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The supply air volume fluctuates in a large range or even interrupts during the switching process of mine main ventilators, which is easy to cause the gas concentration to exceed the limit. The commonly used model-based main ventilator switchover control method is difficult to handle the constraints well. The intelligent algorithm relies on expert knowledge and experience, which is subjective and arbitrary. In order to solve the above problems, taking the switchover process of main ventilators in the No.2 Mine of China Pingmei Energy and Chemical Group Co., Ltd. as the research background, the optimal control of supply air volume in the switchover process of main ventilators is studied. Based on the hydrodynamics equation and the concept of graph theory, the dynamic model of the main ventilator switchover process is established. The Taylor expansion is used to linearize it to reduce the computational complexity. The switchover process of mine main ventilator is strongly nonlinear, and the system state is constrained. It is a discrete multi-input and multi-output system. The model predictive control (MPC) algorithm is used to study the air volume control problem. The MPC system of the main ventilator switchover process is designed, which converts the air volume optimization into a quadratic programming problem. The primal-dual neural network is used to solve the optimization problem online to realize the real-time optimal control of the supply air volume during the main ventilator switchover process. The test results show that the MPC system can effectively switch the main ventilator, and the air volume of four air doors can well track the reference value during the switchover process. The operation time of each sampling time is 0.027 s, which meets the real-time requirements of the switchover process. The maximum fluctuation of supply air volume is only 0.9%, which is significantly better than the traditional PID control effect.

BACKGROUND. Hepatic de novo lipogenesis (DNL) and [beta]-oxidation are tightly coordinated, and their dysregulation is thought to contribute to the pathogenesis of nonalcoholic fatty liver (NAFL). Fasting normally relaxes DNL-mediated inhibition of hepatic [beta]-oxidation, dramatically increasing ketogenesis and decreasing reliance on the TCA cycle. Thus, we tested whether aberrant oxidative metabolism in fasting NAFL subjects is related to the inability to halt fasting DNL. METHODS. Forty consecutive nondiabetic individuals with and without a history of NAFL were recruited for this observational study. After phenotyping, subjects fasted for 24 hours, and hepatic metabolism was interrogated using a combination of [sup.2][H.sub.2]O and [sup.13]C tracers, magnetic resonance spectroscopy, and high- resolution mass spectrometry. RESULTS. Within a subset of subjects, DNL was detectable after a 24-hour fast and was more prominent in those with NAFL, though it was poorly correlated with steatosis. However, fasting DNL negatively correlated with hepatic [beta]- oxidation and ketogenesis and positively correlated with citrate synthesis. Subjects with NAFL but undetectable fasting DNL (25th percentile) were comparatively normal. However, those with the highest fasting DNL (75th percentile) were intransigent to the effects of fasting on the concentration of insulin, non-esterified fatty acid, and ketones. Additionally, they sustained glycogenolysis and were spared the loss of oxaloacetate to gluconeogenesis in favor of citrate synthesis, which correlated with DNL and diminished ketogenesis. CONCLUSION. Metabolic flux analysis in fasted subjects indicates that shared metabolic mechanisms link the dysregulations of hepatic DNL, ketogenesis, and the TCA cycle in NAFL. TRIAL REGISTRATION. Data were obtained during the enrollment/non- intervention phase of Effect of Vitamin E on Non-Alcoholic Fatty Liver Disease, ClinicalTrials.gov NCT02690792. FUNDING. This work was supported by the University of Texas Southwestern NORC Quantitative Metabolism Core (NIH P30DK127984), the NIH/National Institute of Diabetes and Digestive and Kidney Diseases (R01DK078184, R01DK128168, R01DK087977, R01DK132254, and K01DK133630), the NIH/National Institute on Alcohol Abuse and Alcoholism (K01AA030327), and the Robert A. Welch Foundation (I-1804)., Introduction Nonalcoholic fatty liver (NAFL) is a highly prevalent condition associated with obesity and insulin resistance that, in some individuals, will progress to nonalcoholic steatohepatitis (NASH), cirrhosis, and liver failure [...]

