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1,251 results on '"Shaffer, Lisa"'

7. Palindromic GOLGA8 core duplicons promote chromosome 15q13.3 microdeletion and evolutionary instability.

Author

Antonacci, Francesca, Dennis, Megan Y, Huddleston, John, Sudmant, Peter H, Steinberg, Karyn Meltz, Rosenfeld, Jill A, Miroballo, Mattia, Graves, Tina A, Vives, Laura, Malig, Maika, Denman, Laura, Raja, Archana, Stuart, Andrew, Tang, Joyce, Munson, Brenton, Shaffer, Lisa G, Amemiya, Chris T, Wilson, Richard K, and Eichler, Evan E

Subjects
Chromosomes, Artificial, Bacterial, Chromosomes, Human, Pair 15, Animals, Primates, Humans, Seizures, Chromosome Disorders, Chromosome Deletion, In Situ Hybridization, Fluorescence, Cluster Analysis, Sequence Analysis, DNA, Repetitive Sequences, Nucleic Acid, Gene Dosage, Polymorphism, Genetic, Genome, Human, Models, Genetic, Comparative Genomic Hybridization, Segmental Duplications, Genomic, Biological Evolution, Intellectual Disability, Genetics, Biological Sciences, Medical and Health Sciences, Developmental Biology
Abstract

Recurrent deletions of chromosome 15q13.3 associate with intellectual disability, schizophrenia, autism and epilepsy. To gain insight into the instability of this region, we sequenced it in affected individuals, normal individuals and nonhuman primates. We discovered five structural configurations of the human chromosome 15q13.3 region ranging in size from 2 to 3 Mb. These configurations arose recently (∼0.5-0.9 million years ago) as a result of human-specific expansions of segmental duplications and two independent inversion events. All inversion breakpoints map near GOLGA8 core duplicons-a ∼14-kb primate-specific chromosome 15 repeat that became organized into larger palindromic structures. GOLGA8-flanked palindromes also demarcate the breakpoints of recurrent 15q13.3 microdeletions, the expansion of chromosome 15 segmental duplications in the human lineage and independent structural changes in apes. The significant clustering (P = 0.002) of breakpoints provides mechanistic evidence for the role of this core duplicon and its palindromic architecture in promoting the evolutionary and disease-related instability of chromosome 15.

Published
2014

8. Neuropathology of brain and spinal malformations in a case of monosomy 1p36

Author

Shiba, Naoko, Daza, Ray AM, Shaffer, Lisa G, Barkovich, A, Dobyns, William B, and Hevner, Robert F

Abstract

Abstract Monosomy 1p36 is the most common subtelomeric chromosomal deletion linked to mental retardation and seizures. Neuroimaging studies suggest that monosomy 1p36 is associated with brain malformations including polymicrogyria and nodular heterotopia, but the histopathology of these lesions is unknown. Here we present postmortem neuropathological findings from a 10 year-old girl with monosomy 1p36, who died of respiratory complications. The findings included micrencephaly, periventricular nodular heterotopia in occipitotemporal lobes, cortical dysgenesis resembling polymicrogyria in dorsolateral frontal lobes, hippocampal malrotation, callosal hypoplasia, superiorly rotated cerebellum with small vermis, and lumbosacral hydromyelia. The abnormal cortex exhibited “festooned” (undulating) supragranular layers, but no significant fusion of the molecular layer. Deletion mapping demonstrated single copy loss of a contiguous 1p36 terminal region encompassing many important neurodevelopmental genes, among them four HES genes implicated in regulating neural stem cell differentiation, and TP73, a monoallelically expressed gene. Our results suggest that brain and spinal malformations in monosomy 1p36 may be more extensive than previously recognized, and may depend on the parental origin of deleted genes. More broadly, our results suggest that specific genetic disorders may cause distinct forms of cortical dysgenesis.

