Abstract. We present a new method to quantify NOx emissions and corresponding atmospheric lifetimes from OMI NO2 observations together with ECMWF wind fields without further model input for sources located in a polluted background. NO2 patterns under calm wind conditions are used as proxy for the spatial patterns of NOx emissions, and the effective atmospheric NOx lifetime is determined from the change of spatial patterns measured at larger wind speeds. Emissions are subsequently derived from the NO2 mass above the background, integrated around the source of interest. Lifetimes and emissions are estimated for 17 power plants and 53 cities located in non-mountainous regions across China and the USA. The derived lifetimes for the ozone season (May–September) are 3.8 ± 1.0 h (mean ± standard deviation) with a range of 1.8 to 7.5 h. The derived NOx emissions show generally good agreement with bottom-up inventories for power plants and cities. Regional inventory shows better agreement with top-down estimates for Chinese cities compared to global inventory, most likely due to different downscaling approaches adopted in the two inventories.

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Anthropogenic impacts on widespread global soil moisture (SM) drying in the root zone layer during 1948–2005 were evaluated based on the Global Land Data Assimilation System version 2 (GLDAS‐2) and global climate models from the Coupled Model Intercomparison Project Phase 5 using trend analysis and optimal fingerprint methods. Both methods show agreement that natural forcing alone cannot drive significant SM drying. There is a high probability (≥90%) that the anthropogenic climate change signal is detectable in global SM drying. Specifically, anthropogenic greenhouse gas forcing can lead to global SM drying by 2.1 × 10−3 m3/m3, which is comparable to the drying trend seen in Global Land Data Assimilation System version 2 (2.4 × 10−3 m3/m3) over the past 58 years. Global SM drying is expected to continue in the future, given continuous greenhouse gas emissions.

A novel photochromic hybrid has been synthesized by fluorescent POM and viologen molecules, of which the decoloration process can be easily realized by exposure to humid air or heating.

To determine whether memantine as a treatment for glaucoma prevents neuron shrinkage in the lateral geniculate nucleus, the major target for retinal ganglion cells.Methods: Sixteen monkeys with right-eye unilateral experimental glaucoma for 14 months were studied and treated with memantine (n=9) or vehicle only (n=7). Left lateral geniculate nucleus relay neurons (layers 1, 4, and 6) were examined following parvalbumin immunolabeling. Cell body cross-sectional areas and neuron numbers were assessed using unbiased methods. Memantine-and vehicle-treated glaucoma groups were compared using t tests and analysis of covariance.Results: Compared with vehicle-treated animals, memantine-treated animals showed significantly less mean±SD neuron shrinkage in layers 1 (−4.0% ± 13.9% vs 28.2% ± 17.4%; P = .001) and 4 (24.9% ± 10.0% vs 37.2%±12.3%; P=.04). For layer 6, the difference was not statistically significant (34.2%±10.1% vs 45.3%±14.5%; P = .10). Analysis of covariance results showed significantly less neuron shrinkage in the memantine-treated group for layers 1, 4, and 6 (PϽ.001; PϽ.02; and PϽ.04, respectively). This difference was greatest in layer 1. In each of these layers, neuron numbers did not differ significantly between groups. Conclusion:Monkeys with glaucoma that were treated with memantine showed significantly less neuron shrinkage in the lateral geniculate nucleus than the vehicletreated glaucoma group. Clinical Relevance:The finding that memantine protects adult visual neurons from transsynaptic atrophy in experimental glaucoma could have therapeutic value. Currently, memantine is being tested in an ongoing clinical trial as a treatment for glaucoma.

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