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1,413 results on '"Nelson, David L."'

1. Characterization and visualization of tandem repeats at genome scale

Author

Dolzhenko, Egor, English, Adam, Dashnow, Harriet, De Sena Brandine, Guilherme, Mokveld, Tom, Rowell, William J., Karniski, Caitlin, Kronenberg, Zev, Danzi, Matt C., Cheung, Warren A., Bi, Chengpeng, Farrow, Emily, Wenger, Aaron, Chua, Khi Pin, Martínez-Cerdeño, Verónica, Bartley, Trevor D., Jin, Peng, Nelson, David L., Zuchner, Stephan, Pastinen, Tomi, Quinlan, Aaron R., Sedlazeck, Fritz J., and Eberle, Michael A.

Published
2024
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3. Intercepting IRE1 kinase‐FMRP signaling prevents atherosclerosis progression

Author

Yildirim, Zehra, Baboo, Sabyasachi, Hamid, Syed M, Dogan, Asli E, Tufanli, Ozlem, Robichaud, Sabrina, Emerton, Christina, Diedrich, Jolene K, Vatandaslar, Hasan, Nikolos, Fotis, Gu, Yanghong, Iwawaki, Takao, Tarling, Elizabeth, Ouimet, Mireille, Nelson, David L, Yates, John R, Walter, Peter, and Erbay, Ebru

Subjects
Biochemistry and Cell Biology, Biological Sciences, Cardiovascular, Intellectual and Developmental Disabilities (IDD), Brain Disorders, Rare Diseases, Atherosclerosis, Fragile X Syndrome, 2.1 Biological and endogenous factors, Animals, Endoplasmic Reticulum Stress, Endoribonucleases, Fragile X Mental Retardation Protein, Membrane Proteins, Mice, Protein Serine-Threonine Kinases, Signal Transduction, atherosclerosis, cholesterol homeostasis, efferocytosis, ER stress, translational regulation, Medical and Health Sciences, Biochemistry and cell biology
Abstract

Fragile X Mental Retardation protein (FMRP), widely known for its role in hereditary intellectual disability, is an RNA-binding protein (RBP) that controls translation of select mRNAs. We discovered that endoplasmic reticulum (ER) stress induces phosphorylation of FMRP on a site that is known to enhance translation inhibition of FMRP-bound mRNAs. We show ER stress-induced activation of Inositol requiring enzyme-1 (IRE1), an ER-resident stress-sensing kinase/endoribonuclease, leads to FMRP phosphorylation and to suppression of macrophage cholesterol efflux and apoptotic cell clearance (efferocytosis). Conversely, FMRP deficiency and pharmacological inhibition of IRE1 kinase activity enhances cholesterol efflux and efferocytosis, reducing atherosclerosis in mice. Our results provide mechanistic insights into how ER stress-induced IRE1 kinase activity contributes to macrophage cholesterol homeostasis and suggests IRE1 inhibition as a promising new way to counteract atherosclerosis.

Published
2022

4. Functional consequences of postnatal interventions in a mouse model of Fragile X syndrome

Author

Rais, Maham, Lovelace, Jonathan W, Shuai, Xinghao S, Woodard, Walker, Bishay, Steven, Estrada, Leo, Sharma, Ashwin R, Nguy, Austin, Kulinich, Anna, Pirbhoy, Patricia S, Palacios, Arnold R, Nelson, David L, Razak, Khaleel A, and Ethell, Iryna M

Subjects
Biomedical and Clinical Sciences, Neurosciences, Brain Disorders, Pediatric, Fragile X Syndrome, Genetics, Mental Health, Intellectual and Developmental Disabilities (IDD), Rare Diseases, Autism, Behavioral and Social Science, Basic Behavioral and Social Science, 2.1 Biological and endogenous factors, Neurological, Animals, Disease Models, Animal, Fragile X Mental Retardation Protein, Mice, Mice, Knockout, Neurons, Cortical deficits, Neurodevelopmental disorders, Parvalbumin inhibitory interneurons, Sensory processing disorders, Clinical Sciences, Neurology & Neurosurgery, Biochemistry and cell biology
Abstract

