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Background. New-onset atrial fibrillation (AF) in patients with chronic obstructive pulmonary disease (COPD) is associated with an accelerated decline in lung function, and a significant increase in mortality rate. A deeper understanding of the risk factors for new-onset AF during COPD will provide insights into the relationship between COPD and AF and guide clinical practice. This systematic review and meta-analysis is designed to identify risk factors for new-onset AF in patients with COPD, and to formulate recommendations for preventing AF in COPD patients that will assist clinical decision making. Methods. PubMed, Embase, Web of Science and Cochrane Library databases were searched for studies, which reported the results of potential risk factors for new-onset AF in COPD patients. Results. Twenty studies involving 8,072,043 participants were included. Fifty factors were examined as potential risk factors for new-onset AF during COPD. Risk factors were grouped according to demographics, comorbid conditions, and COPDand cardiovascular-related factors. In quantitative analysis, cardiovascular- and demographic-related factors with a greater than 50% increase in the odds of new-onset AF included age (over 65 years and over 75 years), acute care encounter, coronary artery disease, heart failure and congestive heart failure. Only one factor is related to the reduction of odds by more than 33.3%, which is black race (vs white). In qualitative analysis, the comparison of the risk factors was conducted between COPD-associated AF and non-COPD-associated AF. Cardiovascular-related factors for non-COPDassociated AF were also considered as risk factors for new-onset AF during COPD; however, the influence tended to be stronger during COPD. In addition, comorbid factors identified in non-COPD-associated AF were not associated with an increased risk of AF during COPD. Conclusions. New-onset AF in COPD has significant demographic characteristics. Older age (over 65 years), males and white race are at higher risk of developing AF. COPD patients with a history of cardiovascular disease should be carefully monitored for new-onset of AF, and appropriate preventive measures should be implemented. Even patients with mild COPD are at high risk of new-onset AF. This study shows that risk factors for new-onset AF during COPD are mainly those associated with the cardiovascular-related event and are not synonymous with comorbid factors for non-COPD-associated AF. The pathogenesis of COPD-associated AF may be predominantly related to the cardiac dysfunction caused by the chronic duration of COPD, which increases the risk of cardiovascular-related factors and further increases the risk of AF during COPD. [ABSTRACT FROM AUTHOR]

Manganese superoxide dismutase (MNSOD) is one of the major scavengers of reactive oxygen species (ROS) in mitochondria with pivotal regulatory role in ischemic disorders, inflammation and cancer. Here we report oxidative modification of MNSOD in human renal cell carcinoma (RCC) by the shotgun method using data-dependent liquid chromatography tandem mass spectrometry (LC-MS/MS). While 5816 and 5571 proteins were identified in cancer and adjacent tissues, respectively, 208 proteins were found to be up- or down-regulated (p < 0.05). Ontological category, interaction network andWestern blotting suggested a close correlation between RCC-mediated proteins and oxidoreductases such as MNSOD. Markedly, oxidative modifications of MNSOD were identified at histidine (H54 and H55), tyrosine (Y58), tryptophan (W147, W149, W205 and W210) and asparagine (N206 and N209) residues additional to methionine. These oxidative insults were located at three hotspots near the hydrophobic pocket of the manganese binding site, of which the oxidation of Y58, W147 and W149 was up-regulated around three folds and the oxidation of H54 and H55 was detected in the cancer tissues only (p < 0.05). When normalized to MNSOD expression levels, relative MNSOD enzymatic activity was decreased in cancer tissues, suggesting impairment of MNSOD enzymatic activity in kidney cancer due to modifications. Thus, LC-MS/MS analysis revealed multiple oxidative modifications of MNSOD at different amino acid residues that might mediate the regulation of the superoxide radicals, mitochondrial ROS scavenging and MNSOD activity in kidney cancer. [ABSTRACT FROM AUTHOR]

