TY  - JOUR
AB  - OBJECTIVES: To detect the associations of a healthy lifestyle and genetic susceptibility with incident osteoarthritis (OA) in the UK biobank study. METHODS: We included 314 729 participants from UK biobank. Five modifiable lifestyle factors including weight management, diet, physical activity, sleep behavior and sedentary behavior were included to generate an overall lifestyle score. Genetic susceptibility was calculated by using polygenic risk score (PRS) of OA. Participants diagnosed with OA were identified by using ICD-9 and ICD-10. Covariates included age, sex, education, Townsend deprivation index, glucosamine use, analgesics use and comorbidities. Cox regression analyses were performed to examine the associations of genetic susceptibility and healthy lifestyle with incident OA. RESULTS: Adopting a more favorable lifestyle can be beneficial in significantly reducing the risk of incident total, knee and hip OA (all p < 0.01). PRS was significantly associated with greater risks of total, knee and hip OA. Compared with unfavorable lifestyle, favorable lifestyle was significantly associated with a lower risk of total OA across low (HR, 0.64; 95%CI, 0.58-0.70), intermediate (HR, 0.59; 95%CI, 0.56-0.63) and high genetic risk groups (HR, 0.58; 95%CI, 0.53-0.64). Similar results were observed on knee OA and hip OA. No significant interactions were detected between lifestyle and PRS for total, knee or hip OA. CONCLUSION: These data suggest that a healthier lifestyle is consistently associated with a lower risk of OA, regardless of genetic risks. Our findings highlight the importance of adherence to an overall healthy lifestyle in attenuating the risk of OA.
AU  - Chen, S.
AU  - Zhang, Y.*
AU  - Fan, T.*
AU  - Zeng, M.*
AU  - Yang, Q.*
AU  - Yang, H.*
AU  - Fang, X.*
AU  - Jin, X.*
AU  - Cao, P.*
AU  - Wang, Z.*
AU  - Hunter, D.J.*
AU  - Zhou, Y.*
AU  - Ding, C.*
AU  - Zhu, Z.*
C1  - 75037
C2  - 57728
CY  - Great Clarendon St, Oxford Ox2 6dp, England
TI  - Associations of healthy lifestyle and genetic susceptibility with risks of osteoarthritis: A prospective cohort study.
JO  - Rheumatology
PB  - Oxford Univ Press
PY  - 2025
SN  - 1462-0324
ER  - 

TY  - JOUR
AU  - Lorenz, G.*
AU  - Schaaf, C.P.*
AU  - Moog, P.*
AU  - Bachmann, Q.*
AU  - Popp, F.*
AU  - Rech, J.*
AU  - Schorr, J.*
AU  - Gabl, C.*
AU  - Küchle, C.*
AU  - Delbridge, C.*
AU  - Weirich, G.G.*
AU  - Heemann, U.*
AU  - Schneider, G.*
AU  - Lange, N.*
AU  - Wagner, M.
AU  - Berg-Johnson, W.*
C1  - 66471
C2  - 53185
SP  - E188-E190
TI  - Brain oedema due to DIC in a patient with AOSD associated hemophagocytic lymphohistiocytosis-a case report.
JO  - Rheumatology
VL  - 62
IS  - 6
PY  - 2022
SN  - 1462-0324
ER  - 

TY  - JOUR
AU  - Thompson, G.*
AU  - Moura, M.C.*
AU  - Nelson, D.*
AU  - Fussner, L.*
AU  - Hummel, A.*
AU  - Jenne, D.
AU  - Fervenza, F.*
AU  - Hoffman, G.*
AU  - Kallenberg, C.*
AU  - Langford, C.*
AU  - McCune, J.*
AU  - Merkel, P.*
AU  - Monach, P.*
AU  - Seo, P.*
AU  - Spiera, R.*
AU  - St Clair, E.W.*
AU  - Ytterberg, S.*
AU  - Stone, J.*
AU  - Robinson, W.*
AU  - Pang, Y.*
AU  - Specks, U.*
C1  - 56751
C2  - 47281
CY  - Great Clarendon St, Oxford Ox2 6dp, England
SP  - 222
TI  - Preferential binding to an unexpected epitope of a chimeric recombinant proteinase 3 variant by anti-neutrophil cytoplasmic antibodies.
JO  - Rheumatology
VL  - 58
IS  - 2
PB  - Oxford Univ Press
PY  - 2019
SN  - 1462-0324
ER  - 