BackgroundFragile X syndrome (FXS) is a leading genetic cause of autism and intellectual disability with cortical hyperexcitability and sensory hypersensitivity attributed to loss and hypofunction of inhibitory parvalbumin-expressing (PV) cells. Our studies provide novel insights into the role of excitatory neurons in abnormal development of PV cells during a postnatal period of inhibitory circuit refinement.MethodsTo achieve Fragile X mental retardation gene (Fmr1) deletion and re-expression in excitatory neurons during the postnatal day (P)14-P21 period, we generated CreCaMKIIa/Fmr1Flox/y (cOFF) and CreCaMKIIa/Fmr1FloxNeo/y (cON) mice, respectively. Cortical phenotypes were evaluated in adult mice using biochemical, cellular, clinically relevant electroencephalogram (EEG) and behavioral tests.ResultsWe found that similar to global Fmr1 KO mice, the density of PV-expressing cells, their activation, and sound-evoked gamma synchronization were impaired in cOFF mice, but the phenotypes were improved in cON mice. cOFF mice also showed enhanced cortical gelatinase activity and baseline EEG gamma power, which were reduced in cON mice. In addition, TrkB phosphorylation and PV levels were lower in cOFF mice, which also showed increased locomotor activity and anxiety-like behaviors. Remarkably, when FMRP levels were restored in only excitatory neurons during the P14-P21 period, TrkB phosphorylation and mouse behaviors were also improved.ConclusionsThese results indicate that postnatal deletion or re-expression of FMRP in excitatory neurons is sufficient to elicit or ameliorate structural and functional cortical deficits, and abnormal behaviors in mice, informing future studies about appropriate treatment windows and providing fundamental insights into the cellular mechanisms of cortical circuit dysfunction in FXS.

Published
2022

5. Deletion of Fmr1 from Forebrain Excitatory Neurons Triggers Abnormal Cellular, EEG, and Behavioral Phenotypes in the Auditory Cortex of a Mouse Model of Fragile X Syndrome

Author

Lovelace, Jonathan W, Rais, Maham, Palacios, Arnold R, Shuai, Xinghao S, Bishay, Steven, Popa, Otilia, Pirbhoy, Patricia S, Binder, Devin K, Nelson, David L, Ethell, Iryna M, and Razak, Khaleel A

Subjects
Basic Behavioral and Social Science, Neurosciences, Rare Diseases, Intellectual and Developmental Disabilities (IDD), Mental Health, Behavioral and Social Science, Genetics, Pediatric, Fragile X Syndrome, Autism, Brain Disorders, Underpinning research, 1.1 Normal biological development and functioning, Aetiology, 2.1 Biological and endogenous factors, Mental health, Neurological, Acoustic Stimulation, Animals, Auditory Cortex, Behavior, Animal, Disease Models, Animal, Electroencephalography, Female, Fragile X Mental Retardation Protein, Gamma Rhythm, Male, Matrix Metalloproteinase 9, Mice, Inbred C57BL, Mice, Knockout, Neurons, Phenotype, Prosencephalon, Signal Transduction, autism, cortical deficits, fragile X syndrome, perineuronal nets, sensory processing disorders, Psychology, Cognitive Sciences, Experimental Psychology
Abstract

Fragile X syndrome (FXS) is a leading genetic cause of autism with symptoms that include sensory processing deficits. In both humans with FXS and a mouse model [Fmr1 knockout (KO) mouse], electroencephalographic (EEG) recordings show enhanced resting state gamma power and reduced sound-evoked gamma synchrony. We previously showed that elevated levels of matrix metalloproteinase-9 (MMP-9) may contribute to these phenotypes by affecting perineuronal nets (PNNs) around parvalbumin (PV) interneurons in the auditory cortex of Fmr1 KO mice. However, how different cell types within local cortical circuits contribute to these deficits is not known. Here, we examined whether Fmr1 deletion in forebrain excitatory neurons affects neural oscillations, MMP-9 activity, and PV/PNN expression in the auditory cortex. We found that cortical MMP-9 gelatinase activity, mTOR/Akt phosphorylation, and resting EEG gamma power were enhanced in CreNex1/Fmr1Flox/y conditional KO (cKO) mice, whereas the density of PV/PNN cells was reduced. The CreNex1/Fmr1Flox/y cKO mice also show increased locomotor activity, but not the anxiety-like behaviors. These results indicate that fragile X mental retardation protein changes in excitatory neurons in the cortex are sufficient to elicit cellular, electrophysiological, and behavioral phenotypes in Fmr1 KO mice. More broadly, these results indicate that local cortical circuit abnormalities contribute to sensory processing deficits in autism spectrum disorders.