Renal cell carcinoma (RCC) is resistant to standard radiotherapy. Ubenimex, an aminopeptidase N inhibitor, is widely used as an adjunct therapy after surgery to enhance the function of immunocompetent cells and confer antitumor effects. Our previous study demonstrated that ubenimex induces autophagic cell death in RCC cells. Recently, the molecular mechanism of autophagy induction has been associated with radiosensitivity in RCC cells. In the present study, the ability of ubenimex to enhance RCC cell sensitivity to radiation via the induction of autophagic cell death was determined, and the mechanism of action of this effect was investigated. The 786-O and OS-RC-2 human RCC cell lines were treated with 0.5 mg/ml ubenimex and different doses of irradiation (IR). The cell viability was measured using a colony-formation assay and flow cytometry. Acridine orange (AO)-ethidium bromide (EB) staining was assessed by fluorescence microscopy as an indicator of autophagic cell death. Protein expression was assessed by western blotting. Autophagosomes were evaluated using transmission electron microscopy. RCC cells were used to evaluate the sensitivity to radiation using clonogenic survival and lactate dehydrogenase assays. Furthermore, these parameters were also tested at physiological oxygen levels. The AO-EB staining and flow cytometry of the OS-RC-2 cells indicated that the combined treatment significantly enhanced autophagic cell death compared with ubenimex or IR alone. Therefore, treatment with ubenimex did not significantly alter cell cycle progression but increased cell death when combined with radiation. An Akt agonist could significantly weaken this effect, indicating that ubenimex may act as an Akt inhibitor. Furthermore, the western blot analysis indicated that the combined treatment inhibited the Akt signaling pathway compared with ubenimex treatment or IR alone. Ubenimex may enhance RCC cell sensitivity to radiation by inducing cell autophagy. This induction changes the role of autophagy from protective to lethal in vitro, and this switch is associated with the inhibition of the Akt signaling pathway. [ABSTRACT FROM AUTHOR]

[Objective] The effect of bacteriostat (Qianxing No.1) on open tissue culture of sugarcane was discussed in this paper. [Method] The axillary bud explants of Qiantang No.5 were used as experimental material. Different concentrations of Qianxing No.1 were added in the media to determine the optimal bacteriostatic concentrations of Qianxing No.1 for induction and proliferation culture of sugarcane in the open tissue culture. [Result] The results showed Qianxing No.1 with the concentration of 0.5% could effectively inhibit the medium contamination. Under that bacteriostatic concentration, the surviving rate of explants was up to 80%, and the propagation coefficient was 3.1. [Conclusion] This research would provide a theoretic basis for the simplification of sugarcane tissue culture procedure and the reduction of production costs. [ABSTRACT FROM AUTHOR]

To investigate the relationship between Eg5 expression and prognosis of patients with non-muscle invasive bladder urothelial carcinoma. Eg5 expression was examined by immunohistochemistry in non-muscle invasive urothelial carcinoma specimens (grade: G1, 32 cases; G2, 92 cases; and G3, 39 cases. Stage: pTa, 49 cases and pT1, 114 cases). The correlation between clinicopathological characteristics and Eg5 expression was evaluated. The prognostic significance of Eg5 immunoreactivity was analyzed through survival analysis in 163 non-muscle invasive cases that were treated with transurethral resection and adjuvant intravesical instillations. The expression of Eg5 was significantly associated with tumor grade ( P = 0.006), with a trend towards significant association with stage ( P = 0.057). The 163 patients with non-muscle invasive tumors were regularly followed with the mean of 32.52 (from 6 to 72) months. Univariate analysis showed Eg5 overexpression exhibited a significant unfavorable influence on intravesical recurrence ( P = 0.012) while having only a marginal correlation with disease progression ( P = 0.070). Subsequent Cox hazard multivariate analysis showed that both grade ( P = 0.045) and Eg5 expression ( P = 0.029) were independent predictors for early intravesical recurrence. Overexpression of Eg5 correlates with poor differentiation of bladder cancer, and it represents an independent prognostic factor in predicting early intravesical recurrence in non-muscle invasive bladder carcinoma patients. [ABSTRACT FROM AUTHOR]

Titanium (Ti) with nanoscale structure on the surface exhibits excellent biocompatibility and bone integration. Once implanted, the surgical implantation may lead to bacterial infection and inflammatory reaction, which cause the implant failure. In this work, irregular and nanorod-shaped ZnO nanoparticles were doped into TiO2 nanotubes (TNTs) with inner diameter of about 50 nm by electro-deposition. The antibacterial properties of ZnO incorporated into TiO2 nanotubes (TNTs/ZnO) were evaluated using Staphylococcus aureus (S. aureus). Zn ions released from the nanoparticles and the morphology could work together, improving antibacterial effectiveness up to 99.3% compared with the TNTs. Macrophages were cultured on the samples to determine their respective anti-inflammatory properties. The proliferation and viability of macrophages were evaluated by the CCK-8 method and Live&Dead stain, and the morphology of the cells was observed by scanning electron microscopy. Results indicated that TNTs/ZnO has a significant inhibitory effect on the proliferation and adhesion of macrophages, which could be used to prevent chronic inflammation and control the inflammatory reaction. Besides, the release of Zn ions from the ZnO nanoparticles is a long-term process, which could be beneficial for bone integration. Results demonstrate that ZnO deposited into TNTs improved the antibacterial effectiveness and weakened the inflammatory reaction of titanium-based implants, which is a promising approach to enhance their bioactivity. [ABSTRACT FROM AUTHOR]