A Retrospective Analysis of Internet-Based Sharing Nursing Service Appointment Data.

Aims: To investigate the historical data of the "Internet+ Nursing" service platform and provide a theoretical basis to optimize the "Internet+ Nursing" service model by analyzing a population in need of nursing care services, service prices, services in demand, willingness to place orders, and feedback on use. Methods: A retrospective analysis of data related to home care services on the "Jiuzhou Nursing Care" platform from April 2020 to August 2021, a total of 279 person-times, relevant information about the research subjects, and the status of home care services was conducted. SPSS 24.0 software was used for data analyses, such as calculating frequencies and percentages and conducting chi-square tests. Results: The "Jiuzhou Online Nurse" primarily serves elderly patients, and the majority of these patients have lost their ability to care for themselves. The average cost of nursing services was ¥183.45, and the unit cost of services had no effect on the number of service items. This particular internet-based home nursing service has a high level of satisfaction. Patients aged 60 to 74 have the highest number of Internet-based home care service orders (χ 2 = 11.791, P < 0.05). Patients who reuse the platform are more willing to assign people to provide services (χ 2 = 238.078, P < 0.05). Patients who were unable to care for themselves had a higher rate of repeat order (χ 2 = 10.877, P < 0.05). Conclusion: The "Internet+ Nursing" service platform specifically meets the individual needs of elderly patients, provides them with home nursing services, and improves local medical treatment and door-to-door services. This platform also provides convenience for elderly individuals who cannot care for themselves so that they can receive prompt treatment and assistance to improve their quality of life.

Associations between perceived overqualification, transformational leadership and burnout in nurses from intensive care units: A multicentre survey.

AIMS: To explore whether perceived overqualification increases the risk of burnout and whether transformational leadership negatively moderates this relationship. BACKGROUND: Perceived overqualification might contribute to burnout and lead to poor experience of transformational leadership, and transformational leadership might be associated with burnout. However, these relationships have not yet been confirmed. METHODS: A multicentre cross-sectional study. A total of 321 nurses from intensive care units were recruited from six tertiary hospitals. Scale of Perceived OverQualification, Transformational Leadership Questionnaire and emotional exhaustion subscale of the Maslach Burnout Inventory-General Survey were employed to collect the data. Hierarchical multiple regression and bootstrap resampling were applied to analyse the data. RESULTS: Burnout was positively associated with perceived overqualification and negatively associated with transformational leadership (each p < 0.05). Transformational leadership significantly mediated the relationship between perceived overqualification and burnout (b = -0.6389, 95% confidence interval: -0.8706, -0.4072). CONCLUSION: Our findings indicated that perceived overqualification and transformational leadership directly or indirectly affect burnout among nurses from intensive care units. IMPLICATIONS FOR NURSING MANAGERS: Personal and organizational-oriented interventions utilizing nurses' overall qualifications and implementing transformational leadership should be employed by nurse managers to alleviate burnout and promote the work performance of nurses from intensive care units.

Psychometric Properties of the Chinese Version of the Surrogate Decision-Making Self-Efficacy Scale.

Surrogate decision making for patients in the intensive care unit (ICU) can have negative physical and emotional health consequences for the decision-maker. Improving confidence and self-efficacy may reduce these consequences, but a valid instrument is necessary for reliable measurement. Using a cross-sectional design, the current study aimed to translate the Surrogate Decision-Making Self-Efficacy Scale (SDM-SES) into Chinese and evaluate its psychometric properties for surrogate decision-makers (SDMs) of patients in the ICU. The English version of the SDM-SES was translated into Chinese according to Brislin's translation guidelines and tested in 107 Chinese SDMs of patients in the ICU. Cronbach's alpha coefficient was 0.86, and a confirmatory factor analysis yielded acceptably high goodness-of-fit. Scores of the Chinese version of the SDM-SES were positively correlated with General Self-Efficacy Scale scores and 10-item Connor-Davidson Resilience Scale scores. This study indicates that the Chinese version of the SDM-SES has sufficient psychometric properties for assessing self-efficacy of SDMs for patients in the ICU. [Research in Gerontological Nursing, 14(1), 17-23.].

MiR-30a-5p ameliorates LPS-induced inflammatory injury in human A549 cells and mice via targeting RUNX2.

In this study, we aim to investigate the role of miR-30a-5p in acute lung injury/acute respiratory distress syndrome (ALI/ARDS) using LPS-induced A549 cells and mice. We found cell viability was significantly declined accompanied by cell apoptosis and cell cycle arrest at G0/G1 phase in LPS-treated A549 cells. MiR-30a-5p was down-regulated by LPS treatment and miR-30a-5p significantly protected A549 cells from LPS-induced injury by increasing cell viability, reducing cell apoptosis, promoting cell cycle progression, and inhibiting inflammatory reactions. Dual-luciferase activity demonstrated that RUNX2 was a direct target for miR-30a-5p and its expression was negatively and directly regulated by miR-30a-5p. Over-expression of RUNX2 weakened the inhibitory effect of miR-30a-5p on inflammatory injury. In vivo, over-expression of miR-30a-5p alleviated LPS-induced inflammatory responses and lung injury in LPS-administrated mice. Besides, miR-30a-5p repressed LPS-elevated phosphorylation levels of the signal transducer and activator of transcription 3 (STAT3) and c-Jun N-terminal kinase (JNK), IκBα degradation, and NF-κB p65 phosphorylation. In conclusion, miR-30a-5p ameliorates LPS-induced inflammatory injury in A549 cells and mice via targeting RUNX2 and related signaling pathways, thereby influencing the progression of ARDS.

