Search

Your search keyword '"Castellanos, F. X."' showing total 152 results
Start Over Author "Castellanos, F. X."
152 results on '"Castellanos, F. X."'

1. The search behavior of terrestrial mammals

Author

Noonan, M. J., (0000-0003-2765-8147) Martinez Garcia, R., Fleming, C. H., Garcia De Figueiredo, B., Ali, A. H., Attias, N., Belant, J. L., Beyer Jr., D. E., Berteaux, D., Bidner, L. R., Boone, R., Boutin, S., Brito, J., Brown, M., Carter, A., Castellanos, A., Castellanos, F. X., Chitwood, C., Darlington, S., Antonio De La Torre, J., Dekker, J., Deperno, C., Droghini, A., Farhadinia, M., Fennessy, J., Fichtel, C., Ford, A., Gill, R., Goheen, J. R., Gustavo R. Oliveira-Santos, L., Hebblewhite, M., Hodges, K. E., Isbell, L. A., Janssen, R., Kappeler, P., Kays, R., Kaczensky, P., Kauffman, M., Lapoint, S., Alan Lashley, M., Leimgruber, P., Little, A., Macdonald, D. W., Masiaine, S., T. McBride Jr., R., Patricia Medici, E., Mertes, K., Moorman, C., Morato, R. G., Mourão, G., Mueller, T., Neilson, E. W., Pastorini, J., Patterson, B. D., Pereira, J., Petroelje, T. R., Piecora, K., John Power, R., Rachlow, J., Ranglack, D. H., Roshier, D., Safford, K., Scott, D. M., Serrouya, R., Songer, M., Songsasen, N., Stabach, J., Stacy-Dawes, J., Swingen, M. B., Thompson, J., Tucker, M. A., Velilla, M., Yarnell, R. W., Young, J., Fagan, W. F., (0000-0003-0575-6408) Calabrese, J., Noonan, M. J., (0000-0003-2765-8147) Martinez Garcia, R., Fleming, C. H., Garcia De Figueiredo, B., Ali, A. H., Attias, N., Belant, J. L., Beyer Jr., D. E., Berteaux, D., Bidner, L. R., Boone, R., Boutin, S., Brito, J., Brown, M., Carter, A., Castellanos, A., Castellanos, F. X., Chitwood, C., Darlington, S., Antonio De La Torre, J., Dekker, J., Deperno, C., Droghini, A., Farhadinia, M., Fennessy, J., Fichtel, C., Ford, A., Gill, R., Goheen, J. R., Gustavo R. Oliveira-Santos, L., Hebblewhite, M., Hodges, K. E., Isbell, L. A., Janssen, R., Kappeler, P., Kays, R., Kaczensky, P., Kauffman, M., Lapoint, S., Alan Lashley, M., Leimgruber, P., Little, A., Macdonald, D. W., Masiaine, S., T. McBride Jr., R., Patricia Medici, E., Mertes, K., Moorman, C., Morato, R. G., Mourão, G., Mueller, T., Neilson, E. W., Pastorini, J., Patterson, B. D., Pereira, J., Petroelje, T. R., Piecora, K., John Power, R., Rachlow, J., Ranglack, D. H., Roshier, D., Safford, K., Scott, D. M., Serrouya, R., Songer, M., Songsasen, N., Stabach, J., Stacy-Dawes, J., Swingen, M. B., Thompson, J., Tucker, M. A., Velilla, M., Yarnell, R. W., Young, J., Fagan, W. F., and (0000-0003-0575-6408) Calabrese, J.

Abstract

Animals moving through landscapes need to strike a balance between finding sufficient resources to grow and reproduce while minimizing encounters with predators 1,2. Because encounter rates are determined by the average distance over which directed motion persists 1,3–5, this trade-off should be apparent in individuals’ movement. Using GPS data from 1,396 individuals across 62 species of terrestrial mammals, we show how predators maintained directed motion ~7 times longer than for similarly-sized prey, revealing how prey species must trade off search efficiency against predator encounter rates. Individual search strategies were also modulated by resource abundance, with prey species forced to risk higher predator encounter rates when resources were scarce. These findings highlight the interplay between encounter rates and resource availability in shaping broad patterns mammalian movement strategies.

