Objective:To investigate the effect of circular RNA (circRNA)_005987 on contrast-associated acute kidney injury (CA-AKI) and its mechanism, and provide new ideas for the prevention and treatment of CA-AKI.Methods:CA-AKI rat models and HK-2 cell injury models were established using iopromide, and CA-AKI-related circRNA_005987 was screened based on circRNA expression chip and real-time quantitative PCR (RT-qPCR). Knockdown and overexpression of circRNA_005987 were performed in HK-2 cell model, respectively. Cell counting kit-8 (CCK-8) and Edu staining assays were used to evaluate cell proliferation. Western blotting was used to detect the protein expression of autophagy-related protein microtubule-associated protein 1 light chain 3B (LC3B), P62, beclin-1 and autophagy-related gene 14 (ATG14). Immunofluorescence staining was used to detect protein expression of LC3B. Electron microscope was used to observe the autophagosome formation. Autophagy activator rapamycin and autophagy inhibitor 3-methyladenine were used for in vitro rescue experiments to observe the changes of the above indicators. Mechanistically, bioinformatics analysis was applied to analyze the binding site among circRNA_005987, miR-129-5p and ATG14, and dual luciferase reporter assay was used to verify their interactions. CircRNA_005987 was knocked down and overexpressed in HK-2 cell model, and RT-qPCR was used to detect the expression of miR-129-5p. HK-2 cells were treated with miR-129-5p inhibitor and mimic, Western blotting was used to detect the protein expression of ATG14, and CCK8 and Edu staining assays were used to evaluate cell proliferation. Results:CircRNA_005987 expression was up-regulated in vitro and vivo CA-AKI models (both P<0.05). Overexpression of circRNA_005987 inhibited cell proliferation and promoted cell autophagy, while knockdown of circRNA_005987 had opposite effects (all P<0.05). In vitro rescue experiments confirmed that circRNA_005987 inhibited cell proliferation by activating autophagy ( P<0.05). The dual luciferase reporter assay suggested that there was an interaction between circRNA_005987, miR-129-5p and ATG14. Knockdown of circRNA_005987 increased miR-129-5p expression, while overexpression of circRNA_005987 inhibited miR-129-5p expression (both P<0.05). Knockdown of miR-129-5p inhibited cell proliferation, while overexpression of miR-129-5p reversed the effect (both P<0.05). Conclusion:CircRNA_005987 promotes CA-AKI through activating autophagy via sponging miR-129-5p, suggesting that circRNA_005987 plays an important role in the pathological process of CA-AKI.

Objective:To investigate the effect of circular RNA (circRNA)_005987 on contrast-associated acute kidney injury (CA-AKI) and its mechanism, and provide new ideas for the prevention and treatment of CA-AKI.Methods:CA-AKI rat models and HK-2 cell injury models were established using iopromide, and CA-AKI-related circRNA_005987 was screened based on circRNA expression chip and real-time quantitative PCR (RT-qPCR). Knockdown and overexpression of circRNA_005987 were performed in HK-2 cell model, respectively. Cell counting kit-8 (CCK-8) and Edu staining assays were used to evaluate cell proliferation. Western blotting was used to detect the protein expression of autophagy-related protein microtubule-associated protein 1 light chain 3B (LC3B), P62, beclin-1 and autophagy-related gene 14 (ATG14). Immunofluorescence staining was used to detect protein expression of LC3B. Electron microscope was used to observe the autophagosome formation. Autophagy activator rapamycin and autophagy inhibitor 3-methyladenine were used for in vitro rescue experiments to observe the changes of the above indicators. Mechanistically, bioinformatics analysis was applied to analyze the binding site among circRNA_005987, miR-129-5p and ATG14, and dual luciferase reporter assay was used to verify their interactions. CircRNA_005987 was knocked down and overexpressed in HK-2 cell model, and RT-qPCR was used to detect the expression of miR-129-5p. HK-2 cells were treated with miR-129-5p inhibitor and mimic, Western blotting was used to detect the protein expression of ATG14, and CCK8 and Edu staining assays were used to evaluate cell proliferation. Results:CircRNA_005987 expression was up-regulated in vitro and vivo CA-AKI models (both P<0.05). Overexpression of circRNA_005987 inhibited cell proliferation and promoted cell autophagy, while knockdown of circRNA_005987 had opposite effects (all P<0.05). In vitro rescue experiments confirmed that circRNA_005987 inhibited cell proliferation by activating autophagy ( P<0.05). The dual luciferase reporter assay suggested that there was an interaction between circRNA_005987, miR-129-5p and ATG14. Knockdown of circRNA_005987 increased miR-129-5p expression, while overexpression of circRNA_005987 inhibited miR-129-5p expression (both P<0.05). Knockdown of miR-129-5p inhibited cell proliferation, while overexpression of miR-129-5p reversed the effect (both P<0.05). Conclusion:CircRNA_005987 promotes CA-AKI through activating autophagy via sponging miR-129-5p, suggesting that circRNA_005987 plays an important role in the pathological process of CA-AKI.