TY  - JOUR
AB  - In a large-scale ENU (N-ethyl-N-nitrosourea) mouse mutagenesis programme, we previously have identified and characterized a novel mutation Ali18 that causes inflammatory arthritis like lesions in peripheral joints. In this study, we analysed the immune system of Ali18 mice to understand mechanisms underlying the spontaneous inflammation. METHODS: Humoral and cellular components of the immune system were phenotyped by ELISA and flow cytometry. The contribution of the immune system for phenotype expression was analysed in disease transfer experiments. The involvement of the adaptive immune system was investigated in Ali18;Rag1 double mutants and the influence of environmental factors was analysed in Ali18 mice reared under germ-free conditions. RESULTS: Bone marrow cells from Ali18 mice were able to transfer the disease phenotype to naïve wild-type recipients suggesting that cellular components of the reconstituted immune system were sufficient to induce arthritis. Ali18 mice revealed abnormal leucocyte populations including lymphocytes and granulocytes, as well as increased plasma IL-5 and IgE levels. Ali18;Rag1 double homozygous mutants, which lack mature lymphocytes, still developed arthritis, suggesting that the phenotype is independent of the adaptive immune system. In addition, the arthritis phenotype appeared to be independent from environmental conditions as demonstrated in mice reared under germ-free conditions. CONCLUSIONS: The Ali18 mutation induces inflammatory arthritis through bone marrow-derived cells. However, non-pro-inflammatory cytokine cascades and mature lymphocyte independent-mechanisms are crucial for initiation and progression of the phenotype. Ali18 mice may thus represent a model to study mechanisms involved in seronegative arthritis induced by cells of the innate immune system.
AU  - Abe, K.
AU  - Wechs, S.
AU  - Kalaydjiev, S.
AU  - Franz, T.J.
AU  - Busch, D.H.
AU  - Fuchs, H.
AU  - Soewarto, D.
AU  - Behrendt, H.
AU  - Wagner, S.
AU  - Jakob, T.
AU  - Hrabě de Angelis, M.
C1  - 2707
C2  - 25146
SP  - 292-300
TI  - Novel lymphocyte-independent mechanisms to initiate inflammatory arthritis via bone marrow-derived cells of Ali18 mutant mice.
JO  - Rheumatology
VL  - 47
IS  - 3
PB  - Oxford Univ. Press
PY  - 2008
SN  - 1462-0324
ER  - 

TY  - JOUR
AB  - To investigate long-term health effects in AS patients treated with (224)Ra. METHODS: A prospective epidemiological study has been carried out on 1471 AS patients treated with repeated intravenous injections of (224)Ra between 1948 and 1975. These patients have been followed together with a control group of 1324 AS patients not treated with radioactive drugs and/or X-rays. Numbers of malignancies expected in a normal population were computed from German and Danish cancer registry data. RESULTS: After a mean follow-up time of 26 yrs in the exposed group or 25 yrs in the control group, causes of death have been ascertained for 1006 exposed patients and 1072 controls. In particular, 19 cases of leukaemia were observed in the exposure group (vs 6.8 cases expected, P < 0.001) compared to 12 cases of leukaemia in the control group (vs 7.5 cases expected). Further subclassification of the leukaemia cases demonstrated a high increase of myeloid leukaemia in the exposure group (11 cases observed vs 2.9 cases expected, P < 0.001), especially a high excess of acute myeloid leukaemias (7 cases observed vs 1.8 cases expected, P = 0.003), whereas in the controls the observed cases are within the expected range (4 myeloid leukaemias vs 3.1 cases expected). CONCLUSIONS: The enhanced leukaemia incidence in the exposed group is in line with results from experiments in mice injected with varying amounts of the bone-seeking alpha-emitter (224)Ra. In these studies, in animals exposed to lower doses of (224)Ra, i.e. at doses lower than those found to induce osteosarcomas, an increased risk of leukaemia was observed.
AU  - Wick, R.R.
AU  - Nekolla, E.A.*
AU  - Gaubitz, M.*
AU  - Schulte, T.L.*
C1  - 2623
C2  - 25321
SP  - 855-859
TI  - Increased risk of myeloid leukaemia in patients with ankylosing spondylitis following treatment with radium-224.
JO  - Rheumatology
VL  - 47
IS  - 6
PB  - Oxford Univ. Press
PY  - 2008
SN  - 1462-0324
ER  -