Objective To investigate the left atrium (LA) function and structure changes in the paroxysmal atrial fibrillation (AF) patients after catheter ablation using tissue Doppler imaging. Methods After complete pul-monary vein, radiofrequency ablation guided by Ensite NavX System, LA systolic function and LA diameter, volume, mean mitral gradient and mitral annulus early and advanced diastolic peak velocity were assessed in 32 cases of par-oxysmal AF patients,which were compared with age-matched controls before and after 24 hours, 1 week, 1 month) AF ablation. Results AF did not occur again in 32 AF paroxysmal patients after isolation. LA diameter and volume in AF groups before ablation were larger than controls(P<0.01), which were also larger 24 hours after ablation than before (P>0.05 ), but LA volume was larger than before (P<0.05), and decreased in I week after ablation (P< 0.05), but had no significant difference compared with controls in 1 month(P>0.05 ) ;mitral annulus advanced di-astolic peak velocity decreased in AF groups before ablation (P<0.01 )and was lower than that 24 hours after cathe-ter ablation (P<0.05 ), but increased after 1 week (P<0.05 or P <0.01 ), and had no significance after 1 month. Conclusion Catheter ablation is the effective way to manage AF because LA is distended and atrial systolic func-tion is reduced within 24 hours after procedure, then gradually increased in a week and will nearly recover to that be-fore procedure in a month, which may be correlated with LA repair, implicating that postprocedural thromboembollc risk and procedure injury should be taken into consideration.

Objective To investigate the role of genistein (Gen) in the expression of connective tissue growth factor (CTGF) induced by parathyroid hormone (PTH) in human renal tubular epithelia cells. Methods Real-time PCR, Western blotting and reporter gene assay were employed to detect the role of Gen in PTH-induced CTGF expression in HK-2 cells. The activity of NF-κB was measured by EMSA to investigate the mechanism by which PTH induced CTGF expression in HK-2 cells. Inhibitors of NF-κB signaling pathway were used to ascertain which signal pathway was involved. Results HK-2 cells had basic amount of CTGF mRNA and protein, which, however, increased significantly after treatment with PTH, and the luciferase activity increased to a higher level as compared with control group after treatment with 10-10 mol/L PTH for 12 h (1.89±0.08 vs 0.99±0.03, P＜0.01). Gen decreased the expressions of CTGF mRNA and protein induced by PTH in dose-dependent manner. The NF-κB of nucleus was inactivation without PTH, while the activity of NF-κB significantly increased after exposed to PTH, with the maximal response of PTH at a concentration of 10-10 mol/L and the best stimulating time at 30 minute. The NF-κB inhibitor PDTC reduced the increase of CTGF transcript levels in response to PTH stimulation. Gen blunted PTH-mediated NF-κB activation. Conclusion Gen inhibits CTGF expression induced by PTH through bloking NF-κB signaling pathway in human renal tubular epithelial cells.

Objective:To investigate the effect of the intact parathyroid hormone (iPTH) on residual renal function (RRF). Methods: The relationship between iPTH and calcium, phosphorum, product Ca?P, hypertension, triglycende, cholesterol,left ventricular mass index(LVMI) and RRF in 120 hemodialysis patients with chronic renal failure. Results: The results showed that 95. 9% of the hemodialysis patients with chronic renal failure had secondary parathyroldism. It was found that iPTH was positively correlated with SBP,DBP, product Ca?P, triglycende and LVMI, and negatively correlated with endogenous creatinine clearance rate and KT/V. RRF had positive correlation with KT/V and SBP,DBP, calcium, product Ca?P, triglyceride, cholesterol and LVMI. Conclusion: iPTH level is elevated in hemodialysis patients, which may lead to RRF loss.

