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52. Mitigación de campo magnético de líneas de transmisión utilizando bucles pasivos

Author

Cadavid, D. R. (Diego Raúl), Ramírez, D. A. (Diego Alejandro), Lopera, F. (Freddy), and Correa, A. F. (Andrés Felipe)

Subjects
MITIGACIÓN DE CAMPO MAGNÉTICO, GENETIC ALGORITHM, MAGNETIC FIELD MITIGATION, TRANSMISSION LINES, LÍNEAS DE TRANSMISIÓN, REI00120, MATERIAL ELECTROMAGNÉTICO, BUCLE PASIVO, ENERGÍA, ENERGY, ALGORITMO GENÉTICO, ELECTRO - MAGNETIC EQUIPMENT, PASSIVE LOOP
Abstract

En este artículo se presenta un método simple para determinar el campo magnético generado por líneas de transmisión. El cálculo del campo magnético tiene en cuenta los efectos de mitigación de bucles pasivos, incluyendo su ubicación óptima en la línea mediante la aplicación de algoritmos genéticos. Los resultados de los cálculos son validados mediante reportes de casos publicados en el IEEE, software de análisis de campo electromagnético y datos experimentales arrojados de una implementación realizada en las líneas de alimentación de las torres de iluminación en un estadio. Luego del análisis, se demuestra la validez del método y la factibilidad de aplicarlo en líneas de transmisión del sistema de potencia. A simple method to determine the magnetic field generated by transmission lines is presented in this paper. The magnetic field calculation takes into account the mitigating effects of passive loops, including their optimal position in the line by applying genetic algorithms. Calculations results are validated by case reports published in the IEEE Transactions, software package for electromagnetic field analysis, and experimental data obtained from an implementation made in the power lines at a stadium lighting tower. After the analysis, the method’s validity and feasibility of its application to transmission lines power systems are demonstrated.

Published
2009

53. Homozygosity of the autosomal dominant Alzheimer disease presenilin 1 E280A mutation

Author

Kosik, K. S., primary, Munoz, C., additional, Lopez, L., additional, Arcila, M. L., additional, Garcia, G., additional, Madrigal, L., additional, Moreno, S., additional, Rios Romenets, S., additional, Lopez, H., additional, Gutierrez, M., additional, Langbaum, J. B., additional, Cho, W., additional, Suliman, S., additional, Tariot, P. N., additional, Ho, C., additional, Reiman, E. M., additional, and Lopera, F., additional

Published
2014
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55. Meta-analysis of genome-wide linkage scans of attention deficit hyperactivity disorder.

Author

Zhou, K., Dempfle, A., Arcos-Burgos, M., Bakker, S.C., Banaschewski, T., Biederman, J., Buitelaar, J.K., Castellanos, F.X., Doyle, A., Ebstein, R.P., Ekholm, J., Forabosco, P., Franke, B., Freitag, C., Friedel, S., Gill, M., Hebebrand, J., Hinney, A., Jacob, C., Lesch, K.P., Loo, S.K., Lopera, F., McCracken, J.T., McGough, J.J., Meyer, J., Mick, E., Miranda, A., Muenke, M., Mulas, F., Nelson, S.F., Nguyen, T.T., Oades, R.D., Ogdie, M.N., Palacio, J.D., Pineda, D., Reif, A., Renner, T.J., Roeyers, H., Romanos, M., Rothenberger, A., Schafer, H., Sergeant, J.A., Sinke, R.J., Smalley, S.L., Sonuga-Barke, E.J.S., Steinhausen, H.C., Meulen, E. van der, Walitza, S., Warnke, A., Lewis, C.M., Faraone, S.V., Asherson, P., Zhou, K., Dempfle, A., Arcos-Burgos, M., Bakker, S.C., Banaschewski, T., Biederman, J., Buitelaar, J.K., Castellanos, F.X., Doyle, A., Ebstein, R.P., Ekholm, J., Forabosco, P., Franke, B., Freitag, C., Friedel, S., Gill, M., Hebebrand, J., Hinney, A., Jacob, C., Lesch, K.P., Loo, S.K., Lopera, F., McCracken, J.T., McGough, J.J., Meyer, J., Mick, E., Miranda, A., Muenke, M., Mulas, F., Nelson, S.F., Nguyen, T.T., Oades, R.D., Ogdie, M.N., Palacio, J.D., Pineda, D., Reif, A., Renner, T.J., Roeyers, H., Romanos, M., Rothenberger, A., Schafer, H., Sergeant, J.A., Sinke, R.J., Smalley, S.L., Sonuga-Barke, E.J.S., Steinhausen, H.C., Meulen, E. van der, Walitza, S., Warnke, A., Lewis, C.M., Faraone, S.V., and Asherson, P.

