Nurses� perception of patient safety culture and its relationship with adverse events: a national questionnaire survey in Iran

Background: Patient safety culture is an important factor in determining hospitals� ability to address and reduce the occurrence of adverse events (AEs). However, few studies have reported on the impact of nurses� perceptions of patient safety culture on the occurrence of AEs. Our study aimed to assess the association between nurses� perception of patient safety culture and their perceived proportion of adverse events. Methods: A cross-sectional survey was carried out among 2295 nurses employed in thirty-two teaching hospitals in Iran. Nurses completed the Persian version of the hospital survey of patients� safety culture between October 2018 and September 2019. Results: Positive Response Rates of overall patient safety culture was 34.1 and dimensions of patient safety culture varied from 20.9 to 43.8. Also, nurses estimated that the occurrence of six adverse events varied from 51.2�63.0 in the past year. The higher nurses� perceptions of �Staffing�, �Hospital handoffs and transitions�, �Frequency of event reporting�, �Non-punitive response to error�, �Supervisor expectation and actions promoting safety�, �Communication openness�, �Organizational learning continuous improvement�, �Teamwork within units�, and �Hospital management support patient safety� were significantly related to lower the perceived occurrence at least two out of six AEs (OR = 0.69 to 1.46). Conclusions: Our findings demonstrated that nurses� perception regarding patient safety culture was low and the perceived occurrence of adverse events was high. The research has also shown that the higher level of nurses� perception of patient safety culture was associated with lowered occurrence of AEs. Hence, managers could provide prerequisites to improve patient safety culture and reduce adverse events through different strategies, such as encouraging adverse events� reporting and holding training courses for nurses. However, further research is needed to assess how interventions addressing patient safety culture might reduce the occurrence of adverse events. © 2021, The Author(s)

Aspergillus antigen induces robust Th2 cytokine production, inflammation, airway hyperreactivity and fibrosis in the absence of MCP-1 or CCR2

BACKGROUND: Asthma is characterized by type 2 T-helper cell (Th2) inflammation, goblet cell hyperplasia, airway hyperreactivity, and airway fibrosis. Monocyte chemoattractant protein-1 (MCP-1 or CCL2) and its receptor, CCR2, have been shown to play important roles in the development of Th2 inflammation. CCR2-deficient mice have been found to have altered inflammatory and physiologic responses in some models of experimental allergic asthma, but the role of CCR2 in contributing to inflammation and airway hyperreactivity appears to vary considerably between models. Furthermore, MCP-1-deficient mice have not previously been studied in models of experimental allergic asthma. METHODS: To test whether MCP-1 and CCR2 are each required for the development of experimental allergic asthma, we applied an Aspergillus antigen-induced model of Th2 cytokine-driven allergic asthma associated with airway fibrosis to mice deficient in either MCP-1 or CCR2. Previous studies with live Aspergillus conidia instilled into the lung revealed that MCP-1 and CCR2 play a role in anti-fungal responses; in contrast, we used a non-viable Aspergillus antigen preparation known to induce a robust eosinophilic inflammatory response. RESULTS: We found that wild-type C57BL/6 mice developed eosinophilic airway inflammation, goblet cell hyperplasia, airway hyperreactivity, elevations in serum IgE, and airway fibrosis in response to airway challenge with Aspergillus antigen. Surprisingly, mice deficient in either MCP-1 or CCR2 had responses to Aspergillus antigen similar to those seen in wild-type mice, including production of Th2 cytokines. CONCLUSION: We conclude that robust Th2-mediated lung pathology can occur even in the complete absence of MCP-1 or CCR2

Epigenetic Regulation of Myofibroblast Differentiation by DNA Methylation.

DNA methylation, a key mechanism of repressing gene expression, is of particular relevance in controlling development and cell differentiation. We analyzed the extent and regulation of DNA methylation of the α-smooth muscle actin (α-SMA) gene to elucidate its potential role in myofibroblast differentiation. These experiments revealed the presence of three CpG islands that were methylated at different levels in fibroblasts, myofibroblasts, and alveolar epithelial type II cells. Coordinately, these cells expressed low, high, or no α-SMA, respectively. In addition, inhibition of DNA methyltransferase activity or knock down of DNA methyltransferase using specific small interfering RNA caused significant induction of α-SMA in fibroblasts. In contrast, induced overexpression of DNA methyltransferase suppressed α-SMA gene expression. Transforming growth factor β induced myofibroblast differentiation was enhanced or suppressed by knockdown or overexpression of DNA methyltransferase, respectively. Finally, in vitro DNA methylation of the α-SMA promoter suppressed its activity. These findings suggest that DNA methylation mediated by DNA methyltransferase is an important mechanism regulating the α-SMA gene expression during myofibroblast differentiation. Copyright © American Society for Investigative Pathology.http://deepblue.lib.umich.edu/bitstream/2027.42/178293/2/Epigenetic regulation of myofibroblast differentiation by DNA methylation.pdfPublished versionDescription of Epigenetic regulation of myofibroblast differentiation by DNA methylation.pdf : Published versio