This study is aimed at exploring the relationship between green behavior intentions and green behavior and analyzing the moderating role of ethical leadership in this relationship. Nurses' green behavior can directly reduce costs and protect the natural environment and organizational sustainability by saving resources and energy. It is not clear how green behavior intention affects green behavior or how the positive influence of green behavior intention on green behavior can be enhanced. . This is a cross-sectional study, and the surveys are collected from 3 hospitals in China. Of the initial cohort of 489 nurses, 89.6% were female. There were 327 subjects (66.9%) aged 35 or less, 267 subjects (54.6%) with 10 years or less of work experience, and 220 unmarried subjects (44.9%). Data were collected from January to July 2018, using three surveys green behavior intentions, green behavior, and ethical leadership. Green behavior intentions impacted employee green behavior ( = 0.32, = 5.37, < 0.0n when ethical leadership is low. The results of this study can help both academics and practitioners to understand the micromechanism of environmentally sustainable development in more detail and to identify the mechanisms and boundary conditions of green behavioral intentions, green behavior, and ethical leadership. Acute lung injury (ALI) induced by sepsis is a process related to inflammatory reactions, which involves lung cell apoptosis and production of inflammatory cytokine. Here, lipopolysaccharide (LPS) was applied to stimulate the mouse or human normal lung epithelial cell line (BEAS-2B) to construct a sepsis model and , and we also investigated the effect of miR-497-5p on sepsis-induced ALI. . Before LPS treatment, miR-497-5p antagomir was injected intravenously into mice to inhibit miR-497-5p expression . Similarly, miR-497-5p was knocked down in BEAS-2B cells. Luciferase reporter assay was applied to predict and confirm the miR-497-5p target gene. Cell viability, apoptosis, the levels of miR-497-5p, IL2RB, SP1, inflammatory cytokine, and lung injury were assessed. In BEAS-2B cells, a significant increase of apoptosis and inflammatory cytokine was shown after LPS stimulation. In septic mice, increased inflammatory cytokine production and apoptosis in lung cells and pulmonary morphological abnormalities were shown. https://www.selleckchem.com/products/unc2250.html miR-497-5p inhibitor transfection showed antiapoptotic and anti-inflammatory effects on BEAS-2B cells upon LPS stimulation. In septic mice, the miR-497-5p antagomir injection also alleviated ALI, apoptosis, and inflammation caused by sepsis. The downregulation of IL2RB in BEAS-2B cells reversed the protective effects of the miR-497-5p inhibitor against ALI. In conclusion, downregulation of miR-497-5p reduced ALI caused by sepsis through targeting IL2RB, indicating the potential effect of miR-497-5p for improving ALI caused by sepsis. In conclusion, downregulation of miR-497-5p reduced ALI caused by sepsis through targeting IL2RB, indicating the potential effect of miR-497-5p for improving ALI caused by sepsis. Acute coronary syndrome (ACS) is a critical disease encountered in the emergency department (ED). Despite the development of diagnostic tools, it may be difficult to diagnose ACS because of atypical symptoms and equivocal test results. We investigated the difference in the rates of revisit and undetected ACS between adult and elderly patients who visited the ED with chest pain. Data from 11,323 patients who visited the ED with chest pain at university hospitals in Korea were retrospectively analyzed. #link# The cohort was categorized into two age groups the adult (30-64 years) and elderly (>65 years). Baseline characteristic data (age, sex, vital signs, triage category, etc.) were obtained. We selected patients who revisited the ED within 30 d and investigated whether ACS was diagnosed. The revisit rate was higher in the elderly (12%) than in the adult group (8.3%). The rate of undetected ACS among the revisited patients was 2.91% (18/7,186) in adults and 6.08% (16/1,998) in elderly patients. Elderly patients with chest pain had an increased rate of ED revisits and undetected ACS than adult patients. We recommend that old patients should be hospitalized to observe the progression of cardiac complaints or receive short-term follow-up. Elderly patients with chest pain had an increased rate of ED revisits and undetected ACS than adult patients. We recommend that old patients should be hospitalized to observe the progression of cardiac complaints or receive short-term follow-up. Acute kidney injury (AKI) is a common and severe complication in critically ill patients, often caused by renal ischemia-reperfusion (RIR). Previous studies have confirmed that lung injury, rather than renal injury, is one of the leading causes of AKI-induced death. The pathophysiological mechanisms of acute lung injury (ALI) resulting from AKI are very complex and remain unclear. In the present study, we aimed to explore the protective effects and potential mechanism of sodium hydrosulfide (NaHS) on lung injury in RIR mice. The RIR model was established in wild-type and Nrf2 mice. Different groups of mice were treated with NaHS and MCC950. Lung tissues were harvested to detect lung injury, mitochondrial function, cell apoptosis, the NLRP3 inflammasome, and Nrf2 pathway-related molecules. RIR led to a deterioration in lung histology, the wet/dry weight ratio, PaO /FiO , and mitochondrial function, in addition to stimulating the activation of the NLRP3 and Nrf2 pathways. MCC950 alleviated mitochondrial dysfunction, lung apoptosis, and histology injury in the lungs after RIR. NaHS treatment markedly improved the lung histological scores, the wet/dry weight ratio, bronchoalveolar lavage fluid (BALF) cell counts, BALF neutrophil counts, BALF neutrophil elastase activity, BALF protein concentration, PaO /FiO , mitochondrial morphology, the red/green fluorescence intensity that indicates changes in mitochondrial membrane potential, respiratory control rate (RCR), ATP, reactive oxygen species (ROS) release, and cell apoptosis via Nrf2-mediated NLRP3 pathway inhibition. NaHS protected against RIR-induced lung injury, mitochondrial dysfunction, and inflammation, which is associated with Nrf2 activation-mediated NLRP3 pathway inhibition. NaHS protected against RIR-induced lung injury, mitochondrial dysfunction, and inflammation, which is associated with Nrf2 activation-mediated NLRP3 pathway inhibition.