Objective To evaluate the prognostic values of common definition compared to traditional definition of contrast-induced nephropathy (CIN) in patients with normal serum creatinine (SCr). Methods Patients undergoing percutaneous coronary angiology or intervention with normal baseline SCr were enrolled prospectively. Those who were diagnosed as CIN according to common definition were divided into two groups based on the peak increase from baseline in the SCr concentration within 48 ~ 72 hours after the procedure: ≥ 44.2 μmol/L (CIN44.2 group, in common with traditional definition), ≥25% of baseline to < 44.2 μmol/L (CIN25%-44.2 group, interval between the two definitions). Hospital stay and long-term outcomes were compared among CIN44.2, CIN25%-44.2, and non-CIN groups. Results Of all 3,044 patients enrolled, 302 (9.9%) patients developed CIN according to common definition including CIN44.2 occurred in 56 (1.8%) patients and CIN25%-44.2 in 246 (8.1%) patients. Patients in CIN44.2 group indicated significant longer hospital stay and long-term outcomes compared with non-CIN group (P < 0.05). However, patients in CIN25%-44.2 group had similar in-hospital mortality and long-term cumulative risk of major clinical adverse events (MACE) and death with non-CIN group (all, P = 1.00). Multivariate Cox proportional hazard analyses also demonstrated that CIN25%-44.2 did not associate with long-term MACE (HR 1.16, P = 0.645) and death (HR 0.98, P = 0.964) after adjusting for potential confounding factors. Conclusions For patients with normal baseline SCr, common definition based on traditional definition of CIN is unreasonable and overestimates the incidence of CIN, whose extension of traditional denifition proves no significant clinical value.

Objective To observe the different behavior of proliferation and cell cycle of MCF-7 cells when exposured to ropivacaine of different concentrations and further explore its underlying mechanism.Methods Human breast cancer cells MCF-7 were inoculated into culture medium for 24 h,then were randomly divided into four groups:Control group(group C),Ropivacaine 100 μg/ml group(group R1 ),Ropivacaine 200 μg/ml group(group R2),Ropivacaine 400 μg/ml group(group R3).We medicated each group and incubated for 48 h,then detected the cell proliferation and cell cy-cle immediately.The level of protein TCF-4 and beta-catein of groups R3 and C were measured at the same time.Results MCF-7 cell viability of groups R2 and R3 was significantly lowed (P <0.05 ), MCF-7 cell viability of group R1 had no significant difference when compared to group C.G0/G1 phase cells of groups R1,R2 and R3 were significantly less than those of group C,S phase cells of groups R1,R2 and R3 were significantly more than group C,G2/M phase cells of groups R1,R2 and R3 were significantly more than group C (P <0.05).The expression level of TCF-4 and beta-catenin in group R3 was significantly lower than that in group C (P <0.05).Conclusion Ropivacaine inhibits the proliferation of breast cancer cells MCF-7 by down-regulating TCF-4 and beta-cateni.

