RESUMO
Presently, piezoelectric materials are gradually playing a significant role within composites to improve the damping and vibrational attenuation capacities of host composites. Previous studies paid attention to isolating the mechanical damping contribution and piezoelectric contribution of polymer-based piezoelectric composites (PPCs). However, reports detailing the piezoelectric damping of such materials have not paid sufficient attention to the technologies and methods to improve the piezoelectric damping of PPCs. In this study, we propose novel damping polyurethane (PU)-based piezoelectric composites with carbon-coated piezoelectric fillers (PZT@C/PU) with improved piezoelectric damping ability. The mechanical damping and piezoelectric damping of composites were theoretically decoupled, and we elaborate on the mechanism enhancing piezoelectric damping through the carbon coating strategy by comparing with the composites with nonpiezoelectric fillers. The as-fabricated core-shell structure having an optimized interface exhibits the proposed PZT@C/PU composite pads with relatively prominent damping ability (loss factor tan δmax = 1.0, tan δRT = 0.3), ductility (400.63%), and sound isolating behavior (transmission loss TL > 23 dB). Moreover, the vibration test results of as-fabricated sandwich structural PZT@C/PU composite damping devices exhibit outstanding vibration attenuating behavior (damping ratio ζ = 0.198). The study herein validates that the carbon shell coated on piezoelectric fillers would effectively increase damping performance of PU-based piezoelectric composites by the enhancement of piezoelectric performance caused by carbon coating piezoelectric fillers, which indicates that this material has potential for future applications in the field of vibration and noise reduction, thereby driving forward and expanding the fundamental understanding in the area of PPCs damping and vibration attenuation.
RESUMO
Inflammatory bowel disease (IBD) is a group of disorders that cause chronic inflammation in the intestines, with the primary types including ulcerative colitis and Crohn's disease. The link between autophagy, a catabolic mechanism in which cells clear protein aggregates and damaged organelles, and intestinal health has been widely studied. Experimental animal studies and human clinical studies have revealed that autophagy is pivotal for intestinal homeostasis maintenance, gut ecology regulation and other aspects. However, few articles have summarized and discussed the pathways by which autophagy improves or exacerbates IBD. Here, we review how autophagy alleviates IBD through the specific genes (e.g., ATG16L1, IRGM, NOD2 and LRRK2), crosstalk of multiple phenotypes with autophagy (e.g., Interaction of autophagy with endoplasmic reticulum stress, intestinal antimicrobial defense and apoptosis) and autophagy-associated signaling pathways. Moreover, we briefly discuss the role of autophagy in colorectal cancer and current status of autophagy-based drug research for IBD. It should be emphasized that autophagy has cell-specific and environment-specific effects on the gut. One of the problems of IBD research is to understand how autophagy plays a role in intestinal tract under specific environmental factors. A better understanding of the mechanism of autophagy in the occurrence and progression of IBD will provide references for the development of therapeutic drugs and disease management for IBD in the future.