Development of the competency assessment scale for clinical nursing teachers: Results of a Delphi study and validation.

BACKGROUND: Highly competent clinical faculty is a prerequisite for graduating competent nurses, and it is very important to explore the comprehensive ability and post competence of clinical nursing teachers (CNT). OBJECTIVE: To construct the competency evaluation elements of clinical nursing teachers and test the reliability and validity of the scale. DESIGN: A Delphi study. SETTINGS: 34 Grade A tertiary hospitals and eight colleges and universities in China, covering 14 provinces, autonomous regions, and municipalities directly under the Central Government. METHODS: Modified Delphi method was used in this study. Between August 2018 and May 2019, 40 experts participated in three rounds of consultation to build the CNT competency assessment scale. The expert coordination coefficient (W) and the coefficient of variation (CV) were used to examine the level of coordination and concentration of expert advice. Then, the reliability and validity of the scale were tested. Using the convenient sampling method, a total of 190 questionnaires were distributed to nursing teachers, and 187 were recovered. Cronbach's α coefficient was used to evaluate the reliability of the scale. Validity was evaluated using the content validity index. RESULTS: After the three rounds of expert consultation, the questionnaire contained five dimensions and 44 elements. After expert inquiry, the total coefficient of variation index (CVI) value of the scale was 0.992, and the CVI of each item was 0.95-1.00. The Spearman-Brown correlation coefficient was 0.984. By comparing the results of the two surveys 2 months apart, the Pearson correlation coefficient was tested, and the retest reliability was 0.852. The Cronbach's α of the scale was 0.962, indicating excellent internal consistency. CONCLUSIONS: The scale of clinical nursing teachers' competence has high reliability and validity. This tool could be widely used to evaluate and improve nursing teaching.

Impaired wound healing results from the dysfunction of the Akt/mTOR pathway in diabetic rats.

BACKGROUND: Wound healing is impaired in diabetes mellitus. The underlying mechanism involved in this process is still unknown. The Akt/mTOR signaling pathway plays a crucial role in the pathogenesis of diabetes. OBJECTIVE: we investigated the role of the Akt/mTOR pathway in diabetic wounds and the mechanisms that growth factors activate this pathway to promote diabetic wound healing. METHODS: Full-thickness skin excisional wounds were created on the backs of normal and streptozotocin-induced diabetic rats. The expression of key proteins in the Akt/mTOR pathway was assayed using western blotting; topical effects of granulocyte-macrophage colony stimulating factor (GM-CSF) on diabetic wounds and activation of the Akt/mTOR pathway were subsequently investigated. Activation of the Akt/mTOR pathway by GM-SCF in vitro was examined in rat primary fibroblasts. RESULTS: The results indicate that the Akt/mTOR pathway was activated in the wound tissue of both non-diabetic and diabetic rats, as indicated by a remarkable increase in expression of total and phosphorylated key proteins in this pathway. However, the expression level of these proteins was dramatically attenuated in diabetic wounds compared with non-diabetic wounds. Upon topical application of GM-CSF, the diabetic wound healing was remarkably improved concomitantly with increased expression and phosphorylation of key proteins in the Akt/mTOR pathway. In addition, rat fibroblast proliferation induced by GM-CSF depended on the Akt/mTOR pathway activation. CONCLUSION: Impaired wound healing results from the dysfunction of the Akt/mTOR pathway in diabetic rats. The pharmacologic elevation of this pathway may represent an attractive intervention strategy to improve prognosis of diabetic wounds.

Stromal cell-derived factor-1 enhances wound healing through recruiting bone marrow-derived mesenchymal stem cells to the wound area and promoting neovascularization.

Stromal cell-derived factor-1 (SDF-1) is a potent chemokine for bone marrow-derived stromal stem cells (BMSCs) that express CXCR4, the receptor for SDF-1. SDF-1 is considered to play an important role in the trafficking of BMSCs. We investigated the contribution of SDF-1 to the recruitment of BMSCs to the wound area and its promotion of wound repair and neovascularization. BMSCs were pretreated with or without anti-CXCR4 blocking antibody and combined with CM-DiI label, and injected via the tail vein into mice with full-thickness skin wounds on the dorsum. Simultaneously, anti-SDF-1 antibody was injected into local wounds in another group of mice. The results show that blockade of CXCR4 on either infused BMSCs or SDF-1 in the host wounds (1) dramatically impaired the number of infused BMSCs being recruited to the injured tissue, (2) reduced the expression of growth factors involved in the repair of injured tissue such as vascular endothelial growth factor, basic fibroblast growth factor and transforming growth factor beta 1, (3) decreased the resultant neovascularization, and (4) retarded wound healing. Taken together, the findings indicate that the SDF-1/CXCR4 signal pathway facilitates wound healing through augmenting BMSC recruitment to wound tissues, responsive secretion of growth factors by BMSCs and neovascularization in the wound area.

Experimental study on He-Ne laser irradiation to inhibit scar fibroblast growth in culture.

OBJECTIVE: To explore the inhibitory effect of He-Ne laser irradiation on fibroblast growth of hypertrophic scars in culture. METHODS: He-Ne laser with wavelength of 632.8 nm, power density of 50 mW/cm(2) and doses of 3 J/cm(2), 30 J/cm(2), 90 J/cm(2) and 180 J/cm(2) was used to irradiate human scar fibroblasts in culture 1, 3 and 5 times respectively, and then the cell count and cell cycle analysis were done. RESULTS: Repeated irradiation with He-Ne laser at dose of 180 J/cm(2) three and five times led to an evident decrease in total cell number compared with that of the control group and there was a significant difference (P<0.05). The cell cycle analysis showed after three and five times of irradiation with 180 J/cm(2) He-Ne laser the cell number in S-phase decreased from 51% to 20% and 14% respectively, the cell number in G(0)/G(1) phase increased from 28% to 55% and 60% respectively, and the cell percentage in Sub-G1 phase was 6.7% and 9.8% respectively. CONCLUSIONS: Repeated irradiation with 180 J/cm(2) He-Ne laser can inhibit scar fibroblasts growth in culture. It may be that He-Ne laser irradiation causes cell stagnation in G(0)/G(1) phase and apoptosis.