BACKGROUND:Humeral supracondylar fracture is a common fracture occurred in children. The selection of internal fixation for humeral supracondylar fracture remains controversial. OBJECTIVE:To compare the biocompatibility between internal fixation with Kirschner wire and bioabsorbable implants for humeral supracondylar fractures. METHODS: From January 2007 to January 2013, 246 cases of humeral supracondylar fractures, from Affiliated Hospital of Luzhou Medical Colege, were treated by internal fixation with Kirschner wire. Meanwhile, the studies on internal fixation for treating supracondylar fracture of humerus in children were searched. Efficacy was evaluated by preoperative and postoperative elbow range of motion and the incidence of cubitus varus, and the results were statisticaly analyzed, and compared with other therapeutic methods. RESULTS AND CONCLUSION:Al cases were folowed up for 6-36 months, averagely 18 months. According to Mayo elbow performance score, function of the elbow joint was excelent in 194 cases, and good in 48 cases, with good and excelent rate being 98.4%. Four cases suffered < 5° cubitus varus, with incidence rate of 1.63%. The internal fixation with Kirschner wire provided functional recovery of elbow joint, but the second stage operation was needed to pick out the wires. And it might be perplexed by Kirschner wire loosening or needle withdrawal, resulting in instable fixation. Bioabsorbable implants were effective in the treatment of supracondylar fracture of humerus. Bioabsorbable sticks would break down over time, without harming to human body or influencing imaging examination. Elbow function development of the epiphysis would not be affected. However, due to lack of large-sample observation, long-term effects of bioabsorbable implants for treating supracondylar fracture of humerus in children deserve further studies.

[Abstract ] Objective The pathogenesis underlying cognitive dysfunction has yet to be fully elucidated.The article was to investigate the effects of memantine on lipopolysaccharide (LPS)-induced spatial learning and memory impairment in C57BL/6J mice. Methods 36 male C57BL/6J mice were randomly divided into 3 groups:control group (C group), lipopolysaccharide group (L group) and memantine group (M group) (n=12).Mice in C, L and M groups were intraperitoneally injected with the same volume of saline, LPS and LPS plus memantine re-spectively for 7 consecutive days.On the 8th day, mice were tested in the Morris water maze, in which the latency to the platform and the propor-tion of time spent in the target quadrant were recorded .Then the mice were sacrificed and the hippocampi were harvested for the determination of expression levels of Amyloid-β(Aβ), glycogen synthase kinase-3β(GSK-3β) and mammalian target of rapamycin (mTOR). Results Com-pared with C group, L group significantly prolongated the latency to the platform (71.01 ±13.21 vs 50.56 ±9.89, P<0.05), decreased the propor-tion of time spent in the target quadrant (42.58 ±7.85 vs 63.74 ±12.43, P<0.05) and increased the levels of hippocampal Aβand GSK-3β(1.75 ±0.43 vs 1.27 ±0.23, 184.0 ±18.6 vs 100.0 ±12.1, P<0.05), (75.0 ±13.5 vs 100.0 ±10.3, P<0.05), while mTOR levels decreased significantly (97.0 ±14.3 vs 75.0 ±13.5, P<0.05).Compared with L group, M group significantly prolongated the latency to the platform (61.45 ±7.65 vs 71.01 ±13.21, P<0.05), decreased the proportion of time spent in the target quadrant shortened (58.25 ±9.02 vs 42.58 ±7.85, P<0.05) and increased the expression of hippocampal Aβ(1.35 ±0.28 vs 1.75 ±0.43,92.4 ±10.8 vs 184.0 ±18.6, P <0.05). Conclusion Memantine contributes to the improvement of LPS-induced spatial learning and memory impairment, which is probably related to the changes of the expression of GSK-3βand mTOR in hippocampus.