The efficacy of aligning lessons learnt from significant bushfire incidents to the organisational stratum

Australia\u27s bushfire seasons are expected to become longer and more severe due to the effects of climate change and an increasing population living in rural-urban fringes. Social and economic vulnerability to extreme natural hazards means that Australia’s emergency services sector plays a significant role in community safety and wellbeing. Therefore, it is important that the sector continually improves. Australia has a long history of conducting external reviews into significant bushfires. While these reviews receive good support and seek to identify relevant lessons, barriers remain that prevent these lessons from being effectively learnt. It is possible that some of these barriers exist because the stratum of work impedes the capture, codifying and adjustments to systems. This research investigated the premise that lessons learnt in the Australian emergency services sector occurs on a stratum, with different types of lessons learnt at different levels of work. Four significant independent bushfire reviews were analysed to evaluate whether specific lessons could be aligned to the stratum of work. Findings were that not all lessons apply to all levels of organisations. This supports the premise that lessons are learnt on a vertical organisational stratum; for example, some lessons were operational, others were tactical and some were strategic. It was determined that a lack of understanding of the barriers within an organisations stratum could impede the effectiveness of lessons being learnt

Monocyte Subset Recruitment Marker Profile Is Inversely Associated With Blood ApoA1 Levels.

Dyslipidemia promotes development of the atherosclerotic plaques that characterise cardiovascular disease. Plaque progression requires the influx of monocytes into the vessel wall, but whether dyslipidemia is associated with an increased potential of monocytes to extravasate is largely unknown. Here (using flow cytometry) we examined recruitment marker expression on monocytes from generally healthy individuals who differed in lipid profile. Comparisons were made between monocyte subsets, participants and relative to participants' lipid levels. Monocyte subsets differed significantly in their expression of recruitment markers, with highest expression being on either the classical or non-classical subsets. However, these inter-subset differences were largely overshadowed by considerable inter-participant differences with some participants having higher levels of recruitment markers on all three monocyte subsets. Furthermore, when the expression of one recruitment marker was high, so too was that of most of the other markers, with substantial correlations evident between the markers. The inter-participant differences were explained by lipid levels. Most notably, there was a significant inverse correlation for most markers with ApoA1 levels. Our results indicate that dyslipidemia, in particular low levels of ApoA1, is associated with an increased potential of all monocyte subsets to extravasate, and to do so using a wider repertoire of recruitment markers than currently appreciated

Monocyte subset recruitment marker profile is inversely associated with blood apoa1 levels

Dyslipidemia promotes development of the atherosclerotic plaques that characterise cardiovascular disease. Plaque progression requires the influx of monocytes into the vessel wall, but whether dyslipidemia is associated with an increased potential of monocytes to extravasate is largely unknown. Here (using flow cytometry) we examined recruitment marker expression on monocytes from generally healthy individuals who differed in lipid profile. Comparisons were made between monocyte subsets, participants and relative to participants’ lipid levels. Monocyte subsets differed significantly in their expression of recruitment markers, with highest expression being on either the classical or non-classical subsets. However, these inter-subset differences were largely overshadowed by considerable inter-participant differences with some participants having higher levels of recruitment markers on all three monocyte subsets. Furthermore, when the expression of one recruitment marker was high, so too was that of most of the other markers, with substantial correlations evident between the markers. The inter-participant differences were explained by lipid levels. Most notably, there was a significant inverse correlation for most markers with ApoA1 levels. Our results indicate that dyslipidemia, in particular low levels of ApoA1, is associated with an increased potential of all monocyte subsets to extravasate, and to do so using a wider repertoire of recruitment markers than currently appreciated

Nature versus number : monocytes in cardiovascular disease

Monocytes play a key role in cardiovascular disease (CVD) as their influx into the vessel wall is necessary for the development of an atherosclerotic plaque. Monocytes are, however, heterogeneous differentiating from classical monocytes through the intermediate subset to the nonclassical subset. While it is recognized that the percentage of intermediate and nonclassical monocytes are higher in individuals with CVD, accompanying changes in inflammatory markers suggest a functional impact on disease development that goes beyond the increased proportion of these ‘inflammatory’ monocyte subsets. Furthermore, emerging evidence indicates that changes in monocyte proportion and function arise in dyslipidemia, with lipid lowering medication having some effect on reversing these changes. This review explores the nature and number of monocyte subsets in CVD addressing what they are, when they arise, the effect of lipid lowering treatment, and the possible implications for plaque development. Understanding these associations will deepen our understanding of the clinical significance of monocytes in CVD

Monocyte inflammatory profile is specific for individuals and associated with altered blood lipid levels

Background and aims Atherogenesis is dependent upon monocyte influx into the vessel wall. In humans, three monocyte subsets exist, the number and function of which are significantly altered in cardiovascular disease (CVD). Whether such alterations arise in individuals with a perturbed lipid profile remains largely unanswered, but is important to delineate, as adoption of a pro-inflammatory state may promote plaque formation. Here, we compared the inflammatory status of monocyte subsets and determined whether monocyte inflammatory changes are evident in individuals with a perturbed lipid profile. Methods Monocyte subset cytokine production, inflammatory and anti-inflammatory marker expression were determined by whole blood flow cytometry and related to participants' lipid levels. Results The intermediate and non-classical monocytes were more inflammatory than classicals as seen by their higher cytokine production (TNF-α, IL-1β, IL-6) and M1 marker (CD86) expression, but lower levels of M2 markers (CD93, CD163). More importantly, a considerable variation was seen between participants, with all monocytes of one individual being more inflammatory than those of another. Many inter-individual differences were related to participants' lipid levels. IL-1β production correlated negatively with Apo A1 and HDL-C. CD86 and TLR2 correlated positively with Chol:HDL-C but negatively with HDL-C and Apo A1:Apo B. Interestingly, CD163 expression correlated positively with Chol:HDL-C but negatively with Apo A1:Apo B. Conclusions Our data indicates that priming of all monocytes to an inflammatory state occurs in individuals with a perturbed lipid profile, overriding the normal functional distinction attributed to the different monocyte subsets. As such, all monocytes may be important in CVD

Guest Essay: The ultra-urban botanic garden

No abstrac

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http://www.archive.org/details/activationenergi00medbU.S. Navy (U.S.N.) author

Taxonomy and Arboretum Design

Volume: 53Start Page: 13End Page: 2

Heart Failure Transition of Care: An Educational Program for Nurses

Heart failure (HF) is becoming an epidemic as people are living longer and surviving cardiovascular events. According to the 2015 to 2018 data the American Heart Association estimates 6 million American adults aged twenty or older are living with HF (AHA, 2021). Heart failure is the nation\u27s leading 30-day readmission diagnosis costing the nation an estimated $30.7 billion according to the Division of Heart Disease and Stroke Prevention. Heart failure is a chronic progressive disease that if not managed correctly will lead to increased morbidity and decreased quality of life. A review of the literature on transition of care frameworks for HF patients validated the most effective interventions and best practices to reduce hospitalization in patients with heart failure. Nurses need to possess knowledge of heart failure care best practices to optimize patient outcomes. The purpose of this quality improvement project was to determine if implementation of a Heart Failure Transition of Care education program increased nurses’ knowledge of heart failure and heart failure transition of care best practices. The results of the educational program demonstrated improvement in nurses\u27 knowledge in all three categories; Heart failure facts and pathophysiology, best practice nursing interventions, and Heart failure assessment and goal directed medical therapy