Measuring Scope of Practice Enactment among Primary Care Registered Nurses in Ontario

Background: Primary care is the sector of health care in which patients first establish contact with the health system, are provided person-focused care over time for all new or common needs, and receive coordinated integrated health services provided elsewhere by other members of the health care team. Registered Nurses (RNs) in Canada provide care within this sector in varying roles. The extent to which RNs enact their full scope of practice in primary care settings in Canada is not known. The Actual Scope of Practice questionnaire (ASCOP) is a 26 item Likert scale questionnaire developed by researchers in Canada and validated in the acute care setting to measure the extent to which RNs apply the knowledge, skills and competencies of the professional full scope of practice. Similar to the acute care setting, there is a need to measure scope of practice enactment in the primary care setting. Objectives: The overall aim of this thesis was to measure scope of practice enactment in the primary care setting. Two research objectives were addressed: (1) to revise and adapt the ASCOP questionnaire for use in the primary care setting, and (2) to determine internal consistency, construct validity, and sensitivity of the modified instrument, the ASCOP-PC. Methods: To address the first objective, a narrative literature review and synthesis and an expert panel review was conducted. To address the second objective a cross-sectional survey of 178 RNs working in primary care organizations in Ontario was conducted Results: The ASCOP, with few modifications, addressed key attributes of nursing scope of practice in the primary care setting. The ASCOP-PC yielded acceptable alpha coefficients ranging from 0.66 to 0.91 and explained variances from 44.2 to 62.6. Total mean score of 5.16 suggests that RNs within these models of care almost always engage in activities reflected in the ASCOP-PC. Interpretation: Findings from this study support the use of a the modified ASCOP questionnaire as a reliable and valid measure of scope of practice enactment among primary care nurses in the primary care setting.

IMPACT OF RNA VIRUSES ON THE REGULATION OF IL-23 IN MOUSE AND HUMAN MODELS OF INFECTION.

Interluekin-23 (IL-23) is a pro-inflammatory cytokine critical to the regulation of innate and adaptive immune responses. The main role for this cytokine is in the proliferation and differentiation of the IL-17 producing CD4 T helper cell, Th17. Virus infection deregulates IL-23 expression and function, but little is known about the mechanism behind this phenomena. Here, I demonstrate a reduction of Toll like receptor (TLR) ligand-induced IL-23 expression in lymphocytic choriomeningitis virus (LCMV)-infected bone marrow-derived dendritic cells (BMDCs), indicating that a function of these cells is disrupted during virus infection. I propose a mechanism of TLR ligand-induced IL-23 expression inhibition upon LCMV infection via the deactivation of p38, AP-1, and NF-κB. Further analysis revealed a direct relationship between LCMV infection with the IL-10 and SOCS3 expression. To understand IL-23 function, I characterized IL-23-induced JAK/STAT signalling pathway and IL-23 receptor expression on human CD4 T cells. My results demonstrate that IL-23 induces activation of p-JAK2, p-Tyk2, p-STAT1, p-STAT3, and p-STAT4 in CD4 T cells. For the first time I show that IL-23 alone induces the expression of its own receptor components, IL-12Rβ1 and IL-23Rα, in CD4 T cells. Blocking JAK2, STAT1, and STAT3 activation with specific inhibitors detrimentally effected expression of IL-23 receptor demonstrating that activation of JAK/STAT signalling is important for IL-23 receptor expression. I also addressed the effect of viral infection on IL-23 function and receptor expression in CD4 T cells using cells isolated from HIV positive individuals. These studies were based on earlier reports that the expression of IL-23 and the IL-23 receptor are impaired during HIV infection. I demonstrate that the phosphorylation of JAK2, STAT1, and STAT3 induced by IL-23, as well as IL-23 receptor expression are deregulated in CD4 T cells isolated from HIV positive individuals. This study has furthered the understanding of how the expression and function of IL-23 is regulated during viral infections.