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Anodic aluminum oxide (AAO) thin films were fabricated in phosphoric acid electrolyte solution via one-step electrochemical anodic oxidation of an Al sheet. The films displayed minimally saturated rainbow rings of structural colors, and pores with depths that decreased symmetrically outward from the center of the films. AAO thin films embedded with Co nanodots were fabricated using the one-step ac electrodeposition method. The composite films showed highly saturated rainbow rings of structural colors, which is due to the Co nanodots efficiently screening reflected light from the Al substrate. Moreover, magnetic Co nanodots were found to tune the physical properties of AAO thin film as a new degree of freedom. After determining that Co@AAO composite films possess magnetism and highly saturated rainbow rings of structural colors, their magnetic and optical properties were studied based on modification of the oxidation voltage and deposition time required to prepare the films.

AMP-activated protein kinase α1 (AMPK α1) is involved in the tumorigenesis of various cancer types. However, the role of AMPK α1 in non-small cell lung cancer (NSCLC) remains unclear. In the present study, 99 NSCLC tumor tissues and paired normal tissues were obtained. The expression levels of AMPK α1 were significantly upregulated in NSCLC tumor tissues compared with those in adjacent non-tumor lung tissues. The patients were further divided into two groups according to their expression levels of AMPK α1 in tumor tissues. The results outlined that overexpression of AMPK α1 was associated with poor prognosis. In addition, vascular endothelial growth factor (VEGF) expression levels were associated with malignant progression in patients with NSCLC. Patients with NSCLC that overexpressed AMPK α1 and VEGF had the worst outcomes. Moreover, AMPK α1 may positively regulate VEGF expression. These results suggest that AMPK α1 serves a carcinogenic role at least in part through the regulation of VEGF expression, and thus represents a potential treatment target in patients with NSCLC.

Malignant gliomas are the most common and deadly primary brain tumors in adults and the high prolifera- tive ability of these cells is one of the most important causes of the poor prognosis of this cancer. Suppressing the proliferation of malignant gliomas cells by altering effector molecules can significantly improve the prognosis of a patient. microRNAs (miRNAs) are small non‑coding RNA molecules ~22 nucleo- tides in length that are able to function as oncogenes or tumor suppressors in human cancer. In the present study, it was demon- strated that the expression level of miRNA‑218 (miR‑218) is markedly downregulated in glioma cell lines and human primary glioma tissues. Upregulation of miR‑218 in glioma U87 cells dramatically inhibited the proliferation by inducing G1-S checkpoint arrest. Furthermore, it was demonstrated that ectopically expressing miR‑218 in glioma U87 cells results in the downregulation of the expression of cyclin depen- dent kinase (CDK)6 and cyclin D1 and upregulation of the expression of p21 Cip1/Waf1 . In addition, it was identified that miR‑218 inactivated the CDK6/cyclin D1/p21 Cip1/Waf1 pathway by downregulating CDK6 expression through the direct targeting of the 3'‑untranslated region of CDK6. The present results suggest that miR‑218 plays an important role in the prevention of the proliferation of glioma cells, and the present study also revealed a novel mechanism for miRNA‑mediated direct suppression of the CDK6/cyclin D1/p21 Cip1/Waf1 pathway in glioma cells.

Malignant gliomas are the most common and deadly primary brain tumors in adults and the high proliferative ability of these cells is one of the most important causes of the poor prognosis of this cancer. Suppressing the proliferation of malignant gliomas cells by altering effector molecules can significantly improve the prognosis of a patient. microRNAs (miRNAs) are small non-coding RNA molecules ∼22 nucleotides in length that are able to function as oncogenes or tumor suppressors in human cancer. In the present study, it was demonstrated that the expression level of miRNA-218 (miR-218) is markedly downregulated in glioma cell lines and human primary glioma tissues. Upregulation of miR-218 in glioma U87 cells dramatically inhibited the proliferation by inducing G1-S checkpoint arrest. Furthermore, it was demonstrated that ectopically expressing miR-218 in glioma U87 cells results in the downregulation of the expression of cyclin dependent kinase (CDK)6 and cyclin D1 and upregulation of the expression of p21Cip1/Waf1. In addition, it was identified that miR-218 inactivated the CDK6/cyclin D1/p21Cip1/Waf1 pathway by downregulating CDK6 expression through the direct targeting of the 3′-untranslated region of CDK6. The present results suggest that miR-218 plays an important role in the prevention of the proliferation of glioma cells, and the present study also revealed a novel mechanism for miRNA-mediated direct suppression of the CDK6/cyclin D1/p21Cip1/Waf1 pathway in glioma cells.

采用溶胶–凝胶法在多孔氧化铝模板的纳米孔洞中成功地合成了 x NiFe 2 O 4 -(1– x )BiFeO 3 (NFO-BFO)复合纳米管阵列。扫描电镜照片显示纳米管的外径约为70 nm, 内径约为50 nm, 长度约为80 μm。X射线衍射图谱显示, 通过自组装形成了钙钛矿结构的铁电相BFO和尖晶石结构的铁磁相NFO。磁性和铁电性的测试结果表明, 复合纳米管具有明显的室温铁磁性和电极化性能, 且易磁化方向沿着纳米管的长轴方向。随着NFO复合比例的增加, 纳米管阵列的磁性和电极化性能逐渐增强。NFO对复合纳米管阵列铁磁贡献的计算结果表明, NFO-BFO纳米管阵列中存在着磁电耦合效应。

Porous anodic alumina thin films with rainbow rings were fabricated in oxalic acid electrolyte by one-step electrochemical oxidation of Al sheet. The hole depth and aperture diminish symmetrically outward from the center of the films. The relationship between the density of rainbow rings to the oxidation voltage and the time in oxalic acid solution are discussed. Theoretical study on the formation mechanism of porous anodic alumina thin films with rainbow rings indicates that the effect of carbon rod is similar to carbon dot electrode in the process of anode electrochemical reaction. Result of the theoretical study is consistent with the experimental phenomenology.