RESUMEN
Activated carbon (AC) is widely used to removing hazardous pollutants from air and water, owing to its exceptional adsorption properties. However, the high affinity of water molecules with the surface oxygen-containing functional groups can adversely affect the adsorption performance of AC. In this study, a facile and efficient method is presented for fabrication of hydrophobic AC through surface monolayer silanation. Compared to initial AC, the hydrophobic AC improves the water contact angle from 29.7° to 123.5° while maintaining high specific surface area and enhances the removal capacity of multi-phase pollutants (emulsified oil and toluene). Additionally, the hydrophobic AC exhibits excellent adsorption capability to harmful algal bloom species (Chlorella) (97.56%) and algal organic matter (AOM) (96.23%) owing to electrostatic interactions and surface hydrophobicity. The study demonstrates that this method of surface monolayer silanation can effectively weaken the effect of water molecules on AC adsorption capacity, which has significant potential for practical use in air and water purification, as well as in the control of harmful algal blooms.
RESUMEN
Acidosis, a common feature of cerebral ischaemia and hypoxia, plays a key role in these pathological processes by aggravating the ischaemic and hypoxic injuries. To explore the mechanisms, in this research, we cultured primary neurons in an acidic environment (potential of hydrogen [pH]6.2, 24 hours) to mimic the acidosis. By proteomic analysis, 69 differentially expressed proteins in the acidic neurons were found, mainly related to stress and cell death, synaptic plasticity and gene transcription. And, the acidotic neurons developed obvious alterations including increased neuronal death, reduced dendritic length and complexity, reduced synaptic proteins, tau hyperphosphorylation, endoplasmic reticulum (ER) stress activation, abnormal lysosome-related signals, imbalanced oxidative stress/anti-oxidative stress and decreased Golgi matrix proteins. Then, melatonin (1 × 10-4 mol/L) was used to pre-treat the cultured primary neurons before acidic treatment (pH6.2). The results showed that melatonin partially reversed the acidosis-induced neuronal death, abnormal dendritic complexity, reductions of synaptic proteins, tau hyperphosphorylation and imbalance of kinase/phosphatase. In addition, acidosis related the activations of glycogen synthase kinase-3ß and nuclear factor-κB signals, ER stress and Golgi stress, and the abnormal autophagy-lysosome signals were completely reversed by melatonin. These data indicate that melatonin is beneficial for neurons against acidosis-induced injuries.