Vaccination is a key strategy to prevent the pandemic caused by the coronavirus disease 2019 (COVID-19). This study aims to investigate the willingness of Chinese adults to be vaccinated against COVID-19 and further explore the factors that may affect their willingness. We used a self-design anonymous questionnaire to conduct an online survey via the Sojump. A total of 1009 valid questionnaires were analyzed. The age of the participants ranged from 18 to 74. Among them, 609 (60.4%, 95%CI: 57.4–63.4%) were willing to receive the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) vaccine. Logistic regression analysis results showed that the age of 30-49 (OR = 2.042, 95%CI: 1.098–3.799), universities and colleges education (OR = 1.873, 95% CI = 1.016–3.451), master degree or above education (OR = 1.885, 95%CI = 1.367–2.599), previous influenza vaccination history (OR = 2.176, 95%CI: 1.474–3.211), trust in the effectiveness of the vaccine (OR = 6.419, 95%CI: 3.717–11.086), and close attention to the latest news of the vaccine (OR = 1.601, 95%CI: 1.046–2.449) were facilitative factors that affected their willingness to be vaccinated. More than half of the adults in China would be willing to receive a SARS-CoV-2 vaccine. Middle-aged people with higher education, those who had been vaccinated against influenza, and those who believed that COVID-19 vaccine was effective and paid close attention to it were more willing to be vaccinated. Our findings can provide reference for the implementation of vaccination and the prevention of COVID-19 in China. More studies are needed after the vaccine is launched.

SUMMARYRibosomal RNA processing is essential for plastid ribosome biogenesis, but is still poorly understood in higher plants. Here, we show that SUPPRESSOR OF THYLAKOID FORMATION1 (SOT1), a plastid-localized pentatricopeptide repeat (PPR) protein with a small MutS-related domain, is required for maturation of the 23S-4.5S rRNA dicistron. Loss of SOT1 function leads to slower chloroplast development, suppression of leaf variegation, and abnormal 23S and 4.5S processing. Predictions based on the PPR motif sequences identified the 5 0 end of the 23S-4.5S rRNA dicistronic precursor as a putative SOT1 binding site. This was confirmed by electrophoretic mobility shift assay, and by loss of the abundant small RNA 'footprint' associated with this site in sot1 mutants. We found that more than half of the 23S-4.5S rRNA dicistrons in sot1 mutants contain eroded and/or unprocessed 5 0 and 3 0 ends, and that the endonucleolytic cleavage product normally released from the 5 0 end of the precursor is absent in a sot1 null mutant. We postulate that SOT1 binding protects the 5 0 extremity of the 23S-4.5S rRNA dicistron from exonucleolytic attack, and favours formation of the RNA structure that allows endonucleolytic processing of its 5 0 and 3 0 ends.

Psoriasis is an immune-mediated systemic disease with associated comorbidities, including metabolic syndrome (MetS) which contributes substantially to premature mortality in patients with psoriasis. However, the pathological mechanisms underlying this comorbidity are unclear. Studies have shown that the pathological parameters of psoriasis mediate the development of MetS. We reviewed the potential mechanisms which mediate the association between psoriasis and MetS, including endoplasmic reticulum stress, pro-inflammatory cytokine releases, excess production of reactive oxygen species, alterations in adipocytokine levels and gut microbiota dysbiosis. Here, we highlight important research questions regarding this association and offer insights into MetS research and treatment.

Gossypium hirsutum is a high yield cotton species that exhibits only moderate performance in fiber qualities. A promising but challenging approach to improving its phenotypes is interspecific introgression, the transfer of valuable traits or genes from the germplasm of another species such as G. barbadense, an important cultivated extra long staple cotton species. One set of chromosome segment introgression lines (CSILs) was developed, where TM-1, the genetic standard in G. hirsutum, was used as the recipient parent and the long staple cotton G. barbadense Hai7124 was used as the donor parent by molecular marker-assisted selection (MAS) in BC(5)S(1–4) and BC(4)S(1–3) generations. After four rounds of MAS, the CSIL population was comprised of 174 lines containing 298 introgressed segments, of which 86 (49.4%) lines had single introgressed segments. The total introgressed segment length covered 2,948.7 cM with an average length of 16.7 cM and represented 83.3% of tetraploid cotton genome. The CSILs were highly varied in major fiber qualities. By integrated analysis of data collected in four environments, a total of 43 additive quantitative trait loci (QTL) and six epistatic QTL associated with fiber qualities were detected by QTL IciMapping 3.0 and multi-QTL joint analysis. Six stable QTL were detected in various environments. The CSILs developed and the analyses presented here will enhance the understanding of the genetics of fiber qualities in long staple G. barbadense and facilitate further molecular breeding to improve fiber quality in Upland cotton.

Owing to the limitations of the present efforts on drug discovery against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and the lack of the understanding of the biological regulation mechanisms underlying COVID-19, alternative or novel therapeutic targets for COVID-19 treatment are still urgently required. SARS-CoV-2 infection and immunity dysfunction are the two main courses driving the pathogenesis of COVID-19. Both the virus and host factors are potential targets for antiviral therapy. Hence, in this study, the current therapeutic strategies of COVID-19 have been classified into “target virus” and “target host” categories. Repurposing drugs, emerging approaches, and promising potential targets are the implementations of the above two strategies. First, a comprehensive review of the highly acclaimed old drugs was performed according to evidence-based medicine to provide recommendations for clinicians. Additionally, their unavailability in the fight against COVID-19 was analyzed. Next, a profound analysis of the emerging approaches was conducted, particularly all licensed vaccines and monoclonal antibodies (mAbs) enrolled in clinical trials against primary SARS-CoV-2 and mutant strains. Furthermore, the pros and cons of the present licensed vaccines were compared from different perspectives. Finally, the most promising potential targets were reviewed, and the update of the progress of treatments has been summarized based on these reviews.

