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Xiangwei XIE(Xiangwei XIE),Jie PAN(Jie PAN),Jinjing ZHAO(Jinjing ZHAO),Miao SU(Miao SU) 한국유통과학회 2023 유통과학연구 Vol.21 No.8
Purpose: To examine the economic effects of logistics under the influence of policies. Research design, data and methodology: This study is the first to use the panel data of 31 provinces and municipalities in China from 2012 to 2021, and use the OLS and DID models to evaluate whether the New Western Land-Sea Corridor (NWLSC) has promoted the economic development of the regions along the corridor. Results: The NWLSC has stimulated local economic growth by promoting the development of transportation, postal, and telecommunications industries along the corridor. Further, considering the locational differences of the regions along the NWLSC, we examined the differences in economic effects between regions along the Yangtze River and those not along the Yangtze River under the background of NWLSC implementation. We found that waterway and airway transport located along the NWLSC and in the Yangtze River Economic Belt (YREB) region can significantly promote economic growth. However, for regions located along the NWLSC but not in the YREB region, the impact of roadway, railway, and airway transport in these regions on economic growth is more significant. Conclusions: This study has important reference value on how to use logistics to promote the economic and cross-border commerce development of landlocked countries or regions.
miRNA-183 Suppresses Apoptosis and Promotes Proliferation in Esophageal Cancer by Targeting PDCD4
Miao Yang,Ran Liu,Xiajun Li,Juan Liao,Yuepu Pu,Enchun Pan,Lihong Yin,Yi Wang 한국분자세포생물학회 2014 Molecules and cells Vol.37 No.12
In our previous study, miRNA-183, a miRNA in the miR-96-182-183 cluster, was significantly over-expressed in esophageal squamous cell carcinoma (ESCC). In the present study, we explored the oncogenic roles of miR-183 in ESCC by gain and loss of function analysis in an esophageal cancer cell line (EC9706). Genome-wide mRNA microarray was applied to determine the genes that were regulated directly or indirectly by miR-183. 3UTR luciferase reporter assay, RT-PCR, and Western blot were conducted to verify the target gene of miR-183. Cell culture results showed that miR-183 inhibited apoptosis (p < 0.05), enhanced cell proliferation (p < 0.05), and accelerated G1/S transition (p < 0.05). Moreo-ver, the inhibitory effect of miR-183 on apoptosis was rescued when miR-183 was suppressed via miR-183 inhibitor (p < 0.05). Western blot analysis showed that the expression of programmed cell death 4 (PDCD4), which was predicted as the target gene of miR-183 by microarray profiling and bioinformatics predictions, decreased when miR-183 was over-expressed. The 3'UTR luciferase reporter assay confirmed that miR-183 directly regulated PDCD4 by binding to sequences in the 3'UTR of PDCD4. Pearson correlation analysis fur-ther confirmed the significant negative correlation between miR-183 and PDCD4 in both cell lines and in ESCC patients. Our data suggest that miR-183 might play an oncogenic role in ESCC by regulating PDCD4 expression.
Pan, Yan,Zhao, Lei,Chen, Xing-Miao,Gu, Yong,Shen, Jian-Gang,Liu, Lu-Ming Asian Pacific Journal of Cancer Prevention 2013 Asian Pacific journal of cancer prevention Vol.14 No.10
The potential correlation of X-ray repair cross-complementing group 1 (XRCC1) Arg399Gln polymorphism with hepatocellular carcinoma (HCC) susceptibility is ambiguous. Taking account of inconsistent results of previous meta-analyses and new emerging literatures, we conducted a meta-analysis covering 15 case-control datasets to evaluate the relationship. Relevant studies from Medline, Embase and CNKI were retrieved. A fixed-effect model or a random-effect model, depending on between-study heterogeneity, were applied to estimate the association between XRCC1 polymorphism Arg399Gln and HCC risk with the results presented as odds ratios (ORs) and 95% confidence intervals (95% CIs). In accordance with Hardy-Weinberg equilibrium, 15 studies with data for 6,556 individuals were enrolled in this systematic review. For overall HCC,thr XRCC1 polymorphism Arg399Gln was significantly associated with HCC susceptibility in a homozygote model as well as in a dominant model (G/G vs. A/A, OR=1.253, p=0.028; G/G+A/G vs. A/A, OR= 1.281, p=0.047, respectively), but not in a heterozygote model (A/G vs. A/A, OR=1.271, p=0.066) or a recessive model (G/G vs. A/G + A/A, OR= 1.049, p=0.542). Similar results were also observed on stratification analysis by ethnicity (A/G vs. A/A, OR=1.357, p=0.025; G/G vs. A/A, OR=1.310, p=0.011; G/G+A/G vs. A/A, OR= 1.371, p=0.013). However, no potential contribution of XRCC1 Arg399Gln polymorphism to HCC susceptibility in HBV/HCV subgroups was identified. No publication bias was found in this study. In conclusion, the XRCC1 Arg399Gln polymorphism contributes to HCC susceptibility. Due to the lack of studies in Western countries, further large-sample and rigorous studies are needed to validate the findings.
