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[Purpose/Significance] With the further development of the integration of culture and tourism in libraries, the social benefits of the cultural resources of libraries will be created, the bright spots of culture and tourism in libraries will be explored, and the characteristic reading space will be enriched, promoting the transformation and upgrading of smart libraries, and social forces to actively participate in more activities. Some preliminary results have been achieved. In the new era, libraries have been given the request and expectation to provide services for the further innovation and development in the field of culture and tourism. [Method/Process] Based on the relevant research on "The integration of culture and tourism" in China in the past two years, most of them focus on a service mode and a single activity case, and seldom from the perspective of a library's IP construction practice to summarize the development path and strategy research. Based on the earlier culture research, this paper focuses on the practice of a library's IP construction, adding the product value and activity brand influence of the library, and creating the exclusive path of the library, from the aspects of IP personification, library IP story, IP topic event marketing, travel IP service efficiency, digital IP integration, Internet celebrity IP card pulling local consumption, cross-border cooperation to activate IP culture, and practice and operation of brand IP. [Results/Conclusions] Through the library IP construction strategy, point-to-point combination, the cultural expression of the library reflects the library value of the integration of IP-enabled culture and tourism. From the position and cultural goal of the literary brigade embedded in the beginning of the IP planning of the library, the evaluation standard of the literary brigade activities at different stages, the relevance of the literary brigade of the IP application, and the team of personnel running the activities of the literary brigade of the IP, all of which need professional library organization construction and link intervention, but the library IP construction can integrate the development of culture and tourism, which is a new business area of the library. This paper mainly discusses the significance of IP construction and practical case level, but each path has not yet further reflected the impact of IP to the attractiveness of tourism evaluation mechanism. New opportunity creates new value, and the key point of a library's IP construction is not only the rational expression of cultural travel attributes, but also the emotional habits of cultural travel activities. Further research is needed to realize the value of cultural IP traffic.

Histone demethylase JMJD2D (also known as KDM4D) can specifically demethylate H3K9me2/3 to activate its target gene expression. Our previous study has demonstrated that JMJD2D can protect intestine from dextran sulfate sodium (DSS)-induced colitis by activating Hedgehog signaling; however, its involvement in host defense against enteric attaching and effacing bacterial infection remains unclear. The present study was aimed to investigate the role of JMJD2D in host defense against enteric bacteria and its underlying mechanisms. The enteric pathogen Citrobacter rodentium (C. rodentium) model was used to mimic clinical colonic infection. The responses of wild-type and JMJD2D-/- mice to oral infection of C. rodentium were investigated. Bone marrow chimeric mice were infected with C. rodentium. JMJD2D expression was knocked down in CMT93 cells by using small hairpin RNAs, and Western blot and real-time PCR assays were performed in these cells. The relationship between JMJD2D and STAT3 was studied by co-immunoprecipitation and chromatin immunoprecipitation. JMJD2D was significantly up-regulated in colonic epithelial cells of mice in response to Citrobacter rodentium infection. JMJD2D-/- mice displayed an impaired clearance of C. rodentium, more body weight loss, and more severe colonic tissue pathology compared with wild-type mice. JMJD2D-/- mice exhibited an impaired expression of IL-17F in the colonic epithelial cells, which restricts C. rodentium infection by inducing the expression of antimicrobial peptides. Accordingly, JMJD2D-/- mice showed a decreased expression of β-defensin-1, β-defensin-3, and β-defensin-4 in the colonic epithelial cells. Mechanistically, JMJD2D activated STAT3 signaling by inducing STAT3 phosphorylation and cooperated with STAT3 to induce IL-17F expression by interacting with STAT3 and been recruited to the IL-17F promoter to demethylate H3K9me3. Our study demonstrates that JMJD2D contributes to host defense against enteric bacteria through up-regulating IL-17F to induce β-defensin expression. Author summary: Our study aimed to unravel the role of JMJD2D, a histone demethylase also known as KDM4D, in the host's defense against enteric bacterial infections and explore the underlying mechanisms. While we had previously demonstrated JMJD2D's protective effect in DSS-induced colitis by activating Hedgehog signaling, its involvement in defending against enteric attaching and effacing bacterial infections remained unexplored. To address this, we employed a Citrobacter rodentium (C. rodentium) infection model to mimic colonic infections in a clinical context. In response to C. rodentium infection, there was a notable increase in JMJD2D expression within the colonic epithelial cells of mice. Our investigation compared the responses of wild-type mice with those lacking JMJD2D (JMJD2D-/-) following oral C. rodentium infection. Notably, JMJD2D-/- mice exhibited impaired C. rodentium clearance, greater body weight loss, and more severe colonic tissue damage compared to their wild-type counterparts. Subsequent analysis revealed that JMJD2D deficiency resulted in reduced IL-17F expression in colonic epithelial cells. IL-17F is a known regulator that restricts C. rodentium infection by promoting the expression of antimicrobial peptides. Consequently, JMJD2D-/- mice showed diminished expression of critical antimicrobial peptides, including β-defensin-1, β-defensin-3, and β-defensin-4, in their colonic epithelial cells. Mechanistically, we discovered that JMJD2D played a pivotal role in activating STAT3 signaling by enhancing STAT3 phosphorylation. Moreover, JMJD2D collaborated with STAT3 to induce IL-17F expression. This cooperation involved JMJD2D physically interacting with STAT3 and binding to the IL-17F promoter, where it demethylated H3K9me3. In summary, our research reveals that JMJD2D contributes significantly to the host's defense against enteric bacterial infections by up-regulating IL-17F, which in turn induces the expression of antimicrobial peptides such as β-defensins. Our findings provide valuable insights into the molecular mechanisms governing host defense against enteric bacterial infections, emphasizing the potential therapeutic relevance of targeting JMJD2D in such contexts. [ABSTRACT FROM AUTHOR]

