Ultra High Voltage Switch for Bidirectional DC-DC Converter Driving Dielectric Elastomer Actuator

Specific applications, such as dielectric elastomer actuators (DEAs) or electroactive polymers, require to switch voltage levels exceeding the ratings of existing semiconductor devices. In low power application, reversible flyback are widely used to supply DEAs. Lowering the parallel parasitic capacitance of the high voltage switch is important to improve the energy transfer, while it becomes mandatory to increase the output voltage of flyback above 2.5 kV. In this paper, a Pulsed Transformer Gate Driver (PTGD) is used to drive series-connected MOSFET and therefore push the limits from 4.5 kV up to 16 kV. At these high voltage levels, the structure reveals a drastic voltage unbalance related to the transformer interwinding parasitic capacitance. The compensation method proposed to achieve voltage balance only adds few passive components and reduces significantly the additional parallel capacitance of the switch compared to common load side voltage balancing methods. Finally and as proof of concept, a half-bridge bidirectional converter was designed from this switch technology and drove an actual dielectric elastomer actuator at 16 kV

Multi-level high-voltage power supply for dea application

In order to reap the benefits of Dielectric Elastomer Actuator (DEA) high energy density, the electronics powering the actuator should be as small as possible. Knowing that only a small fraction of the energy delivered to DEAs is effectively converted into mechanical energy, the power supply has to be highly efficient and bidirectional in order to recover the unused energy, which requires more volume. Furthermore, DEA applications call for high voltage (up to 18kV for a 200um film), but as the voltage increases, so does the volume. In addition, there are no MOS transistors rated above 4.5kV, which limits our options. Since these goals are contradictory, we need to demonstrate the feasibility of DEA integration and find its limits. Therefore we present a prototype of Multi-Level Converter designed for DEA, which is a bidirectional structure that has proven to be especially effective in the power electronics field. A Multi-Level Converter overcomes the voltage limitation by equally distributing the desired voltage among levels; because the voltage of each level is sufficiently low, smaller available parts can now be used. Our prototype includes 20 levels of 1kV each. A numerical study of this topology has demonstrated that the efficiency is above 90%. Upcoming experimental works will discuss the advantages and the drawbacks of such Multi-Level Converters. Finally, the volume of the DEA will be compared with the volume of electronics

High voltage switch for compact bidirectional dc-dc converter driving dielectric electroactive polymer actuators

Driving DEAs requires time-varying high voltage power supplies, up to 18kV for 200um polymer layers. HV amplifiers are commonly used but bulky and expensive. Designing embedded actuators requires compact and efficient powersupplies. Furthermore, only a little part of the electrical energy delivered to the DEA is converted to mechanical energy. The major part is stored in the capacitance of the actuator and needs to be recollected to maximise the system's efficiency. Low cost integrated bidirectional DC-DC converters (ex. Flyback) have been proven reliable to drive DEAs at voltages up to 2,5kV. To design a reversible converter with an output voltage up to 18kV, a high voltage switch is needed. Yet, the maximum breakdown voltage for a MOSFET with current ratings inferior to 200mA is 4,5kV. Our simulation and experimental work demonstrate a reliable driving circuit for triggering two series connected MOSFETs. A wide voltage switching range is achieved (0 to 8kV) with a 200mA current rating. Using the Transformer Gate Driver topology, galvanic insulation and synchronisation of each gate driver is ensured. To gain an equal distribution of the bus voltage over the MOSFETs, mastering the parasitic capacitances is mandatory. A design method has been developed to compensate these parasites and ensure the reliability of the device. The architecture of the high voltage switch is N-scalable and a switching range from 0 to 18kV could be achieved when stacking five MOSFETs in series

A distinct innate lymphoid cell population regulates tumor-associated T cells.

