Search

Your search keyword '"Rivera, Margarita"' showing total 512 results
Start Over Author "Rivera, Margarita"
512 results on '"Rivera, Margarita"'

151. Morphology-controlled silicon oxide particles produced by red wiggler worms

Author

Torres, Maykel González, primary, Muñoz, Susana Vargas, additional, Martínez, Andrea Ruíz, additional, Hernández, Valentina Segovia, additional, Saucedo, Alejandra Vargas, additional, Cervantes, Eric Reyes, additional, Talavera, Rogelio Rodríguez, additional, Rivera, Margarita, additional, and del Pilar Carreón Castro, María, additional

Published
2017
Full Text
View/download PDF

152. The VAL66MET Bdnf Genetic Polymorphism Does Not Modify The Association Between Major Depression And Body Mass Index (BMI)

Author

Rivera, Margarita, primary, Rovira, Paula, additional, Cervilla, Jorge, additional, Ching-López, Ana, additional, Victoria Martín-Laguna, María, additional, Bandrés-Ciga, Sara, additional, Molina, Esther, additional, Ruiz-Pérez, Isabel, additional, Rodríguez-Barranco, Miguel, additional, Aneiros, Germán, additional, and Gutiérrez, Blanca, additional

Published
2017
Full Text
View/download PDF

155. Comorbid Medical Conditions In Individuals With Major Psychiatric Disorders

Author

Rivera, Margarita, primary, Rovira, Paula, additional, Gutierrez, Blanca, additional, Ching-López, Ana, additional, Molina, Esther, additional, Martín-Laguna, María Victoria, additional, Ibanez-Casas, Inmaculada, additional, McKenney, Kathryn, additional, Ruiz-Pérez, Isabel, additional, Rodríguez-Barranco, Miguel, additional, and Cervilla, Jorge, additional

Published
2017
Full Text
View/download PDF

156. Epidemiological support for genetic variability at hypothalamic-pituitary-adrenal axis and serotonergic system as risk factors for major depression

Author

Ching López, Ana, Cervilla, Jorge, Rivera, Margarita, Molina, Esther, McKenney, Kathryn, Ruiz-Perez, Isabel, Rodríguez-Barranco, Miguel, Gutiérrez, Blanca, and Universidad de Sevilla. Departamento de Enfermería

Subjects
Serotonergic system, HPA axis, Major depression, Genetic association analysis
Abstract

Background Major depressive disorder (MDD) is a serious, and common psychiatric disorder worldwide. By the year 2020, MDD will be the second cause of disability in the world. The GranadΣp study is the first, to the best of our knowledge, epidemiological study of mental disorders carried out in Andalusia (South Spain), being one of its main objectives to identify genetic and environmental risk factors for MDD and other major psychiatric disorders. In this study, we focused on the possible association of 91 candidate single nucleotide polymorphisms (SNPs) with MDD. Methods A total of 711 community-based individuals participated in the GranadΣp study. All individuals were extensively assessed for clinical, psychological, sociodemographic, life style, and other environmental variables. A biological sample was also collected for subsequent genetic analyses in 91 candidate SNPs for MDD. DSM-IV diagnosis of MDD was used as the outcome variable. Logistic regression analysis assuming an additive genetic model was performed to test the association between MDD and the genetic data. The experiment-wide significance threshold adjusted with the SNP spectral decomposition method provided a maximum P-value (8×10−3) required to identify an association. Haplotype analyses were also performed. Results One SNP (rs623580) located in the tryptophan hydroxylase 1 gene (TPH1; chromosome 11), one intergenic variant (rs9526236) upstream of the 5-hydroxytryptamine receptor 2A gene (HTR2A; chromosome 13), and five polymorphisms (rs17689966, rs173365, rs7209436, rs110402, and rs242924) located in the corticotropin-releasing hormone receptor 1 gene (CRHR1; chromosome 17), all showed suggestive trends for association with MDD (P

Published
2015

162. Epidemiological support for genetic variability at hypothalamic-pituitary-adrenal axis and serotonergic system as risk factors for major depression

Author

Universidad de Sevilla. Departamento de Enfermería, Ching López, Ana, Cervilla, Jorge, Rivera, Margarita, Molina, Esther, McKenney, Kathryn, Ruiz-Perez, Isabel, Rodríguez-Barranco, Miguel, Gutiérrez, Blanca, Universidad de Sevilla. Departamento de Enfermería, Ching López, Ana, Cervilla, Jorge, Rivera, Margarita, Molina, Esther, McKenney, Kathryn, Ruiz-Perez, Isabel, Rodríguez-Barranco, Miguel, and Gutiérrez, Blanca

Abstract

Background Major depressive disorder (MDD) is a serious, and common psychiatric disorder worldwide. By the year 2020, MDD will be the second cause of disability in the world. The GranadΣp study is the first, to the best of our knowledge, epidemiological study of mental disorders carried out in Andalusia (South Spain), being one of its main objectives to identify genetic and environmental risk factors for MDD and other major psychiatric disorders. In this study, we focused on the possible association of 91 candidate single nucleotide polymorphisms (SNPs) with MDD. Methods A total of 711 community-based individuals participated in the GranadΣp study. All individuals were extensively assessed for clinical, psychological, sociodemographic, life style, and other environmental variables. A biological sample was also collected for subsequent genetic analyses in 91 candidate SNPs for MDD. DSM-IV diagnosis of MDD was used as the outcome variable. Logistic regression analysis assuming an additive genetic model was performed to test the association between MDD and the genetic data. The experiment-wide significance threshold adjusted with the SNP spectral decomposition method provided a maximum P-value (8×10−3) required to identify an association. Haplotype analyses were also performed. Results One SNP (rs623580) located in the tryptophan hydroxylase 1 gene (TPH1; chromosome 11), one intergenic variant (rs9526236) upstream of the 5-hydroxytryptamine receptor 2A gene (HTR2A; chromosome 13), and five polymorphisms (rs17689966, rs173365, rs7209436, rs110402, and rs242924) located in the corticotropin-releasing hormone receptor 1 gene (CRHR1; chromosome 17), all showed suggestive trends for association with MDD (P<0.05). Within CRHR1 gene, the TATGA haplotype combination was found to increase significantly the risk for MDD with an odds ratio =1.68 (95% CI: 1.16–2.42, P=0.006). Conclusion Although limited, perhaps due to insufficient sample size power, our results seem to support th

