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Objective:To investigate the effects of miR-5011-5p on apoptosis and migration of bladder cancer cell line J82 and the underlying mechanism.Methods:J82 cells were transfected with random sequence molecules (NC group) and miR-5011-5p sequence molecules (miR-5011-5p group). Flow cytometry and scratch experiment were performed to analyze the effects of miR-5011-5p on apoptosis and migration of J82 cells. The target gene of miR-5011-5p was predicted by bioinformatics. Real-time fluorescent quantitative polymerase chain reaction and western blot assay were performed to investigate the effects of miR-5011-5p on target gene expression.Results:The relative expression of miR-5011-5p in J82 cells in the miR-5011-5p group was significantly higher than that in the NC group (10.73 ± 1.67 vs. 1.04 ± 0.16, t = 5.81, P < 0.01). There was significant difference in the apoptosis rate of J82 cells between NC and miR-5011-5p groups [(8.83 ± 1.67)% vs. (34.96 ± 3.80)%, t = 6.30, P < 0.01]. The migration rate of J82 cells differed significantly between NC and miR-5011-5p groups [(71.31 ± 7.69)% vs. (37.43 ± 5.01)%, t = 3.69, P < 0.05]. The target gene of miR-5011-5p may be Yes-related protein 1 (YAP1). Compared with the NC group, miR-5011-5p exhibited an obvious inhibitory effect on the YAP1 expression in J82 cells ( P < 0.01). Conclusion:miR-5011-5p may promote the apoptosis of J82 cells and inhibit their migration in bladder cancer through targeted inhibition of YAP1 gene expression.
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Objective To investigate the effect of long-chain non-coding RNA AL117378.1 on the proliferation and invasion of bladder cancer cells.Methods From August 2016 to December 2017,the tumor tissues and adjacent tissues of 14 patients with bladder cancer treated by Huangshi Central Hospital of Edong Healthcare Group were selected.Real-time quantitative polymerase chain reaction (qRT-PCR) was used to detect the expression level of AL117378.1 in 14 pairs of bladder cancer tissues and corresponding adjacent tissues,bladder cancer cell lines (5637,J82,T24,BIU-87) and corresponding human bladder normal epithelial cells (SV-HUC-1).The negative control plasmid (control group) and the plasmid carrying the AL117378.1 (experimental group) were transfected into the bladder cancer cell line with the lowest expression level.qRT-PCR was used to detect the expression levels of ALl 17378.1 and non-receptor protein tyrosine phosphatase 9 (PTPN9)mRNA in the transfected cells.The expression levels of PTPN9,E-cadherin,o-SMA,CDK4 and Cyclin A2 protein were detected by Western blotting.MTT assay and Transwell invasion assay were used to detect the cell proliferative capacity and invasive ability of the two groups.Measurement data were expressed as mean ± standard deviation(Mean ± SD),and comparison between groups used independent sample t test.Results The expression of AL117378.1 in bladder cancer tissues was lower than that in adjacent tissues (P ＜ 0.01).The expression of AL117378.1 in bladder cancer cell lines was lower than that in human bladder normal epithelial cells (P ＜ 0.01),and the expression level of AL117378.1 was the lowest in J82 cells (P ＜ 0.01).The expression levels of AL117378.1 in the control and experimental groups were 1.02 ± 0.11 and 7.96 ± 1.06,respectively,and the difference was statistically significant (t =6.51,P ＜0.01).The expression of PTPN9 mRNA was 1.01 ± 0.08 and 4.99 ± 0.50,respectively.the difference was statistically significant (t =7.84,P ＜0.01).Western blotting results showed that the expression of PTPN9 and E-cadherin increased,and the expression of α-SMA,CDK4 and Cyclin A2 decreased.MTT experiments showed that the proliferation of cells transfected with AL117378.1 was significantly decreased (P ＜ 0.05).Transwell invasion experiments showed that the number of invasive cells in the control group and the experimental group were 97.96 ± 13.71 and 38.02 ±7.51,respectively,and the difference was statistically significant (t =3.84,P ＜ 0.01).Conclusions The expression of AL117378.1 was significantly decreased in bladder cancer tissues and cell lines (5637,J82,T24,BIU-87).ALl 17378.1 can significantly inhibit the proliferation and invasion of bladder cancer cells by positively regulating the expression of PTPN9 gene.