Antitumor T cells are subject to multiple mechanisms of negative regulation. Recent findings that innate lymphoid cells (ILCs) regulate adaptive T cell responses led us to examine the regulatory potential of ILCs in the context of cancer. We identified a unique ILC population that inhibits tumor-infiltrating lymphocytes (TILs) from high-grade serous tumors, defined their suppressive capacity in vitro, and performed a comprehensive analysis of their phenotype. Notably, the presence of this CD56+CD3- population in TIL cultures was associated with reduced T cell numbers, and further functional studies demonstrated that this population suppressed TIL expansion and altered TIL cytokine production. Transcriptome analysis and phenotypic characterization determined that regulatory CD56+CD3- cells exhibit low cytotoxic activity, produce IL-22, and have an expression profile that overlaps with those of natural killer (NK) cells and other ILCs. NKp46 was highly expressed by these cells, and addition of anti-NKp46 antibodies to TIL cultures abrogated the ability of these regulatory ILCs to suppress T cell expansion. Notably, the presence of these regulatory ILCs in TIL cultures corresponded with a striking reduction in the time to disease recurrence. These studies demonstrate that a previously uncharacterized ILC population regulates the activity and expansion of tumor-associated T cells

Schwann Cell Coculture Improves the Therapeutic Effect of Bone Marrow Stromal Cells on Recovery in Spinal Cord-Injured Mice

Studies of bone marrow stromal cells (MSCs) transplanted into the spinal cord-injured rat give mixed results: some groups report improved locomotor recovery while others only demonstrate improved histological appearance of the lesion. These studies show no clear correlation between neurological improvements and MSC survival. We examined whether MSC survival in the injured spinal cord could be enhanced by closely matching donor and recipient mice for genetic background and marker gene expression and whether exposure of MSCs to a neural environment (Schwann cells) prior to transplantation would improve their survival or therapeutic effects. Mice underwent a clip compression spinal cord injury at the fourth thoracic level and cell transplantation 7 days later. Despite genetic matching of donors and recipients, MSC survival in the injured spinal cord was very poor (~1%). However, we noted improved locomotor recovery accompanied by improved histopathological appearance of the lesion in mice receiving MSC grafts. These mice had more white and gray matter sparing, laminin expression, Schwann cell infiltration, and preservation of neurofilament and 5-HT-positive fibers at and below the lesion. There was also decreased collagen and chondroitin sulphate proteoglycan deposition in the scar and macrophage activation in mice that received the MSC grafts. The Schwann cell cocultured MSCs had greater effects than untreated MSCs on all these indices of recovery. Analyses of chemokine and cytokine expression revealed that MSC/Schwann cell cocultures produced far less MCP-1 and IL-6 than MSCs or Schwann cells cultured alone. Thus, transplanted MSCs may improve recovery in spinal cord-injured mice through immunosuppressive effects that can be enhanced by a Schwann cell coculturing step. These results indicate that the temporary presence of MSCs in the injured cord is sufficient to alter the cascade of pathological events that normally occurs after spinal cord injury, generating a microenvironment that favors improved recovery

A distinct innate lymphoid cell population regulates tumor-associated T cells.

Antitumor T cells are subject to multiple mechanisms of negative regulation. Recent findings that innate lymphoid cells (ILCs) regulate adaptive T cell responses led us to examine the regulatory potential of ILCs in the context of cancer. We identified a unique ILC population that inhibits tumor-infiltrating lymphocytes (TILs) from high-grade serous tumors, defined their suppressive capacity in vitro, and performed a comprehensive analysis of their phenotype. Notably, the presence of this CD56+CD3- population in TIL cultures was associated with reduced T cell numbers, and further functional studies demonstrated that this population suppressed TIL expansion and altered TIL cytokine production. Transcriptome analysis and phenotypic characterization determined that regulatory CD56+CD3- cells exhibit low cytotoxic activity, produce IL-22, and have an expression profile that overlaps with those of natural killer (NK) cells and other ILCs. NKp46 was highly expressed by these cells, and addition of anti-NKp46 antibodies to TIL cultures abrogated the ability of these regulatory ILCs to suppress T cell expansion. Notably, the presence of these regulatory ILCs in TIL cultures corresponded with a striking reduction in the time to disease recurrence. These studies demonstrate that a previously uncharacterized ILC population regulates the activity and expansion of tumor-associated T cells