Objective:To analyze the related factors affecting the use of autogenous arteriovenous fistula (AVF), and provide a theoretical basis for prolonging the service life of AVF in hemodialysis patients.Methods:This was a retrospective study. The patients undergoing AVF and using it to maintain hemodialysis (MHD) in the First Affiliated Hospital of Nanchang University from October 2004 to June 2017 were selected as study subjects to discuss the relevant factors affecting the service life of AVF. The data of general information, dialysis and laboratory examinations were collected through questionnaire surveys, hospital case system and hemodialysis record sheets. The patients were divided into the patency group and the dysfunction group according to the status of AVF, and the related factors were compared. Multivariate Cox proportional hazard model was used to analyze the influencing factors, and Kaplan-Meier survival curve was used to determine the service life of AVF, respectively.Results:A total of 187 subjects were included in the study. The patency group had 140 cases and the dysfunction group had 47 cases. There were statistically significant differences in the proportion of diabetes, the level of serum albumin, uric acid and parathyroid hormone (PTH) between the two groups (all P<0.05). Multivariate Cox proportional hazard regression analysis showed that diabetes ( HR=9.348, 95% CI 3.507-24.918, P<0.001) and hypoalbuminemia ( HR=12.650, 95% CI 2.925-54.714, P=0.001) were risk factors for the short service life of AVF. The results of Kaplan-Meier analysis showed that the service life of AVF in patients with diabetes was significantly shorter than that in MHD patients without diabetes (Log-rank χ2=13.191, P<0.001); the service life of AVF in patients with hypoalbuminemia was significantly shorter than that without hypoalbuminemia (Log-rank χ2=13.591, P<0.001). Conclusions:Diabetes mellitus and hypoalbuminemia are risk factors for the short service life of AVF. Therefore, intervention programs should be formulated to extend the service life of AVF.

Background: Oxidative stress is crucial for the development of ionizing radiation-induced intestinal injuries and inflammation. Taurine is a sulfur-containing amino acid distributed in tissues and organs throughout the body. It possesses several important physiological functions, including anti-oxidative activity and anti-inflammatory effects. Aims: To investigate the therapeutic effect and underlying mechanism of taurine against radiation-induced intestinal injuries. Methods: CCK-8 assay and DCFH-DA, a fluorescence probe of intracellular reactive oxygen species (ROS) were applied to determine the effects of taurine on radiation-induced inhibition of cell viability and ROS accumulation in human intestinal epithelial cell line HIEC-6. The modulatory effects of taurine on expressions of oxidative stress-related genes in intestinal cells after exposure to radiation were measured by real-time PCR in in vitro and in vivo studies. The roles of taurine in maintenance of intestinal morphology and suppression of cell apoptosis in mice receiving whole body radiation were assessed by HE staining and TUNEL staining. Results: In in vitro study, taurine improved the radiation-induced inhibition of cell viability and reduced intracellular ROS accumulation in HIEC-6 cells. The expression levels of catalase (CAT) and glutathione peroxidase 1 (GPx1) in HIEC-6 cells were up-regulated by taurine treatment. In vivo study showed that taurine activated the nuclear factor erythroid 2-related factor 2/heme oxygenase-1 (Nrf2/HO-1) signaling pathway, alleviated intestinal villi disorganization and loss of crypt cells, and suppressed cell apoptosis in mice after radiation. Conclusions: Taurine can reduce the intracellular ROS accumulation via activating Nrf2/HO-1 antioxidant signaling pathway, and thereby, exerts protective effect against radiation-induced intestinal injuries. It might be a candidate for treatment of intestinal injuries in patients undergoing radiotherapy.

