Induction of micronuclei by acute and chronic exposure in vivo to gamma rays in murine polychromatic erythrocytes

AbstractThe effects of ethanol on brain function have been extensively studied using a variety of in vitro and in vivo techniques. For example, electrophysiological studies using brain slices from rodents and nonhuman primates have demonstrated that acute and chronic exposure to ethanol alters the intrinsic excitability and synaptic signaling of neurons within cortical and sub-cortical areas of the brain. In humans, neuroimaging studies reveal alterations in measures of brain activation and connectivity in subjects with alcohol use disorders. While complementary, these methods are inherently limited due to issues related to either disruption of normal sensory input (in vitro slice studies) or resolution (whole brain imaging). In the present study, we used 2-photon laser scanning microscopy in intact animals to assess the impact of chronic ethanol exposure on sensory evoked neuronal and vascular responses. Adult male C57BL/6J mice were exposed to 4 weekly cycles of chronic intermittent ethanol (CIE) exposure while control mice were exposed to air. After withdrawal (≤ 72 hr), a cranial window was placed over the primary visual cortex (V1) and sensory evoked responses were monitored using the calcium indicator OGB-1. CIE exposure produced small but significant changes in response amplitude (decrease) and orientation selectivity of V1 neurons (increase). While arteriole diameter did not differ between control and CIE mice under baseline conditions, sensory-evoked dilation was enhanced in vessels from CIE exposed mice as compared to controls. This was accompanied by a reduced latency in response to stimulation. In separate experiments, pial arteriole diameter was measured in the barrel cortex of control and CIE exposed mice. Baseline diameter of barrel cortex arterioles was similar between control and CIE exposed mice but unlike vessels in V1, sensory-evoked dilation of barrel cortex arterioles was similar between the two groups. Together the results of these studies suggest that chronic exposure to alcohol induces changes in neurovascular coupling that are region dependent.

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Acute and chronic exposure to air pollution in relation with incidence, prevalence, severity and mortality of COVID-19: a rapid systematic review

Environmental Health ◽

10.1186/s12940-021-00714-1 ◽

2021 ◽

Vol 20 (1) ◽

Author(s):

Patrick D. M. C. Katoto ◽

Amanda S. Brand ◽

Buket Bakan ◽

Paul Musa Obadia ◽

Carsi Kuhangana ◽

...

Keyword(s):

Air Pollution ◽

Chronic Exposure ◽

Ambient Air ◽

Short Term ◽

Incidence And Mortality ◽

Acute And Chronic Exposure ◽

Anthropogenic Pollutant ◽

Incident Cases ◽

Incidence Prevalence

Abstract Background Air pollution is one of the world’s leading mortality risk factors contributing to seven million deaths annually. COVID-19 pandemic has claimed about one million deaths in less than a year. However, it is unclear whether exposure to acute and chronic air pollution influences the COVID-19 epidemiologic curve. Methods We searched for relevant studies listed in six electronic databases between December 2019 and September 2020. We applied no language or publication status limits. Studies presented as original articles, studies that assessed risk, incidence, prevalence, or lethality of COVID-19 in relation with exposure to either short-term or long-term exposure to ambient air pollution were included. All patients regardless of age, sex and location diagnosed as having COVID-19 of any severity were taken into consideration. We synthesised results using harvest plots based on effect direction. Results Included studies were cross-sectional (n = 10), retrospective cohorts (n = 9), ecological (n = 6 of which two were time-series) and hypothesis (n = 1). Of these studies, 52 and 48% assessed the effect of short-term and long-term pollutant exposure, respectively and one evaluated both. Pollutants mostly studied were PM2.5 (64%), NO2 (50%), PM10 (43%) and O3 (29%) for acute effects and PM2.5 (85%), NO2 (39%) and O3 (23%) then PM10 (15%) for chronic effects. Most assessed COVID-19 outcomes were incidence and mortality rate. Acutely, pollutants independently associated with COVID-19 incidence and mortality were first PM2.5 then PM10, NO2 and O3 (only for incident cases). Chronically, similar relationships were found for PM2.5 and NO2. High overall risk of bias judgments (86 and 39% in short-term and long-term exposure studies, respectively) was predominantly due to a failure to adjust aggregated data for important confounders, and to a lesser extent because of a lack of comparative analysis. Conclusion The body of evidence indicates that both acute and chronic exposure to air pollution can affect COVID-19 epidemiology. The evidence is unclear for acute exposure due to a higher level of bias in existing studies as compared to moderate evidence with chronic exposure. Public health interventions that help minimize anthropogenic pollutant source and socio-economic injustice/disparities may reduce the planetary threat posed by both COVID-19 and air pollution pandemics.

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