Help Wanted, Experience Preferred, Stamina a Must: A Narrative Review of the Contextual Factors Influencing Nursing Recruitment and Retention in Rural and Remote Western Canada from the Early Twentieth Century to 2023.

Rural and remote communities of Western Canada have struggled to recruit and retain nursing professionals since the turn of the twentieth century. Existing literature has identified the unique challenges of rural nursing due to the shifting context of rural and remote nursing practice. The objective of this narrative review is to explore the history of rural and remote nursing to better understand the contextual influences shaping rural nursing shortages in Western Canada. This narrative review compared 27 sources of scholarly and historical evidence on the nature of rural nursing practices and recruitment and retention methods following the First World War until 2023. The findings suggest that the complex nature of rural nursing practice is a consistent challenge that has intersected with the long-standing power inequities that are inherent in rural marginalization, political influences, the nursing profession, social structures, and organizational design, to perpetuate rural nursing shortages throughout the past century. Integration and collaboration are needed to reduce systemic marginalization and develop effective and sustainable solutions to reduce nursing shortages in rural and remote areas of Western Canada.

Nurses' perceptions of caring for dying patients in an open critical care unit: a descriptive exploratory study.

BACKGROUND: Nurses in critical care areas play a vital part in providing end-of-life care and recognise that an ideal death should be peaceful, dignified, and comfortable. However, environmental restrictions in critical care units can make a peaceful death unachievable and can have a profoundly negative impact on end-of-life care. PURPOSE: To describe the provision of end-of-life care in an open high-dependency unit. METHOD: A descriptive exploratory approach was used involving semi-structured interviews with a purposive sample of five registered nurses working in the high-dependency area at a major teaching hospital. The interviews were audiotaped and transcribed. Thematic analysis was used to code the data and identify themes. RESULTS: Three themes emerged from the data. The core theme was 'the nurse as protector'. The two other themes were 'conflict of care' and 'peace and quiet'. Within these themes, characteristics of an ideal death were identified and barriers to providing an ideal death were acknowledged. CONCLUSION: This study illustrates nurses' perceptions of caring for dying patients in an open critical care unit. This environment influences the development of the nursing role as protector and presents barriers to achieving an ideal death.

Reducing endocannabinoid metabolism with the fatty acid amide hydrolase inhibitor, URB597, fails to modify reinstatement of morphine-induced conditioned floor preference and naloxone-precipitated morphine withdrawal-induced conditioned floor avoidance.

The potential of the fatty acid amide hydrolase (FAAH) inhibitor, URB597, to modify drug prime-induced reinstatement of morphine-induced conditioned floor preference or naloxone-precipitated morphine withdrawal-induced conditioned floor avoidance was evaluated. In Experiment 1, morphine-induced conditioned floor preference was established across 4 conditioning trials. Following extinction training (4 trials), rats were pretreated with URB597 or vehicle prior to a morphine prime or a saline prime. Morphine reinstated the previously extinguished floor preference, but URB597 did not modify the strength of the reinstated preference. In Experiment 2, naloxone-precipitated morphine withdrawal-induced conditioned floor avoidance was established across 2 conditioning trials. Following extinction training (14 trials), rats were pretreated with URB597 or vehicle prior to a saline prime or a morphine withdrawal prime. The morphine withdrawal prime reinstated the previously extinguished floor avoidance, but URB597 did not modify the strength of reinstated avoidance. These results suggest that under the conditions in which URB597 promotes extinction (e.g., Manwell et al. (2009)) it does not interfere with drug-induced reinstatement of either conditioned floor preference or avoidance. That is, although activation of the endocannabinoid (eCB) system promotes extinction of aversive learning, it may not prevent reinstatement of that aversion by re-exposure to the aversive treatment.

Relative contribution of cell contact pattern, specific PKC isoforms and gap junctional communication in tight junction assembly in the mouse early embryo.

