Constraints on the time-scale of nuclear breakup from thermal hard-photon emission

Measured hard photon multiplicities from second-chance nucleon-nucleon collisions are used in combination with a kinetic thermal model, to estimate the break-up times of excited nuclear systems produced in nucleus-nucleus reactions at intermediate energies. The obtained nuclear break-up time for the $^{129}${Xe} + $^{nat}${Sn} reaction at 50{\it A} MeV is $\Delta$$\tau$ $\approx$ 100 -- 300 fm/$c$ for all reaction centralities. The lifetime of the radiating sources produced in seven other different heavy-ion reactions studied by the TAPS experiment are consistent with $\Delta$$\tau$ $\approx$ 100 fm/$c$, such relatively long thermal photon emission times do not support the interpretation of nuclear breakup as due to a fast spinodal process for the heavy nuclear systems studied.Comment: 11 pages, 9 figures, submitted to EPJ

Regulation of NMDA Receptor Signaling at Single Synapses by Human Anti-NMDA Receptor Antibodies

The NMDA receptor (NMDAR) subunit GluN1 is critical for receptor function and plays a pivotal role in synaptic plasticity. Mounting evidence has shown that pathogenic autoantibody targeting of the GluN1 subunit of NMDARs, as in anti-NMDAR encephalitis, leads to altered NMDAR trafficking and synaptic localization. However, the underlying signaling pathways affected by antibodies targeting the NMDAR remain to be fully delineated. It remains unclear whether patient antibodies influence synaptic transmission via direct effects on NMDAR channel function. Here, we show using short-term incubation that GluN1 antibodies derived from patients with anti-NMDAR encephalitis label synapses in mature hippocampal primary neuron culture. Miniature spontaneous calcium transients (mSCaTs) mediated via NMDARs at synaptic spines are not altered in pathogenic GluN1 antibody exposed conditions. Unexpectedly, spine-based and cell-based analyses yielded distinct results. In addition, we show that calcium does not accumulate in neuronal spines following brief exposure to pathogenic GluN1 antibodies. Together, these findings show that pathogenic antibodies targeting NMDARs, under these specific conditions, do not alter synaptic calcium influx following neurotransmitter release. This represents a novel investigation of the molecular effects of anti-NMDAR antibodies associated with autoimmune encephalitis

Postsynaptic Positioning of Endocytic Zones and AMPA Receptor Cycling by Physical Coupling of Dynamin-3 to Homer

Endocytosis of AMPA receptors and other postsynaptic cargo occurs at endocytic zones (EZs), stably positioned sites of clathrin assembly adjacent to the postsynaptic density (PSD). The tight localization of postsynaptic endocytosis is thought to control spine composition and regulate synaptic transmission and plasticity. However, the molecular mechanisms that situate the EZ near the PSD, and the role of local spine endocytosis in synaptic transmission, are unknown. Here we report that a physical link between dynamin-3 and the postsynaptic adaptor Homer positions the EZ near the PSD. Disruption of dynamin-3 or its interaction with Homer uncouples the PSD from the EZ, resulting in synapses devoid of postsynaptic clathrin. This loss of the EZ leads to a loss of synaptic AMPA receptors and reduced excitatory synaptic transmission that corresponds with impaired synaptic recycling. Thus, a physical link between the PSD and the EZ ensures localized endocytosis and recycling by recapturing and maintaining a proximate pool of cycling AMPA receptors

Dispersion Effects in Nucleon Polarisabilities

We present a formalism to extract the dynamical nucleon polarisabilities defined via a multipole expansion of the structure amplitudes in nucleon Compton scattering. In contradistinction to the static polarisabilities, dynamical polarisabilities gauge the response of the internal degrees of freedom of a composed object to an external, real photon field of arbitrary energy. Being energy dependent, they therefore contain additional information about dispersive effects induced by internal relaxation mechanisms, baryonic resonances and meson production thresholds of the nucleon. We give explicit formulae to extract the dynamical electric and magnetic dipole as well as quadrupole polarisabilities from low energy nucleon Compton scattering up to the one pion production threshold and discuss the connection to the definition of static nucleon polarisabilities. As a concrete example, we examine the results of leading order Heavy Baryon Chiral Perturbation Theory for the four leading spin independent iso-scalar polarisabilities of the nucleon. Finally, we consider the possible r{\^o}le of energy dependent effects in low energy extractions of the iso-scalar dipole polarisabilities from Compton scattering on the deuteron.Comment: 17 pages LaTeX2e with 2 figures, using includegraphicx (5 .eps files). Minor corrections, references updated. Contents identical to version to appear in Phys. Rev. C 65, spelling differen

