'Roman' or 'native' bodies in Britain: the evidence of late Roman nail-cleaner strap-ends

This paper reviews late Roman `nail-cleaner strap-ends', a group of objects first discussed by Hawkes and Dunning (1961). The precise function of these objects is unclear as their shape suggests use as toilet instruments but the split socket suggests that they were part of belt-fittings. We suggest a detailed typology and discuss the dating evidence and the spatial distribution of the type. Regardless of their precise function, it is argued in this paper that nail-cleaner strap-ends of this type are unique to late Roman Britain and thus represent a distinct regional type. The use of nail-cleaner strap-ends can be viewed in the context of gender associations, military status and religious beliefs.

History in tatters: bodies and things in Samuel Beckett’s theatre

The article takes a phenomenological approach to the relationship between stage properties and the performing body in Beckett's theatre.

Mutated bodies: stage performances of Beckett's late prose texts by Mabou Mines (1984) and Gare St. Lazare Players, Ireland (2005)

An exploration of the stage adaptations of Beckett's fictional texts by the New York based Mabou Mines theatre company.

Delivery of AAV2/9-microdystrophin genes incorporating helix 1 of the coiled-coil motif in the C-terminal domain of dystrophin improves muscle pathology and restores the level of α1-syntrophin and α-dystrobrevin in skeletal muscles of mdx mice. Level of α1-Syntrophin and α-Dystrobrevin in Skeletal Muscles of mdx Mice

Duchenne muscular dystrophy is a severe X-linked inherited muscle wasting disorder caused by mutations in the dystrophin gene. Adeno-associated virus (AAV) vectors have been extensively used to deliver genes efficiently for dystrophin expression in skeletal muscles. To overcome limited packaging capacity of AAV vectors (<5 kb), truncated recombinant microdystrophin genes with deletions of most of rod and carboxyl-terminal (CT) domains of dystrophin have been developed. We have previously shown the efficiency of mRNA sequence–optimized microdystrophin (ΔR4-23/ΔCT, called MD1) with deletion of spectrin-like repeat domain 4 to 23 and CT domain in ameliorating the pathology of dystrophic mdx mice. However, the CT domain of dystrophin is thought to recruit part of the dystrophin-associated protein complex, which acts as a mediator of signalling between extracellular matrix and cytoskeleton in muscle fibers. In this study, we extended the ΔR4-23/ΔCT microdystrophin by incorporating helix 1 of the coiled-coil motif in the CT domain of dystrophin (MD2), which contains the α1-syntrophin and α-dystrobrevin binding sites. Intramuscular injection of AAV2/9 expressing CT domain–extended microdystrophin showed efficient dystrophin expression in tibialis anterior muscles of mdx mice. The presence of the CT domain of dystrophin in MD2 increased the recruitment of α1-syntrophin and α-dystrobrevin at the sarcolemma and significantly improved the muscle resistance to lengthening contraction–induced muscle damage in the mdx mice compared with MD1. These results suggest that the incorporation of helix 1 of the coiled-coil motif in the CT domain of dystrophin to the microdystrophins will substantially improve their efficiency in restoring muscle function in patients with Duchenne muscular dystrophy.