Search Results - (Author, Cooperation:I. Kockum)
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1Latest Papers from Table of Contents or Articles in PressS. Sawcer ; G. Hellenthal ; M. Pirinen ; C. C. Spencer ; N. A. Patsopoulos ; L. Moutsianas ; A. Dilthey ; Z. Su ; C. Freeman ; S. E. Hunt ; S. Edkins ; E. Gray ; D. R. Booth ; S. C. Potter ; A. Goris ; G. Band ; A. B. Oturai ; A. Strange ; J. Saarela ; C. Bellenguez ; B. Fontaine ; M. Gillman ; B. Hemmer ; R. Gwilliam ; F. Zipp ; A. Jayakumar ; R. Martin ; S. Leslie ; S. Hawkins ; E. Giannoulatou ; S. D'Alfonso ; H. Blackburn ; F. Martinelli Boneschi ; J. Liddle ; H. F. Harbo ; M. L. Perez ; A. Spurkland ; M. J. Waller ; M. P. Mycko ; M. Ricketts ; M. Comabella ; N. Hammond ; I. Kockum ; O. T. McCann ; M. Ban ; P. Whittaker ; A. Kemppinen ; P. Weston ; C. Hawkins ; S. Widaa ; J. Zajicek ; S. Dronov ; N. Robertson ; S. J. Bumpstead ; L. F. Barcellos ; R. Ravindrarajah ; R. Abraham ; L. Alfredsson ; K. Ardlie ; C. Aubin ; A. Baker ; K. Baker ; S. E. Baranzini ; L. Bergamaschi ; R. Bergamaschi ; A. Bernstein ; A. Berthele ; M. Boggild ; J. P. Bradfield ; D. Brassat ; S. A. Broadley ; D. Buck ; H. Butzkueven ; R. Capra ; W. M. Carroll ; P. Cavalla ; E. G. Celius ; S. Cepok ; R. Chiavacci ; F. Clerget-Darpoux ; K. Clysters ; G. Comi ; M. Cossburn ; I. Cournu-Rebeix ; M. B. Cox ; W. Cozen ; B. A. Cree ; A. H. Cross ; D. Cusi ; M. J. Daly ; E. Davis ; P. I. de Bakker ; M. Debouverie ; B. D'Hooghe M ; K. Dixon ; R. Dobosi ; B. Dubois ; D. Ellinghaus ; I. Elovaara ; F. Esposito ; C. Fontenille ; S. Foote ; A. Franke ; D. Galimberti ; A. Ghezzi ; J. Glessner ; R. Gomez ; O. Gout ; C. Graham ; S. F. Grant ; F. R. Guerini ; H. Hakonarson ; P. Hall ; A. Hamsten ; H. P. Hartung ; R. N. Heard ; S. Heath ; J. Hobart ; M. Hoshi ; C. Infante-Duarte ; G. Ingram ; W. Ingram ; T. Islam ; M. Jagodic ; M. Kabesch ; A. G. Kermode ; T. J. Kilpatrick ; C. Kim ; N. Klopp ; K. Koivisto ; M. Larsson ; M. Lathrop ; J. S. Lechner-Scott ; M. A. Leone ; V. Leppa ; U. Liljedahl ; I. L. Bomfim ; R. R. Lincoln ; J. Link ; J. Liu ; A. R. Lorentzen ; S. Lupoli ; F. Macciardi ; T. Mack ; M. Marriott ; V. Martinelli ; D. Mason ; J. L. McCauley ; F. Mentch ; I. L. Mero ; T. Mihalova ; X. Montalban ; J. Mottershead ; K. M. Myhr ; P. Naldi ; W. Ollier ; A. Page ; A. Palotie ; J. Pelletier ; L. Piccio ; T. Pickersgill ; F. Piehl ; S. Pobywajlo ; H. L. Quach ; P. P. Ramsay ; M. Reunanen ; R. Reynolds ; J. D. Rioux ; M. Rodegher ; S. Roesner ; J. P. Rubio ; I. M. Ruckert ; M. Salvetti ; E. Salvi ; A. Santaniello ; C. A. Schaefer ; S. Schreiber ; C. Schulze ; R. J. Scott ; F. Sellebjerg ; K. W. Selmaj ; D. Sexton ; L. Shen ; B. Simms-Acuna ; S. Skidmore ; P. M. Sleiman ; C. Smestad ; P. S. Sorensen ; H. B. Sondergaard ; J. Stankovich ; R. C. Strange ; A. M. Sulonen ; E. Sundqvist ; A. C. Syvanen ; F. Taddeo ; B. Taylor ; J. M. Blackwell ; P. Tienari ; E. Bramon ; A. Tourbah ; M. A. Brown ; E. Tronczynska ; J. P. Casas ; N. Tubridy ; A. Corvin ; J. Vickery ; J. Jankowski ; P. Villoslada ; H. S. Markus ; K. Wang ; C. G. Mathew ; J. Wason ; C. N. Palmer ; H. E. Wichmann ; R. Plomin ; E. Willoughby ; A. Rautanen ; J. Winkelmann ; M. Wittig ; R. C. Trembath ; J. Yaouanq ; A. C. Viswanathan ; H. Zhang ; N. W. Wood ; R. Zuvich ; P. Deloukas ; C. Langford ; A. Duncanson ; J. R. Oksenberg ; M. A. Pericak-Vance ; J. L. Haines ; T. Olsson ; J. Hillert ; A. J. Ivinson ; P. L. De Jager ; L. Peltonen ; G. J. Stewart ; D. A. Hafler ; S. L. Hauser ; G. McVean ; P. Donnelly ; A. Compston
Nature Publishing Group (NPG)
Published 2011Staff ViewPublication Date: 2011-08-13Publisher: Nature Publishing Group (NPG)Print ISSN: 0028-0836Electronic ISSN: 1476-4687Topics: BiologyChemistry and PharmacologyMedicineNatural Sciences in GeneralPhysicsKeywords: Alleles ; Cell Differentiation/immunology ; Europe/ethnology ; Genetic Predisposition to Disease/*genetics ; Genome, Human/genetics ; Genome-Wide Association Study ; HLA-A Antigens/genetics ; HLA-DR Antigens/genetics ; HLA-DRB1 Chains ; Humans ; Immunity, Cellular/genetics/*immunology ; Major Histocompatibility Complex/genetics ; Multiple Sclerosis/*genetics/*immunology ; Polymorphism, Single Nucleotide/genetics ; Sample Size ; T-Lymphocytes, Helper-Inducer/cytology/immunologyPublished by: -
2Latest Papers from Table of Contents or Articles in PressEbenesersdottir, S. S., Sandoval-Velasco, M., Gunnarsdottir, E. D., Jagadeesan, A., Guthmundsdottir, V. B., Thordardottir, E. L., Einarsdottir, M. S., Moore, K. H. S., Sigurthsson, A., Magnusdottir, D. N., Jonsson, H., Snorradottir, S., Hovig, E., Moller, P., Kockum, I., Olsson, T., Alfredsson, L., Hansen, T. F., Werge, T., Cavalleri, G. L., Gilbert, E., Lalueza-Fox, C., Walser, J. W., Kristjansdottir, S., Gopalakrishnan, S., Arnadottir, L., Magnusson, O. T., Gilbert, M. T. P., Stefansson, K., Helgason, A.
American Association for the Advancement of Science (AAAS)
Published 2018Staff ViewPublication Date: 2018-06-01Publisher: American Association for the Advancement of Science (AAAS)Print ISSN: 0036-8075Electronic ISSN: 1095-9203Topics: BiologyChemistry and PharmacologyGeosciencesComputer ScienceMedicineNatural Sciences in GeneralPhysicsKeywords: Anthropology, GeneticsPublished by: -
3Articles: DFG German National LicensesKockum, I. ; Sanjeevi, C.B. ; Eastman, S. ; Landin-Olsson, M. ; Dahlouist, G. ; Lernmark, Å.
