Child As Metaphor: Colonialism, Psy-Governance, and Epistemicide

This paper mobilizes transdisciplinary inquiry to explore and deconstruct the often-used comparison of racialized/colonized people, intellectually disabled people and mad people as being like children. To be childlike is a metaphor that is used to denigrate, to classify as irrational and incompetent, to dismiss as not being knowledge holders, to justify governance and action on others’ behalf, to deem as being animistic, as undeveloped, underdeveloped or wrongly developed, and, hence, to subjugate. We explore the political work done by the metaphorical appeal to childhood, and particularly the centrality of the metaphor of childhood to legitimizing colonialism and white supremacy. The article attends to the ways in which this metaphor contributes to the shaping of the material and discursive realities of racialized and colonized others, as well as those who have been psychiatrized and deemed “intellectually disabled”. Further, we explore specific metaphors of child-colony, and child-mad-“crip”. We then detail the developmental logic underlying the historical and continued use of the metaphorics of childhood, and explore how this makes possible an infantilization of colonized peoples and the global South more widely. The material and discursive impact of this metaphor on children’s lives, and particularly children who are racialized, colonized, and/or deemed mad or “crip”, is then considered. We argue that complex adult-child relations, sane-mad relations and Western-majority world relations within global psychiatry, are situated firmly within pejorative notions of what it means to be childlike, and reproduce multi-systemic forms of oppression that, ostensibly in their “best interests”, govern children and all those deemed childlike

Isentropic Compression for TATB Based HE Samples, Numerical Simulations and Comparison with Experiments

Isentropic compression experiments and numerical simulations on TATB based HE were performed respectively at Z accelerator facility from Sandia National Laboratory and at Lawrence Livermore National Laboratory in order to study the isentrope and associated Hugoniot of this HE [1]. 3D configurations have been calculated here to test the new beta version of the electromagnetism package coupled with the dynamics in Ls-Dyna and compared with the ICE Z shot 1967

One Year Term Review as a Participating Guest in the Detonator and Detonation Physics Group

The one year stay was possible after a long administrative process, because of the fact that this was the first participating guest of B division as a foreign national in HEAF (High Explosives Application Facility) with the Detonator/Detonation Physics Group

Shock Desensitization Effect in the STANAG 4363 Confined Explosive Component Water Gap Test

The Explosive Component Water Gap Test (ECWGT) in the Stanag 4363 has been recently investigated to assess the shock sensitivity of lead and booster components having a diameter less than 5 mm. For that purpose, Pentaerythritol Tetranitrate (PETN) based pellets having a height and diameter of 3 mm have been confined by a steel annulus of wall thickness 1-3.5 mm and with the same height as the pellet. 1-mm wall thickness makes the component more sensitive (larger gap). As the wall thickness is increased to 2-mm, the gap increases a lesser amount, but when the wall thickness is increased to 3.5-mm a decrease in sensitivity is observed (smaller gap). This decrease of the water gap has been reproduced experimentally by many nations. Numerical simulations using Ignition and Growth model have been performed in this paper and have reproduced the experimental results for the steel confinement up to 2 mm thick and aluminum confinement. A stronger re-shock following the first input shock from the water is focusing on the axis due to the confinement. The double shock configuration is well-known to lead in some cases to shock desensitization

The Batten disease protein CLN3 is important for stress granules dynamics and translational activity

