Arterio-Arterial Fistula ; complications ; Coronary Artery Disease ; complications ; Coronary Stenosis ; complications ; Female ; Humans ; Middle Aged

Adult ; Aged ; Cause of Death ; China ; epidemiology ; Female ; Humans ; Male ; Middle Aged ; Pneumoconiosis ; mortality ; Retrospective Studies ; Young Adult

To observe the effect of calycosin on the proliferation and activation of primary hepatic stellate cells (HSCs) in rats, and prove calycosin shows the effects through peroxisome proliferator-activated receptor γ(PPARγ) and farnesoid X receptor (FXR). The results indicated that calycosin could inhibit HSC proliferation and expressions of activation marker smooth muscle actin-α and type I collagen. With the increase in HSC activation time, FXR expression reduced, but with no notable impact from calycosin. Calycosin could up-regulate PPARγ expression and its nuclear transition in a concentration-dependent manner. Its prohibitory effect on HSC activation could be blocked by PPARγ antagonist. In conclusion, calycosin could inhibit HSC activation and proliferation, which may be related with the up-regulation of PPARγ signal pathway.
Animals ; Cell Proliferation ; drug effects ; Cells, Cultured ; Drugs, Chinese Herbal ; pharmacology ; Hepatic Stellate Cells ; cytology ; drug effects ; metabolism ; Isoflavones ; pharmacology ; Male ; PPAR gamma ; genetics ; metabolism ; Rats ; Rats, Sprague-Dawley ; Receptors, Cytoplasmic and Nuclear ; genetics ; metabolism ; Up-Regulation ; drug effects

OBJECTIVETo study the effect of panax notoginsenosides (PNS) on the proliferation of hematopoietic progenitor cells (HPC) in mice with immune-mediated aplastic anemia.

METHODSBalb/c mice model of immune-mediated aplastic anemia was established by radiation with sublethal dose of 60Co following the intravenously infusing lymphocytes of DBA/2 mice. Model mice in the treated groups were treated separately with high, middle and low dose of PNS, 3.2 mg, 1.6 mg and 0.8 mg per day respectively by intraperitoneal injection. Model mice in the control group and normal mice in the normal control group were treated with normal saline. The peripheral white blood cell (WBC) count and pathological examination of bone marrow were carried out 12 days later, the bone marrow was taken to be incubated in semi-solid culture system for observing proliferation of HPC.

RESULTSPNS could (1) increase peripheral WBC count: as compared with that in the model control, WBC in the high, middle and low dose PNS groups was raised by (34.3 +/- 2.9)%, (29.2 +/- 1.7)% and (14.5 +/- 1.6)% respectively, P < 0.01 and P < 0.05; (2) improve the bone marrow inhibition: pathological examination showed in the model group, the hematopoietic structure was destroyed and replaced by fatty tissue, while in the PNS treated groups, the structure of marrow was rather complete and filled with abundant hematopoietic cells; (3) promote the proliferation of HPC: as compared with the model group, the colony formation of CFU-GM were increased by (64.4 +/- 2.8)%, (67.3 +/- 2.4)% and (21.9 +/- 1.8)% respectively and that of CFU-E increased by (31.9 +/- 3.6)%, (20.7 +/- 2.4)% and (12.8 +/- 2.6)% respectively in the three PNS treated group (P < 0.01 and P < 0.05).

CONCLUSIONPNS could enhance hematopoiesis by promoting proliferation of CFU-GM and CFU-E progenitors so as to improve the hematopoietic function in mice of immune-mediated aplastic anemia.

Anemia, Aplastic ; blood ; etiology ; immunology ; Animals ; Cell Division ; drug effects ; Female ; Ginsenosides ; pharmacology ; Hematopoietic Stem Cells ; cytology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred DBA ; Panax ; Radiation Injuries ; Random Allocation

OBJECTIVETo observe the effect of sesamin (Ses) on pulmonary vascular remodeling in rats with monocrotaline ( MCT)-induced pulmonary hypertension (PH).

METHODTotally 48 male Sprague-Dawley (SD) rats were fed adaptively for one week and then divided into the normal control group, the MCT group, the MCT +Ses (50 mg x kg(-1)) group and the MCT + Ses (100 mg x kg(-1)) group, with 12 rats in each group. The PH rat model was induced through the subcutaneous injection with MCT(60 mg x kg(-1)). After the administration for four weeks, efforts were made to measure the right ventricular systolic pressure( RVSP) and mean pulmonary artery pressure (mPAP) through right jugular vein catheterization, and isolate right ventricle( RV) and left ventricle( LV) +septum (S) and measure their length to calculate RV/ ( LV + S) and ratio of RV to tibial length. Pathologic changes in arterioles were observed by HE staining. Masson's trichrome stain was used to demonstrate changes in collagen deposition of arterioles. The alpha-smooth muscle actin (alpha-SMA) expression in pulmonary arteries was measured by immunohistochemisty. The total antioxidative capacity (T-AOC) and malondialdehyde (MDA) content in pulmonary arteries were determined by the colorimetric method. The protein expressions of collagen I, NOX2 and NOX4 were analyzed by Real-time PCR and Western blot.

