1,204 research outputs found

    Introduction

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    Species categories are not simply an invention of the human mind. Plants, animals, fungi, and viruses engage in species making by mingling and separating.1 Yet, at the same time, the boundaries that define or differentiate species are not simply natural ; they are actively made, maintained, politically charged, and fashioned to serve some needs more than others, inviting new essentialisms even as they alert us to important differences. Like other rubrics for organizing social worlds—race, ethnicity, gender, age, ability—the concept of species and the alternative classifications it invites are complicated and controversial. Whether wild or domestic, pet or pest, such categories are subject to temporally fluctuating human motives, shifting values, and cultural diversities

    Introduction

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    Species categories are not simply an invention of the human mind. Plants, animals, fungi, and viruses engage in species making by mingling and separating.1 Yet, at the same time, the boundaries that define or differentiate species are not simply natural ; they are actively made, maintained, politically charged, and fashioned to serve some needs more than others, inviting new essentialisms even as they alert us to important differences. Like other rubrics for organizing social worlds—race, ethnicity, gender, age, ability—the concept of species and the alternative classifications it invites are complicated and controversial. Whether wild or domestic, pet or pest, such categories are subject to temporally fluctuating human motives, shifting values, and cultural diversities

    The Democratic Biopolitics of PrEP

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    PrEP (Pre-Exposure Prophylaxis) is a relatively new drug-based HIV prevention technique and an important means to lower the HIV risk of gay men who are especially vulnerable to HIV. From the perspective of biopolitics, PrEP inscribes itself in a larger trend of medicalization and the rise of pharmapower. This article reconstructs and evaluates contemporary literature on biopolitical theory as it applies to PrEP, by bringing it in a dialogue with a mapping of the political debate on PrEP. As PrEP changes sexual norms and subjectification, for example condom use and its meaning for gay subjectivity, it is highly contested. The article shows that the debate on PrEP can be best described with the concepts ‘sexual-somatic ethics’ and ‘democratic biopolitics’, which I develop based on the biopolitical approach of Nikolas Rose and Paul Rabinow. In contrast, interpretations of PrEP which are following governmentality studies or Italian Theory amount to either farfetched or trivial positions on PrEP, when seen in light of the political debate. Furthermore, the article is a contribution to the scholarship on gay subjectivity, highlighting how homophobia and homonormativity haunts gay sex even in liberal environments, and how PrEP can serve as an entry point for the destigmatization of gay sexuality and transformation of gay subjectivity. ‘Biopolitical democratization’ entails making explicit how medical technology and health care relates to sexual subjectification and ethics, to strengthen the voice of (potential) PrEP users in health politics, and to renegotiate the profit and power of Big Pharma

    Genetic risk and a primary role for cell-mediated immune mechanisms in multiple sclerosis.

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    Multiple sclerosis is a common disease of the central nervous system in which the interplay between inflammatory and neurodegenerative processes typically results in intermittent neurological disturbance followed by progressive accumulation of disability. Epidemiological studies have shown that genetic factors are primarily responsible for the substantially increased frequency of the disease seen in the relatives of affected individuals, and systematic attempts to identify linkage in multiplex families have confirmed that variation within the major histocompatibility complex (MHC) exerts the greatest individual effect on risk. Modestly powered genome-wide association studies (GWAS) have enabled more than 20 additional risk loci to be identified and have shown that multiple variants exerting modest individual effects have a key role in disease susceptibility. Most of the genetic architecture underlying susceptibility to the disease remains to be defined and is anticipated to require the analysis of sample sizes that are beyond the numbers currently available to individual research groups. In a collaborative GWAS involving 9,772 cases of European descent collected by 23 research groups working in 15 different countries, we have replicated almost all of the previously suggested associations and identified at least a further 29 novel susceptibility loci. Within the MHC we have refined the identity of the HLA-DRB1 risk alleles and confirmed that variation in the HLA-A gene underlies the independent protective effect attributable to the class I region. Immunologically relevant genes are significantly overrepresented among those mapping close to the identified loci and particularly implicate T-helper-cell differentiation in the pathogenesis of multiple sclerosis

    Response of littoral chironomid community and organic matter to late glacial lake level and environmental changes at Lago dell'Accesa (Tuscany, Italy).

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    International audienceThis study focuses on the response of lacustrine littoral chironomid communities to late glacial changes in limnological, environmental and climate conditions in the Mediterranean context. Late glacial chironomid (Diptera: Chironomidae) assemblages, organic petrography and geochemistry were analysed in a sediment core from the littoral zone of Lago dell'Accesa (Tuscany, Italy), where the lake-level fluctuations and the vegetation history have been previously reconstructed. Comparison of the chironomid stratigraphy to other proxies (pollen assemblages, organic petrography and geochemistry, lake-level) and regional climate reconstruction suggested the predominant influence of lake-level changes on the littoral chironomid fauna. The main lowering events that occurred during the Oldest and the Younger Dryas were followed by higher proportions of taxa typical of littoral habitats. A complementary study of organic matter suggested the indirect impact of lake-level on the chironomids through changes in humic status and habitat characteristics, such as the type of substrate and aquatic macrophyte development. Several chironomid taxa, such as Glyptotendipes, Microtendipes and Cricotopus type patens, were identified as possible indicators of low lake-level in the late glacial records. Nevertheless, this study suggested that parallel analyses of organic matter and chironomid assemblages may be needed to circumvent misinterpretation of littoral chironomid assemblage stratigraphy. There was a weak response of the chironomid assemblages to small lake-level lowerings that corresponded to the Older Dryas and Preboreal oscillations. A higher level of determination, e.g. to the species group level, may be necessary to increase the sensibility of the indicators to lake-level changes

