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Yu, ChengPeng,Zhou, XiaoYan,Fu, Qiang,Peng, QingHua,Oh, Ki-Wan,Hu, ZhenZhen Frontiers Media S.A. 2017 Frontiers in cellular neuroscience Vol.11 No.-
<P>Cocaine- and amphetamine-regulated transcript (CART) peptides are neuropeptides that are expressed in brain regions associated with reward, such as the nucleus accumbens (NAc), and play a role in cocaine reward. Injection of CART into the NAc can inhibit the behavioral effects of cocaine, and injecting CART into the ventral tegmental area (VTA) reduces cocaine-seeking behavior. However, the exact mechanism of these effects is not clear. Recent research has demonstrated that Ca<SUP>2+</SUP>/calmodulin-dependent protein kinase II (CaMKII) and inhibitory G-protein coupled receptor (GPCR) signaling are involved in the mechanism of the effect of CART on cocaine reward. Hence, we review the role of CaMKII and inhibitory GPCR signaling in the effect of CART on cocaine reward and provide a new insight into the mechanism of that effect. In this article, we will first review the biological function of CART and discuss the role of CART in cocaine reward. Then, we will focus on the role of CaMKII and inhibitory GPCR signaling in cocaine reward. Furthermore, we will discuss how CaMKII and inhibitory GPCR signaling are involved in the mechanistic action of CART in cocaine reward. Finally, we will provide our opinions regarding the future directions of research on the role of CaMKII and inhibitory GPCR signaling in the effect of CART on cocaine reward.</P>
Liu Qi,Yang Jun,Ahmed Waqar,Wan Xiaoyan,Wei Lanfang,Ji Guanghai 한국미생물학회 2022 The journal of microbiology Vol.60 No.5
Bacterial leaf streak caused by Xanthomonas oryzae pv. oryzicola (Xoc) is one of the most destructive diseases affecting rice production worldwide. In this study, we extracted and purified phenazine substances from the secondary metabolites of Lysobacter antibioticus 13-6. The bacteriostatic mechanism of phenazine substances against Xoc was investigated through physiological response and transcriptomic analysis. Results showed that phenazine substances affects the cell membrane permeability of Xoc, which causes cell swelling and deformation, blockage of flagellum synthesis, and imbalance of intracellular environment. The changes in intracellular environment affect the physiological and metabolic functions of Xoc, which reduces the formation of pathogenic factors and pathogenicity. Through transcriptomic analysis, we found that among differentially expressed genes, the expression of 595 genes was induced significantly (275 up-regulated and 320 down-regulated). In addition, we observed that phenazine substances affects three main functions of Xoc, i.e., transmembrane transporter activity, DNA-mediated transposition, and structural molecular activity. Phenazine substances also inhibits the potassium ion transport system that reduces Xoc resistance and induces the phosphate ion transport system to maintain the stability of the internal environment. Finally, we conclude that phenazine substances could retard cell growth and reduce the pathogenicity of Xoc by affecting cell structure and physiological metabolism. Altogether, our study highlights latest insights into the antibacterial mechanism of phenazine substances against Xoc and provides basic guidance to manage the incidence of bacterial leaf streak of rice.
Family History of Cancer and Head and Neck Cancer Risk in a Chinese Population
Huang, Yu-Hui Jenny,Lee, Yuan-Chin Amy,Li, Qian,Chen, Chien-Jen,Hsu, Wan-Lun,Lou, Pen-Jen,Zhu, Cairong,Pan, Jian,Shen, Hongbing,Ma, Hongxia,Cai, Lin,He, Baochang,Wang, Yu,Zhou, Xiaoyan,Ji, Qinghai,Zho Asian Pacific Journal of Cancer Prevention 2015 Asian Pacific journal of cancer prevention Vol.16 No.17
Background: The aim of this study was to investigate whether family history of cancer is associated with head and neck cancer risk in a Chinese population. Materials and Methods: This case-control study included 921 cases and 806 controls. Recruitment was from December 2010 to January 2015 in eight centers in East Asia. Controls were matched to cases with reference to sex, 5-year age group, ethnicity, and residence area at each of the centers. Results: We observed an increased risk of head and neck cancer due to first degree family history of head and neck cancer, but after adjustment for tobacco smoking, alcohol drinking and betel quid chewing the association was no longer apparent. The adjusted OR were 1.10 (95% CI=0.80-1.50) for family history of tobacco-related cancer and 0.96 (95%CI=0.75-1.24) for family history of any cancer with adjustment for tobacco, betel quid and alcohol habits. The ORs for having a first-degree relative with HNC were higher in all tobacco/alcohol subgroups. Conclusions: We did not observe a strong association between family history of head and neck cancer and head and neck cancer risk after taking into account lifestyle factors. Our study suggests that an increased risk due to family history of head and neck cancer may be due to shared risk factors. Further studies may be needed to assess the lifestyle factors of the relatives.