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1دورية أكاديمية
المؤلفون: Gyllenberg, A, Piehl, F, Alfredsson, L, Hillert, J, Bomfim, I L, Padyukov, L, Orho-Melander, M, Lindholm, E, Landin-Olsson, M, Lernmark, Å, Aili, M, Bååth, L E, Carlsson, E, Edenwall, H, Forsander, G, Granström, B W, Gustavsson, I, Hanas, R, Hellenberg, L, Hellgren, H, Holmberg, E, Hörnell, H, Ivarsson, Sten-A, Johansson, C, Jonsell, G, Kockum, K, Lindblad, B, Lindh, A, Ludvigsson, J, Myrdal, U, Neiderud, J, Segnestam, K, Sjö, S, Skogsberg, L, Strömberg, L, Ståhle, U, Thalme, B, Tullus, K, Tuvemo, T, Wallensteen, M, Westphal, O, Åman, J, Arnqvist, H, Björck, E, Eriksson, J, Nyström, L, Ohlson, L O, Scherstén, B, Östman, J, Olsson, T
المصدر: Genes & Immunity ; volume 15, issue 3, page 162-167 ; ISSN 1466-4879 1476-5470
مصطلحات موضوعية: Genetics (clinical), Genetics, Immunology
الإتاحة: https://doi.org/10.1038/gene.2013.71Test
https://www.nature.com/articles/gene201371.pdfTest
https://www.nature.com/articles/gene201371Test -
2دورية أكاديمية
المؤلفون: KOCKUM, I, SANJEEVI, CB, EASTMAN, S, LANDINOLSSON, M, DAHLQUIST, G, LERNMARK, A, AILI, M, BAATH, LE, BACKMAN, H, CARLSSON, E, EDENWALL, H, ELFSTRAND, PO, FORSANDER, G, GRANSTROM, BW, GUSTAVSSON, I, HALLBERG, A, HANAS, R, HELLENBERG, L, HELLGREN, H, HOLMBERG, E, HORNELL, H, JOHANSSON, C, JONSELL, G, JONSSON, C, KOCKUM, K, LINDBERG, U, LINDBLAD, B, LINDH, A, LUDVIGSSON, J, MASRELIEZ, V, MYRDAL, U, NEIDERUD, J, NILSSON, KO, PETZEN, PG, SAMUELSON, G, SEGNESTAM, K, SJOBLAD, S, SKOGSBERG, L, SMITH, T, STROMBERG, L, STAHLE, U, TENSTAM, J, THALME, B, TULLUS, K, TUVEMO, T, WALLENSTEEN, M, WESTPHAL, O, AMAN, J
المصدر: European journal of immunogenetics : official journal of the British Society for Histocompatibility and Immunogenetics. 22(6):443-465
مصطلحات موضوعية: Medicin och hälsovetenskap
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3دورية أكاديمية
المؤلفون: LIMA-DE-FARIA, A., PERO, R., AVANZI, S., DURANTE, M., STÅHLE, U., D'AMATO, F., GRANSTRÖM, H.
المصدر: Hereditas ; volume 79, issue 1, page 5-19 ; ISSN 0018-0661
مصطلحات موضوعية: Genetics, General Medicine
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4
المؤلفون: Resic-Lindehammer, S., Larsson, K., Ortqvist, E., Carlsson, A., Cederwall, E., Cilio, C. M., Ivarsson, S. A., Jonsson, B. A., Larsson, H. E., Lynch, K., Neiderud, J., Nilsson, A., Sjoblad, S., Lernmark, A., Aili, M., Baath, L. E., Carlsson, E., Edenwall, H., Forsander, Gun, 1951, Granstro, B. W., Gustavsson, I., Hanas, R., Hellenberg, L., Hellgren, H., Holmberg, E., Hornell, H., Johansson, C., Jonsell, G., Kockum, K., Lindblad, Bengt, Lindh, A., Ludvigsson, J., Myrdal, U., Segnestam, K., Skogsberg, L., Strömberg, L., Stahle, U., Thalme, B., Tullus, K., Tuvemo, T., Wallensteen, M., Westphal, Otto, 1935, Åman, J.
المصدر: Acta Diabetologica. 45(4):231-5
مصطلحات موضوعية: MEDICAL AND HEALTH SCIENCES, MEDICIN OCH HÄLSOVETENSKAP, HLA-DQ, Genotype, Temporal trends, Age at diagnosis, Autoimmune disease
الوصف: The aim of this study was to compare the frequency of human leukocyte antigen (HLA) genotypes in 1-18-year-old patients with type 1 diabetes newly diagnosed in 1986-1987 (n = 430), 1996-2000 (n = 342) and in 2003-2005 (n = 171). We tested the hypothesis that the HLA DQ genotype distribution changes over time. Swedish type 1 diabetes patients and controls were typed for HLA using polymerase chain reaction amplification and allele specific probes for DQ A1* and B1* alleles. The most common type 1 diabetes HLA DQA1*-B1*genotype 0501-0201/0301-0302 was 36% (153/430) in 1986-1987 and 37% (127/342) in 1996-2000, but decreased to 19% (33/171) in 2003-2005 (P \ 0.0001). The 0501-0201/0501-0201 genotype increased from 1% in 1986-1987 to 7% in 1996-2000 (P = 0.0047) and to 5% in 2003-2005 (P > 0.05). This study in 1-18-year-old Swedish type 1 diabetes patients supports the notion that there is a temporal change in HLA risk.