Published
2013

12. A recurrent 16p12.1 microdeletion supports a two-hit model for severe developmental delay

Author

Girirajan, Santhosh, Rosenfeld, Jill A, Cooper, Gregory M, Antonacci, Francesca, Siswara, Priscillia, Itsara, Andy, Vives, Laura, Walsh, Tom, McCarthy, Shane E, Baker, Carl, Mefford, Heather C, Kidd, Jeffrey M, Browning, Sharon R, Browning, Brian L, Dickel, Diane E, Levy, Deborah L, Ballif, Blake C, Platky, Kathryn, Farber, Darren M, Gowans, Gordon C, Wetherbee, Jessica J, Asamoah, Alexander, Weaver, David D, Mark, Paul R, Dickerson, Jennifer, Garg, Bhuwan P, Ellingwood, Sara A, Smith, Rosemarie, Banks, Valerie C, Smith, Wendy, McDonald, Marie T, Hoo, Joe J, French, Beatrice N, Hudson, Cindy, Johnson, John P, Ozmore, Jillian R, Moeschler, John B, Surti, Urvashi, Escobar, Luis F, El-Khechen, Dima, Gorski, Jerome L, Kussmann, Jennifer, Salbert, Bonnie, Lacassie, Yves, Biser, Alisha, McDonald-McGinn, Donna M, Zackai, Elaine H, Deardorff, Matthew A, Shaikh, Tamim H, Haan, Eric, Friend, Kathryn L, Fichera, Marco, Romano, Corrado, Gécz, Jozef, DeLisi, Lynn E, Sebat, Jonathan, King, Mary-Claire, Shaffer, Lisa G, and Eichler, Evan E

Subjects
Agricultural, Veterinary and Food Sciences, Biological Sciences, Bioinformatics and Computational Biology, Genetics, Agricultural Biotechnology, Neurosciences, Brain Disorders, Pediatric, Aetiology, 2.1 Biological and endogenous factors, Adult, Case-Control Studies, Child, Child, Preschool, Chromosome Deletion, Chromosomes, Human, Pair 16, Comparative Genomic Hybridization, Developmental Disabilities, Family, Gene Frequency, Humans, Infant, Models, Genetic, Oligonucleotide Array Sequence Analysis, Pedigree, Phenotype, Polymorphism, Single Nucleotide, Recurrence, Severity of Illness Index, Medical and Health Sciences, Developmental Biology, Agricultural biotechnology, Bioinformatics and computational biology
Abstract

We report the identification of a recurrent, 520-kb 16p12.1 microdeletion associated with childhood developmental delay. The microdeletion was detected in 20 of 11,873 cases compared with 2 of 8,540 controls (P = 0.0009, OR = 7.2) and replicated in a second series of 22 of 9,254 cases compared with 6 of 6,299 controls (P = 0.028, OR = 2.5). Most deletions were inherited, with carrier parents likely to manifest neuropsychiatric phenotypes compared to non-carrier parents (P = 0.037, OR = 6). Probands were more likely to carry an additional large copy-number variant when compared to matched controls (10 of 42 cases, P = 5.7 x 10(-5), OR = 6.6). The clinical features of individuals with two mutations were distinct from and/or more severe than those of individuals carrying only the co-occurring mutation. Our data support a two-hit model in which the 16p12.1 microdeletion both predisposes to neuropsychiatric phenotypes as a single event and exacerbates neurodevelopmental phenotypes in association with other large deletions or duplications. Analysis of other microdeletions with variable expressivity indicates that this two-hit model might be more generally applicable to neuropsychiatric disease.

Published
2010

13. Human Chromosome 7: DNA Sequence and Biology

Author

Scherer, Stephen W., Cheung, Joseph, MacDonald, Jeffrey R., Osborne, Lucy R., Nakabayashi, Kazuhiko, Herbrick, Jo-Anne, Carson, Andrew R., Parker-Katiraee, Layla, Skaug, Jennifer, Khaja, Razi, Zhang, Junjun, Hudek, Alexander K., Li, Martin, Haddad, May, Duggan, Gavin E., Fernandez, Bridget A., Kanematsu, Emiko, Gentles, Simone, Christopoulos, Constantine C., Choufani, Sanaa, Kwasnicka, Dorota, Zheng, Xiangqun H., Lai, Zhongwu, Nusskern, Deborah, Zhang, Qing, Gu, Zhiping, Lu, Fu, Zeesman, Susan, Nowaczyk, Malgorzata J., Teshima, Ikuko, Chitayat, David, Shuman, Cheryl, Weksberg, Rosanna, Zackai, Elaine H., Grebe, Theresa A., Cox, Sarah R., Kirkpatrick, Susan J., Rahman, Nazneen, Friedman, Jan M., Pelicci, Pier Giuseppe, Lo-Coco, Francesco, Belloni, Elena, Shaffer, Lisa G., Pober, Barbara, Morton, Cynthia C., Gusella, James F., Korf, Bruce R., Quade, Bradley J., Ligon, Azra H., Ferguson, Heather, Higgins, Anne W., Leach, Natalia T., Herrick, Steven R., Lemyre, Emmanuelle, Farra, Chantal G., Kim, Hyung-Goo, Summers, Anne M., Gripp, Karen W., Roberts, Wendy, Szatmari, Peter, Grzeschik, Karl-Heinz, Teebi, Ahmed, Minassian, Berge A., Kere, Juha, Armengol, Lluis, Pujana, Miguel Angel, Estivill, Xavier, Wilson, Michael D., Koop, Ben F., Tosi, Sabrina, Moore, Gudrun E., Boright, Andrew P., Zlotorynski, Eitan, Kerem, Batsheva, Kroisel, Peter M., Petek, Erwin, Oscier, David G., Mould, Sarah J., Döhner, Hartmut, Döhner, Konstanze, Rommens, Johanna M., Vincent, John B., Venter, J. Craig, Li, Peter W., Mural, Richard J., Adams, Mark D., and Tsui, Lap-Chee

