ObjectiveTo evaluate the changes of hepatic blood perfusion in cirrhotic patients undergoing pericardial devascularization (PCDV).MethodsHepatic artery and portal vein perfusion of 22 pre- and post- PCDV cirrhotic patients were evaluated with rheohepatogram(RHG) and ultrasonography (USG).ResultsCompared with normal control, the hepatic artery, portal vein effective perfusion and total hepatic perfusion decreased on RHG 〔(0.053?0.011) vs. (0.031?0.009),(0.033?0.011) vs. (0.018?0.008),〔(7.7?3.0) vs. (3.5?1.7), all P

Objective To study the effects of Qingjinkangkuoyin (QJKKY) on TNF-α and NE in rats with bronchiectasis.Methods Models were established by intrabronchially injecting with pseudomonas aeruginosa,and divided into 5 groups by random:the QJKKY high dose treatment group (given high dose of QJKKY into stomach),the QJKKY low dose treatment group (given low dose of QJKKY),the levofloxacin group (given levofloxacin),the model group (given normal saline),and the normal contrast group (given normal saline).After 2 weeks of treatment,the histopathology of lung tissue,the levels of TNF-α and inflammatory cells in peripheral blood and NE in rats' lung tissue were detected.Results Compared with the model group (160.425±9.9293)ng/L,QJKKY could decrease the level of TNF-α in blood significantly [high dose of QJKKY treatment group was (137.133±6.1646)ng/L,P＜0.05]; the expression of inflammatory cells in serum were decreased significantly by QJKKY [high dose of QJKKY treatment group was (1.106± 0.3580) 109/L,P＜0.05].Low dose of QJKKY treatment group was (1.086 ±0.2433) 109/L,(P＜0.05) ; the expression of NE in lung tissue were decreased remarkably by QJKKY [high dose of QJKKY treatment group(80.697 ±4.5877)ng/L,P＜0.05]; low dose of QJKKY treatment group is (80.747±3.6925)ng/L,(P＜0.05); and the histopathologic change of lung tissue in QJKKY treatment groups were ameliorated under light microscope by HE staining.Conclusion Qingjinkangkuoyin could cure bronchiectasis by decreasing the expression of TNF-αin peripheral blood and NE in rats' lung tissue.

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Objective To evaluate the efficacy and safety of combination therapy with domestic bezafibrate and fluvastatin in patients with combined hyperlipidemia. Methods 180 patients with combined hyperlipidemia were randomly divided into two groups. They were assigned to receive 40 mg fluvastatin (n = 90) or a combination of 400 mg bezafibrate and 40 mg fluvastatin (n = 90) for 24 weeks. Results After 24 weeks treatments, the serum TC, LDL-C levels were reduced (P <0.01) and HDL-C level was increased more significantly (P <0.05) in the combi-nation therapy group. Conclusion Combination therapy with bezafibrate (400 mg) and fluvastatin (40 rag) is more effective than fluvastatin(40 mg) monotherapy.

Aim To investigate the signaling mecha-nisms in endothelial monocyte-activating polypeptide-Ⅱ( EMAP-Ⅱ)-induced increase in blood-tumor barri-er ( BTB ) permeability. Methods Relatively pure cerebral microvessel fragments were obtained from the cortex of 3-5 days old Wistar rats by using careful dis-section, enzyme digestion, and dextran centrifugation. Then, these fragments were seeded on dishes and cul-tured primarily. In vitro BTB models were constructed by co-cultivation of rat brain microvascular endothelial cells ( BMECs) with C6 glioma cells. Confluent mono-layers of co-cultured BMECs were divided randomly in-to 5 groups ( each n=6 ): control, EMAP-Ⅱ, H7 +EMAP-Ⅱ, C3 exoenzyme + EMAP-Ⅱ, and C3 ex-oenzyme + H7 + EMAP-Ⅱ groups. Transendothelial electric resistance values and horseradish peroxidase flux were measured to evaluate changes in the BTB permeability . The expression levels of tight junction-re-lated protein occludin and ZO-1 in BMECs were meas-ured by Western blot. Immunofluorescence was used to identify the expression and distribution of occludin and ZO-1 in BMECs. Also, Western blot were used to de-tect the expression levels of myosin light chain ( MLC) and phosphomyosin light chain ( pMLC ) in BMECs. Results Compared with control group, the BTB per-meability of EMAP-Ⅱ group was increased significant-ly. The expression levels of occludin and ZO-1 in BMECs were significantly decreased, accompanied with marked increase in the expression level of pMLC. These above-mentioned effects of EMAP-Ⅱ were sig-nificantly inhibited by pretreatment with H7 ( an inhib-itor of PKC ) or/and C3 exoenzyme ( an inhibitor of RhoA ) . Conclusion Signaling molecules PKC and RhoA play important roles in EMAP-Ⅱ-induced in-crease in BTB permeability; signaling pathways PKC-pMLC and RhoA-pMLC are involved in this process.

