The Persistence of Utopia: Plasticity and Difference from Roland Barthes to Catherine Malabou

The theorizing of utopia is a persistent theme throughout several generations of the French continental tradition, and alongside the process theory of Alfred North Whitehead to a large degree recuperates the concept of utopia from its supposed dismissal by Marx and his intellectual descendants. Most recently, attention to the notion of plasticity, popularized (relatively speaking) by Catherine Malabou, extends speculation on utopian possibility.  Compelled to answer to Marx’s denigration of utopia as fantasy, the tendency was (still is, for many) to compensate for the absence of a programmatic politics by stressing what is “useful” about utopian dreaming, and therefore where or how exactly a utopian text reveals or creates political drive, or motivates political action. In this essay, I argue that theorists have overlooked the use of utopia as not only the reproduction of difference, or what Malabou calls positive plasticity, but also as, therefore, a disruption; Malabou might prefer the term accident here. Tracing the concept of plasticity from Roland Barthes to Malabou, with a nod at Miguel Abensour, this essay teases out the links between a contemporary notion of plasticity to argue, simply put, that utopia is plastic. This plasticity of the concept ensures its political force. These links, obscured in the essay “Plastic,” Barthes makes only later in his writing. But for Malabou, plasticity underlies a principle of futurity and/as generativity, such that new forms, new meanings, new concepts emerge through difference. Utopia’s horizons of potentiality depend on difference, and on non-achievement. Finally, I argue that the persistence of utopia (Abensour) as a form of thinking is the most important, and political, effect of utopian plasticity

The Persistence of Utopia: Plasticity and Difference from Roland Barthes to Catherine Malabou

The theorizing of utopia is a persistent theme throughout several generations of the French continental tradition, and alongside the process theory of Alfred North Whitehead to a large degree recuperates the concept of utopia from its supposed dismissal by Marx and his intellectual descendants. Most recently, attention to the notion of plasticity, popularized (relatively speaking) by Catherine Malabou, extends speculation on utopian possibility.  Compelled to answer to Marx’s denigration of utopia as fantasy, the tendency was (still is, for many) to compensate for the absence of a programmatic politics by stressing what is “useful” about utopian dreaming, and therefore where or how exactly a utopian text reveals or creates political drive, or motivates political action. In this essay, I argue that theorists have overlooked the use of utopia as not only the reproduction of difference, or what Malabou calls positive plasticity, but also as, therefore, a disruption; Malabou might prefer the term accident here. Tracing the concept of plasticity from Roland Barthes to Malabou, with a nod at Miguel Abensour, this essay teases out the links between a contemporary notion of plasticity to argue, simply put, that utopia is plastic. This plasticity of the concept ensures its political force. These links, obscured in the essay “Plastic,” Barthes makes only later in his writing. But for Malabou, plasticity underlies a principle of futurity and/as generativity, such that new forms, new meanings, new concepts emerge through difference. Utopia’s horizons of potentiality depend on difference, and on non-achievement. Finally, I argue that the persistence of utopia (Abensour) as a form of thinking is the most important, and political, effect of utopian plasticity

Finishing the euchromatic sequence of the human genome

The sequence of the human genome encodes the genetic instructions for human physiology, as well as rich information about human evolution. In 2001, the International Human Genome Sequencing Consortium reported a draft sequence of the euchromatic portion of the human genome. Since then, the international collaboration has worked to convert this draft into a genome sequence with high accuracy and nearly complete coverage. Here, we report the result of this finishing process. The current genome sequence (Build 35) contains 2.85 billion nucleotides interrupted by only 341 gaps. It covers ∼99% of the euchromatic genome and is accurate to an error rate of ∼1 event per 100,000 bases. Many of the remaining euchromatic gaps are associated with segmental duplications and will require focused work with new methods. The near-complete sequence, the first for a vertebrate, greatly improves the precision of biological analyses of the human genome including studies of gene number, birth and death. Notably, the human enome seems to encode only 20,000-25,000 protein-coding genes. The genome sequence reported here should serve as a firm foundation for biomedical research in the decades ahead

