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Numrering	Referens	Omslagsbild	Hitta
81.	Kallberg, H, et al. (författare) Smoking is associated with anti-CCP positive RA in a dose dependent manner, results from the Swedish eira study 2007 Ingår i: ANNALS OF THE RHEUMATIC DISEASES. - 0003-4967. ; 66, s. 291-291 Konferensbidrag (övrigt vetenskapligt/konstnärligt)
82.	Keenan, BT, et al. (författare) Effect of interactions of glutathione S-transferase T1, M1, and P1 and HMOX1 gene promoter polymorphisms with heavy smoking on the risk of rheumatoid arthritis 2010 Ingår i: Arthritis and rheumatism. - : Wiley. - 1529-0131 .- 0004-3591. ; 62:11, s. 3196-3210 Tidskriftsartikel (refereegranskat)
83.	Kivimäki, M., et al. (författare) Job strain as a risk factor for coronary heart disease : A collaborative meta-analysis of individual participant data 2012 Ingår i: The Lancet. - : Elsevier. - 0140-6736 .- 1474-547X. ; 380:9852, s. 1491-1497 Tidskriftsartikel (refereegranskat)abstract Background Published work assessing psychosocial stress (job strain) as a risk factor for coronary heart disease is inconsistent and subject to publication bias and reverse causation bias. We analysed the relation between job strain and coronary heart disease with a meta-analysis of published and unpublished studies. Methods We used individual records from 13 European cohort studies (1985-2006) of men and women without coronary heart disease who were employed at time of baseline assessment. We measured job strain with questions from validated job-content and demand-control questionnaires. We extracted data in two stages such that acquisition and harmonisation of job strain measure and covariables occurred before linkage to records for coronary heart disease. We defined incident coronary heart disease as the first non-fatal myocardial infarction or coronary death. Findings 30 214 (15%) of 197 473 participants reported job strain. In 1•49 million person-years at risk (mean follow-up 7•5 years [SD 1•7]), we recorded 2358 events of incident coronary heart disease. After adjustment for sex and age, the hazard ratio for job strain versus no job strain was 1•23 (95% CI 1•10-1•37). This effect estimate was higher in published (1•43, 1•15-1•77) than unpublished (1•16, 1•02-1•32) studies. Hazard ratios were likewise raised in analyses addressing reverse causality by exclusion of events of coronary heart disease that occurred in the first 3 years (1•31, 1•15-1•48) and 5 years (1•30, 1•13-1•50) of follow-up. We noted an association between job strain and coronary heart disease for sex, age groups, socioeconomic strata, and region, and after adjustments for socioeconomic status, and lifestyle and conventional risk factors. The population attributable risk for job strain was 3•4%. Interpretation Our findings suggest that prevention of workplace stress might decrease disease incidence; however, this strategy would have a much smaller effect than would tackling of standard risk factors, such as smoking. Funding Finnish Work Environment Fund, the Academy of Finland, the Swedish Research Council for Working Life and Social Research, the German Social Accident Insurance, the Danish National Research Centre for the Working Environment, the BUPA Foundation, the Ministry of Social Affairs and Employment, the Medical Research Council, the Wellcome Trust, and the US National Institutes of Health.
