8 results on '"Alemany S"'
Search Results
2. A genome-wide association study of attention function in a population-based sample of children
- Author
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Alemany S, Vilor-Tejedor N, Bustamante M, Pujol J, Macià D, Martínez-Vilavella G, Fenoll R, Alvárez-Pedrerol M, Forns J, Júlvez J, Suades-González E, Llop S, Rebagliato M, and Sunyer J
- Abstract
Background Attention function filters and selects behaviorally relevant information. This capacity is impaired in some psychiatric disorders and has been proposed as an endophenotype for Attention-Deficit/Hyperactivity Disorder; however, its genetic basis remains largely unknown. This study aimed to identify single nucleotide polymorphism (SNPs) associated with attention function. Materials and Methods The discovery sample included 1655 children (7-12 years) and the replication sample included 546 children (5-8 years). Five attention outcomes were assessed using the computerized Attentional Network Test (ANT): alerting, orienting, executive attention, Hit Reaction time (HRT) and the standard error of HRT (HRTSE). A Genome-wide Association Study was conducted for each outcome. Gene set enrichment analyses were performed to detect biological pathways associated with attention outcomes. Additional neuroimaging analyses were conducted to test neural effects of detected SNPs of interest. Results Thirteen loci showed suggestive evidence of association with attention function (P
- Published
- 2016
3. Cot kinase regulation of IL-2 production in Jurkat T cells
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Sara Ballester, Tobeña, R., Lisbona, C., Calvo, V., and Alemany, S.
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Immunology ,Immunology and Allergy - Abstract
tpl-2 is a rat gene that encodes a serine/threonine protein kinase that can act as a novel mitogen-activated protein (MAP) kinase kinase kinase. Tpl-2 is activated in Moloney murine leukemia virus-induced rat T lymphomas, due to a truncation in the C-terminal region of the protein. cot is a very closely related gene, if not the human homologue. The truncated form of Cot has been shown to have a higher transforming activity than the nontruncated form. In this paper we show that an increase in truncated Cot kinase expression correlates with an increase in IL-2 production in anti-CD3-treated Jurkat cells. Truncated Cot expression also cooperates with PHA or phorbol 12,13-dibutyrate (PDBu) and calcium ionophore for IL-2 production in Jurkat cells. Both the truncated and nontruncated Cot forms increased IL-2 transcription because they enhanced transcription of a reporter gene linked to the IL-2 promoter. The expression of a dominant negative form of Cot inhibits transcription directed by the IL-2 promoter in Jurkat cells stimulated by PDBu and ionophore. These data suggest a role of Tpl-2/Cot kinase in IL-2 production during T lymphocyte activation and could also explain its role in Moloney murine leukemia virus-induced lymphomagenesis.
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- 1997
4. The catalytic domain of pp56(lck), but not its regulatory domain, is sufficient for inducing IL-2 production
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Ana Carrera, Calvo, V., R -Borlado, L., Paradis, H., Alemany, S., Roberts, T. M., and Martinez-A, C.
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Immunology ,Immunology and Allergy - Abstract
The lymphoid src kinase pp56lck has been shown to be essential for the induction of different T lymphocyte responses, including CD4-mediated enhancement of Ag-induced T cell activation, early T cell differentiation, induction of IL-2 production, and cytotoxicity. It is assumed that pp56lck acts on these processes by phosphorylating substrates. However, it has been recently reported that the NH2 regulatory domain is sufficient to mediate CD4 accessory function. In this report we address the contribution of the regulatory and catalytic domains of pp56lck to another function of this enzyme independent of CD4: TCR-induced IL-2 production. Two pp56lck mutants lacking either the entire catalytic domain or the entire NH2 regulatory domain were generated, and their abilities to trigger transactivation of the TCR-regulated nuclear factor of activated T cells (NF-AT) region of the IL-2 promoter were compared. Only the catalytic, but not the NH2 regulatory, domain of pp56lck was able to induce NF-AT region transactivation on its own and to cooperate with other intracellular signals to trigger this response. Moreover, the catalytic domain of pp56lck was able to induce IL-2 cytokine production to an extent similar to that of wild-type pp56lck. We conclude that different domains of the pp56lck molecule contribute to regulate distinct biologic functions. In fact, while the NH2 regulatory domain is sufficient to mediate CD4 accessory function, we show here that the catalytic domain of pp56lck is sufficient for induction of IL-2 production, mimicking TCR ligation., This work was supported by the CICyT, Pharmacia, Consejo Superiro de Investigaciones Científicas, and the José Carreras International Foundation.