Published
2020

8. Intellectual and developmental disabilities research centers: Fifty years of scientific accomplishments

Author

Walkley, Steven U, Abbeduto, Leonard, Batshaw, Mark L, Bhattacharyya, Anita, Bookheimer, Susan Y, Christian, Bradley T, Constantino, John N, de Vellis, Jean, Doherty, Daniel A, Nelson, David L, Piven, Joseph, Poduri, Annapurna, Pomeroy, Scott L, Samaco, Rodney C, Zoghbi, Huda Y, Guralnick, Michael J, Bookheimer, Susan, Chang, Qiang, Colombo, John, Gallo, Vittorio, Mahone, E Mark, Neul, Jeffrey, Robinson, Michael B, and Smith, Peter G

Subjects
Brain Disorders, Mental Health, Clinical Research, Neurosciences, Pediatric, Prevention, Intellectual and Developmental Disabilities (IDD), Academies and Institutes, Developmental Disabilities, History, 20th Century, History, 21st Century, Humans, Intellectual Disability, National Institute of Child Health and Human Development (U.S.), United States, Intellectual and Developmental Disabilities Research Centers Directors Committee, Clinical Sciences, Neurology & Neurosurgery
Abstract

Progress in addressing the origins of intellectual and developmental disabilities accelerated with the establishment 50 years ago of the Eunice Kennedy Shriver National Institute of Child Health and Human Development of the National Institutes of Health and associated Intellectual and Developmental Disabilities Research Centers. Investigators at these Centers have made seminal contributions to understanding human brain and behavioral development and defining mechanisms and treatments of disorders of the developing brain. ANN NEUROL 2019;86:332-343.

Published
2019

10. TPT sulfonate, a single, oral dose schistosomicidal prodrug: In vivo efficacy, disposition and metabolic profiling.

Author

Wolfe, Alan R, Neitz, R Jeffrey, Burlingame, Mark, Suzuki, Brian M, Lim, KC, Scheideler, Mark, Nelson, David L, Benet, Leslie Z, and Caffrey, Conor R

Subjects
Liver, Animals, Mice, Schistosoma haematobium, Schistosoma mansoni, Schistosomiasis mansoni, Disease Models, Animal, Arylsulfonates, Praziquantel, Prodrugs, Schistosomicides, Administration, Oral, Female, Male, Metabolomics, Drug Discovery, Alkylaminoalkanethiosulfuric acid, Anthelmintic, Drug disposition, Drug metabolism, Schistosoma, Schistosomiasis, Disease Models, Animal, Administration, Oral, Medical Microbiology
Abstract

Treatment of schistosomiasis relies precariously on just one drug, praziquantel (PZQ). In the search for alternatives, 15 S-[2-(alkylamino)alkane] thiosulfuric acids were obtained from a previous research program and profiled in mice for efficacy against both mature (>42-day-old) and juvenile (21-day-old) Schistosoma mansoni using a screening dose of 100 mg/kg PO QDx4. One compound, S-[2-(tert-butylamino)-1-phenylethane] thiosulfuric acid (TPT sulfonate), was the most effective by decreasing female and male worm burdens by ≥ 90% and ≥46% (mature), and ≥89% and ≥79% (juvenile), respectively. In contrast, PZQ decreased mature female and male worm burdens by 95% and 94%, respectively, but was ineffective against juvenile stages. Against 7-day-old lung-stage worms, TPT sulfonate was only effective at twice the dose decreasing female and male burdens by 95 and 80%, respectively. Single oral doses at 400 and/or 600 mg/kg across various developmental time-points (1-, 7-, 15-, 21- and/or 42 day-old) were consistent with the QD x4 data; efficacy was strongest once the parasites had completed lung migration, and female and male burdens were decreased by at least 90% and 80%, respectively. In vitro, TPT sulfonate is inactive against the parasite suggesting a pro-drug mechanism of action. In mice, TPT sulfonate is fully absorbed and subject to rapid, non-CYP-mediated, first-pass metabolism that is initiated by desulfation and yields a series of metabolites. The initially-formed free thiol-containing metabolite, termed TP thiol, was chemically synthesized; it dose-dependently decreased S. mansoni and Schistosoma haematobium motility in vitro. Also, when administered as a single 50 mg/kg IP dose, TP thiol decreased 33-day-old S. mansoni female and male burdens by 35% and 44%, with less severe organomegaly. Overall, TPT sulfonate's efficacy profile is competitive with that of PZQ. Also, the characterization of a parasiticidal metabolite facilitates an understanding and improvement of the chemistry, and identification of the mechanism of action and/or target.