Objective To investigate the protective effects of atorvastatin on hyperphosphate-induced rat vascular smooth muscle ceils (RVSMCs) calcification and to discuss the mechanism. Methods RVSMCs were placed in various culture media, including normal phosphate medium, high phosphate medium, ZVAD-FMK medium and atorvastatin medium.Calcium content and cell protein content were quantified by the o-cresolphthalein complexone method and BCA protein assay respectively. Calcification was visualized by yon Kossa staining. And cell apoptosis was quantified by ELISA. Results (1)At day 3, 6, 9, RVSMCs calcification occurred more frequently in high phosphate medium than that in normal phosphate medium (P<0.05). (2)At day 6, RVSMCs calcification was significantly inhibited in 1.0 μmol/L and 2.0 μmol/LZVAD-FMK medium (P<0.05). And in 10 nmol/L and I00 nmol/L statin medium, RVSMCscalcium deposition significantly decreased (P<0.05). (3)RVSMCs apoptosis and calcification occurredfrequently in high phosphate medium. And atorvastatin significantly inhibited RVSMCs apoptosisboth in long-term and short-term (P<0.05). Conclusions Hyperphosphate can induce the calcium deposition of RVSMCs in vitro. Atorvastatin protects RVSMCs from phosphate-induced calcification by inhibiting apoptosis.

Objective To evaluate the effect of parathyroid hormone (PTH) on the expression of connective tissue growth factor (CTGF) in human renal tubular epithelial cells, and to explore the role of MAPK signaling pathway. Methods Real time RT-PCR, Western blot, and reporter gene assay were employed to detect PTH-induced CTGF expression in HK-2 cells. Inhibitors (PD98059 and U0126) of MAPK signaling pathway were used to confirm involved signal pathway. Results HK-2 cells had basic expression level of CTGF mRNA and protein, which were increased significantly after treatment with PTH. The luciferase activity was up-regulated to a higher level as compared with control group after treatment with 10-10 mol/L PTH for 12 h [(1.8884±0.0780) vs (0.9891±0.0300) A, P<0.01]. Moreover, a small amount of p-ERK1/2 was detected in normal HK-2 cells, but it was increased significantly in response to PTH activation, most remarkably when treated with 10-10 mol/L PTH for 30 min. Inhibitors of MAPK signaling pathway, PD98059 and U0126, noticeably inhibited the expression of CTGF mRNA and protein as well as gene promoters in HK-2 cells. Conclusion PTH can induce higher expression of CTGF in HK-2 cells probably via MAPK signaling pathway.

Objective To explore the effect of serum uric acid on the clinical manifestations,pathological characteristics and prognosis of IgA nephropathy.Methods Four hundred and fifty-six cases of primary IgA nephropathy confirmed by renal biopsy from Jan 2007 to Oct 2010 in the Ji'nan Military General Hospital were reviewed retrospectively.The clinical manifestations and pathological characteristics of all the patients were analyzed,x2-test and t-test were used for statistical analysis.Results There were 127 cases with hyperuricemia in 456 IgAN patients (27.9％).The mean age,percentage of male patients,number of patients with hypertension,the serum cholesterol and triglyceride level,body mass index (BMI),serum creatinine and 24 hour urine protein level in hyperuricemia group were significantly higher than those with normal serum uric acid (P＜0.01).The renal pathological changes,glomerular score (8.1 ±0.8 v 5.3t0.9 ),tubulointerstitial score (4.2±0.4 vs 2.7±0.4) and vasculopathy score ( 1.43±0.60 vs 0.76±0.29) in the hyperuricemia group were more severe than those with normal serum uric acid (P＜0.01).Conclusion High level of serum uric acid can affect IgA nephropathy significantly.It is effe-ctive to delay the kindey damage and progression of IgA nephropathy by decreasing the level of uric acid and control the clinical parameters listed above.

Objective Delayed xenograft rejection (DXR) is a major barrier to the long-term xenograft survial.This study evaluated the interaction between human peripheral blood mononuelear cells (PBMC) and porcine endothelial cells (PEC),and the effects of new generation of rabbit antihuman leukocyte polyclonal antibody (newRALG) inhibiting xenogeneic cell-mediated immune responses.Methods newRALG was obtained from rabbits after immunization with activated lymphocytes and monoeytes.PEC were isolated from aorta,and human PBMC were isolated from peripheral blood.Co-cultures of PKH-26 labeled PEC with PBMC were established,newRALG,thymoglobulin,isotype Ig and scavenger receptor (SR) ligand poly G were added into the co-cultures.Cells were collected,then FACS analysis was carried out to detect the up-take of PEC membrane by monocytes and the expression of costimulatory molecules.Lymphocyte proliferative responses to PEC with or without antibody were evaluated by a xenogeneie mixed lymphocyte-endothelial cell reaction (xMLER).Results FACS analysis revealed that monocytes from PBMC-PEC co-cultures became positive for PKH-26 following their interaction with PKH-26 labeled PEC,indicating that they engulfed PEC membranes during activation.PKH-26 positive monocytes up-regulated the CD40 and CD80 expression.Furthermore,SR blockade with poly-G prevented PEC membrane up-take by monocytes,newRALG greatly reduced SR-mediated PEC membrane up-take.The effects of thymoglobulin in inhibiting PEC membrane uptake were limited.xMLER demonstrated strong lymphocyte proliferation in response to PEC,and lymphocyte proliferation was dramatically inhibited by newRALG but not isotype Ig at a dosmdependent manner.Conclusions Monocytes play an important role in xenogeneic immune responses.SR ligand poly G inhibits PEC membrane up-take.newRALG inhibits PEC membrane up-take by monocytes,suggesting that newRALG blocks SR.Additionally,newRALG inhibits lymphocyte proliferation in response to PEC.These results suggest that this new polyclonal preparation may thus impair the initiation of xeno-specific immune responses and prevent xenograft rejection.