    Genome Sequence of Brucella abortus Vaccine Strain S19 Compared to Virulent Strains Yields Candidate Virulence Genes

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    The Brucella abortus strain S19, a spontaneously attenuated strain, has been used as a vaccine strain in vaccination of cattle against brucellosis for six decades. Despite many studies, the physiological and molecular mechanisms causing the attenuation are not known. We have applied pyrosequencing technology together with conventional sequencing to rapidly and comprehensively determine the complete genome sequence of the attenuated Brucella abortus vaccine strain S19. The main goal of this study is to identify candidate virulence genes by systematic comparative analysis of the attenuated strain with the published genome sequences of two virulent and closely related strains of B. abortus, 9–941 and 2308. The two S19 chromosomes are 2,122,487 and 1,161,449 bp in length. A total of 3062 genes were identified and annotated. Pairwise and reciprocal genome comparisons resulted in a total of 263 genes that were non-identical between the S19 genome and any of the two virulent strains. Amongst these, 45 genes were consistently different between the attenuated strain and the two virulent strains but were identical amongst the virulent strains, which included only two of the 236 genes that have been implicated as virulence factors in literature. The functional analyses of the differences have revealed a total of 24 genes that may be associated with the loss of virulence in S19. Of particular relevance are four genes with more than 60bp consistent difference in S19 compared to both the virulent strains, which, in the virulent strains, encode an outer membrane protein and three proteins involved in erythritol uptake or metabolism

    The Myosin Va Head Domain Binds to the Neurofilament-L Rod and Modulates Endoplasmic Reticulum (ER) Content and Distribution within Axons

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    The neurofilament light subunit (NF-L) binds to myosin Va (Myo Va) in neurons but the sites of interaction and functional significance are not clear. We show by deletion analysis that motor domain of Myo Va binds to the NF-L rod domain that forms the NF backbone. Loss of NF-L and Myo Va binding from axons significantly reduces the axonal content of ER, and redistributes ER to the periphery of axon. Our data are consistent with a novel function for NFs as a scaffold in axons for maintaining the content and proper distribution of vesicular organelles, mediated in part by Myo Va. Based on observations that the Myo Va motor domain binds to intermediate filament (IF) proteins of several classes, Myo Va interactions with IFs may serve similar roles in organizing organelle topography in different cell types

    Pharmacogenetic meta-analysis of genome-wide association studies of LDL cholesterol response to statins

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    Statins effectively lower LDL cholesterol levels in large studies and the observed interindividual response variability may be partially explained by genetic variation. Here we perform a pharmacogenetic meta-analysis of genome-wide association studies (GWAS) in studies addressing the LDL cholesterol response to statins, including up to 18,596 statin-treated subjects. We validate the most promising signals in a further 22,318 statin recipients and identify two loci, SORT1/CELSR2/PSRC1 and SLCO1B1, not previously identified in GWAS. Moreover, we confirm the previously described associations with APOE and LPA. Our findings advance the understanding of the pharmacogenetic architecture of statin response

    sodC-Based Real-Time PCR for Detection of Neisseria meningitidis

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    Real-time PCR (rt-PCR) is a widely used molecular method for detection of Neisseria meningitidis (Nm). Several rt-PCR assays for Nm target the capsule transport gene, ctrA. However, over 16% of meningococcal carriage isolates lack ctrA, rendering this target gene ineffective at identification of this sub-population of meningococcal isolates. The Cu-Zn superoxide dismutase gene, sodC, is found in Nm but not in other Neisseria species. To better identify Nm, regardless of capsule genotype or expression status, a sodC-based TaqMan rt-PCR assay was developed and validated. Standard curves revealed an average lower limit of detection of 73 genomes per reaction at cycle threshold (Ct) value of 35, with 100% average reaction efficiency and an average R2 of 0.9925. 99.7% (624/626) of Nm isolates tested were sodC-positive, with a range of average Ct values from 13.0 to 29.5. The mean sodC Ct value of these Nm isolates was 17.6±2.2 (±SD). Of the 626 Nm tested, 178 were nongroupable (NG) ctrA-negative Nm isolates, and 98.9% (176/178) of these were detected by sodC rt-PCR. The assay was 100% specific, with all 244 non-Nm isolates testing negative. Of 157 clinical specimens tested, sodC detected 25/157 Nm or 4 additional specimens compared to ctrA and 24 more than culture. Among 582 carriage specimens, sodC detected Nm in 1 more than ctrA and in 4 more than culture. This sodC rt-PCR assay is a highly sensitive and specific method for detection of Nm, especially in carriage studies where many meningococcal isolates lack capsule genes
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