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.
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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