How Does Retailer-Oriented Remanufacturing Affect the OEM’s Quality Choice?

We consider that a supply chain consists of an original equipment manufacturer (OEM) and a retailer. We analyze how the retailer’s remanufacturing decision affects the decision of the new products’ qualities for the OEM. We use a game theory approach to investigate the interactions between the OEM and the retailer with or without remanufacturing operation. We find the retailer’s motivation to develop the remanufacturing industry depends on the profitability of remanufactured products and the OEM’s deterring strategy. When the remanufacturing operation profit margin is low, the retailer voluntarily gives up remanufacturing; when this profit margin is moderate, the OEM induces the retailer to give up remanufacturing by improving the quality of the new product; when this profit margin is sufficiently high, the OEM cannot prevent the retailer from developing remanufacturing. The retailer developing remanufacturing as well as their threat of developing decrease the OEM’s profit because the OEM improves the quality of the new products to induce the retailer to give up remanufacturing, at the expense of its own profit. We explicitly characterize the process of the OEM from preventing to accepting the retailer developing the remanufacturing industry, as well as the changes in supply-chain members’ operating decisions and profits in the process. Finally, using MATLAB numerical analysis, we also found that the retailer’s development of the remanufacturing industry always benefits the whole supply chain, consumer surplus, and social welfare. Furthermore, the retailer’s development of the remanufacturing industry is not always good for the environment. This development is only good for the environment when the new products’ environmental impacts in the EOL stage are larger than the total environmental impacts of the remanufactured products in every stage of their life cycle

How Does Retailer-Oriented Remanufacturing Affect the OEM’s Quality Choice?

We consider that a supply chain consists of an original equipment manufacturer (OEM) and a retailer. We analyze how the retailer’s remanufacturing decision affects the decision of the new products’ qualities for the OEM. We use a game theory approach to investigate the interactions between the OEM and the retailer with or without remanufacturing operation. We find the retailer’s motivation to develop the remanufacturing industry depends on the profitability of remanufactured products and the OEM’s deterring strategy. When the remanufacturing operation profit margin is low, the retailer voluntarily gives up remanufacturing; when this profit margin is moderate, the OEM induces the retailer to give up remanufacturing by improving the quality of the new product; when this profit margin is sufficiently high, the OEM cannot prevent the retailer from developing remanufacturing. The retailer developing remanufacturing as well as their threat of developing decrease the OEM’s profit because the OEM improves the quality of the new products to induce the retailer to give up remanufacturing, at the expense of its own profit. We explicitly characterize the process of the OEM from preventing to accepting the retailer developing the remanufacturing industry, as well as the changes in supply-chain members’ operating decisions and profits in the process. Finally, using MATLAB numerical analysis, we also found that the retailer’s development of the remanufacturing industry always benefits the whole supply chain, consumer surplus, and social welfare. Furthermore, the retailer’s development of the remanufacturing industry is not always good for the environment. This development is only good for the environment when the new products’ environmental impacts in the EOL stage are larger than the total environmental impacts of the remanufactured products in every stage of their life cycle

Study on the Combustion Characteristics and Kinetic Parameters of the Blended Coal Treated with Different Grinding Methods

The presented investigation focused on the combustion characteristics and kinetic parameters of the coals blended using different grinding methods (separated and mixed grinding), via Thermogravimetric analyser. According to the thermogravimetric experiments, with the increase of the proportion of Yangcheng coal, the combustion characteristics of the coal treated with the mixed grinding method are increasingly better than those of the coal treated with the separated grinding method (under the same mixing ratio). Additionally, the methods of Coats-Redfern were applied to calculate kinetic parameters, which indicated that when the proportion of Yangcheng coal is 30%, the activation energy values of the coal treated with two grinding methods are similar; when the proportion of Yangcheng coal is below 30%, the activation energy values of coal treated with the separated grinding method is lower than that of the coal treated with the mixed grinding method; when the proportion of Yangcheng coal is above 30%, the activation energy values of the coal treated with the mixed grinding method is lower than that of the coal treated with the separated grinding method

Metformin’s Effects on Apoptosis of Esophageal Carcinoma Cells and Normal Esophageal Epithelial Cells: An In Vitro Comparative Study

The effect of metformin on human esophageal normal and carcinoma cells remains poorly understood. We aim to investigate the different antiproliferation effects and underlying distinct molecular mechanisms between these two types of cells. Human esophageal squamous cell carcinoma cell line, EC109, and normal esophageal epithelial cell line, HEEC, were used in the experiment. The cell survival rate was determined by cell counting kit-8 (CCK-8). Cell apoptosis was analyzed by flow cytometry. The mRNA and protein levels of signal transducer and activator of transcription 3 (Stat3) were detected by real-time quantitative PCR and western blot. Interleukin-6 (IL-6) was added to activate Stat3. The level of intracellular reactive oxygen species (ROS) was assessed by a DCFH-DA fluorescent probe. Metformin had more significant inhibitory effects on cell proliferation in EC109 cells than HEECs. Metformin induced apoptosis of EC109 cells in a dose-dependent manner instead of HEECs. The expression of Stat3 in both mRNA and protein levels was higher in EC109 cells than HEECs. Further study revealed that metformin may attenuate the phosphorylation of the Stat3 and the Bcl-2 expression, which was restored by IL-6 partly in EC109 cells but not HEECs. On the contrary, metformin increased the level of ROS in both the cell lines, but this intracellular ROS variation had no effect on apoptosis. Metformin has different functional roles on the apoptosis in esophageal carcinoma cells and normal esophageal cells. Therefore, the Stat3/Bcl-2 pathway-mediated apoptosis underlies the cell-type-specific drug sensitivity, suggesting metformin possesses a therapeutic activity and selectivity on esophageal cancer

