How to humiliate and shame: A reporter's guide to the power of the mugshot

This is an Author's Accepted Manuscript of an article published in Social Semiotics, 24(1), 56-87, 2014, copyright Taylor & Francis, available online at: http://www.tandfonline.com/The judicial photograph – the “mugshot” – is a ubiquitous and instantly recognisable form, appearing in the news media, on the internet, on book covers, law enforcement noticeboards and in many other mediums. This essay attempts to situate the mugshot in a historical and theoretical context to explain the explicit and implicit meaning of the genre as it has developed, focussing in particular on their use in the UK media in late modernity. The analysis is based on the author's reflexive practice as a journalist covering crime in the national news media for 30 years and who has used mugshots to illustrate stories for their explicit and specific content. The author argues that the visual limitations of the standardised “head and shoulders” format of the mugshot make it a robust subject for analysing the changing meaning of images over time. With little variation in the image format, arguments for certain accreted layers of signification are easier to make. Within a few years of the first appearance of the mugshot form in the mid-19th century, it was adopted and adapted as a research tool by scientists and criminologists. While the positivist scientists claimed empirical objectivity we can now see that mugshots played a part in the construction of subjective notions of “the other”, “the lesser” or “sub-human” on the grounds of class, race and religion. These dehumanising ideas later informed the theorists and bureaucrats of National Socialist ideology from the 1920s to 1940s. The author concludes that once again the mugshot has become, in certain parts of the media, a signifier widely used to exclude or deride certain groups. In late modernity, the part of the media that most use mugshots – the tabloid press and increasingly tabloid TV – is part of a neo-liberal process that, in a conscious commercial appeal to the paying audience, seeks to separate rather than unify wider society

Potentiation of Synaptic GluN2B NMDAR Currents by Fyn Kinase Is Gated through BDNF-Mediated Disinhibition in Spinal Pain Processing

In chronic pain states, the neurotrophin brain-derived neurotrophic factor (BDNF) transforms the output of lamina I spinal neurons by decreasing synaptic inhibition. Pain hypersensitivity also depends on N-methyl-D-aspartate receptors (NMDARs) and Src-family kinases, but the locus of NMDAR dysregulation remains unknown. Here, we show that NMDAR-mediated currents at lamina I synapses are potentiated in a peripheral nerve injury model of neuropathic pain. We find that BDNF mediates NMDAR potentiation through activation of TrkB and phosphorylation of the GluN2B subunit by the Src-family kinase Fyn. Surprisingly, we find that Cl−-dependent disinhibition is necessary and sufficient to prime potentiation of synaptic NMDARs by BDNF. Thus, we propose that spinal pain amplification is mediated by a feedforward mechanism whereby loss of inhibition gates the increase in synaptic excitation within individual lamina I neurons. Given that neither disinhibition alone nor BDNF-TrkB signaling is sufficient to potentiate NMDARs, we have discovered a form of molecular coincidence detection in lamina I neurons

Paul Nizan: conspiracy and the contemplation of crime

Paul Nizan (1905-1940) is also known in France as the ‘impossible communist’, for his long-term allegiance to the Party and the abrupt cancellation of his membership, in the late 1930s, following the Nazi-Soviet pact. This paper discusses a number of his writings, focusing particularly on his best known novel, The Conspiracy, where a revolutionary cell plans illegal political action. Conflict, nihilism, suicide and betrayal are among the topics stemming from the novel, which will be examined from a criminological perspective. The analysis will primarily address ‘cultural’ aspects of crime and refer to notions such as ‘thrill’ and ‘seductions of crime’ among others. These notions, it will be argued, require some revision in the face of the imagined or actual criminality described in the novel

Targeted Epigenetic Remodeling of the \u3cem\u3eCdk5\u3c/em\u3e Gene in Nucleus Accumbens Regulates Cocain- and Stress-Evoked Behavior

Recent studies have implicated epigenetic remodeling in brain reward regions following psychostimulant or stress exposure. It has only recently become possible to target a given type of epigenetic remodeling to a single gene of interest, and to probe the functional relevance of such regulation to neuropsychiatric disease. We sought to examine the role of histone modifications at the murine Cdk5 (cyclin-dependent kinase 5) locus, given growing evidence of Cdk5 expression in nucleus accumbens (NAc) influencing reward-related behaviors. Viral-mediated delivery of engineered zinc finger proteins (ZFP) targeted histone H3 lysine 9/14 acetylation (H3K9/14ac), a transcriptionally active mark, or histone H3 lysine 9 dimethylation (H3K9me2), which is associated with transcriptional repression, specifically to the Cdk5 locus in NAc in vivo. We gound that Cdk5-ZFP transcription factors are sufficient to bidirectionally regulate Cdk5 gene expression via enrichment of their respective histone modifications. We examined the behavioral consequences of this epigenetic remodeling and found that Cdk5-targeted H3K9/14ac increased cocaine-induced locomotor behavior, as well as resilience to social stress. Conversely, Cdk5-targeted H3K9me2 attenuated both cocaine-induced locomotor behavior and conditioned place preference, but had no effect on stress-induced social avoidance behavior. The current study provides evidence for the causal role of Cdk5 epigenetic remodeling in NAc in Cdk5 gene expression and in the control of reward and stress responses. Moreover, these data are especially compelling given that previous work demonstrated opposite behavioral phenotypes compared with those reported here upon Cdk5 overexpression or knockdown, demonstrating the importance of targeted epigenetic remodeling tools for studying more subtle molecular changes that contribute to neuropsychiatric disease

Down-regulation of BDNF in cell and animal models increases striatal-enriched protein tyrosine phosphatase 61 (STEP61) levels