Analysis of shared heritability in common disorders of the brain

ience, this issue p. eaap8757 Structured Abstract INTRODUCTION Brain disorders may exhibit shared symptoms and substantial epidemiological comorbidity, inciting debate about their etiologic overlap. However, detailed study of phenotypes with different ages of onset, severity, and presentation poses a considerable challenge. Recently developed heritability methods allow us to accurately measure correlation of genome-wide common variant risk between two phenotypes from pools of different individuals and assess how connected they, or at least their genetic risks, are on the genomic level. We used genome-wide association data for 265,218 patients and 784,643 control participants, as well as 17 phenotypes from a total of 1,191,588 individuals, to quantify the degree of overlap for genetic risk factors of 25 common brain disorders. RATIONALE Over the past century, the classification of brain disorders has evolved to reflect the medical and scientific communities' assessments of the presumed root causes of clinical phenomena such as behavioral change, loss of motor function, or alterations of consciousness. Directly observable phenomena (such as the presence of emboli, protein tangles, or unusual electrical activity patterns) generally define and separate neurological disorders from psychiatric disorders. Understanding the genetic underpinnings and categorical distinctions for brain disorders and related phenotypes may inform the search for their biological mechanisms. RESULTS Common variant risk for psychiatric disorders was shown to correlate significantly, especially among attention deficit hyperactivity disorder (ADHD), bipolar disorder, major depressive disorder (MDD), and schizophrenia. By contrast, neurological disorders appear more distinct from one another and from the psychiatric disorders, except for migraine, which was significantly correlated to ADHD, MDD, and Tourette syndrome. We demonstrate that, in the general population, the personality trait neuroticism is significantly correlated with almost every psychiatric disorder and migraine. We also identify significant genetic sharing between disorders and early life cognitive measures (e.g., years of education and college attainment) in the general population, demonstrating positive correlation with several psychiatric disorders (e.g., anorexia nervosa and bipolar disorder) and negative correlation with several neurological phenotypes (e.g., Alzheimer's disease and ischemic stroke), even though the latter are considered to result from specific processes that occur later in life. Extensive simulations were also performed to inform how statistical power, diagnostic misclassification, and phenotypic heterogeneity influence genetic correlations. CONCLUSION The high degree of genetic correlation among many of the psychiatric disorders adds further evidence that their current clinical boundaries do not reflect distinct underlying pathogenic processes, at least on the genetic level. This suggests a deeply interconnected nature for psychiatric disorders, in contrast to neurological disorders, and underscores the need to refine psychiatric diagnostics. Genetically informed analyses may provide important "scaffolding" to support such restructuring of psychiatric nosology, which likely requires incorporating many levels of information. By contrast, we find limited evidence for widespread common genetic risk sharing among neurological disorders or across neurological and psychiatric disorders. We show that both psychiatric and neurological disorders have robust correlations with cognitive and personality measures. Further study is needed to evaluate whether overlapping genetic contributions to psychiatric pathology may influence treatment choices. Ultimately, such developments may pave the way toward reduced heterogeneity and improved diagnosis and treatment of psychiatric disorders

New genetic loci link adipose and insulin biology to body fat distribution.

Body fat distribution is a heritable trait and a well-established predictor of adverse metabolic outcomes, independent of overall adiposity. To increase our understanding of the genetic basis of body fat distribution and its molecular links to cardiometabolic traits, here we conduct genome-wide association meta-analyses of traits related to waist and hip circumferences in up to 224,459 individuals. We identify 49 loci (33 new) associated with waist-to-hip ratio adjusted for body mass index (BMI), and an additional 19 loci newly associated with related waist and hip circumference measures (P < 5 × 10(-8)). In total, 20 of the 49 waist-to-hip ratio adjusted for BMI loci show significant sexual dimorphism, 19 of which display a stronger effect in women. The identified loci were enriched for genes expressed in adipose tissue and for putative regulatory elements in adipocytes. Pathway analyses implicated adipogenesis, angiogenesis, transcriptional regulation and insulin resistance as processes affecting fat distribution, providing insight into potential pathophysiological mechanisms

Genome-wide association study identifies six new loci influencing pulse pressure and mean arterial pressure.

Numerous genetic loci have been associated with systolic blood pressure (SBP) and diastolic blood pressure (DBP) in Europeans. We now report genome-wide association studies of pulse pressure (PP) and mean arterial pressure (MAP). In discovery (N = 74,064) and follow-up studies (N = 48,607), we identified at genome-wide significance (P = 2.7 × 10(-8) to P = 2.3 × 10(-13)) four new PP loci (at 4q12 near CHIC2, 7q22.3 near PIK3CG, 8q24.12 in NOV and 11q24.3 near ADAMTS8), two new MAP loci (3p21.31 in MAP4 and 10q25.3 near ADRB1) and one locus associated with both of these traits (2q24.3 near FIGN) that has also recently been associated with SBP in east Asians. For three of the new PP loci, the estimated effect for SBP was opposite of that for DBP, in contrast to the majority of common SBP- and DBP-associated variants, which show concordant effects on both traits. These findings suggest new genetic pathways underlying blood pressure variation, some of which may differentially influence SBP and DBP

Genetic associations at 53 loci highlight cell types and biological pathways relevant for kidney function.

Reduced glomerular filtration rate defines chronic kidney disease and is associated with cardiovascular and all-cause mortality. We conducted a meta-analysis of genome-wide association studies for estimated glomerular filtration rate (eGFR), combining data across 133,413 individuals with replication in up to 42,166 individuals. We identify 24 new and confirm 29 previously identified loci. Of these 53 loci, 19 associate with eGFR among individuals with diabetes. Using bioinformatics, we show that identified genes at eGFR loci are enriched for expression in kidney tissues and in pathways relevant for kidney development and transmembrane transporter activity, kidney structure, and regulation of glucose metabolism. Chromatin state mapping and DNase I hypersensitivity analyses across adult tissues demonstrate preferential mapping of associated variants to regulatory regions in kidney but not extra-renal tissues. These findings suggest that genetic determinants of eGFR are mediated largely through direct effects within the kidney and highlight important cell types and biological pathways

The Art of Myth-Busting: Barthes' "Plastic" and the Gyre Art Exhibit

Roland Barthes' essay "Plastic" (1957) offers a framework for "reading" the stunning display of eco-artwork feature in GYRE: The Plastic Ocean exhibit coming to the Anchorage Museum. At this event, guest speaker Jennifer Wagner-Lawlor traces Barthes' admiration and skepticism about plastic, a then-new material, and links his insights to themes seen in the genre of found-plastic art. Jennifer Wagner-Lawlor is an associate professor of Women's Studies and English at Penn State. Her most recent book is Postmodern Utopias and Feminist Fictions

MLA 2020 Roundtable Proposal (accepted) - Reading Utopia in Dark Times

Within the context of an increasingly dystopian sense of global crisis, how can the idea of Utopia help us galvanise political literary readings? This special session will present a roundtable discussion in which panelists consider how we can use utopian methods to understand different kinds of literary texts, reflecting upon the importance of the humanities and humanist values in “dark times.