RESULTAfter the administration for 4 weeks, Ses could attenuate RVSP and mPAP induced by MCT, RV/ (LV + S) and ratio of RV to Tibial length, alpha-SMA and collagen I expressions and remodeling of pulmonary vessels and right ventricle. Meanwhile, Ses could obviously inhibit the expressions of NOX2, NOX4 and MDA content and increase T-AOC.

CONCLUSIONSesamin could ameliorate pulmonary vascular remodeling induced by monocrotaline in PH rats. Its mechanism may be related to expressions of NOX2 and NOX4 expression and reduction in oxidative stress injury.

Animals ; Dioxoles ; administration & dosage ; Disease Models, Animal ; Drugs, Chinese Herbal ; administration & dosage ; Humans ; Hypertension, Pulmonary ; drug therapy ; enzymology ; genetics ; physiopathology ; Lignans ; administration & dosage ; Lung ; blood supply ; enzymology ; metabolism ; Male ; Membrane Glycoproteins ; genetics ; metabolism ; Monocrotaline ; adverse effects ; NADPH Oxidase 2 ; NADPH Oxidase 4 ; NADPH Oxidases ; genetics ; metabolism ; Pulmonary Artery ; drug effects ; metabolism ; physiopathology ; Rats ; Rats, Sprague-Dawley ; Vascular Remodeling ; drug effects

Objective To establish an HPLC method for determination of related substances of dexmethylphenidate hydrochloride and their content .Methods The HPLC method was used on an Agilent ZORBAX SB-C18 column with a mo-bile phase of methanol-0.2%triethyl citrate in 25 mmol/L potassium dihydrogen phosphate ( pH was adjusted to 3.5 with phosphoric acid) (35∶65) at a flow rate of 1.0 ml/min.The detection wavelength was 209 nm and column temperature was 40℃.Results Under the selected chromatographic condition , dexmethylphenidate hydrochloride was completely separated from impurity.The limit of detection was 81.12 ng/ml.The calibration curve was linear in the range of 2-30 μg/ml ( r=0.9995).The average recovery of the method was 100.83%, and the stability of the working solution was acceptable in 12 h(RSD=0.10%).Conclusion This method is simple,specific,accurate and suitable for analyzing the related substances and their content in dexmethylphenidate hydrochloride .

Objective To determine the effects of β-estradiol on vasoconstriction in human umbilical artery and vein and its potential mechanisms.Methods Human umbilical cord samples were obtained from 96 term neonates of healthy singleton pregnant women born in the First Hospital of Soochow University between December 2013 and June 2015 (multiple pregnancy,pregnancy complications,cesarean delivery and low birth weight were excluded).Human umbilical arteries and veins were isolated and suspended in 37 2 organ baths containing 5 ml Krebs solution and exposed to β-estradiol followed by phenylephrine (PE) for vasoconstriction test.The subjects were divided into β-estradiol group and control group according to the presence or absence of β-estradiol incubation.To determine the effects and the possible underlying mechanisms of β-estradiol on PE-induced vasoconstriction,human umbilical artery and vein rings were pretreated with N ω-nitro-L-arginine (L-NMMA,nitric oxide synthesis inhibitor),fulvestrant (ICI182780,estradiol receptor antagonist),indomethacin (prostaglandin synthesis blocker),and removal of endothelium,then incubated with β-estradiol for 60 min followed by PE,and the concentration-response curves to PE were recorded.The concentrationresponse curves to phorbol 12,13-dibutyrate (PDBU,protein kinase C agonist) in Krebs solution in the presence or absence of β-estradiol were also obtained.Nonlinear regression and fitting curve were performed,and the two-sample ANOVA was used for analysis.Results (1) β-estradiol suppressed PE-induced vasoconstriction of human umbilical vein and artery.In human umbilical vein and artery of the control group,the maximum contraction intensity induced by PE was (59.17± 5.98)％ and (43.35± 5.02)％ of that induced by potassium chloride,respectively.The maximum contraction induced by PE in β-estradiol group was (5.87± 1.32)％and (4.52±1.22)％ of that induced by potassium chloride.(2) In both groups,incubation with L-NMMA or endothelium removal enhanced the vasoconstriction of human umbilical artery and vein,indicating that the inhibitory effect of β-estradiol was not influenced by the endothelium.(3) The suppression of β-estradiol on PE-induced vasoconstriction in human umbilical artery and vein was not significantly decreased by estrogen receptor antagonist.(4) β-estradiol did not affect human umbilical artery and vein vasoconstriction induced by PDBU.(5) In the control group,incubation with indomethacin did not affect human umbilical artery and vein vasoconstriction induced by PE.In the β-estradiol group,indomethacin significantly enhanced the contraction response induced by PE,suggesting that prostacycline synthesis was partly involved in β-estradiol-suppressed contractility in human umbilical artery and vein.The contractile response induced by phenylephrine was still lower in the β-estradiol group than in the control group,which was induced by indomethacin.Conclusions (1) β-estradiol can suppress vasoconstriction in human umbilical artery and vein,which is not dependent on endothelium and estrogen receptors,or protein kinase C activity,(2) Prostacycline synthesis is partly involved in β-estradiol-suppressed vasoconstriction in human umbilical artery and vein.