Objective To investigate the efficacy of leflunomide combined with prednisone in the induction therapy of proliferative lupus nephritis (LN).Methods A prospective,multicenter,randomized controlled clinical trial was conducted in patients with biopsy-proved proliferative lupus nephritis recruited from 15 renal centers from 2013 to 2015.Patients were randomized to two groups.Oral leflunomide or intravenous cyclophosphamide was given to patients in each group.Both groups received a tapering course of oral prednisone therapy.All patients were followed up for 24 weeks.The blood biochemistry,urine index,clinical curative effect and adverse reaction were recorded and analyzed statistically.Results A total of 100 patients were enrolled in this clinical trial,including 48 patients in leflunomide group and 52 patients in cyclophosphamide group.After 24 weeks,the overall response rate was 79％ (95％ CI 67％-90％) in the leflunomide group and 69％ (95％ CI 56％-82％) in the cyclophosphamide group.23％ (95％CI 11％-35％) of patients in leflunomide group showed complete remission compared with 27％ (95％CI 24％-30％) in cyclophosphamide group (P=0.35).The levels of 24-hr urine protein excretion,SLEDAI and anti-dsDNA antibody titers were decreased in patients treated with leflunomide group after 24-weeks treatment.And the levels of serum albumin and complement 3 after treatment were significantly higher compared with these before treatment.There was also no significant difference in changes of 24-hr urine protein excretion,SLEDAI score,anti-dsDNA antibody titers,serum albumin and complement C3 levels after treatment between two groups.Incidence of adverse events did not differ between the leflunomide and cyclophosphamide group.Conclusions Leflunomide combined with prednisone showed same efficacy compared with cyclophosphamide as induction therapy for lupus nephritis.Leflunomide might be an useful medicine in the induction therapy of lupus nephritis.

Background: Studies showed that aberrant activation of JAK/STAT3 signaling pathway promoted the tumorigenesis and progression of hepatocellular carcinoma (HCC), and transforming growth factor-β1 (TGF-β1) has either tumor-suppressing or tumor-promoting effect in regulation of tumor progression.Aims: To investigate the effect of specific inhibition of JAK/STAT3 signaling pathway on HCC and whether TGF-β1 signaling pathway is involved in this process or not.Methods: Thirty Wistar rats were randomly divided into three groups: control group, HCC group, and HCC+AG490 group.In the latter two groups, diethylnitrosamine was administered in drinking water to induce HCC model, and in HCC+AG490 group, AG490, a specific inhibitor of JAK was injected intraperitoneally in the first week of model establishment.At the end of the 16th week, all rats were sacrificed.The maximum diameter of tumor nodules in the liver was recorded and the number of tumors with maximum diameter greater than 1 cm was counted.Expression and distribution of STAT3 and TGF-β1 in liver tissue were determined by real-time PCR, immunohistochemistry, and immunofluorescence.Results: Compared with the control group, expressions of STAT3 and TGF-β1 mRNA in liver tissue were significantly increased in HCC group (P<0.05).Phosphorylated STAT3 (p-STAT3) and TGF-β1 proteins were absent in liver tissue in control group, and both were up-regulated and co-expressed in HCC group.While in HCC+AG490 group, expressions of STAT3 and TGF-β1 mRNA were significantly lower than those in HCC group (P<0.05);the liver tissue was weakly positive for p-STAT3 and TGF-β1 proteins, and the number of tumor nodules greater than 1 cm and the maximum diameter were markedly reduced when compared with the HCC group [1.20±1.03 and (1.14±0.18) cm vs.4.30±1.06 and (1.78±0.27) cm, P all<0.05].Conclusions: Specific inhibition of JAK/STAT3 signaling pathway may restrain the tumorigenesis and progression of HCC partially by interfering TGF-β1 signaling pathway.

Epithelial-mesenchymal transition (EMT) is a process by which epithelial cells lose their own features and become mesenchymal cells, and more and more studies have shown that EMT plays an important role in the invasion and metastasis of hepatocellular carcinoma (HCC). This article reviews the signaling pathways involved in the progression of HCC and molecules involved in the regulation of EMT, in order to provide a new direction for the treatment of HCC.