84.	Klareskog, L, et al. (författare) A new model for an etiology of RA;: Smoking may trigger HLA-DR (SE)-restricted immune reactions to autoantigens modified by citruillination 2005 Ingår i: ANNALS OF THE RHEUMATIC DISEASES. - 0003-4967. ; 64, s. 165- Konferensbidrag (övrigt vetenskapligt/konstnärligt)
85.	Klareskog, L, et al. (författare) Genes and environment in arthritis: can RA be prevented? 2002 Ingår i: Arthritis research. - : Springer Science and Business Media LLC. - 1465-9905. ; 44 Suppl 3, s. S31-6 Tidskriftsartikel (refereegranskat)
86.	Klareskog, L, et al. (författare) Mechanisms of disease: Genetic susceptibility and environmental triggers in the development of rheumatoid arthritis 2006 Ingår i: Nature clinical practice. Rheumatology. - : Springer Science and Business Media LLC. - 1745-8382 .- 1745-8390. ; 2:8, s. 425-433 Tidskriftsartikel (refereegranskat)
87.	Klareskog, L, et al. (författare) Smoking as a trigger for inflammatory rheumatic diseases 2007 Ingår i: Current opinion in rheumatology. - 1040-8711. ; 19:1, s. 49-54 Tidskriftsartikel (refereegranskat)
88.	Klareskog, L, et al. (författare) Smoking, citrullination and genetic variability in the immunopathogenesis of rheumatoid arthritis 2011 Ingår i: Seminars in immunology. - : Elsevier BV. - 1096-3618 .- 1044-5323. ; 23:2, s. 92-98 Tidskriftsartikel (refereegranskat)
89.	Klareskog, L., et al. (författare) The importance of differences : On environment and its interactions with genes and immunity in the causation of rheumatoid arthritis 2020 Ingår i: Journal of Internal Medicine. - : Wiley. - 0954-6820 .- 1365-2796. ; 287:5, s. 514-533 Forskningsöversikt (refereegranskat)abstract The current review uses rheumatoid arthritis (RA) as a prominent example for how studies on the interplay between environmental and genetic factors in defined subsets of a disease can be used to formulate aetiological hypotheses that subsequently can be tested for causality using molecular and functional studies. Major discussed findings are that exposures to airways from many different noxious agents including cigarette smoke, silica dust and more interact with major susceptibility genes, mainly HLA-DR genetic variants in triggering antigen-specific immune reactions specific for RA. We also discuss how several other environmental and lifestyle factors, including microbial, neural and metabolic factors, can influence risk for RA in ways that are different in different subsets of RA.The description of these processes in RA provides the best example so far in any immune-mediated disease of how triggering of immunity at one anatomical site in the context of known environmental and genetic factors subsequently can lead to symptoms that precede the classical inflammatory disease symptoms and later contribute also to the classical RA joint inflammation. The findings referred to in the review have led to a change of paradigms for very early therapy and prevention of RA and to efforts towards what we have named 'personalized prevention'. We believe that the progress described here for RA will be of relevance for research and practice also in other immune-mediated diseases.
90.	Klareskog, L, et al. (författare) What precedes development of rheumatoid arthritis? 2004 Ingår i: Ann Rheum Dis. - : BMJ. - 0003-4967. ; 63 Suppl 2, s. ii28-ii31 Tidskriftsartikel (refereegranskat)

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Författare/redaktör: Alfredsson, L (596); KLARESKOG, L (249); Olsson, T (174); Padyukov, L (121); Kockum, I. (119); Hillert, J (104); visa fler...; Bengtsson, C (72); Hedstrom, AK (69); Saevarsdottir, S (64); Askling, J (52); Kallberg, H (48); Jiang, X. (44); Alfredsson, Lars (40); Ding, B. (32); Theorell, Töres (29); Westerlund, Hugo (28); Westerlind, H (28); Nordin, Maria (27); Karlson, EW (26); Hammar, N (24); Piehl, F (24); Vahtera, Jussi (23); Stridh, P (23); Plenge, RM (23); Knutsson, Anders (23); Rugulies, Reiner (23); Singh-Manoux, Archan ... (23); Virtanen, Marianna (22); Pentti, Jaana (22); Lundberg, K. (22); Barcellos, LF (21); Ronnelid, J (21); Burr, Hermann (21); Madsen, Ida E. H. (20); Gregersen, PK (19); Schaefer, C (19); Oksanen, Tuula (19); Batty, G. David (19); Manouchehrinia, A (18); Waterboer, T (18); Dragano, Nico (18); Bjorner, Jakob B. (18); Raychaudhuri, S (17); Kivimäki, Mika (17); Holmqvist, M (17); Huang, J. (16); Hansson, M (16); Harbo, HF (16); Butt, J (16); Ferrie, Jane E (16); visa färre...

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