Objective:To evaluate the clinical performance of CAD/CAM zirconia all-ceramic restorations.Methods:287 all-ce-ramic Zirconia restorations in 206 patients were included in a 3-year prospectively survey with California Dental Association Standard (CDA)as a reference.The effects and the related factors such as restoration type,tooth region,fiber reinforced composite application on survival rate were analyzed.Kaplan-Meier survival analysis and Log-Rank test were used for data analysis.Results:Chipping frac-tures in 5 restorations,intense gingivitis at 4 restorations and periapical inflammation for 3 restorations were observed during the obser-vation period.The 3-year cumulative survival rate (CSR)of CAD/CAMzirconia restorations was 95.7%,The differences among the CSR of single crowns(96.3%),linked crowns (93.6%)and fixed partial dentures(95.7%)were not statistically significant(P >0.05).The difference was not statistically significant(P >0.05)between the CSR of the anterior region group(94.5%)and posterior region group(96.3%)as well as difference(P >0.05)between the CSR of fiber reinforced composite group (95.0%)and without fiber reinforced composite group(96.1%).Conclusion:The cumulative survival rate of CAD/CAM zirconia all-ceramic restorations is high.Chipping fracture is the main reason of failure.Restoration type,tooth region and fiber reinforced composite have no significant effect on the survival of zirconia restorations.

Objective To assess the clinical value of pentraxin-3 (PTX-3) in diagnosis and survey of therapeutic effect for lung cancer.Methods The serum level of PTX-3,carcinoembryonic antigen (CEA),cytokeratin 19 fragment (CYFRA 21-1) were measured in 802 patients with lung cancer,462 with benign lung diseases and 522 healthy controls from multiple research centers,using ELISA and electrochemiluminescent assays.The clinical value of PTX-3 was assessed by comparing the area under receiver characteristic curves (AUC) with CEA and CYFRA21-1.The optimum cutoff value for diagnosis of lung cancer was investigated by maximizing the sum of sensitivity and specificity.By following-up,the serum level of PTX-3 was measured at 3 day,7 day,and 14 day in 61 lung cancer patients after surgical resection of lung cancer.Results In test group and validation,the serum levels of PTX-3 (g/L) are significantly higher in lung cancer group [9.21 (6.13-12.80),10.4(5.54-13.11)] than in benign lung diseases [5.28 (3.42-8.53),6.52 (3.84-7.89)] and in healthy controls [2.18 (0.54-5.44),2.44 (0.67-5.87)],[Z =8.161,14.118,(test group,all P ＜ 0.05) ;Z =9.832,17.595 (validation group,all P ＜0.05)].ROC curve showed the optimal cut-off values for PTX-3 was 8.03 g/L [AUC of 0.831,with a sensitivity of 76.1％ and specificity of 75.2％ in the test cohort; 0.828,71.3％,89.2％ in the validation cohort].Similar results were noted for early-stage lung cancer [0.764,79.1％,and 62.2％ in the test cohort; 0.744,71.3％,and 69.6％ in the validation].In the diagnosis of early-stage lung,the AUC and sensitivity and specificity of PTX-3 were 79.1％,0.764,71.3％ (test group),and 75.2％,89.2％,0.824 (validation group) significantly higher in these patients than CEA and CYFRA21-1.In small cell lung cancer,PTX-3 and NSE shared similar AUC differentiating LC from benign lung diseases and health controls.In following-up 61 lung cancer patients,PTX-3 levels before surgical resection of tumours [11.12(9.12-12.59)] was significant high than following 3 day after surgery(Z =4.32,P ＜0.01),and 14 day (5.12 ±2.54) vs.7 day (7.13 ±3.42) (t =2.143,P =0.023).The correlation between PTX-3 and CRP in LC,benign lung diseases,health control was 0.364,0.592,0.512 (all P ＜ 0.05).Conclusion Serum PTX-3 is a valuable biomarker of lung cancer and early-stage lung cancer with high sensitivity and specificity and improved identification of patients with lung cancer from those with non-malignant chronic lung diseases.