Miao Su,Yiyun Yang,Rensheng Pan 국제구조공학회 2021 Structural Engineering and Mechanics, An Int'l Jou Vol.78 No.2
Track-bridge interaction has become an essential part in the design of bridges and rails in terms of modern railways. As a unique ballastless slab track, the longitudinal continuous slab track (LCST) or referred to as the China railway track system Type-II (CRTS II) slab track, demonstrates a complex force mechanism. Therefore, a comprehensive track-bridge interaction study between multi-span simply supported beam bridges and the LCST is presented in this work. In specific, we have developed an integrated finite element model to investigate the overall interaction effects of the LCST-bridge system subjected to the actions of temperature changes, traffic loads, and braking forces. In that place, the deformation patterns of the track and bridge, and the distributions of longitudinal forces and the interfacial shear stress are studied. Our results show that the additional rail stress has been reduced under various loads and the rail’s deformation has become much smoother after the transition of the two continuous structural layers of the LCST. However, the influence of the temperature difference of bridges is significant and cannot be ignored as this action can bend the bridge like the traffic load. The uniform temperature change causes the tensile stress of the concrete track structure and further induce cracks in them. Additionally, the influences of the friction coefficient of the sliding layer and the interfacial bond characteristics on the LCST’s performance are discussed. The systematic study presented in this work may have some potential impacts on the understanding of the overall mechanical behavior of the LCSTbridge system.
miRNA-183 Suppresses Apoptosis and Promotes Proliferation in Esophageal Cancer by Targeting PDCD4
Yang, Miao,Liu, Ran,Li, Xiajun,Liao, Juan,Pu, Yuepu,Pan, Enchun,Yin, Lihong,Wang, Yi Korean Society for Molecular and Cellular Biology 2014 Molecules and cells Vol.37 No.12
In our previous study, miRNA-183, a miRNA in the miR-96-182-183 cluster, was significantly over-expressed in esophageal squamous cell carcinoma (ESCC). In the present study, we explored the oncogenic roles of miR-183 in ESCC by gain and loss of function analysis in an esophageal cancer cell line (EC9706). Genome-wide mRNA micro-array was applied to determine the genes that were regulated directly or indirectly by miR-183. 3'UTR luciferase reporter assay, RT-PCR, and Western blot were conducted to verify the target gene of miR-183. Cell culture results showed that miR-183 inhibited apoptosis (p < 0.05), enhanced cell proliferation (p < 0.05), and accelerated G1/S transition (p < 0.05). Moreover, the inhibitory effect of miR-183 on apoptosis was rescued when miR-183 was suppressed via miR-183 inhibitor (p < 0.05). Western blot analysis showed that the expression of programmed cell death 4 (PDCD4), which was predicted as the target gene of miR-183 by microarray profiling and bioinformatics predictions, decreased when miR-183 was over-expressed. The 3'UTR luciferase reporter assay confirmed that miR-183 directly regulated PDCD4 by binding to sequences in the 3'UTR of PDCD4. Pearson correlation analysis further confirmed the significant negative correlation between miR-183 and PDCD4 in both cell lines and in ESCC patients. Our data suggest that miR-183 might play an oncogenic role in ESCC by regulating PDCD4 expression.
Ke, Pan,Wu, Zhong-De,Wen, Hua-Song,Ying, Miao-Xiong,Long, Huo-Cheng,Qing, Liu-Guo Asian Pacific Journal of Cancer Prevention 2013 Asian Pacific journal of cancer prevention Vol.14 No.4
Matrix metalloproteinases (MMPs) degrade various components of the extracellular matrix and functional polymorphisms in encoding genes may contribute to genetic susceptibility to many cancers. Up to now, associations between MMP-7 (-181A>G) and digestive system cancer risk have remained inconclusive. To better understand the role of the MMP-7 (-181A>G) genotype in digestive cancer development, we conducted this comprehensive meta-analysis encompassing 3,518 cases and 4,596 controls. Overall, the MMP-7 (-181A>G) polymorphism was associated with higher digestive system cancer risk on homozygote comparison (GG vs. AA, OR=1.21, 95% CI = 1.12-1.60) and in a dominant model (GG/GA vs. AA, OR=1.16, 95% CI =1.03-1.46). On subgroup analysis, this polymorphism was significantly linked to higher risks for gastric cancer (GG vs. AA, OR=1.22, 95% CI = 1.02-1.46; GA vs. AA, OR=1.82, 95% CI =1.16-2.87; GG/GA vs. AA, OR=1.13, 95% CI =1.01-1.27; GG vs. GA/AA, OR= 1.25, 95% CI = 1.06-2.39. We also observed increased susceptibility to colorectal cancer and esophageal SCC in both homozygote (OR = 1.13, 95% CI = 1.06-1.26) and heterozygote comparisons (OR = 1.45, 95% CI = 1.11-1.91). In the stratified analysis by controls, significant effects were only observed in population-based studies (GA vs. AA, OR=1.16, 95% CI=1.08-1.50; GA/AA vs. GG, OR=1.10, 95% CI=1.01-1.72). According to the source of ethnicity, a significantly increased risk was found among Asian populations in the homozygote model (GG vs. AA, OR=1.40, 95% CI=1.12-1.69), heterozygote model (GA vs. AA, OR=1.26, 95% CI=1.02-1.51), and dominant model (GG/GA vs. AA, OR=1.18, 95% CI=1.08-1.55). Our findings suggest that the MMP-7 (-181A>G) polymorphism may be a risk factor for digestive system cancer, especially among Asian populations.
