Australasian ED doctors, predominantly specialist emergency physicians or trainees, perform the majority of ED intubations using rapid sequence induction as their preferred technique mainly for medical indications. First attempt success rate was not different between different types of EDs, and is comparable published international data. Complications are not infrequent, and are comparable to other published series. Monitoring and reporting of ED intubation practice will enable continued improvements in the safety of this high-risk procedure.

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Objective We aim to investigate whether a bundle of changes made to the practice of endotracheal intubation in our ED was associated with an improvement in first pass success rate and a reduction in the incidence of complications. Methods We used a prospective observational study. Results The data on 360 patients who were intubated during an 18‐month period following the introduction of these changes were compared with our previously published observational data. Success on first attempt at intubation improved 83.4% to 93.9% (P < 0.0001). The proportion of patients with one or more complication fell from 29.0% to 19.4% (P < 0.042). Oesophageal intubation fell from 4.0% to 0.3% (P < 0.001), and there was a non‐significant reduction in the rate of desaturation, from 15.6% to 10.9% (P < 0.07). Conclusion We have shown that, through the introduction of a bundle of changes that spans the domains of staff training, equipment and practice standardisation, we have made significant improvements in the safety of patients undergoing endotracheal intubation in our ED.

Background: Mast cells modulate events in wound healing. Results: Shorter forms of perlecan are produced by mast cells via proteolytic processing and alternative splicing, which contain domain V and functional endorepellin. Conclusion:The production of these shorter forms modulates endothelial cell adhesion, proliferation, and migration. Significance: Mast cells produce specific forms of perlecan that affect endothelial cell behavior.

CXCL10 (IP10) is involved in mast cell migration to airway smooth muscle (ASM) bundles in asthma. We aimed to investigate the role of cytokine-induced MAPK activation in CXCL10 production by ASM cells from people with and without asthma. Confluent growth-arrested ASM cells were treated with inhibitors of the MAPKs ERK, p38, and JNK and transcription factor NF-κB, or vehicle, and stimulated with IL-1β, TNF-α, or IFN-γ, alone or combined (cytomix). CXCL10 mRNA and protein, JNK, NF-κB p65 phosphorylation, and Iκ-Bα protein degradation were assessed using real-time PCR, ELISA, and immunoblotting, respectively. Cytomix, IL-1β, and TNF-α induced CXCL10 mRNA expression more rapidly in asthmatic than nonasthmatic ASM cells. IL-1β and/or TNF-α combined with IFN-γ synergistically increased asthmatic ASM cell CXCL10 release. Inhibitor effects were similar in asthmatic and nonasthmatic cells, but cytomix-induced release was least affected, with only JNK and NF-κB inhibitors halving it. Notably, JNK phosphorylation was markedly less in asthmatic compared with nonasthmatic cells. However, in both, the JNK inhibitor SP600125 reduced JNK phosphorylation and CXCL10 mRNA levels but did not affect CXCL10 mRNA stability or Iκ-Bα degradation. Together, the JNK and NF-κB inhibitors completely inhibited their CXCL10 release. We concluded that, in asthmatic compared with nonasthmatic ASM cells, JNK activation was reduced and CXCL10 gene expression was more rapid following cytomix stimulation. However, in both, JNK activation did not regulate early events leading to NF-κB activation. Thus JNK and NF-κB provide independent therapeutic targets for limiting CXCL10 production and mast cell migration to the ASM in asthma.