Estimated eye movement profile from model output.

<p>A: Peak saccade speed as a function of saccade distance. Circles are individual trials; solid line is the average per simulated distance; and dotted line is the hypothetical linear relation based on the 2 average. B: Saccade time as a function of angular distance. Circles are individual trials; solid line is average per simulated distance; hashed line is parametrized monkey data from <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0057134#pone.0057134-vanOpstal1" target="_blank">[5]</a>. C: Peak saccade speed as function of horizontal distance for 0 and 60 directions. The oblique saccades show the expected drop in peak speed. D: The estimated final eye position discrepancy as a function of target saccade position for the model with (solid) and without (hashed) deep inhibitory neuron feedback, terminated 300 ms after inhibitory release.</p

The model circuit.

<p>Each neuron model layer is spatially extended and organized in the same relative order as in the neural substrate. Feedback connections to the same node indicate layer intraconnections. Primary functional circuits are indicated by coloured connections. Red connections: Burst neuron burst profile circuit. Blue connections: Spreading inhibition and system reset. Grey shaded connections: inputs common to both circuits. See <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0057134#s4" target="_blank">materials and Methods</a> for further details.</p

Angle-dependent parameter estimation.

<p>A Model peak-to-end burst time (orange contour plot) and equal peak burst rate (blue contour plot) as functions of QVburst NMDA synapse strength (horizontal axis) and cMRF inhibitory feedback strength (vertical axis). Axis values are factors of the nominal NMDA synapse and inhibitory synapse strengths (nS, nS) as specified in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0057134#pone-0057134-t002" target="_blank">Table 2</a>. The selected contour line values correspond to the peak-to-end burst times and peak burst rates from <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0057134#pone-0057134-g002" target="_blank">figure 2</a>. Red marks show intersections of burst time and burst rate for the same magnitude saccade, and signify the combination of parameters that will give us burst neuron activation corresponding to a saccade of that magnitude.B The total peak-to-end spikes (blue contour lines) as a function of NMDA and inhibitory strength. Burst end is determined when activity drops below 10% of peak activity. Red line: the contour line corresponding to the average emitted spikes for all points from 4A (1088 spikes, red marks). Hashed line: the linear approximation of the selected contour line. Cross marks signify the 35 degree and 2 degree points.C NMDA and inhibitory synapse strength across the SC surface is set according to this linear approximation as the radius from the fovea in SC surface coordinates.</p

Model neuron response to a Poisson spike train input.

<p>Input to a regular excitatory synapse (top) and to an NMDA-type synapse (bottom). A 50 pA input current is added between 50 ms and 100 ms. Model parameters in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0057134#pone-0057134-t002" target="_blank">table 2</a>.</p

AEIaF neuron parameters.

<p>Parameters used for the AEIaF neuron for the simulation model. Burst neurons have a membrane capacitance of 40 pF.</p

Model interconnection parameters.

<p>Radius: receptive radius, mm; sd: standard deviation, mm; Wt: weight (in terms of synaptic conductance); ConnP: interneuron connection probability.</p><p> nS: excitatory synapse; nS: inhibitory synapse; nS: NMDA synapse. Connection delays are 1 ms unless otherwise specified.</p><p>input: input source; wide: Wide-field superficial neuron; narrow: Narrow field superficial neuron; QV: Quasivisual neuron; InQV: Quasivisual interneuron; Build: Buildup neuron; InB: Buildup interneuron; Burst: Burst neuron; Inhib: Deep layer inhibitory neuron; INT: cMRF integrator.</p><p>(1): interconnections are rostrally shifted by 0.3 mm, and with a 5 ms delay.</p><p>(2): Connection weight varies by a saccade angular distance-dependent factor; see Results for details.</p><p>(3): Integrator connections have 5 ms delay.</p

Parametrized burst neuron activation profiles based on monkey data.

<p>Curves show peak firing rate and peak-to-end firing time, where the end is taken when the curve drops below 1% of peak. Regenerated from <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0057134#pone.0057134-vanOpstal1" target="_blank">[5]</a>.</p

Core–Shell to Doped Quantum Dots: Evolution of the Local Environment Using XAFS

Internal structure study at an atomic level is a challenging task with far reaching consequences to its material properties, specifically in the field of transition metal doping in quantum dots. Diffusion of transition metal ions in and out of quantum dots forming magnetic clusters has been a major bottleneck in this class of materials. Diffusion of the magnetic ions from the core into the nonmagnetic shell in a core/shell heterostructure architecture to attain uniform doping has been recently introduced and yet to be understood. In this work, we have studied the local structure variation of Fe as a function of CdS matrix thickness and annealing time during the overcoating of Fe₃O₄ core with CdS using X-ray absorption spectroscopy. The data reveals that Fe₃O₄ core initially forms a core/shell structure with CdS followed by alloying at the interface eventually completely diffusing all the way through the CdS matrix to form homogeneously Fe-doped CdS QDs with excellent control over size and size distribution. Study of Fe K-edge shows a complete change of Fe local environment from Fe–O to FeS

MOESM1 of Changes in corneal thickness following combined cataract and vitreous surgery

Additional file 1: Table S1. Degree of the anterior segment inflammation score before and after surgery

Origin of Photoluminescence and XAFS Study of (ZnS)_1–<i>x</i>(AgInS₂)_<i>x</i> Nanocrystals

Donor–Acceptor transition was previously suggested as a mechanism for luminescence in (ZnS)_1–<i>x</i>(AgInS₂)_<i>x</i> nanocrystals. Here we show the participation of delocalized valence/conduction band in the luminescence. Two emission pathways are observed: Path-1 involves transition between a delocalized state and a localized state exhibiting higher energy and shorter lifetime (∼25 ns) and Path-2 (donor–acceptor) involves two localized defect states exhibiting lower emission energy and longer lifetime (>185 ns). Surprisingly, Path-1 dominates (82% for <i>x</i> = 0.33) for nanocrystals with lower <i>x</i>, in sharp difference with prior assignment. Luminescence peak blue shifts systematically by 0.57 eV with decreasing <i>x</i> because of this large contribution from Path-1. X-ray absorption fine structure (XAFS) study of (ZnS)_1–<i>x</i>(AgInS₂)_<i>x</i> nanocrystals shows larger AgS₄ tetrahedra compared with InS₄ tetrahedra with Ag–S and In–S bond lengths 2.52 and 2.45 Å respectively, whereas Zn–S bond length is 2.33 Å along with the absence of second nearest-neighbor Zn–S–metal correlation