Abstract

Contains fulltext : 69243.pdf (publisher's version ) (Closed access), 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 (P(SR) = 0.00034, P(OR) = 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

59. 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
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68. C455R notch3 mutation in a Colombian CADASIL kindred with early onset of stroke

Author

Arboleda–Velasquez, J. F., primary, Lopera, F., additional, Lopez, E., additional, Frosch, M. P., additional, Sepulveda–Falla, D., additional, Gutierrez, J. E., additional, Vargas, S., additional, Medina, M., additional, Martinez de Arrieta, C., additional, Lebo, R. V., additional, Slaugenhaupt, S. A., additional, Betensky, R. A., additional, Villegas, A., additional, Arcos–Burgos, M., additional, Rivera, D., additional, Restrepo, J. C., additional, and Kosik, K. S., additional

Published
2002
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69. Presenilin-1-associated abnormalities in regional cerebral perfusion

Author

Johnson, K.A., primary, Lopera, F., additional, Jones, K., additional, Becker, A., additional, Sperling, R., additional, Hilson, J., additional, Londono, J., additional, Siegert, I., additional, Arcos, M., additional, Moreno, S., additional, Madrigal, L., additional, Ossa, J., additional, Pineda, N., additional, Ardila, A., additional, Roselli, M., additional, Albert, M. S., additional, Kosik, K.S., additional, and Rios, A., additional

Published
2001
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71. 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
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72. 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
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77. 3-12-16 A large geographical focus of early onset familial Alzheimer's disease in Antioquia, Colombia

Author

Lopera̧, F., primary, Martínez, A., additional, Madrigal, L., additional, Arango-Viana, J.C., additional, Lemere, C., additional, Arango-Lasprilla, J.C., additional, Hincapié, L., additional, Arcos-Burgos, M., additional, Ossa, J.E., additional, Lendon, C., additional, Goate, A., additional, Ruiz-Linares, A., additional, and Kosik, K., additional

Published
1997
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78. Clinical features of early-onset Alzheimer disease in a large kindred with an E280A presenilis-1 mutation.

Author

Lopera, F, primary, Ardilla, A, additional, Martinez, A, additional, Madrigal, L, additional, Arango-Viana, JC, additional, Lemere, CA, additional, Arango-Lasprilla, JC, additional, Hincapie, L, additional, Arcos-Burgos, M, additional, Ossa, J, additional, Behrens, IM, additional, Norton, J, additional, Lendon, C, additional, Goate, AM, additional, Ruiz-Linares, A, additional, Roselli, MM, additional, and Kosik, KS, additional

Published
1997
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80. 68 Immunocytochemical characterization of plaques, tangles and vascular amyloid in the brains of 2 FAD patients with an identified psi mutation

Author

Lemere, C.A., primary, Lopera, F., additional, Kosikl, K.S., additional, Ossa, J., additional, Saido, T.C., additional, Ruiz, A., additional, Martinez, A., additional, Madrigol, L., additional, Hincapie, L., additional, Arango L., J.C., additional, Selkoe, D.J., additional, and Arango V., J.C., additional

Published
1996
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81. The structure of the presenilin 1 (S182) gene and identification of six novel mutations in early onset AD families

Author

Clark, R.F., primary, Hutton, M., additional, Fuldner, M., additional, Froelich, S., additional, Karran, E., additional, Talbot, C., additional, Crook, R., additional, Lendon, C., additional, Prihar, G., additional, He, C., additional, Korenblat, K., additional, Martinez, A., additional, Wragg, M., additional, Busfield, F., additional, Behrens, M.I., additional, Myers, A., additional, Norton, J., additional, Morris, J., additional, Mehta, N., additional, Pearson, C., additional, Lincoln, S., additional, Baker, M., additional, Duff, K., additional, Zehr, C., additional, Perez-Tur, J., additional, Houlden, H., additional, Ruiz, A., additional, Ossa, J., additional, Lopera, F., additional, Arcos, M., additional, Madrigal, L., additional, Collinge, J., additional, Humphreys, C., additional, Ashworth, A., additional, Sarner, S., additional, Fox, N., additional, Harvey, R., additional, Kennedy, A., additional, Roques, P., additional, Cline, R.T., additional, Philips, C.A., additional, Venter, J.C., additional, Forsell, L., additional, Axelman, K., additional, Lilius, L., additional, Johnston, J., additional, Cowburn, R., additional, Viitanen, M., additional, Winblad, B., additional, Kosik, K., additional, Haltia, M., additional, Poyhonen, M., additional, Dickson, D., additional, Mann, D., additional, Neary, D., additional, Snowden, J., additional, Lantos, P., additional, Lannfelt, L., additional, Rossor, M., additional, Roberts, G.W., additional, Adams, M.D., additional, Hardy, J., additional, and Goate, A., additional

