R) reduced GABA-evoked current density from whole cells.

Published
2008

38. ER stress increased inflammatory cytokines in an epilepsy mouse model Gabrg2(+/Q390X) knockin: a link between genetic and acquired epilepsy?

Author

Shen, Wangzhen, Poliquin, Sarah, Macdonald, Robert L., Dong, Marco, and Kang, Jing-Qiong

Subjects
Cerebral Cortex, Male, Mice, Knockout, Epilepsy, Endoplasmic Reticulum Stress, Receptors, GABA-A, Article, Mice, Inbred C57BL, Disease Models, Animal, Mice, Animals, Cytokines, Female, Inflammation Mediators, Cells, Cultured
Abstract

OBJECTIVE: Neuroinflammation is a major theme for epilepsy, which has been characterized in acquired epilepsy but is poorly understood in genetic epilepsy. GABA(A) receptor subunit gene mutations are significant causes of epilepsy, and we have studied the pathophysiology directly resulting from defective receptor channels. Here we determined the proinflammatory factors in a genetic mouse model, the Gabrg2(+/Q390X) knockin (KI). We have identified increased cytokines in multiple brain regions of the KI mouse throughout different developmental stages and propose that accumulation of the trafficking deficient mutant protein may increase neuroinflammation, which would be a novel mechanism for genetic epilepsy. METHODS: We used enzyme-linked immunosorbent assay (ELISA), immunoprecipitation, nuclei purification, immunoblot, immunohistochemistry, and confocal microscopy to characterize increased neuroinflammation and its potential causes in a Gabrg2(+/Q390X) knockin mouse and a Gabrg2(+/−) knockout (KO) mouse, each associated with a different epilepsy syndrome with different severities. RESULTS: We found that proinflammatory cytokines such as tumor necrosis factor alpha (TNF), interleukin 1-beta (IL-1β) and IL-6 were increased in the KI mice but not in the KO mice. A major underlying basis for the discrepancy in cytokine expression between the two mouse models is likely due to chronic mutant protein accumulation and endoplasmic reticulum (ER) stress. The presence of mutant protein dampened cytokine induction upon further cellular stimulation or external stress such as elevated temperature. Pharmacological induction of ER stress upregulated cytokine expression in the wildtype and KO but not in the KI mice. The increased cytokine expression was independent of seizure occurrence since it was upregulated in both mice and cultured neurons. SIGNIFICANCE: Together, these data demonstrate a novel pathophysiology for genetic epilepsy, increased neuroinflammation which is common mechanism for acquired epilepsy. The findings thus provide the first link of neuroinflammation between genetic epilepsy associated with an ion channel gene mutation and acquired epilepsy.

Published
2020

39. The GAB[A.sub.A] receptor [alpha]1 subunit epilepsy mutation A322D inhibits transmembrane helix formation and causes proteasomal degradation

Author

Gallagher, Martin J., Ding, Li, Maheshwari, Ankit, and Macdonald, Robert L.

Subjects
Epilepsy -- Genetic aspects, Endoplasmic reticulum -- Chemical properties, Ubiquitin-proteasome system -- Evaluation, Gene mutations -- Evaluation, GABA -- Receptors, GABA -- Genetic aspects, Science and technology
Abstract

A form of autosomal dominant juvenile myoclonic epilepsy is caused by a nonconservative missense mutation, A322D, in the GABA[A.sub.A] receptor [alpha]1 subunit M3 transmembrane helix. We reported previously that the A322D mutation reduced total and surface [alpha]1(A322D) subunit protein and that residual [alpha]1(A322D) subunit resided in the endoplasmic reticulum. Here, we demonstrate that the reduction in [alpha]1(A322D) expression results from rapid endoplasmic reticulum-associated degradation of the [alpha]1(A322D) subunit through the ubiquitin-proteasome system. We provide direct evidence that the [alpha]1(A322D) subunit misfolds and show that in at least 33% of [alpha]1(A322D) subunits, M3 failed to insert into the lipid bilayer. We constructed a series of mutations in the M3 domain and empirically determined the apparent free energy cost ([DELTA][G.Sub.app]) of membrane insertion failure, and we show that the [DELTA][G.sub.app] correlated directly with the recently elucidated transmembrane sequence code ([DELTA][G.sub.Lep]). These data provide a biochemical mechanism for the pathogenesis of this epilepsy mutation and demonstrate that [DELTA][G.sub.Lep] predicts the efficiency of lipid partitioning of a naturally occurring protein's transmembrane domain expressed in vivo. Finally, we calculated the [DELTA][DELTA][G.sub.Lep] for 277 known transmembrane missense mutations associated with Charcot--Marie--Tooth disease, diabetes insipidus, retinitis pigmentosa, cystic fibrosis, and severe myoclonic epilepsy of infancy and showed that the majority of these mutations also are likely to destabilize transmembrane domain membrane insertion, but that only a minority of the mutations would be predicted to be as destabilizing as the A322D mutation. ion channel | peripheral myelin protein | protein folding | sodium channel | translocon

