ZnS coated on N,S co-doped carbon (ZnS/NSC) composite has been prepared utilizing zinc pyrithione (CHNOSZn) as raw material via calcination. Through activation using NaCO salt, ZnS nanoparticles encapsulated in NSC (denoted as A-ZnS/NSC) with mixed-crystal structure has also been obtained, which reveals much larger specific surface area and more bridges between ZnS and NSC. Based on the existence of bridges (C-S-Zn and S-O-Zn bonds) and the modification of carbon from N,S co-doping, the A-ZnS/NSC composite as an anode for sodium-ion batteries (SIBs) displays significantly enhanced electrochemical performances with a high reversible specific capacity of 516.6 mA h g (at 100 mA g), outstanding cycling stability (96.9% capacity retention after 100 cycles at 100 mA g), and high rate behavior (364.9 mA h g even at 800 mA g).

Subarachnoid hemorrhage (SAH) is a devastating disease with high mortality. The mechanisms underlying its pathological complications have not been fully identified. Here, we investigate the potential involvement of the glymphatic system in the neuropathology of SAH. We demonstrate that blood components rapidly enter the paravascular space following SAH and penetrate into the perivascular parenchyma throughout the brain, causing disastrous events such as cerebral vasospasm, delayed cerebral ischemia, microcirculation dysfunction and widespread perivascular neuroinflammation. Clearance of the paravascular pathway with tissue-type plasminogen activator ameliorates the behavioral deficits and alleviates histological injury of SAH. Interestingly, AQP4−/− mice showed no improvements in neurological deficits and neuroinflammation at day 7 after SAH compared with WT control mice. In conclusion, our study proves that the paravascular pathway dynamically mediates the pathological complications following acute SAH independently of glymphatic control.

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Depression is associated with somatic immune changes, and neuroinflammation is now recognized as hallmark for depressive disorders. N-3 (or omega-3) polyunsaturated fatty acids (PUFAs) are well known to suppress neuroinflammation, reduce oxidative stress, and protect neuron from injury. We pretreated animals with fish oil and induced acute depression-like behaviors with systemic lipopolysaccharide (LPS) injection. The levels of cytokines and stress hormones were determined from plasma and different brain areas. The results showed that fish oil treatment prevent LPS-induce depressive behavior by suppression of neuroinflammation. LPS induced acute neuroinflammation in different brain regions, which were prevented in fish oil fed mice. However, neither LPS administration nor fish oil treatment has strong effect on stress hormone secretion in the hypothalamus and adrenal. Fish oil might provide a useful therapy against inflammation-associated depression.

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