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14 results on '"Palatnik, S. A."'

2. No evidence of association between genetic variants of the PDCD1 ligands and SLE

Author

Abelson, A K, Johansson, C M, Kozyrev, S V, Kristjansdottir, H, Gunnarsson, I, Svenungsson, E, Jönsen, A, Lima, G, Scherbarth, H R, Gamron, S, Allievi, A, Palatnik, S A, Alvarellos, A, Paira, S, Graf, C, Guillerón, C, Catoggio, L J, Prigione, C, Battagliotti, C G, Berbotto, G A, García, M A, Perandones, C E, Truedsson, L, Steinsson, K, Sturfelt, G, Pons-Estel, B, and Alarcón-Riquelme, M E

Published
2007
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3. In vitro and ex vivo effect of hyaluronic acid on erythrocyte flow properties

Author

Palatnik S, Volpintesta R, Pistone G, Giorgetti ME, Gennaro AM, Svetaz MJ, Urli L, Luquita A, and Rasia M

Subjects
Medicine
Abstract

Abstract Background Hyaluronic acid (HA) is present in many tissues; its presence in serum may be related to certain inflammatory conditions, tissue damage, sepsis, liver malfunction and some malignancies. In the present work, our goal was to investigate the significance of hyaluronic acid effect on erythrocyte flow properties. Therefore we performed in vitro experiments incubating red blood cells (RBCs) with several HA concentrations. Afterwards, in order to corroborate the pathophysiological significance of the results obtained, we replicated the in vitro experiment with ex vivo RBCs from diagnosed rheumatoid arthritis (RA) patients, a serum HA-increasing pathology. Methods Erythrocyte deformability (by filtration through nucleopore membranes) and erythrocyte aggregability (EA) were tested on blood from healthy donors additioned with purified HA. EA was measured by transmitted light and analyzed with a mathematical model yielding two parameters, the aggregation rate and the size of the aggregates. Conformational changes of cytoskeleton proteins were estimated by electron paramagnetic resonance spectroscopy (EPR). Results In vitro, erythrocytes treated with HA showed increased rigidity index (RI) and reduced aggregability, situation strongly related to the rigidization of the membrane cytoskeleton triggered by HA, as shown by EPR results. Also, a significant correlation (r: 0.77, p < 0.00001) was found between RI and serum HA in RA patients. Conclusions Our results lead us to postulate the hypothesis that HA interacts with the erythrocyte surface leading to modifications in erythrocyte rheological and flow properties, both ex vivo and in vitro.

Published
2010
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4. Erythrocyte aggregation in rheumatoid arthritis: cell and plasma factor’s role

Author

Luquita, A., Urli, L., Svetaz, M. J., Gennaro, Ana Maria, Volpintesta, R., Palatnik, S., and Rasia, M.

Subjects
erythrocyte deformability, Ciencias Biológicas, membrane fluidity, Rheumatoid arthritis activity, erythrocyte aggregation, Biofísica, CIENCIAS NATURALES Y EXACTAS
Abstract