Oxford, UK : Blackwell Publishing Ltd
Published 1995Staff ViewISSN: 1744-313XSource: Blackwell Publishing Journal Backfiles 1879-2005Topics: BiologyMedicineNotes: A negative association between insulin-dependent diabetes mellitus (IDDM) and HLA-DR, DQA1 or DQB1 was found in a large population-based investigation of childhood-onset patients (more than 420 patients) and controls (more than 340 controls) from Sweden. The relative risk was decreased for several haplotypes that were negatively associated with IDDM: DR15-DQA1*0102-DQB1*0602, DR7-DQA1*0201-DQB1*0303, DR14-DQA1*0101-DQB1*0503, DRI1-DQAI*0501-DQB1*0301, DR13-DQA1*0103-DQB1*0603 and DR4-DQA1*0301-DQB1*0301. In a relative predispositional effect (RPE) analysis, however, only the DR15-DQA1*0102-DQB1*0602 haplotype was significantly decreased, which suggests that the major protective effect for IDDM is carried by this haplotype. This was supported by the observation that all genotypes which were negatively associated with IDDM, except DR7/13, included at least one allele from the DR15-DQA1*0102-DQB1*0602 haplotype. Relative predispositional effect (RPE) analysis of genotypes showed further that the DR15-DQA1*0102-DQB1*0602 haplotype was also negatively associated with IDDM when combined with any other haplotype, whether negatively or positively associated with IDDM. This supports previous suggestions that DR15-DQA1*0102-DQB1*0602 acts dominantly. However, both the stratification and the predispositional allele test failed to distinguish the negative association between IDDM and DR15 from that of DQBT0602. On the other hand, these tests indicated that DQA1*0102 was not likely to explain the negative association between IDDM and the DR15-DQA1*0102-DQB1*0602 haplotype. We conclude that theType of Medium: Electronic ResourceURL: -
4Articles: DFG German National LicensesSöderhäll, C. ; Bradley, M. ; Kockum, I. ; Luthman, H. ; Wahlgren, C.-F. ; Nordenskjöld, M.
Oxford, UK : Blackwell Science, Ltd
Published 2002Staff ViewISSN: 1365-2222Source: Blackwell Publishing Journal Backfiles 1879-2005Topics: MedicineNotes: Background Atopic dermatitis (AD) is caused by genetic and environmental factors that interact to determine disease susceptibility and severity. Several lines of evidence suggest that the IL-4 gene and the IL-4-receptor alpha (IL-4Rα) gene are involved in the development of atopic diseases.Objective The objective of this study was to evaluate the possible involvement of the chromosomal regions 5q31 and 16p12, which include the genes coding for the IL-4 and the IL-4Rα in AD.Methods We conducted linkage analysis and association studies using the microsatellite markers D16S298 and D16S403 and a single nucleotide polymorphism in the promoter region of the IL-4 gene (− 590C/T) in 406 Swedish families with at least two siblings affected with AD, in total 1514 individuals.Results and Conclusion We report linkage (P 〈 0.005) to the − 590C/T polymorphism in the promoter of the IL-4 gene for the semiquantitative trait severity score of AD. Neither linkage nor association was found to the IL-4Rα chromosomal region.Type of Medium: Electronic ResourceURL: -
5Articles: DFG German National LicensesWassmuth, R. ; Eastman, S. ; Kockum, I. ; Holmberg, E. ; Starck, M. ; Lindhagen, T. ; Kalden, J. R. ; Lernmark, Å. ; Sundkvist, G. ; Lindgren, S.
Oxford, UK : Blackwell Publishing Ltd
Published 1993Staff ViewISSN: 1744-313XSource: Blackwell Publishing Journal Backfiles 1879-2005Topics: BiologyMedicineNotes: A study of 109 Swedish patients and 85 healthy Swedish controls with Crohn's disease (CD) by HLA class II RFLP genotyping was carried out. There was no significant association for any single DR or DQ specificity or phenotypic combination of DR and/or DO specificities among our study group of Caucasian extraction.Type of Medium: Electronic ResourceURL: -
6Articles: DFG German National LicensesLotfi, K. ; Sund, G. ; Lowe, R. ; Graham, J. ; Landin-Olsson, M. ; Kockum, I. ; Deeb, S. ; Lernmark, Å.
