The Geostationary Environment Monitoring Spectrometer (GEMS) is scheduled for launch in February 2020 to monitor air quality (AQ) at an unprecedented spatial and temporal resolution from a geostationary Earth orbit (GEO) for the first time. With the development of UV–visible spectrometers at sub-nm spectral resolution and sophisticated retrieval algorithms, estimates of the column amounts of atmospheric pollutants (O3, NO2, SO2, HCHO, CHOCHO, and aerosols) can be obtained. To date, all the UV–visible satellite missions monitoring air quality have been in low Earth orbit (LEO), allowing one to two observations per day. With UV–visible instruments on GEO platforms, the diurnal variations of these pollutants can now be determined. Details of the GEMS mission are presented, including instrumentation, scientific algorithms, predicted performance, and applications for air quality forecasts through data assimilation. GEMS will be on board the Geostationary Korea Multi-Purpose Satellite 2 (GEO-KOMPSAT-2) satellite series, which also hosts the Advanced Meteorological Imager (AMI) and Geostationary Ocean Color Imager 2 (GOCI-2). These three instruments will provide synergistic science products to better understand air quality, meteorology, the long-range transport of air pollutants, emission source distributions, and chemical processes. Faster sampling rates at higher spatial resolution will increase the probability of finding cloud-free pixels, leading to more observations of aerosols and trace gases than is possible from LEO. GEMS will be joined by NASA’s Tropospheric Emissions: Monitoring of Pollution (TEMPO) and ESA’s Sentinel-4 to form a GEO AQ satellite constellation in early 2020s, coordinated by the Committee on Earth Observation Satellites (CEOS).

Obesity, caused by a high-fat diet (HFD), leads to insulin resistance, which is a precursor of diabetes and a risk factor for impaired cognitive function, dementia, and brain diseases, such as Alzheimer’s disease. Physical exercise has positive effects on obesity and brain functions. We investigated whether the decline in cognitive function caused by a HFD could be improved through exercise by examining insulin signaling pathways and neuroplasticity in the hippocampus. Four-week-old C57BL/6 male mice were fed a HFD or a regular diet for 20 weeks, followed by 12 weeks of treadmill exercise. To ascertain the effects of treadmill exercise on impaired cognitive function caused by obesity, the present study implemented behavioral testing (Morris water maze, step-down). Moreover, insulin-signaling and neuroplasticity were measured in the hippocampus and dentate gyrus. Our results demonstrated that HFD-fed obesity-induced insulin resistance was improved by exercise. In addition, the HFD group showed a decrease in insulin signaling and neuroplasticity in the hippocampus and the dentate gyrus and increased cognitive function impairment, which were reversed by physical exercise. Overall, our findings indicate that physical exercise may act as a non-pharmacologic method that protects against cognitive dysfunction caused by obesity by improving hippocampal insulin signaling and neuroplasticity.

Background: Exercise promotes brain health and improves cognitive functioning in the elderly, while 40-Hz light flickering through the visual cortex reduces amyloid beta (Aβ) by stabilizing gamma oscillation. We examined whether exercise was associated with hippocampus-mediated improvement in cognitive functioning in the 3xTg-Alzheimer's disease (3xTg-AD) murine model following exposure to 40-Hz light flickering and exercise. Methods: We subjected 12-month-old 3xTg-AD mice to exercise and 40-Hz light flickering for 3 months to investigate spatial learning, memory, long-term memory, Aβ levels, tau levels, mitochondrial functioning including Ca 2+ retention and H 2 O 2 emission, apoptosis, and neurogenesis in the hippocampus. Results: Treatments had a positive effect; however, the combination of exercise and 40-Hz light flickering exposure was most effective in reducing Aβ and tau levels. Reducing Aβ and tau levels by combination of exercise and 40-Hz light flickering improves Ca 2+ homeostasis and reactive oxygen species such as H 2 O 2 in mitochondria and apoptosis including bax, bcl-2, cytochrome c, and cleaved caspase-3 and cell death, cell differentiation, and neurogenesis in the 3xTg-AD model of the hippocampus, resulting in improving cognitive impairment such as spatial learning, memory and long term memory. Conclusion: Our results show that exercising in a 40-Hz light flickering environment may improve cognitive functioning by reducing Aβ and tau levels, thereby enhancing mitochondrial function and neuroplasticity.

