No abstract

Calcium sulfate whiskers (CSWs) were hydroxylated with a sodium hydroxide (NaOH) solution and isolated for subsequent treatment with an ethanolic 3-(methacryloxy)propyltrimethoxysilane (KH570) solution to introduce C=C double bonds on the CSWs’ surfaces. Then, CSW-g-PMMA was prepared by grafting polymethyl methacrylate (PMMA) onto the surface of modified CSW using in situ dispersion polymerization. The CSW-g-PMMA was used as a filler and melt-blended with polyvinyl chloride (PVC) to prepare PVC-based composites. The surface chemical structure, PMMA grafting rate, and hydrophobic properties of CSW-g-PMMA were analyzed using X-ray diffraction, diffuse reflectance Fourier-transform infrared spectroscopy, thermogravimetric analysis, and water contact angle measurements, respectively. The effects of the CSW-g-PMMA filler on the mechanical properties of the CSW-PMMA/PVC composites were also investigated. The results showed that NaOH treatment significantly increased the number of hydroxyl groups on the surface of the CSWs, which facilitated the introduction of KH570. PMMA was successfully grafted onto the KH570 with a grafting rate of 14.48% onto the surface of the CSWs. The CSW-g-PMMA had good interfacial compatibility and adhesion properties with the PVC matrix. The tensile, flexural, and impact strengths of the CSW-g-PMMA/PVC composite reached 39.28 MPa, 45.69 MPa, and 7.05 kJ/m2, respectively, which were 38.55%, 30.99%, and 20.10% higher than those of the CSW/PVC composite and 54.52%, 40.80%, and 32.52% higher than those of pure PVC, respectively. This work provides a new method for surface modification of inorganic fillers, resource utilization, and high value-added application of CSWs from phosphogypsum.

Polyacrylic acid (PAA) has high water absorbency but poor salt resistance. Humic acid (HA) extracted from lignite was introduced into the cross-linked copolymer systems of AA to improve the water absorbency and salt-tolerance. A polyacrylic acid-potassium humate (PAA-KHA) coated ammonium dihydrogen phosphate (ADP) fertilizer with water-preserving, salt-resistant and slow-release properties was prepared. The main properties of HA extracted from lignite oxidized by H2O2 were studied. Furthermore, the synthesis process, water absorbency of PAA-KHA in deionized water and in NaCl solution, morphologies of PAA-KHA, and the slow-release performance of the fertilizer (ADP@PAA-KHA) were investigated. The results showed PAA-KHA had a layered interpenetrating network, which can provide sufficient storage space for water and nutrients. The salty water absorbency of PAA-KHA increased by about 3 times compared to PAA. Both the PO43− and NH4+ cumulative release of ADP@PAA-KHA with a coating rate of 10% in deionized water, were less than 20% within 24 h, and were 55.71% and 28.04% after the 15th day, respectively. The weight change of ADP@PAA-KHA before and after absorbing water was about 53 times in deionized water and about 4 times in 1 wt% of NaCl salty water. The results show that ADP@PAA-KHA has excellent properties of water retention, salt resistance and slow-release. This will efficiently improve the utilization of fertilizer and reduce the irrigation water consumption at the same time.

Cell adhesion molecule 4 (Cadm4) plays important roles on plasma membrane (PM) to regulate myelin formation and the downregulation of Cadm4 is a prominent feature in many demyelination diseases. However, how Cadm4 maintains its level on PM has been elusive. Here, we identify that Cadm4 is palmitoylated at cysteine-347 (C347) and palmitoylation regulates the stable localization of Cadm4 on PM, as blocking palmitoylation by mutating C347 into alanine (C347A) results in the dissociation of Cadm4 from PM and targeting for degradation. Intriguingly, blocking Cadm4 palmitoylation by introducing C347A (Cadm4-KI) causes myelin abnormalities in CNS, characterized by loss of myelination, myelin infoldings and hypermyelination. Moreover, it is uncovered that Cadm4 palmitoylation is catalyzed by DHHC3, reducing Cadm4 palmitoylation by the deletion of DHHC3 renders the redistribution of Cadm4 for degrading. Consistently, the genetic deletion of DHHC3 leads to downregulated Cadm4 palmitoylation and defects in CNS myelination, virtually phenocopies that of the Cadm4-KI mice. Our findings suggest a mechanism that the stable localization of Cadm4 on PM regulated by protein palmitoylation is vital for myelination in CNS.