Psychological stress responses of medical staff after workplace violence: a longitudinal study.

OBJECTIVE: To explore the occurrence and dynamic trends of psychological stress responses of medical staff experiencing workplace violence at different time points. METHODS: A longitudinal study of 23 medical workers who experienced workplace violence was conducted. The perceived stress scale (PSS-4), posttraumatic stress disorder checklist for DSM-5 (PCL-5), and hospital anxiety and depression scale (HADS) were used to measure the medical workers' psychological perception of pressure, posttraumatic stress symptoms, anxiety, and depression at the time of exposure to violence, at 1 month, 2 months, and 4 months after exposure in the workplace, respectively. Repeated measures analysis of variance was applied to analyze psychological stress response and temporal effect. Factors influencing psychological stress responses were analyzed. RESULTS: The scores of PSS-4, PCL-5, HADS-anxiety, and HADS-depression of medical staff exposed to violence began to increase at the time of exposure, peaked 1 month after exposure, and gradually decreased 2 months and 4 months after exposure (all P<0.05). The main influencing factors were being nurses, physical violence, working years ≤5, and being female. CONCLUSION: Effective interventions for medical staff should be made up to 1 month after exposure to workplace violence when the psychological stress responses are the highest.

Silencing of long noncoding RNA H19 alleviates pulmonary injury, inflammation, and fibrosis of acute respiratory distress syndrome through regulating the microRNA-423-5p/FOXA1 axis.

PURPOSE: This study aimed to explore the regulatory effects and mechanisms of long noncoding RNA H19 (H19) on pulmonary injury, inflammation, and fibrosis of acute respiratory distress syndrome (ARDS). MATERIALS AND METHODS: A rat model of ARDS was established by intratracheal instillation of 2 mg/kg lipopolysaccharide (LPS). qRT-PCR was performed to detect the expression of H19, miR-423-5p, tumor necrosis factor-α (TNF-α), interleukin (IL)-1ß, IL-6, monocyte chemoattractant protein (MCP)-1, and vascular endothelial growth factor (VEGF). Histology score was assessed by hematoxylin-eosin (HE) staining. Enzyme-linked immunosorbent assay (ELISA) was used to detect the levels of proinflammatory cytokines and the content of VEGF in bronchoalveolar lavage fluid (BALF). The lung fibrosis was evaluated using western blot and Masson's trichrome staining. Dual-luciferase reporter gene assay was used for confirming the relationship between miR-423-5p and H19/FOXA1 in alveolar macrophage cells (MH-S) and alveolar epithelial cells (MLE-12). The regulatory effects of H19/miR-423-5p/FOXA1 axis on the inflammation and fibrosis were further analyzed in LPS-induced MH-S cells. RESULTS: The expression of H19 and FOXA1 was significantly up-regulated, while the expression of miR-423-5p was down-regulated in LPS-induced ARDS rats. Silencing of H19 decreased the mRNA expression of TNF-α, IL-1ß, IL-6, MCP-1, and VEGF, the contents of TNF-α, IL-1ß, IL-6, and VEGF in BALF, and histology score in LPS-induced ARDS rats. H19 knockdown also reduced the fibrosis scores and the protein expression of vimentin and α-SMA, and elevated the protein expression of E-cadherin in LPS-induced ARDS rats. Furthermore, silencing of miR-423-5p and overexpression of FOXA1 reversed the inhibitory effects of si-H19 on the inflammation and fibrosis of LPS-induced MH-S cells. CONCLUSIONS: Silencing of H19 relieved the pulmonary injury, inflammation and fibrosis of LPS-induced ARDS in rats. Silencing of H19 also alleviated the inflammation and fibrosis of LPS-induced MH-S cells through regulating the miR-423-5p/FOXA1 axis.

The Effect of Angiotensin-Converting Enzyme Gene Polymorphisms on the Clinical Efficacy of Perindopril Prescribed for Acute Myocardial Infarction in Chinese Han Patients.

