Objective To investigate the correlation of serum high-mobility group box-1 (HMG-B1) with the severity of lesion of coronary artery disease (CAD) and its prognosis in elderly patients.Methods A total of 180 CAD patients with coronary stenosis exceeding 50 percent by coronary angiography were divided into three groups:one branch stenosis;two branches stenosis and three branches stenosis.The control group included 50 patients without coronary stenosis.The degrees of coronary stenosis were diagnosed as mild stenosis,moderate stenosis and severe stenosis based on improved Gensini scores.The severity of decrements of left ventricular ejection fraction (LVEF) by echocardiogram were divided into three groups:mild,moderate and severe LVEF.Levels of HMGB1,hs-CRP and glucose were measured in all the patients.According to whether there was a complication of type 2 diabetic mellitus (T2DM),the 180 patients were classified as two groups.The patients were also divided into two groups according to whether there were adverse events.Results The HMGB1 levels of the CAD group were increased along with the number of affected vessels [three bunch group (40.5±6.0) ng/ml,double bunch group (33.1±4.9)μg/L,single bunch group (20.5±3.3)μg/L and control group (6.2±1.4)μg/L (all P＜0.05)].And the HMGB1 levels of the CAD group were increased along with the degrees of CAD stenosis [severe stenosis group (43.0±5.8)μg/L,medium stenosis group (32.1±4.5)μg/L,mild stenosis group(19.3±2.0)μg/L] (all P＜0.05).Meanwhile,the levels of HMGB1 were increased along with the decrement of left ventricular ejection fraction [left ventricular severe dysfunction group (41.0 ± 5.5) μg/L,medium dysfunction group(33.1± 4.3)μg/L,mild dysfunction group (21.3± 2.0)μg/L] (all P＜0.05).CAD with T2DM had a higher HMGB1 level than non-T2DM group[(35.7±5.0) (C)/L vs.(23.3±3.0) (C)/L,P＜0.05].The adverse events group had a higher HMGB1 level than non-adverse events group[(38.7±5.5) (C)/L vs.(25.3±3.3)μg/L,P＜0.05].Besides,HMGB1 had a positive correlation with levels of hs-CRP and glucose(r=0.680,0.571,P＜0.05).Conclusions Serum HMGB1 change is closely related to morbid change degree of elderly CAD patients as well as prognosis.As a new type of inflammatory factor,HMGB1 may serve as a new target for disease treatment.

Objective To investigate the expression of the hsa-miR-155 in serum of endometrial cancer and its clinical significance. Methods Collected 44 cases blood specimens before surgery operation from Sep. 2008 to Dec. 2009, and collected 12 cases blood specimens from the health of volunteers in comparison. Real time quantity PCR was used to detect the expression of hsa-miR-155 in those specimens and analyzed clinical pathological with the expression of hsa-mir-155 in endometrial cancer. Results The expression of hsa-miR-155 was (3.9 ±0.7) in endometrial cancer, which was significantly higher than that in control group( P ＜ 0.01 ). The expressions of hsa-miR-155 were ( 3.7 ± 0.6 ), ( 3.9 ± 0.6 ) and ( 3.7 ±0.6)times in well, moderately and poorly differentiated endometrial cancer, respectively,while there were not significant difference ( P ＞ 0.05 ). The expressions were ( 3.8 ± 0.6 ) and ( 3.9 ± 0.6 ) times between endometrioid adenocarcinoma and non-endometrioid adenocarcinoma, and there were significant difference (P ＞ 0.05). The expressions were ( 2.1 ± 0.4 ) and ( 5.6 ± 0.8 ) times in stage Ⅰ - Ⅱ and Ⅲ - Ⅳ endometrial cancer, respectively, in which there were significant difference (P ＜ 0.05 ). The expressions of hsa-miR-155 were (5.5 ± 0.5 ) and ( 1.9 ± 0.2) times between lymph node metastasis and without lymph node metastasis in endometrial cancer, in which there were significant difference (P ＜ 0.01 ). Conclusion Hsa-miR-155 may play an important role in the proliferation, and metastasis of endometrial cancer, which may be a indicator in the diagnosis and prognosis of endometrial cancer and may be used as a predictive biomarker.