This paper employs algebraic transformation to describe complex social network learning (SNL) behaviors under continuous expected payoff. Three distinct algorithms are then introduced that factor in uncertainty and heterogeneity. We find that individuals' strategies tend to converge through SNL. We then construct a framework for studying the convergence process in the principal–agent relationship by applying our SNL algorithms to distinct scenarios. Our results show that network topology plays a significant role in changes in the payoffs and the convergence speed of individuals' strategies. We also evaluate the impacts of uncertainty, heterogeneity, agents' output efficiency and risk aversion, and individual's centrality on the effectiveness of SNL. [ABSTRACT FROM AUTHOR]

Acrylamide (AA) is an important product of the Maillard reaction. Studies have demonstrated that AA caused oxidative stress damage in liver, which in turn triggered an inflammatory response, and the activation of NOD-like receptor protein-3 (NLRP3) inflammasome played a key factor in regulating inflammation. Therefore, we hypothesized NLRP3 inflammasome activation was involved in AA-induced inflammatory response. AA induced the reactive oxygen species (ROS) overproduction, accompanied by the MAPK pathway activation, which resulted in NLRP3 inflammasome formation, and eventually increased IL-1β and IL-18 release. The activation of the MAPK pathway was inhibited when using ROS scavenger (NAC). And when MAPK selective inhibitors were used, KCs viability was increased though AA-treated. Meanwhile the NLRP3 inflammasome activation was inhibited, which decreased the release of the cellular inflammatory secretion factors IL-1β and IL-18. Overall, the activation of ROS-MAPK-NLRP3-IL-1β signalling axis induced by AA plays an important role in the process of inflammation. Signaling pathways involved in inflammation induced by AA. After AA stimulated KCs, a large amount of ROS were released. ROS activated MAPK signaling pathway to promote the activation of NLRP3 inflammasome. Activation of NLRP3 signaling activated Caspase-1, resulting in the maturation of IL-1β and IL-18. The activation of NLRP3 inflammasome was inhibited and the levels of cytoinflammatory factor IL-1β and IL-18 were decreased when using MAPK selective inhibitors.