Objective: To investigate the differences of biochemical markers between the patients with pulmonary hypertension related to left heart disease (PH-LHD) and LHD; to explore the sensitive bio markers which may predict PH in LHD patients. Methods: A total of 355 LHD patients admitted to our hospital from 2014-01 to 2015-05 were enrolled. According to 2009 ESC/ERS guidelines, PH was deifned by pulmonary artery systolic pressure (PASP)>50 mmHg and patients were divided into 2 groups: LHD group,n=224 and PH-LHD group,n=131. The basic information with blood levels of biomarkers was recorded and their accuracy for predicting PH was analyzed. Results: The pathogenesis of LHD included 184 (51.83%) patients of coronary heart disease, 90 (25.35%) of dilated cardiomyopathy and 81 (22.81%) of cardiac valve heart disease. Compared with LHD group, PH-LHD group had increased ratio of NYHA III and IV degree (89.31% vs 45.54%), decreased LVEF [42.0 (33.0, 59.0) % vs 60.0 (42.0, 65.0) %], all P<0.001; PH-LHD group presented elevated blood levels of BNP, bilirubin, red cell distribution width (RDW), uric acid and cystatin C, while reduced lipoprotein (HDL), allP<0.001. PASP was positively related to biomarkers as BNP, bilirubin, RDW, uric acid and cystatin C, while negatively related to HDL. With the combination of BNP, direct bilirubin and RDW, the predictive value for PH-LHD under ROC curve was 0.828 with the sensitivity at 0.813, speciifcity at 0.708. Conclusion: Blood levels of biochemical markers were statistically different between the patients of PH-LHD and LHD; the combination of BNP, direct bilirubin and RDW showed the higher accuracy for predicting PH occurrence in LHD patients.

ASICs are H+-gated novel cation ion channels, which belong to the epithelial sodium channels (NaC/DEG) superfamily. As recent studies focus, ASICs are expected to be pharmacological targets on protecting the neuron from ischemia and damage, improving the ability of memory and study, curing epilepsy and analgesia. It is not until the most recentness that the subunits of ASICs have been cloned. Now, researchers have paid more attention to the distribution, expression, function and modulation of ASICs in the organism.

Objective To investigate the sequence variations of mitochondrial D-loop region in chronic glomerular nephritis patients and family members and their possible associations with chronic glomerular nephritis.Methods 20 patients with chronic glomerular nephritis and 48 unaffected pedigree members,as well as 122 cases of normal control were recruited.mtDNA extracted from peripheral blood were examined by PCR-based assay for D-loop sequence variations,followed by sequencing analysis.Results Compared with the normal control and standard sequence,a total of 61 sequence variants were detected,among these,three high variations were found,and the base variation rate of patients with chronic glomerular nephritis(CGN)and unaffected pedigree members(UAPM)(0.88%,0.72%)significantly increased compared with the control group(0.61%).The distibutional difference of base variation rate in the experimental groups were significantly higher than those in the control group(x2=21.220,7.964,all P<0.05).Especially in microsatellite variation in D310 region,the mutation frequency and base variation rate in patients with CGN were 100.00% and 30.00%,respectively,which of UAPM were 81.30% and 17.95%,respectively,while those in the normal control group were 53.30% and 6.05%,respectively.Among them,the patients with CGN compared with the control group had statistically significant differences(x2=15.610,150.047,all P<0.05).Likewise,UAPM also had statistically significant difference compared with the control group(x2=11.347,66.188,all P<0.05).Conclusion D-Loop of mitochondrial genome mutations may be related to the development of chronic glomerular nephritis.

Objective: To compare the safety and efifcacy of platelet glycoprotein IIb/IIIa antagonist in treating STEMI patients by intracoronary-intravenous administration and intravenous administration.
Methods: We searched PubMed, Embase, Cochrane library, CNKI, VIPH and Wanfang database, the retrieval stopped at 2014-03. According to 5.0.2 Cochrane handbook, 2 scientists collected 2494 STEMI patients treated by IIb/IIIa antagonist from 20 references, and they were divided into 2 groups. Combination group, the patients received intracoronary, then intravenous administration, n=1258 and Intravenous group, the patients receive only intravenous administration, n=1236. RevMan 5.0 software was used for Meta-analysis.
Results: At 1 month after PCI treatment, compared with Intravenous group, the Combination group had better conditions of TIMI 3, TMP 3, ST segment recovery, MACE occurrence and MI area changes, all P<0.01; Combination group also showed better conditions of angina recurrence, death and post-operative target vessel revascularization, all P<0.05. LVEF was similar between 2 groups at 1 week after PCI. MI recurrence, post-operative bleeding and thrombocytopenia were similar between 2 groups at 1 month after PCI, all P>0.05.
Conclusion: Intracoronary-intravenous administration of platelet glycoprotein IIb/IIIa antagonist had the better effect for treating STEMI patients without increasing the side effects of post-operative bleeding and thrombocytopenia.

