Monomeric Tartrate Resistant Acid Phosphatase Induces Insulin Sensitive Obesity

Obesity is associated with macrophage infiltration of adipose tissue, which may link adipose inflammation to insulin resistance. However, the impact of inflammatory cells in the pathophysiology of obesity remains unclear

The tuberous sclerosis proteins regulate formation of the primary cilium via a rapamycin-insensitive and polycystin 1-independent pathway

Tuberous sclerosis complex (TSC) is a tumor suppressor gene syndrome in which severe renal cystic disease can occur. Many renal cystic diseases, including autosomal dominant polycystic kidney disease (ADPKD), are associated with absence or dysfunction of the primary cilium. We report here that hamartin (TSC1) localizes to the basal body of the primary cilium, and that Tsc1−/− and Tsc2−/− mouse embryonic fibroblasts (MEFs) are significantly more likely to contain a primary cilium than wild-type controls. In addition, the cilia of Tsc1−/− and Tsc2−/− MEFs are 17–27% longer than cilia from wild-type MEFs. These data suggest a novel type of ciliary disruption in TSC, associated with enhanced cilia development. The TSC1 and TSC2 proteins function as a heterodimer to inhibit the activity of the mammalian target of rapamycin complex 1 (TORC1). The enhanced ciliary formation in the Tsc1−/− and Tsc2−/− MEFs was not abrogated by rapamycin, which indicates a TORC1-independent mechanism. Polycystin 1 (PC1), the product of the PKD1 gene, has been found to interact with TSC2, but Pkd1−/− MEFs did not have enhanced ciliary formation. Furthermore, while activation of mTOR has been observed in renal cysts from ADPKD patients, Pkd1−/− MEFs did not have evidence of constitutive mTOR activation, thereby underscoring the independent functions of the TSC proteins and PC1 in regulation of primary cilia and mTOR. Our data link the TSC proteins with the primary cilium and reveal a novel phenotype of enhanced ciliary formation in a cyst-associated disease

Sticky Stories: Joe Orton, Queer History, Queer Dramaturgy

This paper investigates the resonances of Orton’s work for contemporary queer audiences. By presenting potential reasons for the rise and fall in popularity and visibility of Orton’s work for queer and gay audiences through the 1980s and 1990s, this paper looks to the queer context in which Joe Orton’s work developed in order to explore the queer social history into which it fits.  This sense of queer history is linked to contemporary notions of queer theorising about temporalities and queer dramaturgy, which offers potentially novel ways of engaging with Orton’s work queerly without twisting it to fit a ‘neat’ reading, in part because such readings tend to ‘smooth out’ the more difficult elements of the work.  In particular, the paper explores the theatrical form of farce, often articulated as conservative, in relation to queer positions, which are quite the opposite.  In so doing, the paper, by way of queer temporalities and work on queer dramaturgies, sketches out a reading strategy that does not ignore Orton’s more difficult or stickier elements, in particular his treatment of women and race