Restorative benefits of urban green space: Physiological, psychological restoration and eye movement analysis.

Urban life is associated with a range of health risks. However, urban green spaces have been found to promote health recovery and reduce mental stress. This study sought to assess the influence of the spatial and environmental characteristics of urban green space on environmental restoration. We measured physiological and psychological changes among 60 participants to evaluate the restorative benefits of 12 green spaces in Shenyang. The Perceived Restorativeness Scale and two physiological measures (heart rate variation and skin conductance response) were used to analyze the effects of spatial characteristics on restorative benefits. In addition, eye-tracking was used to explore the influence of environmental components on restorative benefits. The results revealed that, although there were slight differences between physiological and psychological findings, both confirmed that urban green space had a restorative benefit. Partially-open green spaces with a high degree of naturalness had more positive effects than open green spaces with a high degree of hard paved spaces. Eye movement analysis results revealed that trees and shrubs, as well as water, had a positive effect on the environmental restoration benefits, whereas buildings and paving had a negative effect. Among environmental features, trees and shrubs, water, and buildings exerted the strongest effects on environment restoration. In the future, combining spatial characteristics and environmental components will aid improvement of the restorative qualities of urban green space.

Bone marrow mesenchymal stem cells protect against n-hexane-induced neuropathy through beclin 1-independent inhibition of autophagy.

Chronic exposure to n-hexane, a widely used organic solvent in industry, induces central-peripheral neuropathy, which is mediated by its active metabolite, 2,5-hexanedione (HD). We recently reported that transplantation of bone marrow-mesenchymal stem cells (BMSC) significantly ameliorated HD-induced neuronal damage and motor deficits in rats. However, the mechanisms remain unclear. Here, we reported that inhibition of HD-induced autophagy contributed to BMSC-afforded protection. BMSC transplantation significantly reduced the levels of microtubule-associated protein 1 light chain 3-II (LC3-II) and the degradation of sequestosome-1 (p62) in the spinal cord and sciatic nerve of HD-intoxicated rats. Downregulation of autophagy by BMSC was also confirmed in VSC4.1 cells exposed to HD. Moreover, inhibition of autophagy by PIK III mitigated the neurotoxic effects of HD and, meanwhile, abolished BMSC-afforded neuroprotection. Furthermore, we found that BMSC failed to interfere with Beclin 1, but promoted activation of mammalian target of rapamycin (mTOR). Unc-like kinse 1 (ULK1) was further recognized as the downstream target of mTOR responsible for BMSC-mediated inhibition of autophagy. Altogether, BMSC transplantation potently ameliorated HD-induced autophagy through beclin 1-independent activation of mTOR pathway, providing a novel insight for the therapeutic effects of BMSC against n-hexane and other environmental toxicants-induced neurotoxicity.

Protection of Taurine Against Arsenic-Induced DNA Damage of Mice Kidneys.

The purpose of this study was to explore the protective capacity of taurine on arsenic (As)-induced neurotoxicity. Thirty mice were used and ten rats in each group. We treated the As exposure group with 4 ppm As2O3 for 60 days by drinking water and the protective group with 4 ppm As2O3 and 150 mg/kg taurine. Drinking water was only given in the control group. Pathologic changes and DNA damage in the mice kidney were examined by HE staining, immunohistochemistry and comet assay. Abnormal morphological changes were found in the kidney of As exposed mouse. Moreover, 8-hydroxy-2-deoxyguanosine (8-OHdG) expression and comet number, tail moment, and tail length of comet were markedly elevated in the As intoxication mice. However, histopathological changes and low expression of 8-OHdG were shown in the protective group. Our results indicate that supplementation of taurine protects against the histopathologic changes and DNA damage of mouse kidneys in As exposure group.