Anomalous Dynamics of Translocation

We study the dynamics of the passage of a polymer through a membrane pore (translocation), focusing on the scaling properties with the number of monomers $N$. The natural coordinate for translocation is the number of monomers on one side of the hole at a given time. Commonly used models which assume Brownian dynamics for this variable predict a mean (unforced) passage time $\tau$ that scales as $N^2$, even in the presence of an entropic barrier. However, the time it takes for a free polymer to diffuse a distance of the order of its radius by Rouse dynamics scales with an exponent larger than 2, and this should provide a lower bound to the translocation time. To resolve this discrepancy, we perform numerical simulations with Rouse dynamics for both phantom (in space dimensions $d=1$ and 2), and self-avoiding (in $d=2$) chains. The results indicate that for large $N$, translocation times scale in the same manner as diffusion times, but with a larger prefactor that depends on the size of the hole. Such scaling implies anomalous dynamics for the translocation process. In particular, the fluctuations in the monomer number at the hole are predicted to be non-diffusive at short times, while the average pulling velocity of the polymer in the presence of a chemical potential difference is predicted to depend on $N$.Comment: 9 pages, 9 figures. Submitted to Physical Review

Lessening the hazards of Florida red tides: a common sense approach

© The Author(s), 2020. This article is distributed under the terms of the Creative Commons Attribution License. The definitive version was published in Hoagland, P., Kirkpatrick, B., Jin, D., Kirkpatrick, G., Fleming, L. E., Ullmann, S. G., Beet, A., Hitchcock, G., Harrison, K. K., Li, Z. C., Garrison, B., Diaz, R. E., & Lovko, V. Lessening the hazards of Florida red tides: a common sense approach. Frontiers in Marine Science, 7, (2020): 538, doi:10.3389/fmars.2020.00538.In the Gulf of Mexico, especially along the southwest Florida coast, blooms of the dinoflagellate Karenia brevis are a coastal natural hazard. The organism produces a potent class of toxins, known as brevetoxins, which are released following cell lysis into ocean or estuarine waters or, upon aerosolization, into the atmosphere. When exposed to sufficient levels of brevetoxins, humans may suffer from respiratory, gastrointestinal, or neurological illnesses. The hazard has been exacerbated by the geometric growth of human populations, including both residents and tourists, along Florida’s southwest coast. Impacts to marine organisms or ecosystems also may occur, such as fish kills or deaths of protected mammals, turtles, or birds. Since the occurrence of a severe Karenia brevis bloom off the southwest Florida coast three-quarters of a century ago, there has been an ongoing debate about the best way for humans to mitigate the impacts of this hazard. Because of the importance of tourism to coastal Florida, there are incentives for businesses and governments alike to obfuscate descriptions of these blooms, leading to the social amplification of risk. We argue that policies to improve the public’s ability to understand the physical attributes of blooms, specifically risk communication policies, are to be preferred over physical, chemical, or biological controls. In particular, we argue that responses to this type of hazard must emphasize maintaining the continuity of programs of scientific research, environmental monitoring, public education, and notification. We propose a common-sense approach to risk communication, comprising a simplification of the public provision of existing sources of information to be made available on a mobile website.The research leading to these results was supported by the US National Science Foundation (NSF) under NSF Grant No. CNH 1009106. PH and DJ acknowledge the complementary support under NSF Grant No. PFI/BIC 1534054

Anomalous Dynamics of Forced Translocation

We consider the passage of long polymers of length N through a hole in a membrane. If the process is slow, it is in principle possible to focus on the dynamics of the number of monomers s on one side of the membrane, assuming that the two segments are in equilibrium. The dynamics of s(t) in such a limit would be diffusive, with a mean translocation time scaling as N^2 in the absence of a force, and proportional to N when a force is applied. We demonstrate that the assumption of equilibrium must break down for sufficiently long polymers (more easily when forced), and provide lower bounds for the translocation time by comparison to unimpeded motion of the polymer. These lower bounds exceed the time scales calculated on the basis of equilibrium, and point to anomalous (sub-diffusive) character of translocation dynamics. This is explicitly verified by numerical simulations of the unforced translocation of a self-avoiding polymer. Forced translocation times are shown to strongly depend on the method by which the force is applied. In particular, pulling the polymer by the end leads to much longer times than when a chemical potential difference is applied across the membrane. The bounds in these cases grow as N^2 and N^{1+\nu}, respectively, where \nu is the exponent that relates the scaling of the radius of gyration to N. Our simulations demonstrate that the actual translocation times scale in the same manner as the bounds, although influenced by strong finite size effects which persist even for the longest polymers that we considered (N=512).Comment: 13 pages, RevTeX4, 16 eps figure

Atomistic modelling of large-scale metal film growth fronts

We present simulations of metallization morphologies under ionized sputter deposition conditions, obtained by a new theoretical approach. By means of molecular dynamics simulations using a carefully designed interaction potential, we analyze the surface adsorption, reflection, and etching reactions taking place during Al physical vapor deposition, and calculate their relative probability. These probabilities are then employed in a feature-scale cellular-automaton simulator, which produces calculated film morphologies in excellent agreement with scanning-electron-microscopy data on ionized sputter deposition.Comment: RevTeX 4 pages, 2 figure

Determination of the Axial-Vector Weak Coupling Constant with Ultracold Neutrons

A precise measurement of the neutron decay $\beta$-asymmetry $A_0$ has been carried out using polarized ultracold neutrons (UCN) from the pulsed spallation UCN source at the Los Alamos Neutron Science Center (LANSCE). Combining data obtained in 2008 and 2009, we report $A_0 = -0.11966 \pm 0.00089_{-0.00140}^{+0.00123}$, from which we determine the ratio of the axial-vector to vector weak coupling of the nucleon $g_A/g_V = -1.27590_{-0.00445}^{+0.00409}$.Comment: 5 pages, 2 figure

Zum biochemischen Wirkungsmechanismus des adrenocorticotropen Hormons

Es wird eine Übersicht über zwei Hypothesen und die dazugehörigen Befunde zum Wirkungsmechanismus des adrenocorticotropen Hormons gegeben: 1. Der Gehalt der Nebenniere an cyclischem Adenosinmonophosphat wird durch ACTH erhöht, die stimulierende Wirkung des Hormons auf die Corticoidsynthese wird durch cyclisches Adenosinmonophosphat imitiert. Die Beschleunigung der Corticoidsynthese dürfte allerdings nicht durch eine Aktivierung der Phosphorylase in der Nebenniere erfolgen. 2. Befunde zum biochemischen Mechanismus der Stimulation der Proteinsynthese in der Nebenniere durch ACTH werden referiert. Die Intaktheit der Proteinsynthese der Nebenniere scheint für den steroidogenen Effekt des ACTH Voraussetzung zu sein.Two current hypotheses on the mechanism of action of ACTH are reviewed: 1. The content of cyclic 3,5-adenosine monophosphate of the adrenals is increased by ACTH, and cyclic AMP or ACTH enhance corticoid synthesis. However, stimulation of corticoid synthesis presumably is not mediated by activation of adrenal phosphorylase. 2. Experiments dealing with the biochemical mechanism of the stimulation of adrenal protein synthesis are reviewed. The integrity of the adrenal protein synthesis appears to be necessary for the enhancement of corticoid synthesis by ACTH