ABSTRACT
Objective to analyze the differences and changes before and after the introduction of supply processing distribution (SPD) supply chain management mode in a public hospital, analyze the typical problems existing in the clinical practice and development of SPD mode, and explore the countermeasures to improve the SPD supply chain management. Methods the changes of 20 management functions before and after the introduction of SPD supply chain management mode were compared. The advantages and disadvantages of SPD management mode were analyzed. The improvement measures and countermeasures were proposed. Results among the 20 management functions, 11 of them were reduced, 5 of them were equal, and 4 of them were increased. The overall efficiency of hospital management was improved. Because the external medicine supplier has not been included in the hospital rules, regulations system and process. The role positioning was not clear. There were defects in institutional and continuous guarantee. Conclusion SPD supply chain management mode can be improved and innovated to promote the supply channel reform of drugs and medical consumables, and improve the fine management level of drugs and medical consumables.
ABSTRACT
Objective To investigate the effect and mechanism of astragalusⅣ (AS-Ⅳ) on the expression of CCL18in U937macrophages.Methods The expression of CCL18mRNA was detected by real time PCR.The expression of CCL18protein was assessed by Elisa.The expression of IL-4receptor was measured by flow cytometry.The STAT 6phosphorylation was measured by Elisa.The activity of JAK kinase was detected by Z″-LYTETMkinase assay.Results AS-Ⅳsignificantly down-regulated the expression of CCL18in U937macrophages stimulated by IL-4with a dose-dependent manner.However, AS-Ⅳhad no significant effect on IL-4receptor subunit expression.The STAT6phosphorylation was inhibited by AS-Ⅳ, but the effect was less than AS1517499;the activity of JAK1, JAK3and TYK2kinase were inhibited by AS-Ⅳ.Conclusion AS-Ⅳcould inhibit the expression of CCL18in U937macrophages stimulated by IL-4.One of the suggested mechanisms was due to inhibition of JAK kinase activity, which caused STAT6transcriptional activity down and inhibited CCL18gene expression.