ncrease in erythrocyte aggregation (EA) is pathognomonic for rheumatoid arthritis (RA), and its estimation through erythrocyte sedimentation rate (ESR) is part of DAS 28-4 activity diagnosis, with low correlation with EA and that does not discriminate the contribution of cell factors that increase aggregation. Objective: To analyse cell and plasma factors that might be involved in EA increase, to understand how RA affects blood components, thus modifying blood fluid behavior. Methodology: One hundred women presenting active RA were compared with age-matched controls (C). EA was measured by transmitted light, obtaining two parameters: 2k2n0, characterizing the aggregation process kinetics and s0/n0, estimating aggregates size. Cell factors assays: erythrocyte deformability, by filtration through nucleopore membranes, cell shape, by microscopy, and membrane fluidity by EPR. Plasma: total proteins and CRP, albumin, fibrinogen (Fb), by gravimetry, and IgG and IgM by single radial immuno-diffusion. Results: AR and C (x ± SE). 2k2n0: 31.83 ± 2.84, 23.75 ± 1.91; s0/n0: 0.92 ± 0.05, 0.87 ± 0.04. Rigidity index (RI): 14.79 ± 4.71, 6.92 ± 1.31. Morphological index: 0.28 ± 0.03, 0.30 ± 0.05, n.s. Fb (mg/dl): 382 ± 80, 299 ± 70. IgG (mg/dl): 1580 ± 219, 1296 ± 158; IgM (mg/dl) 233 ± 28, 183 ± 23; albumin (g/dl) 3.84 ± 0.44, 3.77 ± 0.51 n.s. p < 0.05 accepted. Correlations: 2k2n0 vs. Fb r = 0.66; s0/n0 vs. Fb r = 0.51; 2k2n0 vs. Igs r = 0.65; s0/n0 vs. Igs r = 0.56. 2k2n0 vs. RI r = -0.59; s0/n0 vs. RI = -0.52, p < 0.05. Conclusions: Plasma factors, Igs and Fb increased aggregation, since RI is altered, this reduces the process efficiency regarding aggregation. Patients with active RA present an increased EA, with values modifications associated with the activity index DAS 28-4, thus becoming an RA activity indicator. Fil: Luquita, A.. Universidad Nacional de Rosario; Argentina Fil: Urli, L.. Universidad Nacional de Rosario; Argentina Fil: Svetaz, M. J.. Universidad Nacional de Rosario; Argentina Fil: Gennaro, Ana Maria. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Santa Fe. Instituto de Desarrollo Tecnológico para la Industria Química. Universidad Nacional del Litoral. Instituto de Desarrollo Tecnológico para la Industria Química; Argentina Fil: Volpintesta, R.. Universidad Nacional de Rosario; Argentina Fil: Palatnik, S.. Universidad Nacional de Rosario; Argentina Fil: Rasia, M.. Universidad Nacional de Rosario; Argentina

Published
2009

5. Chromosome 17p12-q11 harbors susceptibility loci for systemic lupus erythematosus

Author

Johansson, C. M., Zunec, R., Garía, M. A., Scherbarth, H. R., Tate, G. A., Paira, S., Navarro, S. M., Perandones, C. E., Gamron, S., Alvarellos, A., Graf, C. E., Manni, J., Berbotto, G. A., Palatnik, S. A., Luis Jose Catoggio, Battagliotti, C. G., Sebastiani, G. D., Migliaresi, S., Galeazzi, M., Pons-Estel, B. A., Alarcón-Riquelme, M. E., Gunnarsson, I., Svennungson, E., Gordon, C., Jonsson, R., Moutsopoulos, H., Doria, A., Marcos, J. C., Marcos, A. I., Marino, P. C., Motta, E. L., Allevi, A., Presas, J. L., Roverano, A., Louteiro, C., Ramos, F. A., Prigione, C. S., Eimon, A., Drenkard, C., Menso, E., Caeiro, F., Bertoli, A., Caprarulo, C., Buchanan, G., Bertero, E., Grimaudo, S., Guillersn, C., Jorfen, M., Romero, E. J., Abdala, M., Bearzotti, M., Soriano, E. R., Santos, C. D., and Battagliotti, C. A.

Subjects
Adult, Male, Candidate gene, Genotype, Argentina, Locus (genetics), Biology, Genome, Systemic lupus erythematosus (SLE), microsatellites, genome scan, Genetics, medicine, Humans, Lupus Erythematosus, Systemic, Genetic Predisposition to Disease, Promoter Regions, Genetic, Gene, Genetics (clinical), Aged, Autoimmune disease, Chromosome Mapping, Middle Aged, medicine.disease, Human genetics, Pedigree, Chromosome 17 (human), Europe, Italy, Microsatellite, Female, Chromosomes, Human, Pair 17, Microsatellite Repeats
Abstract

Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by the presence of autoantibodies against intracellular components, the formation of immune complexes, and inflammation in various organs, typically the skin and kidney glomeruli. The etiology of the disease is not well understood but is most likely the result of the interaction between genetic and environmental factors. In order to identify susceptibility loci for SLE, we have performed genome scans with microsatellite markers covering the whole genome in families from Argentina, Italy, and Europe. The results reveal a heterogeneous disease with different susceptibility loci in different family sets. We have found significant linkage to chromosome 17p12-q11 in the Argentine set of families. The maximum LOD score was given by marker D17S1294 in combination with D17S1293, when assuming a dominant inheritance model (Z = 3.88). We also analyzed a repeat in the promoter region of the NOS2A gene, a strong candidate gene in the region, but no association was found. The locus on chromosome 17 has previously been identified in genetic studies of multiple sclerosis families. Several other interesting regions were found at 1p35, 1q31, 3q26, 5p15, 11q23 and 19q13, confirming previously identified loci for SLE or other autoimmune diseases.

Published
2004

6. Preferential Binding to Elk-1 by SLE-Associated IL10 Risk Allele Upregulates IL10 Expression

Author

Sakurai, D., Zhao, J., Deng, Y., Kelly, J. A., Brown, E. E., Harley, J. B., Bae, S. C., Alarcón-Riquelme, M. E., Edberg, J. C., Kimberly, R. P., Ramsey-Goldman, R., Caeiro, F., Soriano, E. R., Bertoli, A., Prigione, C., Ramos, F. A., Romero, E. J., Tsao, B. P., Chen, W., Truedsson, L., Yu, C. Y., Migliarese, S., García, M. A., Marcos, J. C., Eimon, A., Sánchez-Román, J., Battagliotti, C. G., Kaufman, K. M., Vyse, T. J., Jacob, C. O., Gaffney, P. M., Sebastiani, G. D., Ramón, Enrique de, Hahn, B. H., Song, Y. W., Grossman, J. M., Sivils, K. M., James, J. A., Kamen, D. L., Gilkeson, G. S., Niewold, T. B., D'Alfonso, Sandra, Merrill, J. T., Martín, J., Scofield, R. H., Chang, D. M., Criswell, L. A., Langefeld, C. D., Stevens, A. M., Cantor, R. M., Frostegård, Johan, Boackle, S. A., Kim, J. H., Choi, J., Pons-Estel, B. A., Freedman, Barry I., Sabio, José Mario, Anaya, J. M., Ortego-Centeno, N., Callejas-Rubio, J. L., González-Escribano, María Francisca, Buchanan, G., Graf, C. E., Paira, S., Galeazzi, M., Witte, Torsten, Lauwerys, B. R., Endreffy, E., Kovács, L., Vasconcelos, C., Silva, B. M. da, Scherbarth, H. R., Catoggio, L. J., Manni, J., Caprarulo, C., Guillerón, C., Marino, P. C., Motta, E. L., Gamron, S., Drenkard, C., Menso, E., Allievi, A., Roverano, S., Tate, G. A., Bertero, E., Presas, J. L., Navarro, S. M., Parque, S., Grimaudo, S., Palatnik, S. A., Abdala, M., Acevedo, E., Bearzotti, M., Santos, C. D., Alvarellos, A., Berbotto, G. A., Jorfen, M., Marcos, A. I., Perandones, C. E., Cucho, M., Torre, I. G. de la, Ríos, M. C., Moctezuma, J. F., Ceceña, M. M., Petri, M. A., Vilá, Luis M., Reveille, J. D., Alarcón, G. S., Sakurai, D., Zhao, J., Deng, Y., Kelly, J. A., Brown, E. E., Harley, J. B., Bae, S. C., Alarcón-Riquelme, M. E., Edberg, J. C., Kimberly, R. P., Ramsey-Goldman, R., Caeiro, F., Soriano, E. R., Bertoli, A., Prigione, C., Ramos, F. A., Romero, E. J., Tsao, B. P., Chen, W., Truedsson, L., Yu, C. Y., Migliarese, S., García, M. A., Marcos, J. C., Eimon, A., Sánchez-Román, J., Battagliotti, C. G., Kaufman, K. M., Vyse, T. J., Jacob, C. O., Gaffney, P. M., Sebastiani, G. D., Ramón, Enrique de, Hahn, B. H., Song, Y. W., Grossman, J. M., Sivils, K. M., James, J. A., Kamen, D. L., Gilkeson, G. S., Niewold, T. B., D'Alfonso, Sandra, Merrill, J. T., Martín, J., Scofield, R. H., Chang, D. M., Criswell, L. A., Langefeld, C. D., Stevens, A. M., Cantor, R. M., Frostegård, Johan, Boackle, S. A., Kim, J. H., Choi, J., Pons-Estel, B. A., Freedman, Barry I., Sabio, José Mario, Anaya, J. M., Ortego-Centeno, N., Callejas-Rubio, J. L., González-Escribano, María Francisca, Buchanan, G., Graf, C. E., Paira, S., Galeazzi, M., Witte, Torsten, Lauwerys, B. R., Endreffy, E., Kovács, L., Vasconcelos, C., Silva, B. M. da, Scherbarth, H. R., Catoggio, L. J., Manni, J., Caprarulo, C., Guillerón, C., Marino, P. C., Motta, E. L., Gamron, S., Drenkard, C., Menso, E., Allievi, A., Roverano, S., Tate, G. A., Bertero, E., Presas, J. L., Navarro, S. M., Parque, S., Grimaudo, S., Palatnik, S. A., Abdala, M., Acevedo, E., Bearzotti, M., Santos, C. D., Alvarellos, A., Berbotto, G. A., Jorfen, M., Marcos, A. I., Perandones, C. E., Cucho, M., Torre, I. G. de la, Ríos, M. C., Moctezuma, J. F., Ceceña, M. M., Petri, M. A., Vilá, Luis M., Reveille, J. D., and Alarcón, G. S.

