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Nucleomodulin BspJ as an effector promotes the colonization of Brucella abortus in the host
Zhongchen Ma,Shuifa Yu,Kejian Cheng,Yuhe Miao,Yimei Xu,Ruirui Hu,Wei Zheng,Jihai Yi,Huan Zhang,Ruirui Li,Zhiqiang Li,Yong Wang,Chuangfu Chen 대한수의학회 2022 Journal of Veterinary Science Vol.23 No.1
Background: Brucella infection induces brucellosis, a zoonotic disease. The intracellular circulation process and virulence of Brucella mainly depend on its type IV secretion system (T4SS) expressing secretory effectors. Secreted protein BspJ is a nucleomodulin of Brucella that invades the host cell nucleus. BspJ mediates host energy synthesis and apoptosis through interaction with proteins. However, the mechanism of BspJ as it affects the intracellular survival of Brucella remains to be clarified. Objectives: To verify the functions of nucleomodulin BspJ in Brucella's intracellular infection cycles. Methods: Constructed Brucella abortus BspJ gene deletion strain (B. abortus ΔBspJ) and complement strain (B. abortus pBspJ) and studied their roles in the proliferation of Brucella both in vivo and in vitro. Results: BspJ gene deletion reduced the survival and intracellular proliferation of Brucella at the replicating Brucella-containing vacuoles (rBCV) stage. Compared with the parent strain, the colonization ability of the bacteria in mice was significantly reduced, causing less inflammatory infiltration and pathological damage. We also found that the knockout of BspJ altered the secretion of cytokines (interleukin [IL]-6, IL-1β, IL-10, tumor necrosis factor-α, interferon-γ) in host cells and in mice to affect the intracellular survival of Brucella. Conclusions: BspJ is extremely important for the circulatory proliferation of Brucella in the host, and it may be involved in a previously unknown mechanism of Brucella's intracellular survival.
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Effect of government R&D subsidies on firms’ innovation in China
Wu Ruirui,Liu Zhiying,Ma Chaoliang,Chen Xiafei 기술경영경제학회 2020 ASIAN JOURNAL OF TECHNOLOGY INNOVATION Vol.28 No.1
This study investigates the effects of R&D subsidies on firms’ innovation using panel data of Chinese listed firms from 2008 to 2013. Through propensity score matching method, we determine that recurrent, high-tech firms are more likely to receive public grants. Moreover, firms affiliated with higher-level governments and located in minimally marketised regions have a higher probability of receiving government financial support. China's state intervention to correct market failure related to firms’ R&D activity is confirmed to be reasonable in an observable time given an instantaneous additionality effect. However, the stimulation effect of R&D subsidies on innovation outputs has not been verified. Results obtained through a continuous matching method show no optimal amount of R&D subsidies for firms in China, but a declining yet a positive marginal effect of treatment has been identified given an increase in the amount of R&D subsidies.
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Wang, Shuaifei,Li, Fangyuan,Qiao, Ruirui,Hu, Xi,Liao, Hongwei,Chen, Lumin,Wu, Jiahe,Wu, Haibin,Zhao, Meng,Liu, Jianan,Chen, Rui,Ma, Xibo,Kim, Dokyoon,Sun, Jihong,Davis, Thomas P.,Chen, Chunying,Tian, American Chemical Society 2018 ACS NANO Vol.12 No.12
<P>Ferroptosis, an iron-based cell-death pathway, has recently attracted great attention owing to its effectiveness in killing cancer cells. Previous investigations focused on the development of iron-based nanomaterials to induce ferroptosis in cancer cells by the up-regulation of reactive oxygen species (ROS) generated by the well-known Fenton reaction. Herein, we report a ferroptosis-inducing agent based on arginine-rich manganese silicate nanobubbles (AMSNs) that possess highly efficient glutathione (GSH) depletion ability and thereby induce ferroptosis by the inactivation of glutathione-dependent peroxidases 4 (GPX4). The AMSNs were synthesized <I>via</I> a one-pot reaction with arginine (Arg) as the surface ligand for tumor homing. Subsequently, a significant tumor suppression effect can be achieved by GSH depletion-induced ferroptosis. Moreover, the degradation of AMSNs during the GSH depletion contributed to <I>T</I><SUB>1</SUB>-weighted magnetic resonance imaging (MRI) enhancement as well as on-demand chemotherapeutic drug release for synergistic cancer therapy. We anticipate that the GSH-depletion-induced ferroptosis strategy by using manganese-based nanomaterials would provide insights in designing nanomedicines for tumor-targeted theranostics.</P> [FIG OMISSION]</BR>
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Ying Zhang,Hengyu Lei,Pengchong Wang,Qinyuan Zhou,Jie Yu,Xue Leng,Ruirui Ma,Danyang Wang,Kai Dong,Jianfeng Xing,Yalin Dong 한국생체재료학회 2023 생체재료학회지 Vol.27 No.00
Background Reactive oxygen species (ROS) overproduction and excessive hypoxia play pivotal roles in the initiation and progression of ulcerative colitis (UC). Synergistic ROS scavenging and generating O2 could be a promising strategy for UC treatment. Methods Ceria nanozymes (PEG-CNPs) are fabricated using a modified reverse micelle method. We investigate hypoxia attenuating and ROS scavenging of PEG-CNPs in intestinal epithelial cells and RAW 264.7 macrophages and their effects on pro-inflammatory macrophages activation. Subsequently, we investigate the biodistribution, pharmacokinetic properties and long-term toxicity of PEG-CNPs in mice. PEG-CNPs are administered intravenously to mice with 2,4,6-trinitrobenzenesulfonic acid-induced colitis to test their colonic tissue targeting and assess their anti-inflammatory activity and mucosal healing properties in UC. Results PEG-CNPs exhibit multi-enzymatic activity that can scavenge ROS and generate O2, promote intestinal epithelial cell healing and inhibit pro-inflammatory macrophage activation, and have good biocompatibility. After intravenous administration of PEG-CNPs to colitis mice, they can enrich at the site of colonic inflammation, and reduce hypoxia-induced factor-1α expression in intestinal epithelial cells by scavenging ROS to generate O2, thus further promoting disrupted intestinal mucosal barrier restoration. Meanwhile, PEG-CNPs can effectively scavenge ROS in impaired colon tissues and relieve colonic macrophage hypoxia to suppress the pro-inflammatory macrophages activation, thereby preventing UC occurrence and development. Conclusion This study has provided a paradigm to utilize metallic nanozymes, and suggests that further materials engineering investigations could yield a facile method based on the pathological characteristics of UC for clinically managing UC.
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