Construction and validation of a competency model for hospital operation assistant of public hospitals in China: a cross­sectional study.

BACKGROUND: Hospital operation assistant (HOA) plays an important role in promoting the operation effectiveness and efficiency of hospital. China, as a resource-poor country, urgently needs to train HOA talent. The purpose of this study is to construct and validate a competency model for HOA, which can be used as a tool to select and train HOAs. METHODS: Basic competency items were first constructed through literature review combined with the job analysis of HOA. Then, a questionnaire survey conducted on more than 300 hospital operation management-related staff was used to assess the importance of competency items. Exploratory factor analysis, structural equation model and second-order confirmatory factor analysis were used to construct and validate the competency model of HOA. RESULTS: A total of 23 items were identified as critical to HOA capability, which were further divided into three factors: professional skills, professional knowledge and personality traits. The structural equation model showed that the standardized path coefficients of the three factors were 0.86, 0.82 and 0.98. The competency model passed strict fitting effect tests in several aspects, including root-mean-square error of approximation (RMSEA) = 0.077 (< 0.080), standardized root mean square residual (SRMR) = 0.062 (< 0.080), comparative fit index (CFI) = 0.927 (> 0.900) and Tucker-Lewis index (TLI) = 0.918 (> 0.900), which showed that the fitting validity of the model was ideal. The composite reliability (CR), average variance extracted (AVE) and correlation coefficients of all factors were within the standard range, which showed that the construction validity and discrimination validity of the model were ideal. CONCLUSION: Our study indicates that the competency model of HOA is an instrument with appropriate fit validity, construct validity and discriminant validity, which can provide criteria for selecting and training HOAs.

Sulforaphane alleviated vascular remodeling in hypoxic pulmonary hypertension via inhibiting inflammation and oxidative stress.

Hypoxic pulmonary hypertension (HPH) is a cardiopulmonary disease featured by pulmonary vascular remodeling, which is due to abnormal proliferation of pulmonary artery smooth muscle cells (PASMCs) and dysfunction of endothelial cells (ECs). Sulforaphane (SFN) is a natural isothiocyanate extracted from cruciferous vegetables with promising anti-inflammatory and anti-oxidative activities. This study aimed to explore the effect and mechanism of SFN on HPH. Male mice were exposed to persistent chronic hypoxia for 4 weeks to induce HPH. The results demonstrated that SFN repressed the increased right ventricular systolic pressure (RVSP) and attenuated the right ventricular hypertrophy and pulmonary arteries remodeling in HPH mice. In particular, after SFN treatment, the CD68 positive cells in lung sections were reduced; TNF-α and IL-6 levels in lungs and serum declined; activation of NF-κB in PASMCs was inhibited in response to hypoxia. Besides, SFN enhanced the superoxide dismutase (SOD) activity in serum, SOD2 expression, total glutathione levels, and GSH/GSSG ratio in PASMCs, along with a decrease in malondialdehyde (MDA) contents in serum and ROS production in PASMCs after hypoxia exposure. Notably, SFN, as an Nrf2 activator, reversed the reduction in Nrf2 expression in hypoxic PASMCs. In vitro, SFN treatment inhibited hyperproliferation and promoted apoptosis of PASMCs under hypoxia conditions. SFN also prevented the apoptosis of pulmonary microvascular ECs caused by hypoxia. Therefore, these data suggested that SFN could significantly restrain the inflammation and oxidative stress, thereby inhibiting PASMCs proliferation, promoting PASMCs apoptosis, and reversing hypoxia injury in ECs to improve pulmonary vascular remodeling.

Steroid receptor coactivator-1 enhances the stemness of glioblastoma by activating long noncoding RNA XIST/miR-152/KLF4 pathway.

