Objective: To demonstrate the influence of HMGB34367,a subfamily member of the high-mobility group protein B1(HMGB1),as a transcriptional factor of the ?-SMA gene expression.Methods: We cloned HMGB34367 cDNA from the fibrotic lung tissue of the Balb/C mouse treated with BLM by RT-PCR,sub-cloned it into a eukaryotic expression vector pcDNA 3.0 or pEGF-N2,and constructed a report plasmid,pDsRed-SMA,encoding red fluorescence(RFP) driven by ?-SMA promoter.Following the co-transfection of pDsRed-SMA and HMGB34367-pcDNA3.0/ pEGF-N2-HMGB34367 in the cultured 16HBE cells,we tested the expression of the RFP in the absence and presence of TGF?1 by fluorescence microscopy.After the transfection of HMGB34367-pcDNA3.0,the nucleus extracts from the transfected cells were subjected to electrophoretic mobility shift assay(EMSA) for the detection of the binding activity of HMGB34367 with ?-SMA promoter CarGB motif.RT-PCR was performed for the evaluation of the ?-SMA gene expression in the cells.Results: The over expression of HMGB34367 activated the ?-SMA promoter and enhances the expression of the ?-SMA gene.An increased binding activity of HMGB34367 with CarGB motif was detected by EMSA in the transfected cells.Conclusion:HMGB34367,a member of HMGB1 family,could act as a transcription factor for the transcriptional activation of the ?-SMA gene,which may play an important role in the development of lung fibrosis.

Objective To study the relevance between blood loss, widespread brain contusion injury and consumptive coagulopathy. Methods One hundred and fifty-three cases with severe brain injury was studied about their coagulation data. Analyzed the relationship between blood loss group according to ≥3000 ml and ＜ 3000 ml and coagulation features, the relationship between widespread brain contusion injury and disorder of coagulation;according to whether with brain contusion injury,kinds of bloods transplant and prognosis were asseseed;according to whether with widespread brain contusion injury in ≥ 3000 ml blood loss group,kinds of bloods transplant and prognosis were assessed. Results Compared with ＜ 3000 ml blood loss patients, ≥ 3000 ml patients' blood coagulation changed obviously, with PT prolonging, Fbg and Plt decreasing, the differences were statistically significant (P ＜ 0.05). Compared with no extensive brain contusion injury patients, in extensive brain contusion injury patients, APTT, PT, TT prolonged, Fbg and Plt decreased,and the difference was statistically significant (P ＜0.05). Extensive brain contusion injury patients with blood loss compared with those without such loss, needed more blood transfusion volume,larger amount of input of fresh frozen plasma Plt volume,the former survival rate was lower [68.29%(28/41)vs. 96.43%(108/112)], the difference between them was statistically significant (P＜ 0.05 ). In 41 patients who had brain widespread contusion ,the cases with extensive blood loss ( ≥ 3000 ml) were compared with those ＜ 3000 ml, and the differences in blood transfusion treatment, fresh frozen plasma, Plt volume,survival rate were statistically significant (P ＜ 0.05). Conclusion When blood loss ≥ 3000 ml after trauma,patients show various degrees of coagulopathy,and when accompanied with extensive brain tissue injury,coagulation disorders are more obvious, and the prognosis is even worse.

Objective To investigate the role of HMGB 1 in epithelial-mesenchymal transition .Methods Specific siRNA of HMGB1 was designed and synthesized .Cultured typeⅡalveolar epithelial cell line-A549 cells were divided into 4 groups:1)control group, 2)model group induced by TGF-β1, 3)HMGB1 RNAi group, 4)RNAi negative con-trol group .Cellular morphology changes were observed by phase-contrast microscope .HMGB1 andα-SMA expression in A549 cells was detected by RT-PCR and Western blotting respectively .Results mRNA and protein expression of HMGB1 andα-SMA in TGF-β1 group increased significantly than that in control group (P<0.01).HMGB1,α-SMA mRNA and protein expression in siRNA-treated cells decreased significantly as compared with that in TGF -β1 group (P<0.01).Conclusions HMGB1 may be involved in the TGF-β1 induced EMT.

