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Objective To investigate the changes of peritoneal macrophage function in sepsis mice after hyperbaric oxygen (HO) therapy.Methods One hundred C57BL/6 mice were randomly(random number) divided into four groups in equal number (n=25):control group (normal saline),sepsis group,hyperbaric oxygen group,sepsis+ hyperbaric oxygen group;the sepstic mice were treated by intra-peritoneal injection with zymosan;The mice of hyperbaric oxygen group and sepsis+ hyperbaric oxygen group received hyperbaric oxygen therapy (2 atm,2 h,100％ O2).The number of surviving mice was obsevred at 72 h after the intra-peritoneal injection with zymosan;The percentage of M1 macrophage was detected by flow cytometry.The expression of mRNA of inducible nitric oxide synthase (iNOS) in peritoneal macrophage was detected with RT-PCR.The levels of IL-12 and IL-10 in peripheral blood were measured by ELISA.Results Compared with sepsis group,the number of surviving mice of sepsis+ hyperbaric oxygen group was significantly higher (9 vs.16,P＜0.01).The percentages of M1 macrophage in sepsis+ hyperbaric oxygen group was significantly lower than that in sepsis group [(4.75+0.14)％ vs.(2.25±0.16)％,F=803.438,P＜0.01].The expression of mRNA of inducible nitric oxide synthase(iNOS) in sepsis+ hyperbaric oxygen group were significantly lower than that in sepsis group [(39.62+1.74) vs.(48.32±3.34),F=31.992,P＜0.01].The level of IL-12 in peripheral blood in sepsis+ hyperbaric oxygen group was significantly lower than that in sepsis group [(242.62±19.10) pg/mL vs.(159.51±6.35)pg/mL,F=102.282,P＜0.01].The level of IL-10 was significantly higher than that in sepsis group [(521.26±6.3) pg/mL vs.(188.83±8.53) pg/mL,F=5 896.006,P＜0.01].Conclusions Hyperbaric oxygen therapy had effective effect on increasing the number of surviving mice of sepsis group,reducing the level of IL-12 in peripheral blood and rising the level of IL-10 in peripheral blood.By inhibiting the expression of M1 macrophage and iNOS,hyperbaric oxygen could reduce the excessive inflammatory response and play a role in the protection of mice.
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Objective To investigate the mechanism of inducing production of vascular endothelial growth factors (VEGF) by recombinant human S100 calcium binding protein A4 (rhS100A4) in rheumatoid arthritis fibroblast-like synoviocytes (RAFLSs).Methods Synovial tissue was sampled from the patients with rheumatoid arthritis (RA) undergoing knee arthroplasty for in vitro culture of RAFLSs.CCK-8 assay was conducted to detect the effect of rhS100A4 and the effect of its interaction with Rapamycin (Rap),an inhibitor of mammalian rapamycin target 1 (mTORC1) signaling pathway,on the proliferation of RAFLSs.The effects of rhS100A4 and its interaction with Rap on the expression of VEGF in RAFLSs were detected by immunofluorescence.After rhS100A4 and its cooperation with Rap stimulated the conditioned medium (CM)produced by RAFLSs,the effect of CM on formation of lumen in human unbilical vein endothelial cells (HUVECs) in vitro was observed to detect the angiogenic ability of rhS100A4.Western blot was used to detect the effect of rhS100A4 on the phosphorylation of downstream ribosomal protein S6 (S6) in the mTORC1 signaling pathway in RAFLSs and to analyze the effects of rhS100A4 and Rap on phosphorylation of S6 protein and expression of VEGF protein in RAFLSs.Results rhS100A4 promoted cell proliferation and expression of VEGF protein in RAFLSs,and the CM formed by rhS100A4 promoted HUVECs to form blood vessels in vitro.Rap inhibited the above biological effects of rhS100A4,rhS100A4 activated the downstream protein S6 in the mTORC1 signaling pathway in RAFLSs cells to increase their phosphorylation levels.The effects of rhS100A4 on the phosphorylation of S6 protein and on the expression of VEGF protein in RAFLSs were inhibited by Rap.Conclusion rhS10OA4 promotes production of VEGF in RAFLSs by activating the mTORC 1 signaling pathway.
