‘It’s better than daytime television’: questioning the socio-spatial impacts of massage parlours on residential communities

It has been shown that street sex work is problematic for some communities, but there is less evidence of the effects of brothels. Emerging research also suggests that impact discourses outlined by residential communities and in regulatory policies should be critiqued, because they are often based on minority community voices, and limited tangible evidence is used to masquerade wider moral viewpoints about the place of sex work. Using a study of residents living in close proximity to brothels in Blackpool, this paper argues that impact is socially and spatially fluid. Impact needs to be evaluated in a more nuanced manner, which is considerate of the heterogeneity of (even one type of) sex work, and the community in question. Brothels in Blackpool had a variety of roles in the everyday socio-spatial fabric; thus also questioning the common assumption that sex work only impacts negatively on residential communities

Serum and glucocorticoid-regulated kinase 1 regulates neutrophil clearance during inflammation resolution

The inflammatory response is integral to maintaining health, by functioning to resist microbial infection and repair tissue damage. Large numbers of neutrophils are recruited to inflammatory sites to neutralise invading bacteria through phagocytosis and the release of proteases and reactive oxygen species into the extracellular environment. Removal of the original inflammatory stimulus must be accompanied by resolution of the inflammatory response, including neutrophil clearance, to prevent inadvertent tissue damage. Neutrophil apoptosis and its temporary inhibition by survival signals provides a target for anti-inflammatory therapeutics, making it essential to better understand this process. GM-CSF, a neutrophil survival factor, causes a significant increase in mRNA levels for the known anti-apoptotic protein Serum and Glucocorticoid Regulated Kinase 1 (SGK1). We have characterised the expression patterns and regulation of SGK family members in human neutrophils, and shown that inhibition of SGK activity completely abrogates the anti-apoptotic effect of GM-CSF. Using a transgenic zebrafish model, we have disrupted sgk1 gene function and shown this specifically delays inflammation resolution, without altering neutrophil recruitment to inflammatory sites in vivo. These data suggest SGK1 plays a key role in regulating neutrophil survival signalling, and thus may prove a valuable therapeutic target for the treatment of inflammatory disease