Windmill palm fibers are an abundant lignin-cellulose fiber resource. Single palm fibers can be prepared using an alkali treatment method. However, these fibers have hydrophilic surfaces, and following drying the fibers exhibit serious aggregation. This limits their application as acoustic materials. In this work, both alkali and acetylation treatments were used to modify the characteristics of windmill palm fibers. These treatments caused the surface of the fibers to become hydrophobic and increased the specific area and free vacuum space of the fibers, thus lowering energy loss. Scanning electron microscope observations combined with Fourier-transform infrared spectroscopy showed that the acetylation treatment resulted in the substitution of hydroxyl groups with acetyl groups, and the formation of nanoscale pores (10~50 nm). The results of the moisture-absorption and contact-angle tests showed that the moisture regain value decreased to 3.86%, and the contact angle increased to above 140° after acetylation treatment. The average sound absorption coefficients of the alkalized and acetylated nonwoven fabrics were 0.31 and 0.36, respectively. The masses of the acetylated samples were 50% those of the windmill palm sheath samples.

Aim The aim was to study the role of Rph3A in neuronal injury induced by cerebral ischemia‐reperfusion. Methods The protein and mRNA levels of Rph3A in penumbra were detected by Western blot. The localization of Rph3A in different cell types in penumbra was detected by immunofluorescence. Apoptosis in the brain was detected by TUNEL staining. We tested neurobehavioral evaluation using rotarod test, adhesive‐removal test, and Morris Water maze test. We examined the expression and localization of Rph3A in cultured neurons and astrocytes in vitro by Western blot and ELISA, respectively. Results The mRNA and protein levels of Rph3A had significantly increased in brain penumbra of the rat MCAO/R model. Rph3A was mainly distributed in neurons and astrocytes and was significantly increased by MCAO/R. We downregulated Rph3A and found that it further worsened the cerebral infarct, neuronal death and behavioral, cognitive, and memory impairments in rats after MCAO/R. We also found that ischemia‐reperfusion upregulated the in vitro protein level and secretion of Rph3A in astrocytes but led to a decrease in the protein level of Rph3A in neurons. Conclusion The increase in Rph3A in the brain penumbra may be an endogenous protective mechanism against ischemia‐reperfusion injury, which is mainly dominated by astrocytes.

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