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Motherhood has been described as an identity, a role, and a way of participating in life (Arendell, 2000; Farber, 2004). Motherhood has also been described as 'work', the care taking, nurturing and teaching of children (Francis-Connolly, 2000). Mothers with arthritis have reported difficulty in the tasks of parenting and household work (Allaire et al., 1991; Backman, Kennedy, Chalmers & Singer, 2004; Barlow, Cullen, Foster, Harrison & Wade, 1999; Grant, Cullen & Barlow, 2000; Reisine, Grady, Goodenow & Fifield, 1998), however, we know little about how a mother experiences these challenges. While the subjective experience of being a mother and having a disability is intrinsically linked to participation, health and social interaction (Farber, 2004), research has not been conducted on how mothers with arthritis experience mothering in the presence of arthritis, and how this experience affects their participation, identity and social interaction. This narrative research study asks "How is being a mother and doing motherhood activities affected by your arthritis?" Study objectives include: 1) Describe mothers' experiences of nurturing, teaching and caring for their children. 2) Describe how mothers understand and explain the effect of arthritis on their role of mother. 3) Describe whether or not this understanding changes how mothers participate and interact in their community. Narrative inquiry was used to explore the experiences of eight married mothers with inflammatory arthritis who have at least one child (aged 0-18) living at home. Purposive sampling allowed representation of families from different communities, with children of different ages. Data collection included two in-depth interviews, participant observation, document review, and fine art painting. Data was coded and analyzed using narrative inquiry techniques (Coffey & Atkinson, 1996; Riessman, 1993; Sandelowski, 1991). Overarching storylines are presented as narratives that describe the mother's experiences of identifying with the role of mother, participation, fatigue and the social context in which mothering occurs. This study contributes to the sparse body of literature on the impact of arthritis on participation in maternal practices and social interaction, informing health professionals about the experience of mothering with arthritis.

PG receptor and COX gene expression patterns and LPS induced PG production have been investigated in human macrophages and osteoclasts as cell models to study rheumatoid arthritis. The results suggest that PG receptors DP₂, EP₁ and EP₃ may not be directly involved in macrophage-mediated inflammatory responses and osteoclast-mediated bone erosion due to the absence of receptor expression. Because of the undetectable levels of natural ligand, IP receptor effects are dependent on the availability of PGI₂ secreted from other types of cells in the close vicinity. Meanwhile, DP₁, EP₂, EP₄, FP and TP receptors, and their natural agonists, may play important and diverse roles in these cells. TXA₂ is the most abundant prostanoid found in these cells with or without LPS stimulation. The TP receptor pathway in inflammation and bone resorption may have been previously overlooked. AGN-211377 was discovered with a unique pharmacological profile, which provided antagonism at specific proinflammatory PG receptor subtypes with the rank order of TP > DP₁ ≥FP >EP₁ > DP₂ and no apparent antagonism on EP₂, EP₃, and IP receptors. AGN-211377 significantly and dose-dependently suppresses LPS- or TNFα-induced release of 12 proinflammatory cytokines/ chemokines in macrophages, and osteolysis activity in osteoclasts. Collectively, these results suggest the existence of prostanoid receptors DP₁ FP, and TP in human macrophages and osteoclasts, which are likely to play a proinflammatory role. AGN-211377 is at least as effective as diclofenac (a NSAID) and rofecoxib (a COX1B) in suppression of proinflammatory cytokine/chemokine production in macrophages, and in suppression of osteoclast function. Moreover, AGN-211377 may represent a safer replacement for COX1Bs. The therapeutic advantages of AGN-211377 can be extended beyond RA treatment.

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Neuropsychiatric (NP) symptoms are relatively common in patients with SLE. The diverse and dramatic clinical presentations, the unclear pathogenesis, the lack of diagnostic test/s and uncertainties about the optimal management are some problems facing a clinician. When serum anti P antibodies were claimed to be highly correlated to lupus psychosis, this needed confirmation. An ELISA for measuring anti P antibodies was developed and validated. The prevalence of anti P antibodies was determined in different patient groups in a large retrospective study. Although anti P antibodies were highly specific for SLE, there was no correlation between the presence of these antibodies and lupus psychosis or other NP symptoms. Two prospective studies were carried out to eliminate any bias in our retrospective study. In one, none of the patients developed psychosis and these antibodies were not found to be specific for lupus depression or anxiety. In the other, anti P antibodies were measured in Malaysian Chinese SLE patients. No correlation was found between these antibodies and NP-SLE but a high prevalence of these antibodies was demonstrated in this group. Genetic studies showed that there was an increase in HLA-Dr2w16X subtype allele in anti P-positive patients but this did not reach significance. The usefulness of measuring antineuronal antibodies in helping to diagnose NP-SLE was examined but these antibodies were not better indicators of NP-SLE. Although the clinical correlations of anti P antibodies remain controversial, anti P antibodies were found to selectively bind to neuroblastoma cell surfaces <i>in vitro</i> but the nature of the surface antigen was not determined. Finally, sera from patients with lupus psychosis were found to significantly influence the response of neuroblastoma cells to agonist-induced stimulation and if confirmed, would offer an explanation for the reversible changes in cell function associated with psychiatric lupus.

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