MiR-150 attenuates LPS-induced acute lung injury via targeting AKT3.

Acute lung injury (ALI) and its severe manifestation of acute respiratory distress syndrome (ARDS) in human lung are induced by inflammatory cytokines and endogenous factors such as miRNAs. However, the role of miR-150 in lipopolysaccharide (LPS)-induced ALI is not clear. Here, we found miR-150 expression was significantly reduced in the serum of patients with ARDS, and negatively associated with the disease severity and 28-day survival of ARDS. In vivo, miR-150 decreased total cell and neutrophil counts, and production of inflammatory cytokines interleukin-1ß (IL-1ß), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) as well as levels of total protein, albumin and IgM in the bronchoalveolar lavage (BAL) fluid in LPS-induced ALI mice. Meanwhile, miR-150 improved the 72 h survival rate of LPS-induced ALI mice. In-vitro assays demonstrated that miR-150 alleviated LPS-induced A549 cell apoptosis, autophagy, and release of inflammatory cytokines. Further, AKT3 was a direct target of miR-150. Silencing of AKT3 partially reversed LPS-induced A549 cell injury, and enhanced the protective effects of miR-150. In addition, miR-150 or si-AKT3 effectively inhibited the phosphorylation levels of c-Jun N-terminal kinase (JNK) and nuclear factor-κB (NF-κB) (p65 and IκBα). In conclusion, miR-150 alleviated LPS-induced acute lung injury via directly targeting AKT3 expression or regulating JNK and NF-κB pathways, which may be a promising therapeutic strategy to treat ALI/ARDS.

miR-297 Protects Human Umbilical Vein Endothelial Cells against LPS-Induced Inflammatory Response and Apoptosis.

BACKGROUND/AIMS: Recently, microRNA-297 (miR-297) and signal transducer and activator of transcription 3 (STAT3) have been demonstrated to be involved in dysfunction of vascular endothelial cells and inflammatory conditions, such as sepsis. The present study aimed to investigate the role of miR-297 and STAT3 in lipopolysaccharide (LPS)-induced inflammatory human umbilical vein endothelial cells (HUVECs). METHODS: HUVECs were stimulated by different concentrations of LPS. miR-297 mimics were transfected into HUVECs to overexpress miR-297. The qRT-PCR was used to measure the expression level of miR-297. Western blot was used to detect the expressions of STAT3, inflammatory cytokines, adhesion molecules and apoptosis-related proteins. Cell apoptosis was determined by flow cytometry. RESULTS: Compared with parental HUVECs, the expression of miR-297 was significantly down-regulated, while the expression of STAT3 was obviously up-regulated in LPS-induced HUVECs. The expressions of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and E-selectin were also increased in LPS-induced HUVECs than those in parental HUVECs. In addition, LPS induced apoptosis of HUVECs through up-regulation of Bax and cleaved caspase 3 expressions. Conversely, miR-297 mimics inhibited LPS-activated expressions of STAT3, inflammatory cytokines, and adhesion molecules, and protected HUVECs against LPS-induced apoptosis through inhibition of Bax and cleaved caspase 3 expressions. Mechanistically, the 3'-untranslated region (3'-UTR) of STAT3 mRNA was validated as a direct target of miR-297. Over-expression of STAT3 partially abrogated protective effects of miR-297, whereas silencin g of STAT3 contributed to miR-297-mediated biological effects. CONCLUSION: miR-297 protects HUVECs against LPS-induced inflammatory response and apoptosis by targeting STAT3 pathway. Thus, miR-297 may be a promising therapeutic target for patients with sepsis.

MiR-150 predicts survival in patients with sepsis and inhibits LPS-induced inflammatory factors and apoptosis by targeting NF-κB1 in human umbilical vein endothelial cells.

MiR-150 is involved into some pathological processes, such as tumorigenesis and autoimmune diseases. However, little is known about the involvement of miR-150 in human sepsis. In this study, plasma miR-150 level had a diagnostic and independent prognostic value in patients with sepsis, and negatively correlated with renal dysfunction and 28-day survival as well as plasma levels of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α). MiR-150 expression was also significantly decreased in human umbilical vein endothelial cells (HUVECs) and C57BL/6 mice with sepsis after lipopolysaccharides (LPS) treatment. In-vitro, miR-150 over-expression protected HUVECs from LPS-induced apoptosis and the expressions of nuclear factor-κB1 (NF-κB1), IL-6, TNF-α, intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and E-selectin. Furthermore, NF-κB1 was identified as a direct target of miR-150. Restored NF-κB1 expression antagonized the protective effects of miR-150, while suppression of NF-κB1 enhanced these protective effects. Our findings indicate miR-150 predicts survival in patients with sepsis and inhibits LPS-induced inflammatory factors and apoptosis by targeting NF-κB1 in human umbilical vein endothelial cells. Thus, miR-150 may be a useful biomarker or target in the diagnosis, prognosis and treatment of patients with sepsis.