A transient multiphysics coupling method based on OpenFOAM for heat pipe cooled reactors

Differing from traditional pressurized water reactors(PWRs),heat pipe cooled reactors have the unique characteristics of fuel thermal expansion,expansion reactivity feedback,and thermal contact conductance.These reactors require a new multiphysics coupling method.In this paper,a transient coupling method based on OpenFOAM is proposed.The method considers power variation,thermal expansion,heat pipe operation,thermal contact conductance,and gap conductance.In particular,the reactivity feedback caused by working medium redistribution in a heat pipe is also preliminarily considered.A typical heat pipe cooled reactor KRUSTY(Kilowatt Reactor Using Stirling TechnologY)is chosen as the research object.Compared with experimental results of load following,the calculated results are in good agreement and show the validity of the proposed method.To discuss the self-adjusting capability of this type of reactor system,a hypothetical accident is simulated.It is assumed that at the beginning of this accident,loss of the heat sink occurs.After 1500 s of the transient process,the reactor system recovers immediately.During this hypothetical accident,the control rod is always out of the reactor core,and the reactor only relies on the reactivity feedback to regulate the fission power.According to the simulation,the peak temperature is only about 1112 K,which is far below the safety limit.As for system recovery,the reactor needs approximately 2500 s to return to a steady state and can realize effective power regulation by reactivity feedback.This study confirms the availability of this coupling method and that it can be an effective tool for the simulation of heat pipe cooled reactors.

1 T moderate intensity static magnetic field affects Akt/mTOR pathway and increases the antitumor efficacy of m TOR inhibitors in CNE-2Z cells

Static magnetic field （SMF） has been known to affect cell proliferation in a cell-type-dependent manner, while the mechanism still remains unclear. We found that 1 T moderate intensity SMF inhibits cell proliferation of nasopharyngeal carcinoma CNE-2Z cells and the Akt/ mTOR signaling pathway, which is upregulated in many cancers, roTOR inhibitors are potential chemodrugs, but their clinical effects are limited by the feedback reactiva- tion of other signaling components such as EGFR and Akt. We showed that 1 T SMF increases the antitumor efficacy of mTOR inhibitor Torin 2. In addition, 1 T SMF increases the inhibition efficiency on roTOR substrates phosphorylation and represses the mTOR inhibitor-induced feedback reactivation of EGFR and Akt. Our study not only demonstrates that mTOR/Akt pathway is one of the molecular targets of SMFs in cells, but also reveals the clinical potentials of combinations of roTOR inhibitors and SMFs in cancer treatment.