No fixed item limit in visuospatial working memory.

Investigations of working memory capacity in the visual domain have converged on the concept of a limited supply of a representational medium, flexibly distributed between objects. Current debate centers on whether this medium is continuous, or quantized into 2 or 3 memory "slots". The latter model makes the strong prediction that, if an item in memory is probed, behavioral parameters will plateau when the number of items is the same or more than the number of slots. Here we examine short-term memory for object location using a two-dimensional pointing task. We show that recall variability for items in memory increases monotonically from 1 to 8 items. Using a novel method to isolate only those trials on which a participant correctly identifies the target, we show that response latency also increases monotonically from 1 to 8 items. We argue that both these findings are incompatible with a quantized model.Wellcome Trust (Grant ID: 106926)This is the final version of the article. It first appeared from Elsevier via http://dx.doi.org/10.1016/j.cortex.2016.07.02

Stochastic sampling provides a unifying account of visual working memory limits.

Research into human working memory limits has been shaped by the competition between different formal models, with a central point of contention being whether internal representations are continuous or discrete. Here we describe a sampling approach derived from principles of neural coding as a framework to understand working memory limits. Reconceptualizing existing models in these terms reveals strong commonalities between seemingly opposing accounts, but also allows us to identify specific points of difference. We show that the discrete versus continuous nature of sampling is not critical to model fits, but that, instead, random variability in sample counts is the key to reproducing human performance in both single- and whole-report tasks. A probabilistic limit on the number of items successfully retrieved is an emergent property of stochastic sampling, requiring no explicit mechanism to enforce it. These findings resolve discrepancies between previous accounts and establish a unified computational framework for working memory that is compatible with neural principles

Drift in Neural Population Activity Causes Working Memory to Deteriorate Over Time.

Short-term memories are thought to be maintained in the form of sustained spiking activity in neural populations. Decreases in recall precision observed with increasing number of memorized items can be accounted for by a limit on total spiking activity, resulting in fewer spikes contributing to the representation of each individual item. Longer retention intervals likewise reduce recall precision, but it is unknown what changes in population activity produce this effect. One possibility is that spiking activity becomes attenuated over time, such that the same mechanism accounts for both effects of set size and retention duration. Alternatively, reduced performance may be caused by drift in the encoded value over time, without a decrease in overall spiking activity. Human participants of either sex performed a variable-delay cued recall task with a saccadic response, providing a precise measure of recall latency. Based on a spike integration model of decision making, if the effects of set size and retention duration are both caused by decreased spiking activity, we would predict a fixed relationship between recall precision and response latency across conditions. In contrast, the drift hypothesis predicts no systematic changes in latency with increasing delays. Our results show both an increase in latency with set size, and a decrease in response precision with longer delays within each set size, but no systematic increase in latency for increasing delay durations. These results were quantitatively reproduced by a model based on a limited neural resource in which working memories drift rather than decay with time.SIGNIFICANCE STATEMENT Rapid deterioration over seconds is a defining feature of short-term memory, but what mechanism drives this degradation of internal representations? Here, we extend a successful population coding model of working memory by introducing possible mechanisms of delay effects. We show that a decay in neural signal over time predicts that the time required for memory retrieval will increase with delay, whereas a random drift in the stored value predicts no effect of delay on retrieval time. Testing these predictions in a multi-item memory task with an eye movement response, we identified drift as a key mechanism of memory decline. These results provide evidence for a dynamic spiking basis for working memory, in contrast to recent proposals of activity-silent storage

Machine Protection Considerations for BERLinPro

The Berlin energy recovery linac project BERLinPro at the HZB is a 50 MeV ERL test facility, which addresses physical and technological questions for future superconducting rf based high brightness, high current electron beam sources. The combination of a 100 mA cw beam, electron bunches with normalized emittances lower than 1 mm mrad and the magnet optics of BERLinPro leads to power densities capable to harm the accelerator components within microseconds if total beam loss occurs. Furthermore, continuous beam loss on the level of 10 5 has to be controlled to avoid activation and to protect the SRF, beam diagnostics and other infrastructure components. In this paper, we present the evaluation of the required key parameters of the BERLinPro machine protection system and present its first conceptual desig

Nuclear factor I-A represses expression of the cell adhesion molecule L1

<p>Abstract</p> <p>Background</p> <p>The neural cell adhesion molecule L1 plays a crucial role in development and plasticity of the nervous system. Neural cells thus require precise control of L1 expression.</p> <p>Results</p> <p>We identified a full binding site for nuclear factor I (NFI) transcription factors in the regulatory region of the mouse <it>L1 </it>gene. Electrophoretic mobility shift assay (EMSA) showed binding of nuclear factor I-A (NFI-A) to this site. Moreover, for a brain-specific isoform of NFI-A (NFI-A bs), we confirmed the interaction <it>in vivo </it>using chromatin immunoprecipitation (ChIP). Reporter gene assays showed that in neuroblastoma cells, overexpression of NFI-A bs repressed L1 expression threefold.</p> <p>Conclusion</p> <p>Our findings suggest that NFI-A, in particular its brain-specific isoform, represses <it>L1 </it>gene expression, and might act as a second silencer of L1 in addition to the neural restrictive silencer factor (NRSF).</p

Rift Valley fever outbreak, Mauritania, 1998: seroepidemiologic, virologic, entomologic, and zoologic investigations.

