The cost of mass gatherings during a pandemic.

In June 2020, the U.S., unlike other regions of the world, faced a surge in cases of COVID-19. Immediately prior to this wave of cases, the largest mass protests in U.S. history took place. We show that when holding other factors constant, COVID-19 cases increased most in places where more demonstrations occurred. We exploit variation in rainfall during the protest period as an exogenous source of variation in attendance. We find that good weather coincides with both more people protesting and more subsequent COVID-19 cases and deaths. Mass gatherings during a pandemic thus lead to more contraction and fatalities of COVID-19, and we quantify these effects.

Targeting Forkhead box O1-aquaporin 5 axis mitigates neuropathic pain in a CCI rat model through inhibiting astrocytic and microglial activation.

Forkhead box O1 (FoxO1) is a critical molecule in modulating cell growth, differentiation and metabolism, acting as a vital transcription factor. This study explored the role of FoxO1 in chronic constriction injury (CCI)-induced neuropathic pain (NP). Microglial and astrocyte activation was achieved with lipopolysaccharide (LPS, 100 ng/mL) to establish an in-vitro NP model. Morphological alterations in LPS-induced microglia and astrocytes were assayed by light microscopy. The levels of inflammatory cytokines and proteins in microglia and astrocytes were gauged by enzyme-linked immunosorbent assay (ELISA), and Western blot (WB). The CCI-induced NP rat model was constructed for investigating the FoxO1-AQP5 axis in NP. LPS markedly expanded the expression of inflammatory factors and boosted the expression of FoxO1 and AQP5 in microglia and astrocytes. Inhibition of FoxO1 or AQP5 dramatically decreased the LPS-induced inflammation in microglia and astrocytes. In vivo, CCI exacerbated the inflammatory response and NP symptoms and substantially raised the contents of FoxO1 and AQP5 in rats' spinal cord tissues. Intrathecal administration of the Sirt1 agonist Resveratrol abated CCI-induced activation of FoxO1 and AQP5, abrogated CCI-induced mechanical hyperalgesia and thermal hyperalgesia, depressed microglial and astrocyte activation, and declined the generation of pro-inflammatory mediators in spinal cord tissues. Mechanistically, blocking the FoxO1-AQP5 pathway inactivated the ERK and p38 MAPK pathways. Suppressing the FoxO1-AQP5 axis alleviated CCI-induced NP and inflammatory responses by modulating the ERK and p38 MAPK signaling pathways.

Degradation of non-oxidizing biocide benzalkonium chloride and bulk dissolved organic matter in reverse osmosis concentrate by UV/chlorine oxidation.

Non-oxidizing biocide that is used to inhibit the microorganism growth on RO membrane, are observed to be high concentration and toxic in RO concentrate. The synergistic oxidation process (SOP) of UV/chlorine was investigated to simultaneously reduced the content (60.2 %) and toxicity (57.0 %) of a representative biocide dodecylbenzyldimethylammonium chloride (DDBAC) in real RO concentrate, with a UV fluence 1080 mJ/cm2 and chlorine dose 20 mg/L. Besides eliminating the DDBAC, UV/chlorine reduced the UVA254 and fluorescence of the dissolved organic matters (DOM). The oxidation mechanism was verified to be the radical electrophilic addition rather than the chlorine-electrophilic substitution through the decay of electron-donation moiety and UVA254. As results, high molecular weight fractions of DOM (>2k Da, 79.2 %) was cleaved into low molecular weight fractions (<0.4k Da, 18.4 %) and organic halide was formed. Parallel-factor analysis of the fluorescence components suggested that decomposition of the protein-like fluorophore is most likely to surrogate the biocide removal and organic halide formation compared to other fluorophore components and UVA254. Accordingly, a portable fluorescence probe with 400 nm excitation and 410-600 nm emission wavelengths was developed as an online surrogate for the DDBAC removal and organic halide formation.

In vitro assessment of the toxicity of lead (Pb2+) to phycocyanin.

This work reports the influence of lead (Pb2+) on fluorescence characteristics and protein structure of phycocyanin molecules experimentally in vitro. The fluorescence intensity decreases with the increasing concentration of Pb2+ from 0 to 5 × 10-5 mol L-1, showing the fluorescence quenching of phycocyanin by Pb2+. The quenching process is suggested to be static regarding the calculation results and the experimental results of time-resolved fluorescence decay profiles. The synchronous fluorescence spectra show that the effect of Pb2+ on the Tyr residues of phycocyanin is more significant than the Trp residues. The forming of aggregation by the interaction of Pb2+ with phycocyanin molecules is suggested from the results of resonance light scattering spectra. The UV-Vis spectra of the protein skeleton of phycocyanin have a red-shift of about 10 nm with increasing the Pb2+ concentration from 0 to 5 × 10-5 mol L-1, indicating a change in the protein skeleton and its secondary structure. With the increasing Pb2+ concentration, the two negative peaks (209 nm and 218 nm) on circular dichroism spectra become smaller, showing a decrease of the α-helix structure. These results may give people a deeper understanding of that how the heavy metal (Pb2+) can affect the chemo-physical properties of phycocyanin.

Formation and control of disinfection byproducts and toxicity during reclaimed water chlorination: A review.

Chlorination is essential to the safety of reclaimed water; however, this process leads to concern regarding the formation of disinfection byproducts (DBPs) and toxicity. This study reviewed the formation and control strategies for DBPs and toxicity in reclaimed water during chlorination. Both regulated and emerging DBPs have been frequently detected in reclaimed water during chlorination at a higher level than those in drinking water, indicating they pose a greater risk to humans. Luminescent bacteria and Daphnia magna acute toxicity, anti-estrogenic activity and cytotoxicity generally increased after chlorination because of the formation of DBPs. Genotoxicity by umu-test and estrogenic activity were decreased after chlorination because of destruction of toxic chemicals. During chlorination, water quality significantly impacted changes in toxicity. Ammonium tended to attenuate toxicity changes by reacting with chlorine to form chloramine, while bromide tended to aggravate toxicity changes by forming hypobromous acid. During pretreatment by ozonation and coagulation, disinfection byproduct formation potential (DBPFP) and toxicity formation potential (TFP) occasionally increase, which is accompanied by DOC removal; thus, the decrease of DOC was limited to indicate the decrease of DBPFP and TFP. It is more important to eliminate the key fraction of precursors such as hydrophobic acid and hydrophilic neutrals. During chlorination, toxicities can increase with the increasing chlorine dose and contact time. To control the excessive toxicity formation, a relatively low chlorine dose and short contact time were required. Quenching chlorine residual with reductive reagents also effectively abated the formation of toxic compounds.