Published
2023

4. The autism brain imaging data exchange: towards a large-scale evaluation of the intrinsic brain architecture in autism

Author

Di Martino, A, Yan, C-G, Li, Q, Denio, E, Castellanos, F X, Alaerts, K, Anderson, J S, Assaf, M, Bookheimer, S Y, Dapretto, M, Deen, B, Delmonte, S, Dinstein, I, Ertl-Wagner, B, Fair, D A, Gallagher, L, Kennedy, D P, Keown, C L, Keysers, C, Lainhart, J E, Lord, C, Luna, B, Menon, V, Minshew, N J, Monk, C S, Mueller, S, Müller, R-A, Nebel, M B, Nigg, J T, O'Hearn, K, Pelphrey, K A, Peltier, S J, Rudie, J D, Sunaert, S, Thioux, M, Tyszka, J M, Uddin, L Q, Verhoeven, J S, Wenderoth, N, Wiggins, J L, Mostofsky, S H, and Milham, M P

Published
2014
Full Text
View/download PDF

6. A common variant of the latrophilin 3 gene, LPHN3, confers susceptibility to ADHD and predicts effectiveness of stimulant medication

Author

Arcos-Burgos, M, Jain, M, Acosta, M T, Shively, S, Stanescu, H, Wallis, D, Domené, S, Vélez, J I, Karkera, J D, Balog, J, Berg, K, Kleta, R, Gahl, W A, Roessler, E, Long, R, Lie, J, Pineda, D, Londoño, A C, Palacio, J D, Arbelaez, A, Lopera, F, Elia, J, Hakonarson, H, Johansson, S, Knappskog, P M, Haavik, J, Ribases, M, Cormand, B, Bayes, M, Casas, M, Ramos-Quiroga, J A, Hervas, A, Maher, B S, Faraone, S V, Seitz, C, Freitag, C M, Palmason, H, Meyer, J, Romanos, M, Walitza, S, Hemminger, U, Warnke, A, Romanos, J, Renner, T, Jacob, C, Lesch, K-P, Swanson, J, Vortmeyer, A, Bailey-Wilson, J E, Castellanos, F X, and Muenke, M

Published
2010
Full Text
View/download PDF

8. A cooperative interaction between LPHN3 and 11q doubles the risk for ADHD

Author

Jain, M, Vélez, J I, Acosta, M T, Palacio, L G, Balog, J, Roessler, E, Pineda, D, Londoño, A C, Palacio, J D, Arbelaez, A, Lopera, F, Elia, J, Hakonarson, H, Seitz, C, Freitag, C M, Palmason, H, Meyer, J, Romanos, M, Walitza, S, Hemminger, U, Warnke, A, Romanos, J, Renner, T, Jacob, C, Lesch, K-P, Swanson, J, Castellanos, F X, Bailey-Wilson, J E, Arcos-Burgos, M, and Muenke, M

Published
2012
Full Text
View/download PDF

18. Castellanos replies

Author

Castellanos, F X, Lau, E, Tayebi, N, Lee, P, Long, R E, Giedd, J N, Sharp, W S, Marsh, W L, Walter, J M, Hamburger, S D, Ginns, E I, Rapoport, J L, and Sidransky, E

Published
1999
Full Text
View/download PDF

21. APOE*E2 allele delays age of onset in PSEN1 E280A Alzheimer’s disease

Author

Vélez, J I, primary, Lopera, F, additional, Sepulveda-Falla, D, additional, Patel, H R, additional, Johar, A S, additional, Chuah, A, additional, Tobón, C, additional, Rivera, D, additional, Villegas, A, additional, Cai, Y, additional, Peng, K, additional, Arkell, R, additional, Castellanos, F X, additional, Andrews, S J, additional, Silva Lara, M F, additional, Creagh, P K, additional, Easteal, S, additional, de Leon, J, additional, Wong, M L, additional, Licinio, J, additional, Mastronardi, C A, additional, and Arcos-Burgos, M, additional

Published
2015
Full Text
View/download PDF

22. Linkage and association analysis of ADHD endophenotypes in extended and multigenerational pedigrees from a genetic isolate

