A wideband and compact end-fire antenna with bowtie-shape drivers is proposed. Based on a wideband microstrip-to-coplanar stripline transition and bowtie-shaped drivers, a broadband impedance bandwidth of more than 75% (4.70-10.44 GHz) for return loss less than − 15 dB and a gain of 5.0-9.1 dBi are obtained. What is more, the front-to-back ratio over the frequency of interest is less than − 10 dB. The overall dimensions of the proposed antenna are only 30 × 24.24 mm 2 . A prototype is fabricated and measured. The simulated and measured results of the proposed antenna indicate that it is suitable for phased array and microwave imaging systems.Introduction: Quasi-Yagi antennas with end-fire radiation have attracted huge interest owing to their light weight, small size, simple fabrication, low cost and ease of integration with RF front-end circuits [1]. The main elements of the antenna are the feeding structure or balun, driver, director and reflector. To satisfy the need of some broadband systems, such as microwave imaging systems and modern telecommunications, based on some wideband feeding structures, many broadband antennas have been proposed [2][3][4][5][6][7]. In [8], an antenna with a balun of microstrip-to-slotline transitions was proposed and a bandwidth of more than 70% and a gain around 4 dBi are obtained. Although the bandwidth of the antenna is enough, the gain is relatively low. A modified antenna based on [8] was presented in [9] and a gain of about 4-6 dBi was achieved. In [10], a broadband periodic end-fire antenna with a gain of about 6.2-9.9 dBi in the whole operating band by using split-ring resonator structures was proposed, but the size (28 × 56.5 mm 2 ) is too large for some wireless communication systems or integrated circuits.In this Letter, in order to resolve the problems mentioned above, we combine the advantages of the broadband feeding structure as given in [7] with the merits of the bowtie dipoles [11]. A wideband and compact quasi-Yagi antenna is proposed. By optimising the structure of the feeding structure and the bowtie-shaped drivers, the proposed antenna has an impedance bandwidth of more than 75% (4.70-10.44 GHz) for a return loss less than − 15 dB and a gain of about 5.0-9.1 dBi over the operating frequency. Meanwhile, the overall size is 30 × 24.24 mm 2 . HFSS software based on the finite-element method is used to design this antenna and good agreements between the measured and simulated results are achieved.
In order to effectively solve the risk of safety on power window, an improved pinch detection algorithm based on the fault detection observer estimation is proposed for an anti-pinch window control system. In designing a residual generator, the proposed fault detection algorithm makes use of the pinch torque rate information by establishing the mathematical model of DC, considered as a fault under the pinched condition. By comparing the residual signal with the pre-designed threshold, the occurrence of pinch is detected. The fault detection observer takes into account robustness against disturbances and sensitivity to faults, simultaneously, both of which are regarded as optimization problems. In this study, the mixed H-/H∞ performance index and reference model fault detection method are advanced to solve the optimization problem in the Linear Matrix Inequality (LMI) which transforms a mathematical problem. The simulation results of the detection time obtained from the two methods are 0.15 and 0.07s, respectively, proving that the use of the fault detection algorithm is effective for an anti-pinch window. The co-simulation based on CANoe-MATLAB is proposed to verify the algorithm again. Moreover, under the premise of strong robustness, the reference model method is superior to the mixed H-/H∞ performance.
Background Evading apoptosis by overexpression of anti-apoptotic Bcl-2 family proteins is a hallmark of cancer cells and the Bcl-2 selective inhibitor venetoclax is widely used in the treatment of hematologic malignancies. Mcl-1, another anti-apoptotic Bcl-2 family member, is recognized as the primary cause of resistance to venetoclax treatment. However, there is currently no Mcl-1 inhibitor approved for clinical use. Methods Paired parental and Mcl-1 knockout H1299 cells were used to screen and identify a small molecule named MI-238. Immunoprecipitation (IP) and flow cytometry assay were performed to analyze the activation of pro-apoptotic protein Bak. Annexin V staining and western blot analysis of cleaved caspase 3 were employed to measure the cell apoptosis. Mouse xenograft AML model using luciferase-expressing Molm13 cells was employed to evaluate in vivo therapeutic efficacy. Bone marrow samples from newly diagnosed AML patients were collected to evaluate the therapeutic potency. Results Here, we show that MI-238, a novel and specific Mcl-1 inhibitor, can disrupt the association of Mcl-1 with BH3-only pro-apoptotic proteins, selectively leading to apoptosis in Mcl-1 proficient cells. Moreover, MI-238 treatment also potently induces apoptosis in acute myeloid leukemia (AML) cells. Notably, the combined treatment of MI-238 with venetoclax exhibited strong synergistic anti-cancer effects in AML cells in vitro, MOLM-13 xenografts mouse model and AML patient samples. Conclusions This study identified a novel and selective Mcl-1 inhibitor MI-238 and demonstrated that the development of MI-238 provides a novel strategy to improve the outcome of venetoclax therapy in AML.
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