Antibiotics have received extensive attention due to their sophisticated effects on human health and ecosystems. However, there is an extreme scarcity of information on composition, content, geographic distribution, and risk of riverine antibiotics at a large spatial scale. Based on a systematic review of over 600 pieces of literature (1999-2021), we established a global dataset containing more than 90,000 records covering 169 antibiotics and their metabolites in surface water and sediment across 76 countries. The occurrence of prioritized antibiotics largely depended on socioeconomic developmental levels, and the current "hotspots" of polluted rivers were found mostly in less developed countries or emerging economies (e.g., some in Africa, South America, and Asia). By developing the screening protocol for risk-based prioritization of antibiotics, we advanced a rank list of antibiotics for guiding formulation of region-specific strategies, which highlighted the importance of whole life cycle management of antibiotics in health maintenance of the world's rivers.
Radial glia in the developing optic tectum extend highly dynamic filopodial protrusions within the tectal neuropil, the motility of which has previously been shown to be sensitive to neural activity and nitric oxide (NO) release. Using in vivo two-photon microscopy, we performed time-lapse imaging of radial glial cells and measured filopodial motility in the intact albino Xenopus laevis tadpole. Application of MK801 to block neuronal NMDA receptor (NMDAR) currents confirmed a significant reduction in radial glial filopodial motility. This reduction did not occur in glial cells expressing a dominant-negative form of cGMP-dependent protein kinase 1 (PKG1), and was prevented by elevation of cGMP levels with the phosphodiesterase type 5 inhibitor sildenafil. These results suggest that neuronal NMDAR activation results in the release of NO, which in turn modulates PKG1 activation in glial cells to control filopodial motility. We further showed that interfering with the function of the small GTPases Rac1 or RhoA, known to be regulated by PKG1 phosphorylation, decreased motility or eliminated filopodial processes respectively. These manipulations led to profound defects in excitatory synaptic development and maturation of neighboring neurons.
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