Objective To study and contruct competency characteristic evaluation models of nursing supervisors in secondly hospitals.Methods Using the matron semi-structured interviews,literature review,questionnaire survey and expert questionnaires to discuss the competency of nursing supervisors in secodary hospitals.Results We found that the competency model of nursing supervisors in secondary hospitals could better reflect the competency of nursing supervisors.The model had 16 competencies which included knewleage skills.management and individual characters.Conclusions Through the study of the model of competency nursing supervisors in secondary hospitals,we form a set of standard for nursing supervisor selection based on their competency.The standard can help to select the most suited nursing supervisors who have great potentials.

OBJECTIVE: To investigate the effects of compound preparation of Cordyceps sinensis and Tripterygium hypoglaucum (CSTHC) on survival time of grafted pigskin after allogeneic transplantation and its mechanism. METHODS: The pigskin was treated with CSTHC solution before allogeneic transplantation, and CSTHC ointment was applied for external use on the grafted pigskin after skin transplantation. Cyclosporine A (CsA) and normal saline were served as control. The survival time, the appearance and the histomorphological changes of the grafted pigskin were observed. The histomorphological changes of testicles in pigs were also examined. The CD4 and CD8 expressions in the grafted pigskins were measured by immunohistochemical method. The white blood cell count in peripheral blood and the liver and renal functions were also examined. RESULTS: The survival time of the grafted pigskin in the CSTHC-treated group was (28.50+/-3.26)d, which was much longer as compared with (10.60+/-1.52)d in the untreated group (P<0.01). The survival time of the grafted pigskin in the CsA-treated group was (28.33+/-3.50)d, and there was no remarkable difference in the survival time of the grafted pigskin between the CsA-treated group and the CSTHC-treated group. The expressions of CD4 and CD8 were lower in the CSTHC-treated group than those in the untreated group on the 7th and 14th day after skin graft (P<0.05), while there was no significant difference in the indices between the CSTHC-treated group and the CsA-treated group. The WBC count was higher in the untreated group than that in the CSTHC-treated group or CsA-treated group on the 7th day after skin graft (P<0.05). CONCLUSION: CSTHC can prolong the survival time of allogeneic grafted pigskin. Its mechanism of inhibiting the immunological rejection may relate to decreasing the expressions of CD4(+) and CD8(+) in the grafted pigskin and reducing the local inflammatory reaction.

Severe acute pancreatitis-associated acute lung injury (SAP-ALI) is a serious disease associated with high mortality. Emodin has been applied to alleviate SAP-ALI; however, the mechanism remains unclear. We report that the therapeutic role of emodin in attenuating SAP-ALI is partly dependent on an exosomal mechanism. SAP rats had increased levels of plasma exosomes with altered protein contents compared to the sham rats. These infused plasma exosomes tended to accumulate in the lungs and promoted the hyper-activation of alveolar macrophages and inflammatory damage. Conversely, emodin treatment decreased the plasma/pancreatic exosome levels in the SAP rats. Emodin-primed exosomes showed less pro-inflammatory effects in alveolar macrophages and lung tissues than SAP exosomes. In detail, emodin-primed exosomes suppressed the NF-κB pathway to reduce the activation of alveolar macrophage and ameliorate lung inflammation by regulating PPARγ pathway, while these effects were amplified/abolished by PPARγ agonist/antagonist. Blockage of pancreatic acinar cell exosome biogenesis also exhibited suppression of alveolar macrophage activation and reduction of lung inflammation. This study suggests a vital role of exosomes in participating inflammation-associated organ-injury, and indicates emodin can attenuate SAP-ALI by reducing the pancreatic exosome-mediated alveolar macrophage activation.