Published
2015

163. Molecular signatures of major depression.

Author

Cai, Na, Cai, Na, Chang, Simon, Li, Yihan, Li, Qibin, Hu, Jingchu, Liang, Jieqin, Song, Li, Kretzschmar, Warren, Gan, Xiangchao, Nicod, Jerome, Rivera, Margarita, Deng, Hong, Du, Bo, Li, Keqing, Sang, Wenhu, Gao, Jingfang, Gao, Shugui, Ha, Baowei, Ho, Hung-Yao, Hu, Chunmei, Hu, Jian, Hu, Zhenfei, Huang, Guoping, Jiang, Guoqing, Jiang, Tao, Jin, Wei, Li, Gongying, Li, Kan, Li, Yi, Li, Yingrui, Li, Youhui, Lin, Yu-Ting, Liu, Lanfen, Liu, Tiebang, Liu, Ying, Liu, Yuan, Lu, Yao, Lv, Luxian, Meng, Huaqing, Qian, Puyi, Sang, Hong, Shen, Jianhua, Shi, Jianguo, Sun, Jing, Tao, Ming, Wang, Gang, Wang, Guangbiao, Wang, Jian, Wang, Linmao, Wang, Xueyi, Wang, Xumei, Yang, Huanming, Yang, Lijun, Yin, Ye, Zhang, Jinbei, Zhang, Kerang, Sun, Ning, Zhang, Wei, Zhang, Xiuqing, Zhang, Zhen, Zhong, Hui, Breen, Gerome, Wang, Jun, Marchini, Jonathan, Chen, Yiping, Xu, Qi, Xu, Xun, Mott, Richard, Huang, Guo-Jen, Kendler, Kenneth, Flint, Jonathan, Cai, Na, Cai, Na, Chang, Simon, Li, Yihan, Li, Qibin, Hu, Jingchu, Liang, Jieqin, Song, Li, Kretzschmar, Warren, Gan, Xiangchao, Nicod, Jerome, Rivera, Margarita, Deng, Hong, Du, Bo, Li, Keqing, Sang, Wenhu, Gao, Jingfang, Gao, Shugui, Ha, Baowei, Ho, Hung-Yao, Hu, Chunmei, Hu, Jian, Hu, Zhenfei, Huang, Guoping, Jiang, Guoqing, Jiang, Tao, Jin, Wei, Li, Gongying, Li, Kan, Li, Yi, Li, Yingrui, Li, Youhui, Lin, Yu-Ting, Liu, Lanfen, Liu, Tiebang, Liu, Ying, Liu, Yuan, Lu, Yao, Lv, Luxian, Meng, Huaqing, Qian, Puyi, Sang, Hong, Shen, Jianhua, Shi, Jianguo, Sun, Jing, Tao, Ming, Wang, Gang, Wang, Guangbiao, Wang, Jian, Wang, Linmao, Wang, Xueyi, Wang, Xumei, Yang, Huanming, Yang, Lijun, Yin, Ye, Zhang, Jinbei, Zhang, Kerang, Sun, Ning, Zhang, Wei, Zhang, Xiuqing, Zhang, Zhen, Zhong, Hui, Breen, Gerome, Wang, Jun, Marchini, Jonathan, Chen, Yiping, Xu, Qi, Xu, Xun, Mott, Richard, Huang, Guo-Jen, Kendler, Kenneth, and Flint, Jonathan

Abstract

Adversity, particularly in early life, can cause illness. Clues to the responsible mechanisms may lie with the discovery of molecular signatures of stress, some of which include alterations to an individual's somatic genome. Here, using genome sequences from 11,670 women, we observed a highly significant association between a stress-related disease, major depression, and the amount of mtDNA (p = 9.00 × 10(-42), odds ratio 1.33 [95% confidence interval [CI] = 1.29-1.37]) and telomere length (p = 2.84 × 10(-14), odds ratio 0.85 [95% CI = 0.81-0.89]). While both telomere length and mtDNA amount were associated with adverse life events, conditional regression analyses showed the molecular changes were contingent on the depressed state. We tested this hypothesis with experiments in mice, demonstrating that stress causes both molecular changes, which are partly reversible and can be elicited by the administration of corticosterone. Together, these results demonstrate that changes in the amount of mtDNA and telomere length are consequences of stress and entering a depressed state. These findings identify increased amounts of mtDNA as a molecular marker of MD and have important implications for understanding how stress causes the disease.

Published
2015

164. Inspección eléctrica y lumínica en la Institución Educativa la Victoria

Author

Alarcón Rivera, Margarita Elizabeth, Ramírez Ramírez, Germán Iván, Alarcón Rivera, Margarita Elizabeth, and Ramírez Ramírez, Germán Iván

Abstract

En este trabajo tiene como objetivo hacer una inspección a las redes eléctricas de la institución educativa La Victoria para así detectar anomalías que se encuentren en la instalación, ya que se puede poner en riesgo a las personas y a los equipos que se encuentren conectados a esa red, también se realizara la medición del nivel de iluminación en cada uno de los espacios de puesto de trabajo de la institución. Para la realización de esta inspección se tendrá en cuenta las normas exigidas por la Norma Técnica Colombiana NTC 2050, Reglamento Técnico de Instalaciones Eléctricas RETIE y Reglamento Técnico de Iluminación y Alumbrado Público RETILAP. Esta inspección eléctrica se realizó ya que la institución educativa La Victoria fue construida antes que se exigiera las normas, por esto se decidió hacer este proyecto para que la institución cuente con lo estipula de dicha norma y así pueda cumplir. Adicionalmente se le entregara a la institución educativa La Victoria los planos eléctricos y se anexara fotos, tablas de datos medidos y otros más que dan soporte al trabajo realizado y brindan información más detallada del trabajo realizado.

