Relaxation Time, Diffusion, and Viscosity Analysis of Model Asphalt Systems Using Molecular Simulation

Molecular dynamics simulation was used to calculate rotational relaxation time, diffusion coefficient, and zero-shear viscosity for a pure aromatic compound naphthalene and for aromatic and aliphatic components in model asphalt systems over a temperature range of 298–443 K. The model asphalt systems were chosen previously to represent real asphalt. Green–Kubo and Einstein methods were used to estimate viscosity at high temperature 443.15 K. Rotational relaxation times were calculated by nonlinear regression of orientation correlation functions to a modified Kohlrausch–Williams–Watts function. The Vogel–Fulcher–Tammann equation was used to analyze the temperature dependences of relaxation time, viscosity, and diffusion coefficient. The temperature dependences of viscosity and relaxation time were related using the Debye–Stokes–Einstein equation, enabling viscosity at low temperatures of two model asphalt systems to be estimated from high temperature 443.15 K viscosity and temperature-dependent relaxation time results. Semiquantitative accuracy of such an equivalent temperature dependence was found for naphthalene. Diffusion coefficient showed a much smaller temperature dependence for all components in the model asphalt systems. Dimethylnaphthalene diffused the fastest while asphaltene molecules diffused the slowest. Neat naphthalene diffused faster than any component in model asphalts. © 2007 American Institute of Physics. DOI: 10.1063/1.279918

Rotational Relaxation Times of Individual Compounds With Simulations of Molecular Asphalt Models

The dynamical properties of a complex system incorporate contributions from the diverse components from which it is constituted. To study this relationship in a multicomponent system, relaxation times based on rotation autocorrelation functions in molecular dynamics simulations were analyzed for molecules in two sets of unmodified and polymer-modified model asphalt/bitumen systems over 298–473 K. The model asphalt systems were proposed previously to approximate the chemical and mechanical properties of real asphalts. Relaxations were modeled using a modified Kaulrausch–Williams–Watts function and were based on the third Legendre polynomial of normal vector time correlation functions for aromatic species asphaltene, polar aromatic, naphthene aromatic. Both the end-to-end vector and the longest axis eigenvector of the radius of gyration matrix were used for time correlation functions of chain molecules C22, polystyrene. Decreases in temperature induced large increases in relaxation time consistent with the Vogel–Fulcher–Tammann equation. The presence of a polymer slowed the decay of each correlation function to some extent. The product of relaxation time and diffusion coefficient revealed qualitative differences between larger and smaller molecules in the same system. These relaxation mechanisms remained coupled for small molecules, while the larger asphaltene and polymer molecules revealed significant slowdowns in rotation compared to translational diffusion at lower temperatures. Smaller values of the stretched exponential parameter for asphaltenes compared to smaller molecules suggested a broader range of relaxation times and were consistent with this distinction. Difficulties in converging polymer chain relaxation times are discussed in terms of fluctuations in the magnitude and orientation of the end-to-end vector and chain axis eigenvector. Viscosity results suggested by the Debye–Stokes–Einstein relationship are consistent with trends shown in the literature for true bitumen systems

Censoring Unbiased Regression Trees and Ensembles

This paper proposes a novel approach to building regression trees and ensemble learning in survival analysis. By first extending the theory of censoring unbiased transformations, we construct observed data estimators of full data loss functions in cases where responses can be right censored. This theory is used to construct two specific classes of methods for building regression trees and regression ensembles that respectively make use of Buckley-James and doubly robust estimating equations for a given full data risk function. For the particular case of squared error loss, we further show how to implement these algorithms using existing software (e.g., CART, random forests) by making use of a related form of response imputation. Comparisons of these methods to existing ensemble procedures for predicting survival probabilities are provided in both simulated settings and through applications to four datasets. It is shown that these new methods either improve upon, or remain competitive with, existing implementations of random survival forests, conditional inference forests, and recursively imputed survival trees

Isolation of cationic and neutral (allenylidene)(carbene) and bis(allenylidene)gold complexes.

The one-electron reduction of a cationic (allenylidene)[cyclic(alkyl) (amino)carbene]gold(i) complex leads to the corresponding neutral, paramagnetic, formally gold(0) complex. DFT calculations reveal that the spin density of this highly robust coinage metal complex is mainly located on the allenylidene fragment, with only 1.8 and 3.1% on the gold center and the CAAC ligand, respectively. In addition, the first homoleptic bis(allenylidene)gold(i) complex has been prepared and fully characterized

Experimental examination of a method to estimate temporal effect by neutrons and γ-rays on scintillation light in scintillator-based soft x-ray diagnostic of experimental advanced superconducting tokamak and large helical device

