RESUMO
Introduction Workplace violence is a common problem that is encountered by healthcare workers worldwide; however, it is still under-studied in Saudi Arabia. This study aims to determine the prevalence of workplace violence and to explore reasons for not reporting it among healthcare workers in a tertiary medical city in Riyadh. Methods This cross-sectional study was conducted among 404 healthcare workers who had direct contact with patients or their relatives in a tertiary care medical city in Riyadh, Saudi Arabia. Data were analyzed using Statistical Analysis Software Package (SPSS; IBM, Armonk, NY, USA). Results Most participants (81.4%) had experienced verbal, physical, academic, or sexual violence. Approximately 39.6% of those who experienced workplace violence did not report the incident, and the most common reason for not reporting was identified as "reporting would not accomplish anything" (49.4%). About 27.5% of violence victims did not know how to report the incidents. Patients or their relatives were the main sources of violence across all violence categories except academic violence, in which consultant physicians were the main source. Conclusions The prevalence of workplace violence in the population studied was higher than anticipated compared to similar studies both in Saudi Arabia and globally. Almost half of those who were subjected to violence did not report the incident, believing that reporting would not change anything. There is arguably an urgent need to develop strategies that reduce workplace violence and facilitate reporting it in hospitals. Moreover, awareness programs regarding the negative impacts of violence against healthcare workers on the quality of care are necessary.
RESUMO
BACKGROUND: Although there is increasing evidence showing that cell senescence is increased in circulating PBMC in type 2 diabetes mellitus (T2DM), the data are contradictory. This study examined several senescence biomarkers, including LMNA/C transcript variants, p16INK4a, p53, and p21Cip1/WAF, in PBMC of T2DM patients and the effect of Metformin on these senescence markers. METHODS: Blood samples were obtained from 30 lean, 30 obese, 20 newly diagnosed type 2 diabetes mellitus (T2DM), and 30 T2DM on Metformin. PBMC were isolated and mRNA expression of the senescence biomarkers were quantified by RT-qPCR. The effect of ectopic expression of LMNA and LMNC in human monocytic cells lines (THP-1 and U937) on several inflammatory mediators were also examined. RESULTS: LMNA expression was significantly higher in PBMC of obese and T2DM patients. LMNC expression was significantly inhibited in T2DM patients. LMNAΔ10 and Progerin mRNA expression was not detected in PBMC of all groups. Expression of p16INK4a, p21Cip1/WAF and p53 were inhibited significantly in T2DM. Metformin treatment reverted LMNA, LMNC, and p53 expression levels to normal levels. Upregulation of LMNA in monocytic THP-1 and U937 cell lines induced CD68, TNFα, CCL2, IL-6 and NOS2. CONCLUSIONS: These data support the notion that LMNA may mediate senescence in PBMCs of T2DM by upregulating inflammatory pathways. Metformin may exert its anti-inflammatory property by modulation of senescence mediator LMNA.