Eliciting Tacit Knowledge with a Grammar-targeted Interview Method

Tacit knowledge represents a challenge to knowledge elicitation due to the assumption that this type of knowledge cannot be articulated. We argue that Polanyi's (1966:4) widely cited notion that “we know more than we can tell” represents a weak model of language that does not acknowledge the grammatical patterns in spoken discourse that we, as speakers, apply tacitly. We investigate the hypothesis that individuals articulate what they know through grammatical patterns, referred to as under-representation, without direct awareness. This thesis develops and pilots a grammar-targeted interview method aimed at unpacking specific grammatical features that occur in spoken discourse. The model of language from which these features are derived is Systemic Functional Linguistics. We report findings from three empirical studies of tacit knowledge in corporate organisations where we used the grammar-targeted interview technique to elicit tacit knowledge in the areas of knowledge management, requirements analysis and performance reviews. We compare this interview method with a content-targeted approach. The results show that the grammar-targeted technique produces less under-represented discourse thus allowing tacit knowledge held by the interviewees to be made visible. Based on the linguistic analyses undertaken in these field studies we propose that Polanyi’s expression “we know more than we tell” be reformulated to “we tell more than we realise we know”

Impaired dendritic cell proinflammatory cytokine production in psoriatic arthritis

Item does not contain fulltextOBJECTIVE: The pathogenesis of psoriatic arthritis (PsA) remains poorly understood. The underlying chronic inflammatory immune response is thought to be triggered by unknown environmental factors potentially arising from a defective immune function. We undertook this study to determine whether an impaired acute inflammatory response by dendritic cells (DCs) might compromise the clearance of bacteria and predispose to chronic inflammation. METHODS: We determined cytokine production by DCs from healthy controls and from patients with rheumatoid arthritis, PsA, and psoriasis in response to Mycobacterium tuberculosis, Mycobacterium avium paratuberculosis, and a range of other bacteria and Toll-like receptor (TLR) ligands. Phenotypic differences involved in cellular responses against (myco)bacteria were determined by quantitative polymerase chain reaction and flow cytometry. RESULTS: The secretion of proinflammatory cytokines by PsA DCs was impaired upon in vitro challenge with mycobacteria and TLR-2 ligands. This impairment was associated with elevated serum levels of C-reactive protein. The expression of TLR-2 and other receptors known to mediate mycobacterial recognition was unaltered. In contrast, the intracellular TLR inhibitors suppressor of cytokine signaling 3 and A20 were more highly expressed in DCs from PsA patients. PsA DCs further demonstrated up-regulated levels of ATG16L1, NADPH oxidase 2, and LL37, which are molecules implicated in the immune response against intracellular bacteria. CONCLUSION: Our findings indicate that DCs from PsA patients have a disordered immune response toward some species of (myco)bacteria. This might predispose to impaired immune responses to, and in turn impaired clearance of, these bacteria, setting the stage for the chronic inflammation of joints, entheses, skin, and the gut

Onset of rheumatoid arthritis after COVID-19: coincidence or connected?

Immunogenetics and cellular immunology of bacterial infectious disease

Arthritis flare after stopping TNF inhibitor in RA: frequency, predictability and radiography

Contains fulltext : 213929.pdf (publisher's version ) (Open Access)Radboud University, 10 januari 2020Promotor : Riel, P.L.C.M. van Co-promotores : Jansen, T.L.Th.A., Jacobs, J.W.G., Luime, J.J

Flare Rate in Patients with Rheumatoid Arthritis in Low Disease Activity or Remission When Tapering or Stopping Synthetic or Biologic DMARD: A Systematic Review

Objective. To evaluate the risk of having a disease flare in patients with rheumatoid arthritis (RA) with low disease activity (LDA) or in remission when deescalating (tapering or stopping) disease-modifying antirheumatic drug (DMARD) therapy. Methods. A search in medical databases including publications from January 1950 to February 2015 was performed. Included were trials and observational studies in adults with RA who were in LDA or remission, evaluating >= 20 patients tapering or stopping DMARD. Flare rates had to have been reported. A metaanalysis was performed on studies deescalating tumor necrosis factor (TNF) blockers. Results. Four studies evaluated synthetic DMARD. Flare rates ranged from 8% at 24 weeks to 63% at 4 months after deescalation. Fifteen studies reported on TNF blockers. Estimated flare rates by metaanalysis on studies tapering or stopping TNF blockers were 0.26 (95% CI 0.17-0.39) and 0.49 (95% CI 0.27-0.73) for good-quality and moderate-quality studies, respectively. Flare rates in 3 studies stopping tocilizumab were 41% after 6 months, 55% at 1 year, and 87% at 1 year. Flare rates in 3 studies deescalating abatacept were 34% at 1 year, 41% at 1 year, and 72% at 6 months. Five studies evaluating radiographic progression in patients deescalating treatment all found limited to no progression. Conclusion. Results suggest that more than one-third of patients with RA with LDA or in remission may taper or stop DMARD treatment without experiencing a disease flare within the first year. Dose reduction of TNF blockers results in lower flare rates than stopping and may be noninferior to continuing full dose. Radiological progression after treatment deescalation remains low, but may increase slightly

Is radiographic progression a downside of stopping TNF-inhibitor in RA patients with low disease activity, if this is followed by flare? A sub-study of the POET-US trial

Contains fulltext : 225880.pdf (Publisher’s version ) (Open Access