Published
1995
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83. Brain potentials reflect residual face processing in a case of prosopagnosia.

Author

Bobes, M.A., Lopera, F., Coma, L. Díaz, Galan, L., Carbonell, F., Bringas, M.L., and Valdés-Sosa, M.

Subjects
*PROSOPAGNOSIA, *AGNOSIA, *FACE perception, *MEMORY, *RECOGNITION (Psychology), *NEUROPSYCHOLOGY
Abstract

Here, ERPs were employed to characterise the residual face processing of FE, a patient with extensive damage to the ventral temporal-occipital cortex and a dense prosopagnosia. Alarge N170 was present in FE and he performed well in tests of face structural processing. Covert recognition of the faces of personal acquaintances was demonstrated with P300 oddball experiments. The onset latency of the P300 effect was normal, indicating fast availability of covert memory. The scalp topography of this component in FE was different from that of the P3b, presenting a centro-frontal maximum. FE also presented larger skin conductance responses to familiar than to unfamiliar faces. The amplitudes of both the single-trial P300s and the SCRs triggered by familiar faces were positively correlated with the degree of person-familiarity that FE had for the poser. He performed at chance when asked to select between the face of a familiar person and that of an unfamiliar person on the basis of explicit recognition, whereas he selected more the previously known face if the forced choice was based on trustworthiness or a vague sense of familiarity. The results suggest that in FE, early face processing was relatively intact and covert recognition was fast. Neural structures involved in the processing of emotional or social cues possibly mediate the covert recognition present in FE. [ABSTRACT FROM AUTHOR]

Published
2004
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84. Nongenetic factors as modifiers of the age of onset of familial Alzheimer's disease.

Author

Mejía S, Giraldo M, Pineda D, Ardila A, Lopera F, Mejía, Silvia, Giraldo, Margarita, Pineda, David, Ardila, Alfredo, and Lopera, Francisco

Abstract

Objective: The purpose of this research was to identify environmental and personal factors that could be related to the variability in the age of onset of familial Alzheimer's disease (FAD) (36-62 years).Methods: A sample was taken of 49 subjects with FAD and with the mutation E280A in the presenilin-1 gene on chromosome 14; the sample was divided into two subgroups: 27 individuals with age of onset of the disease between 36 and 46 years (early onset) and 22 individuals whose disease began between 47 and 62 years (late onset). Information on environmental and personal factors was collected by means of a questionnaire answered by the patients if their clinical condition allowed it, or by their relatives; such information was organized in a categorical way. Comparisons between the two groups for each categorical variable were done by means of the chi-square test. Noncollinear variables that showed statistical significance were included as independent variables in a logistic regression analysis to predict their association with early onset of the disease.Results: Only 5 of the 140 studied variables were different between the two groups in univariate analysis: education, surgical history, type of stressful event, depression, and affective losses. The logistic regression model was constituted by education, depression, and affective losses. High-level education had approximately 15 times more probability of association with an early onset of the disease; both the history of affective losses and depressive symptoms had 4 times more probability of a similar association.Conclusions: The association of high-level education and early onset of the disease could be related to an earlier detection of symptoms, in turn determined by greater intellectual and environmental demands. The occurrence of depression and affective losses has been considered a prodromic manifestation of the disease. Our findings are evidence of high clinical heterogeneity even in a genetically homogeneous group. [ABSTRACT FROM AUTHOR]

Published
2003
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86. Neuropsychological study of familial Alzheimer's disease caused by mutation E280A in the presenilin 1 gene.

