Combining finite element and reinforcement learning methods to design superconducting coils of saturated iron-core superconducting fault current limiter in the DC power system.

A saturated iron-core type superconducting fault current limiter (SI-SFCL) can effectively restrict the magnitude of the fault current and alleviate the strain on circuit breakers in DC power systems. Design of a superconducting coil (SC), which is one of the key tasks in the SI-SFCL design, requires guaranteeing a sufficient magnetic field, ensuring optimization of the shape and size, minimizing the wire cost, and satisfying the safety and stability of operation. Generally, finite element method (FEM) is used to calculate and evaluate the operating characteristics of SCs, from which it is possible to determine their optimal design parameters. When the coil is complex and large, the simulation time may range from hours to days, and if input parameters change even slightly, the simulations have to be redone from scratch. Recent advances in deep learning represent the ability to be effective for modeling and optimizing complex problems from training data or in real-time. In this paper, we presented a combination of the FEM simulation and deep Q-network (DQN) algorithm to optimize the SC design of a lab-scale SI-SFCL for a DC power system. The detailed design process and options for the SC of SI-SFCL were proposed. In order to analyze the characteristics related to the electromagnetic properties and operational features of the SC, a 3D FEM model was developed. Then, a DQN model was constructed and integrated with the FEM simulation for training and optimizing the design parameters of the SC in real-time. The obtained results of this study have the potential to effectively optimize the design parameters of large-scale SI-SFCL development for high-voltage DC power systems.

Preservation of keratinized mucosa around implants using a prefabricated implant-retained stent: a case-control study.

PURPOSE: The aim of this study was to clinically assess the impact of a prefabricated implant-retained stent clipped over healing abutments on the preservation of keratinized mucosa around implants after implant surgery, and to compare it with horizontal external mattress sutures. METHODS: A total of 50 patients were enrolled in this study. In the test group, a prefabricated implant-retained stent was clipped on the healing abutment after implant surgery to replace the keratinized tissue bucco-apically. In the control group, horizontal external mattress sutures were applied instead of using a stent. After the surgical procedure, the width of the buccal keratinized mucosa was measured at the mesial, middle, and distal aspects of the healing abutment. The change in the width of the buccal keratinized mucosa was assessed at 1 and 3 months. RESULTS: Healing was uneventful in both groups. The difference of width between baseline and 1 month was -0.26±0.85 mm in the test group, without any statistical significance (P=0.137). Meanwhile, the corresponding difference in the control group was -0.74±0.73 mm and it showed statistical significance (P<0.001). The difference of width between baseline and 3 months was -0.57±0.97 mm in the test group and -0.86±0.71 mm in the control group. These reductions were statistically significant (P<0.05); however, there was no difference between the 2 groups. CONCLUSIONS: Using a prefabricated implant-retained stent was shown to be effective in the preservation of the keratinized mucosa around implants and it was simple and straightforward in comparison to the horizontal external mattress suture technique.

TRAIL restores DCA/metformin-mediated cell death in hypoxia.

Previous studies have shown that hypoxia can reverse DCA/metformin-induced cell death in breast cancer cells. Therefore, targeting hypoxia is necessary for therapies targeting cancer metabolism. In the present study, we found that TRAIL can overcome the effect of hypoxia on the cell death induced by treatment of DCA and metformin in breast cancer cells. Unexpectedly, DR5 is upregulated in the cells treated with DCA/metformin, and sustained under hypoxia. Blocking DR5 by siRNA inhibited DCA/metformin/TRAIL-induced cell death, indicating that DR5 upregulation plays an important role in sensitizing cancer cells to TRAIL-induced cell death. Furthermore, we found that activation of JNK and c-Jun is responsible for upregulation of DR5 induced by DCA/metformin. These findings support the potential application of combining TRAIL and metabolism-targeting drugs in the treatment of cancers under hypoxia.

Combined effects of EGFR tyrosine kinase inhibitors and vATPase inhibitors in NSCLC cells.

Despite excellent initial clinical responses of non-small cell lung cancer (NSCLC) patients to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs), many patients eventually develop resistance. According to a recent report, vacuolar H+ ATPase (vATPase) is overexpressed and is associated with chemotherapy drug resistance in NSCLC. We investigated the combined effects of EGFR TKIs and vATPase inhibitors and their underlying mechanisms in the regulation of NSCLC cell death. We found that combined treatment with EGFR TKIs (erlotinib, gefitinib, or lapatinib) and vATPase inhibitors (bafilomycin A1 or concanamycin A) enhanced synergistic cell death compared to treatments with each drug alone. Treatment with bafilomycin A1 or concanamycin A led to the induction of Bnip3 expression in an Hif-1α dependent manner. Knock-down of Hif-1α or Bnip3 by siRNA further enhanced cell death induced by bafilomycin A1, suggesting that Hif-1α/Bnip3 induction promoted resistance to cell death induced by the vATPase inhibitors. EGFR TKIs suppressed Hif-1α and Bnip3 expression induced by the vATPase inhibitors, suggesting that they enhanced the sensitivity of the cells to these inhibitors by decreasing Hif-1α/Bnip3 expression. Taken together, we conclude that EGFR TKIs enhance the sensitivity of NSCLC cells to vATPase inhibitors by decreasing Hif-1α/Bnip3 expression. We suggest that combined treatment with EGFR TKIs and vATPase inhibitors is potentially effective for the treatment of NSCLC.