Why is there no queer international theory?

Over the last decade, Queer Studies have become Global Queer Studies, generating significant insights into key international political processes. Yet, the transformation from Queer to Global Queer has left the discipline of International Relations largely unaffected, which begs the question: if Queer Studies has gone global, why has the discipline of International Relations not gone somewhat queer? Or, to put it in Martin Wight’s provocative terms, why is there no Queer International Theory? This article claims that the presumed non-existence of Queer International Theory is an effect of how the discipline of International Relations combines homologization, figuration, and gentrification to code various types of theory as failures in order to manage the conduct of international theorizing in all its forms. This means there are generalizable lessons to be drawn from how the discipline categorizes Queer International Theory out of existence to bring a specific understanding of International Relations into existence

Safety and Efficacy of Ombitasvir, Paritaprevir With Ritonavir ± Dasabuvir With or Without Ribavirin in Patients With Human Immunodeficiency Virus-1 and Hepatitis C Virus Genotype 1 or Genotype 4 Coinfection: TURQUOISE-I Part 2.

BACKGROUND: Ombitasvir, paritaprevir with ritonavir, and dasabuvir (OBV/PTV/r ± DSV) ±ribavirin (RBV) are approved to treat hepatitis C virus (HCV) genotype 1 and 4 infection. Here, we investigate the safety and efficacy of OBV/PTV/r + DSV ±RBV for HCV genotype 1, and OBV/PTV/r + RBV for HCV genotype 4, in human immunodeficiency virus (HIV)-1 coinfected patients with or without compensated cirrhosis. METHODS: TURQUOISE-I, Part 2 is a phase 3 multicenter study. Patients with or without cirrhosis were HCV treatment-naive or -experienced, on an HIV-1 antiretroviral regimen containing atazanavir, raltegravir, dolutegravir, or darunavir (for genotype 4 only), and had plasma HIV-1 ribonucleic acid <40 copies/mL at screening. Patients received OBV/PTV/r ± DSV ±RBV for 12 or 24 weeks. RESULTS: In total, 228 patients were treated according to guidelines. Sustained virologic response at posttreatment week 12 (SVR12) was achieved by 194 of 200 (97%) and 27 of 28 (96%) patients with HCV genotype 1 and genotype 4 infection, respectively. There were 2 virologic failures: 1 breakthrough and 1 relapse in a cirrhotic and a noncirrhotic patient with genotype 1b and 1a infection, respectively. One reinfection occurred at posttreatment week 12 in a genotype 1a-infected patient. Excluding nonvirologic failures, the SVR12 rates were 98% (genotype 1) and 100% (genotype 4). Adverse events were mostly mild in severity and did not lead to discontinuation. Laboratory abnormalities were rare. CONCLUSIONS: The OBV/PTV/r ±DSV was well tolerated and yielded high SVR12 rates in patients with HCV genotype 1 or genotype 4/HIV-1 coinfection. The OBV/PTV/r ± DSV ±RBV is a potent HCV treatment option for patients with HIV-1 coinfection, regardless of treatment experience

Using fMRI Brain Activation to Identify Cognitive States Associated with Perception of Tools and Dwellings

Previous studies have succeeded in identifying the cognitive state corresponding to the perception of a set of depicted categories, such as tools, by analyzing the accompanying pattern of brain activity, measured with fMRI. The current research focused on identifying the cognitive state associated with a 4s viewing of an individual line drawing (1 of 10 familiar objects, 5 tools and 5 dwellings, such as a hammer or a castle). Here we demonstrate the ability to reliably (1) identify which of the 10 drawings a participant was viewing, based on that participant's characteristic whole-brain neural activation patterns, excluding visual areas; (2) identify the category of the object with even higher accuracy, based on that participant's activation; and (3) identify, for the first time, both individual objects and the category of the object the participant was viewing, based only on other participants' activation patterns. The voxels important for category identification were located similarly across participants, and distributed throughout the cortex, focused in ventral temporal perceptual areas but also including more frontal association areas (and somewhat left-lateralized). These findings indicate the presence of stable, distributed, communal, and identifiable neural states corresponding to object concepts

Glecaprevir-Pibrentasvir for 8 or 12 Weeks in HCV Genotype 1 or 3 Infection

The trials (NCT02604017, NCT02640157) were funded by AbbVie Inc

The Stress Response Factors Yap6, Cin5, Phd1, and Skn7 Direct Targeting of the Conserved Co-Repressor Tup1-Ssn6 in S. cerevisiae

Maintaining the proper expression of the transcriptome during development or in response to a changing environment requires a delicate balance between transcriptional regulators with activating and repressing functions. The budding yeast transcriptional co-repressor Tup1-Ssn6 is a model for studying similar repressor complexes in multicellular eukaryotes. Tup1-Ssn6 does not bind DNA directly, but is directed to individual promoters by one or more DNA-binding proteins, referred to as Tup1 recruiters. This functional architecture allows the Tup1-Ssn6 to modulate the expression of genes required for the response to a variety of cellular stresses. To understand the targeting or the Tup1-Ssn6 complex, we determined the genomic distribution of Tup1 and Ssn6 by ChIP-chip. We found that most loci bound by Tup1-Ssn6 could not be explained by co-occupancy with a known recruiting cofactor and that deletion of individual known Tup1 recruiters did not significantly alter the Tup1 binding profile. These observations suggest that new Tup1 recruiting proteins remain to be discovered and that Tup1 recruitment typically depends on multiple recruiting cofactors. To identify new recruiting proteins, we computationally screened for factors with binding patterns similar to the observed Tup1-Ssn6 genomic distribution. Four top candidates, Cin5, Skn7, Phd1, and Yap6, all known to be associated with stress response gene regulation, were experimentally confirmed to physically interact with Tup1 and/or Ssn6. Incorporating these new recruitment cofactors with previously characterized cofactors now explains the majority of Tup1 targeting across the genome, and expands our understanding of the mechanism by which Tup1-Ssn6 is directed to its targets