Abundant user‐generated content has increasingly driven consumers to form or modify their purchasing decisions based on interactions with other consumers, although the extant research overlooks the customer‐to‐customer (C2C) interaction touchpoints. Based on the customer journey characteristics of cross‐channel and multi‐frequency interactions, this study explores the impact of interaction valence and interaction channel sequence on Generation Z consumers' purchase attitudes from the perspective of attitude modification process. Using a scenario‐based experimental design in a restaurant setting, we sample 616 Generation Z students. Findings suggest that C2C interactions that have the same valence at each touchpoint strengthen Generation Z consumers' initial purchase attitude, whereas inconsistent valences modify purchase attitudes. Our results reveal that a negative‐to‐positive ordering is more conducive to the formation of a positive purchase attitude than a positive‐to‐negative ordering. Moreover, the cross‐channel sequence of a customer journey moderates the inconsistent valence order such that the positive‐to‐negative order improves purchase attitude more than the negative‐to‐positive order. This study explains theoretically the difference of ambivalent experiences on Generation Z consumer attitudes. We provide practical suggestions for multi‐channel restaurant enterprises to successfully employ customer journey touchpoint management. [ABSTRACT FROM AUTHOR]

Mitochondria are critical for respiration in all tissues; however, in liver, these organelles also accommodate high-capacity anaplerotic/cataplerotic pathways that are essential to gluconeogenesis and other biosynthetic activities. During nonalcoholic fatty liver disease (NAFLD), mitochondria also produce ROS that damage hepatocytes, trigger inflammation, and contribute to insulin resistance. Here, we provide several lines of evidence indicating that induction of biosynthesis through hepatic anaplerotic/cataplerotic pathways is energetically backed by elevated oxidative metabolism and hence contributes to oxidative stress and inflammation during NAFLD. First, in murine livers, elevation of fatty acid delivery not only induced oxidative metabolism, but also amplified anaplerosis/cataplerosis and caused a proportional rise in oxidative stress and inflammation. Second, loss of anaplerosis/cataplerosis via genetic knockdown of phosphoenolpyruvate carboxykinase 1 (Pck1) prevented fatty acid-induced rise in oxidative flux, oxidative stress, and inflammation. Flux appeared to be regulated by redox state, energy charge, and metabolite concentration, which may also amplify antioxidant pathways. Third, preventing elevated oxidative metabolism with metformin also normalized hepatic anaplerosis/cataplerosis and reduced markers of inflammation. Finally, independent histological grades in human NAFLD biopsies were proportional to oxidative flux. Thus, hepatic oxidative stress and inflammation are associated with elevated oxidative metabolism during an obesogenic diet, and this link may be provoked by increased work through anabolic pathways., Introduction Hepatic mitochondria support a broad range of metabolic activities, many of which are unique to liver and contribute to the pathophysiology of insulin resistance, diabetes, and fatty liver disease. [...]

E-referral incentive programs are key instruments to carry out relationship marketing on social platforms. This study explores the effect of e-referral incentive programs on customer loyalty and its mechanisms. Two theories, the cognitive dissonance theory and the attention resource theory are adopted in this study, and therefore, referral dissonance and audience size are introduced as a mediator and a context variable separately. The results show that (1) the reward size and reward scheme have a significant interaction effect on customers' repurchase intention and their re-referral intention; (2) this kind of interaction effect can be mediated by cognitive dissonance; and (3) the effect of referral incentive programs on customer loyalty will be influenced by the audience size. This study also explains how the referral incentive programs influence customer loyalty in social platforms and therefore can serve as a theoretical guidance for enterprises aiming to develop e-referral incentive programs. [ABSTRACT FROM AUTHOR]

Hepatic ketogenesis provides a vital systemic fuel during fasting because ketone bodies are oxidized by most peripheral tissues and, unlike glucose, can be synthesized from fatty acids via mitochondrial [beta]-oxidation. Since dysfunctional mitochondrial fat oxidation may be a cofactor in insulin-resistant tissue, the objective of this study was to determine whether diet-induced insulin resistance in mice results in impaired in vivo hepatic fat oxidation secondary to defects in ketogenesis. Ketone turnover ([micro]mol/min) in the conscious and unrestrained mouse was responsive to induction and diminution of hepatic fat oxidation, as indicated by an eightfold rise during the fed (0.50+/-0.1)-to-fasted (3.8+/-0.2) transition and a dramatic blunting of fasting ketone turnover in PPAR[alpha]-/- mice (1.0 +/-0.1). C57BL/6 mice made obese and insulin resistant by high-fat feeding for 8 wk had normal expression of genes that regulate hepatic fat oxidation, whereas 16 wk on the diet induced expression of these genes and stimulated the function of hepatic mitochondrial fat oxidation, as indicated by a 40% induction of fasting ketogenesis and a twofold rise in short-chain acylcarnitines. Together, these findings indicate a progressive adaptation of hepatic ketogenesis during high-fat feeding, resulting in increased hepatic fat oxidation after 16 wk of a high-fat diet. We conclude that mitochondrial fat oxidation is stimulated rather than impaired during the initiation of hepatic insulin resistance in mice. hepatic insulin resistance; liquid chromatography-tandem mass spectrometry; nuclear magnetic resonance doi: 10.1152/ajpendo.00033.2010.