No abstract

China is facing intense coastal eutrophication. Large-scale seaweed aquaculture in China is popular, now accounting for over 2/3’s of global production. Here, we estimate the nutrient removal capability of large-scale Chinese seaweed farms to determine its significance in mitigating eutrophication. We combined estimates of yield and nutrient concentration of Chinese seaweed aquaculture to quantify that one hectare of seaweed aquaculture removes the equivalent nutrient inputs entering 17.8 ha for nitrogen and 126.7 ha for phosphorus of Chinese coastal waters, respectively. Chinese seaweed aquaculture annually removes approximately 75,000 t nitrogen and 9,500 t phosphorus. Whereas removal of the total N inputs to Chinese coastal waters requires a seaweed farming area 17 times larger than the extant area, one and a half times more of the seaweed area would be able to remove close to 100% of the P inputs. With the current growth rate of seaweed aquaculture, we project this industry will remove 100% of the current phosphorus inputs to Chinese coastal waters by 2026. Hence, seaweed aquaculture already plays a hitherto unrealized role in mitigating coastal eutrophication, a role that may be greatly expanded with future growth of seaweed aquaculture.

Physical exercise improves learning and memory, but little in vivo evidence has been provided to illustrate the molecular mechanisms. Here, we show that chronic treadmill exercise activates the mechanistic target of rapamycin (mTOR) pathway in mouse motor cortex. Both ex vivo and in vivo recordings suggest that mTOR activation leads to potentiated postsynaptic excitation and enhanced neuronal activity of layer 5 pyramidal neurons after exercise, in association with increased oligodendrogenesis and axonal myelination. Exercise training also increases dendritic spine formation and motor learning. Together, exercise activates mTOR pathway, which is necessary for spinogenesis, neuronal activation, and axonal myelination leading to improved motor learning. This model provides new insights for neural network adaptations through exercises and supports the intervention of cognitive deficits using exercise training.

Type 2 helper T cells (T(H)2) are critically involved in allergies and asthma. Here we demonstrate that extracellular matrix protein-1 (ECM1) is highly and selectively expressed in T(H)2 cells. ECM1 deficiency caused impaired T(H)2 responses and reduced allergic airway inflammation in vivo. Functional analysis demonstrated that although the T(H)2 polarization of ECM1-deficient cells was unimpaired, these cells had a defect in migration and were retained in peripheral lymphoid organs. This was associated with reduced expression of KLF2 and S1P(1). We also found that ECM1 could directly bind the interleukin-2 (IL-2) receptor to inhibit IL-2 signaling and activate S1P(1) expression. Our data identify a previously unknown function of ECM1 in regulating T(H)2 cell migration through control of KLF2 and S1P(1) expression.