Published
2015

165. Epidemiological support for genetic variability at hypothalamic–pituitary–adrenal axis and serotonergic system as risk factors for major depression

Author

Ching-López,Ana, Cervilla,Jorge, Rivera,Margarita, Molina,Esther, McKenney,Kathryn, Ruiz-Perez,Isabel, Rodríguez-Barranco,Miguel, Gutiérrez,Blanca, Ching-López,Ana, Cervilla,Jorge, Rivera,Margarita, Molina,Esther, McKenney,Kathryn, Ruiz-Perez,Isabel, Rodríguez-Barranco,Miguel, and Gutiérrez,Blanca

Abstract

Ana Ching-López,1 Jorge Cervilla,1–3 Margarita Rivera,1–3 Esther Molina,4 Kathryn McKenney,2 Isabel Ruiz-Perez,3,5,6 Miguel Rodríguez-Barranco,5 Blanca Gutiérrez1,21Department of Psychiatry, Institute of Neurosciences, School of Medicine, University of Granada, Granada, 2CIBER en Salud Mental (CIBERSAM), University of Granada, Granada, 3Instituto de Investigación Biosanitaria Ibs. Granada, Granada, 4Department of Nursing, University of Seville, Seville, 5Andalusian School of Public Health, Granada, 6CIBER de Epidemiología y Salud Pública (CIBERESP), Granada, SpainBackground: Major depressive disorder (MDD) is a serious, and common psychiatric disorder worldwide. By the year 2020, MDD will be the second cause of disability in the world. The Granad∑p study is the first, to the best of our knowledge, epidemiological study of mental disorders carried out in Andalusia (South Spain), being one of its main objectives to identify genetic and environmental risk factors for MDD and other major psychiatric disorders. In this study, we focused on the possible association of 91 candidate single nucleotide polymorphisms (SNPs) with MDD.Methods: A total of 711 community-based individuals participated in the Granad∑p study. All individuals were extensively assessed for clinical, psychological, sociodemographic, life style, and other environmental variables. A biological sample was also collected for subsequent genetic analyses in 91 candidate SNPs for MDD. DSM-IV diagnosis of MDD was used as the outcome variable. Logistic regression analysis assuming an additive genetic model was performed to test the association between MDD and the genetic data. The experiment-wide significance threshold adjusted with the SNP spectral decomposition method provided a maximum P-value (8×10-3) required to identify an association. Haplotype analyses were also performed.Resu

Published
2015

166. Reduction in the levels of CoQ biosynthetic proteins is related to an increase in lifespan without evidence of hepatic mitohormesis.

Author

Rodríguez-Hidalgo, María, Luna-Sánchez, Marta, Hidalgo-Gutiérrez, Agustín, Barriocanal-Casado, Eliana, Mascaraque, Cristina, Acuña-Castroviejo, Darío, Rivera, Margarita, Escames, Germaine, and López, Luis C.

Abstract

Mitohormesis is an adaptive response induced by a mild mitochondrial stress that promotes longevity and metabolic health in different organisms. This mechanism has been proposed as the cause of the increase in the survival in Coq7+/− (Mclk1+/−) mice, which show hepatic reduction of COQ7, early mitochondrial dysfunction and increased oxidative stress. Our study shows that the lack of COQ9 in Coq9Q95X mice triggers the reduction of COQ7, COQ6 and COQ5, which results in an increase in life expectancy. However, our results reveal that the hepatic CoQ levels are not decreased and, therefore, neither mitochondrial dysfunction or increased oxidative stress are observed in liver of Coq9Q95X mice. These data point out the tissue specific differences in CoQ biosynthesis. Moreover, our results suggest that the effect of reduced levels of COQ7 on the increased survival in Coq9Q95X mice may be due to mitochondrial mechanisms in non-liver tissues or to other unknown mechanisms. [ABSTRACT FROM AUTHOR]

Published
2018
Full Text
View/download PDF

167. A Cross-Sectional Study on the Prevalence and Risk Correlates of Mental Disorders: The GRANADΣP Study.

Author

Cervilla, Jorge A., Gutiérrez, Blanca, Rodríguez-Barranco, Miguel, Ibanez-Casas, Inmaculada, Pérez-García, Miguel, Valmisa, Eulalio, Carmona, José, Molina, Esther, Moreno-Kustner, Berta, Rivera, Margarita, Lozano, Vanessa, Muñoz-Negro, José Eduardo, Ching, Ana, Guerrero, Margarita, Porras-Segovia, Alejandro, Ruiz-Pérez, Isabel, Gutiérrez, Blanca, Rodríguez-Barranco, Miguel, Pérez-García, Miguel, and Carmona, José

Published
2018
Full Text
View/download PDF

168. Electrochemical deposition of poly[ethylene-dioxythiophene] (PEDOT) films on ITO electrodes for organic photovoltaic cells: control of morphology, thickness, and electronic properties.

