关键词： inulin   intestinal inflammation   microbiota  

摘要： Background: Lack of dietary fiber has been suggested to increase the risk of developing various chronic inflammatory diseases, whereas supplementation of diets with fiber might offer an array of health-promoting benefits. Consistent with this theme, we recently reported that in mice, compositionally defined diets that are made with purified ingredients and lack fermentable fiber promote low-grade inflammation and metabolic syndrome, both of which could be ameliorated by supplementation of such diets with the fermentable fiber inulin. Methods: Herein, we examined if, relative to a grain-based mouse diet (chow), compositionally defined diet consumption would impact development of intestinal inflammation induced by dextran sulfate sodium (DSS) and moreover, whether DSS-induced colitis might also be attenuated by diets supplemented with inulin. Results: Analogous to their promotion of low-grade inflammation, compositionally defined diet of high-and low-fat content with cellulose increased the severity of DSS-induced colitis relative to chow. However, in contrast to the case of low-grade inflammation, addition of inulin, but not the insoluble fiber cellulose, further exacerbated the severity of colitis and its associated clinical manifestations (weight loss and bleeding) in both low-and high-fat diets. Conclusions: While inulin, and perhaps other fermentable fibers, can ameliorate low-grade inflammation and associated metabolic disease, it also has the potential to exacerbate disease severity in response to inducers of acute colitis.

关键词： Predictive maintenance   Internet of Things   radio-frequency identification   remote maintenance   e-maintenance   Wireless Network Systems   reliability   availability   quality  

摘要： This study covers new trends and techniques in the field of predictive maintenance, which has been superseding traditional management policies, at least in part. It also presents suggestions for how to implement a predictive maintenance programme in a factory/premise and so on. Predictive maintenance primarily involves foreseeing breakdown of the system to be maintained by detecting early signs of failure in order to make maintenance work more proactive. In addition to the aim of acting before failure, it also aims to attend to any fault, even if there is no immediate danger of failure, to ensure smooth operation and reduce energy consumption. Predictive maintenance has been adopted by various sectors in manufacturing and service industries in order to improve reliability, safety, availability, efficiency and quality as well as to protect the environment. It also has created a separate sector, which specializes in developing predictive maintenance instruments, offering dedicated predictive maintenance solutions and training predictive maintenance experts. Predictive maintenance techniques are closely associated with sensor technologies but for efficient predictive maintenance applications, a comprehensive approach, which integrates sensing with subsequent maintenance activities, is needed to be adapted in accordance with the needs of the particular organization. Recent advances in information, communication and computer technologies, such as Internet of Things and radio-frequency identifications, have been enabling predictive maintenance applications to be more efficient, applicable, affordable, and consequently more common and available for all sorts of industries. Researches on remote maintenance and e-maintenance have been supporting predictive maintenance activities especially in unsafe working environments and scattered locations.

关键词： INTESTINAL BARRIER FUNCTION   INFLAMMATORY MECHANISMS   INFLAMMATORY BOWEL DISEASE   REACTIVE OXYGEN SPECIES   IMMUNE RESPONSE  

摘要： Objective Western lifestyle and diet are major environmental factors playing a role in the development of IBD. Titanium dioxide (TiO2) nanoparticles are widely used as food additives or in pharmaceutical formulations and are consumed by millions of people on a daily basis. We investigated the effects of TiO2 in the development of colitis and the role of the nucleotide-binding oligomerisation domain receptor, pyrin domain containing (NLRP) 3 inflammasome. Design Wild-type and NLRP3-deficient mice with dextran sodium sulfate-induced colitis were orally administered with TiO2 nanoparticles. The proinflammatory effects of TiO2 particles in cultured human intestinal epithelial cells (IECs) and macrophages were also studied, as well as the ability of TiO2 crystals to traverse IEC monolayers and accumulate in the blood of patients with IBD using inductively coupled plasma mass spectrometry. Results Oral administration of TiO2 nanoparticles worsened acute colitis through a mechanism involving the NLRP3 inflammasome. Importantly, crystals were found to accumulate in spleen of TiO2-administered mice. In vitro, TiO2 particles were taken up by IECs and macrophages and triggered NLRP3-ASC-caspase-1 assembly, caspase-1 cleavage and the release of NLRP3-associated interleukin (IL)-1 beta and IL-18. TiO2 also induced reactive oxygen species generation and increased epithelial permeability in IEC monolayers. Increased levels of titanium were found in blood of patients with UC having active disease. Conclusion These findings indicate that individuals with a defective intestinal barrier function and preexisting inflammatory condition, such as IBD, might be negatively impacted by the use of TiO2 nanoparticles.

关键词： CD4   NKG2D   colitis   NK1   1   regulatory  

摘要： CD4(+) NKG2D(+) T cells are associated with tumour, infection and autoimmune diseases. Some CD4(+) NKG2D(+) T cells secrete IFN- and TNF- to promote inflammation, but others produce TGF- and FasL to facilitate tumour evasion. Here, murine CD4(+) NKG2D(+) T cells were further classified into NK1.1(-) CD4(+) NKG2D(+) and NK1.1(+) CD4(+) NKG2D(+) subpopulations. The frequency of NK1.1(-) CD4(+) NKG2D(+) cells decreased in inflamed colons, whereas more NK1.1(+) CD4(+) NKG2D(+) cells infiltrated into colons of mice with DSS-induced colitis. NK1.1(-) CD4(+) NKG2D(+) cells expressed TGF- and FasL without secreting IFN-, IL-21 and IL-17 and displayed no cytotoxicity. The adoptive transfer of NK1.1(-) CD4(+) NKG2D(+) cells suppressed DSS-induced colitis largely dependent on TGF-. NK1.1(-) CD4(+) NKG2D(+) cells did not expressed Foxp3, CD223 (LAG-3) and GITR. The subpopulation was distinct from NK1.1(+) CD4(+) NKG2D(+) cells in terms of surface markers and RNA transcription. NK1.1(-)CD4(+) NKG2D(+) cells also differed from Th2 or Th17 cells because the former did not express GATA-3 and ROR-t. Thus, NK1.1(-) CD4(+) NKG2D(+) cells exhibited immune regulatory functions, and this T cell subset could be developed to suppress inflammation in clinics.