Published
2003

14. Saving Venice: Engineering and ecology in the Venice lagoon

Author

Deheyn, Dimitri D and Shaffer, Lisa R

Subjects
Environment, Sustainability, Interdisciplinary Research, Venice, Lagoon, Sediment management, Sustainability, SIOSED
Abstract

This paper describes some of the challenges of sustainability, and shows how they are manifested in coastal environments. It reviews the problems facing Venice and its lagoon, as a particularly interesting and complex example, and describes the technological, environmental, and scientific actions taken to address the problems of sustainability. Specifically, the actions and interdisciplinary research supporting management of the Venice lagoon environment are discussed, with a particular focus on the sediment. Conclusions are drawn regarding the integration of science, technology, and the environment, including the interactions of industry, the international scientific community, and governments.

Published
2007

15. Identification of a novel polymorphism—the duplication of the NPHP1 (nephronophthisis 1) gene

Author

Baris, Hagit, Bejjani, Bassem A, Tan, Wen‐Hann, Coulter, David L, Martin, Judith A, Storm, Andrea L, Burton, Barbara K, Saitta, Sulagna C, Gajecka, Marzena, Ballif, Blake C, Irons, Mira B, Shaffer, Lisa G, and Kimonis, Virginia E

Subjects
Adaptor Proteins, Signal Transducing, Child, Child, Preschool, Chromosomes, Human, Pair 2, Cytoskeletal Proteins, Developmental Disabilities, Female, Gene Duplication, Humans, In Situ Hybridization, Fluorescence, Infant, Male, Membrane Proteins, Polymorphism, Genetic, Proteins, Speech Disorders, Genetics, Clinical Sciences
Published
2006

16. Molecular mechanism for duplication 17p11.2— the homologous recombination reciprocal of the Smith-Magenis microdeletion

Author

Potocki, Lorraine, Chen, Ken-Shiung, Park, Sung-Sup, Osterholm, Doreen E, Withers, Marjorie A, Kimonis, Virginia, Summers, Anne M, Meschino, Wendy S, Anyane-Yeboa, Kwame, Kashork, Catherine D, Shaffer, Lisa G, and Lupski, James R

Subjects
Biological Sciences, Genetics, Rare Diseases, Neurosciences, Human Genome, Peripheral Neuropathy, Neurodegenerative, Abnormalities, Multiple, Chromosome Aberrations, Chromosomes, Human, Pair 17, Female, Genotype, Humans, In Situ Hybridization, Fluorescence, Intellectual Disability, Male, Pedigree, Recombination, Genetic, Syndrome, Medical and Health Sciences, Developmental Biology, Agricultural biotechnology, Bioinformatics and computational biology
Abstract