Author

Del-Oso, José Alfredo, Frontana-Uribe, Bernardo Antonio, Maldonado, José-Luis, Rivera, Margarita, Tapia-Tapia, Melina, and Roa-Morales, Gabriela

Subjects
PHOTOVOLTAIC cells, ELECTRIC properties of indium tin oxide, ELECTROPOLYMERIZATION, POLYMER films, POLARITY (Chemistry)
Abstract

In this article, controlled changes on morphology, thickness, and band gap of poly[ethylenedioxythiophene] (PEDOT) polymer films fabricated by electrochemical polymerization (potentiostatically) are analyzed. Electropolymerization of the monomer ethylenedioxythiophene (EDOT) was carried out on indium tin oxide (ITO) electrodes, in different dry organic electrolytic media, such as acetonitrile, acetonitrile-dichloromethane, and toluene-acetonitrile mixtures. It was found that electropolymerization kinetics can be controlled by changing the polarity of the electrolytic media, and kinetics is slower for those with low polarity. This fact combined with an accurate control of EDOT monomer concentration and electropolymerization at Epeak/2 potential, allows to control the morphology and thickness of the electropolymerized PEDOT films (E-PEDOT:ClO4); toluene/ACN (4:1, v/v) and [EDOT] = 0.3 mM gave the best films for application in organic photovoltaic (OPV) cells. The performance of the E-PEDOT:ClO4 films was tested on ITO electrodes as anode buffer layer in OPV cells with the configuration ITO/E-PEDOT:ClO4/P3HT:PC61BM/Field’s metal, where Field’s metal (cathode) is a eutectic alloy that lets to fabricate OPV devices easily and in a fast and economical way at free vacuum conditions. The performance of these devices was compared with an OPV device constructed with a buffer layer anode, prepared using the classical spin coating of PEDOT:PSS on ITO. Results showed that OPV cells fabricated with E-PEDOT:ClO4 have a slightly increased PV performance. [ABSTRACT FROM AUTHOR]

Published
2018
Full Text
View/download PDF

169. Genetic Association of Major Depression With Atypical Features and Obesity-Related Immunometabolic Dysregulations.

Author

Milaneschi, Yuri, Lamers, Femke, Peyrot, Wouter J., Baune, Bernhard T., Breen, Gerome, Dehghan, Abbas, Forstner, Andreas J., Grabe, Hans J., Homuth, Georg, Kan, Carol, Lewis, Cathryn, Mullins, Niamh, Nauck, Matthias, Pistis, Giorgio, Preisig, Martin, Rivera, Margarita, Rietschel, Marcella, Streit, Fabian, Strohmaier, Jana, and Teumer, Alexander

Subjects
MENTAL depression, OBESITY, BODY mass index, C-reactive protein, MENTAL health services, DIAGNOSIS of mental depression, OBESITY & psychology, COMPARATIVE studies, DESIRE, DISEASE susceptibility, INTERNATIONAL relations, RESEARCH methodology, MEDICAL cooperation, CLASSIFICATION of mental disorders, PSYCHOLOGICAL tests, RESEARCH, RESEARCH funding, WEIGHT gain, EVALUATION research, SEQUENCE analysis, DIAGNOSIS
Abstract

Importance: The association between major depressive disorder (MDD) and obesity may stem from shared immunometabolic mechanisms particularly evident in MDD with atypical features, characterized by increased appetite and/or weight (A/W) during an active episode.Objective: To determine whether subgroups of patients with MDD stratified according to the A/W criterion had a different degree of genetic overlap with obesity-related traits (body mass index [BMI] and levels of C-reactive protein [CRP] and leptin).Design, Setting, and Patients: This multicenter study assembled genome-wide genotypic and phenotypic measures from 14 data sets of the Psychiatric Genomics Consortium. Data sets were drawn from case-control, cohort, and population-based studies, including 26 628 participants with established psychiatric diagnoses and genome-wide genotype data. Data on BMI were available for 15 237 participants. Data were retrieved and analyzed from September 28, 2015, through May 20, 2017.Main Outcomes and Measures: Lifetime DSM-IV MDD was diagnosed using structured diagnostic instruments. Patients with MDD were stratified into subgroups according to change in the DSM-IV A/W symptoms as decreased or increased.Results: Data included 11 837 participants with MDD and 14 791 control individuals, for a total of 26 628 participants (59.1% female and 40.9% male). Among participants with MDD, 5347 (45.2%) were classified in the decreased A/W and 1871 (15.8%) in the increased A/W subgroups. Common genetic variants explained approximately 10% of the heritability in the 2 subgroups. The increased A/W subgroup showed a strong and positive genetic correlation (SE) with BMI (0.53 [0.15]; P = 6.3 × 10-4), whereas the decreased A/W subgroup showed an inverse correlation (-0.28 [0.14]; P = .06). Furthermore, the decreased A/W subgroup had a higher polygenic risk for increased BMI (odds ratio [OR], 1.18; 95% CI, 1.12-1.25; P = 1.6 × 10-10) and levels of CRP (OR, 1.08; 95% CI, 1.02-1.13; P = 7.3 × 10-3) and leptin (OR, 1.09; 95% CI, 1.06-1.12; P = 1.7 × 10-3).Conclusions and Relevance: The phenotypic associations between atypical depressive symptoms and obesity-related traits may arise from shared pathophysiologic mechanisms in patients with MDD. Development of treatments effectively targeting immunometabolic dysregulations may benefit patients with depression and obesity, both syndromes with important disability. [ABSTRACT FROM AUTHOR]

