32 research outputs found
Here one year, gone the next? Investigating persistence of frequent emergency department attendance: a retrospective study in Australia
Objectives Patients are presenting to emergency departments (EDs) with increasing complexity at rates beyond population growth and ageing. Intervention studies target patients with 12 months or less of frequent attendance. However, these interventions are not well targeted since most patients do not remain frequent attenders. This paper quantifies temporary and ongoing frequent attendance and contrasts risk factors for each group.
Design Retrospective population-based study using 10 years of longitudinal data.
Setting An Australian geographic region that includes metropolitan and rural EDs.
Participants 332 100 residents visited any ED during the study period.
Main outcome measure Frequent attendance was defined as seven or more visits to any ED in the region within a 12-month period. Temporary frequent attendance was defined as meeting this threshold only once, and ongoing more than once. Risk factors for temporary and ongoing frequent attenders were identified using logistic regression models for adults and children.
Results Of 8577 frequent attenders, 80.1% were temporary and 19.9% ongoing (12.9% repeat, 7.1% persistent). Among adults, ongoing were more likely than temporary frequent attenders to be young to middle aged (aged 25-64 years), and less likely to be from a high socioeconomic area or be admitted. Ongoing frequent attenders had higher rates of non-injury presentations, in particular substance-related (OR=2.5, 99% CI 1.1 to 5.6) and psychiatric illness (OR=2.9, 99% CI 1.8 to 4.6). In comparison, children who were ongoing were more likely than temporary frequent attenders to be aged 5-15 years, and were not more likely to be admitted (OR=2.7, 99% CI 0.7 to 10.9).
Conclusions Future intervention studies should distinguish between temporary and ongoing frequent attenders, develop specific interventions for each group and include rigorous evaluation
Functional modelling of complex multi‑disciplinary systems using the enhanced sequence diagram
YesThis paper introduces an Enhanced Sequence Diagram (ESD) as the basis for a structured framework for the functional analysis of complex multidisciplinary systems. The ESD extends the conventional sequence diagrams (SD) by introducing a rigorous functional flow-based modelling schemata to provide an enhanced basis for model-based functional requirements and architecture analysis in the early systems design stages. The proposed ESD heuristics include the representation of transactional and transformative functions required to deliver the use case sequence, and fork and join nodes to facilitate analysis of combining and bifurcating operations on flows. A case study of a personal mobility device is used to illustrate the deployment of the ESD methodology in relation to three common product development scenarios: (i) reverse engineering, (ii) the introduction of a specific technology to an existent system; and (iii) the introduction of a new feature as user-centric innovation for an existing system, at a logical design level, without reference to any solution. The case study analysis provides further insights into the effectiveness of the ESD to support function modelling and functional requirements capture, and architecture development. The significance of this paper is that it establishes a rigorous ESD-based functional analysis methodology to guide the practitioner with its deployment, facilitating its impact to both the engineering design and systems engineering communities, as well as the design practice in the industry
Functional modelling of complex multi‑disciplinary systems using the enhanced sequence diagram
YesThis paper introduces an Enhanced Sequence Diagram (ESD) as the basis for a structured framework for the functional analysis of complex multidisciplinary systems. The ESD extends the conventional sequence diagrams (SD) by introducing a rigorous functional flow-based modelling schemata to provide an enhanced basis for model-based functional requirements and architecture analysis in the early systems design stages. The proposed ESD heuristics include the representation of transactional and transformative functions required to deliver the use case sequence, and fork and join nodes to facilitate analysis of combining and bifurcating operations on flows. A case study of a personal mobility device is used to illustrate the deployment of the ESD methodology in relation to three common product development scenarios: (i) reverse engineering, (ii) the introduction of a specific technology to an existent system; and (iii) the introduction of a new feature as user-centric innovation for an existing system, at a logical design level, without reference to any solution. The case study analysis provides further insights into the effectiveness of the ESD to support function modelling and functional requirements capture, and architecture development. The significance of this paper is that it establishes a rigorous ESD-based functional analysis methodology to guide the practitioner with its deployment, facilitating its impact to both the engineering design and systems engineering communities, as well as the design practice in the industry
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The H1 receptor agonist 2-(3-chlorophenyl)histamine activates Gi proteins in HL-60 cells through a mechanism that is independent of known histamine receptor subtypes
In dibutyryl-cAMP-differentiated HL-60 cells, histamine H1 and formyl peptide receptors mediate increases in the cytosolic Ca2+ concentration ([Ca2+]i) via pertussis toxin-sensitive G proteins of the Gi family. We compared the effects of 2-(3-chlorophenyl)-histamine (CPH) [2-[2-(3-chlorophenyl)-1H-imidazol-4-yl] ethanamine], one of the most potent and selective H1 receptor agonists presently available, with those of histamine and N-formyl-L-methionyl-L-leucyl-L-phenylalanine (fMLP) in these cells. CPH increased [Ca2+]i through Ca2+ mobilization and Ca2+ influx. Unlike histamine-induced rises in [Ca2+]i, those induced by CPH were not desensitized in a homologous manner, and there was no cross-desensitization between CPH and histamine. Like fMLP, CPH activated phospholipases C and D, tyrosine phosphorylation, superoxide anion formation, and azurophilic granule release. The effects of CPH on [Ca2+]i, phospholipase D, and superoxide anion formation were inhibited by pertussis toxin. CPH and fMLP stimulated high affinity GTP hydrolysis by Gi proteins in HL-60 membranes. They also enhanced binding of guanosine-5'-O-(3-thio)triphosphate and GTP azidoanilide to, and cholera toxin-catalyzed ADP-ribosylation of, Gi protein alpha subunits. Histamine receptor antagonists did not inhibit the stimulatory effects of CPH, and CPH did not reduce fMLP binding in HL-60 membranes. Our data suggest that CPH activates Gi proteins in HL-60 cells through a receptor agonist-like mechanism that is, however, independent of known histamine receptor subtypes and formyl peptide receptors. CPH may be an agonist at an as yet unknown histamine receptor subtype or, by analogy with other cationic-amphiphilic substances, may activate G proteins directly. Future studies will have to take into consideration the fact that CPH, in addition to activating H1 receptors, may show other, most unexpected, stimulatory effects on G protein-mediated signal transduction processes
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