Published
2018

13. Mouse models of the fragile X premutation and fragile X-associated tremor/ataxia syndrome

Author

Berman, Robert F, Buijsen, Ronald AM, Usdin, Karen, Pintado, Elizabeth, Kooy, Frank, Pretto, Dalyir, Pessah, Isaac N, Nelson, David L, Zalewski, Zachary, Charlet-Bergeurand, Nicholas, Willemsen, Rob, and Hukema, Renate K

Subjects
Biomedical and Clinical Sciences, Neurosciences, Genetics, Intellectual and Developmental Disabilities (IDD), Orphan Drug, Pediatric, Brain Disorders, Clinical Research, Fragile X Syndrome, Mental Health, Neurodegenerative, Behavioral and Social Science, Rare Diseases, Aetiology, 2.1 Biological and endogenous factors, Mental health, Neurological, CGG trinucleotide repeat, FMR1, FMRP, Fragile X premutation, FXTAS, Intranuclear inclusions, Mouse models, RNA toxicity, Psychology
Abstract

Carriers of the fragile X premutation (FPM) have CGG trinucleotide repeat expansions of between 55 and 200 in the 5'-UTR of FMR1, compared to a CGG repeat length of between 5 and 54 for the general population. Carriers were once thought to be without symptoms, but it is now recognized that they can develop a variety of early neurological symptoms as well as being at risk for developing the late onset neurodegenerative disorder fragile X-associated tremor/ataxia syndrome (FXTAS). Several mouse models have contributed to our understanding of FPM and FXTAS, and findings from studies using these models are summarized here. This review also discusses how this information is improving our understanding of the molecular and cellular abnormalities that contribute to neurobehavioral features seen in some FPM carriers and in patients with FXTAS. Mouse models show much of the pathology seen in FPM carriers and in individuals with FXTAS, including the presence of elevated levels of Fmr1 mRNA, decreased levels of fragile X mental retardation protein, and ubiquitin-positive intranuclear inclusions. Abnormalities in dendritic spine morphology in several brain regions are associated with neurocognitive deficits in spatial and temporal memory processes, impaired motor performance, and altered anxiety. In vitro studies have identified altered dendritic and synaptic architecture associated with abnormal Ca(2+) dynamics and electrical network activity. FPM mice have been particularly useful in understanding the roles of Fmr1 mRNA, fragile X mental retardation protein, and translation of a potentially toxic polyglycine peptide in pathology. Finally, the potential for using these and emerging mouse models for preclinical development of therapies to improve neurological function in FXTAS is considered.

Published
2014

14. Personal journeys to and in human genetics and dysmorphology.

Author

Schwartz, Charles E., Aylsworth, Arthur S., Allanson, Judith, Battaglia, Agatino, Carey, John C., Curry, Cynthia J., Davies, Kay E., Eichler, Evan E., Graham, John M., Hall, Bryan, Hall, Judith G., Holmes, Lewis B., Hoyme, H. Eugene, Hunter, Alasdair, Innis, Jeffrey, Johnson, John, Keppler‐Noreuil, Kim M., Leroy, Jules G., Moore, Cynthia, and Nelson, David L.

Abstract

Genetics has become a critical component of medicine over the past five to six decades. Alongside genetics, a relatively new discipline, dysmorphology, has also begun to play an important role in providing critically important diagnoses to individuals and families. Both have become indispensable to unraveling rare diseases. Almost every medical specialty relies on individuals experienced in these specialties to provide diagnoses for patients who present themselves to other doctors. Additionally, both specialties have become reliant on molecular geneticists to identify genes associated with human disorders. Many of the medical geneticists, dysmorphologists, and molecular geneticists traveled a circuitous route before arriving at the position they occupied. The purpose of collecting the memoirs contained in this article was to convey to the reader that many of the individuals who contributed to the advancement of genetics and dysmorphology since the late 1960s/early 1970s traveled along a journey based on many chances taken, replying to the necessities they faced along the way before finding full enjoyment in the practice of medical and human genetics or dysmorphology. Additionally, and of equal importance, all exhibited an ability to evolve with their field of expertise as human genetics became human genomics with the development of novel technologies. [ABSTRACT FROM AUTHOR]

Published
2024
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21. The Genome Sequence of Drosophila melanogaster

