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Virtual enterprise is a dynamic enterprise alliance for the purpose of reacting to drastic market and improving core competence. Knowledge sharing is crucial to the virtual enterprise. The case of knowledge sharing between two member enterprises without participant of hegemony enterprise has been discussed using Prisoner Dilemma Game Model. There are many factors may affect the strategy of member enterprise like utility of monopolizing the knowledge, the lost monopolizing benefit when sharing the knowledge and the cost of the knowledge sharing. The theory of complete and perfect two-stage dynamic game of knowledge sharing based on work competition model has been applied to the analysis on knowledge sharing in virtual enterprise. The member enterprise will choose knowledge sharing level to make marginal income equal to the value of negative utility by sharing its knowledge at Nash Equilibrium. The hegemony enterprise should formulate a reasonable stimulation policy and give enough bounty to the member enterprise who has contributed more knowledge to the virtual enterprise through knowledge sharing. There is a positive correlation between stimulation level and the variance of random item probability distribution of production function.

Virtual enterprise is the outcome of fierce competition in the world market. The selection of partners is one of the key factors for the success of virtual enterprises. Multi-agent system is an incompact agent federation composed of many agents, with its characteristics identical to virtual enterprises. It is, therefore, reasonable and effective to apply to the selection of enterprises' partner. The issue of trust is a hot topic in multi-agent system. The present trust model cannot well solve the problem of identifying the initial trust value of applicant agents. Moreover, there is room for improvement as to the calculation of agent trust value. This study puts forward a new trust management model based on multi-agent system. In the model, a fuzzy algorithm is used to calculate the initial value of the agent instead of a static definition. In addition, an independent validation module is used to test information reliability. Therefore, the problems of identifying initial trust value can be solved. Through system simulation, it is noted that based on the trust management model the cooperation rate has been enhanced and individual agent's income has risen by a big margin.

Due to the convenience of Internet, people can search for whatever information they need and buy whatever they want on the web. In the age of E- Commerce, it is difficult to provide support for customers to find the most valuable products that match their heterogeneous needs. Traditional approaches to this so-called personalization problem adopt pre-defined formats to describe the customer requirements. This always leads to distortion in eliciting requirement information and thus inaccurate recommendations. In this paper,we propose a personalized recommendation system using association rule mining and classification in e-commerce. Customer requirements are extracted from text documents and transformed into a set of significant phrases. Allowing the transformed transaction records, a set of association rule are mined from database using Apriori algorithm. CBA-CB algorithm is applied to produce the best rules out of the whole set of rules. The best classifiers are then generated after the test and validation of those rules, aimed to predict the item labels for new customer requirements and thus assigns the corresponding class labels to the customer. The system analysis and design of the proposed recommendation system as well as the implementation of prototype are also presented.

Some modeling methods of virtual enterprise have been proposed such as workflow coordination modeling, supply chain modeling and agent-based modeling. But they all have some insufficient in some aspects to be improved. For example, they are difficult to be realized in process dynamic optimization. This paper proposes a service-based model for Virtual Enterprise workflows. Modeling the workflow execution as a cooperation of services allows different organizations to interact via well-defined interfaces. The paper primarily covers three models: the conceptual model of workflow for virtual enterprise, the service model and the execution model, it discusses the agile service choice and transfer mechanism of the virtual enterprise and shows how the execution can be optimized by selecting services depending on their contribution to quality criteria of the workflow. The model proposed in this paper has referenced and practical value for the thorough research and realization of the system.

Replenishment of pancreatic beta cells is a key to the cure for diabetes. Beta cells regeneration is achieved predominantly by self-replication especially in rodents, but it was also shown that pancreatic duct cells can transdifferentiate into beta cells. How pancreatic duct cells undergo transdifferentiated and whether we could manipulate the transdifferentiation to replenish beta cell mass is not well understood. Using a genome-wide CRISPR screen, we discovered that loss-of-function of ALDH3B2 is sufficient to transdifferentiate human pancreatic duct cells into functional beta-like cells. The transdifferentiated cells have significant increase in beta cell marker genes expression, secrete insulin in response to glucose, and reduce blood glucose when transplanted into diabetic mice. Our study identifies a novel gene that could potentially be targeted in human pancreatic duct cells to replenish beta cell mass for diabetes therapy.

Type 1 diabetes (T1D) arises from autoimmune-mediated destruction of insulin-producing pancreatic beta cells. Recent advancements in the technology of generating pancreatic beta cells from human pluripotent stem cells (SC-beta cells) have facilitated the exploration of cell replacement therapies for treating T1D. However, the persistent threat of autoimmunity poses a significant challenge to the survival of transplanted SC-beta cells. Genetic engineering is a promising approach to enhance immune resistance of beta cells as we previously showed by inactivating of the Renalase ( Rnls ) gene. Here we demonstrate that Rnls loss-of-function in beta cells shape autoimmunity by mediating a regulatory Natural Killer (NK) cell phenotype important for the induction of tolerogenic antigen presenting cells. Rnls -deficient beta cells mediate cell-cell-contact-independent induction of hallmark anti-inflammatory cytokine Tgfβ1 in NK cells. In addition, surface expression of key regulatory NK immune checkpoints CD47 and Ceacam1 are markedly elevated on beta cells deficient for Rnls . Enhanced glucose metabolism in Rnls mutant beta cells is responsible for upregulation of CD47 surface expression. These findings are crucial to a better understand how genetically engineered beta cells shape autoimmunity giving valuable insights for future therapeutic advancements to treat and cure T1D., Competing Interests: Duality of Interest. P.Y. and S.K. are inventors on a patent application filed by the Joslin Diabetes Center that relates to the targeting of RNLS for the protection of transplanted SC-islets. The authors declare no other conflicts of interest.

Brown adipose tissue (BAT) has the capacity to regulate systemic metabolism through the secretion of signaling lipids. N6-methyladenosine (m 6 A) is the most prevalent and abundant post-transcriptional mRNA modification and has been reported to regulate BAT adipogenesis and energy expenditure. In this study, we demonstrate that the absence of m 6 A methyltransferase-like 14 (METTL14), modifies the BAT secretome to initiate inter-organ communication to improve systemic insulin sensitivity. Importantly, these phenotypes are independent of UCP1-mediated energy expenditure and thermogenesis. Using lipidomics, we identified prostaglandin E2 (PGE2) and prostaglandin F2a (PGF2a) as M14 KO -BAT-secreted insulin sensitizers. Notably, circulatory PGE2 and PGF2a levels are inversely correlated with insulin sensitivity in humans. Furthermore, in vivo administration of PGE2 and PGF2a in high-fat diet-induced insulin-resistant obese mice recapitulates the phenotypes of METTL14 deficient animals. PGE2 or PGF2a improves insulin signaling by suppressing the expression of specific AKT phosphatases. Mechanistically, METTL14-mediated m 6 A installation promotes decay of transcripts encoding prostaglandin synthases and their regulators in human and mouse brown adipocytes in a YTHDF2/3-dependent manner. Taken together, these findings reveal a novel biological mechanism through which m 6 A-dependent regulation of BAT secretome regulates systemic insulin sensitivity in mice and humans., Highlights: Mettl14 KO -BAT improves systemic insulin sensitivity via inter-organ communication; PGE2 and PGF2a are BAT-secreted insulin sensitizers and browning inducers;PGE2 and PGF2a sensitize insulin responses through PGE2-EP-pAKT and PGF2a-FP-AKT axis; METTL14-mediated m 6 A installation selectively destabilizes prostaglandin synthases and their regulator transcripts; Targeting METTL14 in BAT has therapeutic potential to enhance systemic insulin sensitivity.