The assembly of membrane-less organelles such as stress granules (SGs) is emerging as central in helping cells rapidly respond and adapt to stress. Following stress sensing, the resulting global translational shutoff leads to the condensation of stalled mRNAs and proteins into SGs. By reorganizing cytoplasmic contents, SGs can modulate RNA translation, biochemical reactions, and signaling cascades to promote survival until the stress is resolved. While mechanisms for SG disassembly are not widely understood, the resolution of SGs is important for maintaining cell viability and protein homeostasis. Mutations that lead to persistent or aberrant SGs are increasingly associated with neuropathology and a hallmark of several neurodegenerative diseases. Mutations in CLN3 are causative of juvenile neuronal ceroid lipofuscinosis, a rare neurodegenerative disease affecting children also known as Batten disease. CLN3 encodes a transmembrane lysosomal protein implicated in autophagy, endosomal trafficking, metabolism, and response to oxidative stress. Using a HeLa cell model lacking CLN3, we now show that CLN3KO is associated with an altered metabolic profile, reduced global translation, and altered stress signaling. Furthermore, loss of CLN3 function results in perturbations in SG dynamics, resulting in assembly and disassembly defects, and altered expression of the key SG nucleating factor G3BP1. With a growing interest in SG-modulating drugs for the treatment of neurodegenerative diseases, novel insights into the molecular basis of CLN3 Batten disease may reveal avenues for disease-modifying treatments for this debilitating childhood disease

Magnetic fields in noncommutative quantum mechanics

We discuss various descriptions of a quantum particle on noncommutative space in a (possibly non-constant) magnetic field. We have tried to present the basic facts in a unified and synthetic manner, and to clarify the relationship between various approaches and results that are scattered in the literature.Comment: Dedicated to the memory of Julius Wess. Work presented by F. Gieres at the conference `Non-commutative Geometry and Physics' (Orsay, April 2007

Microbiological, histological, immunological, and toxin response to antibiotic treatment in the mouse model of Mycobacterium ulcerans disease.

Mycobacterium ulcerans infection causes a neglected tropical disease known as Buruli ulcer that is now found in poor rural areas of West Africa in numbers that sometimes exceed those reported for another significant mycobacterial disease, leprosy, caused by M. leprae. Unique among mycobacterial diseases, M. ulcerans produces a plasmid-encoded toxin called mycolactone (ML), which is the principal virulence factor and destroys fat cells in subcutaneous tissue. Disease is typically first manifested by the appearance of a nodule that eventually ulcerates and the lesions may continue to spread over limbs or occasionally the trunk. The current standard treatment is 8 weeks of daily rifampin and injections of streptomycin (RS). The treatment kills bacilli and wounds gradually heal. Whether RS treatment actually stops mycolactone production before killing bacilli has been suggested by histopathological analyses of patient lesions. Using a mouse footpad model of M. ulcerans infection where the time of infection and development of lesions can be followed in a controlled manner before and after antibiotic treatment, we have evaluated the progress of infection by assessing bacterial numbers, mycolactone production, the immune response, and lesion histopathology at regular intervals after infection and after antibiotic therapy. We found that RS treatment rapidly reduced gross lesions, bacterial numbers, and ML production as assessed by cytotoxicity assays and mass spectrometric analysis. Histopathological analysis revealed that RS treatment maintained the association of the bacilli with (or within) host cells where they were destroyed whereas lack of treatment resulted in extracellular infection, destruction of host cells, and ultimately lesion ulceration. We propose that RS treatment promotes healing in the host by blocking mycolactone production, which favors the survival of host cells, and by killing M. ulcerans bacilli

Measurement of the ratio of branching fractions BR(B0 -> K*0 gamma)/BR(Bs0 -> phi gamma)

The ratio of branching fractions of the radiative B decays B0 -> K*0 gamma and Bs0 -> phi gamma has been measured using 0.37 fb-1 of pp collisions at a centre of mass energy of sqrt(s) = 7 TeV, collected by the LHCb experiment. The value obtained is BR(B0 -> K*0 gamma)/BR(Bs0 -> phi gamma) = 1.12 +/- 0.08 ^{+0.06}_{-0.04} ^{+0.09}_{-0.08}, where the first uncertainty is statistical, the second systematic and the third is associated to the ratio of fragmentation fractions fs/fd. Using the world average for BR(B0 -> K*0 gamma) = (4.33 +/- 0.15) x 10^{-5}, the branching fraction BR(Bs0 -> phi gamma) is measured to be (3.9 +/- 0.5) x 10^{-5}, which is the most precise measurement to date.Comment: 15 pages, 1 figure, 2 table