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Objective@#To investigate the effect of long-chain non-coding RNA AL117378.1 on the proliferation and invasion of bladder cancer cells.@*Methods@#From August 2016 to December 2017, the tumor tissues and adjacent tissues of 14 patients with bladder cancer treated by Huangshi Central Hospital of Edong Healthcare Group were selected. Real-time quantitative polymerase chain reaction (qRT-PCR) was used to detect the expression level of AL117378.1 in 14 pairs of bladder cancer tissues and corresponding adjacent tissues, bladder cancer cell lines (5637, J82, T24, BIU-87) and corresponding human bladder normal epithelial cells (SV-HUC-1). The negative control plasmid (control group) and the plasmid carrying the AL117378.1 (experimental group) were transfected into the bladder cancer cell line with the lowest expression level. qRT-PCR was used to detect the expression levels of AL117378.1 and non-receptor protein tyrosine phosphatase 9 (PTPN9) mRNA in the transfected cells. The expression levels of PTPN9, E-cadherin, α-SMA, CDK4 and Cyclin A2 protein were detected by Western blotting. MTT assay and Transwell invasion assay were used to detect the cell proliferative capacity and invasive ability of the two groups. Measurement data were expressed as mean± standard deviation(Mean±SD), and comparison between groups used independent sample t test.@*Results@#The expression of AL117378.1 in bladder cancer tissues was lower than that in adjacent tissues (P<0.01). The expression of AL117378.1 in bladder cancer cell lines was lower than that in human bladder normal epithelial cells (P<0.01), and the expression level of AL117378.1 was the lowest in J82 cells (P<0.01). The expression levels of AL117378.1 in the control and experimental groups were 1.02 ± 0.11 and 7.96 ± 1.06, respectively, and the difference was statistically significant (t=6.51, P<0.01). The expression of PTPN9 mRNA was 1.01 ± 0.08 and 4.99 ± 0.50, respectively. the difference was statistically significant (t=7.84, P<0.01). Western blotting results showed that the expression of PTPN9 and E-cadherin increased, and the expression of α-SMA, CDK4 and Cyclin A2 decreased. MTT experiments showed that the proliferation of cells transfected with AL117378.1 was significantly decreased (P<0.05). Transwell invasion experiments showed that the number of invasive cells in the control group and the experimental group were 97.96±13.71 and 38.02±7.51, respectively, and the difference was statistically significant (t=3.84, P<0.01).@*Conclusions@#The expression of AL117378.1 was significantly decreased in bladder cancer tissues and cell lines (5637, J82, T24, BIU-87). AL117378.1 can significantly inhibit the proliferation and invasion of bladder cancer cells by positively regulating the expression of PTPN9 gene.
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Objective :To study correlation between serum level of lipoprotein—associated phospholipase A2 (Lp—PLA2 ) and carotid atherosclerosis (AS) in patients with morning hypertension (MH ).Methods : A total of 160 MH pa—tients ,who visited or hospitalized in our department from Dec 2014 to Mar 2017 ,were selected .According to diag—nostic standard of MH ,patients were divided into MH group (n＝85) and non—MH group (n＝75).Levels of blood lipids ,fasting blood glucose (FBG ) ,serum Lp—PLA2 ,carotid intima—media thickness (IMT ) and plaque detection rate were measured and compared between two groups ,and the correlation between serum Lp—PLA2 level and carot—id AS was analyzed .Results : There were no significant difference in levels of blood lipids and FBG between two groups , P＞0.05 all.Compared with non—MH group ,there were significant rise in serum Lp—PLA2 level [ (47. 50 ± 3.15) μg／L vs.(156. 87 ± 18.56) μg／L ] ,plaque detection rate (66. 6% vs.90.6%) and carotid IMT [ (0.96 ± 0.12) mm vs.(1.26 ± 0.16) mm] in MH group , P＝0.001 all.Spearman rank correlation analysis indicated that serum Lp—PLA2 level was significant positively correlated with carotid plaque detection rate ( r＝0.532 , P＝0.003). Conclusion : Serum Lp—PLA2 level of MH patients is significantly higher than that of non—MH patients ,and it＇s sig—nificant positively correlated with carotid AS .Therefore ,the Lp—PLA2 level and atherosclerosis detections should be enhanced for early diagnosis and treatment .
