Objectives: Although COVID-19 is known to be caused by human-to-human transmission, it remains largely unclear whether ambient air pollutants and meteorological parameters could promote its transmission. Methods: A retrospective study was conducted to study whether air quality index (AQI), four ambient air pollutants (PM 2.5 , PM 10 , NO 2 and CO) and five meteorological variables (daily temperature, highest temperature, lowest temperature, temperature difference and sunshine duration) could increase COVID-19 incidence in Wuhan and XiaoGan between Jan 26th to Feb 29th in 2020. Results: First, a significant correlation was found between COVID-19 incidence and AQI in both Wuhan (R 2 = 0.13, p < 0.05) and XiaoGan (R 2 = 0.223, p < 0.01). Specifically, among four pollutants, COVID-19 incidence was prominently correlated with PM 2.5 and NO 2 in both cities. In Wuhan, the tightest correlation was observed between NO 2 and COVID-19 incidence (R 2 = 0.329, p < 0.01). In XiaoGan, in addition to the PM 2.5 (R 2 = 0.117, p < 0.01) and NO 2 (R 2 = 0.015, p < 0.05), a notable correlation was also observed between the PM 10 and COVID-19 incidence (R 2 = 0.105, p < 0.05). Moreover, temperature is the only meteorological parameter that constantly correlated well with COVID-19 incidence in both Wuhan and XiaoGan, but in an inverse correlation (p < 0.05). Conclusions: AQI, PM 2.5 , NO 2 , and temperature are four variables that could promote the sustained transmission of COVID-19.

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The receptor for advanced glycation end products (RAGE) is associated with several pathological states including Alzheimer's disease (AD) pathology, while its soluble form (sRAGE) acts as a decoy receptor. We have tested for association of AD with a functional single-nucleotide polymorphism (SNP) in the RAGE gene (G82S; rs2070600), a SNP associated with increased ligand affinity of RAGE. Analysis of a Chinese cohort (276 cases; 254 controls) showed a higher prevalence of the RAGE 82S allele and GS + SS genotype in the patients [82S vs. 82G: P = 0.017, odds ratio (OR) = 1.431; GS + SS vs. GG: P = 0.025, OR = 1.490]. Further stratification analysis revealed that the association of the RAGE G82S polymorphism with AD was significant in early onset AD stratum. Moreover, plasma sRAGE levels were lower in AD than in normal elderly controls, and the presence of the risk allele was associated with further plasma sRAGE reduction and a fast cognitive deterioration. The present study provides preliminary evidence that the RAGE G82S variant is involved in genetic susceptibility to AD.

These results indicated that Sphk1/S1P regulates the expression of IL-17A in activated microglia, inducing neuronal apoptosis in cerebral ischemia/reperfusion. The microglial Sphk1/S1P pathway may thus be a potential therapeutic target to control neuroinflammation in brain IR.

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Pentatricopeptide repeat (PPR) proteins were identified as site-specific recognition factors for RNA editing in plant mitochondria and plastids. In this study, we characterized maize (Zea mays) kernel mutant defective kernel 46 (dek46), which has lethal embryo and collapsed endosperm. Dek46 encodes an E-subgroup PPR protein which possesses a short PLS repeat region of only seven repeats. Subcellular localization analysis indicated that DEK46 is localized in mitochondrion. The strand- and transcript-specific RNA-seq (STS-PCRseq) analysis showed that the dek46 mutation impacted C-to-U RNA editing at over 60 mitochondrial C targets. Biochemical analysis of mitochondrial protein complexes revealed significant reduced assembly of mitochondrial complex III in dek46. Transmission electron microscopy (TEM) observation showed severe morphological defects of mitochondria in dek46 endosperm cells. In addition, Yeast two-hybrid (Y2H) and luciferase complementation image (LCI) assays indicated that DEK46 can interact with mitochondria-targeting non-PPR RNA editing factor, ZmMORF1, suggesting that DEK46 might be a functional component in organellar RNA editosome.

Recent breakthroughs in transcriptome analysis and gene characterization have provided valuable resources and information about the maize endosperm developmental program. The high temporal‐resolution transcriptome analysis has yielded unprecedented access to information about the genetic control of seed development. Detailed spatial transcriptome analysis using laser‐capture microdissection has revealed the expression patterns of specific populations of genes in the four major endosperm compartments: the basal endosperm transfer layer (BETL), aleurone layer (AL), starchy endosperm (SE), and embryo‐surrounding region (ESR). Although the overall picture of the transcriptional regulatory network of endosperm development remains fragmentary, there have been some exciting advances, such as the identification of OPAQUE11 (O11) as a central hub of the maize endosperm regulatory network connecting endosperm development, nutrient metabolism, and stress responses, and the discovery that the endosperm adjacent to scutellum (EAS) serves as a dynamic interface for endosperm‐embryo crosstalk. In addition, several genes that function in BETL development, AL differentiation, and the endosperm cell cycle have been identified, such as ZmSWEET4c, Thk1, and Dek15, respectively. Here, we focus on current advances in understanding the molecular factors involved in BETL, AL, SE, ESR, and EAS development, including the specific transcriptional regulatory networks that function in each compartment during endosperm development.