BackgroundAlthough several key molecules have been identified to modulate SARS-CoV-2 invasion of human host cells, the molecules correlated with outcomes in COVID-19 caused by SARS-CoV-2 infection remain insufficiently explored.MethodsThis study analyzed three RNA-Seq gene expression profiling datasets for COVID-19 and identified differentially expressed genes (DEGs) between COVID-19 patients and normal people, commonly in the three datasets. Furthermore, this study explored the correlation between the expression of these genes and clinical features in COVID-19 patients.ResultsThis analysis identified 13 genes significantly upregulated in COVID-19 patients’ leukocyte and SARS-CoV-2-infected nasopharyngeal tissue compared to normal tissue. These genes included OAS1, OAS2, OAS3, OASL, HERC6, SERPING1, IFI6, IFI44, IFI44L, CMPK2, RSAD2, EPSTI1, and CXCL10, all of which are involved in antiviral immune regulation. We found that these genes’ downregulation was associated with worse clinical outcomes in COVID-19 patients, such as intensive care unit (ICU) admission, mechanical ventilatory support (MVS) requirement, elevated D-dimer levels, and increased viral loads. Furthermore, this analysis identified two COVID-19 clusters based on the expression profiles of the 13 genes, termed COV-C1 and COV-C2. Compared with COV-C1, COV-C2 more highly expressed the 13 genes, had stronger antiviral immune responses, were younger, and displayed more favorable clinical outcomes.ConclusionsA strong antiviral immune response is essential in reducing severity of COVID-19.

Hepatocellular carcinoma (HCC) is characterized by a poor prognosis because of its insensitivity to radiation and chemotherapy. Recently, circular RNAs (circRNAs) have been found to serve important roles in hepatocellular carcinogenesis. circ-CCT3, a novel circRNA, was screened from the differential tissue expression results of a circRNA microarray. Relative expression levels of circ-CCT3 in specimens and cell lines were evaluated by reverse transcription-quantitative PCR and the relationship between circ-CCT3 and prognosis was analyzed by Kaplan-Meier curves. The oncogenic role of circ-CCT3 was confirmed in HCC cells through a cell counting kit-8 (CCK-8) assay, a colony formation assay, acridine orange/ethidium bromide double fluorescence staining, flow cytometry, a wound-healing assay and a Transwell assay. Bioinformatics prediction and luciferase reporter assays validated that circ-CCT3 facilitated HCC progression through the miR-1287-5p/TEA domain transcription factor 1 (TEAD1) axis. TEAD1 could then directly activate patched 1 and lysyl oxidase transcription, as analyzed by chromatin immunoprecipitation and luciferase reporter assays. The present study identified a novel circRNA, circ-CCT3, which may be used as a potential therapeutic target for HCC.

The main task of the Top Tracker detector of the neutrino reactor experiment Jiangmen Underground Neutrino Observatory (JUNO) is to reconstruct and extrapolate atmospheric muon tracks down to the central detector. This muon tracker will help to evaluate the contribution of the cosmogenic background to the signal. The Top Tracker is located above JUNO's water Cherenkov Detector and Central Detector, covering about 60% of the surface above them. The JUNO Top Tracker is constituted by the decommissioned OPERA experiment Target Tracker modules. The technology used consists in walls of two planes of plastic scintillator strips, one per transverse direction. Wavelength shifting fibres collect the light signal emitted by the scintillator strips and guide it to both ends where it is read by multianode photomultiplier tubes. Compared to the OPERA Target Tracker, the JUNO Top Tracker uses new electronics able to cope with the high rate produced by the high rock radioactivity compared to the one in Gran Sasso underground laboratory. This paper will present the new electronics and mechanical structure developed for the Top Tracker of JUNO along with its expected performance based on the current detector simulation.

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We discuss JUNO sensitivity to the annihilation of MeV dark matter in the galactic halo via detecting inverse beta decay reactions of electron anti-neutrinos resulting from the annihilation. We study possible backgrounds to the signature, including the reactor neutrinos, diffuse supernova neutrino background, charged- and neutral-current interactions of atmospheric neutrinos, backgrounds from muon-induced fast neutrons and cosmogenic isotopes. A fiducial volume cut, as well as the pulse shape discrimination and the muon veto are applied to suppress the above backgrounds. It is shown that JUNO sensitivity to the thermally averaged dark matter annihilation rate in 10 years of exposure would be significantly better than the present-day best limit set by Super-Kamiokande and would be comparable to that expected by Hyper-Kamiokande.