Jianguo Niu

The Ozone Mapping and Profiler Suite (OMPS) has been onboard the Suomi National Polar-orbiting Partnership (S-NPP) satellite since October 2011, and was followed by an OMPS on NOAA-20 (N20) in November 2017, as part of the US Joint Polar Satellite System (JPSS) program. The OMPS measurements are processed to yield various products of atmospheric composition data for near-real-time monitoring and off-line study, including retrievals of total column ozone (TCO) and an Ultraviolet absorbing aerosol index (AI) based on the version-8 total ozone (V8TOZ) algorithm. With the implementation of changes to employ a broadband channel approach in the NOAA OMPS V8TOZ, the retrieved TCO and AI products become more stable and consistent between S-NPP and N20. Two particular regions have been chosen for building soft-calibration adjustments for both OMPS S-NPP and N20, which force the V8TOZ retrievals to be in quite good agreement from both sensors with little change by seasons. However, bias analysis shows that some noticeable errors / differences still exist after soft-calibration, and those errors appear to be quite persistently associated with solar zenith angle (SZA) and satellite viewing angle (SVA) in the retrievals of TCO and AI for both OMPS S-NPP and N20. Comparisons of TCO and AI from NOAA OMPS retrievals with other products such as those from the Tropospheric Monitoring Instrument (TROPOMI) and the Earth Polychromatic Imaging Camera (EPIC), show that, although the sensor, algorithm and solar spectra are different among them, the overall retrievals from those products are quite similar and consistent.

Cerebral ischemia‐reperfusion (I‐R) transiently increased autophagy by producing excessively reactive oxygen species (ROS); on the other hand, activated autophagy would remove ROS‐damaged mitochondria and proteins, which led to cell survival. However, the regulation mechanism of autophagy activity during cerebral I‐R is still unclear. In this study, we found that deficiency of the TRPM2 channel which is a ROS sensor significantly decreased I‐R‐induced neuronal damage. I‐R transiently increased autophagy activity both in vitro and in vivo. More importantly, TRPM2 deficiency decreased I‐R‐induced neurological deficit score and infarct volume. Interestingly, our results indicated that TRPM2 deficiency could further activate AMPK rather than Beclin1 activity, suggesting that TRPM2 inhibits autophagy by regulating the AMPK/mTOR pathway in I‐R. In conclusion, our study reveals that ROS‐activated TRPM2 inhibits autophagy by downregulating the AMPK/mTOR pathway, which results in neuronal death induced by cerebral I‐R, further supporting that TRPM2 might be a potential drug target for cerebral ischemic injury therapy.