The main impacting factors on implementing clinical pathway were analyzed by applying fishbone diagram.The factors include policy factors,organizational factors and personal factors.It was suggested to improve the trial work of implementing clinical pathway management by reforming the medical care payment system,putting the clinical pathway management into the evaluation system,building up medical information system,putting more efforts on promotion and enhancing cooperation among related departments.

Objective To observe the effects of Fuyanshu Capsule on phenol mucilage-induced endometritis rats and the possible anti-inflammation mechanism of the therapeutic effects.Methods Chronic endometritis in rats was induced by injection of phenol mucilage suspension into the uterus.Sixty female SD rats were randomly divided into 6 groups,namely,sham-operation group (distilled water,10mL/kg),model group,Jinji capsule group (0.65 g/kg),and Fuyanshu Capsule groups (1.8 g/kg,0.9 g/kg and 0.45 g/kg).After the rats were treated 28 days with corresponding medicine by intragastric administration,the pathology of the endometrium and changes of tumor necrosis factor α(TNF-α)and interleukin-2 (IL-2)levels were detected to evaluate the effects of Fuyanshu Capsule. Results Fuyanshu Capsule (1.8 g/kg and 0.9 g/kg)ameliorated the body weight reduction caused by endometritis in rats.Fuyanshu Capsule (1.8 g/kg,0.9 g/kg and 0.45 g/kg)reduced the ratio of the swelling uterus and ovaries to body weight of the rats.It ameliorated obviously the hyperplasia,necrosis and degeneration of endometrial epithelia and infiltration of inflammatory cells.The capsule (1.8 g/kg)decreased the serum IL-2 level in the rats with phenol mucilage-induced endometritis. Conclusion The anti-inflammatory effect of Fuyanshu Capsule on chronic endometritis induced by phenol mucilage in rats may be related to the decrease of IL-2 level.

Objective To investigate the effect of human CD47 (hCD47) in inducing the immune tolerance of human macrophages to porcine endothelial cells. Methods The porcine iliac endothelial cell (PIEC) transfected with pCDH-hCD47-FLAG plasmid was assigned into the pCDH-hCD47 group, PIEC transfected with pCDH-FLAG empty vector plasmid was assigned into the pCDH group, PIEC transfected with hCD47-dN was assigned into the pCDH-hCD47-dN group and human umbilical vein endothelial cell (HUVEC) was assigned into the positive control group. The cells were co-cultured with human macrophages to detect and analyze the phosphorylation of signal regulatory protein α (SIRPα) and the killing effect of human macrophages on PIEC. Furthermore, porcine arteriae endothelial cell (PAEC) was isolated from GT^－/－ and GT^－/－/ hCD 47 gene editing pigs to analyze the phosphorylation of SIRPα and the killing effect of human macrophages on PAEC. Results The pCDH group cells could not induce the phosphorylation of SIRPα, whereas the pCDH-hCD47 group cells could activate the phosphorylation of SIRPα after 10 min co-culture with human macrophages, and the degree of phosphorylation of SIRPα was increased with the prolongation of the co-culture time. The pCDH-hCD47-dN group cells failed to activate the phosphorylation of SIRPα. Human macrophages exerted significant effect on killing the pCDH group cells. The pCDH-hCD47 group cells could evidently inhibit the killing effect of human macrophages (P < 0.05), whereas the pCDH-hCD47-dN cells failed to suppress the killing effect of human macrophages. GT^－/－-PAEC could not activate the phosphorylation of SIRPα after co-culture with human macrophages. However, GT^－/－/hCD47-PAEC significantly activated the phosphorylation of SIRPα after co-culture with human macrophages. Human macrophages exerted significant killing effect on GT^－/－-PAEC, and GT^－/－/hCD47-PAEC could obviously inhibit the killing effect of human macrophages (P < 0.05). Conclusions The expression of hCD47 in the porcine endothelial cells can inhibit the killing effect of human macrophages on endothelial cells by activating the phosphorylation of SIRPα.

OBJECTIVETo assess the association of copy number variations (CNVs) of exon 11 of IL-23 receptor gene with susceptibility to active pulmonary tuberculosis among Chinese Uygurs.

METHODSIn this study, 250 subjects with active pulmonary tuberculosis (PTB) and 250 normal controls were recruited. A paired case-control study was conducted in the Chinese Uygur population in Xinjiang and the CNV of IL-23R was analyzed using Taqman real-time PCR.

RESULTSThe study showed that the frequencies of different copy number in exon 11 of IL-23R between PTB and control groups were statistically significant (χ(2)=13.35, P<0.01). There were significant difference in CNV of exon 11 in IL-23R between PTB patients and controls (χ(2)=14.95, P<0.01, OR=2.875, 95%CI: 1.655-4.994). The increase of copy number in exon 11 of IL-23R showed significantly different between PTB and control groups (χ(2)=10.475, P=0.0012, OR=2.611, 95%CI: 1.437-4.744).

CONCLUSIONThe CNV of exon 11 in IL-23R is associated with PTB in the Chinese Uygur population. The increase of the copy number in exon 11 of IL-23R may be a risk factor for PTB in Chinese Uygurs.

Adult ; Aged ; Asian Continental Ancestry Group ; ethnology ; genetics ; Case-Control Studies ; China ; ethnology ; DNA Copy Number Variations ; Exons ; Female ; Genetic Predisposition to Disease ; ethnology ; Humans ; Male ; Middle Aged ; Receptors, Interleukin ; genetics ; Tuberculosis, Pulmonary ; ethnology ; genetics ; Young Adult