Chloroplast biogenesis and development are highly complex processes requiring interaction between plastid and nuclear genomic products. Using a high-throughput screen for chloroplast biogenesis suppressors in Arabidopsis (), we identified a () that displays virescent and serrated leaves. Further characterization revealed that mutants are defective in leaf adaxial and abaxial polarity and act as enhancers of Map-based cloning identified as a gene previously named that encodes a plastid-targeted pentatricopeptide repeat (PPR) protein with 11 PPR motifs. A G-to-A mutation in leads to a significant decrease in splicing efficiency, generating two additional mRNA variants. As reported previously, the null mutation is embryo lethal. SOT5 is predicted to bind to specific RNA sequences found in plastid and genes, and we found decreased splicing efficiency of the and genes in mutants. Together, our results reveal that the PPR protein SOT5/EMB2279 is required for intron splicing of plastid and , providing insights into the role of plastid translation in the coupled development between chloroplasts and leaves.

Immune checkpoint inhibitors (ICIs) that target cytotoxic T lymphocyte antigen 4, programmed cell death-1, and PD-ligand 1 have revolutionized cancer treatment, achieving unprecedented efficacy in multiple malignancies. ICIs are increasingly being used in early cancer settings and in combination with various other types of therapies, including targeted therapy, radiotherapy, and chemotherapy. However, despite the excellent therapeutic effect of ICIs, these medications typically result in a broad spectrum of toxicity reactions, termed immune-related adverse events (irAEs). Of all irAEs, cardiotoxicity, uncommon but with high mortality, has not been well recognized. Herein, based on previous published reports and current evidence, we summarize the incidence, diagnosis, clinical manifestations, underlying mechanisms, treatments, and outcomes of ICI-associated cardiotoxicity and discuss possible management strategies. A better understanding of these characteristics is critical to managing patients with ICI-associated cardiotoxicity.

UDP-glucose:glycoprotein glucosyltransferase 1 (UGT1) serves as a folding sensor in the calnexin/calreticulin glycoprotein quality control cycle. UGT1 recognizes disordered or hydrophobic patches near asparagine-linked nonglucosylated glycans in partially misfolded glycoproteins and reglucosylates them, returning folding intermediates to the cycle. In this study, we examine the contribution of the UGT1-regulated quality control mechanism to MHC I antigen presentation. Using UGT1-deficient mouse embryonic fibroblasts reconstituted or not with UGT1, we show that, although formation of the peptide loading complex is unaffected by the absence of UGT1, the surface level of MHC class I molecules is reduced, MHC class I maturation and assembly are delayed, and peptide selection is impaired. Most strikingly, we show using purified soluble components that UGT1 preferentially recognizes and reglucosylates MHC class I molecules associated with a suboptimal peptide. Our data suggest that, in addition to the extensively studied tapasin-mediated quality control mechanism, UGT1 adds a new level of control in the MHC class I antigen presentation pathway.antigen processing | chaperones M ajor histocompatibility complex (MHC) class I-mediated antigen presentation is critical for adaptive immune responses to intracellular pathogens. MHC class I assembly and peptide loading constitute a specialized case of glycoprotein folding, using general chaperones and enzymes involved in the endoplasmic reticulum (ER) quality control machinery as well as MHC class I-specific cofactors. Like other glycoproteins, MHC class I heavy chains (HCs) are modified during translocation by asparagine (N)-linked glycosylation with the glycan Glc 3 Man 9 GlcNAc 2 . After the first two glucose residues are trimmed by glucosidases I (GlsI) and II (GlsII), the monoglucosylated (Glc 1 Man 9 GlcNAc 2 ) glycan interacts with the lectin chaperone calnexin (CNX) for oxidative folding (1). The maturing HCs are partially stabilized by β 2 -microglobulin (β 2 m) association, and the HC/β 2 m dimers are recruited by the second lectin chaperone calreticulin (CRT) into the peptide loading complex (PLC) via their monoglucosylated glycans (2, 3). The PLC is composed of the HC/β 2 m dimer, CRT, the transporter associated with antigen processing (TAP), and a disulfide-linked tapasin-ERp57 conjugate (reviewed in ref. 4). It facilitates peptide loading onto MHC class I molecules and functions in quality control by retaining empty and suboptimally loaded MHC class I molecules in the ER.The glycosylation status of ER MHC class I molecules is highly regulated. Monoglucosylation is not detectable in free human MHC class I HCs (5), whereas PLC-associated HCs are virtually all monoglucosylated (3, 5). Inhibiting deglucosylation of the monoglucosylated glycan prolongs the interaction of MHC class I molecules with the PLC (3, 6), and, in vitro, GlsII can trim the monoglucosylated glycans of free HCs but not PLC-associated HCs (3). This suggests that only when MHC class I molecules dis...