Objective To observe the PML protein expression of hepatocellar carcinoma tissue and cells lines and As 2 O3 regulate its expression .Methods Immunohistochemistry was used to examine the PML protein expression of hepatocellar carcinoma tissue . Western blot analysis were used to observe PML protein expression of hepatocellar carcinoma tissue of 12 cases ,5 hepatocellar car-cinoma cell lines ,such as HuH7 ,HepG2 ,Hep3B ,SMMC-7721 ,MHC97H .Western blot analysis was used to detected the PML pro-tein expression of these hepatocellar carcinoma cell lines after 72-96 h treated with 0 .25 μg/mL of As2 O3 .Results Immunohisch-enmical staining showed that the PML protein was expressed in both cytoplasm and nucleus ,did not well-distributed in hepatocellar carcinoma cells .There was no significant differences of PML protein expressed among differently differentiated stages of hepatocel-lar carcinoma cells .Western blot analysis found that hepatocellar carcinoma tissues of 12 cases with hepatocellar carcinoma ex-pressed PML protein ,and there was significant difference of PML protein expressed among 12 cases suffer with hepatocellar carci-noma .hepatocellar carcinoma cell lines ,such as HuH7 ,HepG2 ,Hep3B ,SMMC-7721 and MHC97H all expressed PML protein ,and there was little difference of PML protein expressed among hepatocellar carcinoma cell lines .The PML protein expression of HuH7 ,HepG2 ,Hep3B ,SMMC-7721 and MHC97H cell after 72-96 h treated with 0 .25 μg/mL of As2O3 significant decreased . Conclusion Hepatocellar carcinoma tissue and cells may express PML protein ,and As2 O3 may regulate this protein expression as well .PML protein may be the target molecule of As2 O3 treating HCC .

BACKGROUND: As a micro-injurying and reduplicative treatment of osteoarthritis,the arthroscopic debridement has got the affirmation of numerous scholars. But as one of the standard procedures in artnroscopic debridement,synovectomy is called in question recently.OBJECTIVE: To explore the applied value of synovectomy in the arthroscopic debridement of osteoarthritis.DESIGN: Retrospective controlled analysis.SETTING: Department of Orthopaedics, Fushun Central Hospital.PARTICIPANTS: Sixty-five patients received synovectomy in the arthroscopic debridement of knee joint osteoarthritis in the Department of Orthopaedics,Fushun Central Hospital from February 1997 to December 2000.Thirty-two among them,with complete data and over 1 year's followup,were taken for synovectomy group. Forty-eight patients received the arthroscopic debridement of knee joint osteoarthritis without synovectomy in the Department of Orthopaedics,Fushun Central Hospital from January 2001 to November 2003.Thirty among them,with complete data and over 1 year's follow-up,were taken for control group.METHODS: Synovectomy was taken as the factor of intervention in the operation to perform grouping. The analysis of curative effect was performed to control with joint douching,corpus liberum removal,osteophyma cleaning,meniscus fitting,cartilage gouging,synovectomy and without synovectomy or part synovectomy. Lysholm evaluation standard of knee joint osteoarthritis was used to the knee joint functional evaluation beween preoperation and postoperative 1 year in two groups. And operative time,postoperative draining quantity,postoperative 7-day visual analog score,postoperative 1-year Lysholm score of knee joint, were recorded.MAIN OUTCOME MEASURES: Preoperative and postoperative 1-year Lysholm score of knee joint,operative time,postoperative draining quantity,postoperative 7-day visual analog score.RESULTS: Sixty-two patients were included and all of them entered the result analysis.The preoperative patients in two groups were comparable with each other and the differences of Lysholm score were not significant (t=0.127,P=0.899).The operative time was longer in synovectomy group than in control group,the differences were significant (t=9.547,P ＜ 0.001)and the postoperative draining quantity was more in synovectomy group.The postoperative visual analog score was bigger in synovectomy group than in control group and the differences were significant [the scores of synovectomy and control groups were respectively (4.6±1.1),(2.8±1.4),t=6.206,P ＜ 0.001].The differences of knee joint score in 1-year follow-up were not significant [the scores of synovectomy and control groups were respectively (77.6±11.9),(79.0± 10.3),t=0.562,P=0.576].CONCLUSION: Synovectomy can not increase the curative effect in the near future in the arthroscopic debridement of osteoarthritis. On the contrary,the operative time was longer,the operative wound was larger and postoperative reaction was more serious. It should not be used in the debridement generally.

