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Objective: Stress is a known trigger for seizures in patients with epilepsy (PWE). However, the association between stress and seizures has not been thoroughly investigated. In December 2019, an outbreak of coronavirus disease (COVID-19) occurred in Wuhan, Hubei province, China, causing tremendous collateral stress. This study was designed to evaluate the influence of the COVID-19 outbreak on seizures in PWE in the most severely affected area, Wuhan, and its surrounding cities. Methods: In this single-center, cross-sectional study, PWE were surveyed via online questionnaires between February 23 and March 5, 2020. Collected data included demographic information, epilepsy-related characteristics (seizure type, frequency, antiepileptic drugs [AEDs], and medication management), direct and perceived threat of COVID-19, and changes in seizures during the outbreak. Psychological comorbidities were evaluated by the Patient Health Questionnaire-9, Generalized Anxiety Disorder-7 items, and Insomnia Severity Index (ISI). Multivariate logistic regression was used to identify precipitants for seizure exacerbation. Results: We received 362 completed questionnaires after excluding 12 duplicates (response rate = 63.51%). A total of 31 (8.56%) patients had increased seizures during the outbreak. Exposure history to COVID-19 (P = .001), uncontrolled seizure after AED therapy (P = .020), seizure frequency of two or more times per month before the outbreak (P = .005), change of AED regimen during the outbreak (AED reduction, withdrawal, replacement, skipping altogether; P = .002), and worry about the adverse effect of the outbreak on overall seizure-related issues (severity = moderate to critical; P = .038) were risk factors for increased seizures. Significance: A minority of PWE experienced seizure exacerbation during the outbreak of COVID-19. Stress, uncontrolled seizures, and inappropriate change in AED regimen were associated with increased seizures. Based on these findings, stress might be an independent precipitant for triggering seizures in some PWE.

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Nitrous acid (HONO) is a precursor of the hydroxyl radical (OH), a key oxidant in the degradation of most air pollutants. Field measurements indicate a large unknown source of HONO during the day time. Release of nitrous acid (HONO) from soil has been suggested as a major source of atmospheric HONO. We hypothesize that nitrite produced by biological nitrate reduction in oxygen-limited microzones in wet soils is a source of such HONO. Indeed, we found that various contrasting soil samples emitted HONO at high water-holding capacity (75-140%), demonstrating this to be a widespread phenomenon. Supplemental nitrate stimulated HONO emissions, whereas ethanol (70% v/v) treatment to minimize microbial activities reduced HONO emissions by 80%, suggesting that nitrate-dependent biotic processes are the sources of HONO. Highthroughput Illumina sequencing of 16S rRNA as well as functional gene transcripts associated with nitrate and nitrite reduction indicated that HONO emissions from soil samples were associated with nitrate reduction activities of diverse Proteobacteria. Incubation of pure cultures of bacterial nitrate reducers and gene-expression analyses, as well as the analyses of mutant strains deficient in nitrite reductases, showed positive correlations of HONO emissions with the capability of microbes to reduce nitrate to nitrite. Thus, we suggest biological nitrate reduction in oxygen-limited microzones as a hitherto unknown source of atmospheric HONO, affecting biogeochemical nitrogen cycling, atmospheric chemistry, and global modeling.