Recombination between repeated sequences at various loci of the human genome are known to give rise to DNA rearrangements associated with many genetic disorders. Perhaps the most extensively characterized genomic region prone to rearrangement is 17p12, which is associated with the peripheral neuropathies, hereditary neuropathy with liability to pressure palsies (HNPP) and Charcot-Marie-Tooth disease type 1A (CMT1A;ref. 2). Homologous recombination between 24-kb flanking repeats, termed CMT1A-REPs, results in a 1.5-Mb deletion that is associated with HNPP, and the reciprocal duplication product is associated with CMT1A (ref. 2). Smith-Magenis syndrome (SMS) is a multiple congenital anomalies, mental retardation syndrome associated with a chromosome 17 microdeletion, del(17)(p11.2p11.2) (ref. 3,4). Most patients (>90%) carry deletions of the same genetic markers and define a common deletion. We report seven unrelated patients with de novo duplications of the same region deleted in SMS. A unique junction fragment, of the same apparent size, was identified in each patient by pulsed field gel electrophoresis (PFGE). Further molecular analyses suggest that the de novo17p11.2 duplication is preferentially paternal in origin, arises from unequal crossing over due to homologous recombination between flanking repeat gene clusters and probably represents the reciprocal recombination product of the SMS deletion. The clinical phenotype resulting from duplication [dup(17)(p11.2p11.2)] is milder than that associated with deficiency of this genomic region. This mechanism of reciprocal deletion and duplication via homologous recombination may not only pertain to the 17p11.2 region, but may also be common to other regions of the genome where interstitial microdeletion syndromes have been defined.

Published
2000

25. TM4SF20 Ancestral Deletion and Susceptibility to a Pediatric Disorder of Early Language Delay and Cerebral White Matter Hyperintensities

Author

Wiszniewski, Wojciech, Hunter, Jill V., Hanchard, Neil A., Willer, Jason R., Shaw, Chad, Tian, Qi, Illner, Anna, Wang, Xueqing, Cheung, Sau W., Patel, Ankita, Campbell, Ian M., Gelowani, Violet, Hixson, Patricia, Ester, Audrey R., Azamian, Mahshid S., Potocki, Lorraine, Zapata, Gladys, Hernandez, Patricia P., Ramocki, Melissa B., Santos-Cortez, Regie L.P., Wang, Gao, York, Michele K., Justice, Monica J., Chu, Zili D., Bader, Patricia I., Omo-Griffith, Lisa, Madduri, Nirupama S., Scharer, Gunter, Crawford, Heather P., Yanatatsaneejit, Pattamawadee, Eifert, Anna, Kerr, Jeffery, Bacino, Carlos A., Franklin, Adiaha I.A., Goin-Kochel, Robin P., Simpson, Gayle, Immken, Ladonna, Haque, Muhammad E., Stosic, Marija, Williams, Misti D., Morgan, Thomas M., Pruthi, Sumit, Omary, Reed, Boyadjiev, Simeon A., Win, Kay K., Thida, Aye, Hurles, Matthew, Hibberd, Martin Lloyd, Khor, Chiea Chuen, Van Vinh Chau, Nguyen, Gallagher, Thomas E., Mutirangura, Apiwat, Stankiewicz, Pawel, Beaudet, Arthur L., Maletic-Savatic, Mirjana, Rosenfeld, Jill A., Shaffer, Lisa G., Davis, Erica E., Belmont, John W., Dunstan, Sarah, Simmons, Cameron P., Bonnen, Penelope E., Leal, Suzanne M., Katsanis, Nicholas, Lupski, James R., and Lalani, Seema R.

Published
2013
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27. ZC4H2 Mutations Are Associated with Arthrogryposis Multiplex Congenita and Intellectual Disability through Impairment of Central and Peripheral Synaptic Plasticity

Author

Hirata, Hiromi, Nanda, Indrajit, van Riesen, Anne, McMichael, Gai, Hu, Hao, Hambrock, Melanie, Papon, Marie-Amélie, Fischer, Ute, Marouillat, Sylviane, Ding, Can, Alirol, Servane, Bienek, Melanie, Preisler-Adams, Sabine, Grimme, Astrid, Seelow, Dominik, Webster, Richard, Haan, Eric, MacLennan, Alastair, Stenzel, Werner, Yap, Tzu Ying, Gardner, Alison, Nguyen, Lam Son, Shaw, Marie, Lebrun, Nicolas, Haas, Stefan A., Kress, Wolfram, Haaf, Thomas, Schellenberger, Elke, Chelly, Jamel, Viot, Géraldine, Shaffer, Lisa G., Rosenfeld, Jill A., Kramer, Nancy, Falk, Rena, El-Khechen, Dima, Escobar, Luis F., Hennekam, Raoul, Wieacker, Peter, Hübner, Christoph, Ropers, Hans-Hilger, Gecz, Jozef, Schuelke, Markus, Laumonnier, Frédéric, and Kalscheuer, Vera M.