Objective To observe the changes of serum complements and proinflammatory cytokines in rats with sepsis, and to explore the possible mechanism.Methods 120 healthy male Wistar rats were randomly divided into three groups: normal control group (n = 15), sham operation group (n = 15) and sepsis group [cecum ligation and puncture (CLP) operation,n = 90]. The sepsis rats were sacrificed on 24, 48 and 72 hours after modeling. The level of serum complements (C5, C5a) and cytokines tumor necrosis factor-α (TNF-α), interleukin (IL-1, IL-6), high mobility group box 1 (HMGB1), macrophage migration inhibitory factor (MIF) were detected by enzyme linked immunosorbent assay (ELISA).Results Compared with normal control group and sham operation group, the levels of serum complements C5, C5a and IL-1β were significantly increased at 24 hours after CLP in sepsis group [C5 (ng/L): 1.60±0.19 vs. 1.04±0.20, 1.09±0.09; C5a (ng/L): 0.20±0.02 vs. 0.18±0.01, 0.18±0.02; IL-1β (ng/L): 700.20±111.41 vs. 475.87±108.96, 592.29±121.57; allP < 0.05]; then the levels of C5, C5a and IL-1β declined, the level of serum C5 were also higher than normal control group at 48 hours and 72 hours after CLP (ng/L: 1.17±0.24, 1.27±0.24 vs. 1.04±0.20, bothP < 0.05). In sepsis group the level of serum TNF-α (ng/L: 51.33±1.96, 51.06±1.64) was lower than that in normal control group (59.53±3.06) and sham operation group (57.91±2.72) at 48 hours and 72 hours (allP < 0.05). There was a time dependent rise of serum HMGB1 in sepsis group, which level was much higher than that in normal control group and sham operation group at 72 hours after CLP (ng/L: 472.21±20.94 vs. 406.00±43.16, 404.41±35.39, bothP < 0.05). There were no significant differences of MIF, and IL-6 level between groups at each time points.Conclusions Complement system led to uncontrolled inflammatory response and immune dysfunction through the release of proinflammatory cytokines and inflammatory mediators, which maybe one of the important mechanism of the pathology of sepsis.

AIM:MicroRNAs ( miRNAs) were recognized to play significant roles in cardiac hypertrophy .But, it remains unknown whether cyclin/Rb pathway is modulated by miRNAs during cardiac hypertrophy .This study investigates the potential roles of microRNA-1 (miR-1) and microRNA-16 (miR-16) in modulating cyclin/Rb pathway during cardiomyocyte hypertrophy .METHODS:An animal model of hypertrophy was established in a rat with abdominal aortic constriction (AAC).In addition, a cell model of hypertrophy was also achieved based on PE-promoted neonatal rat ventricular cardiomyocyte .RESULTS:miR-1 and-16 expression were markedly de-creased in hypertrophic myocardium and hypertrophic cardiomyocytes in rats .Overexpression of miR-1 and -16 suppressed rat cardiac hypertrophy and hypertrophic phenotype of cultured cardiomyocytes .Expression of cyclins D1, D2 and E1, CDK6 and phosphorylated pRb was increased in hypertrophic myocardium and hypertrophic cardiomyocytes , but could be reversed by enforced expression of miR-1 and -16.CDK6 was validated to be modulated post-transcriptionally by miR-1, and cyclins D1, D2 and E1 were further validated to be modulated post-transcriptionally by miR-16.CONCLUSION: Attenuations of miR-1 and -16 provoke cardiomyocyte hypertrophy via derepressing the cyclins D1, D2, E1 and CDK6, and activating cyclin/Rb pathway.