Superficial simplicity of the 2010 El Mayor–Cucapah earthquake of Baja California in Mexico

The geometry of faults is usually thought to be more complicated at the surface than at depth and to control the initiation, propagation and arrest of seismic ruptures. The fault system that runs from southern California into Mexico is a simple strike-slip boundary: the west side of California and Mexico moves northwards with respect to the east. However, the M_w 7.2 2010 El Mayor–Cucapah earthquake on this fault system produced a pattern of seismic waves that indicates a far more complex source than slip on a planar strike-slip fault. Here we use geodetic, remote-sensing and seismological data to reconstruct the fault geometry and history of slip during this earthquake. We find that the earthquake produced a straight 120-km-long fault trace that cut through the Cucapah mountain range and across the Colorado River delta. However, at depth, the fault is made up of two different segments connected by a small extensional fault. Both segments strike N130° E, but dip in opposite directions. The earthquake was initiated on the connecting extensional fault and 15 s later ruptured the two main segments with dominantly strike-slip motion. We show that complexities in the fault geometry at depth explain well the complex pattern of radiated seismic waves. We conclude that the location and detailed characteristics of the earthquake could not have been anticipated on the basis of observations of surface geology alone

Optimization of Cell Morphology Measurement via Single-Molecule Tracking PALM

In neurons, the shape of dendritic spines relates to synapse function, which is rapidly altered during experience-dependent neural plasticity. The small size of spines makes detailed measurement of their morphology in living cells best suited to super-resolution imaging techniques. The distribution of molecular positions mapped via live-cell Photoactivated Localization Microscopy (PALM) is a powerful approach, but molecular motion complicates this analysis and can degrade overall resolution of the morphological reconstruction. Nevertheless, the motion is of additional interest because tracking single molecules provides diffusion coefficients, bound fraction, and other key functional parameters. We used Monte Carlo simulations to examine features of single-molecule tracking of practical utility for the simultaneous determination of cell morphology. We find that the accuracy of determining both distance and angle of motion depend heavily on the precision with which molecules are localized. Strikingly, diffusion within a bounded region resulted in an inward bias of localizations away from the edges, inaccurately reflecting the region structure. This inward bias additionally resulted in a counterintuitive reduction of measured diffusion coefficient for fast-moving molecules; this effect was accentuated by the long camera exposures typically used in single-molecule tracking. Thus, accurate determination of cell morphology from rapidly moving molecules requires the use of short integration times within each image to minimize artifacts caused by motion during image acquisition. Sequential imaging of neuronal processes using excitation pulses of either 2 ms or 10 ms within imaging frames confirmed this: processes appeared erroneously thinner when imaged using the longer excitation pulse. Using this pulsed excitation approach, we show that PALM can be used to image spine and spine neck morphology in living neurons. These results clarify a number of issues involved in interpretation of single-molecule data in living cells and provide a method to minimize artifacts in single-molecule experiments

Photon asymmetry measurements of γ→ p→ π0p for Eγ= 320-650 MeV

High-statistics measurements of the photon asymmetry Σ for the γ→ p→ π0p reaction have been made in the center-of-mass energy range W= 1214 - 1450 MeV. The data were measured with the MAMI A2 real photon beam and Crystal Ball/TAPS detector systems in Mainz, Germany. The results significantly improve the existing world data and are shown to be in good agreement with previous measurements, and with the MAID, SAID, and Bonn-Gatchina predictions. We have also combined the photon asymmetry results with recent cross-section measurements from Mainz to calculate the profile functions, Σˇ (= σ0Σ) , and perform a moment analysis. Comparison with calculations from the Bonn-Gatchina model shows that the precision of the data is good enough to further constrain the higher partial waves, and there is an indication of interference between the very small F-waves and the N(1520) 3 / 2 - and N(1535) 1 / 2 - resonances