Nicotine withdrawal symptoms comprise insomnia, depression, anxiety, attention disorders, and increased craving. We evaluated the ameliorating effect of treadmill exercise on nicotine withdrawal symptoms. The rats in the nicotine withdrawal groups received subcutaneous injection with 6-mg/kg nicotine hydrogen tartrate salt for 17 days. And then, the injection of nicotine hydrogen tartrate salt was stopped next for 2 weeks. The rats in the exercise groups performed treadmill running once a day, 5 days per week, for 31 days. In the present results, activity was decreased and anxiety-like behavior was observed in the nicotine withdrawal rats. Treadmill running increased activity and ameliorated anxiety-like behavior in the nicotine-withdrawal rats. Expressions of tryptophan hydroxylase (TPH) and 5-hydroxytryptamine (5-HT) in the dorsal raphe were decreased in the nicotine withdrawal rats, in contrast, treadmill running increased TPH and 5-HT expressions. Impaired short-term memory and deteriorated spatial learning ability were observed in the nicotine withdrawal rats, in contrast, treadmill running ameliorated impairment of short-term memory and spatial learning ability. Expressions of brain-derived neurotrophic factor and tyrosine kinase B (TrkB) were decreased in the nicotine withdrawal rats, in contrast, treadmill running increased brain-derived neurotrophic factor and TrkB expressions. The numbers of the dou¬blecortin (DCX)-positive cells and 5-bromo-2´-deoxyuridine (BrdU)-positive cells in the dentate gyrus were suppressed in the nicotine withdrawal rats, in contrast, treadmill running enhanced the numbers of DCX-positive cells and BrdU-positive cells. The present study demonstrate that treadmill exercise ameliorated nicotine withdrawal-induced anxiety, depression, and memory impairment.

Effect of swimming exercise on serotonin (5-hydroxytryptamine, 5-HT) expression and apoptosis in social isolation rats during old age was investigated. Rats in the old social isolation groups were housed alone per cage for 4 weeks. Rats in the swimming exercise groups were allowed to swim for 30 min once daily for 4 weeks. Morris water maze task determined spatial working memory and elevated plus maze test determined anxiety. Immunohistochemistry for tryptophan hydroxylase (TPH) and 5-HT in the dorsal raphe and for doublecortin (DCX) in the hippocampal dentate gyrus was conducted. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining in the hippocampal dentate gyrus was performed. Western blot analysis for Bax, Bcl-2, and cytochrome c in the hippocampus was conducted. Social isolation in rats of old age reduced spatial working memory and increased anxiety level. Swimming exercise enhanced spatial working memory and suppressed anxiety level. Social isolation in rats of old age inhibited TPH and 5-HT expression in dorsal rape. Swimming exercise increased TPH and 5-HT expression. Social isolation in rats of old age inhibited DCX-positive cells in the hippocampal dente gyrus. Swimming exercise increased DCX-positive cells. Social isolation in rats of old age increased TUNEL-positive cells, Bax and cytochrome c expression, and decreased Bcl-2 expression, which promoted apoptosis. Swimming exercise suppressed TUNEL-positive cells, Bax and cytochrome c expression, and increased Bcl-2 expression, which inhibited apoptosis. Swimming exercise improved 5-HT expression and suppressed apoptosis to alleviate anxiety and memory impairment during old age.

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Social isolation during adolescence is associated with anxiety, depression, and memory impairment. Exercise has been reported as a positive effect on brain function, especially hippocampus. The present study examined the effect of swimming exercise on apoptosis, cell proliferation, and serotonin expression in social isolation rats during adolescence stage. Social isolation started at postnatal day 21 and continued for 6 weeks. The rats in the swimming group were forced to swim for 60 min once daily during 6 days per week for 6 consecutive weeks. The rats in the social isolation during adolescence showed anxiety, depression, short-term memory impairment. Social isolation facilitated apoptosis and inhibited cell proliferation and differentiation. Social isolation suppressed expression of serotonin, brain-derived neurotrophic factor, and tyrosine kinase B. Swimming exercise alleviated anxiety, depression, short-term impairment. Swimming exercise suppressed apoptosis, enhanced neurogenesis, and increased serotonin expression. In our study, swimming exercise ameliorates mood disorder and memory impairment by enhancing neurogenesis and serotonin expression and inhibiting apoptosis in social isolation.

PurposeRotenone is the most widely used neurotoxin for the making Parkinson disease (PD) animal model. The neurodegenerative disorder PD shows symptoms, such as slowness of movements, tremor at resting, rigidity, disturbance of gait, and instability of posture. We investigated whether treadmill running improves motor ability using rotenone-caused PD rats. The effect of treadmill running on PD was also assessed in relation with apoptosis of cerebellar Purkinje cells. MethodsTreadmill running was applied to the rats in the exercise groups for 30 minutes once a day for 4 weeks, starting 4 weeks after birth. We used rota-rod test for the determination of motor coordination and balance. In this experiment, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining, immunohistochemistry for calbindin, glial fibrillary acidic protein (GFAP), Iba-1, and western blot analysis for Bax and Bcl-2 were performed. ResultsTreadmill running enhanced motor balance and coordination by preventing the loss of Purkinje cells in the cerebellar vermis. Treadmill running suppressed PD-induced expression of GFAP-positive reactive astrocytes and Iba-1-positive microglia, showing that treadmill running suppressed reactive astrogliosis and microglia activation. Treadmill running suppressed TUNEL-positive cell number and Bax expression and enhanced Bcl-2 expression, demonstrating that treadmill running inhibited the progress of apoptosis in the cerebellum of rotenone-induced PD rats. ConclusionsTreadmill running improved motor ability of the rotenone-induced PD rats by inhibiting apoptosis in the cerebellum. Apoptosis suppressing effect of treadmill running on rotenone-induced PD was achieved via suppression of reactive astrocyte and inhibition of microglial activation.