Objective: Perindopril is an angiotensin-converting enzyme (ACE) inhibitor that is commonly used in the treatment of Chinese Han patients with acute myocardial infarction (AMI). However, there have been few studies on whether polymorphisms of the ACE gene affect the efficacy of perindopril or the prognosis of AMI patients. The purpose of this study was to analyze the relationship among the ACE rs121912703 (C>T), rs767880620 (C>A), and rs397514689 (C>T) gene polymorphisms and the prognosis of AMI patients and the clinical efficacy of perindopril in the treatment of AMI. Methods: The ACE genotypes at the rs121912703, rs767880620, and rs397514689 loci in 225 AMI patients treated with perindopril were determined by polymerase chain reaction/Sanger sequencing. Differences in cardiac structure, functional indicators, hemodynamic parameters, and related laboratory indicators were detected before and after treatment. Results: After administration of perindopril, improved ventricular remodeling in AMI patients with wild-type ACE was better than in patients with the ACE rs121912703, rs767880620, and rs397514689 minor variant alleles. The patients harboring wild-type ACE had lower systolic blood pressure and diastolic blood pressure than the patients harboring the minor variant alleles (p < 0.01). The contents of serum ACE and Ang II (angiotensin II) in AMI patients carrying the wild-type ACE alleles were lower than those of patients harboring any of the minor variant alleles (p < 0.01). The 3-year survival time of AMI patients carrying the wild-type ACE alleles was markedly greater compared with AMI patients carrying the mutant genes (p < 0.01). Conclusion: Mutations at the ACE rs121912703, rs767880620, and rs397514689 loci affect the efficacy of perindopril on ventricular remodeling and hemodynamics in Chinese Han AMI patients. The 3-year survival of AMI patients harboring the variant alleles is less than that of the patients harboring the wild-type gene.

Aldehyde Dehydrogenase 2 (ALDH2) Glu504Lys Polymorphism Affects Collateral Circulation and Short-Term Prognosis of Acute Cerebral Infarction Patients.

BACKGROUND Acute cerebral infarction is a major clinical subtype of ischemic stroke that has become a leading cause of death and disability worldwide. Aldehyde dehydrogenase 2 (ALDH2) is an important oxidative enzyme in alcohol metabolism. The polymorphism of ALDH2 Glu504Lys polymorphism modifies the activity of this enzyme. However, the potential association between the allelic variation of ALDH2 Glu504Lys with collateral circulation and short-term prognosis of acute cerebral infarction remains unclear. MATERIAL AND METHODS A total of 394 patients with acute cerebral infarction were recruited for ALDH2 genotyping using direct sequencing. Cerebrovascular stenosis and collateral circulation were evaluated by digital subtraction angiography (DSA). Short-term prognosis was assessed in accordance with the modified Ranking Scale (mRS). RESULTS We identified 297 as EAS and 394 as IAS. There were more patients with occluded blood vessel in the opened group and far fewer in the unopened group. ALDH2 polymorphism was significantly different among the primary, secondary, and tertiary opened groups. ALDH2 gene Glu504Lys was significantly associated with short-term prognosis. The genotype GA+AA of ALDH2 gene Glu504Lys locus was an independent risk factor of poor 90-day prognosis. CONCLUSIONS ALDH2 Glu504Lys could be a risk factor for collateral circulation and a negative predictor for short-term prognosis in acute cerebral infarction in Han Chinese. ALDH2 Glu504Lys could be a new therapeutic target for patients with acute cerebral infarction.

Curcumin protects against cerebral ischemia-reperfusion injury by activating JAK2/STAT3 signaling pathway in rats.

Curcumin (Cur) is the active component in Curcuma longa, and it has been reported to exhibit a variety of biological effects such as anti-inflammation and anti-oxidation. This study aims to investigate the effect of Cur on cerebral ischemia-reperfusion injury and whether the Janus kinase 2 and signal transducer and activator 3 of transcription (JAK2/STAT3) signaling pathway is involved in the neuroprotective effects of Cur. Rats were subjected to 2 h transient middle cerebral artery occlusion (MCAO), followed by 24 h reperfusion. Rats were randomly assigned into sham group, MCAO group, MCAO + Cur group. AG490, a JAK2 inhibitor, was utilized to throw light upon the underlying mechanism. The results suggested that compared to MCAO, Cur attenuated neurological deficits, reduced cerebral infarction area and lowered brain water content. In addition, Cur reduced the activity of IL-1ß and IL-8. The results of western blot indicated that Cur enhanced the expression of p-JAK2 and p-STAT3, which was abolished by AG490 administration. Our results suggested that Cur protects effects against cerebral I/R injury through the activation of JAK2/STAT3 signaling pathway.