Published
2017
Full Text
View/download PDF

174. Molecular Signatures of Major Depression

Author

Cai, Na, primary, Chang, Simon, additional, Li, Yihan, additional, Li, Qibin, additional, Hu, Jingchu, additional, Liang, Jieqin, additional, Song, Li, additional, Kretzschmar, Warren, additional, Gan, Xiangchao, additional, Nicod, Jerome, additional, Rivera, Margarita, additional, Deng, Hong, additional, Du, Bo, additional, Li, Keqing, additional, Sang, Wenhu, additional, Gao, Jingfang, additional, Gao, Shugui, additional, Ha, Baowei, additional, Ho, Hung-Yao, additional, Hu, Chunmei, additional, Hu, Jian, additional, Hu, Zhenfei, additional, Huang, Guoping, additional, Jiang, Guoqing, additional, Jiang, Tao, additional, Jin, Wei, additional, Li, Gongying, additional, Li, Kan, additional, Li, Yi, additional, Li, Yingrui, additional, Li, Youhui, additional, Lin, Yu-Ting, additional, Liu, Lanfen, additional, Liu, Tiebang, additional, Liu, Ying, additional, Liu, Yuan, additional, Lu, Yao, additional, Lv, Luxian, additional, Meng, Huaqing, additional, Qian, Puyi, additional, Sang, Hong, additional, Shen, Jianhua, additional, Shi, Jianguo, additional, Sun, Jing, additional, Tao, Ming, additional, Wang, Gang, additional, Wang, Guangbiao, additional, Wang, Jian, additional, Wang, Linmao, additional, Wang, Xueyi, additional, Wang, Xumei, additional, Yang, Huanming, additional, Yang, Lijun, additional, Yin, Ye, additional, Zhang, Jinbei, additional, Zhang, Kerang, additional, Sun, Ning, additional, Zhang, Wei, additional, Zhang, Xiuqing, additional, Zhang, Zhen, additional, Zhong, Hui, additional, Breen, Gerome, additional, Wang, Jun, additional, Marchini, Jonathan, additional, Chen, Yiping, additional, Xu, Qi, additional, Xu, Xun, additional, Mott, Richard, additional, Huang, Guo-Jen, additional, Kendler, Kenneth, additional, and Flint, Jonathan, additional

Published
2015
Full Text
View/download PDF

175. The risk for major depression conferred by childhood maltreatment is multiplied by BDNF and SERT genetic vulnerability: a replication study

Author

Gutiérrez, Blanca, primary, Bellón, Juan Ángel, additional, Rivera, Margarita, additional, Molina, Esther, additional, King, Michael, additional, Marston, Louise, additional, Torres-González, Francisco, additional, Moreno-Küstner, Berta, additional, Moreno-Peral, Patricia, additional, Motrico, Emma, additional, Montón-Franco, Carmen, additional, GildeGómez-Barragán, María Josefa, additional, Sánchez-Celaya, Marta, additional, Díaz-Barreiros, Miguel Ángel, additional, Vicens, Catalina, additional, de Dios Luna, Juan, additional, Nazareth, Irwin, additional, and Cervilla, Jorge, additional

Published
2015
Full Text
View/download PDF

176. A genetic risk score combining 32 SNPs is associated with body mass index and improves obesity prediction in people with major depressive disorder

Author

Hung, Chi-Fa, primary, Breen, Gerome, additional, Czamara, Darina, additional, Corre, Tanguy, additional, Wolf, Christiane, additional, Kloiber, Stefan, additional, Bergmann, Sven, additional, Craddock, Nick, additional, Gill, Michael, additional, Holsboer, Florian, additional, Jones, Lisa, additional, Jones, Ian, additional, Korszun, Ania, additional, Kutalik, Zoltan, additional, Lucae, Susanne, additional, Maier, Wolfgang, additional, Mors, Ole, additional, Owen, Michael J, additional, Rice, John, additional, Rietschel, Marcella, additional, Uher, Rudolf, additional, Vollenweider, Peter, additional, Waeber, Gerard, additional, Craig, Ian W, additional, Farmer, Anne E, additional, Lewis, Cathryn M, additional, Müller-Myhsok, Bertram, additional, Preisig, Martin, additional, McGuffin, Peter, additional, and Rivera, Margarita, additional

Published
2015
Full Text
View/download PDF

179. Cytotoxic effect of Annona cherimola seeds on cell cultures of cervical and breast cancer and chronic myeloid leukemia

Author

Quispe-Mauricio, Angel, Callacondo Riva, David, Rojas-Camayo, Jose, Zavala Curzo, David, Posso Rivera, Margarita C., and Vaisberg Wolach, Abraham J.

Subjects
Annona cherimola, medicinal plant, cáncer, planta medicinal, cytotoxic effect, cancer, efecto citotóxico
Abstract

Introducción: Diversos productos naturales del género Annona han sido utilizados en el tratamiento del cáncer. Annona cherimola posee diversos compuestos puros de sus semillas y tallos que han demostrado actividad antitumoral frente a células de carcinoma nasofaríngeo. Objetivo: Determinar el efecto citotóxico del extracto etanólico de semillas de Annona cherimola en las líneas celulares MCF-7(adenocarcinoma de mama humano), ME-180(carcinoma epidermoide de cervix), K562 (leucemia mieloide crónica) y 3T3 (fibroblastos normales de ratón). Materiales y métodos: Las líneas MCF-7, ME-180, K562 y 3T3, fueron expuestas a cuatro concentraciones del extracto etanólico de semillas de Annona cherimola (0,125, 0,031, 0,008, 0,002mg/mL), asimismo a diferentes concentraciones de 5-fluorouracilo (5-FU) (0,01563, 0,00391, 0,00098, 0,00024mg/mL) y Cisplatino (0,00250, 0,00063, 0,00016, 0,00004mg/mL) como controles positivos. Se hallaron los porcentajes de crecimiento en 48 horas. Luego se determinó la concentración inhibitoria de crecimiento 50 (CI50) mediante correlación lineal, asimismo se obtuvieron los coeficientes de determinación r2 utilizando Microsoft Office Excel 2007. Finalmente se precisó el Índice de Selectividad de cada muestra. Resultados: Los CI50 en μg/mL del extracto etanσlico de semillas de Annona cherimola fueron 9,4(r2 =0,96) para MCF-7; 6,6(r2 =0.99) para ME-180; 2,2(r2 =0,96) para K562 y 29,5(r2 =0,98) para 3T3. Los CI50 de 5-FU fueron 3,4(r2 =0,95) para MCF-7; 3,8(r2 =0,96) para K562 y 0,2(r2 =0,98) para 3T3 y los CI50 del Cisplatino fueron 12,1(r2 =0,96) para MCF-7; 0.1(r2 =0,96) para K562 y 0,3(r2 =0,99) para 3T3. La relación dosis respuesta del extracto para la línea celular 3T3 fue de -0,98 (p

Published
2009

180. An epidemiological survey on personality disorder in Andalusia (the PISMA-ep PD study).

Author

Muñoz-Negro, José Eduardo, Gutiérrez, Blanca, Rivera, Margarita, Molina, Esther, González Díaz, Manuel, Jabalera Ruz, Paula, and Cervilla, Jorge A.