Abstract

Immunoregulatory cytokine interleukin-10 (IL-10) is elevated in sera from patients with systemic lupus erythematosus (SLE) correlating with disease activity. The established association of IL10 with SLE and other autoimmune diseases led us to fine map causal variant(s) and to explore underlying mechanisms. We assessed 19 tag SNPs, covering the IL10 gene cluster including IL19, IL20 and IL24, for association with SLE in 15,533 case and control subjects from four ancestries. The previously reported IL10 variant, rs3024505 located at 1 kb downstream of IL10, exhibited the strongest association signal and was confirmed for association with SLE in European American (EA) (P = 2.7×10-8, OR = 1.30), but not in non-EA ancestries. SNP imputation conducted in EA dataset identified three additional SLE-associated SNPs tagged by rs3024505 (rs3122605, rs3024493 and rs3024495 located at 9.2 kb upstream, intron 3 and 4 of IL10, respectively), and SLE-risk alleles of these SNPs were dose-dependently associated with elevated levels of IL10 mRNA in PBMCs and circulating IL-10 protein in SLE patients and controls. Using nuclear extracts of peripheral blood cells from SLE patients for electrophoretic mobility shift assays, we identified specific binding of transcription factor Elk-1 to oligodeoxynucleotides containing the risk (G) allele of rs3122605, suggesting rs3122605 as the most likely causal variant regulating IL10 expression. Elk-1 is known to be activated by phosphorylation and nuclear localization to induce transcription. Of interest, phosphorylated Elk-1 (p-Elk-1) detected only in nuclear extracts of SLE PBMCs appeared to increase with disease activity. Co-expression levels of p-Elk-1 and IL-10 were elevated in SLE T, B cells and monocytes, associated with increased disease activity in SLE B cells, and were best downregulated by ERK inhibitor. Taken together, our data suggest that preferential binding of activated Elk-1 to the IL10 rs3122605-G allele upregulates IL10 expressio

