Objective To investigate the effects of mitochondrial DNA (mtDNA) on the pathopoiesis mechanisms of paraquat poisoning in vitro.Methods Firstly,the survival rate of A549 cells (human type Ⅱ alveolar epithelial cells) was measured with cell counting kit-8 after exposure to paraquat.Afterwards,the concentration of mtDNA in supernant of culture medium for culturing A549 and the chauge of mitochondrial membrance potential were detected with absolute quantitative PCR and confocal laser microscopy,respectively.Then,The chemotactic activity of mtDNA in peripheral blood mononuclear cells (PBMC) and neutrophils (PMN) were detected by transwell chemotaxis,and the subtype of chemotactic cells was measured with flow cytometry.Meanwhile,the role of mtDNA in vascular permeability was measured by using Xcelligence system and in vitro using vascular permeability kits.Finally,the effects of mtDNA in cell proliferation were to verify.Results The 50％ of lethal concentration (LD50) of paraquat for A549 was 600 μmol/L.Cell viability and concentration of mtDNA following challenge of PQ revealed in a concentration-and time-dependent manner (P ＜ 0.05).The mtDNA had a power in aggregating PBMC nonspecifically,but there was no effect on the vascular permeability was found.Moreover,the proliferation of human fibroblasts was not stimulated directly by mtDNA,but TGF-β1 (transforming growth factor-beta 1),a major pro-fibrotic factor,was increased compared to control group (P ＜ 0.05).Conclusions The mtDNA could play an important role in the inflammatory and proliferation responses to paraquat poisoning.

To review the experience in surgical management of cor triatriatum, fourteen patients underwent open heart surgery under hypothermic cardiopulmonary bypass (CPB) from 1986 to 2001 for their cor triatiatum were studied retrospectively. The mean age of the patients was 6 6 years, with a range of 1 to 26 years. Eight patients were men and six were women. Eleven cases were diagnosed by two dimensioned echo cardiography with colour Dopplar imaging. Eleven patients with complete cor triatriatum were operate on enlarging ASD, resecting the fiboromuscular membrane and patching ASD and one patient with incomplete cor triatriatum were operated on through similar techniques and the associated abnormalities were corrected at a time. Nine patients were followed up after surgery from 5 months to 15 years, no patient died and had salutary results. It suggested that two dimensional echo cardiography with colour Doppler imaging can diagnose this condition accurately, surgical treatment of cor triatriatum was satisfactory in longterm follow up.

To investigate the role of calcineurin dependent signal pathway in cardiac hypertrophy of cold stress induced hypertensive rats, 3 months old Wistar rats were exposed to cold (4?2℃) for 4 hours per day for 8 weeks to produce cold stress induced hypertension and cardiac hypertrophy. The systolic blood pressure(SBP), heart rate and hemodynamic parameters were measured using a force transducer.The heart/body weight ratio, CaN activity, CaN, c fos expression protein of cardiac tissure were also investigated. The results showed that SBP and heart rate in cold stress rats were significantly increased than that in nomal rats during the whole experiment( P

Objective　To explore the effect of hypoxia on the apoptosis of cultured human umbilical vein endothelial cells（HUVECs） and the role of vascular endothelial growth factor（VEGF） in inhibition of apoptosis． Methods　①Culture and identification of HUVECs．②Establishment of hypoxic model（0，12，24，48 h）in HUVECs．③Incubation of HUVECs with VEGF(0 ng, 100 ng) under hypoxic condition for 24 h. ④Detection of apoptosis of HUVECs with TUNEL method． Results　The percentages of apoptosis were different under different hypoxic conditions． The longer hypoxic time was，the higher apoptosis percentage was．VEGF reduced the apoptosis of HUVECs induced by hepoxia． Conclusion　Over-apoptosis EVCs in one of the important factors for the impairment of endothelial function. HEGF inhibits the apoptosis of HVCs and having a pretive function on them.

