Objective To study the association between metabolic syndrome (MS) and prognosis of endometrioid carcinoma.Methods A total of 256 patients with endometrioid carcinoma at,Zhejiang Cancer Hospital between January,2001 and December,2008 were chosen.The deadline for follow up was December 2008.The general conditions(including age and body mass index),whether coupled with MS and it's risk factors(including waist circumference,fasting plasma glucose,triglycerides,high-densitylipoprotein,systolic and diastolic blood pressure) were analyzed.The outcome of 256 patients whether coupled with MS were analyzed using Kaplan-Meier curve.Relative risks were estimated using Cox proportional hazards regression model.Results A total of 256 cases were followed-up successfully.Sixtyfour (33.0％) cases coupled with MS among the 194 patients survived,while thirty-two (51.6％)coupled with MS from 62 cases died,there was significant difference between them (x2=6.953,P=0.008).The total fiveyear survival rate was 75.8％,the survival time was (78.0±3.4) months.The rate and the survival time of patients coupled with MS [66.7％,(67.0±2.4) months] were significatly lower than those coupled with no MS [81.3％,(85.0±4.0) months;P＜0.05].The Cox proportional hazards regression results showed that coupled with MS,body mass index ≥25 kg/m2,waist circumference＞80 cm,abnormol systolic and diastolic blood pressure,abnormal fasting plasma glucose and more than two components of definitions of MS were related to bad prognosis of endometrioid carcinoma(P＜0.05).Conclusion Metabolic syndrome may be lead to a bad prognosis of endometrioid carcinoma.

Objective To investigate the role of miR-223 in the pathogenesis of acute gouty inflammation.Methods The subjects were divided into 3 groups:65 acute gout patients (AG),50 inter-critical gout patients (IG),and 45 healthy controls (HC).The peripheral blood mononuclear cells (PBMCs) and the clinical laboratory parameters were all collected.The expression of miR-223 in the PBMCs was detected using realtime fluorescent quantitative polymerase chain reaction (RT-qPCR) (TaqMan probe).The PBMCs of 5 healthy people were stimulated with monosodium urate (MSU) (100 μg/ml) for 12 h,and then,miR-223,NLRP3 mRNA and IL-1β production were all measured using RT-qPCR and ELISA respectively.All data were analyzed by SPSS 17.0 statistical software,Wilcoxon rank sum test,t test and Spearman's correlations analysis were used for statistical analysis.Results ① The expression of miR-223 in AG and IG groups was both significantly decreased than that in the HC group (8±17 vs 26±76,P＜0.05;9±17 vs 26±76,P＜0.05;respectively),AG group was significantly decreased than that in the IG group [8(17) vs 9(17),Z=11.387,P＜0.01].② After stimulated with MSU in healthy controls,IL-1β production and NLRP3 mRNA were both significantly increased [(86±5) pg/ml vs (13±6) pg/ml,t=21.042,P＜0.01;5.2±0.4 vs 1.2±0.4,t=14.640,P＜0.01;respectively],while the expression of miR-223 was significantly decreased (0.34±0.20 vs 1.05±0.24,t=-5.164,P＜0.01).Conclusion The data suggests that miR-223 might be involved in the patho-genesis of spontaneous regulation,but further study is needed to discover the exact mechanism.

Objective To investigate the impact of ropivacaine on apoptosis of lippolysaccharide(LPS)-induced ulcerative colitis cell line NCM-460 and on activity of nucleotide oligomerization domain(NOD)-like receptor protein-3(NLRP3)inflammatome.Methods Human colon epithelial cell line NCM-460 was cultured in vitro and divided into control group(no intervention),model group(10 μg/mL LPS treatment),low/medium/high concentration ropivacaine group(10 μg/mL LPS and 0.5,1,1.5 mmol/L ropivacaine co-treatment,respectiv-oly).Cell viability was determined by cell counting kit 8(CCK-8)and the appropriate concentration was selected.The cells were then divided into control group,model group,ropivacaine group(10 μg/mL LPS and 1.5 mmol/L ropivacaine treatment)and ropivacaine+inhibitor group(10 μg/mL LPS,1.5 mmol/L ropiva-caine and 1 μmol/L NF-κB pathway inhibitor BAY 11-7082 treatment),inhibitor group(10 μg/mL LPS+1 μmol/L NF-κB pathway inhibitor BAY 11-7082 treatment)and ropivacaine+activator group(10 μg/mL LPS,1.5 mmol/L ropivacaine and 1 μmol/L NF-κB pathway activator Prostratin),all groups were treated for 24 h.The level of IL-6,IL-8 and TNF-α were detected by enzyme-linked immunosorbent assay(ELISA).The proliferation rate was detected by EdU incorporation.Hoechst 33258 staining microscopy was used to detect the apoptosis rate.Level of cyclinD1,caspase-3,NLRP3 and NF-κB pathway-related proteins were detected by Western blot.Results Compared with the control group,the cell viability of the model group was significantly decreased and the cell viability of high-concentration experimental group was increased after adding ropivacaine(P＜0.05).So,1.5 mmol/L ropivacaine was selected for the follow-up experiment.Compared with the control group,the concentration of inflammatory cytokines IL-6,IL-8,TNF-α,apoptosis rate and the protein expression of caspase-3,NLRP3 and phosphorylated p-NF-κB in model group were all significantly increased(P＜0.05),while the proliferation rate and cycilnD1 protein expression were decreased(P＜0.05).Com-pared with model group,the concentrations of IL-6,IL-8,TNF-α,apoptosis rate and the expression of caspase-3,NLRP3 and p-NF-κB protein in ropivacaine group and inhibitor group were significantly decreased(P＜0.05),while the proliferation and cycilnD1 protein expression were increased(P＜0.05).Compared with ropivacaine group,the trend of the above indexes in ropivacaine+inhibitor group was more significant(P＜0.05),and the trend of these indexes in ropivacaine+agonist group was significantly reversed(P＜0.05).Conclusions Ropivacaine can inhibit the activation of NLRP3 inflammasome and block the signal transduction of NF-κB pathway,further inhibit LPS-induced apoptosis of NCM-460 cells and promote proliferation.

