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1دورية أكاديمية
المؤلفون: Skogsberg, L, Fors, H, Hanas, R, Chaplin, JE, Lindman, E, Skogsberg, J
المصدر: Pediatric diabetes. 9(5):472-479
مصطلحات موضوعية: Medicin och hälsovetenskap
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2دورية 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 -
3دورية 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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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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المؤلفون: Sanjeevi, Carani B., Sedimbi, Saikiran K., Landin-Olsson, Mona, Kockum, Ingrid, Lernmark, Åke, Aili, M., Bååth, L.E., Carlsson, E., Edenwall, H., Forsander, G., Granström, B.W., Gustavsson, I., Hanås, 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., Sjöblad, S., Skogsberg, L., Strömberg, L., Ståhle, U., Thalme, B., Tullus, K., Tuvemo, Torsten, Wallensteen, M., Westphal, O., Dahlquist, G., Åman, J.
المصدر: Annals of the New York Academy of Sciences. 1150:106-11
مصطلحات موضوعية: type 1 diabetes, HLA-DR and DQ, environmental factors, genetic susceptibility, MEDICINE, MEDICIN
الوصف: HLA DR4-DQ8 and DR3-DQ2 haplotypes account for 89% of newly diagnosed cases of type 1 diabetes (T1D) in Sweden. The presence of a single copy of DQ6 confers protection. The aim of the present study is to evaluate whether the risk conferred by high risk HLA DR and DQ to T1D is similar in all regions of Sweden and see whether there are any significant regional differences. The subjects comprised 799 consecutively diagnosed T1D patients and 585 age-, sex-, and geography-matched healthy controls in the age group 0-35 years. HLA typing for high-risk haplotypes was previously performed using PCR-SSOP and RFLP. The results showed that HLA DR3-DR4 gave an odds ratio of 8.14 for the whole of Sweden. However, when the study group was divided into six geographical regions, subjects from Stockholm had the highest OR, followed by those from Lund, Linköping, Gothenburg, Umeå, and Uppsala. Absolute protection was conferred by the presence of DQ6 in subjects from the Linköping region, but varied in the other regions. The frequency of DR3 and DQ2, DR4 and DQ8, DR15, and DQ6 in patients showed high linkage for each region, but were different between regions. In conclusion: The risk conferred by high-risk HLA varies in different regions for a homogenous population in Sweden. The results highlight the important role played by the various environmental factors in the precipitation of T1D.
وصف الملف: print
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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
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المؤلفون: Landin-Olsson, Mona, Borgstrom, Anders, Blom, Leif, Sundkvist, Goran, Lernmark, Ake, Nyström, L., Sandström, A., Wall, S., Aili, M., Bäckman, H., Carlsson, E., Edenwall, H., Elfstrand, P. O., Granström, B. W., Gustavsson, I., Gustavsson, L. E., Hallberg, A., Hansing, B., Hanås, R., Hellenberg, L., Holmberg, E., Hornell, H., Jonsell, G., Jönsson, C., Kockum, K., Lindberg, U., Lindblad, B., Ludvigsson, J., Mazreliez, V., Myrdal, U., Neiderud, J., Nilsson, K. O., Persson, B., Petzén, P. G., Samuelsson, G., Segnestam, K., Sigurs, N., Sjöblad, S., Sjögren, S., Skogsberg, L., Smith, T., Snellman, K., Strömberg, L., Ståle, U., Tenstam, J., Thalme, B., Thilén, A., Tullus, K., Tuvemo, T., Westphal, O.
المصدر: Pancreas. 5(3):241-247
مصطلحات موضوعية: Anodal trypsin-(ogen), Case-control study, Cathodal trypsin(ogen), Exocrine pancreatic function, Insulin-dependent diabetic children
الوصف: To evaluate the exocrine pancreatic function at the time of diagnosis of insulin-dependent diabetes mellitus, we determined immunoreactive an-odal and cathodal trypsin(ogen) levels in sera from almost all children (n = 375) 0-14 years of age in Sweden in whom diabetes developed during 1 year, and in sex-, age-, and geographically matched control subjects (n = 312). The median level of anodal trypsin(ogen) was 5 (quartile range, 3-7) µg/L in children with newly diagnosed diabetes, compared with a median level of 7 (quartile range, 4-8) µg/L in control subjects (p < 0.0001). Similarly, the median level of cathodal trypsin(ogen) was 8 (quartile range, 4-10) µg/L in children with diabetes, compared with a median level of 11 (quartile range, 7-15) µg/L in control subjects (p < 0.0001). The median of the individual ratios between cathodal and anodal trypsin(ogen) was 1.4 in the diabetic patients and 1.7 in the control children (p < 0.001). In a multivariate test, however, only the decrease in cathodal trypsin(ogen) concentration was associated with diabetes. The levels of trypsin(ogen)s did not correlate with levels of islet cell antibodies, present in 81% of the diabetic children. Several mechanisms may explain our findings, for example, similar pathogenetic factors may affect both the endocrine and exocrine pancreas simultaneously, a failing local trophic stimulation by insulin on the exocrine cells may decrease the trypsinogen production, and there may be an increased elimination of trypsin(ogen) because of higher filtration through the kidneys in the hyperglycemic state.
الوصول الحر: https://lup.lub.lu.se/record/829ae736-8136-4d5a-aeb2-63766383fbc4Test
http://dx.doi.org/10.1097/00006676-199005000-00001Test -
9دورية أكاديمية
المؤلفون: Lindqvist, B., Ahlberg, E., Skogsberg, L.
المصدر: Applied Ergonomics ; volume 22, issue 6, page 421-422 ; ISSN 0003-6870
مصطلحات موضوعية: Physical Therapy, Sports Therapy and Rehabilitation, Engineering (miscellaneous), Safety, Risk, Reliability and Quality, Human Factors and Ergonomics
الإتاحة: https://doi.org/10.1016/0003-6870Test(91)90121-w
https://api.elsevier.com/content/article/PII:000368709190121W?httpAccept=text/xmlTest
https://api.elsevier.com/content/article/PII:000368709190121W?httpAccept=text/plainTest -
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المؤلفون: Ludvigsson, J, Dahlqvist, G, Edenvall, H, Lundmark, KM, Samuelson, Gösta, 1930, Skogsberg, L, Thilén, A
وصف الملف: print