Chemically cross-linked polymers are inherently limited by stresses that are introduced by post-gelation volume changes during polymerization. It is also difficult to change a cross-linked polymer's shape without a corresponding loss of material properties or substantial stress development. We demonstrate a cross-linked polymer that, upon exposure to light, exhibits stress and/or strain relaxation without any concomitant change in material properties. This result is achieved by introducing radicals via photocleavage of residual photoinitiator in the polymer matrix, which then diffuse via addition-fragmentation chain transfer of midchain functional groups. These processes lead to photoinduced plasticity, actuation, and equilibrium shape changes without residual stress. Such polymeric materials are critical to the development of microdevices, biomaterials, and polymeric coatings.

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Inhibitor of apoptosis (IAP) proteins cIAP1, cIAP2, and XIAP (X-linked IAP) regulate apoptosis and cytokine receptor signalling, but their overlapping functions make it difficult to distinguish their individual roles. To do so, we deleted the genes for IAPs separately and in combination. While lack of any one of the IAPs produced no overt phenotype in mice, deletion of cIap1 with cIap2 or Xiap resulted in mid-embryonic lethality. In contrast, Xiap(-/-)cIap2(-/-) mice were viable. The death of cIap2(-/-)cIap1(-/-) double mutants was rescued to birth by deletion of tumour necrosis factor (TNF) receptor 1, but not TNFR2 genes. Remarkably, hemizygosity for receptor-interacting protein kinase 1 (Ripk1) allowed Xiap(-/-)cIap1(-/-) double mutants to survive past birth, and prolonged cIap2(-/-)cIap1(-/-) embryonic survival. Similarly, deletion of Ripk3 was able to rescue the mid-gestation defect of cIap2(-/-)cIap1(-/-) embryos, as these embryos survived to E15.5. cIAPs are therefore required during development to limit activity of RIP kinases in the TNF receptor 1 signalling pathway.

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