关键词： 船长   应急决策   支持系统  

摘要： 随着航海科技的发展和航道环境的日益复杂,船舶的安全行驶受到了广泛关注。一旦发生紧急情况,船长和船员的反应速度和应急对策将对应急处理结果产生重要影响。船长应急决策支持系统的应用,通过对船舶数据的全面监控和数字化的显示,能够为船长迅速掌握船舶情况并制定有效的解决对策提供方便。本文将对船长应急决策支持系统进行研究,并提出几点应用建议。

标准号: DB44/T 2019-2017

摘要： 本标准规定了供应链业务协同服务系统(简称:“供应链协同系统”)的术语和定义、业务流程、系统交易参与方业务规范和监督管理。 本标准适用于使用区域供应链协同系统的零售商、分销商/品牌商、第三方物流商规范电子商务业务。

摘要： Uridine, one of the four components that comprise RNA, has attracted attention as a novel therapeutic modulator of inflammation. However, very little is known about its effect on intestinal inflammation. The aim of the present study was to investigate the potential protective effect of intracolonic administered uridine against DSS induced colitis in male C57BL/6 mice. Intracolonic instillation of 3 doses of uridine 1 mg/Kg (lower dose), 5 mg/Kg (medium dose), and 10 mg/Kg (higher dose) in saline was performed daily. Uridine at medium and high dose significantly reduced the severity of colitis (DAI score) and alleviated the macroscopic and microscopic signs of the disease. The levels of proinflammatory cytokines IL-6, IL-1 beta and TNF in serum as well as mRNA expression in colon were significantly reduced in the uridine treated groups. Moreover, colon tissue myloperoxidase activities, protein expression of IL-6, TNF-alpha, COX-2, P-NFkB and P-Ikk-alpha beta in the colon tissues were significantly reduced in medium and high dose groups. These findings demonstrated that local administration of uridine alleviated experimental colitis in male C57BL/6 mice accompanied by the inhibition of neutrophil infiltration and NF-kappa B signaling. Thus, Uridine may be a promising candidate for future use in the treatment of inflammatory bowel disease.

关键词： miR-155   Jarid2   Th17 cells differentiation   Ulcerative colitis (UC)  

摘要： MicroRNAs (miRNAs) play an important role in regulating immune system function by mRNA destabilisation or inhibition of translation. Recently, miR-155 was detected to be significantly up-regulated in colonic tissues of patients with active UC. However, it is unknown whether miR-155 is involved in the pathogenesis of UC and how it influences immune response in dextran sulfate sodium (DSS)-induced colitis mice. Here, we investigated the role of miR-155 in UC. Firstly, through bioinformatics analysis and luciferase report assay, we found Jarid2 was a direct target of miR-155;then, we carried out in situ hybridization, immunofluorescence and flow cytometry, and revealed that miR-155 levels were increased, Jarid2 levels were decreased and the frequency of Th17 cells was elevated in DSS-induced mice;we also used lentiviral vector to deliver miR-155 inhibition sequences to silence miR-155 that was effectively taken up by epithelial cells. MiR-155 inhibition attenuated DSS-induced colonic damage and inhibited Th17 cells differentiation. This study suggests that miR-155 plays a host-damaging role during DSS-induced colitis mice and induces Th17 differentiation by targeting Jarid2. (C) 2017 Elsevier Inc. All rights reserved.

关键词： SIRT5   PKM2   succinylation   IL-1β   macrophages   colitis  

摘要： LPS-activated macrophages undergo a metabolic shift from dependence on mitochondria-produced ATP to reliance on aerobic glycolysis, where PKM2 is a critical determinant. Here, we show that PKM2 is a physiological substrate of SIRT5 and that SIRT5-regulated hypersuccinylation inhibits the pyruvate kinase activity of PKM2 by promoting its tetramer-to-dimer transition. Moreover, a succinylation- mimetic PKM2 K311E mutation promotes nuclear accumulation and increases protein kinase activity. Furthermore, we show that SIRT5-dependent succinylation promotes PKM2 entry into nucleus, where a complex of PKM2-HIF1 alpha is formed at the promoter of IL-1 beta gene in LPS-stimulated macrophages. Activation of PKM2 using TEPP-46 attenuates Sirt5-deficiency-mediated IL-1 beta upregulation in LPS-stimulated macrophages. Finally, we find that Sirt5-deficient mice are more susceptible to DSS-induced colitis, which is associated with Sirt5 deficiency prompted PKM2 hypersuccinylation and boosted IL-1 beta production. In conclusion, our findings reveal a mechanismby which SIRT5 suppresses the pro-inflammatory response in macrophages at least in part by regulating PKM2 succinylation, activity, and function.