Author

Adams, Mark D., Celniker, Susan E., Holt, Robert A., Evans, Cheryl A., Gocayne, Jeannine D., Amanatides, Peter G., Scherer, Steven E., Li, Peter W., Hoskins, Roger A., Galle, Richard F., George, Reed A., Lewis, Suzanna E., Richards, Stephen, Ashburner, Michael, Henderson, Scott N., Sutton, Granger G., Wortman, Jennifer R., Yandell, Mark D., Zhang, Qing, Chen, Lin X., Brandon, Rhonda C., Rogers, Yu-Hui C., Blazej, Robert G., Champe, Mark, Pfeiffer, Barret D., Wan, Kenneth H., Doyle, Clare, Baxter, Evan G., Helt, Gregg, Nelson, Catherine R., Abril, Josep F., Agbayani, Anna, An, Hui-Jin, Andrews-Pfannkoch, Cynthia, Baldwin, Danita, Ballew, Richard M., Basu, Anand, Baxendale, James, Bayraktaroglu, Leyla, Beasley, Ellen M., Beeson, Karen Y., Benos, P. V., Berman, Benjamin P., Bhandari, Deepali, Bolshakov, Slava, Borkova, Dana, Botchan, Michael R., Bouck, John, Brokstein, Peter, Brottier, Phillipe, Burtis, Kenneth C., Busam, Dana A., Butler, Heather, Cadieu, Edouard, Chandra, Ishwar, Cherry, J. Michael, Cawley, Simon, Dahlke, Carl, Davenport, Lionel B., Davies, Peter, de Pablos, Beatriz, Delcher, Arthur, Deng, Zuoming, Mays, Anne Deslattes, Dew, Ian, Dietz, Suzanne M., Dodson, Kristina, Doup, Lisa E., Downes, Michael, Dugan-Rocha, Shannon, Dunkov, Boris C., Dunn, Patrick, Durbin, Kenneth J., Evangelista, Carlos C., Ferraz, Concepcion, Ferriera, Steven, Fleischmann, Wolfgang, Fosler, Carl, Gabrielian, Andrei E., Garg, Neha S., Gelbart, William M., Glasser, Ken, Glodek, Anna, Gong, Fangcheng, Gorrell, J. Harley, Gu, Zhiping, Guan, Ping, Harris, Michael, Harris, Nomi L., Harvey, Damon, Heiman, Thomas J., Hernandez, Judith R., Houck, Jarrett, Hostin, Damon, Houston, Kathryn A., Howland, Timothy J., Wei, Ming-Hui, Ibegwam, Chinyere, Jalali, Mena, Kalush, Francis, Karpen, Gary H., Ke, Zhaoxi, Kennison, James A., Ketchum, Karen A., Kimmel, Bruce E., Kodira, Chinnappa D., Kraft, Cheryl, Kravitz, Saul, Kulp, David, Lai, Zhongwu, Lasko, Paul, Lei, Yiding, Levitsky, Alexander A., Li, Jiayin, Li, Zhenya, Liang, Yong, Lin, Xiaoying, Liu, Xiangjun, Mattei, Bettina, McIntosh, Tina C., McLeod, Michael P., McPherson, Duncan, Merkulov, Gennady, Milshina, Natalia V., Mobarry, Clark, Morris, Joe, Moshrefi, Ali, Mount, Stephen M., Moy, Mee, Murphy, Brian, Murphy, Lee, Muzny, Donna M., Nelson, David L., Nelson, David R., Nelson, Keith A., Nixon, Katherine, Nusskern, Deborah R., Pacleb, Joanne M., Palazzolo, Michael, Pittman, Gjange S., Pan, Sue, Pollard, John, Puri, Vinita, Reese, Martin G., Reinert, Knut, Remington, Karin, Scheeler, Frederick, Shen, Hua, Shue, Bixiang Christopher, Sidén-Kiamos, Inga, Simpson, Michael, Skupski, Marian P., Smith, Tom, Spier, Eugene, Spradling, Allan C., Stapleton, Mark, Strong, Renee, Sun, Eric, Svirskas, Robert, Tector, Cyndee, Turner, Russell, Venter, Eli, Wang, Aihui H., Wang, Xin, Wang, Zhen-Yuan, Wassarman, David A., Weinstock, George M., Weissenbach, Jean, Williams, Sherita M., Woodage, Trevor, Worley, Kim C., Wu, David, Yang, Song, Yao, Q. Alison, Ye, Jane, Yeh, Ru-Fang, Zaveri, Jayshree S., Zhan, Ming, Zhang, Guangren, Zhao, Qi, Zheng, Liansheng, Zheng, Xiangqun H., Zhong, Fei N., Zhong, Wenyan, Zhou, Xiaojun, Zhu, Shiaoping, Zhu, Xiaohong, Smith, Hamilton O., Gibbs, Richard A., Myers, Eugene W., Rubin, Gerald M., and Venter, J. Craig

