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Experimental study on creep behavior of fly ash concrete filled steel tube circular arches
Wu T. Yan,Bing Han,Jin Q. Zhang,Hui B. Xie,Li Zhu,Zhong J. Xue 국제구조공학회 2018 Steel and Composite Structures, An International J Vol.27 No.2
Fly ash can significantly improve concrete workability and performance, and recycling fly ash in concrete can contribute to a cleaner environment. Since fly ash influences pozzolanic reactions in concrete, mechanical behaviors of concrete containing fly ash differ from traditional concrete. Creep behaviors of fly ash concrete filled steel tube arch were experimentally investigated for 10% and 30% fly ash replacement. The axes of two arches are designed as circular arc with 2.1 m computed span, 0.24 m arch rise, and their cross-sections are all in circular section. Time dependent deflection and strain of loading and mid-span steel tube were measured, and long term deflection of the model arch with 10% fly ash replacement was significantly larger than with 30% replacement. Considering the steel tube strain, compressive zone height, cross section curvature, and internal force borne by the steel tube, the compressive zone height and structural internal forces increased gradually over time due to concrete creep. Increased fly ash content resulted in more significant neutral axis shift. Mechanisms for internal force effects on neutral axis height were analyzed and verified experimentally.
Liu, Fen,Wei, Wen-Qiang,Cormier, Robert T.,Zhang, Shu-Tian,Qiao, You-Lin,Li, Xin-Qing,Zhu, Sheng-Tao,Zhai, Yan-Chun,Peng, Xiao-Xia,Yan, Yu-Xiang,Wu, Li-Juan,He, Dian,He, Yan Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.4
Background: The prostaglandin-endoperoxide synthase 2 (PTGS2) and phospholipase A2 group IIA (PLA2G2A) genes encode enzymes that are involved in arachidonic acid and prostaglandin biosynthesis. Dysregulation of both genes is associated with inflammation and carcinogenesis, including esophageal squamous cell carcinoma (ESCC). We therefore hypothesized that there is an association between single nucleotide polymorphisms (SNPs) in these genes and susceptibility to ESCC. Methods: We performed a gene-wide tag SNP-based association study to examine the association of SNPs in PTGS2 and PLA2G2A with ESCC in 269 patients and 269 healthy controls from Taihangshan Mountain, Henan and Hebei Provinces, the rural area of China which has the highest incidence of esophageal cancer in the world. Thirteen tag SNPs in PLA2G2A and 4 functional SNPs in PTGS2 were selected and genotyped using a high-throughput Mass Array genotyping platform. Results: We found a modest increased risk of ESCC in subjects with the PTGS2 rs12042763 AA genotype (OR=1.23; 95% CI, 1.00-3.04) compared with genotype GG. For PLA2G2A, a decreased risk of ESCC was observed in subjects with the rs11677 CT (OR=0.51, 95%CI, 0.29-0.85) or TT genotype (OR=0.51, 95%CI, 0.17-0.96) or the T carriers (CT+TT) (OR=0.52, 95%CI, 0.31-0.85) when compared with the CC genotype. Also for PLA2G2A, rs2236771 C allele carriers were more frequent in the control group (P=0.02). Subjects with the GC (OR=0.55, 95%CI, 0.33-0.93) or CC genotype (OR=0.38, 95% CI, 0.16-0.94) or the C carriers (GC+CC) (OR=0.52, 95%CI, 0.32-0.85) showed a negative association with ESCC susceptibility. Conclusions: Our results suggest that PTGS2 and PLA2G2A gene polymorphisms may modify the risk of ESCC development.
EVI1 acts as an inducible negative-feedback regulator of NF-κB by inhibiting p65 acetylation.
Xu, Xiangbin,Woo, Chang-Hoon,Steere, Rachel R,Lee, Byung Cheol,Huang, Yuxian,Wu, Jing,Pang, Jinjiang,Lim, Jae Hyang,Xu, Haidong,Zhang, Wenhong,Konduru, Anuhya S,Yan, Chen,Cheeseman, Michael T,Brown, S Williams Wilkins 2012 JOURNAL OF IMMUNOLOGY Vol.188 No.12
<P>Inflammation is a hallmark of many important human diseases. Appropriate inflammation is critical for host defense; however, an overactive response is detrimental to the host. Thus, inflammation must be tightly regulated. The molecular mechanisms underlying the tight regulation of inflammation remain largely unknown. Ecotropic viral integration site 1 (EVI1), a proto-oncogene and zinc finger transcription factor, plays important roles in normal development and leukemogenesis. However, its role in regulating NF-κB-dependent inflammation remains unknown. In this article, we show that EVI1 negatively regulates nontypeable Haemophilus influenzae- and TNF-α-induced NF-κB-dependent inflammation in vitro and in vivo. EVI1 directly binds to the NF-κB p65 subunit and inhibits its acetylation at lysine 310, thereby inhibiting its DNA-binding activity. Moreover, expression of EVI1 itself is induced by nontypeable Haemophilus influenzae and TNF-α in an NF-κB-dependent manner, thereby unveiling a novel inducible negative feedback loop to tightly control NF-κB-dependent inflammation. Thus, our study provides important insights into the novel role for EVI1 in negatively regulating NF-κB-dependent inflammation, and it may also shed light on the future development of novel anti-inflammatory strategies.</P>