军事飞行人员疲劳与社会支持及特质焦虑的关系研究

目的探讨特质焦虑与社会支持对疲劳的影响以及特质焦虑的中介作用,为维护军事飞行人员心理健康提供数据支持。方法按照随机数字表法抽取100名健康疗养的军事飞行人员,采用疲劳量表-14(Fatigue Scale-14,FS-14)、特质焦虑量表(Trait Anxiety Inventory,T-AI)及领悟社会支持量表(Perceived Social Support Scale,PSSS)进行测评,分析特质焦虑与社会支持对疲劳的影响。结果不同年龄、军龄、飞行时间、军衔等级、婚姻状态、受教育程度及是否独生子女对疲劳的影响差异均无统计学意义(P值均>0.05)。疲劳与特质焦虑呈正相关(r=0.412、0.311,P值均<0.001),与社会支持呈负相关(r=-0.247、-0.236、-0.226、-0.314、-0.337、-0.235,P=0.013、0.018、0.024、0.001、0.001、0.019);特质焦虑与社会支持呈负相关(r=-0.345、-0.350、-0.325,P<0.001、<0.001、P=0.001)。特质焦虑不仅对疲劳有直接路径影响效应(β=0.423、0.246,P<0.001、P=0.012),而且还作为社会支持的多重中介对疲劳有间接路径影响效应(β=-0.143、-0.088,P=0.026、0.037)。结论特质焦虑与社会支持共同影响军事飞行人员疲劳,且特质焦虑在这种影响关系中起多重中介作用。

Facile fabrication of micro-grooves based photonic crystals towards anisotropic angle-independent structural colors and polarized multiple reflections

In nature,many living organisms exhibit low-angle-dependent or even angle-independent structural colors for wide viewing angle,such as the blue skin of mandrill,feather of blue bird and shell of longhorn beetle,etc.To mimic these structural colors,based on periodic semicircular micro-grooved(PSMG) substrate,silica colloidal photonic crystals provide anisotropic angle-independent structural colors.The PSMG photonic crystals were fabricated by self-assembling monodispersed silica nanoparticles on a micro-grooved template,which can be easily prepared in large scale by a hot embossing method,and no additional materials are needed in the whole preparation process.The PSMG photonic crystals exhibit identical structural colors around the groove axis,whereas it is angle-dependent along the groove axis.In addition,this PSMG surface of photonic crystal also leads to color separation effect and monocolor polarization conversion.This system provides a facile and scalable means to prepare anisotropically angleindependent colloidal photonic crystal,which is considered important in applications in the field of anti-counterfeiting or the manufacture of monochromatic light reflector with wide viewing angles and other novel optical devices.

Mex3a promotes oncogenesis through the RAP1/MAPK signaling pathway in colorectal cancer and is inhibited by hsa-miR-6887-3p

Background:Although Mex3 RNA-binding family member A(Mex3a)has demonstrated an important role in multiple cancers,its role and regulatory mechanism in CRC is unclear.In this study,we aimed to investigate the role and clinical significance of Mex3a in CRC and to explore its underlying mechanism.Methods:Western blotting and quantitative real-time polymerase chain reaction(qRT-PCR)were performed to detect the expression levels of genes.5-Ethynyl-2’-deoxyuridine(EDU)and transwell assays were utilized to examine CRC cell proliferation and metastatic ability.The R software was used to do hierarchical clustering analysis and Kyoto Encyclopedia of Genes and Genomes(KEGG)pathway analysis.Overexpression and rescue experiments which included U0126,a specific mitogen activated protein kinase kinase/extracellular regulated protein kinase(MEK/ERK)inhibitor,and PX-478,a hypoxia-inducible factor 1 subunit alpha(HIF-1α)inhibitor,were used to study the molecularmechanisms of Mex3a in CRC cells.Co-immunoprecipitation(Co-IP)assay was performed to detect the interaction between two proteins.Bioinformatics analysis including available public database and Starbase software(starbase.sysu.edu.cn)were used to evaluate the expression and prognostic significance of genes.TargetScan(www.targetscan.org)and the miRDB(mirdb.org)website were used to predict the combination site between microRNA and target mRNA.BALB/c nude micewere used to study the function of Mex3a and hsa-miR-6887-3p in vivo.Results:Clinicopathological and immunohistochemical(IHC)studies of 101 CRC tissues and 79 normal tissues demonstrated that Mex3a was a significant prognostic factor for overall survival(OS)in CRC patients.Mex3a knockdown substantially inhibited the migration,invasion,and proliferation of CRC cells.Transcriptome analysis and mechanism verification showed that Mex3a regulated the RAP1 GTPase activating protein(RAP1GAP)/MEK/ERK/HIF-1αpathway.Furthermore,RAP1GAP was identified to interact with Mex3a in Co-IP experiments.Bioinformatics and dual-luciferase reporter experiments revealed that hsa-miR-6887-3p could bind to the 3’-untranslated regions(3’-UTR)of the Mex3amRNA.hsa-miR-6887-3p downregulated Mex3a expression and inhibited the tumorigenesis of CRC both in vitro and in vivo.Conclusions:Our study demonstrated that the hsa-miR-6887-3p/Mex3a/RAP1GAP signaling axis was a key regulator of CRC and Mex3a has the potential to be a new diagnostic marker and treatment target for CRC.