Glioblastoma (GBM) recurrence is attributed to the presence of therapy-resistant glioblastoma stem cells. Steroid receptor coactivator-1 (SRC-1) acts as an oncogenic regulator in many human tumors. The relationship between SRC-1 and GBM has not yet been studied. Herein, we investigate the role of SRC-1 in GBM. In this study, we found that SRC-1 expression is positively correlated with grades of glioma and inversely correlated with glioma patient's prognosis. Steroid receptor coactivator-1 promotes the proliferation, migration, and tumor growth of GBM cells. Notably, SRC-1 knockdown suppresses the stemness of GBM cells. Mechanistically, long noncoding RNA X-inactive specific transcript (XIST) is regulated by SRC-1 at the posttranscriptional level and mediates the function of SRC-1 in promoting stemness-like properties of GBM. Steroid receptor coactivator-1 can promote the expression of Kruppel-like factor 4 (KLF4) through the XIST/microRNA (miR)-152 axis. Additionally, arenobufagin and bufalin, SRC small molecule inhibitors, can reduce the proliferation and stemness of GBM cells. This study reveals SRC-1 promotes the stemness of GBM by activating the long noncoding RNA XIST/miR-152/KLF4 pathway and provides novel markers for diagnosis and therapy of GBM.

Aqp-1 Gene Knockout Attenuates Hypoxic Pulmonary Hypertension of Mice.

Objective- Hypoxic pulmonary hypertension (HPH) is characterized by proliferative vascular remodeling. Abnormal pulmonary artery smooth muscle cells proliferation and endothelial dysfunction are the primary cellular bases of vascular remodeling. AQP1 (aquaporin-1) is regulated by oxygen level and has been observed to play a role in the proliferation and migration of pulmonary artery smooth muscle cells. The role of AQP1 in HPH pathogenesis has not been directly determined to date. To determine the possible roles of AQP1 in the pathogenesis of HPH and explore its possible mechanisms. Approach and Results- Aqp1 knockout mice were used, and HPH model was established in this study. Primary pulmonary artery smooth muscle cells, primary mouse lung endothelial cells, and lung tissue sections from HPH model were used. Immunohistochemistry, immunofluorescence and Western blot, cell cycle, apoptosis, and migration analysis were performed in this study. AQP1 expression was upregulated by chronic hypoxia exposure, both in pulmonary artery endothelia and medial smooth muscle layer of mice. Aqp1 deficiency attenuated the elevation of right ventricular systolic pressures and mitigated pulmonary vascular structure remodeling. AQP1 deletion reduced abnormal cell proliferation in pulmonary artery and accompanied with accumulation of HIF (hypoxia-inducible factor). In vitro, Aqp1 deletion reduced hypoxia-induced proliferation, apoptosis resistance, and migration ability of primary cultured pulmonary artery smooth muscle cells and repressed HIF-1α protein stability. Furthermore, Aqp1 deficiency protected lung endothelial cells from apoptosis in response to hypoxic injury. Conclusions- Our data showed that Aqp1 deficiency could attenuate hypoxia-induced vascular remodeling in the development of HPH. AQP1 may be a potential target for pulmonary hypertension treatment.

Susceptibility-weighted imaging: the value in cerebral astrocytomas grading.

OBJECTIVE: To investigate the value of susceptibility weighted imaging (SWI) in evaluating the histopathologic grade of cerebral astrocytomas and compare the relative value of SWI and conventional magnetic resonance imaging (MRI) sequences. MATERIALS AND METHODS: This is an analysis of 26 untreated patients with pathologically confirmed astrocytomas. The tumors were classified as low grade (grade I-II: 12 cases) or high grade (grade III-IV: 14 cases). Imaging was performed with a 3.0 T MRI scanner. Conventional sequences [T1-weighted imaging (T1WI), contrast enhanced T1WI (CE-T1WI), T2-weighted imaging (T2WI), and T2 FLuid Attenuated Inversion Recovery (T2FLAIR)] and SWI sequence (including CE-SWI) were done. The number of small vessels and the amount of blood products in the tumors were determined for each sequence. Differences between the two groups were analyzed statistically. RESULTS: SWI was more sensitive than conventional sequences (T1WI, CE-T1WI, T2WI, and T2FLAIR) in visualizing small vessels and microhemorrhages in cerebral astrocytomas (P < 0.01). CE-SWI was better than CE-T1WI sequences for visualizing tumor small vessels and microhemorrhages. SWI visualized greater numbers of small vessels and areas of microhemorrhages in high-grade tumors than in low-grade tumors (P < 0.01). This was especially true after contrast administration (P < 0.01). CONCLUSION: SWI plays an important role in astrocytoma grading, especially for enhanced astrocytomas after contrast injection. CE-SWI was better than CE-T1WI in visualizing tumor architecture.