Springer
Published 1997Staff ViewISSN: 1432-0428Keywords: Keywords IDDM ; NIDDM ; glucokinase gene ; polymerase chain reaction ; single strand conformational polymorphism ; islet cell antibodies ; GAD65 antibodies.Source: Springer Online Journal Archives 1860-2000Topics: MedicineNotes: Summary Glucokinase plays an important role in the regulation of insulin secretion and is therefore an attractive candidate gene for both insulin dependent (IDDM) and non-insulin-dependent (NIDDM) diabetes mellitus. A single G-A nucleotide polymorphism at the –30 position of the beta-cell specific promoter region of the glucokinase gene was previously associated with reduced beta-cell function. In the present study we analysed 268 consecutive newly diagnosed Swedish patients classified with either IDDM (n = 205), NIDDM (n = 31) or unclassifiable (n = 32) diabetes between the ages of 15 and 35 years along with a group of 158 age- and sex-matched control subjects. The beta-cell promoter region was amplified by the polymerase chain reaction and the G-A variant identified by single strand conformational polymorphism. There was no significant difference in allele frequencies of G and A between any of the subject groups and likewise, no significant difference in the frequencies of the G/G, G/A, or A/A genotypes. Eight subjects were homozygous for the less common A allele, five had IDDM and three were control subjects. Our results suggest that the –30 beta-cell glucokinase promoter variant is not associated with IDDM. [Diabetologia (1997) 40: 959–962)Type of Medium: Electronic ResourceURL: -
7Articles: DFG German National LicensesCiccarese, M. ; Tonolo, G. ; Delin, I. ; Wong, F. K. ; Holm, P. ; Atzeni, M. M. ; Lichtenstein, P. ; Kockum, I. ; Maioli, M. ; Luthman, H.
Springer
Published 1997Staff ViewISSN: 1432-0428Source: Springer Online Journal Archives 1860-2000Topics: MedicineType of Medium: Electronic ResourceURL: -
8Articles: DFG German National LicensesStaff View
ISSN: 1432-0428Keywords: Key words Transmission rates ; non-inherited maternal haplotypes ; non-inherited paternal haplotypes ; HLA-DR ; HLA-DQ.Source: Springer Online Journal Archives 1860-2000Topics: MedicineNotes: Summary The transmission of HLA-DR and DQ was compared between 46 families with at least one child affected by insulin dependent diabetes mellitis (IDDM) and 43 healthy control families. In the patient families, there was an increased transmission of DR4 (p 〈 0.025) and DQB1*0302 (p 〈 0.01) from both parents to the index patient. There was an increased transmission of DQB1*0302 (p 〈 0.03) from the mothers only. The non-inherited maternal haplotypes showed a significantly decreased frequency (p 〈 0.01) of positively associated haplotypes (DR4-DQA1* 0301-DQB1*0302, DR3-DQA1*0501-DQB1*0201) compared to all parental haplotypes in the control families. In the control families neither transmission rates nor frequencies of non-inherited haplotypes differed from those expected in the control families. In conclusion, the observed reduction of IDDM-positively associated haplotypes in patient non-inherited maternal haplotypes, but not in non-inherited paternal haplotypes, suggests that tolerance during fetal life to maternal non-inherited HLA molecules may be important to diabetes development. [Diabetologia (1994) 37: 1105–1112]Type of Medium: Electronic ResourceURL: -
9Articles: DFG German National LicensesStaff View
ISSN: 1432-0428Keywords: Transmission rates ; non-inherited maternal haplotypes ; non-inherited paternal haplotypes ; HLA-DR ; HLA-DQSource: Springer Online Journal Archives 1860-2000Topics: MedicineNotes: Summary The transmission of HLA-DR and DQ was compared between 46 families with at least one child affected by insulin dependent diabetes mellitis (IDDM) and 43 healthy control families. In the patient families, there was an increased transmission of DR4 (p〈0.025) and DQB1*0302 (p〈0.01) from both parents to the index patient. There was an increased transmission of DQB1*0302 (p〈0.03) from the mothers only. The non-inherited maternal haplotypes showed a significantly decreased frequency (p〈0.01) of positively associated haplotypes (DR4-DQA1* 0301-DQB1*0302, DR3-DQA1*0501-DQB1*0201) compared to all parental haplotypes in the control families. In the control families neither transmission rates nor frequencies of non-inherited haplotypes differed from those expected in the control families. In conclusion, the observed reduction of IDDM-positively associated haplotypes in patient non-inherited maternal haplotypes, but not in non-inherited paternal haplotypes, suggests that tolerance during fetal life to maternal non-inherited HLA molecules may be important to diabetes development.Type of Medium: Electronic ResourceURL: -
