User-Friendly MES Interfaces:Recommendations for an AI-Based Chatbot Assistance in Industry 4.0 Shop Floors

The purpose of this paper is to study an Industry 4.0 scenario of ‘technical assistance’ and use manufacturing execution systems (MES) to address the need for easy information extraction on the shop floor. We identify specific requirements for a user-friendly MES interface to develop (and test) an approach for technical assistance and introduce a chatbot with a prediction system as an interface layer for MES. The chatbot is aimed at production coordination by assisting the shop floor workforce and learn from their inputs, thus acting as an intelligent assistant. We programmed a prototype chatbot as a proof of concept, where the new interface layer provided live updates related to production in natural language and added predictive power to MES. The results indicate that the chatbot interface for MES is beneficial to the shop floor workforce and provides easy information extraction, compared to the traditional search techniques. The paper contributes to the manufacturing information systems field and demonstrates a human-AI collaboration system in a factory. In particular, this paper recommends the manner in which MES based technical assistance systems can be developed for the purpose of easy information retrieval

Evaluation of 2-deoxy-D-glucose as a chemotherapeutic agent: mechanism of cell death

Nutrient deprivation has been shown to cause cancer cell death. To exploit nutrient deprivation as anti-cancer therapy, we investigated the effects of the anti-metabolite 2-deoxy-D-glucose on breast cancer cells in vitro. This compound has been shown to inhibit glucose metabolism. Treatment of human breast cancer cell lines with 2-deoxy-D-glucose results in cessation of cell growth in a dose dependent manner. Cell viability as measured by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide conversion assay and clonogenic survival are decreased with 2-deoxy-D-glucose treatment indicating that 2-deoxy-D-glucose causes breast cancer cell death. The cell death induced by 2-deoxy-D-glucose was found to be due to apoptosis as demonstrated by induction of caspase 3 activity and cleavage of poly (ADP-ribose) polymerase. Breast cancer cells treated with 2-deoxy-D-glucose express higher levels of Glut1 transporter protein as measured by Western blot analysis and have increased glucose uptake compared to non-treated breast cancer cells. From these results we conclude that 2-deoxy-D-glucose treatment causes death in human breast cancer cell lines by the activation of the apoptotic pathway. Our data suggest that breast cancer cells treated with 2-deoxy-D-glucose accelerate their own demise by initially expressing high levels of glucose transporter protein, which allows increased uptake of 2-deoxy-D-glucose, and subsequent induction of cell death. These data support the targeting of glucose metabolism as a site for chemotherapeutic intervention by agents such as 2-deoxy-D-glucose

Properties of baryon resonances from a multichannel partial wave analysis

Properties of nucleon and $\Delta$ resonances are derived from a multichannel partial wave analysis. The statistical significance of pion and photo-induced inelastic reactions off protons are studied in a multichannel partial-wave analysis.Comment: 12 pages, 8 Table

Nucleon resonances in the fourth resonance region

Nucleon and $\Delta$ resonances in the fourth resonance region are studied in a multichannel partial-wave analysis which includes nearly all available data on pion- and photo-induced reactions off protons. In the high-mass range, above 1850\,MeV, several alternative solutions yield a good description of the data. For these solutions, masses, widths, pole residues and photo-couplings are given. In particular, we find evidence for nucleon resonances with spin-parities $J^P=1/2^+...7/2^+$. For one set of solutions, there are four resonances forming naturally a spin-quartet of resonances with orbital angular momentum L=2 and spin S=3/2 coupling to $J=1/2,...,7/2$. Just below 1.9\,GeV we find a spin doublet of resonances with $J^P=1/2^-$ and $3/2^-$. Since a spin partner with $J^P=5/2^-$ is missing at this mass, the two resonances form a spin doublet which must have a symmetric orbital-angular-momentum wave function with L=1. For another set of solutions, the four positive-parity resonances are accompanied by mass-degenerate negative-parity partners -- as suggested by the conjecture of chiral symmetry restoration. The possibility of a $J^P=1/2^+, 3/2^+$ spin doublet at 1900\,MeV belonging to a 20-plet is discussed.Comment: 16 page

Regulation of immune cell function and differentiation by the NKG2D receptor

NKG2D is one of the most intensively studied immune receptors of the past decade. Its unique binding and signaling properties, expression pattern, and functions have been attracting much interest within the field due to its potent antiviral and anti-tumor properties. As an activating receptor, NKG2D is expressed on cells of the innate and adaptive immune system. It recognizes stress-induced MHC class I-like ligands and acts as a molecular sensor for cells jeopardized by viral infections or DNA damage. Although the activating functions of NKG2D have been well documented, recent analysis of NKG2D-deficient mice suggests that this receptor may have a regulatory role during NK cell development. In this review, we will revisit known aspects of NKG2D functions and present new insights in the proposed influence of this molecule on hematopoietic differentiation

Loss of Toll-Like Receptor 4 Function Partially Protects against Peripheral and Cardiac Glucose Metabolic Derangements During a Long-Term High-Fat Diet

We would like to acknowledge Matt Priest for excellent technical assistance.Diabetes is a chronic inflammatory disease that carries a high risk of cardiovascular disease. However, the pathophysiological link between these disorders is not well known. We hypothesize that TLR4 signaling mediates high fat diet (HFD)-induced peripheral and cardiac glucose metabolic derangements. Mice with a loss-of-function mutation in TLR4 (C3H/HeJ) and age-matched control (C57BL/6) mice were fed either a high-fat diet or normal diet for 16 weeks. Glucose tolerance and plasma insulin were measured. Protein expression of glucose transporters (GLUT), AKT (phosphorylated and total), and proinflammatory cytokines (IL-6, TNF-α and SOCS-3) were quantified in the heart using Western Blotting. Both groups fed a long-term HFD had increased body weight, blood glucose and insulin levels, as well as impaired glucose tolerance compared to mice fed a normal diet. TLR4-mutant mice were partially protected against long-term HFD-induced insulin resistance. In control mice, feeding a HFD decreased cardiac crude membrane GLUT4 protein content, which was partially rescued in TLR4-mutant mice. TLR4-mutant mice fed a HFD also had increased expression of GLUT8, a novel isoform, compared to mice fed a normal diet. GLUT8 content was positively correlated with SOCS-3 and IL-6 expression in the heart. No significant differences in cytokine expression were observed between groups, suggesting a lack of inflammation in the heart following a HFD. Loss of TLR4 function partially restored a healthy metabolic phenotype, suggesting that TLR4 signaling is a key mechanism in HFD-induced peripheral and cardiac insulin resistance. Our data further suggest that TLR4 exerts its detrimental metabolic effects in the myocardium through a cytokine-independent pathway.Yeshttp://www.plosone.org/static/editorial#pee