Control of transmembrane protein diffusion within the postsynaptic density assessed by simultaneous single-molecule tracking and localization microscopy

Postsynaptic transmembrane proteins are critical elements of synapses, mediating trans-cellular contact, sensitivity to neurotransmitters and other signaling molecules, and flux of Ca and other ions. Positioning and mobility of each member of this large class of proteins is critical to their individual function at the synapse. One critical example is that the position of glutamate receptors within the postsynaptic density (PSD) strongly modulates their function by aligning or misaligning them with sites of presynaptic vesicle fusion. In addition, the regulated ability of receptors to move in or out of the synapse is critical for activity-dependent plasticity. However, factors that control receptor mobility within the boundaries of the synapse are not well understood. Notably, PSD scaffold molecules accumulate in domains much smaller than the synapse. Within these nanodomains, the density of proteins is considerably higher than that of the synapse as a whole, so high that steric hindrance is expected to reduce receptor mobility substantially. However, while numerical modeling has demonstrated several features of how the varying protein density across the face of a single PSD may modulate receptor motion, there is little experimental information about the extent of this influence. To address this critical aspect of synaptic organizational dynamics, we performed single-molecule tracking of transmembrane proteins using uPAINT over PSDs whose internal structure was simultaneously resolved using PALM. The results provide important experimental confirmation that PSD scaffold density protein strongly influences the mobility of transmembrane proteins. Tracking a protein with a cytosolic domain that does not bind PSD-95 still was slowed in regions of high PSD-95 density, suggesting that crowding by scaffold molecules and perhaps other proteins is sufficient to stabilize receptors even in the absence of binding. Because numerous proteins thought to be involved in establishing PSD structure are linked to disorders including autism and depression, this motivates further exploration of how PSD nanostructure is created. The combined application uPAINT-PALM should be invaluable for distinguishing the interactions of mobile proteins with their nanoenvironment both in synapses and other cellular compartments

More accurate morphology of living neurons using short, pulsed excitation during acquisition.

<p><b>A</b>. Cultured hippocampal neurons grown 10 days in vitro (DIV) expressing membrane-mEos2 were imaged at 50 Hz using excitation pulses of two durations (t_e = 2 ms and 10 ms) delivered in random order. The distribution of localized positions was plotted (A, enlarged in B), demonstrating a thinner appearance of neuronal processes imaged with longer t_e. <b>C</b>. Intensity profile of line scans drawn perpendicular to the neuronal process as in B. <b>D</b>. Cumulative frequency plot of the line scan full width at half maximum intensity. <b>E</b>. Paired comparison showed that the width of the processes was consistently diminished in the longer exposure. <b>F</b>. Measured spine neck widths (red) and spine lengths (blue) in neurons grown 11 to 12 DIV. Neurons were imaged at 50 Hz for 10,000 frames with t_e = 4 ms.</p

Effect of motion during image acquisition on single molecule photon distribution and localization precision.

<p><b>A</b>. Examples of random walks taken by a molecule over various timescales. Blue lines depict the path taken by the molecules, with green and red dots denoting the starting and ending position, respectively. <b>B</b>. Examples of photon distributions emitted from moving molecules of the indicated D over integration times ranging from 0 to 50 ms. <b>C</b>. The mean value of the brightest pixel (N = 1000 molecules) is plotted against integration time for molecules emitting 100, 250, or 1000 photons over the course of the integration time. <b>D</b>. Histogram of calculated precisions for molecules with D = 1.0 µm²/sec. <b>E</b>. The mean calculated precision for molecules with D = 0.1 µm²/sec (<b>red line</b>) and D = 1.0 µm²/sec (<b>black line</b>). Points represent mean of 1000 molecules. <b>F</b>. To examine the interaction of movement-induced error with photon-dependent precision, the mean error of molecules emitting 100 photons (<b>black line</b>), 250 photons (<b>red line</b>), and 1000 photons (<b>blue line</b>) were plotted as a function of exposure duration.</p