Published
2013
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28. Mouse model implicates GNB3 duplication in a childhood obesity syndrome

Author

Unique Rare Chromosome Disorder Support Group, Goldlust, Ian S., Hermetz, Karen E., Catalano, Lisa M., Barfield, Richard T., Cozad, Rebecca, Wynn, Grace, Ozdemir, Alev Cagla, Conneely, Karen N., Mulle, Jennifer G., Dharamrup, Shikha, Hegde, Madhuri R., Kim, Katherine H., Angle, Brad, Colley, Alison, Webb, Amy E., Thorland, Erik C., Ellison, Jay W., Rosenfeld, Jill A., Ballif, Blake C., Shaffer, Lisa G., Demmer, Laurie A., and Rudd, M. Katharine

Published
2013

30. Novel 9q34.11 gene deletions encompassing combinations of four Mendelian disease genes: STXBP1, SPTAN1, ENG, and TOR1A

Author

Campbell, Ian M., Yatsenko, Svetlana A., Hixson, Patricia, Reimschisel, Tyler, Thomas, Matthew, Wilson, William, Dayal, Usha, Wheless, James W., Crunk, Amy, Curry, Cynthia, Parkinson, Nicole, Fishman, Leona, Riviello, James J., Nowaczyk, Malgorzata J.M., Zeesman, Susan, Rosenfeld, Jill A., Bejjani, Bassem A., Shaffer, Lisa G., Cheung, Sau Wai, Lupski, James R., Stankiewicz, Pawel, and Scaglia, Fernando

Published
2012
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31. Genetic and environmental risk factors in congenital heart disease functionally converge in protein networks driving heart development

Author

Lage, Kasper, Greenway, Steven C., Rosenfeld, Jill A., Wakimoto, Hiroko, Gorham, Joshua M., Segrè, Ayellet V., Roberts, Amy E., Smoot, Leslie B., Pu, William T., Pereira, Alexandre C., Mesquita, Sonia M., Tommerup, Niels, Brunak, Søren, Ballif, Blake C., Shaffer, Lisa G., Donahoe, Patricia K., Daly, Mark J., Seidman, Jonathan G., Seidman, Christine E., and Larsen, Lars A.

Published
2012

32. Translocations Disrupting PHF21A in the Potocki-Shaffer-Syndrome Region Are Associated with Intellectual Disability and Craniofacial Anomalies

Author

Kim, Hyung-Goo, Kim, Hyun-Taek, Leach, Natalia T., Lan, Fei, Ullmann, Reinhard, Silahtaroglu, Asli, Kurth, Ingo, Nowka, Anja, Seong, Ihn Sik, Shen, Yiping, Talkowski, Michael E., Ruderfer, Douglas, Lee, Ji-Hyun, Glotzbach, Caron, Ha, Kyungsoo, Kjaergaard, Susanne, Levin, Alex V., Romeike, Bernd F., Kleefstra, Tjitske, Bartsch, Oliver, Elsea, Sarah H., Jabs, Ethylin Wang, MacDonald, Marcy E., Harris, David J., Quade, Bradley J., Ropers, Hans-Hilger, Shaffer, Lisa G., Kutsche, Kerstin, Layman, Lawrence C., Tommerup, Niels, Kalscheuer, Vera M., Shi, Yang, Morton, Cynthia C., Kim, Cheol-Hee, and Gusella, James F.

Published
2012
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36. Sequencing Chromosomal Abnormalities Reveals Neurodevelopmental Loci that Confer Risk across Diagnostic Boundaries

Author

Talkowski, Michael E., Rosenfeld, Jill A., Blumenthal, Ian, Pillalamarri, Vamsee, Chiang, Colby, Heilbut, Adrian, Ernst, Carl, Hanscom, Carrie, Rossin, Elizabeth, Lindgren, Amelia M., Pereira, Shahrin, Ruderfer, Douglas, Kirby, Andrew, Ripke, Stephan, Harris, David J., Lee, Ji-Hyun, Ha, Kyungsoo, Kim, Hyung-Goo, Solomon, Benjamin D., Gropman, Andrea L., Lucente, Diane, Sims, Katherine, Ohsumi, Toshiro K., Borowsky, Mark L., Loranger, Stephanie, Quade, Bradley, Lage, Kasper, Miles, Judith, Wu, Bai-Lin, Shen, Yiping, Neale, Benjamin, Shaffer, Lisa G., Daly, Mark J., Morton, Cynthia C., and Gusella, James F.