Brain-derived neurotrophic factor (BDNF) regulates synaptic strengthening and memory consolidation, and altered BDNF expression is implicated in a number of neuropsychiatric and neurodegenerative disorders. BDNF potentiates N-methyl-D-aspartate receptor function through activation of Fyn and ERK1/2. STriatal-Enriched protein tyrosine Phosphatase (STEP) is also implicated in many of the same disorders as BDNF but, in contrast to BDNF, STEP opposes the development of synaptic strengthening. STEP-mediated dephosphorylation of the NMDA receptor subunit GluN2B promotes internalization of GluN2B-containing NMDA receptors, while dephosphorylation of the kinases Fyn, Pyk2, and ERK1/2 leads to their inactivation. Thus, STEP and BDNF have opposing functions. In this study, we demonstrate that manipulation of BDNF expression has a reciprocal effect on STEP61 levels. Reduced BDNF signaling leads to elevation of STEP61 both in BDNF(+/-) mice and after acute BDNF knockdown in cortical cultures. Moreover, a newly identified STEP inhibitor reverses the biochemical and motor abnormalities in BDNF(+/-) mice. In contrast, increased BDNF signaling upon treatment with a tropomyosin receptor kinase B agonist results in degradation of STEP61 and a subsequent increase in the tyrosine phosphorylation of STEP substrates in cultured neurons and in mouse frontal cortex. These findings indicate that BDNF-tropomyosin receptor kinase B signaling leads to degradation of STEP61 , while decreased BDNF expression results in increased STEP61 activity. A better understanding of the opposing interaction between STEP and BDNF in normal cognitive functions and in neuropsychiatric disorders will hopefully lead to better therapeutic strategies. Altered expression of BDNF and STEP61 has been implicated in several neurological disorders. BDNF and STEP61 are known to regulate synaptic strengthening, but in opposite directions. Here, we report that reduced BDNF signaling leads to elevation of STEP61 both in BDNF(+/-) mice and after acute BDNF knockdown in cortical cultures. In contrast, activation of TrkB receptor results in the degradation of STEP61 and reverses hyperlocomotor activity in BDNF(+/-) mice. Moreover, inhibition of STEP61 by TC-2153 is sufficient to enhance the Tyr phosphorylation of STEP substrates and also reverses hyperlocomotion in BDNF(+/-) mice. These findings give us a better understanding of the regulation of STEP61 by BDNF in normal cognitive functions and in neuropsychiatric disorders

The genomics of visuospatial neurocognition in obsessive-compulsive disorder: A preliminary GWAS

Background: The study of Obsessive-Compulsive Disorder (OCD) genomics has primarily been tackled by Genome-wide association studies (GWAS), which have encountered troubles in identifying replicable single nucleotide polymorphisms (SNPs). Endophenotypes have emerged as a promising avenue of study in trying to elucidate the genomic bases of complex traits such as OCD.Methods: We analyzed the association of SNPs across the whole genome with the construction of visuospatial information and executive performance through four neurocognitive variables assessed by the Rey-Osterrieth Complex Figure Test (ROCFT) in a sample of 133 OCD probands. Analyses were performed at SNP- and genelevel.Results: No SNP reached genome-wide significance, although there was one SNP almost reaching significant association with copy organization (rs60360940; P = 9.98E-08). Suggestive signals were found for the four variables at both SNP- (P < 1E-05) and gene-levels (P < 1E-04). Most of the suggestive signals pointed to genes and genomic regions previously associated with neurological function and neuropsychological traits. Limitations: Our main limitations were the sample size, which was limited to identify associated signals at a genome-wide level, and the composition of the sample, more representative of rather severe OCD cases than a population-based OCD sample with a broad severity spectrum.Conclusions: Our results suggest that studying neurocognitive variables in GWAS would be more informative on the genetic basis of OCD than the classical case/control GWAS, facilitating the genetic characterization of OCD and its different clinical profiles, the development of individualized treatment approaches, and the improvement of prognosis and treatment response

Liberal governmentality in Spain: bodies, minds, and the medical construction of the “outsider,” 1870–1910

This paper traces the fragility of the subject in the period extending from the aftermath of the Sexenio through to the early twentieth century. In particular, two case studies are focused upon: the question of gender “deviance” and the figure of the genius, in order to understand how medicine participated in the construction of “outsider” identities within the context of the emerging liberal order. How did liberal rationales exclude or curtail certain wayward expressions of identity and subjectivity? What consequences did the marking of “excessive” figures or outsiders have for notions of inclusiveness and citizenship within the late-nineteenth-century liberal order? By concentrating primarily on medical texts and journals published during the period, this study builds on existing research to tease out answers to these questions

Fragile X Syndrome in Korea: A Case Series and a Review of the Literature

The purposes of this study were to present DNA analysis findings of our case series of fragile X syndrome (FXS) based on methylation-specific polymerase chain reaction (MS-PCR), PCR, and Southern blotting alongside developmental characteristics including psychological profiles and to review the literature on FXS in Korea. The reports of 65 children (male:female, 52:13; age, 6.12±4.00 yrs) referred for the diagnosis of FXS over a 26-months period were retrospectively reviewed for the identification of full mutation or premutation of fragile X mental retardation 1 (FMR1). Among the 65 children, there were 4 boys with full mutation, and one boy showed premutation of FMR1, yielding a 6.15% positive rate of FXS. All 4 children with full mutation showed significant developmental delay, cognitive dysfunction, and varying degrees of autistic behaviors. The boys with premutation showed also moderate mental retardation, severe drooling, and behavioral problems as severe as the boys with full mutation. Thirteen articles on FXS in Korea have been published since 1993, and they were reviewed. The positive rate of FXS was in the range of 0.77-8.51%, depending on the study groups and the method of diagnosis. Finally, the population-based prevalence study on FXS in Korea is required in the near future