الوصول الحر: https://gup.ub.gu.se/publication/84609Test
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5
المؤلفون: Sedimbi, S. K., Luo, X. R., Sanjeevi, C. B., Lernmark, A., Landin-Olsson, M., Arnqvist, H., Björck, E., Nyström, L., Ohlson, L. O., Schersten, B., Östman, J., Aili, M., Baath, L. E., Carlsson, E., Edenwall, H., Forsander, Gun, 1951, Granström, B. W., Gustavsson, I., Hanas, R., Hellenberg, L., Hellgren, H., Holmberg, E., Hornell, H., Ivarsson, S. A., Johansson, C., Jonsell, G., Kockum, K., Lindblad, B., Lindh, A., Ludvigsson, J., Myrdal, U., Neiderud, J., Segnestam, K., Sjöblad, S., Skogsberg, L., Strömberg, L., Stahle, U., Thalme, B., Tullus, K., Tuvemo, T., Wallensteen, M., Westphal, Otto, 1935, Dahlquist, G., Aman, J.
المصدر: Genes Immun. 8(6):518-21
مصطلحات موضوعية: MEDICAL AND HEALTH SCIENCES, MEDICIN OCH HÄLSOVETENSKAP, Adolescent, Adult, Alleles, Case-Control Studies, Child, Preschool, Cohort Studies, Diabetes Mellitus, Type 1/*genetics/immunology, Female, Genetic Predisposition to Disease, Genotype, HLA-DR3 Antigen/*genetics/immunology, HLA-DR4 Antigen/*genetics/immunology, Haplotypes, Humans, Infant, Newborn, Male, Polymorphism, Single Nucleotide, Small Ubiquitin-Related Modifier Proteins/*genetics/immunology, Sweden
الوصف: SUMO4 M55V, located in IDDM5, has been a focus for debate because of its association to type I diabetes (TIDM) in Asians but not in Caucasians. The current study aims to test the significance of M55V association to TIDM in a large cohort of Swedish Caucasians, and to test whether M55V is associated in those carrying human leukocyte antigen (HLA) class II molecules. A total of 673 TIDM patients and 535 age- and sex-matched healthy controls were included in the study. PCR-RFLP was performed to identify the genotype and allele variations. Our data suggest that SUMO4 M55V is not associated with susceptibility to TIDM by itself. When we stratified our patients and controls based on heterozygosity for HLA-DR3/DR4 and SUMO4 genotypes, we found that presence of SUMO4 GG increased further the relative risk conferred by HLA-DR3/DR4 to TIDM, whereas SUMO4 AA decreased the risk. From the current study, we conclude that SUMO4 M55V is associated with TIDM in association with high-risk HLA-DR3 and DR4, but not by itself.
الوصول الحر: https://gup.ub.gu.se/publication/66317Test
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المؤلفون: Shin, J. H., Janer, M., McNeney, B., Blay, S., Deutsch, K., Sanjeevi, C. B., Kockum, I., Lernmark, A., Graham, J., Arnqvist, H., Björck, E., Eriksson, J., Nystrom, L., Ohlson, L. O., Schersten, B., Östman, J., Aili, M., Baath, L. E., Carlsson, E., Edenwall, H., Forsander, Gun, 1951, Granström, B. W., Gustavsson, I., Hanas, R., Hellenberg, L., Hellgren, H., Holmberg, E., Hornell, H., Ivarsson, S. A., Johansson, C., Jonsell, G., Kockum, K., Lindblad, B., Lindh, A., Ludvigsson, J., Myrdal, U., Neiderud, J., Segnestam, K., Sjöblad, S., Skogsberg, L., Stromberg, L., Stahle, U., Thalme, B., Tullus, K., Tuvemo, T., Wallensteen, M., Westphal, O., Aman, J.
المصدر: Genes Immun. 8(6):503-12
مصطلحات موضوعية: MEDICAL AND HEALTH SCIENCES, MEDICIN OCH HÄLSOVETENSKAP, Adolescent, Adult, Autoantibodies/blood/*immunology, Case-Control Studies, Child, Preschool, Diabetes Mellitus, Type 1/*genetics/*immunology/metabolism, Female, GTP-Binding Proteins/*genetics/metabolism, Humans, Infant, Newborn, Male, Polymorphism, Single Nucleotide, Sweden
الوصف: In a large case-control study of Swedish incident type I diabetes patients and controls, 0-34 years of age, we tested the hypothesis that the GIMAP5 gene, a key genetic factor for lymphopenia in spontaneous BioBreeding rat diabetes, is associated with type I diabetes; with islet autoantibodies in incident type I diabetes patients or with age at clinical onset in incident type I diabetes patients. Initial scans of allelic association were followed by more detailed logistic regression modeling that adjusted for known type I diabetes risk factors and potential confounding variables. The single nucleotide polymorphism (SNP) rs6598, located in a polyadenylation signal of GIMAP5, was associated with the presence of significant levels of IA-2 autoantibodies in the type I diabetes patients. Patients with the minor allele A of rs6598 had an increased prevalence of IA-2 autoantibody levels compared to patients without the minor allele (OR=2.2; Bonferroni-corrected P=0.003), after adjusting for age at clinical onset (P=8.0 x 10(-13)) and the numbers of HLA-DQ A1*0501-B1*0201 haplotypes (P=2.4 x 10(-5)) and DQ A1*0301-B1*0302 haplotypes (P=0.002). GIMAP5 polymorphism was not associated with type I diabetes or with GAD65 or insulin autoantibodies, ICA, or age at clinical onset in patients. These data suggest that the GIMAP5 gene is associated with islet autoimmunity in type I diabetes and add to recent findings implicating the same SNP in another autoimmune disease.
الوصول الحر: https://gup.ub.gu.se/publication/66312Test