"Author! Author!" : Shakespeare and biography

Original article can be found at: http://www.informaworld.com/smpp/title~content=t714579626~db=all Copyright Informa / Taylor & Francis Group. DOI: 10.1080/17450910902764454Since 1996, not a year has passed without the publication of at least one Shakespeare biography. Yet for many years the place of the author in the practice of understanding literary works has been problematized, and even on occasions eliminated. Criticism reads the “works”, and may or may not refer to an author whose “life” contributed to their meaning. Biography seeks the author in the works, the personality that precedes the works and gives them their characteristic shape and meaning. But the form of literary biography addresses the unusual kind of “life” that puts itself into “works”, and this is particularly challenging where the “works” predominate massively over the salient facts of the “life”. This essay surveys the current terrain of Shakespeare biography, and considers the key questions raised by the medium: can we know anything of Shakespeare's “personality” from the facts of his life and the survival of his works? What is the status of the kind of speculation that inevitably plays a part in biographical reconstruction? Are biographers in the end telling us as much about themselves as they tell us about Shakespeare?Peer reviewe

Identifying an indoor air exposure limit for formaldehyde considering both irritation and cancer hazards

Formaldehyde is a well-studied chemical and effects from inhalation exposures have been extensively characterized in numerous controlled studies with human volunteers, including asthmatics and other sensitive individuals, which provide a rich database on exposure concentrations that can reliably produce the symptoms of sensory irritation. Although individuals can differ in their sensitivity to odor and eye irritation, the majority of authoritative reviews of the formaldehyde literature have concluded that an air concentration of 0.3 ppm will provide protection from eye irritation for virtually everyone. A weight of evidence-based formaldehyde exposure limit of 0.1 ppm (100 ppb) is recommended as an indoor air level for all individuals for odor detection and sensory irritation. It has recently been suggested by the International Agency for Research on Cancer (IARC), the National Toxicology Program (NTP), and the US Environmental Protection Agency (US EPA) that formaldehyde is causally associated with nasopharyngeal cancer (NPC) and leukemia. This has led US EPA to conclude that irritation is not the most sensitive toxic endpoint and that carcinogenicity should dictate how to establish exposure limits for formaldehyde. In this review, a number of lines of reasoning and substantial scientific evidence are described and discussed, which leads to a conclusion that neither point of contact nor systemic effects of any type, including NPC or leukemia, are causally associated with exposure to formaldehyde. This conclusion supports the view that the equivocal epidemiology studies that suggest otherwise are almost certainly flawed by identified or yet to be unidentified confounding variables. Thus, this assessment concludes that a formaldehyde indoor air limit of 0.1 ppm should protect even particularly susceptible individuals from both irritation effects and any potential cancer hazard

Genome-wide mega-analysis identifies 16 loci and highlights diverse biological mechanisms in the common epilepsies.

The epilepsies affect around 65 million people worldwide and have a substantial missing heritability component. We report a genome-wide mega-analysis involving 15,212 individuals with epilepsy and 29,677 controls, which reveals 16 genome-wide significant loci, of which 11 are novel. Using various prioritization criteria, we pinpoint the 21 most likely epilepsy genes at these loci, with the majority in genetic generalized epilepsies. These genes have diverse biological functions, including coding for ion-channel subunits, transcription factors and a vitamin-B6 metabolism enzyme. Converging evidence shows that the common variants associated with epilepsy play a role in epigenetic regulation of gene expression in the brain. The results show an enrichment for monogenic epilepsy genes as well as known targets of antiepileptic drugs. Using SNP-based heritability analyses we disentangle both the unique and overlapping genetic basis to seven different epilepsy subtypes. Together, these findings provide leads for epilepsy therapies based on underlying pathophysiology