Subjects
*MENTAL illness risk factors, *PERSONALITY disorders, *LIFE change events, *CONFIDENCE intervals, *SOCIAL support, *CROSS-sectional method, *MULTIVARIATE analysis, *CHILD abuse, *IMPULSIVE personality, *INTERVIEWING, *SURVEYS, *RISK assessment, *QUALITY of life, *DESCRIPTIVE statistics, *QUESTIONNAIRES, *STATISTICAL sampling, *ODDS ratio, *COMORBIDITY, *PSYCHOSOCIAL factors
Abstract

Background: Despite a significant clinical and social burden, there is a relative scarcity of epidemiological studies on Personality Disorder (PD). Aim: To determine the current prevalence of PD and the psychosocial correlates associated with this in the Andalusian population. Method: We carried out a cross-sectional population mental-health survey in Andalusia, southern Spain. Thus, 4,518 randomly selected participants were interviewed following sampling using different standard stratification levels. We used the Spanish version of the SAPAS to estimate PD prevalence. In addition, a full battery of other instruments was utilized to explore global functionality, childhood abuse, maltreatment, threatening life events, personality traits (neuroticism, impulsivity and paranoia), medical and psychiatric comorbidities, family history of psychological problems and other potential risk factors for PD. Results: PD prevalence (10.8%; 95% CI [9.8, 11.7]) and ran two different multivariate models for PD. We obtained the highest PD prevalence in those affected by any mental disorder plus those reporting having suffered childhood abuse, particularly sexual abuse. Additional potential risk factors or correlates of PD identified were: younger age, lower levels of functioning, less social support, poorer general health, having suffered maltreatment, threatening life events, higher suicidal risk scores and higher levels of both neuroticism and impulsivity. Conclusions: This study reports PD prevalence and risk correlates in consonance with similar findings reported in other Western populations. However, longitudinal studies are needed to elicit a more thorough group of prospective determinants of PD. [ABSTRACT FROM AUTHOR]

Published
2024
Full Text
View/download PDF

185. Interaction between the gene, body mass index and depression: meta-analysis of 13701 individuals.

Author

Rivera, Margarita, Locke, Adam E., Corre, Tanguy, Czamara, Darina, Wolf, Christiane, Ching-Lopez, Ana, Milaneschi, Yuri, Kloiber, Stefan, Cohen-Woods, Sara, Rucker, James, Aitchison, Katherine J., Bergmann, Sven, Boomsma, Dorret I., Craddock, Nick, Gill, Michael, Holsboer, Florian, Hottenga, Jouke-Jan, Korszun, Ania, Kutalik, Zoltan, and Lucae, Susanne

Subjects
MENTAL depression genetics, OBESITY, BODY mass index, PUBLIC health, META-analysis, ALLELES, MENTAL depression, DISEASE susceptibility, GENETIC polymorphisms, RESEARCH funding, COMORBIDITY, CASE-control method
Abstract

BackgroundDepression and obesity are highly prevalent, and major impacts on public health frequently co-occur. Recently, we reported that having depression moderates the effect of the FTO gene, suggesting its implication in the association between depression and obesity.AimsTo confirm these findings by investigating the FTO polymorphism rs9939609 in new cohorts, and subsequently in a meta-analysis.MethodThe sample consists of 6902 individuals with depression and 6799 controls from three replication cohorts and two original discovery cohorts. Linear regression models were performed to test for association between rs9939609 and body mass index (BMI), and for the interaction between rs9939609 and depression status for an effect on BMI. Fixed and random effects meta-analyses were performed using METASOFT.ResultsIn the replication cohorts, we observed a significant interaction between FTO, BMI and depression with fixed effects meta-analysis (β = 0.12, P = 2.7 × 10-4) and with the Han/Eskin random effects method (P = 1.4 × 10-7) but not with traditional random effects (β = 0.1, P = 0.35). When combined with the discovery cohorts, random effects meta-analysis also supports the interaction (β = 0.12, P = 0.027) being highly significant based on the Han/Eskin model (P = 6.9 × 10-8). On average, carriers of the risk allele who have depression have a 2.2% higher BMI for each risk allele, over and above the main effect of FTOConclusionsThis meta-analysis provides additional support for a significant interaction between FTO, depression and BMI, indicating that depression increases the effect of FTO on BMI. The findings provide a useful starting point in understanding the biological mechanism involved in the association between obesity and depression. [ABSTRACT FROM AUTHOR]

Published
2017
Full Text
View/download PDF

187. Investigating the genetic variation underlying episodicity in major depressive disorder: Suggestive evidence for a bipolar contribution

Author

Ferentinos, Panagiotis, primary, Rivera, Margarita, additional, Ising, Marcus, additional, Spain, Sarah L., additional, Cohen-Woods, Sarah, additional, Butler, Amy W., additional, Craddock, Nicholas, additional, Owen, Michael J., additional, Korszun, Ania, additional, Jones, Lisa, additional, Jones, Ian, additional, Gill, Michael, additional, Rice, John P., additional, Maier, Wolfgang, additional, Mors, Ole, additional, Rietschel, Marcella, additional, Lucae, Susanne, additional, Binder, Elisabeth B., additional, Preisig, Martin, additional, Tozzi, Federica, additional, Muglia, Pierandrea, additional, Breen, Gerome, additional, Craig, Ian W., additional, Farmer, Anne E., additional, Müller-Myhsok, Bertram, additional, McGuffin, Peter, additional, and Lewis, Cathryn M., additional

