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This article presents a novel frequency-tapered Ring Bar Slow Wave Structure (RBSWS) for high-gain and wide-bandwidth Traveling Wave Tubes (TWTs) operating in the K-band for space applications. Starting from an analytical circuit model of the RBSWS, a conical-cut geometry is introduced to reduce the phase velocity. Our proposed novel RBSWS operates over a frequency range of 18.8 to 20.1 GHz, under a cathodic voltage and current of 19.8 kV and 0.3 A, respectively. Particle-In-Cell (PIC) results, carried out by CST Studio 2023, show a very high output peak power of 840.5 W at a gain of 20.2 dB, for an input power of 8 W, and an electron efficiency of 15.3%. The tapered RBSWS-TWT achieves a wider bandwidth, higher output power, and higher electron efficiency with respect to the untapered RBSWS-TWT, demonstrating the effectiveness of the proposed structure.

In this article, a sheet-beam type ring bar slow wave structure (RBSWS) capable of working at very low-voltage value is proposed. The structure is designed to work over the frequency range from 14 to 18 GHz with a cathodic voltage of 2.050 kV and a current of 100 mA. Simulation results for two 50-period sections, carried out by CST Studio Suite 2023, show a saturated output power of 30 W, a maximum gain of 0.795 dB/mm, and a radio frequency (RF) electronic efficiency higher than 15 %. The proposed structure is ideal for aerospace applications that usually require compact size, low weight and power consumption, while maintaining very high output power levels. Furthermore, this device is relatively easy to manufacture, making it a more accessible option than other structures that require complex and expensive manufacturing processes. Finally, the mechanical and thermal dissipation problems are kept under control thanks to the large surface contact between the slow wave structure and the dielectric rod realized in Boron Nitride.

Purpose: Myeloproliferative neoplasms (MPN) dysregulate JAK2 signaling. Because clinical JAK2 inhibitors have limited disease-modifying effects, type II JAK2 inhibitors such as CHZ868 stabilizing inactive JAK2 and reducing MPN clones, gain interest. We studied whether MPN cells escape from type ll inhibition., Experimental Design: MPN cells were continuously exposed to CHZ868. We used phosphoproteomic analyses and ATAC/RNA sequencing to characterize acquired resistance to type II JAK2 inhibition, and targeted candidate mediators in MPN cells and mice., Results: MPN cells showed increased IC50 and reduced apoptosis upon CHZ868 reflecting acquired resistance to JAK2 inhibition. Among >2,500 differential phospho-sites, MAPK pathway activation was most prominent, while JAK2-STAT3/5 remained suppressed. Altered histone occupancy promoting AP-1/GATA binding motif exposure associated with upregulated AXL kinase and enriched RAS target gene profiles. AXL knockdown resensitized MPN cells and combined JAK2/AXL inhibition using bemcentinib or gilteritinib reduced IC50 to levels of sensitive cells. While resistant cells induced tumor growth in NOD/SCID gamma mice despite JAK2 inhibition, JAK2/AXL inhibition largely prevented tumor progression. Because inhibitors of MAPK pathway kinases such as MEK are clinically used in other malignancies, we evaluated JAK2/MAPK inhibition with trametinib to interfere with AXL/MAPK-induced resistance. Tumor growth was halted similarly to JAK2/AXL inhibition and in a systemic cell line-derived mouse model, marrow infiltration was decreased supporting dependency on AXL/MAPK., Conclusions: We report on a novel mechanism of AXL/MAPK-driven escape from type II JAK2 inhibition, which is targetable at different nodes. This highlights AXL as mediator of acquired resistance warranting inhibition to enhance sustainability of JAK2 inhibition in MPN., (©2023 The Authors; Published by the American Association for Cancer Research.)