- Published
- 1996
5. Induction of NGFI-B gene expression during T cell activation: Role of protein phosphatases
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Garcia, I., Pipaon, C., Alemany, S., and Ana Perez-Castillo
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Immunology ,Immunology and Allergy - Abstract
mRNA expression of the immediate-early gene NGFI-B was investigated in T cells during the G0/G1 transition as well as throughout the G1 phase. After stimulation of T lymphocytes with Con A or phorbol 12,13 dibutyrate (PDBu), NGFI-B gene expression showed an induction of at least sevenfold within 3 h of stimulation. Twenty-four h later, however, the level of NGFI-B transcripts had fallen to almost basal levels. Activation of the Ca2+ signaling pathway also produced an induction of this gene, although to a lesser extent than the one obtained after protein kinase C activation. Similar transient kinetics of NGFI-B mRNA were also observed after PDBu stimulation of G1 lymphoblasts. However, the induction of NGFI-B by IL-2 is dependent on the presence of cycloheximide. Con A-induced activation of NGFI-B gene expression was not overcome by cyclosporin A or by 8Br-cAMP, but was partially prevented by dexamethasone. In lymphoblasts, okadaic acid caused the induction of NGFI-B gene expression, indicating a role for the serine/threonine protein phosphatases PP1 and PP2A in the regulation of this gene in resting cells. Okadaic acid-induced NGFI-B transcripts were significantly more stable than PDBu-induced NGFI-B mRNA. Thus, the level of NGFI-B transcripts in T cells might be determined by the balance between the activities of several serine/threonine protein kinases and phosphatases. Together, these findings indicate that the transient induction of NGFI-B transcripts is associated with normal lymphocyte activation. Because the mRNA for NGFI-B codes for a zinc-finger DNA-binding protein, these results suggest that NGFI-B participates in transcriptional regulation during T cell activation.
6. Optimization of methods of chondrocyte cell culture from human disc hernia subjects and testing the presence of Toll-like receptor 4 (TLR 4),Optimización de la metodología de cultivo de condrocitos de discos procedentes de hernias discales y comprobación de la presencia del Toll-like receptor 4 (TLR 4)
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Krzyzanowska, A., Cabrerizo, M., Alemany, S., Pablo Munarriz, and Lagares, A.
7. A statistical approach to build 3D prototypes from a 3D anthropometric survey of the Spanish female population
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Ibáñez, M. V., Simó, A., Domingo, J., Durá, E., Guillermo Ayala, Alemany, S., Vinué, G., and Solves, C.
8. Air Pollution Exposure During Pregnancy and Childhood, Apoe Ε4 Status and Alzheimer Polygenic Risk Score, and Brain Structural Morphology in Preadolescents
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Esmée Essers, Anne-Claire Binter, Alexander Neumann, Tonya White, Silvia Alemany, Mònica Guxens, Child and Adolescent Psychiatry / Psychology, Radiology & Nuclear Medicine, Institut Català de la Salut, [Essers E] ISGlobal, Barcelona, Spain. Universitat Pompeu Fabra, Barcelona, Spain. Spanish Consortium for Research on Epidemiology and Public Health (CIBERESP), Instituto de Salud Carlos III, Madrid, Spain. Department of Child and Adolescent Psychiatry/Psychology, Erasmus MC, University Medical Centre, Rotterdam, the Netherlands. [Binter AC] ISGlobal, Barcelona, Spain. Universitat Pompeu Fabra, Barcelona, Spain. Spanish Consortium for Research on Epidemiology and Public Health (CIBERESP), Instituto de Salud Carlos III, Madrid, Spain. [Neumann A] Department of Child and Adolescent Psychiatry/Psychology, Erasmus MC, University Medical Centre, Rotterdam, the Netherlands. Complex Genetics of Alzheimer's Disease Group, VIB Center for Molecular Neurology, VIB, Antwerp, Belgium. Department of Biomedical Sciences, University of Antwerp, Antwerp, Belgium. [White T] Department of Child and Adolescent Psychiatry/Psychology, Erasmus MC, University Medical Centre, Rotterdam, the Netherlands. Department of Radiology and Nuclear Medicine, Erasmus Medical Centre, Rotterdam, the Netherlands. [Alemany S] Unitat de Genètica Psiquiàtrica, Grup de Recerca de Psiquiatria, Salut Mental i Addiccions, Vall d’Hebron Institut de Recerca (VHIR), Barcelona, Spain. Biomedical Network Research Centre on Mental Health (CIBERSAM), Barcelona, Spain. Departament de Psiquiatria i Medicina Forense, Universitat Autònoma de Barcelona, Bellaterra, Spain. [Guxens M] ISGlobal, Barcelona, Spain. Universitat Pompeu Fabra, Barcelona, Spain. Department of Child and Adolescent Psychiatry/Psychology, Erasmus MC, University Medical Centre, Rotterdam, the Netherlands, and Vall d'Hebron Barcelona Hospital Campus