Author

Mastronardi, C A, primary, Pillai, E, additional, Pineda, D A, additional, Martinez, A F, additional, Lopera, F, additional, Velez, J I, additional, Palacio, J D, additional, Patel, H, additional, Easteal, S, additional, Acosta, M T, additional, Castellanos, F X, additional, Muenke, M, additional, and Arcos-Burgos, M, additional

Published
2015
Full Text
View/download PDF

23. Association of the dopamine receptor D4 (DRD4) gene 7-repeat allele with children with attention-deficit/hyperactivity disorder (ADHD): An update

Author

Gornick, M. C., Addington, Anjene, Shaw, P., Bobb, A. J., Sharp, W., Greenstein, D., Arepalli, S., Castellanos, F. X., and Rapoport, J. L.

Subjects
mental disorders
Abstract

Polymorphisms of the dopamine receptor D4 gene DRD4, 11p15.5, have previously been associated with attention‐deficit/hyperactivity disorder (ADHD) [Bobb et al., 2005; Am J Med Genet B Neuropsychiatr Genet 132:109–125; Faraone et al., 2005; Biol Psychiatry 57:1313–1323; Thapar et al., 2005; Hum Mol Genet 14 Spec No. 2:R275‐R282]. As a follow up to a pilot study [see Castellanos et al., 1998; Mol Psychiatry 3:431–434] consisting of 41 probands and 56 controls which found no significant association between the DRD4 7‐repeat allele in exon 3 and ADHD, a greatly expanded study sample (cases n = 166 and controls n = 282) and long term follow‐up (n = 107, baseline mean age n = 9, follow‐up mean age of n = 15) prompted reexamination of this gene. The DRD4 7‐repeat allele was significantly more frequent in ADHD cases than controls (OR = 1.2; P = 0.028). Further, within the ADHD group, the 7‐repeat allele was associated with better cognitive performance (measured by the WISC‐III) (P = 0.013–0.07) as well as a trend for association with better long‐term outcome. This provides further evidence of the role of the DRD4 7‐repeat allele in the etiology of ADHD and suggests that this allele may be associated with a more benign form of the disorder.

Published
2007

25. Meta-analysis of genome-wide linkage scans of attention deficit hyperactivity disorder

Author

Zhou, K., Dempfle, A., Arcos-Burgos, Mauricio, Bakker, S. C., Banaschewski, T., Biederman, J., Buitelaar, J., Castellanos, F. X., Doyle, A., Ebstein, R. P., Zhou, K., Dempfle, A., Arcos-Burgos, Mauricio, Bakker, S. C., Banaschewski, T., Biederman, J., Buitelaar, J., Castellanos, F. X., Doyle, A., and Ebstein, R. P.

Abstract

Genetic contribution to the development of attention deficit hyperactivity disorder (ADHD) is well established. Seven independent genome-wide linkage scans have been performed to map loci that increase the risk for ADHD. Although significant linkage signals were identified in some of the studies, there has been limited replications between the various independent datasets. The current study gathered the results from all seven of the ADHD linkage scans and performed a Genome Scan Meta Analysis (GSMA) to identify the genomic region with most consistent linkage evidence across the studies. Genome-wide significant linkage (PSR = 0.00034, POR = 0.04) was identified on chromosome 16 between 64 and 83 Mb. In addition there are nine other genomic regions from the GSMA showing nominal or suggestive evidence of linkage. All these linkage results may be informative and focus the search for novel ADHD susceptibility genes.

Published
2008

26. Latent class subtyping of attention-deficit/hyperactivity disorder and comorbid conditions

Author

Acosta, M. T., Castellanos, F. X., Bolton, Kelly L., Balog, J., Eagen, P., Nee, L., Janet, Jones, Luis Guillermo, Palacio, Sarampote, C., Russell, H. F., Berg, kate, Arcos-Burgos, Mauricio, Muenke, Maximilian, Acosta, M. T., Castellanos, F. X., Bolton, Kelly L., Balog, J., Eagen, P., Nee, L., Janet, Jones, Luis Guillermo, Palacio, Sarampote, C., Russell, H. F., Berg, kate, Arcos-Burgos, Mauricio, and Muenke, Maximilian