Objective To observe the efficacy and safety of different initial doses of nebulized budesonide inhalation (BI) in infants and young children with moderate to severe asthma exacerbations.Methods A multi-center,parallel controlled clinical trial was performed during Sep 2008 to Apr 2010 in three hospitals,which were Department of Pediatrics,Shanghai Jiaotong University Affiliated Shanghai First People's Hospital,Department of Pediatrics,Shanghai Jiaotong University School of Medicine Affiliated Xinhua Hospital,and Department of Respiratory,Fudan University Affiliated Children's Hospital.One hundred and fifty children aged 6 to 36 month with moderate to severe asthma exacerbations were randomly divided into two groups.The high-starting-dose group was treated with a dose of 1 mg nebulized BI every 8 h for 2 days,while the conventional-starting-dose group was treated with a dose of 0.5 mg cvcry 8 h for 4 days.The terbutaline sulfate aerosol liquid was administered with a dose of 2.5 mg each time as needed.The primary outcome measures were severity scores,which were assessed at admission (0 h),and 8 h,16 h,24 h,48 h,72 h after treatment separately.The secondary outcome measures included the use of β2 receptor agonist,the systemic use of corticosteroids,average length of hospital stay and total cost.The data was analyzed with SPSS 13.0.Results (1) The clinical severity scores were significantly decreased at all time points after treatment in both groups (P ＜ 0.05).Compared with conventional starting-dose of BI,high starting-dose of 3.25 ± 1.82,P ＜ 0.01).(2) The terbutaline doses and the systemic corticosteroids do-ses were significantly reduced in high-starting-dose group compared with conventional-starting-dose group [(16.27 ± 12.99) mg vs (22.90 ± 18.27) mg,P ＜ 0.05 ; (4.54 ± 18.18) mg vs (11.16 ± 21.34) mg,P ＜ 0.05).The average length of hospital stay and the total cost of the two groups showed no significant differences (P ＞ 0.05).(3) There were no side effects associated with BI.Conclusion Compared with conventional treatment,high-starting-dose of BI can control symptoms fast and reduce the use of systemic corticosteroid without any side effects.BI improved symptoms more quickly at 8 h (2.87 ± 1.60 vs 4.48 ± 2.24,P ＜ 0.01) and 16 h (2.48 ± 1.56 vs

Aim To express the fusion protein hTNFα -hPgnK5 in E.Coli and to identify its activity. Methods The hTNFα -hPgnK5 gene express vector was constructed and the fusion protein was expressed in E.coli. The activity of fusion protein to inhibit the proliferation of tumor cells or angioendothelial cells in vitro was determined by MTT. Results Fusion protein hTNFα -hPgnK5 possessed immunoactivity in Western blot analysis and could inhibit proliferation of tumor cells or angioendothelial cells in vitro test. Conclusion The hTNFα gene and hPgnk5 gene can be coexpressed in prokaryotic system and expression products can inhibit the proliferation of tumor cells or angioendothelial cells in vitro.

Aim To explore the effect of shikonin on stemness maintance of glioma stem cells ( GSCs ). Methods After the U87-MG cells were cultured and isolated, the sphere cells were identified by immuno-fluorescent staining. The alteration of stemness of GSCs by shikonin treatment(2 μmol·L - 1 ) for 12 h, 24 h and 48 h was valued by morphological detection using optical microscope and sub-sphere forming assay. Mo-reover, the related markers of stem cells, such as CD133, were detected in shikonin treated GSCs by western blot assay. Protein expression of PI3K, p-PI3K, Akt and p-Akt was detected by western blot af-ter shikonin treatment alone. Furthermore, by combi-nation with insulin-like growth factor-1 ( IGF-1), we observed the alteration of stemness maintance of shiko-nin-treated GSCs. Results The presence of neural stem cell related markers CD133 and nestin proved the characteristics of GSCs. Shikonin treatment significant-ly inhibited the morphology of GSCs and the sub-sphere forming. Besides, the reduced expression of CD133 was detected in shikonin treated GSCs. Though, the expression of PI3K and Akt did not change compared with the control group, the expression of p-PI3K and p-Akt was reduced. Furthermore, the combination of IGF-1 markedly attenuated the inhibitory effect of shikonin on stemness maintance of GSCs. Conclusion The stemness maintance of GSCs can be significantly inhibited by shikonin treatment, in which PI3K/ Akt pathway is involved.

Objective To discuss the impact of repeated contrast media exposure on renal function in patients who received coronary angiography ( CAG) or percutaneous coronary intervention ( PCI) within 1 week after CTA of coronary ateries. Methods A total of 258 patients who received CAG or PCI after coronary CTA were divided into the study group ( n=132, patients had CAG/PCI within 1 week after CTA) and the control group ( n=126, patients had CAG/PCI 1-2 weeks after CTA). Serum creatinine, cystatin C and estimated GFR were tested before and on day 1, 2 and 3 after procedures. The occurance of contrast-induced nephropathy ( CIN ) was recorded. Resu1ts The baseline clinical characteristics of the patients between the two groups had no significant difference. Preoperative and postoperative serum creatinine, cystatin C and eGFR values on day 1, 2 and 3 had no significant difference between the two groups (all P﹥0. 05). There was no significant difference in the incidence of CIN between two groups (5. 3% in the study group vs. 4. 8% in the control group, P﹥0. 05 ) . Conc1usions It is safe and feasible for patients with eGFR≥60 ml/( min?1. 73 m2 ) to undergo CAG or PCI within 1 week after coronary CTA.