Author

Lasprilla JCA, Iglesias J, and Lopera F

Abstract

In Antioquia, Colombia, investigators have recently discovered the largest family with the E280A mutation in the presenilin 1 gene that causes one type of familial Alzheimer's disease (FAD). The current study compares two groups within this family: those diagnosed with Alzheimer's disease (AD) in its early stage (nine subjects) and relatives (carriers) who did not show any signs of dementia (nine subjects). A battery of the following neuropsychological tests was administered to subjects in both groups: the Consortium to Establish a Registry for Alzheimer's Disease (CERAD), a Phonological Verbal Fluency test, the Visual 'A' Cancellation Test, memory of three phrases, the Rey-Osterrieth Complex Figure, and the Trail Making Test Part A. Statistical analyses of the average test scores of each group showed that the AD group scored significantly (p < 0.01 or p < 0.05) lower on 29 of the 43 neuropsychological variables measured (67 percent). Therefore, this specific battery was useful in discriminating subjects with AD from their healthy relatives who are carriers of the disease. The AD group as a whole presented slight dementia with predominant deficits in memory, language, praxis, and attention. This profile is similar to those reported in subjects with sporadic AD in its early stage and confirms the findings found in other neuropsychological studies of subjects with FAD linked to mutations in chromosome 14. [ABSTRACT FROM AUTHOR]

Published
2003
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87. DNA Damage does not Correlate with Amyloid-beta-Plaques and Neurofibrillary Tangles in Familial Alzheimer's Disease Presenilin-1 [E280A] Mutation.

Author

Velez-Pardo, C., Lopera, F., and Jimenez Del Rio, M.

Abstract

Recent studies have shown that the missense mutation in presenilin-1 [E280A] increases deposition of amyloid-beta (Abeta) and neurofibrillary tangle (NFT) formation. Indeed, we only observed 10 out of 48 FAD brain sections displaying TUNEL (+) labeling, and none with the classical apoptotic morphology. These results may indicate that DNA fragmentation is not a generalized phenomenon in early-onset FAD PS1 [E280A] patients or that neuronal cells are dying by a different mechanism of cell death. Taking together these findings suggest that Abeta and NFTs are not per se a causative factor to damage neuronal cells but their damage could be more related with individual neuronal vulnerability and brain aging [ABSTRACT FROM AUTHOR]

Published
2000
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91. C455R notch3mutation in a Colombian CADASIL kindred with early onset of stroke

Author

Arboleda–Velasquez, J. F., Lopera, F., Lopez, E., Frosch, M. P., Sepulveda–Falla, D., Gutierrez, J. E., Vargas, S., Medina, M., Martinez de Arrieta, C., Lebo, R. V., Slaugenhaupt, S. A., Betensky, R. A., Villegas, A., Arcos–Burgos, M., Rivera, D., Restrepo, J. C., and Kosik, K. S.

Abstract

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is caused by mutations in the notch3epidermal growth factor–like repeats. A Colombian kindred carries a novel C455R mutation located in the predicted ligand-binding domain. Stroke occurred in the patients at an unusually early age (median age 31 years) in comparison to the more frequent onset in the fourth decade of life in other CADASIL populations, including a second Colombian kindred with an R1031C mutation.

Published
2002

96. Attention deficit hyperactivity behavioral phenotype dimensions of adults from antioquian families using the Wender-Utah scale -Spanish version | Dimensiones del fenotipo conductual del trastorno por déficit de atención/hiperactividad en adultos de familias antioqueñas utilizando la escala Wender-Utah en español

Author

Trujillo-Orrego, N., Pineda, D. A., Arango, C. P., Puerta, I. C., Lopera, F., Daniel Camilo Aguirre-Acevedo, Hincapié-Henao, L., Pineda-Álvarez, D. E., Arcos-Burgos, M., and Muenke, M.

100. Successful Object Encoding Induces Increased Directed Connectivity in Presymptomatic Early-Onset Alzheimer's Disease

Author

Jf, Ochoa, Jf, Alonso, Je, Duque, Carlos Andrés Tobón, Ma, Mañanas, Lopera F, and Am, Hernández

Subjects
Alzheimer’s disease, autosomal-dominant, electroencephalography, functional neuroimaging, memory encoding, presenilin-1
Abstract

Recent studies report increases in neural activity in brain regions critical to episodic memory at preclinical stages of Alzheimer's disease (AD). Although electroencephalography (EEG) is widely used in AD studies, given its non-invasiveness and low cost, there is a need to translate the findings in other neuroimaging methods to EEG.

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