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Abstract:The atmospheric propagation delay of radar signals is a systematic error that occurs in the atmospheric environment, and is a key issue in the high-precision geometric calibration of spaceborne SAR. A multimode hybrid geometric calibration method for spaceborne SAR that considers the atmospheric propagation delay is proposed in this paper. Error sources that affect the accuracy of the geometric calibration were systematically analyzed. Based on correction of the atmospheric propagation delay, a geometric calibration model for spaceborne SAR was established. The high precision geometric calibration scheme for spaceborne SAR was explored by considering the pulse-width and bandwidth of the signal. A series of experiments were carried out based on high-resolution Yaogan 13 (YG-13) SAR satellite data and ground control data. The experimental results demonstrated that the proposed method is effective. The plane positioning accuracy of YG-13 in stripmap mode without control points is better than 3 m, and the accuracy of the sliding spotlight mode is better than 1.5 m.

* ese authors contributed equally to this work PEG10 promotes the migration of human Burkitt's lymphoma cells by up-regulating the expression of matrix metalloproteinase-2 and -9 Abstract Purpose: Paternally expressed gene 10 (PEG10) is important for apoptosis resistance in cancer cells; however, the e ect of PEG10 on tumor cell migration remains poorly understood. In this study, we investigated the e ects of PEG10 on proliferation, apoptosis, adhesion and migration in the Burkitt's lymphoma cell line, Raji.Methods: Apoptosis was induced by 5-uorouracil (5-FU) in pcDNA3.0/PEG10 transiently transfected HEK293T cells and PEG10-suppressed Raji cells. siRNAPEG10 was used to inhibit PEG10 expression. Fluorescence-activated cell sorting (FACS) were performed to analyze the e ect of PEG10 on apoptosis. CCK-8 were performed to detect cell proliferation and adhesion. Matrigel invasion were performed using PEG10-suppressed Raji cells to investigate cell migration. e expression levels of matrix metalloproteinases -2 and -9 (MMP-2 and MMP-9) were analyzed in PEG10-suppressed Raji cells using both real-time RT-PCR and Western blot analysis.Results: HEK293T cells that overexpressed PEG10 exhibited greater viability 48 h following treatment with 5-FU, relative to control cells. Speci c inhibition of PEG10 expression by siRNA resulted in inhibition of growth and apoptosis in Raji cells. Adherence and invasion capabilities were downregulated and expression levels of MMP-2 and MMP-9 were reduced in PEG10-suppressed Raji cells.Conclusions: Our ndings demonstrated that PEG10 enhances the apoptotic resistance and viability of Raji cells. e migration and adherence invasion capacity of Raji cells could potentially be a ected by regulation of the expression of MMP-2 and MMP-9. Our research provides a promising strategy for cancer immunotherapy of lymphoma.

The coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is bringing an unprecedented health crisis to the world. To date, our understanding of the interaction between SARS-CoV-2 and host innate immunity is still limited. Previous studies reported that SARS-CoV-2 non-structural protein 12 (NSP12) was able to suppress interferon-β (IFN-β) activation in IFN-β promoter luciferase reporter assays, which provided insights into the pathogenesis of COVID-19. In this study, we demonstrated that IFN-β promoter mediated luciferase activity was reduced during co-expression of NSP12. However, we could show NSP12 did not affect IRF3 or NF-κB activation. Moreover, IFN-β production induced by Sendai virus (SeV) infection or other stimulus was not affected by NSP12 at mRNA or protein level. Additionally, type I IFN signaling pathway was not affected by NSP12, as demonstrated by the expression of interferon stimulated genes (ISGs). Further experiments revealed that different experiment systems, including protein tags and plasmid backbones, could affect the readouts of IFN-β promoter luciferase assays. In conclusion, unlike previously reported, our study showed SARS-CoV-2 NSP12 protein is not an IFN-β antagonist. It also rings the alarm on the general usage of luciferase reporter assays in studying SARS-CoV-2. Importance Previous studies investigated the interaction between SARS-CoV-2 viral proteins and interferon signaling, and proposed that several SARS-CoV-2 viral proteins, including NSP12, could suppress IFN-β activation. However, most of these results were generated from IFN-β promoter luciferase reporter assay, and have not been validated functionally. In our study, we found that although NSP12 could suppress IFN-β promoter luciferase activity, it showed no inhibitory effect on IFN-β production or it downstream signaling. Further study revealed that contradictory results could generated from different experiment systems. On one hand, we demonstrated that SARS-CoV-2 NSP12 could not suppress IFN-β signaling. On the other hand, our study suggests that cautions need to be taken with the interpretation of SARS-CoV-2 related luciferase assays.