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Objective To observe the effect of mitofusion 2 (MFN2) on the proliferation of prostate cancer cells and its molecular mechanism. Methods Lentivirus containing the MFN2 coding sequence (Lenti-MFN2) were used to infect the prostate cancer cell lines DU-145 and LNCaP, and the lentivirus containing the green fluorescent protein gene (Lenti-GFP) were defined as the control. Real-time quantitative PCR (qRT-PCR) and Western blot were used to detect the expression of MFN2 mRNA and protein in the infected cells. MTT assay and colony formation assay were used to detect the cell proliferation. Cell cycle distribution was measured by flow cytometry.Western blot was used to detect the expression of Ras,p-Raf and p-Erk1/2 proteins in infected cells. Results The expressions of MFN2 mRNA in DU-145 and LNCaP cells of Lenti-MFN2 group were 2.79±0.91 and 3.87±1.06, which were higher than those in Lenti-GFP group (1.02± 0.27 and 1.13±0.59),the differences were statistically significant(t=3.726,P=0.010;t=5.209,P =0.002). Compared with Lenti-GFP group, the expression of MFN2 protein in Lenti-MFN2 group was increased. The number of colonies formed in DU-145 and LNCaP cells of Lenti-MFN2 group was 147.42±32.91 and 130.26± 62.47, respectively, which was lower than that of the Lenti-GFP group (255.46±50.91 and 238.10±49.77), the differences were statistically significant (t =3.565, P=0.012; t =2.700, P=0.036). The cell cycle was arrested at G0/G1phase,and the expressions of Ras, p-Raf and p-Erk1/2 proteins were significantly decreased. Conclusion MFN2 can inhibit the proliferation of prostate cancer cells,and its mechanism may be related to the inhibition of activation of Ras-Raf1-Erk1/2 signaling pathway.
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Objective To investigate the regulatory effect of miRNA-370(miR-370)on the expression of tumor suppressor gene p21 in renal cell carcinoma cell lines ACHN and 786-O and its effect on cell growth. Methods RCC cells were transfected with dsRNA known lack homology to human genes (control group) and miR-370 (experimental group) by Lipofectamine 3000 respectively. Real-time fluorescence quantitative polynucleotide chain reaction (RT-qPCR) and Western blot were used to detect the expression of p21 mRNA and protein. The cell cycle distribution was identified by flow cytometry (FCM). Cell viability and proliferation ability were measured by cell viability assay (MTS) and colony culture assay. Results The expression of p21 mRNA in ACTN and 786-O cells in control group was 1.04±0.33, 1.04±0.31, respectively. The expression of p21 mRNA in experimental group was significantly increased by 3.68±0.62 (t=7.535, P<0.001), 3.15±0.29 (t=9.975, P<0.001). Western blot further demonstrated that the increased expression of p21 protein in both renal cell lines was consistent with the upregulation of p21 mRNA level. FCM results showed that the cell cycle of more cells was blocked in G0-G1phase after transfection of miR-370.MTS results showed that after transfection of miR-370,the number of colonies formed by ACHN and 786-O cells in the control group was 113±30 and 106±27 respectively. The number of colonies formed by experimental group was significantly reduced by 53±17 (t=2.982, P=0.041) and 50±16 (t=3.089, P=0.037). Conclusion miR-370 can significantly up-regulate the expression of tumor suppressor gene p21 in renal cell carcinoma and inhibit the growth of renal cell carcinoma.
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Objective To investigate the regulatory effect of miRNA-370(miR-370)on the expression of tumor suppressor gene p21 in renal cell carcinoma cell lines ACHN and 786-O and its effect on cell growth. Methods RCC cells were transfected with dsRNA known lack homology to human genes (control group) and miR-370 (experimental group) by Lipofectamine 3000 respectively. Real-time fluorescence quantitative polynucleotide chain reaction (RT-qPCR) and Western blot were used to detect the expression of p21 mRNA and protein. The cell cycle distribution was identified by flow cytometry (FCM). Cell viability and proliferation ability were measured by cell viability assay (MTS) and colony culture assay. Results The expression of p21 mRNA in ACTN and 786-O cells in control group was 1.04±0.33, 1.04±0.31, respectively. The expression of p21 mRNA in experimental group was significantly increased by 3.68±0.62 (t=7.535, P<0.001), 3.15±0.29 (t=9.975, P<0.001). Western blot further demonstrated that the increased expression of p21 protein in both renal cell lines was consistent with the upregulation of p21 mRNA level. FCM results showed that the cell cycle of more cells was blocked in G0-G1phase after transfection of miR-370.MTS results showed that after transfection of miR-370,the number of colonies formed by ACHN and 786-O cells in the control group was 113±30 and 106±27 respectively. The number of colonies formed by experimental group was significantly reduced by 53±17 (t=2.982, P=0.041) and 50±16 (t=3.089, P=0.037). Conclusion miR-370 can significantly up-regulate the expression of tumor suppressor gene p21 in renal cell carcinoma and inhibit the growth of renal cell carcinoma.
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Objective To investigate the effect of dsP21-555 transfection on the expression of tumor suppressor gene p21 in renal clear cell carcinoma cell lines ACHN and 786-O.Methods Renal clear cell carcinoma cells were transfected with dsControl and dsP21-555 with Lipofectamine 3000 respectively.Real-time quantitative PCR (RT-qPCR) and Western blotting were used to detect the expression of p21 mRNA and protein.Cell cycle distribution was detected by flow cytometry (FCM).Cell viability and proliferation were analyzed by cell viability assay (MTS method) and colony culture assay.Results In ACHN and 786-O cells, the expressions of p21 mRNA in dsP21-555 group (2.86±0.33, 1.96±0.35) were significantly higher than those in dsControl group (1.05±0.34, 1.01±0.14), which were increased to 2.72 times (t=7.640, P<0.001) and 1.95 times (t=5.058, P=0.002).Western blotting showed that the expressions of P21 protein were up-regulated in both renal cell lines, which was consistent with p21 mRNA up-regulation.The result of FCM showed that the cell cycle was blocked in G0-G1 phase (57.08%±5.66% vs.46.06%±4.60%, t=3.023, P=0.023;61.58%±6.23% vs.42.25%±6.08%, t=4.444, P=0.004) after transfection of dsP21-555 in renal clear cell carcinoma cells.MTS result showed that the vitality of both cell lines after transfection of dsP21-555 decreased compared with dsControl group, their absorbance values were 0.85±0.20 vs.1.27±0.13, t=3.410, P=0.014;1.04±0.25 vs.1.55±0.10, t=3.758, P=0.009.Colony culture experiments showed that the numbers of colonies formed by ACHN and 786-O in the dsControl group were 110.91±26.21 and 129.99±22.87 respectively, and the numbers of colonies formed in the dsP21-555 group were 59.37±14.23 (t=3.456, P=0.014) and 71.26±21.38 (t=3.745, P=0.010), indicating that the proliferation of cells in the dsP21-555 group was significantly reduced.Conclusion dsP21-555 can up-regulate the expression of p21 gene in renal clear cell carcinoma cells and inhibit the growth of carcinoma cells, suggesting that dsP21-555 may become a new gene therapy tool.
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Objective To investigate the effect of microRN-206 (miR-206) on the expression of Cyclin-dependent kinase 4 (CDK4) and Cyclin G-associated protein kinase (GAK), and the growth of prostate cancer cells.Methods Prostate cancer cell lines DU-145 and PC-3 were transfected with miR-NC (the control group) or miR-206 (the experimental group).The expressions of CDK4 and GAK mRNA were detected by real-time quantitative PCR (qRT-PCR).The expressions of CDK4 and GAK protein were detected by Western blotting.Cell cycle distribution was detected by flow cytometry.EdU proliferation assay and colony forming assay were used to analyze the cell proliferation ability.Results In DU-145 and PC-3 cells, the expressions of CDK4 mRNA in miR-NC group were 1.00±0.09, 1.00±0.10, the expressions of GAK mRNA were 1.00±0.05, 1.00±0.06.The expressions of CDK4 mRNA in miR-206 group were significantly decreased in DU-145 (0.36±0.18;t=6.572, P=0.001) and PC-3 cell lines (0.43±0.17;t=5.794, P=0.001).The expressions of GAK mRNA were also significantly decreased in DU-145 (0.23±0.04;t=22.420, P<0.001) and PC-3 cell lines (0.32±0.08;t=14.500, P<0.001).Western blotting results were consistent with qRT-PCR results.The results of flow cytometry showed that compared with the miR-NC group of DU-145 and PC-3 cell lines, the percentage of cells in S phase (23.60%±5.68% vs.32.53%±4.52%, t=2.462, P=0.049;22.09%±4.35% vs.30.96%±4.86%, t=2.720, P=0.035) and G2-M phase (16.28%±7.12% vs.26.63%±4.33%, t=2.484, P=0.048;14.60%±1.62% vs.24.68%±7.13%, t=2.758, P=0.033) decreased after transfection of miR-206, and the percentage of cells in G0-G1 phase (60.13%±5.82% vs.40.84%±5.37%, t=4.872, P=0.003;63.31%±3.27% vs.44.36%±3.82%, t=7.533, P<0.001) increased.The results of EdU proliferation assay showed that the proliferation abilities were significantly attenuated after transfection of miR-206 (22.56±3.81 vs.38.90±8.51, t=3.503, P=0.013;25.12±6.42 vs.48.45±8.92, t=4.244, P=0.005).The results of colony formation experiments showed that the numbers of colonies formed by DU-145 and PC-3 in miR-NC group were 218.66±44.59 and 177.35±24.49, respectively.The numbers of colonies formed in miR-206 group were 125.38±32.80 (t=3.370, P=0.015) and 82.65±14.05 (t=6.708, P=0.001), suggesting that cell proliferation ability in miR-206 group was reduced.Conclusion miR-206 significantly inhibits the growth of prostate cancer cells by interfering with the expressions of CDK4 and GAK, suggesting that miR-206 may be a molecular targeted therapy tool for prostate cancer.
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Objective To evaluate the clinical efficacy of sodium tanshinone IIA sulfonate(STS)in the treatment of ad-vanced schistosomiasis. Methods Fifty cases with advanced schistosomiasis admitted to the Touzao Township Hospital of Dong-tai City during the period from November 2012 to November 2013 were treated with STS for 10 days,and the internal diameter of the portal vein,levels of ALT,AST,γ-GT,PIIIP,CIV,HA and LN were measured and compared before and after the adminis-tration of STS. Results The mean levels of all serological parameters except HA were within the normal range before STS treat-ment,while the highest positive rate was detected inγ-GT(26.0%)and HA(54.0%). Following the STS treatment,the mean lev-els of all parameters and the positive rates reduced,with the greatest reduction observed inγ-GT(36.7%)and HA(37.8%);how-ever,the mean HA level was still higher than the normal range. The mean internal diameter of the portal vein reduced from(10.5± 1.7)mm before the STS treatment to(9.8±1.3)mm after the STS administration,with a significant diffrtence(P<0.05). Conclu-sion STS appears effective in the treatment of advanced schistosomiasis.
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Objective To observe the effects of trimetazidine (TMZ) on the cardiac function and neurohormonal of heart failure model in rats.Methods Partially banding abdominal aortic artery to achieve congestive heart failure rats model.Interventricular septum thickness(IVST),left ventricular posterior wall thickness(LVPWT),left ventricular end-diastolic diameter(LVEDD),left ventricular end-systolic diameter (LVESD),left ventricular ejection fraction(LVEF) and shortening fraction(FS) were measured by echocardiogram,Pathological changes of myocardial cells was observed,B-type natriuretic peptide (BNP)、C-type natriuretic peptide receptor (NPRC),atrial natriuretic peptide (ANP),myosin heavy chain (β-MHC) and angiotensinl (AT1) were measured by Real-Time PCR,superoxide dismutase (SOD) was measured by immunohistochemistry method.Results Trimetazidine treatment of the high-dose group and the model group compare IVST LVPWT,LVESD,LVEDD were (0.63 ± 0.05) mn,(0.73 ± 0.06) mm,(0.73 ±0.05)mm,(0.87 ±0.06)mm and (1.07 ±0.06)mm,(1.13 ±0.06) mm,(0.93 ±0.06)mm,(1.33 ±0.06) mm,was significantly reduced (P ＜ 0.05),LVEF,FS increased to (27.75 ± 1.83) ％,(11.44 ± 0.76) ％ and (11.78 ±0.56)％,(4.27 ± 0.22)％ (P ＜ 0.01),Myocardial cell structure were remarkably improved.The expression of BNP,ANP,NPRC,ATI,β-MHC were remarkably decreased.The expression of SOD was elevated.Conclusion TMZ treatment group can improve the secretion of neurohormonal of heart failure model in rats,and also obviously improve the cardiac contractility.
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Objective To investigate the effects of 6-minutes of walking exercise (6-MWE) on the exercise tolerance and left ventricular diastolic function (LVDF) of heart failure patients with a normal ejection fraction (HFNEFs).Methods Ninety grade Ⅱ or Ⅲ HFNEFs of the New York heart association (NYHA) were randomly divided into an exercise training group and a control group with 45 cases in each.The control group was treated with routine drugs.The exercise training group was treated with the same drugs plus 6-MWE.Before and after the sixmonth period of treatment,plasma N-terminal pro-brain natriuretic peptide (NT-proBNP) levels were determined,each subject's left atrial volume index (LAVI) was measured with a color ultrasonic cardiogram (UCG),and their 6-minute walk distance (6-MWD) was measured.Results Plasma NT-proBNP levels and 6-MWD improved significantly comparing with before treatment in both groups.The average 6-MWD,LAVI and plasma NT-proBNP level all improved significantly more in the experimental group.Conclusion 6-MWE can significantly improve the exercise tolerance and LVDF of HFNEFs,and improve their quality of life.Walking can be helpful in delaying the development of HFNEF.
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Objective To evaluate the expression of epidermal growth factor-like domain 7 (Egfl7) in atherosclerotic plaques and effects of its small interference RNA (siRNA) on angiogenesis gene expression in human endothelial cell line (HUVEC). MethodsEgfl7 expression in atheroscleroticplaquesweredetectedinhumaniliacarteryandmousearteriaeusing immunohistochemistry and immunofluorescence stainings.The siRNA targeting Egfl7 was transfected into HUVEC by lipofectamine with non-transfected cells and unconcerned siRNA as controls.At 0 h,12 h,24 h and 48 h after intervention,the levels of mRNA and protein of Egf17,vascular endothelial growth factor(VEGF),platelet derived growth factor-A (PDGF-A),platelet derived growth factor-B (PDGF-B),vascular cell adhesion molecule(VCAM) and intercellular adhesion molecule (ICAM)were measured by RT-PCR and Western blotting,respectively. ResultsThe expressions of Egfl7 in human iliac artery and mouse arteriae were increased.The expressions of Egfl7 in HUVEC at the levels of mRNA were[(0.14±0.02),(0.09±0.01),(0.02±0.01)]and the levels of protein[(0.71±0.11),(0.39±0.09),(0.07±0.01)]at 12 h,24 h and 48 h after siRNA intervention,respectively,which were decreased as compared with 0 h intervention [(0.31 ±0.05) and (0.93±0.08) ].Other genes such as VEGF,PDGF-A and PDGF-B were reduced or silenced at the levels of protein and mRNA in HUVEC with siRNA longer interventions(all P＜0.05).ConclusionsThe expression of Egfl7 in atherosclerotic plaques is increased.The siRNA inhibiting Egfl7 gene expression results in silence of other factors involved in angiogenesis.
