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196 results on '"Gratacòs M"'

8. Prediabetes is independently associated with subclinical carotid atherosclerosis: An observational study in a non-urban mediterranean population

Author

Vilanova M.B., Franch-Nadal J., Falguera M., Marsal J.R., Canivell S., Rubinat E., Miró N., Molló À., Mata-Cases M., Gratacòs M., Castelblanco E., and Mauricio D.

Subjects
leukocyte count, obesity, systolic blood pressure, hypertension, estimated glomerular filtration rate, carotid intima-media thickness, glucose tolerance, alanine aminotransferase, carotid atherosclerosis, prevalence, tobacco, Article, low density lipoprotein cholesterol, disease burden, male, high density lipoprotein cholesterol, human, glucose, kidney function, hemoglobin A1c, adult, dyslipidemia, creatinine, diastolic blood pressure, echography, arterial wall thickness, waist circumference, major clinical study, female, impaired glucose tolerance, risk factor, diabetes mellitus, observational study, coronary artery disease, prospective study, uric acid blood level
Abstract

This was a prospective, observational study to compare the burden of subclinical atherosclerosis as measured by carotid ultrasonography in a cohort of subjects with prediabetes vs. subjects with normal glucose tolerance (NGT) from a non-urban Mediterranean population. Atherosclerosis was assessed through carotid intima-media thickness (c-IMT), the presence/absence of carotid plaques, and plaque number. Among 550 subjects included, 224 (40.7%) had prediabetes. The mean c-IMT and the prevalence of carotid plaque were significantly higher in the prediabetes group compared to the NGT group (0.72 vs. 0.67 mm, p < 0.001; and 37.9% vs. 19.6%; p < 0.001, respectively). Older age, male gender, and increased systolic blood pressure were positively correlated with c-IMT and were independent predictors of the presence of plaques. In contrast, prediabetes and low-density lipoprotein (LDL)-c were predictors of the presence of plaque (odds ratio [OR] = 1.64; 95% confidence interval [CI] = 1.05–2.57; p = 0.03 and OR = 1.01; 95% CI = 1.00–1.02; p = 0.006, respectively) together with tobacco exposure and the leukocyte count (OR = 1.77; 95% CI = 1.08–2.89; p = 0.023 and OR = 1.20; 95% CI = 1.05–1.38; p = 0.008, respectively). In a non-urban Mediterranean population, prediabetes was associated with established subclinical carotid atherosclerosis. These findings could have implications for the prevention and treatment of CV risk in these subjects before the first symptoms of cardiovascular disease appear. © 2020 by the authors. Licensee MDPI, Basel, Switzerland.

Published
2020

26. Fat mass and obesity-associated gene (FTO) in eating disorders : Evidence for association of the rs9939609 obesity risk allele with Bulimia nervosa and anorexia nervosa

Author

Müller, T.D., Greene, B.H., Bellodi, L., Cavallini, M.C., Cellini, E., di Bella, D., Ehrlich, S., Erzegovesi, S., Estivill, X., Fernández-Aranda, F., Fichter, M., Fleischhaker, C., Scherag, S., Gratacòs, M., Grallert, H., Herpertz-Dahlmann, B., Herzog, W., Illig, T., Lehmkuhl, U., Nacmias, B., Ribasés, M., Ricca, V., Schäfer, H., Scherag, A., Sorbi, S., Wichmann, H.-E., Hebebrand, J., Hinney, A., Universitat de Barcelona, Müller, Td, Greene, Bh, Bellodi, Laura, Cavallini, Mc, Cellini, E, Di Bella, D, Ehrlich, S, Erzegovesi, S, Estivill, X, Fernández Aranda, F, Fichter, M, Fleischhaker, C, Scherag, S, Gratacòs, M, Grallert, H, Herpertz Dahlmann, B, Herzog, W, Illig, T, Lehmkuhl, U, Nacmias, B, Ribasés, M, Ricca, V, Schäfer, H, Scherag, A, Sorbi, S, Wichmann, He, Hebebrand, J, and Hinney, A.

Subjects
Adult, Male, Risk, Anorexia Nervosa, Adolescent, Genotype, Medizin, Alpha-Ketoglutarate-Dependent Dioxygenase FTO, Polymorphism, Single Nucleotide, Young Adult, 610 Medical sciences Medicine, Confidence Intervals, Odds Ratio, Humans, Obesity, Bulímia, Bulimia, Bulimia Nervosa, Child, Trastorns de la conducta alimentària, Alleles, Proteins, Anorèxia nerviosa, Fat Mass And Obesity-associated Gene, Fto, Eating Disorders, Association Study, Anorexia nervosa, Middle Aged, anorexia, Eating disorders, Obesitat, Female
Abstract