AIM:To investigate the effect of miR-214 on cardiomyocyte hypertrophy and the expression of the potential target genes . METHODS:A cell model of hypertrophy was established based on angiotensin-Ⅱ( Ang-Ⅱ)-induced neonatal mouse ventricular car-diomyocytes (NMVCs).Dual luciferase reporter assay was performed to verify the interaction between miR-214 and the 3’ UTR of MEF2C.The expression of MEF2C and hypertrophy-related genes at mRNA and protein levels was determined by RT-qPCR and Wes-tern blotting, respectively.RESULTS:The expression of ANP, ACTA1,β-MHC and miR-214 was markedly increased in Ang-Ⅱ-in-duced hypertrophic cardiomyocytes .Dual luciferase reporter assay revealed that miR-214 interacted with the 3’ UTR of MEF2C, and miR-214 was verified to inhibit MEF2C expression at the transcriptional level .The protein expression of MEF2C was markedly in-creased in the hypertrophic cardiomyocytes .Moreover, miR-214 mimic, in parallel to MEF2C siRNA, inhibited the expression of hy-pertrophy-related genes in Ang-Ⅱ-induced NMVCs.CONCLUSION:MEF2C is a target gene of miR-214, which mediates the effect of miR-214 on attenuating cardiomyocyte hypertrophy .

Objective To summary the therapy outcome of retroperitoneal laparoscopic treatment on upper ureteral calculi.Methods The retroperitoneal laparoscopic treatment were performed to all cases from Jun.2011 to Jun.2012 in our hospital.All cases were treated with 3-hold method (two 10 mm and one 5 mm ports).The retroperitoneal space was made by a combination of blunt and balloon dissection,and the space was maintained with CO2 Ureteral longitudinal incision was made to remove the stones,and double J catheter was served as stent drainage.Absorbable suture was used to suture ureteral incision.Results A retroperitoneal approach was performed in 12 patients,and another patient was conducted the open surgery because the stone cower in the kidney calices.Operative periods ranged from 55 to 132 min (average was 85 min).There were no significant postoperative complications.Conclusion It is a minimally invasive and effective approach in the therapy of upper urerteral calculi with laparoscopic.

Objective To explore the effect and mechanism of CD4+CD25+Tregs(Tregs)on the protective efficacy of glutha?tione?S?transferase(GST)against Schistosoma japonicum in mice. Methods Female BALB/c mice were divided randomly into five groups:a normal control group,an infected control group,an anti?CD25mAb group,a GST immunization group and a com?bination group with GST immunization and anti?CD25 mAb. The GST group and combination group were injected percutaneously with GST 50μg each mouse,the other two groups were injected with equal volume PBS. The immunization was performed for 3 times for two?week interval,and 2 weeks after the last immunization,each mouse was challenged with 40 S. japonicum cercaria. Two weeks post?infection,the combination group and anti?CD25 mAb group were injected intraperitoneally with 300μg anti?CD25 mAb each mouse. The mice were succumbed 2 weeks,3 weeks,4 weeks and 5 weeks post?infection respectively. The per?centages of CD4+CD25+Tregs in splenocytes of mice were measured with flow cytometer. The levels of IFN?γ,IL?2,IL?4,IL?5 and TGF?βin cell cultural supernatants were determined by sandwich?ELISA after stimulation with Con A. The liver sections were stained with hematoxylin and eosin. Results The worm burden in the combination group(15.80 ± 2.74)was significantly lower than those of the infected control group(27.78 ± 3.15),anti?CD25 mAb group(21.50 ± 4.21),and GST group(20.84 ± 6.46). Compared to those of the infected control group,the percentages of CD4+CD25+Tregs were significantly higher in the GST group,while the percentages of CD4+CD25+Tregs were significantly lower post?anti?CD25 mAb?administration. Regardless of GST administration,the levels of IFN?γ,IL?2,IL?4 and IL?5 after anti?CD25 mAb were significantly higher than those of the in?fected control groups. There were no significant differences of egg granuloma and the level of TGF?βbetween each group. Con?clusion CD4+CD25+Tregs could be partially blocked by anti?CD25 mAb while Th1 and Th2 type immunization response could be enhanced,which plays a role in improving the protective efficacy of GST against of S. japonicum.

