Autonomic self-healing materials, where initiation of repair is integral to the material, are being developed for engineering applications. This bio-inspired concept offers the designer an ability to incorporate secondary functional materials capable of counteracting service degradation whilst still achieving the primary, usually structural, requirement. Most materials in nature are themselves self-healing composite materials. This paper reviews the various self-healing technologies currently being developed for fibre reinforced polymeric composite materials, most of which are bioinspired, inspired by observation of nature. The most recent self-healing work has attempted to mimic natural healing through the study of mammalian blood clotting and the design of vascular networks found in biological systems. A perspective on current and future self-healing approaches using this biomimetic technique is offered. The intention is to stimulate debate outside the engineering community and reinforce the importance of a multidisciplinary approach in this exciting field.

Impact damage can degrade the flexural strength of composite sandwich structures by over 50% due to a loss of skin support inducing localized skin buckling. Various self-healing methodologies have been applied to laminated composites but the concept of delivering a healing agent from a remote reservoir to a region of damage via a vascular network offers the potential for a robust and replenishable system housed in the core of a sandwich structure. In this pilot study a vascular sandwich structure that appears as a conventional sandwich composite has been developed and tested. The network has been shown to have negligible influence on the innate static mechanical properties of the host panel. Infiltration of the vascular network with a pre-mixed epoxy resin system after impact damage demonstrated a complete recovery of flexural failure mode and load. Infiltration with the same resin system from separate unmixed networks, where self-healing is initiated autonomously via mixing within the damage, has also been shown to fully recover undamaged failure load when both networks are successfully breached.

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We aimed to identify novel molecular mechanisms for muscle growth during administration of anabolic agents. Growing pigs (Duroc/(Landrace/Large-White)) were administered Ractopamine (a beta-adrenergic agonist; BA; 20 ppm in feed) or Reporcin (recombinant growth hormone; GH; 10 mg/48 hours injected) and compared to a control cohort (feed only; no injections) over a 27-day time course (1, 3, 7, 13 or 27-days). Longissimus Dorsi muscle gene expression was analyzed using Agilent porcine transcriptome microarrays and clusters of genes displaying similar expression profiles were identified using a modified maSigPro clustering algorithm. Anabolic agents increased carcass (p = 0.002) and muscle weights (Vastus Lateralis: p < 0.001; Semitendinosus: p = 0.075). Skeletal muscle mRNA expression of serine/one-carbon/glycine biosynthesis pathway genes (Phgdh, Psat1 and Psph) and the gluconeogenic enzyme, phosphoenolpyruvate carboxykinase-M (Pck2/PEPCK-M), increased during treatment with BA, and to a lesser extent GH (p < 0.001, treatment x time interaction). Treatment with BA, but not GH, caused a 2-fold increase in phosphoglycerate dehydrogenase (PHGDH) protein expression at days 3 (p < 0.05) and 7 (p < 0.01), and a 2-fold increase in PEPCK-M protein expression at day 7 (p < 0.01). BA treated pigs exhibit a profound increase in expression of PHGDH and PEPCK-M in skeletal muscle, implicating a role for biosynthetic metabolic pathways in muscle growth.