Objective To assess the diagnostic predictive value of Wells score and modified Geneva score for acute pulmonary embolism by prospective case series and to explore a more suitable scoring system for Chinese population.Methods All the patients suspected of pulmonary embolism (PE) and received CT pulmonary angiography (CTPA) were enrolled consecutively in Fuxing Hospital,Capital Medical University,China,from June 2009 to August 2011.Before CTPA test or on condition that test results were unknown,clinical scoring was assessed prospectively by the Wells score and the modified Geneva score.The probability of PE in each patient was assessed and the patients were divided into low,moderate and high probability groups according to the clinical scores.The result of CTPA was used as the diagnostic gold standard for PE.Diagnostic accuracy in each group was analyzed.The predictive accuracy of both scores was compared by AUCROC curve.Results A total of 139 patients met our enrollment criteria and 117 eligible patients entered our study at last.PE was diagnosed in 47 patients by CTPA with an overall prevalence of 40.2％.Prevalence of PE in the low,moderate and high pretest probability groups assessed by the Wells score and by the simplified modified Geneva score were 7.1％ (3/42),42.9％ (21/49),88.5％ (23/26)and 10.0％ (3/30),48.1％ (37/77),7/10,respectively.AUCROC curves for the Wells score and the simplified modified Geneva score were 0.872 ( 95％ CI 0.810-0.933 ) and 0.734 ( 95％ CI 0.643-0.825 )respectively,with a significant difference ( P =0.005 ).Conclusion The Wells score is more accurate for clinical predicting acute PE than the modified Geneva score.

Objective To investigate the molecular mechanism of epithelial-mesenchymal transition (EMT) induced by activated vascular endothelial growth factor receptor-1 ( VEGFR-I ) in cell line MHCC97-H.Methods MHCC97-H cells were cultured in DMEM with 1％ fetal bovine serum (control group),10 μmol/L PP2 (PP2 group),10 μmol/L PBS (PBS group),50 μmol/L VEGF-B (VEGF-B group),l0μmol/L PP2 and 50 μmol/L VEGF-B (PP2 +VEGF group),10 μmol/L PBS and 50 μmol/L VEGF-B (PBS + VEGF-B group),respectively.Protein expressions of epithelial marker E-cadherin,α-catenin and mesenchymal marker vimentin and N-cadherin were detected by Western blot.The expression sites of E-cadherin,α-catenin and mesenchymal marker vimentin and N-cadherin were detected by cell immunofluorescence.The ability of invasion and migration of cell line MHCC97-H were assessed by cell invasion and migration test.All data were analyzed by the t test.Results The expressions of E-cadherin,α-catenin,vimentin and N-cadherin were 3.23 +0.76,3.01 ±0.25,3.01 +0.22 and 2.63 +0.40 in the control group,4.18 +0.32,3.29 +0.11,4.85 +0.36 and 3.02 +0.52 in the PP2 group,2.83 +0.65,3.03 +0.27,1.37 ±0.24 and 2.98 ±0.36 in the PBS group,2.06 ±0.15,2.84 ±0.76,5.79 ± 0.38 and 5.54 ± 0.28 in the VEGF-B group,6.12 ± 0.08,5.45 ± 0.37,3.36 ± 0.42 and 3.26 ±0.13 in the PP2 + VEGF-B group and 1.36 ±0.54,1.26 ±0.45,4.05 ±0.17 and 1.05 ±0.33 in the PBS +VEGF-B group.There was a significant difference in the expressions of E-cadherin and α-catenin between the PP2 +VEGF-B group and the VEGF-B group (t =7.625,9.931,P ＜ 0.05 ).The expressions of vimentin and N-cadherin in the PP2 + VEGF-B group were significantly lower than those in the VEGF-B group (t =12.001,11.910,P ＜ 0.05).Six hours after the treatment with VEGF-B,the numbers of MHCC97-H migrated were 19 ± 1,5 ± 2and 16 ± 1 in the VEGF-B group,PP2 + VEGF-B group and PBS + VEGF-B group,respectively.The number of MHCC97-H cells migrated in the VEGF-B group was greater than that in the PP2 ± VEGF-B group ( t =13.566,P ＜ 0.05 ).The number of MHCC97-H cells passed through the Boyden chamber was 4 + 2,which was significantly less than 16 ± 1 of the VEGF-B group (t =12.350,P ＜0.05).Conclusion EMT induced by activated VEGFR-1 was mediated via c-Src kinase signal transduction in MHCC91-H cell line,and c-Src may be a potential target to interfere the invasion and migration of hepatic cancer cells.