Published
2007

43. Epilepsies

Author

Abou-Khalil, Bassel W., primary, Gallagher, Martin J., additional, and Macdonald, Robert L., additional

Published
2012
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44. Contributors

Author

Abou-Khalil, Bassel W., primary, Adamczyk, Peter, additional, Ajtai, Bela, additional, Allen, Jeffrey C., additional, Amato, Anthony A., additional, Aminoff, Michael J., additional, Apostolova, Liana G., additional, Avidan, Alon Y., additional, Baehring, Joachim M., additional, Balcer, Laura J., additional, Baloh, Robert W., additional, Barkhoudarian, Garni, additional, Bartleson, J.D., additional, Batchelor, Tracy T., additional, Beckham, J. David, additional, Beglinger, Leigh, additional, Berger, Joseph R., additional, Bergsneider, Marvin, additional, Bethoux, Francois, additional, Biller, José, additional, Black, David F., additional, Boes, Christopher J., additional, Boulis, Nicholas, additional, Bramlett, Helen M., additional, Brooke, Michael H., additional, Bruni, Joseph, additional, Burnette, W. Bryan, additional, Buttner, Edgar A., additional, Capobianco, David J., additional, Carson, Alan, additional, Cavaliere, Robert, additional, Chad, David A., additional, Chelimsky, Gisela, additional, Chelimsky, Thomas, additional, Cheshire, William P., additional, Chitnis, Tanuja, additional, Chokroverty, Sudhansu, additional, Cooper, Paul E., additional, Cummings, Jeffrey L., additional, Cutrer, F. Michael, additional, Dalmau, Josep, additional, Daroff, Robert B., additional, DasGupta, Ranan, additional, DeKosky, Steven T., additional, Dietrich, W. Dalton, additional, Dobkin, Bruce H., additional, Doty, Richard L., additional, Duckwiler, Gary, additional, Dusick, Joshua R., additional, Emerson, Ronald G., additional, Fenichel, Gerald M., additional, Fessler, Richard G., additional, Flores-Sarnat, Laura, additional, Fogel, Brent L., additional, Fowler, Clare J., additional, Fugate, Jennifer E., additional, Gallager, Martin J., additional, Gardner, Sharon L., additional, Garza, Ivan, additional, Gehl, Carissa, additional, Geldmacher, David S., additional, Geschwind, Daniel H., additional, Geschwind, Michael D., additional, Golomb, Meredith R., additional, Gonzalez, Nestor, additional, Hallett, Mark, additional, Hamati, Aline I., additional, Havton, Leif A., additional, Heffner, Reid R., additional, Hill, Alan, additional, Hochberg, Fred H., additional, Houtchens, Maria K., additional, Islam, Monica P., additional, Jankovic, Joseph, additional, Jansen, Michael, additional, Josephson, S. Andrew, additional, Karajannis, Matthias A., additional, Kase, Carlos S., additional, Katirji, Bashar, additional, Kerber, Kevin A., additional, Kerchner, Geoffrey A., additional, Khoury, Samia J., additional, Kirshner, Howard S., additional, Koontz, Daniel, additional, Koshy, Anita, additional, Kremen, Sarah A., additional, Kula, Roger W., additional, Kumar, Abhay, additional, Kurtzke, John F., additional, Lang, Anthony E., additional, Lavin, Patrick J.M., additional, Liebeskind, David S., additional, Lindzen, Eric, additional, Lockwood, Alan H., additional, Louis, David N., additional, Love, Betsy B., additional, Lublin, Fred D., additional, Macdonald, Robert L., additional, Mack, William, additional, Martin, Neil, additional, Masdeu, Joseph C., additional, Mazziotta, John C., additional, Mendez, Mario F., additional, Meriggioli, Matthew N., additional, Meyer, Philipp T., additional, Michaud, Dominique S., additional, Miller, Aaron E., additional, Misulis, Karl E., additional, Mitsumoto, Hiroshi, additional, Murray, Brian, additional, Murray, Evan D., additional, Nass, Ruth, additional, Nutt, John G., additional, Nuwer, Marc R., additional, Okun, Michael S., additional, O’Rourke, Justin J.F., additional, Pandey, Ajay K., additional, Panicker, Jalesh N., additional, Pastores, Gregory M., additional, Paulsen, Jane S., additional, Pedley, Timothy A., additional, Perry, Arie, additional, Pestronk, Alan, additional, Pfeiffer, Ronald F., additional, Prasad, Sashank, additional, Preston, David C., additional, Price, Bruce H., additional, Ptáček, Louis J., additional, Rabinstein, Alejandro A., additional, Reimschisel, Tyler, additional, Remler, Bernd F., additional, Rijntjes, Michel, additional, Roach, E. Steve, additional, Robertson, David, additional, Rogers, Lisa R., additional, Ronthal, Michael, additional, Roos, Karen, additional, Rosenbaum, Richard B., additional, Rosenberg, Gary A., additional, Rosenfeld, Myrna R., additional, Ross, Gail, additional, Rucker, Janet C., additional, Sanders, Donald B., additional, Sarnat, Harvey B., additional, Savani, Aman, additional, Schapira, Anthony H.V., additional, Schiff, David, additional, Schmidley, James W., additional, Schneck, Michael J., additional, Shaner, D. Malcolm, additional, Shapiro, Barbara E., additional, Shih, Patrick, additional, Simon, Roger P., additional, So, Yuen T., additional, Sohn, Young H., additional, Solbrig, Marylou V., additional, Stippler, Martina, additional, Stoessl, A. Jon, additional, Stone, Jon, additional, Subramony, S.H., additional, Swanson, Jerry W., additional, Tateshima, Satoshi, additional, Thompson, Philip D., additional, Thurtell, Matthew J., additional, Tomsak, Robert L., additional, Tsai, Po-Heng, additional, Tsao, Bryan, additional, Turner, Chris, additional, Tyler, Kenneth L., additional, Vargas, Bert B., additional, Verma, Ashok, additional, Vinuela, Fernando, additional, Wall, Michael, additional, Wallin, Mitchell T., additional, Wang, Leo H., additional, Weiller, Cornelius, additional, Wen, Patrick, additional, Wijdicks, Eelco F.M., additional, Xia, Guangbin, additional, Zenteno, Marco, additional, Zhou, Jiachen, additional, and Zhou, YiLi, additional

