Rheumatoid arthritis (RA) is a chronic disease characterized by an overactive immune system and joint inflammation. Population-based administrative health data (AHD) are widely used for RA outcomes research and surveillance. However, AHD may not completely capture all cases of RA in the population. Capture-recapture (CR) methods have been proposed to describe the completeness of AHD for estimating disease population size, but AHD may not conform to the assumptions that underlie CR models. A Monte Carlo simulation study was used to investigate the effects of violations of the assumptions for two-source CR methods: dependence between data sources and heterogeneity of capture probabilities. We compared the Chapman estimator and an estimator based on the multinomial logistic regression model (MLRM) to study relative bias (RB), coverage probability (CP) of 95% confidence intervals, width of 95% confidence intervals (WCI), and root-mean-square-error (RMSE) in prevalence estimates. The effects of misspecification of the MLRM were also investigated. In addition, the Chapman and MLRM estimators were used to estimate RA prevalence using AHD data from Saskatchewan, Canada. Population sizes were consistently underestimated for CR methods when the assumptions were violated. The estimated population size for both of the estimators did not differ substantially except for the RMSE values. Parameter estimates became biased when the MLRM model was misspecified, but there was little impact on population size estimates. In conclusion, CR methods are recommended to reduce bias in prevalence estimates based on AHDS. Because these methods may be sensitive to assumption violations, researchers should consider potential dependence between data sources. As well, sufficient overlap in the cases captured by each data source (e.g., 50% of the cases are captured by both data sources) or balanced capture probability in each data source is needed to effectively implement these methods. Researchers who estimate population size using CR methods in AHDs should favour the MLRM estimator over the Chapman estimator.

<p>This study explored women's perceptions of how their illness (Rheumatoid Arthritis- RA) affects their relationship with their intimate life partner. RA is a chronic, inflammatory, auto-immune illnes, which mainly affects the synovial membranes of multiple joints. This highly inflammatory poly-arthritis may lead to joint destruction, chronic pain, deformity and loss of functioning as unfortunate outcomes of the established illness. RA affects key life domains such as psychological well-being, social well-being, family and couple relationships, employment, loss of independence and restrictions in daily functioning.</p>

The Leukocyte Immunoglobulin-like Receptors (LILRs) are a family of receptors that is broadly expressed on all leukocytes and have the ability to regulate their function. A substantial amount of evidence suggests that LILRs may be involved in immune homeostasis but also immune dysregulation. We therefore studied the role of LILRs in relation to the autoimmune disease, rheumatoid arthritis (RA). RA is a chronic and systemic inflammatory disease involving inflammation of the joints affecting the synovial membrane, cartilage and bone. Much of the tissue damage is a result of an inappropriate immune response within the joint space caused by the unwarranted activation of leukocytes. Here were report that LILRA2 (an activating receptor) that has been previously shown to be highly expressed in the rheumatoid synovium, induces the production of pro-inflammatory cytokines TNF-α, IL-1, IL-6, IFN-γ and IL-10 in primary monocytes. These cytokines are known to have an important role in the pathogenesis of RA indicating a pathway by which LILRA2 exacerbates RA. Co-ligation of LILRB4 (an inhibitory receptor) with LILRA2 abolishes cytokine production suggesting that LILRB4 is able to suppress the function of LILRA2. Expression of both LILRA2 and LILRB4 are regulated by inflammatory cytokines and LPS, indicative of a feedback mechanism. There is also cross-talk between LILRs and TLR4 as co-stimulation with LPS and either LILRA2 or LILRB4 inhibits cytokine production. A differential expression of LILRs has also been identified on lymphocytes of patients with RA whereby an increase of LILRA1 (activating) and LILRB1 (inhibitory) expressing circulating lymphocytes is present in RA patients when compared to healthy control subjects. From these studies, we propose that LILRs have a functional role in RA by regulating local and systemic inflammation. The presence of LILRA2 in the RA joint is detrimental since its potent ability to induce inflammatory cytokines, particularly TNF-α, can initiate leukocyte recruitment and activation of proteases. Along with TLR4, LILRA2 and LILRB4 have the potential to moderate the innate immune system via regulation of cytokine production. Furthermore, suppression of LILRA2 function may serve as a therapeutic tool in many inflammatory diseases.

Project (D. Min.)--Perkins School of Theology, Southern Methodist University, 1977. / Includes bibliographical references (leaves 62-63).

Diss. (sammanfattning) Stockholm : Karol. inst., 2003. / Härtill 4 uppsatser.

Diss. (sammanfattning) Stockholm : Karol. inst., 2003. / Härtill 4 uppsatser.

Thesis (Ph.D.)--University of Adelaide, Dept. of Medicine, 2001. / Includes bibliographical references (leaves 182-240).

Thesis (Psy.D.)--California School of Professional Psychology, 1999. / Includes bibliographical references (leaves 107-117).

Diss. (sammanfattning) Stockholm : Karolinska institutet, 2005. / Härtill 4 uppsatser.

Thesis--Lund University, 1995.