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Objective To evaluate the performance of D-dimer in the differential diagnosis between acute aortic dissection (AAD)with elevated troponin-I(TNI)and acute myocardial infarction (AMI) in patients with acute chest pain diseases with elevated TNI.Methods The data of the 547 patients complaining acute chest pain who were diagnosed as acute myocardial infarction by thoracic and abdominal aorta CTA examination from January 2013 to September 2015 were analyzed.The comparison of data of D-dimer mass concentration and the general clinical information between 44 patients diagnosed as AAD with elevated TNI and without other underlying diseases which could cause increase in D-dimer mass concentration(AAD with elevated TNI group) and 50 patients diagnosed as acute myocardial infarction confirmed by using coronary angiography(AMI group) were carried out.Results Compared with AMI group,in the AAD with elevated TNI group,the type of Stanford A was 38 cases, accounting for 86.4%;the proportion of the patients with a history of hypertension was higher, and the average age was younger;the D-dimer mass concentration levels and the positive ratio of the D-dimer test were much higher[11.27 μg/mL(3.95,20)μg/mL vs.0.28 μg/mL(0.22,0.40)μg/mL,P<0.01;100%vs.14%,P<0.01.The area under the ROC curve to diagnosis of the AAD with elevated TNI was 0.997,and the optimal diagnostic threshold was 1.095 μg/mL.When the D-dimer mass concentration level was 1.095 μg/mL,the sensitivity,specificity,positive predictive value(PPV),negative predictive value(NPV),positive likelihood ratio(PLR),negative likelihood ratio(NLR)were 97.7%,98%,97.7%,98%,48.86,and 0.02,respctively.When the D-dimer mass concentration level was 0.5 μg/mL,which meant the D-dimer test was positive,the sensitivity,specificity,PPV,NPV,PLR,NLR were 100%,86%,86.3%,100%,7.14,and 1.16,respctively.Conclusion D-dimer is helpful to the differential diagnosis between the AAD with elevated TNI and the AMI in acute chest pain patients with elevated TNI.
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BACKGROUND:Atorvastatin has been shown to reduce bone loss and fracture, but its effects on implant osseointegration remain unknown. OBJECTIVE:To investigate the effects of atorvastatin on implant osseointegration in osteoporotic rats and the underlying mechanisms. METHODS:Forty-eight Sprague-Dawley rats were randomized into sham-surgery, ovariectomy, and atorvastatin (10 and 20 mg/kg per day) treatment groups, respectively. Al rats received ovariectomy and implant surgery except those in the sham-surgery group. Bone mineral density of the lumbar vertebra, osseointegration ratio and pul-out strength of implants were measured after 12-week treatment.Levels of bone formation and resorption markers in osteoblasts treated with atorvastatin were determined by ELISA. Wnt pathway-relatedgene expression was detected by RT-PCR. RESULTS AND CONCLUSION:Bone mineral density, osseointegration ratio and pul-out strength of implants were significantly increased in 20 mg/kg per day of atorvastatin treatment group compared with ovariectomy group (P< 0.05). Levels of alkaline phosphatase, osteocalcinand osteoprotegerinwere significantly increased in osteoblasts treated with atorvastatinin vitro(P<0 .05), and the level of osteoclast differentiation factor RANKL was significantly inhibited (P< 0.05). Meanwhile, atorvastatin significantly promoted the mRNA expression of low-density lipoprotein associated protein 5and β-catenin, and inhibited the mRNA expression of dickkopfWnt signal pathway inhibitor 1and sclerostin. Our results suggest that atorvastatin promotes implant osseointegration in osteoporotic rats by activating Wnt/β-catenin signal pathway.
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Objective:To investigate the relation between the expression of proliferating cell nuclear antigen (PCNA) and prognosis in lung squamous cell.Methods:The expression of PCNA on 51 cases carcinoma tissues were detected by immunohistochemical SP technique. Thet test and F test was used to analyze the difference of expression of PCNA in different pathological grades and clinic stages.Spearman Grade-relation test was used to analyze the relation between PCNA expression and pathological grades.The difference of survival time was compared by Kaplan-Meier curve and Long-rank test in different PCNA expression.Rusults:The position of PCNA expression almostl located in the nuclear,some in cytoplasm.There was difference of PCNA expression in different clinical stages and pathological grades.( P