Published
2014
Full Text
View/download PDF

189. Genome-wide association analyses identify 44 risk variants and refine the genetic architecture of major depression

Author

Wray, Naomi, Ripke, Stephan, Mattheisen, Manuel, Trzaskowski, Maciej, Byrne, Enda, Abdellaoui, Abdel, Adams, Mark, Agerbo, Esben, Air, Tracy, Andlauer, Till, Bacanu, Silviu-Alin, Bækvad-Hansen, Marie, Beekman, Aartjan, Bigdeli, Tim, Binder, Elisabeth, Blackwood, Douglas, Bryois, Julien, Buttenschøn, Henriette, Bybjerg-Grauholm, Jonas, Cai, Na, Castelao, Enrique, Christensen, Jane, Clarke, Toni-Kim, Coleman, Jonathan, Colodro-Conde, Lucía, Couvy-Duchesne, Baptiste, Craddock, Nick, Crawford, Gregory, Crowley, Cheynna, Dashti, Hassan, Davies, Gail, Deary, Ian, Degenhardt, Franziska, Derks, Eske, Direk, Nese, Dolan, Conor, Dunn, Erin, Eley, Thalia, Eriksson, Nicholas, Escott-Price, Valentina, Kiadeh, Farnush, Finucane, Hilary, Forstner, Andreas, Frank, Josef, Gaspar, Héléna, Gill, Michael, Giusti-Rodríguez, Paola, Goes, Fernando, Gordon, Scott, Grove, Jakob, Hall, Lynsey, Hannon, Eilis, Hansen, Christine, Hansen, Thomas, Herms, Stefan, Hickie, Ian, Hoffmann, Per, Homuth, Georg, Horn, Carsten, Hottenga, Jouke-Jan, Hougaard, David, Hu, Ming, Hyde, Craig, Ising, Marcus, Jansen, Rick, Jin, Fulai, Jorgenson, Eric, Knowles, James, Kohane, Isaac, Kraft, Julia, Kretzschmar, Warren, Krogh, Jesper, Kutalik, Zoltán, Lane, Jacqueline, Li, Yihan, Li, Yun, Lind, Penelope, Liu, Xiaoxiao, Lu, Leina, MacIntyre, Donald, MacKinnon, Dean, Maier, Robert, Maier, Wolfgang, Marchini, Jonathan, Mbarek, Hamdi, McGrath, Patrick, McGuffin, Peter, Medland, Sarah, Mehta, Divya, Middeldorp, Christel, Mihailov, Evelin, Milaneschi, Yuri, Milani, Lili, Mill, Jonathan, Mondimore, Francis, Montgomery, Grant, Mostafavi, Sara, Mullins, Niamh, Nauck, Matthias, Ng, Bernard, Nivard, Michel, Nyholt, Dale, O’Reilly, Paul, Oskarsson, Hogni, Owen, Michael, Painter, Jodie, Pedersen, Carsten, Pedersen, Marianne, Peterson, Roseann, Pettersson, Erik, Peyrot, Wouter, Pistis, Giorgio, Posthuma, Danielle, Purcell, Shaun, Quiroz, Jorge, Qvist, Per, Rice, John, Riley, Brien, Rivera, Margarita, Saeed Mirza, Saira, Saxena, Richa, Schoevers, Robert, Schulte, Eva, Shen, Ling, Shi, Jianxin, Shyn, Stanley, Sigurdsson, Engilbert, Sinnamon, Grant, Smit, Johannes, Smith, Daniel, Stefansson, Hreinn, Steinberg, Stacy, Stockmeier, Craig, Streit, Fabian, Strohmaier, Jana, Tansey, Katherine, Teismann, Henning, Teumer, Alexander, Thompson, Wesley, Thomson, Pippa, Thorgeirsson, Thorgeir, Tian, Chao, Traylor, Matthew, Treutlein, Jens, Trubetskoy, Vassily, Uitterlinden, André, Umbricht, Daniel, Van der Auwera, Sandra, van Hemert, Albert, Viktorin, Alexander, Visscher, Peter, Wang, Yunpeng, Webb, Bradley, Weinsheimer, Shantel, Wellmann, Jürgen, Willemsen, Gonneke, Witt, Stephanie, Wu, Yang, Xi, Hualin, Yang, Jian, Zhang, Futao, Arolt, Volker, Baune, Bernhard, Berger, Klaus, Boomsma, Dorret, Cichon, Sven, Dannlowski, Udo, de Geus, E., DePaulo, J., Domenici, Enrico, Domschke, Katharina, Esko, Tõnu, Grabe, Hans, Hamilton, Steven, Hayward, Caroline, Heath, Andrew, Hinds, David, Kendler, Kenneth, Kloiber, Stefan, Lewis, Glyn, Li, Qingqin, Lucae, Susanne, Madden, Pamela, Magnusson, Patrik, Martin, Nicholas, McIntosh, Andrew, Metspalu, Andres, Mors, Ole, Mortensen, Preben, Müller-Myhsok, Bertram, Nordentoft, Merete, Nöthen, Markus, O’Donovan, Michael, Paciga, Sara, Pedersen, Nancy, Penninx, Brenda, Perlis, Roy, Porteous, David, Potash, James, Preisig, Martin, Rietschel, Marcella, Schaefer, Catherine, Schulze, Thomas, Smoller, Jordan, Stefansson, Kari, Tiemeier, Henning, Uher, Rudolf, Völzke, Henry, Weissman, Myrna, Werge, Thomas, Winslow, Ashley, Lewis, Cathryn, Levinson, Douglas, Breen, Gerome, Børglum, Anders, and Sullivan, Patrick

