From civic place to digital space: The design of public libraries in Britain from past to present

Inaugurated as, at once, an antidote to the social problems of industrialization and a cultural and “scientific” helpmate to progress in an industrial society, public libraries in Britain first appeared in 1850 and soon became a familiar feature, not only on the sociocultural, but also the urban-architectural, landscape. Over the past century and a half, changes in the public library built form have reflected changes in the aims of the public library movement, in architectural style and planning and in wider society. The development and symbolism of the public library built form is analyzed in five periods, stretching from the pre–First World War phases of civic architecture and large-scale philanthropic eclecticism, through the interwar period of embryonic modernism, to the post–Second World War era of full-blown modernism and the subsequent postmodernism of the digital age. In each of these periods, the public library building can be “read” as readily as the books they contained.published or submitted for publicationOpe

Opto-mechanical micro-macro entanglement

We propose to create and detect opto-mechanical entanglement by storing one component of an entangled state of light in a mechanical resonator and then retrieving it. Using micro-macro entanglement of light as recently demonstrated experimentally, one can then create opto-mechanical entangled states where the components of the superposition are macroscopically different. We apply this general approach to two-mode squeezed states where one mode has undergone a large displacement. Based on an analysis of the relevant experimental imperfections, the scheme appears feasible with current technology.Comment: 7 pages, 6 figures, to appear in PRL, submission coordinated with Sekatski et al. who reported on similar result

Optomechanical superpositions via nested interferometry

We present a scheme for achieving macroscopic quantum superpositions in optomechanical systems by using single photon postselection and detecting them with nested interferometers. This method relieves many of the challenges associated with previous optical schemes for measuring macroscopic superpositions, and only requires the devices to be in the weak coupling regime. It requires only small improvements on currently achievable device parameters, and allows observation of decoherence on a timescale unconstrained by the system's optical decay time. Prospects for observing novel decoherence mechanisms are discussed.Comment: 5 pages, 3 figure

P1266: Flow cytometry combined with systems biology enables rational targeting of NFKB in DLBCL

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NF-kB and the CLL microenvironment

Chronic lymphocytic leukemia (CLL) is the most prevalent type of leukemia in the western world. Despite the positive clinical effects of new targeted therapies, CLL still remains an incurable and refractory disease and resistance to treatments are commonly encountered. The Nuclear Factor-Kappa B (NF-κB) transcription factor has been implicated in the pathology of CLL, with high levels of NF-κB associated with disease progression and drug resistance. This aberrant NF-κB activation can be caused by genetic mutations in the tumor cells and microenvironmental factors, which promote NF-κB signaling. Activation can be induced via two distinct pathways, the canonical and non-canonical pathway, which result in tumor cell proliferation, survival and drug resistance. Therefore, understanding how the CLL microenvironment drives NF-κB activation is important for deciphering how CLL cells evade treatment and may aid the development of novel targeting therapeutics. The CLL microenvironment is comprised of various cells, including nurse like cells, mesenchymal stromal cells, follicular dendritic cells and CD4+ T cells. By activating different receptors, including the B cell receptor and CD40, these cells cause overactivity of the canonical and non-canonical NF-κB pathways. Within this review, we will explore the different components of the CLL microenvironment that drive the NF-κB pathway, investigating how this knowledge is being translated in the development of new therapeutics

Macroscopic superpositions via nested interferometry: finite temperature and decoherence considerations

Recently there has been much interest in optomechanical devices for the production of macroscopic quantum states. Here we focus on a proposed scheme for achieving macroscopic superpositions via nested interferometry. We consider the effects of finite temperature on the superposition produced. We also investigate in detail the scheme's feasibility for probing various novel decoherence mechanisms.Comment: 12 pages, 2 figure

Inhibition of the classical pathway of the complement cascade prevents early dendritic and synaptic degeneration in glaucoma

BACKGROUND: Glaucoma is a complex, multifactorial disease characterised by the loss of retinal ganglion cells and their axons leading to a decrease in visual function. The earliest events that damage retinal ganglion cells in glaucoma are currently unknown. Retinal ganglion cell death appears to be compartmentalised, with soma, dendrite and axon changes potentially occurring through different mechanisms. There is mounting evidence from other neurodegenerative diseases suggesting that neuronal dendrites undergo a prolonged period of atrophy, including the pruning of synapses, prior to cell loss. In addition, recent evidence has shown the role of the complement cascade in synaptic pruning in glaucoma and other diseases. RESULTS: Using a genetic (DBA/2J mouse) and an inducible (rat microbead) model of glaucoma we first demonstrate that there is loss of retinal ganglion cell synapses and dendrites at time points that precede axon or soma loss. We next determine the role of complement component 1 (C1) in early synaptic loss and dendritic atrophy during glaucoma. Using a genetic knockout of C1qa (D2.C1qa (-/-) mouse) or pharmacological inhibition of C1 (in the rat bead model) we show that inhibition of C1 is sufficient to preserve dendritic and synaptic architecture. CONCLUSIONS: This study further supports assessing the potential for complement-modulating therapeutics for the prevention of retinal ganglion cell degeneration in glaucoma. Mol Neurodegener 2016 Apr 6; 11(2):2