Objective To explore the risk factors of cognitive function in out-patients with depression in order to direct clinical therapy.Methods The clinical data of 180 cases of epileptic patients with depression from September 2005 to March 2009 were analyzed retrospectively.Results In 180 cases of epileptic patients with depression,82 cases(45.6%) of cognitive function were found,the occurrence with sex,marital status,the site of epileptic foci,the types of epileptic seizures were no significant correlation(P＞0.05),but related with onset age,educational level,disease course,the frequency of epileptic seizures and duration of attack (P＜0.05).Conclusion The risk factors of cognitive function in epileptic patients with depression were onset age,educational level,disease course,seizure frequency and duration of attack,it should avoid the occurrence of these risk factors and improve the quality of life of patients in clinical practice.

Objective To explore the risk factors of cognitive function in out-patients with depression in order to direct clinical therapy.Methods The clinical data of 180 cases of epileptic patients with depression from September 2005 to March 2009 were analyzed retrospectively.Results In 180 cases of epileptic patients with depression,82 cases(45.6%)of cognitive function were found,the occurrence with sex,marital status,the site of epileptic foci,the types of epileptic seizures was no significant correlation(P＞0.05),but related with onset age.educational levd,disease course,the frequency of epileptic seizures and duration of attack(P＜0.05).Conclusion The risk factors of cognitive function in epileptic patients with depression were onset age,educational level,disease course,seizure frequency and duration of attack,it should avoid the occurrence of these risk factors and improve the quality of life of patients in clinical practice.

Adult ; Aged ; Alopecia ; chemically induced ; Antineoplastic Combined Chemotherapy Protocols ; adverse effects ; therapeutic use ; Bone Neoplasms ; drug therapy ; pathology ; secondary ; Carcinoma, Non-Small-Cell Lung ; drug therapy ; pathology ; secondary ; Cisplatin ; adverse effects ; therapeutic use ; Humans ; Leukopenia ; chemically induced ; Liver Neoplasms ; drug therapy ; pathology ; secondary ; Lung Neoplasms ; drug therapy ; pathology ; Lymphatic Metastasis ; Middle Aged ; Neoplasm Staging ; Organoplatinum Compounds ; administration & dosage ; Paclitaxel ; administration & dosage ; Remission Induction ; Survival Rate ; Taxoids ; adverse effects ; therapeutic use ; Young Adult

Objective To study the effect of postoperative anticoagulant therapy after splenectomy in patients with cirrhosis and portal hypertension.Methods One hundred and forty patients with cirrhosis and portal hypertension receiving splenectomy and periesophagastric devascularization were divided into anticoagulant group (76 cases) and control group (64 cases) by random number table,patients in anticoagulant group received postoperative anticoagulant therapy,principally according to the platelet count,gave ligustrazine,aspirin,low molecular heparin after operation; patients in control group without postoperative anticoagulant therapy.Postoperative monitoring platelet count and D-dimer,ultrasound or CT check the presence of portal vein thrombosis.Results Platelet count,D-dimer levels in anticoagulant group and control group in 2 days after operation were significantly increased,the difference was significant compared with preoperative [anticoagulant group:(95.73 ± 28.06) × 109/L vs.(38.41 ± 11.96) × 109/L,(3.61 ± 0.18) mg/L vs.(0.42 ± 0.09) mg/L;control group:(92.56 ± 27.75) × 109/L vs.(35.13 ± 11.38) × 109/L,(3.26 ± 0.16) mg/L vs.(0.37 ± 0.09) mg/L,P ＜ 0.05].Platelet count and D-dimer levels between two groups at preoperative and postoperative in 2 days had no statistical significance (P ＞ 0.05).Ten cases of control group occurred postoperative portal vein thrombosis,anticoagulant group were 3 cases,portal vein thrombosis incidence of anticoagulant group [3.95％ (3/76)] compared with control group [15.62％(10/64)] was statistically significant (P ＜ 0.05).Conclusion Postoperative anticoagulant therapy after splenectomy in patients with cirrhosis and portal hypertension is an effective method to prevent portal vein thrombosis.