ObjectiveTo investigate the preventive effects of rosiglitazone on nonalcoholic steatohepatitis (NASH) rats and to explore the potential mechanisms in modulating peroxisome proliferator-activated receptor gamma (PPARγ),nuclear factor kappa B (NF-κB),and cyclooxygenase-2 (COX-2) expression.Methods Thirty male SD rats were assigned into the normal group ( n =10),the model group ( n =10),rosiglitazone prevention group [ n =10,simultaneously 4mg/( kg · d) gavage daily at beginning].Liver appearance,liver index,and histological changes were assessed.Serum tumor necrosis factor-o (TNF-c) and prostaglandin E2 (PGE2) were determined using enzyme-linked immunosorbent assay.The expressions of PPARγ,NF-κB,and COX-2 in liver were determined using immunohistochemical methods.The mRNA and protein expressions of COX-2 were disclosed by real-time polymerase chain reaction and Western blot analysis.ResultsCompared with the normal group,the liver index significantly increased in model group (3.92 ±0.72 vs.5.71 ± 1.05,P =0.004).HE and Masson staining showed significantly increased steatosis,inflammation,and fibrosis.The serum levels of TNF-α,PGE2 in high-fat-diet-fed rats were significantly increased ( 11.72 ± 2.47 vs.29.39 ± 5.32,P =0.002 ; 236.60 ± 24.90vs.288.24 ± 17.17,P =0.004).Immunohistochemistry showed NF-κB and COX-2 in livers were significantly elevated,but PPARγ wasdecreased in nonalcoholic steatohepatitis rats.Real-time polymerase chain reaction and Western blot found mRNA and protein expressions of COX-2 were increased in the model group (0.57 ± 0.08 vs.2.83 ± 0.24,P =0.0007 ; 0.38 ± 0.03 vs.1.00 ± 0.03,P =0.004).Compared with the model group,the expressions of PPARγsignificantly increased and the expressions of NF-κB and COX-2 significantly decreased ( mRNA:2.83 ± 0.24 vs.0.46 ± 0.11,P =0.002 ; protein: 1.00 ± 0.03 vs.0.62 ± 0.02,P =0.006 ) in the rosiglitazone prevention group.ConclusionBy inhibiting NF-κB and COX-2 expressions,rosiglitazone can reduce insulin resistance and then prevent the occurrence and deve lopment of nonalcoholic steatohepatitis.

AIM To explore the effect of hypoxia on apoptosis in human umbilical vein endothelial cells(HUVECs) and the role of ecdysterone(EDS)in inhibition of apoptosis. METHODS ① Culture and identification of HUVECs;② Hypoxic model(0,12,24,48 h) in HUVECs was established. While HUVECs was incubated 24 h with EDS(100 mg?L -1 ) under hypoxic condition. Apoptosis in HUVECs was detected by TUNEL;③ HUVECs received EDS 100 mg?L -1 in normal and hypoxic condition. After 24 h, vascular endothelial growth factor (VEGF) was detected with immunohistochemical technique. RESULTS The apoptosis percentages are different under different hypoxic condition. The longer hypotic the time was, the higher the apoptosis percentage was. EDS reduced apoptosis of HUVECs. EDS could enhance expression of VEGF protein in cardiac myocytes of rat in normal and hypoxic condition. CONCLUSION The role of hypoxia in HUVECs apoptosis is more significant along with prolonging of hypoxic time. VEGF play an important role in protective effect of EDS on endothelial cell apoptosis.

0.05).After 30 minutes treatment,93% patients in labetalol group reached goal blood pressure(0.05).However,tachycardia was significantly(P

OBJECTIVE To study the effects of levofloxacin on QT correction dispersion(QTcd) interval in elderly patients hospitalized with acute exacerbations of COPD(AECOPD).METHODS Totally 124 patients received IV levofloxacin(500 mg qd) for 10-14 days.Evaluations included of 12-lead ECGs at baseline and blood examination before treatment,day 5 and after treatment.RESULTS QT correction(QTc) interval was no significant changes,but the QTcd interval was with significant prolongation.CONCLUSIONS IV levofloxacin could not cause QTc interval prolongation,but could make QTcd interval prolongation,which is a potential risk of arrhythmia in elderly patients with AECOPD.

0.05).CONCLUSIONS Levofloxacin 500mg orally administered is effective in the treatment of acute suppurative tonsillitis.

Objective To investigate the effect of total saponins of panax notoginseng(PNS)on the production of collagen Ⅰ,Ⅲ and TGF-?1 in rats with experimental fibrosis.Methods Experimental fibrosis model was copied by intracutaneous injection of BSA and rats feeding on diet rich in lipid.From the 1st day after BSA injection,SPN(60 or 30 mg/kg)or Colchicine were given intracutaneously once a day for 42 days.All animals were sacrificed on the 43rd day.Their hepatic function was evaluated by determining the levels of ALT,AST,ALB in serum.The progression of hepatic fibrosis was confirmed by pathological analysis.Then type collagenⅠ,Ⅲ and TGF-?1 were observed with immunohistochemical method.Results The BSA injection significantly elevated the levels of ALT and AST,while SPN treatment significantly down-regulated them.But the level of ALB was opposite to that of ALT or AST in SPN treatment group.The positive staining of the collagenⅠ,Ⅲ and TGF-?1 was stronger in hepatic fibrosis model group than in SPN treatment group.The contents of the collagen were identical to the immunohistochemical results.Conclusion SPN has the protective effect against liver fibrosis.