Publications by authors named "Sarah Ashton"

Purpose: Participation in Brazilian jiu-jitsu and mixed martial arts has increased over the last three decades. These sports feature submission attacks, including strangles. These strangles, termed "chokes" in this context, primarily limit blood flow to the brain via compression of neck vasculature.

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Peripheral intravenous cannulation (PIVC) is one of the most commonly performed invasive procedures in healthcare and can be a stressful experience for patients. Co-creating a patient journey map of intravenous therapy (IVT) together with patients highlighted the need to better understand patient experiences of IVT and informed the development of a patient-reported experience measure of intravenous therapy (IVT). The British Columbia (BC) Lower Mainland IVT Working Group, the BC Office of Patient-Centred Measurement and the provincial supplier of IVT products, hypothesized patient feedback about their IVT experiences would garner new insights to improve both patient experiences and outcomes related to IVT.

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Background: End-of-life (EOL) discussions remain difficult in non-terminal patients as death is often perceived as a taboo and uncertainty. However, the call for proper EOL discussions has recently received public attention and media coverage. Evidence also reveals that non-terminal patients are more satisfied with health-care encounters when EOL has been discussed.

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The chemokine CXC receptor 4 (CXCR4) is activated by stromal cell-derived factor (SDF-1α). CXCR4 may be part of a lipopolysaccharide (LPS) sensing co-clustering complex that modulates TLR4 activation and evidence suggest that SDF-1α can activate anti-inflammatory signaling pathways and suppress inflammation. In the present study we examined the hypothesis that the SDF-1α peptide analog and CXCR4 agonist CTCE-0214 is anti-inflammatory in three distinct models of murine systemic inflammation.

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Peroxisome proliferator activated receptor-gamma (PPARgamma) has been reported to exert anti-inflammatory properties in endotoxic shock and sepsis. One phenomenon that alters the inflammatory response to endotoxin [lipopolysaccharide (LPS)] is endotoxin tolerance, which is caused by previous exposure to endotoxin. Here, we investigate whether changes in endogenous PPARgamma function regulate this phenomenon using three different models of LPS-induced tolerance in macrophages.

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Previous studies have suggested that heterotrimeric G(i) proteins, Src tyrosine kinase and phosphatidylinositol-3 kinase (PI3 Kinase) are involved in signaling events induced by lipopolysaccharide (LPS) leading to pro-inflammatory cytokines gene expression. To investigate the involvement of these mediators in Gram-positive bacteria induced pro-inflammatory cytokine expression, LPS (10 ng/ml), heat killed group B Streptococci (GBS 1 microg/ml) and Staphylococcus aureus (SA 10 microg/ml) were used to induce TNFalpha production in the murine J774A.1 macrophage (MØ) cell line and human promonocytic THP-1 cell line.

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Bacterial products, such as lipopolysaccharide (LPS) or heat-killed Escherichia coli (EC), and heat-killed Staphylococcus aureus (SA) are potent activators of macrophages (MØ). When stimulated by these bacterial components, MØ produce inflammatory mediators, such as nitric oxide (NO) and thromboxane (Tx) B(2). Bacterial mediator production is preceded by the activation of various signal transduction pathways.

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Previous studies have suggested that heterotrimeric G proteins and tyrosine kinases may be involved in lipopolysacchaide (LPS) signaling events. Signal transduction pathways activated by LPS we examined in human pomonocytic THP-l cells. We hypothesized that Gi proteins and Src tyrosine kinase differentially affect mitogen-activated protein (MAP) kinases (MAPK) and nuclear factor kappa(NF-kappaB) activation.

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