Objective To assess the effects of eszopiclone (ESZ) on the pentobarbital sodium-induced sleeping time and spontaneous activity in mice exposed to acute hypobaric hypoxia.Methods 120 mice were randomly divided into 6 groups by using two factors 2×3 levels factorial design,in which two factors were interventions (ESZ and 0.9％ sodium chloride,2 levels) and altitudes (800 m,3500 m and 6000 m,3 levels).The pentobarbital sodium-induced sleeping test and the open field test were engaged to assess the effects of ESZ on sleeping time and spontaneous activity.Results (1) The drug and altitude had no interaction in the results of both the pentobarbital sodium-induced sleeping test and the open field test(P＞0.05).(2)The time of pentobarbital sodium-induced sleeping of mice in the groups of ESZ at each altitudes were (37.77± 18.22) min,(37.02± 13.67) min,(95.67±47.68)min and in the groups of NS were(17.78± 14.10) min,(15.09± 12.46) min,(39.54±28.24) min respectively,and the sleep time in ESZ groups were significantly longer than those in the groups of NS (P＜0.05).The time of pentobarbital sodium-induced sleeping were longer in group of 6000 m than those in the other two groups,both the ESZ and NS groups (P＜0.05).(3)No significant difference was found in the open field test between the ESZ and NS groups in the same altitude(P＞0.05) ; while the mice at the altitude of 6000 m in groups of ESZ and NS decreased compared with the groups at the altitude of 800 m after the relevant drugs intra-perineally for 6 h (P＜0.05).Conclusion ESZ may prolong pentobarbital sodium-induced sleeping time especially at the altitude of 6000 m and with no influence on the spontaneous activity in mice exposed to acute hypobaric hypoxia.High altitude at 6000 m may prolong the sleep time induced by pentobarbital sodium and reduce the spontaneous activities.

Objective To study the protein binding rate of brucine in plasma of rats.Methods The plasma balance dialysis was used.HPLC was performed for the quantitative determination of brucine,and then the protein binding rate of brucine in rats plasma was calculated.Results The protein binding rate was 59.679 %,59.935 %,and 56.387 %when the concentration of plasma brucine was 2.5,1,and 0.4 ?g?mL-1 respectivley.Conclusion The HPLC method used to determine brucine is simple,rapid,and sensitive,and with good specificity,precision and accuracy.Brucine has medium capacity in binding to plasma protein.

AIM:To investigate the effect of oleuropein on interleukin-1β( IL-1β)-induced SD rat articular chondrocytes .METHODS:The SD rat articular chondrocytes were isolated by 2 step enzyme digestions .The chondrocytes were cultured in vitro.Inverted microscopic observation was performed during the culture .Alcian blue staining and type II collagen immunohistochemical staining were used to identify the chondrocytes .The effects of oleuropein on the viability of chondrocytes were determined by CCK-8 assay.The cells in 3rd passage were pretreated with oleuropein at 10, 50 or 100 μmol/L and subsequently stimulated with IL-1βat 10 μg/L for 24 h.Production of prostaglandin E 2 ( PGE2 ) and ni-tric oxide (NO) were evaluated by the Griess reaction and an enzyme linked immunosorbent assay (ELISA).The mRNA expression of matrix metalloproteinase ( MMP)-1 and MMP-13 was measured by real-time PCR.The protein levels of in-ducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2) and nuclear factor-kappa B (NF-κB) were detected by Western blotting .RESULTS:The cell viability of chondrocytes was not significantly impaired by treating with oleuropein at concentration of 10, 50 or 100μmol/L for 24 h compared with control group .Pretreatment with oleuropein significantly in-hibited the production of PGE 2 and NO induced by IL-1β.Oleuropein also significantly decreased the IL-1β-stimulated MMP-1 and MMP-13 mRNA expression in articular chondrocytes .Pretreatment with oleuropein inhibited the IL-1β-media-ted activation of NF-κB by suppressing the degradation of its inhibitory protein IκBαin the cytoplasm .CONCLUSION:Oleuropein inhibits IL-1β-induced inflammatory gene expression by suppressing NF-κB activation at the transcriptional le-vel, suggesting a new mechanism for the anti-inflammatory effects of oleuropein as a novel agent on treating with osteoarthri-tis.