Scintillators, which are more tolerant of neutrons or γ-rays than semiconductors, are a promising candidate for soft X-ray (SX) diagnostics in high neutron flux environments such as JT-60SA or ITER. Although scintillators are tolerant of radiations, neutrons and γ-rays can cause scintillation light and become noise on SX signals. Therefore, a method to estimate the temporal effect by the radiations on SX signals and an appropriate design of the radiation shield based on the estimation are required. In previous studies, it has been proposed for estimating the effect by the radiations to calculate the absorption powers due to SXs, neutrons, and γ-rays in scintillators assuming that amplitudes of scintillation light are proportional to the absorption powers. In this study, an experimental examination of this proposal is conducted in the Experimental Advanced Superconducting Tokamak (EAST). It is shown that the proposal may be valid in the examination of EAST. In addition to results in EAST, initial results of a multi-channel scintillator-based SX diagnostic in the Large Helical Device (LHD) are introduced. Although a scintillator-based SX diagnostic in LHD observes oscillations of SXs by magnetohydrodynamic (MHD) phenomena successfully, the observed temporal effect on SX signals by neutrons or γ-rays is more significant than the expected effect, which is estimated by calculating the absorption powers. One of the possible reasons for the contradiction between the results in EAST and LHD is unexpected γ-rays around the scintillators in LHD. Although the temporal effect by the radiations is significant in the current system of LHD, the degradation of amplitudes of SX signals after the deuterium plasma experiments is not observed with the current level of the fluence. The scintillator-based SX diagnostic in LHD may work as a diagnostic to research MHD instabilities in deuterium plasma experiments without additional maintenance during an experimental campaign by making the pinhole larger or setting an additional radiation shield

Nitric oxide mediates glial-induced neurodegeneration in Alexander disease

Glia play critical roles in maintaining the structure and function of the nervous system; however, the specific contribution that astroglia make to neurodegeneration in human disease states remains largely undefined. Here we use Alexander disease, a serious degenerative neurological disorder caused by astrocyte dysfunction, to identify glial-derived NO as a signalling molecule triggering astrocyte-mediated neuronal degeneration. We further find that NO acts through cGMP signalling in neurons to promote cell death. Glial cells themselves also degenerate, via the DNA damage response and p53. Our findings thus define a specific mechanism for glial-induced non-cell autonomous neuronal cell death, and identify a potential therapeutic target for reducing cellular toxicity in Alexander disease, and possibly other neurodegenerative disorders with glial dysfunction

Matrix stiffness controls lymphatic vessel formation through regulation of a GATA2-dependent transcriptional program

Tissue and vessel wall stiffening alters endothelial cell properties and contributes to vascular dysfunction. However, whether extracellular matrix (ECM) stiffness impacts vascular development is not known. Here we show that matrix stiffness controls lymphatic vascular morphogenesis. Atomic force microscopy measurements in mouse embryos reveal that venous lymphatic endothelial cell (LEC) progenitors experience a decrease in substrate stiffness upon migration out of the cardinal vein, which induces a GATA2-dependent transcriptional program required to form the first lymphatic vessels. Transcriptome analysis shows that LECs grown on a soft matrix exhibit increased GATA2 expression and a GATA2-dependent upregulation of genes involved in cell migration and lymphangiogenesis, including VEGFR3. Analyses of mouse models demonstrate a cell-autonomous function of GATA2 in regulating LEC responsiveness to VEGF-C and in controlling LEC migration and sprouting in vivo. Our study thus uncovers a mechanism by which ECM stiffness dictates the migratory behavior of LECs during early lymphatic development.Peer reviewe

A genome-wide library of MADM mice for single-cell genetic mosaic analysis

Mosaic analysis with double markers (MADM) offers one approach to visualize and concomitantly manipulate genetically defined cells in mice with single-cell resolution. MADM applications include the analysis of lineage, single-cell morphology and physiology, genomic imprinting phenotypes, and dissection of cell-autonomous gene functions in vivo in health and disease. Yet, MADM can only be applied to 96% of the entire mouse genome can now be subjected to single-cell genetic mosaic analysis. Beyond a proof of principle, we apply our MADM library to systematically trace sister chromatid segregation in distinct mitotic cell lineages. We find striking chromosome-specific biases in segregation patterns, reflecting a putative mechanism for the asymmetric segregation of genetic determinants in somatic stem cell division

Rabies screen reveals GPe control of cocaine-triggered plasticity.

Identification of neural circuit changes that contribute to behavioural plasticity has routinely been conducted on candidate circuits that were preselected on the basis of previous results. Here we present an unbiased method for identifying experience-triggered circuit-level changes in neuronal ensembles in mice. Using rabies virus monosynaptic tracing, we mapped cocaine-induced global changes in inputs onto neurons in the ventral tegmental area. Cocaine increased rabies-labelled inputs from the globus pallidus externus (GPe), a basal ganglia nucleus not previously known to participate in behavioural plasticity triggered by drugs of abuse. We demonstrated that cocaine increased GPe neuron activity, which accounted for the increase in GPe labelling. Inhibition of GPe activity revealed that it contributes to two forms of cocaine-triggered behavioural plasticity, at least in part by disinhibiting dopamine neurons in the ventral tegmental area. These results suggest that rabies-based unbiased screening of changes in input populations can identify previously unappreciated circuit elements that critically support behavioural adaptations