The new generation particle accelerator requires a highly stable radio frequency (RF) system. The stability of the RF system is realized by the Low Level RF (LLRF) subsystem which controls the amplitude and phase of the RF signal. The detection of the RF signal's amplitude and phase is fundamental to LLRF controls. High-speed ADC (Analog to Digital Converter), DAC (Digital to Analog Converter) and FPGA (Field Programmable Gate Array) play very important roles in digital LLRF control systems. This paper describes the implementation of real-time amplitude and phase detection based of the FPGA with an analysis of the main factors that affect the detection accuracy such as jitter, algorithm's defects and non-linearity of devices, which is helpful for future work on high precision detection and control.
The Superconducting Proton Linac (SPL) is the project for a superconducting, high current H-accelerator at CERN. To find dangerous higher order modes (HOMs) in the SPL superconducting cavities, simulation and analysis for the cavity model using simulation tools are necessary. The existing TESLA 9-cell cavity geometry data have been used for the initial construction of the models in HFSS. Monopole, dipole and quadrupole modes have been obtained by applying different symmetry boundaries on various cavity models. In calculation, scripting language in HFSS was used to create scripts to automatically calculate the parameters of modes in these cavity models (these scripts are also available in other cavities with different cell numbers and geometric structures). The results calculated automatically are then compared with the values given in the TESLA paper. The optimized cavity model with the minimum error will be taken as the base for further simulation of the SPL cavities.
Background: Infantile pneumonia is a respiratory infection disease, seriously threatening the life of neonatal patients. Circular RNA (circRNA) dysregulation is reported to be involved in pneumonia pathogenesis. Circ_0012535 was previously displayed to be upregulated in blood samples of patients with community-acquired pneumonia. However, circ_0012535’s role in this disorder remains unclear. We thus aim to unveil the functions of circ_0012535 in infantile pneumonia. Methods: Fetal lung fibroblasts (WI38) treated with LPS were used as pneumonia cell models. Expression analysis for circ_0012535, miR-338-3p and IL6R was performed using quantitative real-time polymerase chain reaction. Cell counting kit 88), 5-ethynyl-2′-deoxyuridine, and flow cytometry assays were implemented for cell function detection. The release of inflammatory factors, and superoxide dismutase activity and malonaldehyde content were ascertained using commercial kits. The putative binding between miR-338-3p and circ_0012535 or IL6R was validated by dual-luciferase analysis, RIP analysis, and pull-down analysis. Results: Circ_0012535 was highly expressed in LPS-treated WI38 cells. Knockdown of circ_0012535 recovered LPS-inhibited cell viability and proliferation and attenuated LPS-induced cell apoptosis, cell cycle arrest, inflammation, and oxidative stress. Circ_0012535 bound to miR-338-3p and negatively regulated miR-338-3p expression. Inhibition of miR-338-3p reversed the role of circ_0012535 knockdown, thereby recovering LPS-induced WI38 cell apoptosis and inflammation. MiR-338-3p bound to IL6R 3′UTR, and circ_0012535 shared miR-338-3p binding site with IL6R. IL6R overexpression reversed the role of miR-338-3p, thereby recovering LPS-induced WI38 cell apoptosis and inflammation. Conclusion: Circ_0012535 supported LPS-induced WI38 cell apoptosis and inflammation to promote the progression of infantile pneumonia, and circ_0012535 functioned partly by targeting the miR-338-3p/IL6R signaling.
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