Gui Miao,Guo Junliang,Kong Huanjun,Wu Pan,Shan Jianqiang,Peng Yujiao 한국원자력학회 2023 Nuclear Engineering and Technology Vol.55 No.9
A phenomenological study on CHF in a bilaterally heated annulus with equal heat flux on both sides was experimentally performed. The working fluid of the present test was R-134a. Variation characteristics of CHF and transition of CHF occurrence location were investigated under different pressure, mass flux and quality conditions. With the increase of critical thermodynamic quality, it was found that CHF first occurred on the outer surface of the annulus, then simultaneously occurred on both sides, and finally occurred on the inner surface at relatively high critical quality. After the CHF location transitioned to the inner rod, the sharp fall of CHF in the limiting critical quality region was observed. The critical quality corresponding to the CHF location transition decreased with the increase of mass flux and pressure. Besides, CHF in tube, internally heated, externally heated and bilaterally heated annuli were compared under the same hydraulic diameter conditions. The present study is conducive to improving the understanding of complicated CHF mechanism in bilaterally heated annulus, enriching the experimental database, and providing evidence for developing accurate CHF mechanism model for annuli.
Sitagliptin attenuates endothelial dysfunction independent of its blood glucose controlling effect
Xin-Miao Chang,Fei Xiao,Qi Pan,Xiao-Xia Wang,Li-Xin Guo 대한생리학회-대한약리학회 2021 The Korean Journal of Physiology & Pharmacology Vol.25 No.5
Although the contributions of sitagliptin to endothelial dysfunction in diabetes mellitus were previously reported, the mechanisms still undefined. Autophagy plays an important role in the development of diabetes mellitus, but its role in diabetic macrovascular complications is unclear. This study aims to observe the effect of sitagliptin on macrovascular endothelium in diabetes and explore the role of autophagy in this process. Diabetic rats were induced through administration of high-fat diet and intraperitoneal injection of streptozotocin. Then diabetic rats were treated with or without sitagliptin for 12 weeks. Endothelial damage and autophagy were measured. Human umbilical vein endothelial cells were cultured either in normal glucose or in high glucose medium and intervened with different concentrations of sitagliptin. Rapamycin was used to induce autophagy. Cell viability, apoptosis and autophagy were detected. The expressions of proteins in c-Jun N-terminal kinase (JNK)-Bcl-2-Beclin-1 pathway were measured. Sitagliptin attenuated injuries of endothelium in vivo and in vitro. The expression of microtubuleassociated protein 1 light chain 3 II (LC3II) and beclin-1 were increased in aortas of diabetic rats and cells cultured with high-glucose, while sitagliptin inhibited the over-expression of LC3II and beclin-1. In vitro pre-treatment with sitagliptin decreased rapamycin-induced autophagy. However, after pretreatment with rapamycin, the protective effect of sitagliptin on endothelial cells was abolished. Further studies revealed sitagliptin increased the expression of Bcl-2, while inhibited the expression of JNK in vivo. Sitagliptin attenuates injuries of vascular endothelial cells caused by high glucose through inhibiting over-activated autophagy. JNK-Bcl-2-Beclin-1 pathway may be involved in this process.
Luqing Pan,Jiaying Li,Jingjing Miao 한국유전학회 2016 Genes & Genomics Vol.38 No.3
Chlamys farreri (C. farreri), as an economic species of marine bivalves, can tolerate manifold anthropogenic stressors including persistent organic pollutants (POPs) stress. A systematic study of transcriptome after POPs exposure may provide insights into the mechanism of acquired pollution tolerance. In this study, we compared C. farreri transcriptome by reanalyzing DGE (digital gene expression) data from previous study. Our results revealed a toxicant-dependent pattern of global transcriptional responses, with 108, 126 and 138 DEGs regulated by BaP, TBBPA and PAHs cocktail (mixed by benzo(a)pyrene, benz(a)anthracene, benzo(b)fluoranthene and chrysene with the ratio of 5:3:1:1) exposure, respectively. Among these DEGs, 219 were commonly regulated by all pollutants, whereas the minority of differences were conditionspecific. In addition, we performed the first hierarchical cluster analysis of the common transcripts throughout three types of contaminants stress ulteriorly, leading to new discoveries of genes’ association information with dynamical gene expression data of C. farreri, which goes beyond the focus on individuals. It revealed a cascade of gene expression patterns in the response of C. farreri to different environmental stresses and may be beneficial for further analysis of novel environmental metrics.