The dark cloud with a silver lining: Assessing the impact of the SARS COVID-19 pandemic on the global environment.

The Severe Acute Respiratory Syndrome-Coronavirus Disease 2019 (COVID-19) pandemic caused by a novel coronavirus known as SARS-CoV-2 has caused tremendous suffering and huge economic losses. We hypothesized that extreme measures of partial-to-total shutdown might have influenced the quality of the global environment because of decreased emissions of atmospheric pollutants. We tested this hypothesis using satellite imagery, climatic datasets (temperature, and absolute humidity), and COVID-19 cases available in the public domain. While the majority of the cases were recorded from Western countries, where mortality rates were strongly positively correlated with age, the number of cases in tropical regions was relatively lower than European and North American regions, possibly attributed to faster human-to-human transmission. There was a substantial reduction in the level of nitrogen dioxide (NO2: 0.00002 mol m-2), a low reduction in CO (<0.03 mol m-2), and a low-to-moderate reduction in Aerosol Optical Depth (AOD: ~0.1-0.2) in the major hotspots of COVID-19 outbreak during February-March 2020, which may be attributed to the mass lockdowns. Our study projects an increasing coverage of high COVID-19 hazard at absolute humidity levels ranging from 4 to 9 g m-3 across a large part of the globe during April-July 2020 due to a high prospective meteorological suitability for COVID-19 spread. Our findings suggest that there is ample scope for restoring the global environment from the ill-effects of anthropogenic activities through temporary shutdown measures.

Stress-induced changes in the expression of the clock protein PERIOD1 in the rat limbic forebrain and hypothalamus: role of stress type, time of day, and predictability.

Stressful events can disrupt circadian rhythms in mammals but mechanisms underlying this disruption remain largely unknown. One hypothesis is that stress alters circadian protein expression in the forebrain, leading to functional dysregulation of the brain circadian network and consequent disruption of circadian physiological and behavioral rhythms. Here we characterized the effects of several different stressors on the expression of the core clock protein, PER1 and the activity marker, FOS in select forebrain and hypothalamic nuclei in rats. We found that acute exposure to processive stressors, restraint and forced swim, elevated PER1 and FOS expression in the paraventricular and dorsomedial hypothalamic nuclei and piriform cortex but suppressed PER1 and FOS levels exclusively in the central nucleus of the amygdala (CEAl) and oval nucleus of the bed nucleus of the stria terminalis (BNSTov). Conversely, systemic stressors, interleukin-1ß and 2-Deoxy-D-glucose, increased PER1 and FOS levels in all regions studied, including the CEAl and BNSTov. PER1 levels in the suprachiasmatic nucleus (SCN), the master pacemaker, were unaffected by any of the stress manipulations. The effect of stress on PER1 and FOS was modulated by time of day and, in the case of daily restraint, by predictability. These results demonstrate that the expression of PER1 in the forebrain is modulated by stress, consistent with the hypothesis that PER1 serves as a link between stress and the brain circadian network. Furthermore, the results show that the mechanisms that control PER1 and FOS expression in CEAl and BNSTov are uniquely sensitive to differences in the type of stressor. Finally, the finding that the effect of stress on PER1 parallels its effect on FOS supports the idea that Per1 functions as an immediate-early gene. Our observations point to a novel role for PER1 as a key player in the interface between stress and circadian rhythms.