In mouse early development, cell contact patterns regulate the spatial organization and segregation of inner cell mass (ICM) and trophectoderm epithelium (TE) during blastocyst morphogenesis. Progressive membrane assembly of tight junctional (TJ) proteins in the differentiating TE during cleavage is upregulated by cell contact asymmetry (outside position) and suppressed within the ICM by cell contact symmetry (inside position). This is reversible, and immunosurgical isolation of the ICM induces upregulation of TJ assembly in a sequence that broadly mimics that occurring during blastocyst formation. The mechanism relating cell contact pattern and TJ assembly was investigated in the ICM model with respect to PKC-mediated signaling and gap junctional communication. Our results indicate that complete cell contact asymmetry is required for TJ biogenesis and acts upstream of PKC-mediated signaling. Specific inhibition of two PKC isoforms, PKCdelta and zeta, revealed that both PKC activities are required for membrane assembly of ZO-2 TJ protein, while only PKCzeta activity is involved in regulating ZO-1alpha+ membrane assembly, suggesting different mechanisms for individual TJ proteins. Gap junctional communication had no apparent influence on either TJ formation or PKC signaling but was itself affected by changes of cell contact patterns. Our data suggest that the dynamics of cell contact patterns coordinate the spatial organization of TJ formation via specific PKC signaling pathways during blastocyst biogenesis.

Specific PKC isoforms regulate blastocoel formation during mouse preimplantation development.

During early mammalian development, blastocyst morphogenesis is achieved by epithelial differentiation of trophectoderm (TE) and its segregation from the inner cell mass (ICM). Two major interrelated features of TE differentiation required for blastocoel formation include intercellular junction biogenesis and a directed ion transport system, mediated by Na+/K+ ATPase. We have examined the relative contribution of intercellular signalling mediated by protein kinase C (PKC) and gap junctional communication in TE differentiation and blastocyst cavitation. The distribution pattern of four (delta, theta, iota/lambda, zeta) PKC isoforms and PKCmicro/PKD1 showed partial colocalisation with the tight junction marker ZO-1alpha+ in TE and all four PKCs (delta, theta, iota/lambda, zeta) showed distinct TE/ICM staining patterns (predominantly at the cell membrane within the TE and cytoplasmic within the ICM), indicating their potential contribution to TE differentiation and blastocyst morphogenesis. Specific inhibition of PKCdelta and zeta activity significantly delayed blastocyst formation. Although modulation of these PKC isoforms failed to influence the already established programme of epithelial junctional differentiation within the TE, Na+/K+ ATPase alpha1 subunit was internalised from membrane to cytoplasm. Inhibition of gap junctional communication, in contrast, had no influence on any of these processes. Our results demonstrate for the first time that distinct PKC isotypes contribute to the regulation of cavitation in preimplantation embryos via target proteins including Na+/K+ ATPase.

PKC signalling regulates tight junction membrane assembly in the pre-implantation mouse embryo.

Epithelial differentiation including tight junction (TJ) formation occurs exclusively within the trophectoderm (TE) lineage of the mouse blastocyst. Here we examine mechanisms by which TJ protein membrane assembly might be regulated by protein kinase C (PKC) in the embryo. To overcome the inherent staging asynchrony of individual blastomeres within intact embryos, we have used isolated inner cell masses (ICMs) from early blastocysts to induce epithelial differentiation in their outer cells responding to their new cell contact pattern. Two TJ proteins examined retain their order of membrane assembly in isolated ICMs in culture as during normal development (early-assembling ZO-2 and late-assembling ZO-1alpha(+)), but this process is highly accelerated. Using six chemical modulators of PKC activity, we show here that PKC signalling is involved in the regulation of TJ membrane assembly. While indolactam-mediated PKC activation stimulates membrane assembly of both TJ proteins, TPA-mediated PKC activation stimulates only that of ZO-1alpha(+). The PKC inhibitors Ro-31-8220, Ro-31-8425 and Gö 6983 suppress the stimulatory effect of both PKC activators on membrane assembly to varying extents according to inhibitor and TJ protein examined. Gö 6983 similarly inhibits ZO-2 and ZO-1alpha(+) membrane assembly. PKC inhibition by Gö 6976 appeared to stimulate TJ membrane assembly. Despite the broad PKC isotype specificity of the inhibitors used, these data suggest that the two TJ proteins are differently regulated by PKC isotypes or subfamilies. As Gö 6983 uniquely affects aPKC (particularly PKCzeta) and we find that both PKCdelta and zeta relocate upon activator treatment to colocalise partially with the TJ proteins in isolated ICMs, we suggest that at least PKCdelta and zeta may play a central role in regulating TJ membrane assembly.