Published
2000

23. Recessive mutations in muscle-specific isoforms of FXR1 cause congenital multi-minicore myopathy

Author

Estañ, María Cristina, Fernández-Núñez, Elisa, Zaki, Maha S., Esteban, María Isabel, Donkervoort, Sandra, Hawkins, Cynthia, Caparros-Martin, José A., Saade, Dimah, Hu, Ying, Bolduc, Véronique, Chao, Katherine Ru-Yui, Nevado, Julián, Lamuedra, Ana, Largo, Raquel, Herrero-Beaumont, Gabriel, Regadera, Javier, Hernandez-Chico, Concepción, Tizzano, Eduardo F., Martinez-Glez, Victor, Carvajal, Jaime J., Zong, Ruiting, Nelson, David L., Otaify, Ghada A., Temtamy, Samia, Aglan, Mona, Issa, Mahmoud, Bönnemann, Carsten G., Lapunzina, Pablo, Yoon, Grace, and Ruiz-Perez, Victor L.

Published
2019
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25. Trigger Finger: Assessment of Surgeon and Patient Preferences and Priorities for Decision Making

Author

Adams, Julie, Abzug, Joshua M., Akabudike, Ngozi M., Bainbridge, L.C., Balfour, George W., Bamberger, H.Brent, Barreto, Camilo Jose Romero, Baskies, Michael, Baxamusa, Taizoon, Behrman, Michael, Benhaim, Prosper, Blazar, Philip, Boler, James M., Boretto, Jorge G., Boyer, Martin, Calfee, Ryan P., Cassidy, Charles, Costanzo, Ralp M., Darowish, Michael, de Bedout, Ramon, Desilva, Gregory, Di Giovanni, Jose Fernando, Dodds, Seth, Erickson, John M., Luis Felipe, Naquira Escobar, Fernandes, C.H., Fricker, Renato M., Frykman, Gary K., Garcia, Aida E., Gaston, R. Glenn, Gilbert, Richard S., Grafe, Michael W., Greenberg, Jeffrey A., Grunwald, H.W., Guidera, Paul, Hammert, Warren C., Hauck, Randy, Helgemo, Steve, Hernandez, German Ricardo, Hofmeister, Eric, Hutchison, Richard L., Ilyas, Asif, Jacoby, Sidney M., Jebson, Peter, Jones, Christopher M., Kakar, Sanjeev, Kaplan, F. Thomas D., Kaplan, Saul, Katolik, Leonid, Kennedy, Stephen A., Kessler, Michael W., Kimball, Hervey L., Kirkpatrick, D. Kay, Klinefelter, Ryan, Kraan, G.A., Lane, Lewis B., Lattanza, Lisa, Lee, Kendrick, Malone, Kevin J., Manke, Chad, Martineau, Paul A., Matiko, Jim, McAuliffe, John, McCabe, Steven J., McKee, Desirae M., Metzger, Charles, Mitchell, Scott, Wolf, Jennifer Moriatis, Nancollas, Michael, Nelson, David L., Nolla, Jose, Nyszkiewicz, Ralf, Ortiz, Jose A., Jr., Overbeck, Joachim P., Owens, Patrick W., Papandrea, Rick, Paz, Lior, Castillo, Alberto Pérez, Polatsch, Daniel, Press, Gary M., Richard, Marc J., Rizzo, Marco, Rozental, Tamara D., Ruchelsman, David, Semenkin, Oleg M., Shatford, Russell, Sierra, Fransisco Javier Aguilar, Siff, Todd, Spath, Catherine, Spruijt, Sander, Sutker, Ben, Swigart, Carrie, Taras, John, Tavakolian, Jason D., Terrono, Andrew L., Tolo, Eric T., Walsh, Christopher J., Walter, Frank L., Watkins, Barry, Weiss, Lawrence, Wills, Brian P.D., Wilson, Chris, Wilson, Christophe J., Wint, Jeffrey, Young, Colby, Döring, Anne-Carolin D., Hageman, Michiel G.J.S., Mulder, Frans J., Guitton, Thierry G., and Ring, David

Published
2014
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27. Carpal Tunnel Syndrome: Assessment of Surgeon and Patient Preferences and Priorities for Decision-Making

