Towards a Harm-Minimising Approach to Sex Work: A Call for Decriminalisation in England and Wales

This thesis has developed a harm-minimising framework to analyse the regulation of sex work in England and Wales and propose a system of reform. In so doing, it defines the ‘harm’ in sex work as that of stigma, violence and exploitation, using this categorisation to judge the effectiveness of any (new) system of legal regulation. This thesis demonstrates how sex workers are frequently cast as a deviant population and separated from the rest of society, facing extreme forms of violence and exploitation. Using my harm-framework of analysis, this thesis examines the regulation of sex work in England and Wales, starting with the Contagious Disease Acts of the 1860’s through to modern day. In doing this, it will demonstrate the ability of the law to maintain, shape and create the conditions for the violence, exploitation and stigma faced by women selling sex. The thesis then explores alternative means of regulating sex work. It will look towards the alternatives of criminalising the clients, regimes of legalisation and of decriminalisation. It concludes that in order to provide the sex worker with sufficient protections against violence, stigma and exploitation, England and Wales should adopt a regime of decriminalisation. It is only under such a regime that sex workers could be provided with effective and realistic safeguards against the harm currently endemic in their work, and within which, crucial steps can be made towards altering their stigmatised and marginalised status

The cDNA and deduced amino acid sequence of the γ subunit of the L-type calcium channel from rabbit skeletal muscle

Complementary DNAs for the γ subunit of the calcium channel of rabbit skeletal muscle were isolated on the basis of peptide sequences derived from the purified protein. The deduced primary structure is without homology to other known protein sequences and is consistent with the γ subunit being an integral membrane protein

Abnormal ryanodine receptor channels in malignant hyperthermia.

Previous studies have demonstrated a defect associated with the calcium release mechanism of sarcoplasmic reticulum (SR) from individuals susceptible to malignant hyperthermia (MH). To examine whether SR calcium release channels were indeed altered in MH, SR vesicles were purified from normal and MH susceptible (MHS) porcine muscle. The Ca2+ dependence of calcium efflux rates from 45Ca2(+)-filled SR vesicles was then compared with the Ca2+ dependence of single-channel recordings of SR vesicles incorporated into planar lipid bilayers. The rate constants of 45Ca2+ efflux from MHS SR were two to threefold larger than from normal SR over a wide range of myoplasmic Ca2+. Normal and MHS single channels were progressively activated in a similar fashion by cis Ca2+ from pCa 7 to 4. However, below pCa 4, normal channels were inactivated by cis Ca2+, whereas MHS channels remained open for significantly longer times. The altered Ca2+ dependence of channel inactivation in MHS SR was also evident when Ca2+ was increased on the trans side while cis Ca2+ was held constant. We propose that a defect in a low-affinity Ca2+ binding site is responsible for the altered gating of MHS SR channels. Such a defect could logically result from a mutation in the gene encoding the calcium release channel, providing a testable hypothesis for the molecular basis of this inherited disorder