Metformin Induced AMPK Activation, G0/G1 Phase Cell Cycle Arrest and the Inhibition of Growth of Esophageal Squamous Cell Carcinomas In Vitro and In Vivo.

Esophageal squamous cell carcinomas (ESCC) have become a severe threat to health and the current treatments for ESCC are frequently not effective. Recent epidemiological studies suggest that the anti-hyperglycemic agent metformin may reduce the risk of developing cancer, including ESCC, among diabetic patients. However, the antitumor effects of metformin on ESCC and the mechanisms underlying its cell cycle regulation remain elusive. The findings reported herein show that the anti-proliferative action of metformin on ESCC cell lines is partially mediated by AMPK. Moreover, we observed that metformin induced G0/G1 phase arrest accompanied by the up-regulation of p21CIP1 and p27KIP1. In vivo experiments further showed that metformin inhibited tumor growth in a ESCC xenograft model. Most importantly, the up-regulation of AMPK, p53, p21CIP1, p27KIP1 and the down-regulation of cyclinD1 are involved in the anti-tumor action of metformin in vivo. In conclusion, metformin inhibits the growth of ESCC cells both in cell cultures and in an animal model. AMPK, p53, p21CIP1, p27KIP1 and cyclinD1 are involved in the inhibition of tumor growth that is induced by metformin and cell cycle arrest in ESCC. These findings indicate that metformin has the potential for use in the treatment of ESCC

The effect of metformin for ESCC prevention.

<p>Animals were treated with metformin (250 mg/kg) or physiological saline (control) 7 days before tumor cell implantation. Tumor volumes were measured every 2 days. Graphs representing the average tumor volumes of EC109 cell xenografts. Data represent mean ± SE. Pre: metformin pretreatment; Con: control group (n = 12; * <i>P</i><0.05; ** <i>P</i>< 0.01; vs. control).</p

Metformin up-regulated p21CIP1 and p27KIP1 in ESCC cells.

<p>EC109 cells were treated with 1.0 mM AICAR or 10 mM metformin for 24h. (A) A representative Western blot of p21^CIP1 and p27^KIP1 in EC109 cells (B) The histogram represents the gray value ratio of the target protein to β-actin which was normalized to the control group. Data is from three independent experiments.</p

Metformin inhibited the growth of EC109 cell xenografts in nude mice.

<p>Xenografts were generated by the subcutaneous implantation of EC109 cells. Two weeks later, physiological saline (control) or metformin (250 mg/kg) were intragastrically administered and the feeding continued until the end of the study. Tumor volumes were measured every 2 days. (A) Photographs showing the representative xenograft tumors on metformin-treated or vehicle-treated nude mice (bar = 1centimetre). (B) Average tumor volumes of the EC109 cell xenografts. (C) Paraffin sections of excised tumors were assessed by H&E stain showing large necrosis area in both experiment and control groups. In necrotic area there were very few nuclei that were well stained by hematoxylin, and tissue was disintegrating and the morphologic details were not preserved (200× magnification; bar = 100 microns). (D) The body weight of all mice were measured the day before intragastric administration, and before euthanasia. Histograms show the average weight from the different groups. There was no difference before and after intragastric administration. (E) After intragastric administration, water and food were withdrawn.for 3h. The serum glucose was detected by blood glucose monitor. The serum glucose levels were not statistically different between the control and treated groups. Data represent mean ± SE. Tre: metformin treated group; Con: control group (n = 10; * <i>P</i><0.05; ** <i>P</i>< 0.01; NS: no significance; vs. control).</p

The effects of metformin on cell cycle regulators in vivo, including cyclinD1, p53, p21^CIP1 and p27^KIP1.

<p>(A) Tissue extracts from 8 different samples of metformin-treated or vehicle-treated mice were immunoblotted with antibodies against cyclinD1, p53, p21^CIP1 and p27^KIP1. β-actin was used as a loading control. Western blot analysis was performed. (B) Histograms represent the ratio of target protein to β-actin which was normalized to the control group. (C) Representative microscopic image of the immunohistochemiscal staining of p53 and p21 ^CIP1 (200× magnification; bar = 100 microns).</p

Metformin induced cell cycle arrest in ESCC cells.

<p>(A) Cells treated with 1mM AICAR or 10mM metformin for 24h were stained with propidium iodide, and analyzed by flow cytometry to estimate the amount of cells in each phase of the cell cycle. (B) The histogram represents the percentage of cells in each cell cycle phase. Data represent the means±SE from three independent experiments. * <i>P</i><0.05, ** <i>P</i><0.01, vs Control.</p