10Articles: DFG German National LicensesStaff View
ISSN: 1420-908XKeywords: Key words: Aminoguanidine — Diamine oxidase — Putrescine releaseSource: Springer Online Journal Archives 1860-2000Topics: MedicineNotes: Abstract. Objective: To determine if putrescine and the higher polyamines spermidine and spermine are released from cultured vascular smooth muscle cells.¶Material: Vascular smooth muscle cell line A7r5.¶Treatment: Cells were treated with aminoguanidine (10 or 100 μM) for 1 to 24 h with or without fetal calf serum (10%) present in the culture medium.¶Methods: Cellular and medium concentrations of polyamines were determined by liquid chromatography. Total cellular protein was determined by the Bradford procedure. Student's two-tailed t-test was used for statistical calculations.¶Results: A constitutive release of putrescine was disclosed within 5 h if serum diamine oxidase was inhibited by 10 μM aminoguanidine. The release was linear with time for 24 h and specific for putrescine in the sense that the higher polyamines spermidine and spermine, despite similar cellular concentrations, were not released. Similar amounts of putrescine were released from the smooth muscle cells whether or not culture medium contained serum. Cells, that had been cultured in medium from which fetal calf serum had been omitted for last 48 h, contained less putrescine, spermidine and protein than those that persisted in medium that contained serum.¶Conclusion: A constitutive putrescine release from vascular smooth muscle cells is disclosed in the presence of aminoguanidine.Type of Medium: Electronic ResourceURL: -
11Articles: DFG German National LicensesStaff View
ISSN: 1420-908XSource: Springer Online Journal Archives 1860-2000Topics: MedicineNotes: Abstract Rat parotid gland and liver cells were cultured for 6 and 24 h. The cells as well as their growth medium were analyzed on their content of the polyamines putrescine, spermidine and spermine. In control medium the content of polyamines was very low but already after 6 h substantial amounts of all three polyamines under study had been released into the medium from parotid as well as from liver cells. The release was much more pronounced from parotid compared to liver cells. Putrescine was accumulated in parotid cells as well as in the medium indicating that a new synthesis of this amine occurred in these cells.Type of Medium: Electronic ResourceURL: -
12Articles: DFG German National LicensesStaff View
ISSN: 1420-908XKeywords: Diamine oxidase ; Histamine ; Putrescine ; Small intestineSource: Springer Online Journal Archives 1860-2000Topics: MedicineNotes: Abstract In blood from the portal vein of anaesthetized rats the levels of histamine and putrescine were 2–3-fold lower compared to arterial blood. Putrescine concentration was increased severalfold and the difference between portal and arterial blood abolished in animals pretreated with the specific diamine oxidase inhibitor aminoguanidine. Histamine concentration was 40% lower in portal compared to arterial blood in animals treated with the mast cell degranulator compound 48/80. In animals pretreated with aminoguanidine, compound 48/80 enhanced the level of histamine and no difference was observed between arterial and portal blood. The amounts of intravenously injected [14C]-labeled histamine was about 15% lower in portal compared to arterial blood. The uptake of [14C]-putrescine from the small intestine was estimated. In urine from animals pretreated with aminoguanidine the concentration of [14C]-putrescine was more than 40-times higher than in control animals corresponding to a calculated uptake of about 7% in aminoguanidine treated animals. Our results suggest that intestinal diamine oxidase clears the blood from diamines and prevents luminal uptake of putrescine.Type of Medium: Electronic ResourceURL: