Objective To investigate the effects of celastrol on the expressions of macrophage migration inhibitory factor(MIF)and matrix metalloproteinase-9(MMP-9)in the aorta of apoE gene knockout mice with earlier atherosclerosis.Methods Eight-week-old ApoE gene knockout male mice were divided randomly into control group and celastrol treatment group(n=6 in each group).The mice in celastrol group were given.celastrol(2 mg?kg-1?d-1)by intraperitoneal injection for 4 weeks;and the mice in control group were only given equivalent amount of dimethyl sulfoxide(DMSO).HE staining of root aorta were used to observe the histomorphological changes and measure the size of plaque in ApoE-/-mice.The expressions of MIF and MMP-9 were detected by immunological histochemical method.Results The area of lipid plaque in the mice treated with celastrol was significantly smaller than that of the control(P

Objective To investigate the effects of liver X receptor agonist on the expressions of C-reactive protein and CD40 ligand and smooth muscle cell ?-actin in the aorta of ApoE gene knockout mice with earlier atherosclerosis. Methods Male ApoE gene knockout mice (8-week old) were divided randomly into control group and T0901317 treatment group (n=6 in each group). The mice in T0901317 group were administered intraperitoneally with T0901317 at the dose of 20 mg?kg-1?d-1 for 4 weeks. Mice in the control group were only given equivalent amount of dimethyl sulfoxide (DMSO). The expressions of C-reactive protein and CD40 ligand and smooth muscle cell ?-actin were detected by immunological histochemical method. Results The expressions of C-reactive protein and CD40 ligand in the atherosclerotic plaque in the aortic wall were significantly lower in T0901317 group as compared with those in the DMSO control group (P0.05). Conclusion Liver X receptor agonist may reduce the formation of atherosclerotic lesions by inhibiting the inflammation and the expressions of C-reactive protein and CD40 ligand in the aorta of ApoE gene knockout mice.

Objective To evaluate the effect of fluid load on the prognosis of severe hand , foot and mouth disease in children. Methods The patients with severe hand foot and mouth disease in the emergency department of PICU in our hospital were enrolled as the research object. We would collect demographic characteristics , labora-tory tests and clinical data: age, gender, focus, basic disease, and simplified acute severity score (SAPS)Ⅱ and record the cumulative amount of fluid balance at 24, 48, 72 hours after admission. Results There was a signifi-cant difference on fluid balance at 48 and 72 hours between the survival group and the death group , the death group appeared the positive liquid balance , and there were significant differences in PICU retention time , mechani-cal ventilation rate, MODF involved organs, mortality and other prognostic indicators between the negative fluid balance group and the positive fluid balance group. Conclusion Fluid balance is an important treatment for severe hand foot and mouth disease, and positive liquid balance is related to mortality and other adverse prognosis.

Urinary prothrombin fragment 1 (UPTF1) is a potent inhibitor of urinary stone formation. UPTF1 exerts such inhibitory effect by effective γ-carboxylation in which vitamin K epoxide reductase complex subunit 1 (VKORC1), the rate-limiting enzyme, is involved. This study examined the correlation between VKORC1 expression and calcium oxalate urolithiasis. The renal cortex samples were obtained from patients undergoing nephrectomy and then divided into 3 groups: urolithiasis group, control group A [hydronephrosis-without-stone (HWS) group], control group B (normal control group). The localization and expression of VKORC1 in renal tissues were determined by using immunohistochemistry, immunofluorescence microscopy, Western blotting and SYBR Green I real-time reverse-transcription PCR. The rapid amplification of cDNA ends (RACE) were conducted to obtain the 3'- and 5'-untranslated region (UTR) of VKORC1. The results showed that VKORC1 was located in the cytoplasm of renal tubular epithelial cells. The expression of VKORC1 in the urolithiasis group was significantly lower than that in the other two control groups (P<0.05). Moreover, the 3'- and 5'-UTR sequence of the VKORC1 gene was successfully cloned. No insertion or deletion was found in the 3'- and 5'-UTR. However, a 171-bp new base sequence was discovered in the upstream of 5'-UTR end in the urolithiasis group. It was concluded that the decreased expression of VKORC1 may contribute to the development of calcium oxalate urolithiasis in the kidney.

OBJECTIVETo investigate aberrant methylation in the promoter of p16 gene in the sediment cells of pleural effusion and evaluate its clinical significance in the differentiating benign and malignant pleural effusion.

METHODSUsing methylation-specific PCR (MSP), aberrant promoter methylation of p16 gene was detected in the sedimental cells of pleural effusion samples from 66 patients with pleural effusion.

RESULTSOf the 66 patients with pleural effusion, 36 had a definite diagnosis of malignant pleural effusion, and the rest were confirmed to have benign pleural effusion. The positivity rate of p16 gene promoter methylation was 69.4% (25/36) in malignant pleural effusion and 13.3% (4/30) in benign pleural effusion specimens, showing a significant difference between them (χ² = 20.915, P < 0.01). The diagnostic sensitivity, specificity and accuracy of aberrant promoter methylation of p16 gene in the 36 malignant cases were 69.4%, 86.7% and 77.3%, respectively. The positive expression of p16 gene promoter methylation in malignant pleural effusion was not correlated to the histological type or the pathological grade of the tumor (P > 0.05).

CONCLUSIONDetection of aberrant methylation in p16 gene promoter in the sediment cells of pleural effusion specimens by MSP method allows differentiation between benign and malignant pleural effusion.

Adult ; Aged ; Aged, 80 and over ; Base Sequence ; DNA Methylation ; Female ; Genes, p16 ; Humans ; Male ; Middle Aged ; Molecular Sequence Data ; Pleural Effusion, Malignant ; diagnosis ; genetics ; Promoter Regions, Genetic ; genetics ; Sensitivity and Specificity

This study was purpose to investigate the role of reactive oxygen species (ROS) in apoptosis and autophagy induced by FTY720 in multiple myeloma cell line U266. U266 cells were treated by different concentrations of FTY720 for 24 h, the apoptotic rates were detected by flow cytometry, and the expression of LC3B was detected by Western blot. The results indicated that apoptosis and autophagy were induced by FTY720 in U266 cells. Autophagy induced by FTY720 could lead to cell death. Bafilomycin A1, the inhibitor of autophagy, could enhance the cell viability in U266 cells treated with FTY720. NAC or Tiron, ROS scavenger, could decrease the FTY720 induced apoptosis and the expression of LC3B-II was reduced in combination of FTY720 with NAC or Tiron as compared with treatment with FTY720 only. It is concluded that FTY720 can induce U266 cell apoptosis and autophagy. ROS is the mediator that regulates both the apoptosis and autophagy in multiple myeloma cells.
1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium Salt ; Apoptosis ; drug effects ; Autophagy ; drug effects ; Cell Line, Tumor ; Fingolimod Hydrochloride ; Humans ; Macrolides ; Microtubule-Associated Proteins ; metabolism ; Multiple Myeloma ; metabolism ; pathology ; Propylene Glycols ; pharmacology ; Reactive Oxygen Species ; metabolism ; Sphingosine ; analogs & derivatives ; pharmacology

This study was aimed to investigate the influence of TIEG1 on apoptosis of HL-60 cells and the expression of Bcl-2/Bax. Different concentration of TIEG1 were used to treat HL-60 cells, the cell growth inhibition rate was detected by MTT method. After treating HL-60 cells with 12.03 ng/ml TIEG1, cell apoptosis was detected with flow cytometry. Bcl-2 and Bax was detected with RT-PCR. The results showed that TIEG1 had inhibitory effect on HL-60 cell proliferation, and in time-and dose-dependent manners. The more obvious inhibitory effect was observed in HL-60 cells treated with TIEG1 of 12.03 ng/ml. During the course of cell apoptosis, Bax expression increased, but Bcl-2 expression decreased (P < 0.05). It is concluded that TIEG1 inhibits HL-60 cell proliferation and induces apoptosis in time and dose-dependent manners. During the course of HL-60 cells apoptosis induced by TIEG1, Bcl-2/Bax are associated with HL-60 cell apoptosis induced by TIEG1.
Apoptosis ; drug effects ; Cell Proliferation ; drug effects ; Early Growth Response Transcription Factors ; pharmacology ; Gene Expression Regulation, Leukemic ; HL-60 Cells ; Humans ; Kruppel-Like Transcription Factors ; pharmacology ; Proto-Oncogene Proteins c-bcl-2 ; metabolism ; bcl-2-Associated X Protein ; metabolism

This study was aimed to investigate the effects of valproic acid sodium (VPA) on the proliferation and apoptosis of acute T-lymphoblastic leukemia Jurkat cells. Jurkat cells were treated with different concentration of VPA. Proliferation-inhibition curve was assayed and plotted by CCK-8 method and the cell apoptosis was detected by flow cytometry with Annexin V/PI double staining. The expression level of anti-apoptotic gene BCL-2 and pro-apoptosis gene Bak1 were detected by semi-quantitative RT-PCR. The results showed that the VPA inhibited the proliferation of Jurkat cells in concentration-dependent manner. As compared with the control group, the apoptosis of cells increased along with adding concentration of VPA; VPA could decrease the expression of BCL-2 gene, but did not show obvious effect on the expression of Bak1. It is concluded that the VPA can inhibit proliferation of Jurkat cells which possibly associates with the decrease of BCL-2 expression.
Apoptosis ; drug effects ; Cell Proliferation ; drug effects ; Humans ; Jurkat Cells ; Proto-Oncogene Proteins c-bcl-2 ; metabolism ; Sodium ; pharmacology ; Valproic Acid ; pharmacology ; bcl-2 Homologous Antagonist-Killer Protein ; metabolism

OBJECTIVETo investigate the clinical value of monitoring the serum cardiac biomarkers in patients with pulmonary thromboembolism (PTE) and secondary myocardial injury.

METHODSThe serum cardiac biomarkers including aspartate aminotransferase (AST), lactate dehydrogenase (LDH), alpha-hydroxybutyrate dehydrogenase (HBDH), creatine kinase (CK), creatine kinase isoenzyme (CK-MB), cardiac tropnin I (cTnI) and myoglobin (Myo) were measured using immunochemiluminescent assays in 36 patients with PTE, who were diagnosed according to imaging findings in the recent 5 years. The measurements in concomitant non-PTE patients free of heart, liver, or kidney diseases were used as the baseline values of the biomarkers. Correlation analysis of the measurements was conducted in relation to the pulmonary embolism area, pulmonary hypertension and mortality rate.

RESULTSThe PTE patients exhibited significantly elevated levels of the serum cardiac biomarkers including AST (56.14-/+15.73 U/L), LDH (303.06-/+94.99 U/L), HBDH (234.67-/+87.86 U/L), CK-MB (26.19-/+12.39 U/L), CK (129.25-/+76.14 U/L), Myo (70.63-/+45.75 ng/ml), and cTnI (0.45-/+0.41 ng/ml) in comparison with the baseline values (P < 0.01). Of these biomarkers, AST and CK-MB showed a significant correlation to the mortality, cTnI was correlated to pulmonary hypertension, and Myo was correlated to pulmonary hypertension and massive pulmonary embolism.

CONCLUSIONMeasurements of these serum cardiac biomarkers may serve as indicators for diagnosis of myocardial injury secondary to PTE. AST, CK-MB, cTnI, and Myo can help assess the prognosis of the patients.

Adult ; Aged ; Aspartate Aminotransferases ; blood ; Biomarkers ; blood ; Creatine Kinase, MB Form ; blood ; Female ; Humans ; L-Lactate Dehydrogenase ; blood ; Male ; Middle Aged ; Myocardial Ischemia ; blood ; etiology ; Pulmonary Embolism ; blood ; complications

Adolescent ; Adult ; Aged ; Aged, 80 and over ; Carcinoma, Renal Cell ; genetics ; metabolism ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Kidney Neoplasms ; genetics ; metabolism ; Male ; Matrix Metalloproteinase 2 ; genetics ; metabolism ; Middle Aged ; Transforming Growth Factor beta1 ; genetics ; metabolism ; Tumor Cells, Cultured ; Young Adult