Abstract

Objective: Genetic studies of attention-deficit/hyperactivity disorder (ADHD) generally use discrete DSM-IV subtypes to define diagnostic status. To improve correspondence between phenotypic variance and putative susceptibility genes, multivariate classif

Published
2008

28. The autism brain imaging data exchange: towards a large-scale evaluation of the intrinsic brain architecture in autism

Author

Di Martino, A, primary, Yan, C-G, additional, Li, Q, additional, Denio, E, additional, Castellanos, F X, additional, Alaerts, K, additional, Anderson, J S, additional, Assaf, M, additional, Bookheimer, S Y, additional, Dapretto, M, additional, Deen, B, additional, Delmonte, S, additional, Dinstein, I, additional, Ertl-Wagner, B, additional, Fair, D A, additional, Gallagher, L, additional, Kennedy, D P, additional, Keown, C L, additional, Keysers, C, additional, Lainhart, J E, additional, Lord, C, additional, Luna, B, additional, Menon, V, additional, Minshew, N J, additional, Monk, C S, additional, Mueller, S, additional, Müller, R-A, additional, Nebel, M B, additional, Nigg, J T, additional, O'Hearn, K, additional, Pelphrey, K A, additional, Peltier, S J, additional, Rudie, J D, additional, Sunaert, S, additional, Thioux, M, additional, Tyszka, J M, additional, Uddin, L Q, additional, Verhoeven, J S, additional, Wenderoth, N, additional, Wiggins, J L, additional, Mostofsky, S H, additional, and Milham, M P, additional

Published
2013
Full Text
View/download PDF

31. A cooperative interaction between LPHN3 and 11q doubles the risk for ADHD

Author

Jain, M, primary, Vélez, J I, additional, Acosta, M T, additional, Palacio, L G, additional, Balog, J, additional, Roessler, E, additional, Pineda, D, additional, Londoño, A C, additional, Palacio, J D, additional, Arbelaez, A, additional, Lopera, F, additional, Elia, J, additional, Hakonarson, H, additional, Seitz, C, additional, Freitag, C M, additional, Palmason, H, additional, Meyer, J, additional, Romanos, M, additional, Walitza, S, additional, Hemminger, U, additional, Warnke, A, additional, Romanos, J, additional, Renner, T, additional, Jacob, C, additional, Lesch, K-P, additional, Swanson, J, additional, Castellanos, F X, additional, Bailey-Wilson, J E, additional, Arcos-Burgos, M, additional, and Muenke, M, additional

Published
2011
Full Text
View/download PDF

33. Contribution of LPHN3 to the genetic susceptibility to ADHD in adulthood: a replication study

Author

Ribasés, M., primary, Ramos-Quiroga, J. A., additional, Sánchez-Mora, C., additional, Bosch, R., additional, Richarte, V., additional, Palomar, G., additional, Gastaminza, X., additional, Bielsa, A., additional, Arcos-Burgos, M., additional, Muenke, M., additional, Castellanos, F. X., additional, Cormand, B., additional, Bayés, M., additional, and Casas, M., additional

Published
2010
Full Text
View/download PDF

37. Linkage and association analysis of ADHD endophenotypes in extended and multigenerational pedigrees from a genetic isolate

Author

Mastronardi, C A, Pillai, E, Pineda, D A, Martinez, A F, Lopera, F, Velez, J I, Palacio, J D, Patel, H, Easteal, S, Acosta, M T, Castellanos, F X, Muenke, M, and Arcos-Burgos, M

Abstract

Attention-deficit/hyperactivity disorder (ADHD) is a heritable, chronic, neurodevelopmental disorder with serious long-term repercussions. Despite being one of the most common cognitive disorders, the clinical diagnosis of ADHD is based on subjective assessments of perceived behaviors. Endophenotypes (neurobiological markers that cosegregate and are associated with an illness) are thought to provide a more powerful and objective framework for revealing the underlying neurobiology than syndromic psychiatric classification. Here, we present the results of applying genetic linkage and association analyses to neuropsychological endophenotypes using microsatellite and single nucleotide polymorphisms. We found several new genetic regions linked and/or associated with these endophenotypes, and others previously associated to ADHD, for example, loci harbored in the LPHN3, FGF1, POLR2A, CHRNA4 and ANKFY1 genes. These findings, when compared with those linked and/or associated to ADHD, suggest that these endophenotypes lie on shared pathways. The genetic information provided by this study offers a novel and complementary method of assessing the genetic causes underpinning the susceptibility to behavioral conditions and may offer new insights on the neurobiology of the disorder.