Author

Abzug, Joshua M., Adams, Julie, Arbelaez, Gallo Fabio, Aspard, T., Balfour, George W., Bamberger, H. Brent, Barreto, Romero Jose Camilo, Baskies, Michael, Batson, W. Arnold, Baxamusa, Taizoon, de Bedout, Ramon, Beldner, Steven, Benhaim, Prosper, Benson, Leon, Boretto, G. Jorge, Boyer, Martin, Dee Byrd, Gregory, Calfee, Ryan P., Zambrano, Gladys Cecilia, Cassidy, Charles, Catalano, Louis, III, Chivers, Karel, Costanzo, Ralph M., Dantuluri, Phani, DeSilva, Gregory, Dodds, Seth, Evans, John P., Felipe, Naquira Escobar Luis, Fernandes, C.H., Fischer, Thomas J., Fischer, Jochen, Fricker, M. Renato, Frykman, Gary K., Garcia, Aida E., Gaston, R. Glenn, Di Giovanni, José Fernando, Goldfarb, Charles A., Grafe, Michael W., Grunwald, H.W., Hammert, Warren C., Hauck, Randy, Hernandez, Ricardo German, Hofmeister, Eric, Hutchison, Richard L., Ilyas, Asif, Isaacs, Jonathan, Jacoby, Sidney M., Jebson, Peter, Jones, Christopher M., Jones, Michael, Kakar, Sanjeev, Kalainov, David M., Kaplan, Thomas D., Kaplan, Saul, Katolik, Leonid, Kennedy, Stephen A., Kessler, Michael W., Kimball, Hervey L., Kraan, G.A., Martineau, Paul A., McAuliffe, John, McCabe, Steven J., McKee, Desirae M., Merrell, Greg, Metzger, Charles, Nancollas, Michael, Nelson, David L., Nyszkiewicz, Ralf, Ortiz, Jose A., Owens, Patrick W., Palmer, Jason M., Paz, Lior, Pess, Gary, Polatsch, Daniel, Raia, Frank J., Richard, Marc J., Rizzo, Marco, Rozental, Ruchelsman, David, Semenkin, Oleg M., Sierra, Aguilar Javier Francisco, Siff, Todd, Sodha, Samir, Spath, Catherine, Spruijt, Sander, Stackhouse, Thomas F., Swigart, Carrie, Szabo, Robert, Taras, John, Tavakolian, Jason, Terrono, Andrew, Varecka, Thomas F., Wahegaonkar, Abhijeet L., Walsh, Christopher J., Walter, Frank L., Weiss, Lawrence, Wills, Brian P.D., Wilson, Chris, Wilson, Christopher, Wolf, Jennifer Moriatis, Wood, Megan, Young, Colby, Hageman, Michiel G.J.S., Kinaci, Ahmet, Ju, Kevin, Guitton, Thierry G., Mudgal, Chaitanya S., and Ring, David

Published
2014
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30. Contributors

Author

Bao, Han, primary, Bear, Mark F., additional, Ben-Hur, Tamir, additional, Benvenisty, Nissim, additional, Berry-Kravis, Elizabeth, additional, Bhattacharya, Aditi, additional, Chiurazzi, Pietro, additional, Cohen, Jeffrey, additional, El-Hassar, Lynda, additional, Ethell, Douglas W., additional, Frick, Andreas, additional, Gall, Christine M., additional, Gasparini, Fabrizio, additional, Gazy, Inbal, additional, Ginger, Melanie, additional, Gross, Christina, additional, Guy, Jacalyn, additional, Hagerman, Randi, additional, Hardiman, Becky, additional, Hoeffer, Charles, additional, Hunter, Jessica E., additional, Huntsman, Molly M., additional, Jønch, Aia E., additional, Jacquemont, Sébastien, additional, Jin, Peng, additional, Jope, Richard S., additional, Kaczmarek, Leonard K., additional, Kind, Peter, additional, Kooy, R. Frank, additional, Lauterborn, Julie C., additional, Ligsay, Andrew, additional, Lindemann, Lothar, additional, Manzoni, Olivier J.J., additional, Martin, Henry G.S., additional, Milà, Montserrat, additional, Nelson, David L., additional, Neri, Giovanni, additional, Neuhofer, Daniela, additional, Osterweil, Emily K., additional, Richstein, Jörg, additional, Santoro, Michael R., additional, Scerif, Gaia, additional, Scharf, Sebastian S., additional, Sherman, Stephanie L., additional, Sidhu, Harpreet, additional, Spooren, Will, additional, Stoppel, Laura J., additional, Suhl, Joshua, additional, Tabolacci, Elisabetta, additional, Tassone, Flora, additional, Till, Sally, additional, Usdin, Karen, additional, Vershkov, Dan, additional, Warren, Stephen T., additional, Willemsen, Rob, additional, and Zhao, Xiao-Nan, additional

Published
2017
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33. LLPS of FXR1 drives spermiogenesis by activating translation of stored mRNAs