Abstract

Major depressive disorder (MDD) is a common illness accompanied by considerable morbidity, mortality, costs, and heightened risk of suicide. We conducted a genome-wide association meta-analysis based in 135,458 cases and 344,901 controls and identified 44 independent and significant loci. The genetic findings were associated with clinical features of major depression and implicated brain regions exhibiting anatomical differences in cases. Targets of antidepressant medications and genes involved in gene splicing were enriched for smaller association signal. We found important relationships of genetic risk for major depression with educational attainment, body mass, and schizophrenia: lower educational attainment and higher body mass were putatively causal, whereas major depression and schizophrenia reflected a partly shared biological etiology. All humans carry lesser or greater numbers of genetic risk factors for major depression. These findings help refine the basis of major depression and imply that a continuous measure of risk underlies the clinical phenotype. A genome-wide association meta-analysis of individuals with clinically assessed or self-reported depression identifies 44 independent risk loci. Comparisons with other psychiatric disorders and candidate gene analyses provide new insights into major depressive disorder.

Published
2018
Full Text
View/download PDF

195. Structural and morphological studies of meso-ethylcarbazole F-BODIPY thin films.

Author

Corona-Sánchez, Ricardo, Arcos-Ramos, Rafael, Maldonado-Domínguez, Mauricio, Amelines-Sarria, Oscar, Jerezano-Domínguez, Alberto, García-Ortega, Héctor, Rivera, Margarita, Pilar Carreón-Castro, María, and Farfán, Norberto

Abstract

In this work, we describe the synthesis of meso-(9-ethyl-9 H-carbazol-3-yl)-4,4-difluoro-4-bora-3a,4a-diaza- s-indacene and its incorporation as thin film by vapor deposition on indium tin oxide. The morphology of the film was analyzed by scanning electron microscopy and atomic force microscopy showing a granular and homogeneous structure, contact angle measurements revealed that this film exhibits a hydrophobic surface. Packing of the compound was simulated through molecular dynamics and Monte Carlo sampling, and the electronic features of aggregates were modeled with plane-wave DFT. A semiconductor behavior for the featured compound in aggregated state, which compares well with systems applied on electronic devices, is predicted for the featured F-BODIPY. Graphical Abstract: [ABSTRACT FROM AUTHOR]

Published
2016
Full Text
View/download PDF

196. Immune signatures and disorder-specific patterns in a cross-disorder gene expression analysis.

Author

de Jong, Simone, Newhouse, Stephen J., Patel, Hamel, Lee, Sanghyuck, Dempster, David, Curtis, Charles, Paya-Cano, Jose, Murphy, Declan, Wilson, C. Ellie, Horder, Jamie, Mendez, M. Andreina, Asherson, Philip, Rivera, Margarita, Costello, Helen, Maltezos, Stefanos, Whitwell, Susannah, Pitts, Mark, Tye, Charlotte, Ashwood, Karen L., and Bolton, Patrick

Subjects
GENE expression, AUTISM spectrum disorders, ATTENTION-deficit hyperactivity disorder, PATHOLOGICAL physiology, MOLECULAR genetics, MENTAL depression, DISEASE susceptibility, RESEARCH funding, CASE-control method, GENE expression profiling, DISEASE complications
Abstract

Background: Recent studies point to overlap between neuropsychiatric disorders in symptomatology and genetic aetiology.Aims: To systematically investigate genomics overlap between childhood and adult attention-deficit hyperactivity disorder (ADHD), autism spectrum disorder (ASD) and major depressive disorder (MDD).Method: Analysis of whole-genome blood gene expression and genetic risk scores of 318 individuals. Participants included individuals affected with adult ADHD (n = 93), childhood ADHD (n = 17), MDD (n = 63), ASD (n = 51), childhood dual diagnosis of ADHD-ASD (n = 16) and healthy controls (n = 78).Results: Weighted gene co-expression analysis results reveal disorder-specific signatures for childhood ADHD and MDD, and also highlight two immune-related gene co-expression modules correlating inversely with MDD and adult ADHD disease status. We find no significant relationship between polygenic risk scores and gene expression signatures.Conclusions: Our results reveal disorder overlap and specificity at the genetic and gene expression level. They suggest new pathways contributing to distinct pathophysiology in psychiatric disorders and shed light on potential shared genomic risk factors. [ABSTRACT FROM AUTHOR]

Published
2016
Full Text
View/download PDF

198. Genome-Wide Association Study of Major Recurrent Depression in the U.K. Population

Author

Lewis, Cathryn M., primary, Ng, Mandy Y., additional, Butler, Amy W., additional, Cohen-Woods, Sarah, additional, Uher, Rudolf, additional, Pirlo, Katrina, additional, Weale, Michael E., additional, Schosser, Alexandra, additional, Paredes, Ursula M., additional, Rivera, Margarita, additional, Craddock, Nicholas, additional, Owen, Mike J., additional, Jones, Lisa, additional, Jones, Ian, additional, Korszun, Ania, additional, Aitchison, Katherine J., additional, Shi, Jianxin, additional, Quinn, John P., additional, MacKenzie, Alasdair, additional, Vollenweider, Peter, additional, Waeber, Gerard, additional, Heath, Simon, additional, Lathrop, Mark, additional, Muglia, Pierandrea, additional, Barnes, Michael R., additional, Whittaker, John C., additional, Tozzi, Federica, additional, Holsboer, Florian, additional, Preisig, Martin, additional, Farmer, Anne E., additional, Breen, Gerome, additional, Craig, Ian W., additional, and McGuffin, Peter, additional

Published
2010
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results