Published
2013

7. Amerindian ancestry in Argentina is associated with increased risk for systemic lupus erythematosus

Author

Seldin, M. F., Qi, L., Scherbarth, H. R., Tian, C., Ransom, M., Silva, G., Belmont, J. W., Gamron, S., Allievi, A., Palatnik, S. A., Saurit, V., Paira, S., Graf, C., Guillerón, C., Catoggio, L. J., Prigione, C., Berbotto, G. A., García, M. A., Perandones, C. E., Truedsson, L., Abderrahim, H., Battagliotti, C. G., Pons-Estel, B. A., Alarcon-Riquelme, Marta E., Seldin, M. F., Qi, L., Scherbarth, H. R., Tian, C., Ransom, M., Silva, G., Belmont, J. W., Gamron, S., Allievi, A., Palatnik, S. A., Saurit, V., Paira, S., Graf, C., Guillerón, C., Catoggio, L. J., Prigione, C., Berbotto, G. A., García, M. A., Perandones, C. E., Truedsson, L., Abderrahim, H., Battagliotti, C. G., Pons-Estel, B. A., and Alarcon-Riquelme, Marta E.

Abstract

Previous studies have demonstrated that in admixed populations, West African ancestry is associated with an increased prevalence of systemic lupus erythematosus (SLE). In the current study, the effect of Amerindian ancestry in SLE was examined in an admixed population in Argentina. The Argentine population is predominantly European with approximately 20% Amerindian admixture, and a very small (<2%) contribution from West Africa. The results indicate that Amerindian admixture in this population is associated with a substantial increase in SLE susceptibility risk (Odds Ratio=7.94, P=0.00006). This difference was not due to known demographic factors, including site of collection, age and gender. In addition, there were trends towards significance for Amerindian ancestry influencing renal disease, age of onset and anti-SSA antibodies. These studies suggest that populations with Amerindian admixture, like those with West African admixture, should be considered in future studies to identify additional allelic variants that predispose to SLE.

Published
2008
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10. Haemorheological variables as a rheumatoid arthritis activity indicator.

Author

Luquita, A., Urli, L., Dominighini, A., Svetaz, M.J., Gennaro, A.M., Volpintesta, R., Palatnik, S., and Rasia, M.

Subjects
BLOOD hyperviscosity syndrome, RHEUMATOID arthritis, ERYTHROCYTES, BLOOD cells, HEMORHEOLOGY, MICROCIRCULATION
Abstract

Objective: To investigate if blood hyperviscosity in RA patients is due to a reduced erythrocyte deformability and, therefore, turning it into a reliable activity indicator, as well as a therapy follow‐up marker for this pathology. Methods: (1) The haemorheological profile consisting of erythrocyte deformability, blood and plasma viscosity, and erythrocyte membrane fluidity was determined in 24 AR patients and 17 healthy controls. (2) A 4 year follow‐up was carried on in 16 patients monitoring blood viscosity, erythrocyte deformability and biochemical variables in relation to clinical assessment of disease activity (Disease Activity Score “DAS 28‐4”). Results: Erythrocyte deformability and membrane fluidity were impaired in RA patients compared to controls (p<0.001). Blood viscosity was significantly increased and correlated with the cell rigidity index (r=0.85, p<0.0000) in RA patients. The follow‐up showed a good correlation between haemorheological parameters and DAS 28‐4 during disease evolution. Conclusion: our results support the hypothesis that in RA, blood hyperviscosity is determined by deformability loss, which in turn is due to a membrane rigidization. This could evidenced that a widespread cell membrane damage is expressed through an impaired erythrocyte deformability, turning haemorheological parameters into reliable tools to study disease evolution. The follow‐up study enabled us to confirm that erythrocyte deformability is an efficient indicator of rheumatoid arthritis activity. [ABSTRACT FROM AUTHOR]

Published
2004

11. Haemorheological variables as a rheumatoid arthritis activity indicator

Author

Luquita, A., Urli, L., Dominighini, A., Svetaz, M. J., Ana María Gennaro, Volpintesta, R., Palatnik, S., and Rasia, M.