Author

Kang, Jun-Yan, primary, Wen, Ze, additional, Pan, Duo, additional, Zhang, Yuhan, additional, Li, Qing, additional, Zhong, Ai, additional, Yu, Xinghai, additional, Wu, Yi-Chen, additional, Chen, Yu, additional, Zhang, Xiangzheng, additional, Kou, Peng-Cheng, additional, Geng, Junlan, additional, Wang, Ying-Yi, additional, Hua, Min-Min, additional, Zong, Ruiting, additional, Li, Biao, additional, Shi, Hui-Juan, additional, Li, Dangsheng, additional, Fu, Xiang-Dong, additional, Li, Jinsong, additional, Nelson, David L., additional, Guo, Xuejiang, additional, Zhou, Yu, additional, Gou, Lan-Tao, additional, Huang, Ying, additional, and Liu, Mo-Fang, additional

Published
2022
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35. An Imaging Roadmap for Biology Education: From Nanoparticles to Whole Organisms

Author

Kelley, Daniel J., Davidson, Richard J., and Nelson, David L.

Abstract

Imaging techniques provide ways of knowing structure and function in biology at different scales. The multidisciplinary nature and rapid advancement of imaging sciences requires imaging education to begin early in the biology curriculum. Guided by the National Institutes of Health (NIH) Roadmap initiatives, we incorporated a nanoimaging, molecular imaging, and medical imaging teaching unit into three 1-h class periods of an introductory course on ways of knowing biology. Activities were derived from NIH Roadmap initiatives in nanomedicine, regenerative medicine, and nuclear medicine. The course materials we describe contributed positively to student learning gains in quantifying and interpreting images, in characterizing imaging methods that provide ways of knowing biological structure and function, and in understanding scale in biology and imaging. The NIH Roadmap provides a useful context to educate students about the multidisciplinary imaging continuum. (Contains 3 tables and 4 figures.)

Published
2008
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37. Identification of PSMB5 as a genetic modifier of fragile X–associated tremor/ataxia syndrome

Author

Kong, Ha Eun, primary, Lim, Junghwa, additional, Linsalata, Alexander, additional, Kang, Yunhee, additional, Malik, Indranil, additional, Allen, Emily G., additional, Cao, Yiqu, additional, Shubeck, Lisa, additional, Johnston, Rich, additional, Huang, Yanting, additional, Gu, Yanghong, additional, Guo, Xiangxue, additional, Zwick, Michael E., additional, Qin, Zhaohui, additional, Wingo, Thomas S., additional, Juncos, Jorge, additional, Nelson, David L., additional, Epstein, Michael P., additional, Cutler, David J., additional, Todd, Peter K., additional, Sherman, Stephanie L., additional, Warren, Stephen T., additional, and Jin, Peng, additional

Published
2022
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40. The Effect of Hands-on Occupation on Recall Memory in Men with Traumatic Brain Injuries.

Author

Eakman, Aaron M. and Nelson, David L.

Abstract

Males with closed head injuries (n=30) participated in a study of their ability to follow simple written and verbal instructions, upper extremity function for a simple meal task, and ability to attend to a task for 30 minutes. Hands-on tasks resulted in greater recall of instructions than verbal training only. (Contains 15 references.) (JOW)

Published
2001

45. Polycyclic aromatic hydrocarbons in cachaças packed in bottles of polyethylene terephthalate

Author

Souza, Rafaella H. Z., primary, Cardoso, Maria das Graças, additional, Machado, Ana Maria R., additional, Santiago, Wilder D., additional, Pedroso, Márcio P., additional, Brandão, Rafaela M., additional, Oliveira, Renan E. S., additional, Barbosa, Richard B., additional, Alvarenga, Gabriela F., additional, Caetano, Alex R. S., additional, and Nelson, David L., additional

Published
2022
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46. Functional consequences of postnatal interventions in a mouse model of Fragile X syndrome

Author

Rais, Maham, primary, Lovelace, Jonathan W., additional, Shuai, Xinghao S., additional, Woodard, Walker, additional, Bishay, Steven, additional, Estrada, Leo, additional, Sharma, Ashwin R., additional, Nguy, Austin, additional, Kulinich, Anna, additional, Pirbhoy, Patricia S., additional, Palacios, Arnold R., additional, Nelson, David L., additional, Razak, Khaleel A., additional, and Ethell, Iryna M., additional

Published
2022
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47. Stephen T. Warren, Ph.D. (1953–2021): A remembrance

Author

Nelson, David L., primary, Clark, Janelle, additional, Garber, Kathryn, additional, Glover, Thomas, additional, Hassold, Terry, additional, Jin, Peng, additional, Orr, Harry T., additional, Sherman, Stephanie L., additional, Zoghbi, Huda, additional, and Warren, Karen L., additional

Published
2022
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