This paper demonstrates the fi rst steps towards self-healing composites that exploit a design philosophy inspired by the damage tolerance and self-repair functions of bone. Cracking in either fi bre reinforced polymers (FRP) or bone, if left unattended, can grow under subsequent cyclic stresses eventually leading to catastrophic failure of the structure. On detection of cracks, an FRP component must be repaired or completely replaced, whereas bone utilises a series of complex processes to repair such damage. Under normal circumstances, these processes allow the skeleton to continually perform over the lifespan of the organism, a highly desirable aspiration for engineering materials. A simple vasculature design incorporated into a FRP via a "lost wax" process was found to facilitate a self-healing function which resulted in an outstanding recovery ( ≥ 96%) in post-impact compression strength. The process involved infusion of a healing resin through the vascule channels. Resin egress from the backface damage, ultrasonic C-scan testing, and microscopic evaluation all provide evidence that suffi cient vascule-damage connectivity exists to confer a reliable and effi cient self-healing function.

Inspired by the ability of biological systems to sense and autonomously heal damage, this research has successfully demonstrated the first autonomous, stimulus triggered, self-healing system in a structural composite material. Both the sensing and healing mechanisms are reliant on microvascular channels incorporated within a laminated composite material. For the triggering mechanism, a single air filled vessel was pressurized, sealed and monitored. Upon drop weight impact (10 J), delamination and microcrack connectivity between the pressurized vessel and those open to ambient led to a pressure loss which, with the use of a suitable sensor, triggered a pump to deliver a healing agent to the damage zone. Using this autonomous healing approach, near full recovery of post-impact compression strength was achieved (94% on average). A simplified alternative system with healing agent continuously flowing through the vessels, akin to blood flow, was found to offer 100% recovery of the material's virgin strength. Optical microscopy and ultrasonic C-scanning provided further evidence of large-scale infusion of matrix damage with the healing agent. The successful implementation of this bioinspired technology could substantially enhance the integrity and reliability of aerospace structures, whilst offering benefits through improved performance/weight ratios and extended lifetimes.

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Inspired by the sensory and autonomous healing processes of living organisms, whether from the Animalia or Plantae biological kingdoms, a microvascular network that undertakes a dual role of sensing structural damage before initiating a triggered healing response has been developed and embedded within an advanced fibre-reinforced composite [−45/90/45/0]2S laminate. In this study, a single vascule is used as a sensing pathway, which detects the introduction of ply delamination and matrix microcracking following a 10-J low-velocity impact event. Once damage connectivity between the sensing vascule and those open to the ambient environment is established, the delivery of a healing agent to the damage zone is triggered. An investigation into a commercially available epoxy healing agent (RT151) and an in-house healing resin formation (diglycidyl ether of bisphenol-A/diethylenetriamine) epoxy system has been evaluated. The pressure-assisted delivery of the liquid epoxy healing agent to the damage zone was observed to occur within 49 s across all specimens. The recovery of compression strength post impact was 91% and 94% for the RT151 and diglycidyl ether of bisphenol-A healing agents, respectively. This study provides further confirmation on how a bio-inspired vascular healing network could substantially enhance the reliability and robustness of advanced composite materials.

A vancomycin regimen of 1 g i.v. every 12 hours in critically ill trauma patients with MRSA pneumonia and normal renal function is unlikely to achieve trough concentrations of 15 to 20 mg/L. Doses of at least 1 g i.v. every 8 hours are needed.