Descriptor Number: 6.01 Word Count: 3,295 At a Glance Commentary:Scientific Knowledge on the Subject: Short-term exposure to air pollution has been associated with increased risk of mortality from a variety of causes including respiratory diseases. As a common chronic respiratory disease, asthma affects 339 million people worldwide. Substantial evidence suggests that short-term exposure to air pollution causes asthma symptoms and leads to exacerbation and increased health-care use of asthma, but its effect on asthma mortality remains largely unknown. What This Study Adds to the Field:In this large case-crossover study, we found that short-term exposures to PM 2.5 , NO 2 and O 3 were positively associated with asthma mortality. For each IQR increase of exposures to PM 2.5 , NO 2 and O 3 , the odds of asthma mortality significantly increased by 7%, 11% and 9%, respectively. Our findings suggest that air pollution increase the risk of asthma mortality and highlight the needs to take effect measures to protect asthmatic individuals by reducing exposure to air pollution.This article has an online data supplement, which is accessible from this issue's table of content online at www.atsjournals.org. AbstractRationale: Short-term exposure to air pollution has been associated with asthma exacerbation and increased health-care use due to asthma, but its effect on asthma mortality remains largely unknown. Objectives:To quantitatively assess the association between short-term exposure to air pollution and asthma mortality. Methods:We investigated 4,454 individuals who lived in Hubei province, China and died from asthma between 2013 and 2018. A case-crossover design and conditional logistic regression models were applied for data analyses. Exposures to particulate matter ≤ 2.5 µm in aerodynamic diameter (PM 2.5 ), PM 10 , sulfur dioxide (SO 2 ), nitrogen dioxide (NO 2 ), carbon monoxide (CO) and ozone (O 3 ) were estimated by inverse distance weighted averages of all monitoring stations within 50 km from each case's home address. Measurements and Main Results:Each interquartile range (IQR) increase of PM 2.5 (lag 3; IQR: 47.1 µg/m 3 ), NO 2 (lag 03; IQR: 26.3 µg/m 3 ) and O 3 (lag 3; IQR: 52.9 µg/m 3 ) were positively associated with asthma mortality, with odds ratios (ORs) of 1.07 (95% confidence interval [CI]: 1.01-1.12), 1.11 (95% CI: 1.01-1.22) and 1.09 (95% CI: 1.01-1.18), respectively. There was no evidence of departure from linearity for these associations. Further adjustment for other pollutants did not change the associations materially. We did not observe significant associations between PM 10 , SO 2 , CO exposures and asthma mortality. Overall, the estimates remained consistent in various sensitivity analyses. Conclusions:Our results provide new evidence that short-term exposures to PM 2.5 , NO 2 and O 3 may increase asthma mortality risk. Further studies are needed to confirm our findings in other populations. Page 4 of 47 2 Word Count: 249

Objectives-The use of different technologies, such as mobile phones, internet, social media networks, and computer-based electronic devices cause a great deal of mental stress. However, few evidence-based studies have investigated ways to overcome this stress. In the present study, we examined the physiological and psychological effects of working environments containing indoor plants on stress. Methods-In total, 50 participants (age 20 years) were recruited. Experiments were performed to evaluate the physiological and psychological responses during a 5-min computer task in the presence or absence of indoor plants. Psychophysiological evaluations were based on blood pressure, electroencephalography (EEG) results, and State-Trait Anxiety Inventory (STAI) scores. Results-EEG analysis revealed that the presence of plants induced a significant change in brain activity, relative to that observed in the absence of plants. The participants exhibited lower STAI scores for tasks performed in the presence of plants than that performed in their absence. Conclusions-Thus, performing tasks in the presence of indoor plants for 5 minutes may lower mental stress.

Efficient syntheses and characterization of a platinum metallacyclyne containing one cyclic enyne pocket (3), the first dinuclear platinum metallacyclyne containing two cyclic enyne pockets (4), and 2,2‘,6,6‘-tetraethynyltolan (2) are reported. Syntheses of 3 and 4 employ bidentate phosphines or cis-platinum starting materials and high dilution techniques to effect high yields.

The syntheses of three strained silicon or germanium heterocyclotriynes, from the dilithium dianion of 2,2‘-diethynyltolane (Li2(OBET)) and the dialkyldichlorosilanes or dialkyldichlorogermane, are described. Reactions of the heterocyclynes with Ni(COD)2 give the nickel(0) complexes in very high yield. The heterocyclynes and their nickel complexes have been characterized by a variety of spectral techniques, and the X-ray crystal structures of compounds Si(i-Pr)2(OBET), Ni[Si(i-Pr)2(OBET)], SiPh2(OBET), Ni[SiPh2(OBET)], GePh2(OBET), and Ni[GePh2(OBET)] are reported. The heterocyclynes and their nickel complexes possess isomorphous structures.