Effect of ultrasonically-assisted drilling on carbon-fibre-reinforced plastics

NOTICE: this is the author’s version of a work that was accepted for publication in Journal of Sound and Vibration. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in Journal of Sound and Vibration, Volume 333, Issue 23, 24 November 2014, Pages 5939–5952 DOI: 10.1016/j.jsv.2014.05.042This research focuses on the effect of ultrasonically-assisted drilling (UAD) on carbon fibre-reinforced plastics. High-frequency vibration was used to excite a drill bit during its standard operation. An extensive experimental study of drilling forces, temperature, chip formation, surface finish, circularity, delamination and tool wear was conducted using ∅3 mm drill and presented here. UAD showed a significant improvement in drill quality when compared to conventional drilling processes. A finite-element study was also conducted to understand the nature of drilling-force reduction in UAD

Histone deacetylase 9 promotes endothelial to mesenchymal transition and an unfavorable atherosclerotic plaque phenotype

Endothelial-mesenchymal transition (EndMT) is associated with various cardiovascular diseases and in particular with atherosclerosis and plaque instability. However, the molecular pathways that govern EndMT are poorly defined. Specifically, the role of epigenetic factors and histone deacetylases (HDACs) in controlling EndMT and the atherosclerotic plaque phenotype remains unclear. Here, we identified histone deacetylation, specifically that mediated by HDAC9 (a class IIa HDAC), as playing an important role in both EndMT and atherosclerosis. Using in vitro models, we found class IIa HDAC inhibition sustained the expression of endothelial proteins and mitigated the increase in mesenchymal proteins, effectively blocking EndMT. Similarly, ex vivo genetic knockout of Hdac9 in endothelial cells prevented EndMT and preserved a more endothelial-like phenotype. In vivo, atherosclerosis-prone mice with endothelial-specific Hdac9 knockout showed reduced EndMT and significantly reduced plaque area. Furthermore, these mice displayed a more favorable plaque phenotype, with reduced plaque lipid content and increased fibrous cap thickness. Together, these findings indicate that HDAC9 contributes to vascular pathology by promoting EndMT. Our study provides evidence for a pathological link among EndMT, HDAC9, and atherosclerosis and suggests that targeting of HDAC9 may be beneficial for plaque stabilization or slowing the progression of atherosclerotic disease