Subjects
Ciencias Físicas, Otras Ciencias Físicas, CIENCIAS NATURALES Y EXACTAS
Abstract

Objective: To investigate if blood hyperviscosity in RA patients is due to a reduced erythrocyte deformability and, therefore, turning it into a reliable activity indicator, as well as a therapy follow-up marker for this pathology. Methods: (1) The haemorheological profile consisting of erythrocyte deformability, blood and plasma viscosity, and erythrocyte membrane fluidity was determined in 24 AR patients and 17 healthy controls. (2) A 4 year follow-up was carried on in 16 patients monitoring blood viscosity, erythrocyte deformability and biochemical variables in relation to clinical assessment of disease activity (Disease Activity Score “DAS 28-4”). Results: Erythrocyte deformability and membrane fluidity were impaired in RA patients compared to controls (p

12. Genetic associations of leptin-related polymorphisms with systemic lupus erythematosus

Author

Marta E. Alarcón-Riquelme, Ignacio García-De La Torre, Luis J. Catoggio, Timothy B. Niewold, Ana I. Marcos, Barry I. Freedman, Pilar C. Marino, Marisa Jorfen, Griselda Buchanan, Marcelo Abdala, Anne M. Stevens, Fernando A. Ramos, Emoke Endreffy, Sandra M. Navarro, Ana M. Bertoli, Sergio Migliarese, Jorge Manni, Jose L. Presas, César Graf, László Kovács, Hye jin Jeong, John B. Harley, Berta Martins da Silva, Cesar Caprarulo, Guillermo Tate, Jennifer M. Grossman, Julio Sánchez-Román, Jian Zhao, Javier Martin, Cristina G. Battagliotti, Estela Bertero, Chaim O. Jacob, Carlos E. Perandones, Kenneth M. Kaufman, Guillermo A. Berbotto, Alberto Allievi, John D. Reveille, Sebastian Grimaudo, Estela L. Motta, Susana Gamron, Yeong Wook Song, Mario Cardiel Ríos, José Luis Callejas, Gary S. Gilkeson, Mercedes A. García, Hugo R. Scherbarth, Kathy Moser Sivils, María Francisca González-Escribano, Alejandro Alvarellos, Antonio La Cava, Mariano Cucho, Joan T. Merrill, Carlos D. Santos, Torsten Witte, Cristina Drenkard, R. Hal Scofield, Seung Taek Song, Cristina Prigione, Lindsey A. Criswell, Mariela Bearzotti, Deh Ming Chang, José Mario Sabio, Francisco Caeiro, Mauro Galeazzi, Rosalind Ramsey-Goldman, Simon A. Palatnik, Lennart Truedsson, Marco Maradiaga Ceceña, Johan Frostegård, Susan A. Boackle, Sanatorio Parque, Francisco Moctezuma, Hui Wu, Juan Carlos Marcos, Eduardo Acevedo, Timothy J. Vyse, Jennifer A. Kelly, Michelle Petri, Carlos Vasconcelos, Sandra D'Alfonso, Elizabeth E. Brown, Norberto Ortego-Centeno, Betty P. Tsao, Enrique de Ramón, Juan-Manuel Anaya, Diane L. Kamen, Emilia Menso, Gian Domenico Sebastiani, Patrick M. Gaffney, Judith A. James, Sang Cheol Bae, Susana Roverano, Carolina Guillerón, Jeffrey C. Edberg, Enrique R. Soriano, Carl D. Langefeld, Elisa J. Romero, Alicia Eimon, Bevra H. Hahn, Robert P. Kimberly, Luis M. Vilá, Graciela S. Alarcón, Sergio Paira, Bernard Lauwerys, Zhao, J., Wu, H., Langefeld, C. D., Kaufman, K. M., Kelly, J. A., Bae, S. -C., Alarcon-Riquelme, M. E., Alarcon, G. S., Anaya, J. -M., Criswell, L. A., Freedman, B. I., Kamen, D. L., Gilkeson, G. S., Jacob, C. O., James, J. A., Merrill, J. T., Gaffney, P. M., Sivils, K. M., Niewold, T. B., Petri, M. A., Song, S. T., Jeong, H. -J., Ramsey-Goldman, R., Reveille, J. D., Hal Scofield, R., Stevens, A. M., Boackle, S. A., Vila, L. M., Chang, D. -M., Song, Y. W., Vyse, T. J., Harley, J. B., Brown, E. E., Edberg, J. C., Kimberly, R. P., Hahn, B. H., Grossman, J. M., Tsao, B. P., La Cava, A., Frostegard, J., Truedsson, L., de Ramon, E., Sabio, J. M., Gonzalez-Escribano, M. F., Martin, J., Ortego-Centeno, N., Callejas, J. L., Sanchez-Roman, J., D'Alfonso, S., Migliarese, S., Sebastiani, G. -D., Galeazzi, M., Witte, T., Lauwerys, B. R., Endreffy, E., Kovacs, L., Vasconcelos, C., da Silva, B. M., Scherbarth, H. R., Marino, P. C., Motta, E. L., Gamron, S., Drenkard, C., Menso, E., Allievi, A., Tate, G. A., Presas, J. L., Palatnik, S. A., Abdala, M., Bearzotti, M., Alvarellos, A., Caeiro, F., Bertoli, A., Paira, S., Roverano, S., Graf, C. E., Bertero, E., Caprarulo, C., Buchanan, G., Guilleron, C., Grimaudo, S., Manni, J., Catoggio, L. J., Soriano, E. R., Santos, C. D., Prigione, C., Ramos, F. A., Navarro, S. M., Berbotto, G. A., Jorfen, M., Romero, E. J., Garcia, M. A., Marcos, J. C., Marcos, A. I., Perandones, C. E., Eimon, A., Parque, S., Battagliotti, C. G., Acevedo, E., Cucho, M., de la Torre, I. G., Rios, M. C., Moctezuma, F., and Maradiaga Cecena, M.