Objective: The common single nucleotide polymorphism (SNP) rs9939609 in the fat mass and obesity-associated gene (FTO) is associated with obesity. As genetic variants associated with weight regulation might also be implicated in the etiology of eating disorders, we evaluated whether SNP rs9939609 is associated with bulimia nervosa (BN) and anorexia nervosa (AN). Methods: Association of rs9939609 with BN and AN was assessed in 689 patients with AN, 477 patients with BN, 984 healthy non-population-based controls, and 3,951 population-based controls (KORA-S4). Based on the familial and premorbid occurrence of obesity in patients with BN, we hypothesized an association of the obesity risk A-allele with BN. Results: In accordance with our hypothesis, we observed evidence for association of the rs9939609 A-allele with BN when compared to the non-population-based controls (unadjusted odds ratio (OR) = 1.142, one-sided 95% confidence interval (CI) 1.001-infinity; one-sided p = 0.049) and a trend in the population-based controls (OR = 1.124, one-sided 95% CI 0.932-infinity; one-sided p = 0.056). Interestingly, compared to both control groups, we further detected a nominal association of the rs9939609 A-allele to AN (OR = 1.181, 95% CI 1.027-1.359, two-sided p = 0.020 or OR = 1.673, 95% CI 1.101-2.541, two-sided p = 0.015,). Conclusion: Our data suggest that the obesity-predisposing FTO allele might be relevant in both AN and BN. Copyright (C) 2012 S. Karger GmbH, Freiburg

Published
2012

33. P-708 - Genetic risk factors for interferon-alpha induced depression

Author

Martín-Santos, R., primary, Navinés, R., additional, Udina, M., additional, Giménez, D., additional, Moreno, J., additional, Castellví, P., additional, Langhor, K., additional, Gutiérrez, F., additional, Gómez, E., additional, Gratacòs, M., additional, Valdés, M., additional, and Solà, R., additional

Published
2012
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35. Association of NTRK3 and its interaction with NGF suggest an altered cross-regulation of the neurotrophin signaling pathway in eating disorders

Author

Mercader, J.M., primary, Saus, E., additional, Agüera, Z., additional, Bayés, M., additional, Claudette, B., additional, Carreras, A., additional, de Cid, R., additional, Dierssen, M., additional, Fernández-Aranda, F., additional, Forcano, L., additional, Gorwood, P., additional, Hebebrand, J., additional, Hinney, A., additional, Puig, A., additional, Ribases, M., additional, Gratacòs, M., additional, and Estivill, X., additional

Published
2008
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46. A haplotype of glycogen synthase kinase 3 β is associated with early onset of unipolar major depression.

Author

Saus, E., Soria, V., Escaramís, G., Crespo, J. M., Valero, J., Gutiérrez-Zotes, A., Martorell, L., Viella, E., Menchón, J. M., Estivill, X., Gratacòs, M., and Urretavizcaya, M.

Subjects
AFFECTIVE disorders, GLYCOGEN synthase kinase-3, PATHOLOGICAL physiology, NUCLEOTIDE sequence, MENTAL illness, POLYMERASE chain reaction
Abstract

Recent findings suggest that glycogen synthase kinase 3 β ( GSK3β) may play a role in the pathophysiology and treatment of mood disorders. Various genetic studies have shown the association of GSK3β polymorphisms with different mood disorder phenotypes. We hypothesized that genetic variants in the GSK3β gene could partially underlie the susceptibility to mood disorders. We performed a genetic case-control study of 440 psychiatrically screened control subjects and 445 mood disorder patients [256 unipolar major depressive disorder (MDD) and 189 bipolar disorder (BD)]. We genotyped a set of 11 single nucleotide polymorphisms (SNPs) and determined the relative frequency of a known copy number variant (CNV) overlapping the GSK3β by quantitative real-time polymerase chain reaction (PCR). We found no evidence of association with MDD or BD diagnosis, and we further investigated the age at onset (AAO) of the disorder and severity of depressive index episode. We found that rs334555, located in intron 1 of GSK3β, was nominally associated with an earlier AAO of the disease in MDD ( P = 0.001). We also identified a haplotype containing three SNPs (rs334555, rs119258668 and rs11927974) associated with AAO of the disorder (permutated P = 0.0025). We detected variability for the CNV, but we could not detect differences between patients and controls for any of the explored phenotypes. This study presents further evidence of the contribution of GSK3β to mood disorders, implicating a specific SNP and a haplotype with an earlier onset of the disorder in a group of well-characterized patients with unipolar MDD. Further replication studies in patients with the same phenotypic characteristics should confirm the results reported here. [ABSTRACT FROM AUTHOR]

Published
2010
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48. HMG20A and HMG20B map to human chromosomes 15q24 and 19p13.3 and constitute a distinct class of HMG-box genes with ubiquitous expression.

Author

Sumoy, L., Carim, L., Escarceller, M., Nadal, M., Gratacòs, M., Pujana, M. A., Estivill, X., and Peral, B.

Subjects
HUMAN genetics, GENE expression, NUCLEOTIDE sequence, NUCLEOPROTEINS, HOMOLOGY (Biology), HUMAN gene mapping
Abstract

The HMG box encodes a conserved DNA binding domain found in many proteins and is involved in the regulation of transcription and chromatin conformation. We describe HMG20A and HMG20B, two novel human HMG box-containing genes, discovered within the EURO-IMAGE Consortium full-length cDNA sequencing initiative. The predicted proteins encoded by these two genes are 48.4% identical (73.9% within the HMG domain). The HMG domain of both HMG20 proteins is most similar to that of yeast NHP6A (38% to 42%). Outside of this domain, HMG20 proteins lack any significant homology to other known proteins. We determined the genomic structure and expression pattern of HMG20A and HMG20B. Both genes have several alternative transcripts, expressed almost ubiquitously. HMG20A maps to chromosome 15q24 (near D15S1227) and HMG20B to 19p13.3 (between D19S209 and D19S216). The HMG20 genes define a distinct class of mammalian HMG box genes. Copyright © 2000 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Published
2000
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