Objective:To study the inhibitory effect of endothelial progenitor cells (EPCs) on aortic injury in mice with systemic lupus erythematosus (SLE) arteriosclerosis.Methods:APOE -/- mice were injected with norphytane and high fat diet to establish lupus vascular injury model. Then the mice were divided into normal control group (ND group), high fat diet group (HFD group), high fat diet+ SLE vascular injury group (HFD+ SLE group), high fat diet+ SLE vascular injury+ hydroxychloroquine treatment group (HFD+ SLE+ Hydro group), high fat diet+ SLE vascular injury+ EPCs treatment group (HFD+ SLE+ EPCs group). At the end of the experiment, urine, blood and aortic tissues of mice in each group were collected, and the content of urinary protein and the depth of serum type I interferon (IFN-Ⅰ) were detected by enzyme linked immunosorbent assay (ELISA). The activation of cyclic guanosine monophosphate synthase/interferon gene stimulating factor/type I interferon (cGAS/STING/IFN-Ⅰ) pathway, the levels of inflammatory factors, adhesion fractions and chemokines in the aorta of mice in each group were detected by immunohistochemistry and Western blotting (WB). The lipid deposition in the aorta was detected by oil red staining. Results:The results of ELISA showed that the levels of urinary protein and serum IFN-Ⅰ in HFD+ SLE group were higher than those in normal control group. EPCs treatment could reduce the levels of urinary protein and serum IFN-Ⅰ in SLE atherosclerotic mice. WB results showed that the expression of CD19, CD68, CD34, chemokine, cGAS, p-STING, phosphorylated TANK binding kinase 1 (p-TBK1), phosphorylated interferon regulatory factor 3 (p-IRF3) and IFN-Ⅰ increased in HFD+ SLE group, and hydroxychloroquine and EPCs decreased the levels of these factors. CGAS/STING/IFN-Ⅰ signal pathway is involved in the occurrence and development of atherosclerosis in SLE patients; both EPCs and hydroxychloroquine can inhibit the activation of cGAS/STING/IFN-Ⅰ signal, thus reducing atherosclerosis in SLE mice.Conclusions:cGAS/STING/IFN-Ⅰ pathway is involved in the development of SLE atherosclerosis. EPCs can inhibit the activation of cGAS/STING signal, reduce the expression and secretion of IFN-Ⅰ, and then reduce vascular inflammation and inhibit the development of SLE-related atherosclerosis.

Objective:To study the inhibitory effect of endothelial progenitor cells (EPCs) on aortic injury in mice with systemic lupus erythematosus (SLE) arteriosclerosis.Methods:APOE -/- mice were injected with norphytane and high fat diet to establish lupus vascular injury model. Then the mice were divided into normal control group (ND group), high fat diet group (HFD group), high fat diet+ SLE vascular injury group (HFD+ SLE group), high fat diet+ SLE vascular injury+ hydroxychloroquine treatment group (HFD+ SLE+ Hydro group), high fat diet+ SLE vascular injury+ EPCs treatment group (HFD+ SLE+ EPCs group). At the end of the experiment, urine, blood and aortic tissues of mice in each group were collected, and the content of urinary protein and the depth of serum type I interferon (IFN-Ⅰ) were detected by enzyme linked immunosorbent assay (ELISA). The activation of cyclic guanosine monophosphate synthase/interferon gene stimulating factor/type I interferon (cGAS/STING/IFN-Ⅰ) pathway, the levels of inflammatory factors, adhesion fractions and chemokines in the aorta of mice in each group were detected by immunohistochemistry and Western blotting (WB). The lipid deposition in the aorta was detected by oil red staining. Results:The results of ELISA showed that the levels of urinary protein and serum IFN-Ⅰ in HFD+ SLE group were higher than those in normal control group. EPCs treatment could reduce the levels of urinary protein and serum IFN-Ⅰ in SLE atherosclerotic mice. WB results showed that the expression of CD19, CD68, CD34, chemokine, cGAS, p-STING, phosphorylated TANK binding kinase 1 (p-TBK1), phosphorylated interferon regulatory factor 3 (p-IRF3) and IFN-Ⅰ increased in HFD+ SLE group, and hydroxychloroquine and EPCs decreased the levels of these factors. CGAS/STING/IFN-Ⅰ signal pathway is involved in the occurrence and development of atherosclerosis in SLE patients; both EPCs and hydroxychloroquine can inhibit the activation of cGAS/STING/IFN-Ⅰ signal, thus reducing atherosclerosis in SLE mice.Conclusions:cGAS/STING/IFN-Ⅰ pathway is involved in the development of SLE atherosclerosis. EPCs can inhibit the activation of cGAS/STING signal, reduce the expression and secretion of IFN-Ⅰ, and then reduce vascular inflammation and inhibit the development of SLE-related atherosclerosis.

Objective:To study the effects of plan-do-check-action (PDCA) cycle in quality improvement of neonatal resuscitation.Methods:From 2016 to 2020, the clinical data of neonates born in our hospital were analyzed. Neonates born during 2016 to 2017 were pre-PDCA group and neonates born during 2018 to 2020 were post-PDCA group. PDCA quality improvement included step-by-step, high-frequency and low-dose training, strengthening teamwork and adding equipment.Results:A total of 7 728 live-birth neonates were delivered before PDCA with 319 cases (4.1%) of asphyxia. 10 174 live-birth neonates were delivered after PDCA with 422 cases (4.1%) of asphyxia. The asphyxia rates showed no significant difference between the two groups ( P>0.05). The incidences of severe asphyxia before and after PDCA were both 0.8% without significant difference ( P>0.05). The success rates of resuscitation for severe asphyxia before and after PDCA was 27.9% and 44.9%, respectively, and the differences were statistically significant ( P<0.05). The mortality rates within 7 d before and after PDCA were 0.5‰ and 0.1‰ respectively, without significant differences ( P>0.05). Conclusions:The implementation of PDCA cycle and step-by-step, high-frequency, low-dose neonatal resuscitation training can effectively improve the success rate of resuscitation in newborns with severe asphyxia.

To estimate the protective effect of removing circulatory TNF-a immunoadsorpnon or Amberlite XAD-7 absorption respectively on endotoxin shock. Methods New Zealand white rabbits injected with lethal dose of endotoxin underwent hemoper-fusion through immunoadsorbent or Amberh'te XAD-7 respectively. Plasma TNF-a levels were detected, and the sorbent efficiency and survival rate were observed. Results After 2 hours hemoperfusion through immunoadsorbent or Amberlite XAD-7 respectively, plasma TNF levels were significandy lower than those in die control group, especially, die sorbent efficiency of immunoadsorp-tion was higher dian dial of Amberlite XAD-7 adsorption. Conclusion Compared widi die nonspecific Amberlite XAD-7 adsorption, immunoadsorption might be a specific and more effective therapy of endotoxin shock.