Objective To investigate the effect of parathyroid hormone (PTH) on the transition and connective tissue growth factor (CTGF) expression of human renal proximal tubular epithelial cell line HK-2 . Methods The expression of CTGF mRNA and protein of HK-2 cells were measured by real time RT-PCR and Western blot respectively . The effect of PTH on the phenotypic transformation of HK-2 cells was examined by light microscopy . The expression of α-smooth muscle actin (α-SMA) in HK-2 cells was detected by immunofluorescence . Results Basal level of CTGF mRNA and the protein expression were detected in HK-2 ceils . PTH upregulated the expression of CTGF mRNA and protein with the maximal response at the concentration of 10-10 mol/L and the best stimulating time was at 72 h . After exposure to PTH (10-10tool/L) for 12 hours, the highest level of luciferase activity was 1 .96 fold as compared to control (1 .888±0 .078 vs 0 .989±0 .030, P＜0 .01 ) . Untreated cells showed negligible expression of ±-SMA,whereas ±-SMA expression was significantly increased in cells treated with PTH . Conclusion PTH up-regulates CTGF expression and induces transition of HK-2 cells .

Objective To investigate the effect of parathyroid hormone (PTH) on the epithelial to mesenchymal transition (EMT) in human renal proximal tubular epithelial cells (HK-2 cells),and determine the role of β-catenin signaling pathway.Method The expression of α-smooth muscle actin (α-SMA),E-cadherin and β-catenin in HK-2 cells was measured by real-time PCR,Western blotting and immunofluorescence technique.The signaling pathway by which PTH activated EMT in HK -2 cells was identified by using synthetic β-catenin siRNA.Results Parathyroid hormone (10-10mol/ L) increased α-SMA expression and decreased E-cadherin expression in HK-2 cells (P＜ 0.01,respectively).Untreated cells showed the expression of E-cadherin,whereas α-SMA staining was noticeably increased in cells treated with PTH.β-catenin activity was significantly increased after exposed to PTH.Theα-SMA expression was decreased strongly and E-cadherin expression was increased after β-catenin siRNA transfection (all P ＜ 0.05).Conclusion PTH significantly induces epithelial to mesenchymal transition in HK-2 cells throughβ-catenin signaling pathway.

AIM: To set up a method of inducing mouse embryonic stem cells (mESC) to differentiate into cardiomyocyte after treatment with 5-azacytidine. METHODS: Cytotoxicity of 5-azacytidine was measured by MTT assay. Treatment of mESC with conditioned culture mediums, which were composed of 5-azacytidine alone or combined with retinoic acid, induced the cell differentiation to cardiomyocytes. The cells induced were identified by detecting the expression of cardiac proteins (myosin, desmin, ?-actin and ?-actinin). Gene MLC-2v, a specific gene of ventricular-like cardiomyocyte, was also detected by RT-PCR. RESULTS: The non-cytotoxic dose of 5-azacytidine was 8 ?mol/L, which was able to induce mESC to differentiate into cardiac syncytiums. Cells induced expressed many cardiac proteins and MLC-2v mRNA. However, combined with retinoic acid inhibited mESC differentiation into cardiomyocyte. CONCLUSION: 5-azacytidine is able to promote mESC differentiation into cardiomyocytes. A method of inducing mESC to differentiate into cardiomyocytes in vitro has been established.