Subjects
Leptin, Hispanic, Gene, Dna determination, immune system diseases, Lep gene, Genotype, 2.1 Biological and endogenous factors, Lupus Erythematosus, Systemic, Immunology and Allergy, Medicine, Aetiology, skin and connective tissue diseases, Priority journal, Leptin pathway, Gene polymorphism, Gene polymorphisms, Single Nucleotide, East asian, Case-Control Studie, Human, Lepr gene, Immunology, Case control study, Lupus, Single-nucleotide polymorphism, Major clinical study, Systemic lupus erythematosu, Autoimmune Disease, Polymorphism, Single Nucleotide, Article, European american, Systemic lupus erythematosus, Clinical Research, Genetic susceptibility, Genetics, Genetic predisposition, Humans, Genetic Predisposition to Disease, Genetic Testing, African american, Polymorphism, Genetic risk, Inflammation, Lupus Erythematosus, business.industry, Inflammatory and immune system, Pparg gene, Marta E. Alarcón-Riquelme for the BIOLUPUS and GENLES networks, Systemic, Case-control study, Single nucleotide polymorphism, Case-Control Studies, Multiple comparisons problem, Genetic association, Ghsr gene, business, Controlled study
Abstract

Leptin is abnormally elevated in the plasma of patients with systemic lupus erythematosus (SLE), where it is thought to promote and/or sustain pro-inflammatory responses. Whether this association could reflect an increased genetic susceptibility to develop SLE is not known, and studies of genetic associations with leptin-related polymorphisms in SLE patients have been so far inconclusive. Here we genotyped DNA samples from 15,706 SLE patients and healthy matched controls from four different ancestral groups, to correlate polymorphisms of genes of the leptin pathway to risk for SLE. It was found that although several SNPs showed weak associations, those associations did not remain significant after correction for multiple testing. These data do not support associations between defined leptin-related polymorphisms and increased susceptibility to develop SLE. © 2015 Elsevier Inc.

Published
2015

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