Structural polymers are susceptible to damage in the form of cracks, which form deep within the structure where detection is difficult and repair is almost impossible. Cracking leads to mechanical degradation of fibre-reinforced polymer composites; in microelectronic polymeric components it can also lead to electrical failure. Microcracking induced by thermal and mechanical fatigue is also a long-standing problem in polymer adhesives. Regardless of the application, once cracks have formed within polymeric materials, the integrity of the structure is significantly compromised. Experiments exploring the concept of self-repair have been previously reported, but the only successful crack-healing methods that have been reported so far require some form of manual intervention. Here we report a structural polymeric material with the ability to autonomically heal cracks. The material incorporates a microencapsulated healing agent that is released upon crack intrusion. Polymerization of the healing agent is then triggered by contact with an embedded catalyst, bonding the crack faces. Our fracture experiments yield as much as 75% recovery in toughness, and we expect that our approach will be applicable to other brittle materials systems (including ceramics and glasses).

Autonomic healing of polymer composites

An Antidiabetic Thiazolidinedione Is a High Affinity Ligand for Peroxisome Proliferator-activated Receptor γ (PPARγ)

Stimulation of adipogenesis in fibroblasts by PPAR gamma 2, a lipid-activated transcription factor.

Gene regulation by steroid hormones.

The RXR heterodimers and orphan receptors

We have cloned a member of the steroid hormone receptor superfamily of ligand-activated transcription factors. The receptor homologue is activated by a diverse class of rodent hepatocarcinogens that causes proliferation of peroxisomes. Identification of a peroxisome proliferator-activated receptor should help elucidate the mechanism of the hypolipidaemic effect of these hepatocarcinogens and aid evaluation of their potential carcinogenic risk to man.

Activation of a member of the steroid hormone receptor superfamily by peroxisome proliferators

Receptor-mediated mechanisms of peroxisome proliferators.

Modulation of oestrogen receptor activity by oestrogens and anti-oestrogens.

Nuclear receptors and chemical carcinogenesis

Cloning of novel members of the steroid hormone receptor superfamily

Stephen Green

Papers

Activation of a member of the steroid hormone receptor superfamily by peroxisome proliferators

Receptor-mediated mechanisms of peroxisome proliferators.

Modulation of oestrogen receptor activity by oestrogens and anti-oestrogens.

Nuclear receptors and chemical carcinogenesis

Cloning of novel members of the steroid hormone receptor superfamily