Published
2012
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37. The Genetic Architecture of down Syndrome Phenotypes Revealed by High-Resolution Analysis of Human Segmental Trisomies

Author

Korbel, Jan O., Tirosh-Wagner, Tal, Urban, Alexander Eckehart, Chen, Xiao-Ning, Kasowski, Maya, Dal, Li, Grubert, Fabian, Erdman, Chandra, Gao, Michael C., Lange, Ken, Sobel, Eric M., Barlow, Gillian M., Aylsworth, Arthur S., Carpenter, Nancy J., Clark, Robin Dawn, Cohen, Monika Y., Doran, Eric, Falik-Zaccai, Tzipora, Lewin, Susan O., Lott, Ira T., McGillivray, Barbara C., Moeschler, John B., Pettenati, Mark J., Pueschel, Slegfried M., Raol, Kathleen W., Shaffer, Lisa G., Shohat, Mordechai, van Riper, Alexander J., Warburton, Dorothy, Weissman, Sherman, Gerstein, Mark B., Snyder, Michael, Korenberg, Julie R., and Ecker, Joseph R.

Published
2009
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44. Assessment of 2q23.1 Microdeletion Syndrome Implicates MBD5 as a Single Causal Locus of Intellectual Disability, Epilepsy, and Autism Spectrum Disorder

Author

Talkowski, Michael E., Mullegama, Sureni V., Rosenfeld, Jill A., van Bon, Bregje W.M., Shen, Yiping, Repnikova, Elena A., Gastier-Foster, Julie, Thrush, Devon Lamb, Kathiresan, Sekar, Ruderfer, Douglas M., Chiang, Colby, Hanscom, Carrie, Ernst, Carl, Lindgren, Amelia M., Morton, Cynthia C., An, Yu, Astbury, Caroline, Brueton, Louise A., Lichtenbelt, Klaske D., Ades, Lesley C., Fichera, Marco, Romano, Corrado, Innis, Jeffrey W., Williams, Charles A., Bartholomew, Dennis, Van Allen, Margot I., Parikh, Aditi, Zhang, Lilei, Wu, Bai-Lin, Pyatt, Robert E., Schwartz, Stuart, Shaffer, Lisa G., de Vries, Bert B.A., Gusella, James F., and Elsea, Sarah H.

Published
2011
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45. Mutations in Prickle Orthologs Cause Seizures in Flies, Mice, and Humans

Author

Tao, Hirotaka, Manak, J. Robert, Sowers, Levi, Mei, Xue, Kiyonari, Hiroshi, Abe, Takaya, Dahdaleh, Nader S., Yang, Tian, Wu, Shu, Chen, Shan, Fox, Mark H., Gurnett, Christina, Montine, Thomas, Bird, Thomas, Shaffer, Lisa G., Rosenfeld, Jill A., McConnell, Juliann, Madan-Khetarpal, Suneeta, Berry-Kravis, Elizabeth, Griesbach, Hilary, Saneto, Russell P., Scott, Matthew P., Antic, Dragana, Reed, Jordan, Boland, Riley, Ehaideb, Salleh N., El-Shanti, Hatem, Mahajan, Vinit B., Ferguson, Polly J., Axelrod, Jeffrey D., Lehesjoki, Anna-Elina, Fritzsch, Bernd, Slusarski, Diane C., Wemmie, John, Ueno, Naoto, and Bassuk, Alexander G.

Published
2011
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46. Implication of LRRC4C and DPP6 in neurodevelopmental disorders

Author

Maussion, Gilles, Cruceanu, Cristiana, Rosenfeld, Jill A., Bell, Scott C., Jollant, Fabrice, Szatkiewicz, Jin, Collins, Ryan L., Hanscom, Carrie, Kolobova, Ilaria, de Champfleur, Nicolas Menjot, Blumenthal, Ian, Chiang, Colby, Ota, Vanessa, Hultman, Christina, OʼDushlaine, Colm, McCarroll, Steve, Alda, Martin, Jacquemont, Sebastien, Ordulu, Zehra, Marshall, Christian R., Carter, Melissa T., Shaffer, Lisa G., Sklar, Pamela, Girirajan, Santhosh, Morton, Cynthia C., Gusella, James F., Turecki, Gustavo, Stavropoulos, Dimitri J., Sullivan, Patrick F., Scherer, Stephen W., Talkowski, Michael E., and Ernst, Carl

Published
2017
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