Published
2016
Full Text
View/download PDF

38. APOE*E2 allele delays age of onset in PSEN1 E280A Alzheimer’s disease

Author

Vélez, J I, Lopera, F, Sepulveda-Falla, D, Patel, H R, Johar, A S, Chuah, A, Tobón, C, Rivera, D, Villegas, A, Cai, Y, Peng, K, Arkell, R, Castellanos, F X, Andrews, S J, Silva Lara, M F, Creagh, P K, Easteal, S, de Leon, J, Wong, M L, Licinio, J, Mastronardi, C A, and Arcos-Burgos, M

Abstract

Alzheimer’s disease (AD) age of onset (ADAOO) varies greatly between individuals, with unique causal mutations suggesting the role of modifying genetic and environmental interactions. We analyzed ~50 000 common and rare functional genomic variants from 71 individuals of the ‘Paisa’ pedigree, the world’s largest pedigree segregating a severe form of early-onset AD, who were affected carriers of the fully penetrant E280A mutation in the presenilin-1 (PSEN1) gene. Affected carriers with ages at the extremes of the ADAOO distribution (30s–70s age range), and linear mixed-effects models were used to build single-locus regression models outlining the ADAOO. We identified the rs7412 (APOE*E2 allele) as a whole exome-wide ADAOO modifier that delays ADAOO by ~12 years (β=11.74, 95% confidence interval (CI): 8.07–15.41, P=6.31 × 10−8, PFDR=2.48 × 10−3). Subsequently, to evaluate comprehensively the APOE (apolipoprotein E) haplotype variants (E1/E2/E3/E4), the markers rs7412 and rs429358 were genotyped in 93 AD affected carriers of the E280A mutation. We found that the APOE*E2 allele, and not APOE*E4, modifies ADAOO in carriers of the E280A mutation (β=8.24, 95% CI: 4.45–12.01, P=3.84 × 10−5). Exploratory linear mixed-effects multilocus analysis suggested that other functional variants harbored in genes involved in cell proliferation, protein degradation, apoptotic and immune dysregulation processes (i.e., GPR20, TRIM22, FCRL5, AOAH, PINLYP, IFI16, RC3H1 and DFNA5) might interact with the APOE*E2 allele. Interestingly, suggestive evidence as an ADAOO modifier was found for one of these variants (GPR20) in a set of patients with sporadic AD from the Paisa genetic isolate. This is the first study demonstrating that the APOE*E2 allele modifies the natural history of AD typified by the age of onset in E280A mutation carriers. To the best of our knowledge, this is the largest analyzed sample of patients with a unique mutation sharing uniform environment. Formal replication of our results in other populations and in other forms of AD will be crucial for prediction, follow-up and presumably developing new therapeutic strategies for patients either at risk or affected by AD.

Published
2016
Full Text
View/download PDF

49. [Functional cerebral activity in a state of rest: connectivity networks]

Author

Proal, E., Alvarez-Segura, M., Maria de la Iglesia Vaya, Marti-Bonmati, L., Castellanos, F. X., and Srsn

Subjects
Functional connectivity, Low frequency fluctuations, State of rest, Connectivity networks, Intrinsic cerebral activity, ICA, Spontaneous fluctuations, Functional MRI
Abstract

Functional connectivity can be measured during task-based functional magnetic resonance imaging (fMRI), or in the absence of specific stimuli or tasks. Analyses of fMRI data from statistical, mathematical and physical perspectives have been found to be reliable and reproducible in detecting activated voxels. In a complementary manner, the study of low frequency fluctuations in the BOLD signal recorded during resting state reveals patterns of synchronization which delineate the intrinsic functional architecture of the brain. The scientific community now has available shared resources to accelerate the exploitation of resting state fMRI with the objective of improving diagnostic methods and leading to better treatments grounded in neuroscience.

Catalog

Books, media, physical & digital resources
See catalog results