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AIM: To explore the expressive role of lipoprotein-associated phospholipase A_2, high sensitive C-reactive protein and matrix metalloproteinase-9 in vulnerable atherosclerotic plaques in a rabbit model. METHODS: Forty eight New Zealand white male rabbits were randomly divided into 4 groups (12 rabbits each): control group, stable plaque group, p53 group, and p53+drug group. Rabbits in control group were fed with a regular diet and underwent sham operation. Rabbits in stable plaque group, p53 group and p53+drug group underwent balloon induced arterial wall injury and then were fed on a diet with 1% cholesterol. The animals were all fed for 3 months, then the rabbits in p53 group and p53+drug group underwent Ad5-CMV p53 transfection at 10th week. Before killed, the animals in p53+drug group underwent pharmacological triggering with Russell's viper venom (RVV) and histamine to induce the rupture of the atherosclerotic plaques. At the 1st day and before sacrifice, the serum was collected for measuring Lp-PLA_2, hs-CRP, MMP-9, HDL, LDL and VLDL. The expressions of Lp-PLA_2, hs-CRP and MMP-9 in tissues were determined by the methods of hybridization and immunohistochemistry. RESULTS: At the end of 12th week, the serum and tissue levels of Lp-PLA_2 and MMP-9 in stable plaque group, p53 group and p53+drug group were significant different from those in control group and in each group at the first day (P<0.05). The serum levels of Lp-PLA_2 and hs-CRP in p53 group and p53+drug group were significantly higher than those in control group and stable group (P<0.05). The serum levels of Lp-PLA_2, hs-CRP and MMP-9 were all significantly different between p53 group and p53+drug group (P<0.05). At the end of 12th week, pathological results showed that 4 groups were normal artery, stable plaque, vulnerable plaque and rupture plaque, respectively. The fabric cap was thicker in plaque groups than that in normal group (P<0.05). The rupture and formation of thrombus were more significant in p53+drug group than those in p53 group. The serum level of Lp-PLA_2 had negative interrelated relationship with fabric cap in plaque groups (r=-0.710, P<0.01), and hs-CRP, MMP-9 had no interrelated relationships with fabric cap in plaque groups. CONCLUSION: Base on the successful establishment of the atherosclerotic plaque animal model, serum Lp-PLA_2 shows better interrelated relationships to plaques stability. Combination with hs-CRP and MMP-9, we can exactly evaluate the nature of plaques.
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w biomarker to predict the presence of vulnerable plaque.
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Objective To study the effects of mild hypothermia on secondary cerebral vasospasm and levels of endothelin (ET),calcitonin gene related peptide (CGRP) in cerebrospinal fluid (CSF)and plasma in patients with severe brain injury(SBI).Methods Sixty-five patients with SBI were randomly divided into mild hypothermia group(30 cases)and control group(35 cases).Based on the routine treating method,the patients of mild hypothermia group were treated with local mild hypothennia.The levels of ET,CGRP in CSF and plasma were detected before and after treatment.And the incidence rates of secondary cerebral vasospasm cases were compared between the two groups.Results (1)At 7,14 day after treatment,ET levels in CSF and plasma in mild hypothermia group were significantly lower than these in control group (P＜0.05or＜0.01).The CGRP levels in CSF and plasma were the lowest at 7 day,then gradually increased in two groups.However,the CGRP levels in mild hypothermia group at 7,14 day were higher than those in control group (P＜0.05 or＜0.01).(2) The rate of secondary cerebral vasospasm in mild hypothermia group was 6.67% which significantly less than that in control group (22.86%) (P＜0.05).Conclusion Mild hypothermia can prevent the increasing of ET and the decreasing of CGRP in CSF and plasma,and decrease the incidence rate of secondary cerebral vasespasm in patients with SBI.
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Objective To investigate the HOMA-IR and HOMA-? index in the diagnosis and judge the patients with vesting traumatic hemorrhagic MODS in the clinical and prognostic value,as well as the role of insulin resistance and decreased insulin secretion in energy metabolism disorder of patients with MODS.Early prevention and treatment of clinical provided for MODS.Methods 60 patients with traumatic MODS and 30 healthy adults participated in the study,were measured and compared their fasting blood glucose,insulin,lactate and pyruvicacad,glucagon and cortisol levels,calculated HOMA-IR,HOMA-?,and the lung,liver,kidney,pancreatic ? cells,and other major organ function in MODS patients parameters and indicators of the level of cells,HOMA-IR index were relevant and regression analysis.Results MODS group HOMA-IR index,fasting plasma glucagon and cortisol were significantly higher than the normal control group(P
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Extracellular matrix remodeling plays a role in the pathogenesis of variety of diseases.Among these extracellular proteinases,Cathepsin is a key member.In this review,the relationships between Cathepsins and many diseases associated with extracellular matrix remodeling is discussed.
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0.05).The prognosis was worse with increase in Dukes stage,negative expression of gene nm23,and positive expression of gene p53 and C-erb-2.Reverse expressions had better prognosis.Conclusions It can be likely to get a more reliable prognosis predication if a combine examination together with p53,C-erb-2,nm23 and their clinical pathology such as Dukes stages,was done in colorectal cancer patients.