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Genetic modifiers ,Nervous System Diseases::Central Nervous System Diseases::Brain Diseases::Dementia::Alzheimer Disease [DISEASES] ,Multifactorial Inheritance ,History ,Polymers and Plastics ,Neurodevelopment ,Embaràs ,Reproductive and Urinary Physiological Phenomena::Reproductive Physiological Phenomena::Reproduction::Pregnancy [PHENOMENA AND PROCESSES] ,Apolipoprotein E4 ,Neuroimaging ,Biochemistry ,Environmental pollution ,Industrial and Manufacturing Engineering ,fenómenos fisiológicos reproductivos y urinarios::fenómenos fisiológicos de la reproducción::reproducción::embarazo [FENÓMENOS Y PROCESOS] ,Pregnancy ,Alzheimer Disease ,Risk Factors ,Air Pollution ,Other subheadings::Other subheadings::/genetics [Other subheadings] ,Humans ,Business and International Management ,Child ,Biology ,Aire - Contaminació - Aspectes ambientals ,General Environmental Science ,SDG 15 - Life on Land ,Air Pollutants ,Otros calificadores::Otros calificadores::/genética [Otros calificadores] ,salud ambiental::aire::contaminación del aire [SALUD PÚBLICA] ,Brain ,Environmental Health::Air::Air Pollution [PUBLIC HEALTH] ,Chemistry ,Alzheimer, Malaltia d' - Aspectes genètics ,enfermedades del sistema nervioso::enfermedades del sistema nervioso central::enfermedades cerebrales::demencia::enfermedad de Alzheimer [ENFERMEDADES] ,Female ,Apolipoprotein E ,Human medicine ,Cohort study - Abstract
Apolipoprotein E; Genetic modifiers; Neurodevelopment Apolipoproteïna E; Modificadors genètics; Neurodesenvolupament Apolipoproteína E; Modificadores genéticos; Neurodesarrollo Background Air pollution exposure is associated with impaired neurodevelopment, altered structural brain morphology in children, and neurodegenerative disorders. Differential susceptibility to air pollution may be influenced by genetic features. Objectives To evaluate whether the apolipoprotein E (APOE) genotype or the polygenic risk score (PRS) for Alzheimer's Disease (AD) modify the association between air pollution exposure during pregnancy and childhood and structural brain morphology in preadolescents. Methods We included 1186 children from the Generation R Study. Concentrations of fourteen air pollutants were calculated at participants’ home addresses during pregnancy and childhood using land-use-regression models. Structural brain images were collected at age 9–12 years to assess cortical and subcortical brain volumes. APOE status and PRS for AD were examined as genetic modifiers. Linear regression models were used to conduct single-pollutant and multi-pollutant (using the Deletion/Substitution/Addition algorithm) analyses with a two-way interaction between air pollution and each genetic modifier. Results Higher pregnancy coarse particulate matter (PMcoarse) and childhood polycyclic aromatic hydrocarbons exposure was differentially associated with larger cerebral white matter volume in APOE ε4 carriers compared to non-carriers (29,485 mm3 (95% CI 6,189; 52,781) and 18,663 mm3 (469; 36,856), respectively). Higher pregnancy PMcoarse exposure was differentially associated with larger cortical grey matter volume in children with higher compared to lower PRS for AD (19436 mm3 (825, 38,046)). Discussion APOE status and PRS for AD possibly modify the association between air pollution exposure and brain structural morphology in preadolescents. Higher air pollution exposure is associated with larger cortical volumes in APOE ε4 carriers and children with a high PRS for AD. This is in line with typical brain development, suggesting an antagonistic pleiotropic effect of these genetic features (i.e., protective effect in early-life, but neurodegenerative effect in adulthood). However, we cannot discard chance findings. Future studies should evaluate trajectorial brain development using a longitudinal design. The Generation R Study is conducted by the Erasmus Medical Center in close collaboration with the Faculty of Social Sciences of the Erasmus University Rotterdam, the Municipal Health Service Rotterdam area, Rotterdam, the Rotterdam Homecare Foundation, Rotterdam, and the Stichting Trombosedienst & Artsenlaboratorium Rijnmond (STAR-MDC), Rotterdam. We gratefully acknowledge the contribution of children and parents, general practitioners, hospitals, midwives, and pharmacies in Rotterdam. The general design of the Generation R Study is made possible by financial support from the Erasmus Medical Center, Rotterdam; the Erasmus University Rotterdam; the Netherlands Organization for Health Research and Development (ZonMw); the Netherlands Organization for Scientific Research (NWO); and the Ministry of Health, Welfare and Sport. A.N. was supported by a grant of the Dutch Ministry of Education, Culture, and Science and the Netherlands Organization for Scientific Research (024.001.003, Consortium on Individual Development), a grant of the Canadian Institutes of Health Research team, and by the Research Foundation Flanders (FWO). S.A. was supported by the Programa Talen_UAB-Banc de Santander. The geocodification of the addresses of the study participants and the air pollution estimations were done within the framework of a project funded by the Health Effects Institute (HEI) (Assistance Award No. R-82811201). We received funding from the Spanish Institute of Health Carlos III (CPII18/00018), the EU Commission (733,206, 824,989), and the Agence Nationale de Securite Sanitaire de l’Alimentation de l’Environnement et du Travail (EST-18 RF-25). We acknowledge support from the Spanish Ministry of Science and Innovation and State Research Agency through the “Centro de Excelencia Severo Ochoa 2019–2023” Program (CEX2018-000806-S), and support from the Generalitat de Catalunya through the CERCA Program”.
- Published
- 2022
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