AIM: To investigate the effect of venous marker chicken ovalbumin upstream promoter-transcription factor Ⅱ (COUP-TFⅡ) expression on vascular endothelial cell senescence and its molecular mechanism.METHODS: The mRNA expression of COUP-TFⅡ in the human coronary artery endothelial cells (HCAEC) and human umbilical vein endothelial cells (HUVEC) was detected by RT-qPCR.After transfection with a COUP-TFⅡ siRNA (siCOUP-TFⅡ) to inhibit COUP-TFⅡ expression in the HUVEC, the senescence and proliferation of endothelial cells were evaluated by β-galactosidase staining, Western blot, CCK-8 assay and cell counting after treatment with 10-5 mol/L angiotensin Ⅱ (AngⅡ).The protein levels of Akt and p-Akt were determined by Western blot.RESULTS: Compared with the HCAEC, COUP-TFⅡ was significantly highly expressed in the HUVEC.Knockdown of COUP-TFⅡ via siCOUP-TFⅡ significantly induced endothelial cell senescence and inhibited endothelial cell proliferation and p-Akt level after treatment with AngⅡ at 10-5 mol/L.Furthermore, an Akt activator SC79 at 4 mg/L partly reversed the effect of siCOUP-TFⅡ on AngⅡ-induced endothelial cell senescence and proliferation.CONCLUSION: Knockdown of COUP-TFⅡ promotes endothelial cell senescence and inhibits endothelial cell proliferation, which might be partly regulated by Akt signaling.

Objective To evaluate the role of Janus kinase 2-signal transducer and activator of transcription 3 (JAK2-STAT3) signaling pathway in sevoflurane postconditioning-induced inhibition of mitochondrial permeability transition pore (mPTP) opening during myocardial ischemia-reperfusion (I/R)in rats.Methods Sixty pathogen-free healthy male Sprague-Dawley rats,weighing 250-300 g,were divided into 4 groups (n=15 each) using a random number table:I/R group,sevoflurane postconditioning group (group SP),AG-490 group (group AG) and sevoflurane postconditioning plus AG-490 group (group SP+AG).Myocardial I/R was induced by 30 min ligation of the left anterior descending branch of coronary artery followed by 120 min reperfusion.In group SP,2.8％ sevoflurane was inhaled for 15 min starting from 2 min before reperfusion.JAK2 inhibitor AG-490 3 mg/kg was intravenously injected at 10 min before reperfusion in group AG.In group SP+AG,AG-490 3 mg/kg was intravenously injected at 10 min before reperfusion,and 2.8％ sevoflurane was inhaled for 15 min starting from 2 min before reperfusion.At 15 min of reperfusion,5 rats were sacrificed and myocardial specimens were obtained for determination of the expression of JAK2,phosphorylated JAK2 (p-JAK2),STAT3 and phosphorylated STAT3 (p-STAT3)in myocardial tissues by Western blot.The ratios of p-JAK2 to JAK2 expression (p-JAK2/JAK2) and pSTAT3 to STAT3 expression (p-STAT3/STAT3) were calculated.Five rats were sacrificed at the end of reperfusion for measurement of myocardial infarct size.The left 5 rats were selected and sacrificed,myocardial specimens were obtained,and the opening of mPTP was detected by a calcein-cobalt quenching method.Results Compared with group I/R,the myocardial infarct size and mPTP opening were significantly decreased,and JAK2/p-JAK2 and STAT3/p-STAT3 were increased in group SP (P＜0.05),and no significant change was found in the parameters mentioned above in SP+AG and AG groups (P＞0.05).Compared with group SP,the myocardial infarct size was significantly enlarged,the extent of mnPTP opening was aggravated,and JAK2/p-JAK2 and STAT3/p-STAT3 were decreased in SP+AG and AG groups (P＜0.05).Conclusion The mechanism by which sevoflurane postconditioning inhibits the opening of mPTP during myocardial I/R is related to activation of JAK2-STAT3 signaling pathway in rats.