ObjectiveTo investigate the risk genes for predicting the development of chronic hepatitis B (CHB) cirrhosis using gene chip technology. MethodsA total of 40 CHB patients who visited Shanghai First People′s Hospital from April 2008 to December 2010 were enrolled as a clinical cohort and were divided into S0, S1, S2, S3, and S4 groups, with 8 patients in each group. Liver biopsy was performed to determine fibrosis stage with the Scheuer pathological score as the criteria, and clinical data and liver tissue samples were reserved. The Human Affymetrix GeneChip was used to establish the gene expression profiles of liver tissues in CHB patients, and the significance analysis of microarrays (SAM) and prediction analysis of microarrays (PAM) were used to screen out the risk genomes for predicting the development of CHB cirrhosis. Quantitative real-time PCR was used to measure the mRNA expression of risk genes in liver tissue. The chi-square test was used for comparison of categorical data. The t-test and a one-way analysis of variance were used for comparison of normally distributed continuous data, and SNK-q test was used for further comparison between any two groups; the Mann-Whitney U rank sum test was used for comparison of non-normally distributed continuous data. ResultsA total of 1674 differentially expressed genes were screened out by Affymetrix GeneChip. A cluster analysis of these genes showed that gene expression showed differences between groups with different fibrosis stages, which suggested that the gene expression profile was well consistent with fibrosis stage. Four different classification methods were used for analysis, and 87 significant genes were screened out by SAM and 14 “high-risk” genes were screened out by PAM. The quantitative real-time PCR showed the expression of 6 risk genes (CD24, CXCL6, EHF, ITGBL1, LUM, and SOX9) differed significantly between groups S0, S1-3, and S4 (P＜0.05), and the S1-3 and S4 groups showed significantly upregulated expression of these genes compared with the S0 group (all P＜0.05). ConclusionThe 6 high-risk factors screened out and verified by gene chip technology help to predict the probability of developing liver cirrhosis in CHB patients and can be used as the diagnostic genes for predicting hepatitis B cirrhosis.

Objective To investigate the effect and mechanism of chitosan on vascular smooth muscle cell proliferation of uremia patients with arteriovenous fistula.Methods Primarily culturing the VSMCs of uremia patients with arteriovenous fistula and patients without uremia by explants adherent method,and taking the second generation.VSMCs from patients without uremia cultured with 20％ FBS medium were non-uremia group,VSMCs of uremia patients cultured with 20％ FBS medium were uremia group,VSMCs of uremia patients with 100 pg/ml chitosan were uremia+ chitosan group.The expression of α-SMA was detected by immunohistochemistry.The changes of migration and invasion of VSMCs were detected by scratches and transwell migration assays.The mRNA expressions of TLR4 and PCNA were measured by real-time PCR.VSMCs of uremia patients with arteriovenous fistula were intervened with different doses of chitosan (0,100 and 500 μg/ml),and the protein expressions of TLR4,MyD88 and NF-κB were detected by Western blotting.Results Compared with those in non-uremia group,in uremia group and uremia+chitosan group α-SMA was upregulated,migration and invasion of VSMCs were enhanced,and mRNA expressions of TLR4 and PCNA were increased (all P ＜ 0.05).Compared with those in uremia group,the level of α-SMA was significantly decreased,the ability of migration and invasion of VSMCs were decreased,and the mRNA expressions of TLR4 and PCNA were decreased (all P ＜ 0.05).TLR4,MyD88 and NF-κB protein expressions were reduced in concentration-dependent manner by 100 and 500 μg/ml chitosan.Conclusions (1) In vitro,chitosan decreases the ability of migration and invasion of VSMCs of uremia patients with arteriovenous fistula.(2) Chitosan inhibits the proliferation of VSMCs,which may be relevant in the decreased expressions of TLR4,MyD88 and NF-κB.

