Occupational violence and aggression in urgent and critical care in rural health service settings: A systematic review of mixed studies.

Rural/remote health services are vulnerable to occupational violence and aggression due to factors such as weapon accessibility, poor network coverage and distance to backup. This systematic review investigated (1) the nature of occupational violence and aggression perpetrated in rural/remote health service urgent care settings and (2) the availability and effectiveness of policies/interventions/recommendations that address occupational violence and aggression in this context. We searched Business Source Complete, CINAHL Complete, Health & Society, APAIS Health, Health Collection, PsycINFO, PubMed, Scopus, SocIndex and Web of Science. Included articles (peer-reviewed, no grey literature and English language) addressed occupational violence and aggression in rural health service urgent care settings. Fifteen articles matched these criteria (total [rural/remote only, where specified] N ~ 2555) and were included in the final analysis. The Mixed Methods Appraisal Tool was applied to assess the risk of bias. A data extraction table and narrative synthesis are presented. The most common occupational violence and aggression type was verbal aggression. The primary perpetrator was patients. Risk factors reflected practitioner age, remoteness, sector, staffing, shift type and area of practice. Precipitating factors were alcohol/drugs, dissatisfaction and mental health conditions. Policy content and limitations and education/training programme effectiveness were not addressed. Community collaboration supported occupational violence and aggression prevention/management. Organisational culture should promote reporting, debriefing and post-incident care for staff well-being. Work environment and job/task design are priorities for safety, but with possible limitations for traumatised clients. Occupational violence and aggression policies/interventions in rural health settings must be systematically evaluated to inform best practices. Co-funded by Swinburne Social Innovation Research Institute Interdisciplinary Seed Funding Scheme and SMART Rural Health Network.

Weight stigmatisation in antiobesity campaigns: The role of images.

ISSUE ADDRESSED: Antiobesity campaigns may inadvertently stigmatise individuals with obesity via the use of images that portray negative obesity stereotypes. This study investigated the impact of images on weight stigma using mock antiobesity campaigns featuring different types of images. METHODS: Participants (N = 240) were randomly assigned to one of four campaign conditions: stereotypical images, counter-stereotypical images, neutral images, or no images. All four conditions used the same nonstigmatising message text. Participants indicated their attitudes towards being in social situations (desired social distance) with the target featured in the images, or individuals with obesity (no images), rated the target or individuals with obesity on various traits, and indicated to what extent the campaign was motivating and stigmatising. RESULTS: Analysis of variance revealed that the stereotypical images were rated as the most stigmatising and were also associated with higher negative and lower positive trait ratings of the target and more desired social distance from the target. Neutral images generally produced the least weight stigma. CONCLUSION: It is important to consider the impact of antiobesity campaign images that depict common obesity stereotypes. Developing, testing and disseminating nonstigmatising campaigns is important to reduce stigma and better engage individuals with antiobesity public health messages. SO WHAT?: Weight stigma has negative consequences for physical and psychological health, which may undermine obesity intervention efforts. Stereotypical images that blame individuals for their weight reinforce obesity stigma and are likely to be in-effective in increasing healthier behaviour and reducing obesity. The development of effective antiobesity campaigns should be a public health priority.

Myocardial infarction increases ACE2 expression in rat and humans.

AIMS: Angiotensin converting enzyme (ACE) 2 catalyses the cleavage of angiotensin (Ang) I to Ang 1-9 and of Ang II to Ang 1-7. ACE2 deficiency impairs cardiac contractility and upregulates hypoxia-induced genes, suggesting a link with myocardial ischaemia. We studied the expression of ACE2 after myocardial infarction (MI) in the rat as well as in human failing hearts. METHODS AND RESULTS: Rats were killed at days 1, 3, and 28 after MI, or treated for 4 weeks with the ACE inhibitor ramipril (1 mg/kg). Cardiac gene and protein expression of ACE and ACE2 were assessed by quantitative real-time reverse transcriptase-polymerase chain reaction and immunohistochemistry/activity assays/in vitro autoradiography, respectively. Both ACE (P = 0.022) and ACE2 (P = 0.015) mRNA increased in the border/infarct area compared with the viable area at day 3 after MI. By day 28, increases in ACE (P = 0.005) and ACE2 (P = 0.006) mRNA were also seen in the viable myocardium of MI rats compared with myocardium of control rats. ACE2 protein localized to macrophages, vascular endothelium, smooth muscle, and myocytes. Ramipril attenuated cardiac hypertrophy and inhibited cardiac ACE. In contrast, ramipril had no effect on cardiac ACE2 mRNA, which remained elevated in all areas of the MI rat heart. Immunoreactivity of both ACE and ACE2 increased in failing human hearts. CONCLUSION: The increase in ACE2 after MI suggests that it plays an important role in the negative modulation of the renin angiotensin system in the generation and degradation of angiotensin peptides after cardiac injury.

Reduction of the accumulation of advanced glycation end products by ACE inhibition in experimental diabetic nephropathy.

The effect of ACE inhibition on the formation of advanced glycation end products (AGEs) and oxidative stress was explored. Streptozocin-induced diabetic animals were randomized to no treatment, the ACE inhibitor ramipril (3 mg/l), or the AGE formation inhibitor aminoguanidine (1 g/l) and followed for 12 weeks. Control groups were followed concurrently. Renal AGE accumulation, as determined by immunohistochemistry and both serum and renal fluorescence, were increased in diabetic animals. This was attenuated by both ramipril and aminoguanidine to a similar degree. Nitrotyrosine, a marker of protein oxidation, also followed a similar pattern. The receptor for AGEs, gene expression of the membrane-bound NADPH oxidase subunit gp91phox, and nuclear transcription factor-kappaB were all increased by diabetes but remained unaffected by either treatment regimen. Two other AGE receptors, AGE R2 and AGE R3, remained unchanged for the duration of the study. The present study has identified a relationship between the renin-angiotensin system and the accumulation of AGEs in experimental diabetic nephropathy that may be linked through oxidative stress