Background Research on non-target organ damage of biological pesticides has attracted much attention. Rotenone exposure may be far beyond the occupational environment, and the exposureduring pregnancy may be increased through bioaccumulation, fruit or vegetable residues, and other forms of oral intake. At present, the effects of rotenone on placental development and its mechanism are still unknown. Objective To investigate the developmental damage of rat placenta and evaluate the expression levels of glycogen synthase kinase (GSK-3β) and beta catenin (β-catenin) followed by rotenone exposure through the placental barrier during pregnancy, as well as to propose possible associated mechanisms. Methods Eighteen sexually mature SD female infertile rats without specific pathogens were selected and divided into three groups: blank control group (0.9% saline), corn oil group, and rotenone group (corn oil + 2 mg·kg⁻¹ rotenone) by random number method, six female animals in each group. Another six male rats were selected and mated to the female rats at night with a female to male ratio of 3:1 per cage. Pregnant rats were given 0.9% saline, corn oil, and 2 mg·kg⁻¹ rotenone preparation by isovolumetric gavage once daily for the entire gestation period (19 d), and their conditions were observed after the last dose. The pregnant rats were anesthetized, and the size of the placenta and blood perfusion were detected by ultrasound the next day of the last dose of rotenone. Then, 3 pregnant rats in each group were sacrificed immediately and the placenta and umbilical cord tissues were dissected. The remaining 9 pregnant rats gave birth naturally, and the fetuses were observed for developmental evaluation and weighed. The histopathological changes of umbilical cord and placenta were observed by hematoxylin-eosin staining. The reactive oxygen species levels of placenta tissues were detected by flow cytometry. The Ca²⁺-ATPase activity of placenta tissues was detected by colorimetric method. The localization and levels of GSK-3β and β-catenin expression of placenta were detected by immunohistochemistry. The p-GSK-3β/GSK-3β and p-β-catenin/β-catenin protein expression in placental tissues were measured by Western blotting. Results No injury or death was recorded during the pregnant rats receiving rotennon administration. Adverse pregnancy outcomes such as fetal absorption and postpartum stillbirth were found in the rotenone group, and the weight of the fetal mice decreased (P<0.05). The B-ultrasound showed disc-shaped placenta with a thick middle and thin edge, smooth fetal surface, rough maternal surface, visible placental lobules, granular echotexture of the placenta with comma-like echogenic densities, and chorionic plate showing deep indentations, no calcification, degeneration, or necrosis in each group. Compared with the corn oil group, the fetal surface diameter of the placenta was reduced in the rotenone group (P<0.05). The Doppler color ultrasound showed that interplacental blood flow was reduced in the rotenone group, while interplacental blood flow was abundant in the blank control and the corn oil groups. The hematoxylin-eosin staining results showed that smooth muscle cells in the umbilical cord tissues of rats were loosely arranged, with fuzzy nuclei and inflammatory infiltration in the rotenone group. The placental trophoblast cells were small in size, disorderly arranged with nuclear fragmentation and cytoplasm turbidity. The tissue reactive oxygen species level in the rotenone group was higher than those in the other two groups (P<0.05). The Ca²⁺-ATPase activity of placental tissues was reduced in the rotenone group (P<0.05). The immunofluorescence low-magnification observation showed that GSK-3β and β-catenin were expressed in placental tissue, weak fluorescence expression in the decidua basalis, strong fluorescence expression in the labyrinthine layer structure. The labyrinthine layer under high magnification showed that compared with the blank control group and the corn oil group, the brightness of β-catenin fluorescence expression in the rotenone group decreased (P<0.05), and the brightness of GSK-3β expression increased (P<0.05). The Western blotting results showed that the expression of β-catenin and p-GSK-3β proteins decreased (P<0.01), and the expression of GSK-3β protein increased (P<0.01) in the rotenone group. No significant expression of p-β-catenin protein was detected in the placenta tissue of each group. Conclusion Rotenone exposure during pregnancy induces placental hypoperfusion, growth retardation, and oxidative stress in rats, as well as down-regulation of β-catenin and p-GSK-3β protein expression, and up-regulation of GSK-3β protein expression, which may further lead to abnormal pregnancy and fetal restricted growth.