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are heavy, bulky, and immovable and are generally situated near dams, coasts, or river banks. [3-5] Furthermore, generating electricity using a traditional electromagnetic apparatus is difficult under low water supply, such as rainwater or fog. [6] Therefore, a small, novel, and portable electromagnetic system that can harvest energy from tiny water drops can act as a water-electricity transducer; such a system is an alternative to traditional hydropower equipment. Bioinspired superhydrophobic materials have low surface energy and microor nano-scale surface roughness, [7-9] rendering their unique capability to manipulate water droplets. By carefully designing and controlling the superhydrophobic surfaces, water drops can pin, [10] roll, [11] separate, [12] jump, [13] and react [14] and, therefore, can possess a variety of

A novel method based on selective laser sintering (SLS) process is proposed for the first time to prepare complex and high-performance carbon fibres/polyamide12/epoxy (CF/PA12/EP) ternary composites. The procedures are briefly described as follows: prepare polyamide12 (PA12) coated carbon fibre (CF) composite powder; build porous green parts by SLS; infiltrate the green parts with high-performance thermosetting epoxy (EP) resin; and finally cure the resin at high temperature. The obtained composites are a ternary composite system consisting of the matrix of novolac EP resin, the reinforcement of CFs and the transition thin layer of PA12 with a thickness of 595 nm. The SEM images and micro-CT analysis prove that the ternary system is a three-dimensional co-continuous structure and the reinforcement of CFs are well dispersed in the matrix of EP with the volume fraction of 31%. Mechanical tests show that the composites fabricated by this method yield an ultimate tensile strength of 101.03 MPa and a flexural strength of 153.43 MPa, which are higher than those of most of the previously reported SLS materials. Therefore, the process proposed in this paper shows great potential for manufacturing complex, lightweight and high-performance CF reinforced composite components in aerospace, automotive industries and other areas.

Background The intervertebral disc (IVD) degeneration is the leading cause of low back pain, which accounts for a main cause of disability. N6‐methyladenosine (m6A) is the most abundant internal modification in eukaryotic messenger RNAs and is involved in various diseases and cellular processes by modulating mRNA fate. However, the critical role of m6A regulation in IVD degeneration remains unclear. Nucleus pulposus cell (NPC) senescence is critical for the progression of IVD degeneration. Here, we uncovered the role and explored the regulatory mechanism of m6A in NPC senescence during IVD degeneration. Methods Identification of NPC senescence during IVD degeneration was based on the analysis of tissue samples and the cellular model. ALKBH5 upregulation inducing cellular senescence was confirmed by functional experiments in vivo and in vitro. ChIP‐qPCR and DNA‐Pulldown were used to reveal increased ALKBH5 was regulated by KDM4A‐mediated H3K9me3. Furthermore, Me‐RIP‐seq was performed to identify m6A hypomethylation of DNMT3B transcripts in senescent NPCs. Stability analysis showed that DNMT3B expression was enhanced for less YTHDF2 recognition and increased DNMT3B promoted NPC senescence and IVD degeneration via E4F1 methylation by in vivo and in vitro analyses. Results Expression of ALKBH5 is enhanced during IVD degeneration and NPC senescence, due to decreased KDM4A‐mediated H3K9me3 modification. Functionally, ALKBH5 causes NPC senescence by demethylating DNMT3B transcripts and in turn promoting its expression via less YTHDF2 recognition and following degradation due to transcript hypomethylation in vitro and in vivo. Increased DNMT3B promotes the development of IVD degeneration and NPC senescence, mechanistically by methylating CpG islands of E4F1 at the promoter region and thus restraining its transcription and expression. Conclusions Collectively, our findings reveal an epigenetic interplay mechanism in NPC senescence and IVD degeneration, presenting a critical pro‐senescence role of ALKBH5 and m6A hypomethylation, highlighting the therapeutic potential of targeting the m6A/DNMT3B/E4F1 axis for treating IVD degeneration.