Objective To study the susceptibility of Neisseria gonorrhoeae to antibiotic agents from 1988 to 2002 in Shanghai. Methods The clinical isolates from patients with gonorrhea were collected and tested for their susceptibility to five antibiotics. Agarose-dilution-method was used to detect minimal inhibitory concentration (MIC) of anti-microbial agents including penicillin, tetracycline, spectinomycin, ciprofloxacin and ceftriaxone, and penicillinase producing Neisseria gonorrhoeae (PPNG) were tested with acidometric method. Results Susceptible strains to penicillin decreased from 11.28% in 1988 to 0 in 2002, MIC50 and MIC90 increased 8 and 4 times, respectively, the resistant rate and proportion of PPNG were 94.29% and 50.95%, respectively in 2002. The strains of high resistance to tetracycline increased from 0 in 1995 to 20.95% in 2002. The susceptible strains to ceftriaxone decreased from 100% in 1995 to 23.80% in 2002. The susceptibility to ciprofloxacin decreased significantly and resistant rate reached 99.05% in 2002. However, these strains were kept highly susceptible to spectionmycin. Concerning the multi-drug resistance, we found that the strains resistant to penicillin, ciprofloxacin and tetracycline simultaneously increased from 20.87% in 2001 to 23.30% in 2002, those resistant to both penicillin and ciprofloxacin reached to 70% in the past 2 years. Conclusions In Shanghai the resistant rates of Neisseria gonorrhoeae to antibiotics increased year by year in the past 15 years. The study indicates that spectinomycin and ceftriaxone should be the first choice for the treatment of gonorrhea at present and new sensitive antibiotic should be developed for the treatment of gonorrhea.

AIM:To investigate the effect of microRNA-214 ( miR-214) on cardiomyocyte hypertrophy and the expression of the potential target genes .METHODS:A cell model of hypertrophy was established based on angiotensin-Ⅱ( Ang-Ⅱ)-induced neonatal mouse ventricular cardiomyocytes ( NMVCs) .Dual luciferase reporter assay was performed to verify the interaction between miR-214 and the 3’ UTR of MEF2C.The expression of MEF2C and hypertrophy-related genes at mRNA and protein levels was determined by RT-qPCR and Western blot , respectively .RESULTS:The expression of ANP, ACTA1,β-MHC and miR-214 was markedly increased in Ang-Ⅱ-induced hypertrophic cardiomyocytes .Dual lu-ciferase reporter assay revealed that miR-214 interacted with the 3’ UTR of MEF2C, and miR-214 was verified to inhibit MEF2C expression at the transcriptional level .The protein expression of MEF2C was markedly increased in the hypertro-phic cardiomyocytes .Moreover, miR-214 mimic, in parallel to MEF2C siRNA, inhibited the expression of hypertrophy-re-lated genes in Ang-Ⅱ-induced NMVCs.CONCLUSION:MEF2C is a target gene of miR-214, which mediates the effect of miR-214 on attenuating cardiomyocyte hypertrophy .

The aim of the present studies was to investigate the cardioprotection of late IP at 72 h and determine the involvement of iNOS, nNOS and COX-2 in this protection. Conscious rabbits were preconditioned with three cycles of 5-minute coronary occlusion/5-minute reperfusion. The myocardial infarct area in the rabbits preconditioned 72 h earlier was significantly smaller than that in control rabbits. The activity of lactate dehydrogenase (LDH) and the level of 6-Keto-PGF1alpha in the rabbits preconditioned 72 h earlier were lower than those in control rabbits. The left ventricular systolic pressure (LVSP) and maximal velocity of contraction and relaxation (+/- dP/dtmax) were improved in rabbits preconditioned 72 h earlier. The nNOS-selective inhibitors N-propyl-L-arginine and selective cyclooxygenase-2 (COX-2) inhibitor celecoxib completely blocked the protection of late IP at 72 h, whereas the iNOS selective inhibitor S-methybisothiourea had no effect. In conclusion, the cardioprotection observed in the final stage of late IP (72 hours) is mediated by nNOS or COX-2, but not by iNOS.
Animals ; Cyclooxygenase 2 ; metabolism ; physiology ; Ischemic Preconditioning, Myocardial ; Male ; Myocardial Infarction ; enzymology ; pathology ; prevention & control ; Myocardial Reperfusion Injury ; enzymology ; metabolism ; prevention & control ; Nitric Oxide Synthase Type I ; metabolism ; physiology ; Rabbits ; Random Allocation ; Time Factors