Published
2012
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48. List of Contributors

Author

Adragna, Norma C., primary, Akaike, Norio, additional, Alvarez-Leefmans, Francisco Javier, additional, Augustine, George J., additional, Berglund, Ken, additional, Botzolakis, Emmanuel J., additional, Britton, Fiona C., additional, Brown, Peter D., additional, Chang, Min-Hwang, additional, Davies, Sarah L., additional, De Koninck, Yves, additional, Delpire, Eric, additional, Di Fulvio, Mauricio, additional, Dutta, Amal K., additional, Clive Ellory, J., additional, Frings, Stephan, additional, Gagnon, Kenneth, additional, Gamba, Gerardo, additional, Garbarini, Nicole, additional, Gibson, John S., additional, Hamann, Steffen, additional, Criss Hartzell, H., additional, Inoue, Hana, additional, Jentsch, Thomas J., additional, Kahle, Kristopher T., additional, Kenyon, James L., additional, Kintner, Douglas B., additional, Kuner, Thomas, additional, Lauf, Peter K., additional, Leblanc, Normand, additional, MacAulay, Nanna, additional, Macdonald, Robert L., additional, Marcus, Daniel C., additional, Millar, Ian D., additional, Mount, David, additional, Novarino, Gaia, additional, O’Donnell, Martha, additional, Okada, Yasunobu, additional, Payne, John A., additional, Pond, Brooks B., additional, Romero, Michael F., additional, Russell, John M., additional, Sabirov, Ravshan Z., additional, Sato, Kaori, additional, Sontheimer, Harald, additional, Staley, Kevin J., additional, Stauber, Tobias, additional, Sun, Dandan, additional, Suzuki, Makoto, additional, Toychiev, Abduqodir H., additional, Vardi, Noga, additional, Verkman, Alan S., additional, Wangemann, Philine, additional, Zeuthen, Thomas, additional, and Zhang, Ling-Li, additional

Published
2010
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