Objective To investigate the effete of chitosan on rabbit carotid artery internal jugular vein fistula intimal hyperplasia and its regulation on TLR4/NF-κB signaling.Methods A total of 28 New Zealand white rabbits were randomly divided into the control group(n=4),the model group(n=12) and the chitosan group(n=12).Model group and chitosan group rabbits were established respectively carotid artery internal jugular vein fistula models.After AVF surgery,chitosan was smeared on venous blood vessels and anastomosis.After 4,6 and 8 weeks,the rabbits were separately sacrificed and the AVF venous vascular tissues were taken.The pathological changes of AVF venous vascular tissue in each group were observed.The changes of α-SMA were detected by immunohistochemistry method.The mRNA expressions of PCNA and TLR4 in the tissues were measured by Real-time PCR.At the same time,the protein expressions of PCNA,TLR4,MyD88 and NF-κB were detected by Western blotting.The experimental data were processed by two-factor analysis of variance in statistics.Results (1) After 4 weeks,vascular intimal was thicked in mdel group.In intimal hyperplasia,α-SMA was staining,and then proliferation of vascular smooth muscle cell was significant.As time increasing,more intimal hyperplasia shown obviously,the expression of α-SMA significantly increased.Compared with model group,chitosan group significantly reduced the degree of intimal hyperplasia,the level of α-SMA was significantly decreased,vascular smooth muscle cell proliferation was also extraordinarily decreased.(2) Compared with control group,the expression levels of PCNA,TLR4,MyD88 and NF-κB increased with time.The indices of Chitosan group were markedly higher than control group,but significantly lower than model groups.Conclusion Chitosan can inhibit the proliferation of rabbit VSMCs.The mechanism may be concerned in down regulating TLR4-mediated signaling pathway,reducing the possibility of intimal hyperplasia of rabbit AVF venous blood vessels.

Objective To analyze the risk factors for hypertension in patients with chronic kidney disease stage 5(CKD5) . Methods The basic information of 390 CKD5 patients complicated with hypertension was collected for univariate analysis ,in‐cluding gender ,age ,primary disease ,dialysis method ,body mass index(BMI) ,complications(hyperlipidemia ,high uric acid ,car‐diac insufficiency) ,level of education ,parathyroid hormone(PTH)level.Univariate variables that showed statistical significance were then subjected to the multivariate analysis(Logistic regression)to identify the risk factors for hypertension in CKD5 pa‐tients.The defined daily dose(DDD)that satisfied the criteria interms of different stages was evaluated.Results Overall hyper‐tension control rate was 22.8%.Univariate analysis showed that the following variables were significantly associated with hy‐pertension in CKD5 patients :>40 years old ,male ,diabetic nephropathy ,hypertensive nephropathy ,hemodialysis ,hyperlipemia , high uric acid level ,and high PTH level(P<0.05).Logistic multivariate analysis showed that diabetic nephropathy ,hyperlipi‐demia ,high PT H level were the independent risk factors for hypertension in patients with CKD5.In hypertension segmented standard ,there was no difference in the DDD between stage 0 and 1(P>0.05) ,and DDD at stage 2 and 3 was increased signifi‐cantly when compared with that at 0 and 1 standard(P<0.05).Conclusion Overall hypertension control rate is very low in pa‐tients with CKD5.Diabetics ,hyperlipidemia ,high PTH level are independent risk factors for hypertension in patients with CKD5.

This paper is aimed to study the feasibility of myocardial infarction risk assessment by noninvasive multivariable trend analysis, including heart rate variability (HRV), deceleration capacity (DC) of heart rate and pulse wave velocity (PWV). Thirty five patients with cardiovascular diseases (11 Myocardial infarction (MI), 8 coronary artery disease (CAD), 6 artery atherosclerosis (AA) and 10 hypertension), and 31 healthy subjects were randomly selected into a control group for this research as comparison. 15 min ECG and 1 min pulse wave data were collected based on the analysis workbench developed by our Lab. HRV, DC and PWV between the cardiovascular group and the control group were analyzed and compared. The results showed that the HRV indices, DC and PWV were significantly higher than those in the control group. The DC and the HRV indices including NN50, PNN50 and TINN especially presented a decline trend that was consistent with the regularity of cardiovascular development process. This noninvasive multivariable trend analysis of HRV, DC and PWV can be a reference for the earlier risk prediction of MI.
Aged ; Electrocardiography ; Female ; Forecasting ; Heart Rate ; Humans ; Male ; Middle Aged ; Multivariate Analysis ; Myocardial Infarction ; physiopathology ; Pulse ; Risk Assessment