Objective To investigate the effect of low molecular weight heparin on lipid parameters in hemodialysis patients. Methods The trial was double blind, open, controlled and randomized for one year. 35 pre-dialysis patients were divided into two groups: UFH(unfractionated heparin) group(n = 13) and LMWH(low molecular weight heparin ) group(n = 22), UFH or Fragmin according to individual dosage was infused to patients of two groups respectively. The level of serum lipid, lipoprotein, apolipoprotein and activity of lipase were measured at months 0, 6 and 12 of trial. Results Significant increases in serum concentrations of TG, LDL, VLDL, Lp(a) and apo-B were observed, whereas serum concentrations of HDL, apo-Al and activity of plasma LCAT or LDL were decreased in both groups before hemodialysis. As dialysis time went by, in LMWH group, activities of plasma LPL and LCAT elevated; TG concentration decreased; VLDL and LDL were not significantly different compared with that of pre-dialysis, but were statistically different in contrast to UFH group. Conclusion The long-term use of LMWH instead of conventional heparin for anticoagulation during dialysis has beneficial effects on the lipid profile, especially in patients with dyslipidemia.

Objective To investigate the effects of arteriovenous fistula on structure and function of left ventricle in patients with maintained hemodialysis. Methods Levels of hemoglobin, inter-hemodialysis weight increase, blood pressure, diameter and blood flow of the fistula, structure and function of left ventricle were examined before and 12, 24 months after hemodialysis treatment in 44 patients who were divided into group A(low flow group, 900 ml/min) based on the fistula flow at the 24th month. Results Left ventricular end-diastolic diameter (LVDd), interventriculare septal thickness (IVST) and left ventricular mass index (LVMI) increased gradually as the time of hemodialysis going on. The cardio-cheat proportion also increased as well as ejection fraction (EF) and the peak velocity ratio of early and late diastolic period(E/A), especially significantly increased in group B. Cardio-chest proportion , LVDd and LVMI were higher and E/A lower in patients with severe sodium retention than those with mild sodium retention in both groups. The fistula flow was positively related to LVDd and LVMI( P

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 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 role of p27 in the inhibition of emodin on the mesangial cell (MC) proliferation induced by tumor necrosis factor-alpha(TNF-alpha). METHODS: p27 protein of MC was detected with western blotting analysis. The degree of MC proliferation was estimated through [(3)H] thymidine ([(3)H] TdR) incorporation. Different dosage of emodin (50 mg/L,100 mg/L) was added into MC stimulated by TNF-alpha. RESULTS: TNF-alpha (200 kU/L) decreased p27 level of MC cultured in serum-free DMEM for 24 hours and increased[(3)H] TdR incorporation. Emodin increased p27 level of MC stimulated by TNF-alpha and decreased [(3)H] TdR incorporation. The more the emodin was added, the greater the above-mentioned effect of emodin. CONCLUSION: The increment of p27 level maybe play an important role in the inhibition of emodin on MC proliferation induced by TNF-alpha.

Objective:To meet the demand of medical system for talents, the training of medical students' competency has become a new direction of medical education. This study aims to evaluate the effectiveness of training quality in medical graduates through the competency scale.Methods:Taking "attitude", "skill" and "knowledge" as the evaluation dimensions, the competency development was divided into four levels of "state", "explain", "apply" and "transfer", and we proposed the competence concept of "A.S.K.-SEAT" and formulated an evaluation scale. Questionnaires and behavior event interviews (BEI) were conducted in medical graduates of Shantou University in 2018. Reliability and validity of the questionnaire were evaluated and current situation of different competency items were analyzed.Results:A total of 155 questionnaires were collected with good reliability and validity, and 15 graduates participated in BEI. A total of 21 A.S.K. competency items (including five basic competency items and two discriminating competency items) and SEAT textual descriptions were finally established.Conclusion:A.S.K.-SEAT scale can provide valid references for the competency evaluation of medical graduates.

Objective Circular RNAs (circRNAs) are non-coding RNAs (ncRNA) circularized without a 3' polyadenylation [poly-(A)] tail or a 5' cap, resulting in a covalently closed loop structure. circRNAs were first discovered in RNA viruses in the 1970s, but only a small number of circRNAs were discovered at that time due to limitations in traditional polyadenylated transcriptome analyses. With the development of specific biochemical and computational methods, recent studies have shown the presence of abundant circRNAs in eukaryotic transcriptomes. circRNAs play vital roles in many physiological and pathological processes, such as acting as miRNA sponges, binding to RNA-binding proteins (RBPs), acting as transcriptional regulatory factors, and even serving as translation templates. Current evidence has shown that circRNAs can be potentially used as excellent biomarkers for diagnosis, therapeutic effect evaluation, and prognostic assessment of a variety of diseases, and they may also provide effective therapeutic targets due to their stability and tissue and development-stage specificity. This review focuses on the properties of circRNAs and their immune relationship to disease, and explores the role of circRNAs in immune-related diseases and the directions of future research.
Biomarkers ; MicroRNAs/genetics* ; RNA, Circular ; Transcriptome