This study presents an algorithm for deriving the long-term polices of quality level, price and advertisement for a product. The diVusion models and cost functions are combined to formulate pro® t functions capable of determining future pro® t trends. The algorithm ® rst implements the optimal control theory to derive the optimal conditions of the pro® t function. Then the genetic algorithm is employed to search for the approximate solutions of quality level, price and advertising expenditure at each period on the planning horizon (life cycle). Examples of diVerent scenarios of the model parameters are presented to describe the results obtained herein. Sensitivity analysis for the major parameters is performed to specify their eVects on pro® ts. Results in this study allow us, ® rstly, to obtain explicit solutions simultaneously with respect to quality, price and advertising policies, secondly, to propose an appropriate algorithm for solving the diVerent scenarios of the dynamic pro® t function, which consists of the diVusion function and cost function, and thirdly, to enhance the long-term pro® t performance via the polices proposed herein, that is the approximation of the best solution.
NomenclatureA…t † rate of advertising expenditure at time t C…x…t †; q…t † † total cost per unit at time t for a cumulative sales volume x…t † and quality level q…t † d price parameter h quality parameter M total number of potential purchasers over the life cycle of the product P…t † unit price at time t q…t † quality level at time t, 0 < q…t † 4 1 r discount rate T period of the life cycle x…t † cumulative sales volume by time t x 0 …t †ˆg…x…t †; p…t †; q…t †; A…t † †, sales rate at time t for a cumulative sales volume x…t †, price p…t †, quality level q…t † and advertising expenditure A…t † ¬ innovation coe cient reaction coe cient for advertising ® imitation coe cient
Oral cancer is a fatal disease, and its incidence in Taiwan is increasing. Thyroid hormone as L-thyroxine (T4) stimulates cancer cell proliferation via a receptor on integrin αvβ3 of plasma membranes. It also induces the expression of programmed death-ligand 1 (PD-L1) and cell proliferation in cancer cells. Thyroid hormone also activates β-catenin-dependent cell proliferation in cancer cells. However, the relationship between PD-L1 and cancer proliferation is not fully understood. In the current study, we investigated the role of inducible thyroid hormone-induced PD-L1-regulated gene expression and proliferation in oral cancer cells. Thyroxine bound to integrin αvβ3 to induce PD-L1 expressions via activation of ERK1/2 and signal transducer and activator of transcription 3 (STAT3). Inactivated STAT3 inhibited PD-L1 expression and nuclear PD-L1 accumulation. Inhibition of PD-L1 expression reduced β-catenin accumulation. Furthermore, nuclear PD-L1 formed a complex with nuclear proteins such as p300. Suppression PD-L1 expression by shRNA blocked not only expression of PD-L1 and β-catenin but also signal transduction, proliferative gene expressions, and cancer cell growth. In summary, thyroxine via integrin αvβ3 activated ERK1/2 and STAT3 to stimulate the PD-L1-dependent and β-catenin-related growth in oral cancer cells.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.