A Rift Valley fever outbreak occurred in Mauritania in 1998. Seroepidemiologic and virologic investigation showed active circulation of the Rift Valley fever virus, with 13 strains isolated, and 16% (range 1.5%-38%) immunoglobulin (Ig) M-positivity in sera from 90 humans and 343 animals (sheep, goats, camels, cattle, and donkeys). One human case was fatal

Location-independent feature binding in visual working memory for sequentially presented objects

Abstract: Spatial location is believed to have a privileged role in binding features held in visual working memory. Supporting this view, Pertzov and Husain (Attention, Perception, & Psychophysics, 76(7), 1914–1924, 2014) reported that recall of bindings between visual features was selectively impaired when items were presented sequentially at the same location compared to sequentially at different locations. We replicated their experiment, but additionally tested whether the observed impairment could be explained by perceptual interference during encoding. Participants viewed four oriented bars in highly discriminable colors presented sequentially either at the same or different locations, and after a brief delay were cued with one color to reproduce the associated orientation. When we used the same timing as the original study, we reproduced its key finding of impaired binding memory in the same-location condition. Critically, however, this effect was significantly modulated by the duration of the inter-stimulus interval, and disappeared if memoranda were presented with longer delays between them. In a second experiment, we tested whether the effect generalized to other visual features, namely reporting of colors cued by stimulus shape. While we found performance deficits in the same-location condition, these did not selectively affect binding memory. We argue that the observed effects are best explained by encoding interference, and that memory for feature binding is not necessarily impaired when memoranda share the same location

Staphylococcus aureus induces tolerance in human monocytes accompanied with expression changes of cell surface markers

Exposure of human monocytes to lipopolysaccharide (LPS) or other pathogen-associated molecular pattern (PAMPs) induces a temporary insensitivity to subsequent LPS challenges, a cellular state called endotoxin tolerance (ET), associated with the pathogenesis of sepsis. In this study, we aimed to characterize the cellular state of human monocytes from healthy donors stimulated with Staphylococcus aureus in comparison to TLR2-specific ligands. We analyzed S. aureus induced gene expression changes after 2 and 24 hours by amplicon sequencing (RNA-AmpliSeq) and compared the pro-inflammatory response after 2 hours with the response in re-stimulation experiments. In parallel, glycoprotein expression changes in human monocytes after 24 hours of S. aureus stimulation were analyzed by proteomics and compared to stimulation experiments with TLR2 ligands Malp-2 and Pam3Cys and TLR4 ligand LPS. Finally, we analyzed peripheral blood monocytes of patients with S. aureus bloodstream infection for their ex vivo inflammatory responses towards S. aureus stimulation and their glycoprotein expression profiles. Our results demonstrate that monocytes from healthy donors stimulated with S. aureus and TLR ligands of Gram-positive bacteria entered the tolerant cell state after activation similar to LPS treatment. In particular reduced gene expression of pro-inflammatory cytokines (TNF, IL1β) and chemokines (CCL20, CCL3, CCL4, CXCL2, CXCL3 and CXCL8) could be demonstrated. Glycoprotein expression changes in monocytes tolerized by the different TLR agonists were highly similar while S. aureus -stimulated monocytes shared some of the PAMP-induced changes but also exhibited a distinct expression profile. 11 glycoproteins (CD44, CD274, DSC2, ICAM1, LAMP3, LILRB1, PTGS2, SLC1A3, CR1, FGL2, and HP) were similarly up- or downregulated in all four comparisons in the tolerant cell state. Monocytes from patients with S. aureus bacteremia revealed preserved pro-inflammatory responsiveness to S. aureus stimulation ex vivo, expressed increased CD44 mRNA but no other glycoprotein of the tolerance signature was differentially expressed

Radiation hardness qualification of PbWO4 scintillation crystals for the CMS Electromagnetic Calorimeter

This is the Pre-print version of the Article. The official published version can be accessed from the link below - Copyright @ 2010 IOPEnsuring the radiation hardness of PbWO4 crystals was one of the main priorities during the construction of the electromagnetic calorimeter of the CMS experiment at CERN. The production on an industrial scale of radiation hard crystals and their certification over a period of several years represented a difficult challenge both for CMS and for the crystal suppliers. The present article reviews the related scientific and technological problems encountered