The cost and risk impacts of rerouting railroad shipments of hazardous materials

Cataloged from PDF version of article.Rail shipments of hazardous materials expose the population near the routes to the possibility of an accident resulting in a spill. Rail routes are determined by economic concerns such as route length and the revenue generated for the originating carrier. In this paper we consider an alternate routing strategy that takes accident risks into account. We employ a model to quantify rail transport risk and then use a weighted combination of cost and risk and generate alternate routes. In some cases the alternate routes achieve significantly lower risk values than the practical routes at a small incremental cost. While there are generally fewer rerouting alternatives for rail than for road transport, considering the possible consequences of a train derailment we argue that risk should be taken into account when selecting rail routes and that the cost–risk tradeoffs should be evaluated. © 2007 Elsevier Ltd. All rights reserved

High-fidelity state detection and tomography of a single ion Zeeman qubit

We demonstrate high-fidelity Zeeman qubit state detection in a single trapped 88 Sr+ ion. Qubit readout is performed by shelving one of the qubit states to a metastable level using a narrow linewidth diode laser at 674 nm followed by state-selective fluorescence detection. The average fidelity reached for the readout of the qubit state is 0.9989(1). We then measure the fidelity of state tomography, averaged over all possible single-qubit states, which is 0.9979(2). We also fully characterize the detection process using quantum process tomography. This readout fidelity is compatible with recent estimates of the detection error-threshold required for fault-tolerant computation, whereas high-fidelity state tomography opens the way for high-precision quantum process tomography

Variation in the Use of 12-Lead Electrocardiography for Patients With Chest Pain by Emergency Medical Services in North Carolina

BackgroundPrehospital 12‐lead electrocardiography (ECG) is critical to timely STEMI care although its use remains inconsistent. Previous studies to identify reasons for failure to obtain a prehospital ECG have generally only focused on individual emergency medical service (EMS) systems in urban areas. Our study objective was to identify patient, geographic, and EMS agency‐related factors associated with failure to perform a prehospital ECG across a statewide geography.Methods and ResultsWe analyzed data from the Prehospital Medical Information System (PreMIS) in North Carolina from January 2008 to November 2010 for patients >30 years of age who used EMS and had a prehospital chief complaint of chest pain. Among 3.1 million EMS encounters, 134 350 patients met study criteria. From 2008–2010, 82 311 (61%) persons with chest pain received a prehospital ECG; utilization increased from 55% in 2008 to 65% in 2010 (trend P<0.001). Utilization by health referral region ranged from 22.9% to 74.2% and was lowest in rural areas. Men were more likely than women to have an ECG performed (63.0% vs 61.3%, adjusted RR 1.02, 95% CI 1.01 to 1.04). The certification‐level of the EMS provider (paramedic vsbasic/intermediate) and system‐level ECG equipment availability were the strongest predictors of ECG utilization. Persons in an ambulance with a certified paramedic were significantly more likely to receive a prehospital ECG than nonparamedics (RR 2.15, 95% CI 1.55, 2.99).ConclusionsAcross a large geographic area prehospital ECG use increased significantly, although important quality improvement opportunities remain. Increasing ECG availability and improving EMS certification and training levels are needed to improve overall care and reduce rural‐urban treatment differences

Proteasome Lid Bridges Mitochondrial Stress with Cdc53/Cullin1 NEDDylation Status

Cycles of Cdc53/Cullin1 rubylation (a.k.a NEDDylation) protect ubiquitin-E3 SCF (Skp1-Cullin1-F-box protein) complexes from self-destruction and play an important role in mediating the ubiquitination of key protein substrates involved in cell cycle progression, development, and survival. Cul1 rubylation is balanced by the COP9 signalosome (CSN), a multi-subunit derubylase that shows 1:1 paralogy to the 26 S proteasome lid. The turnover of SCF substrates and their relevance to various diseases is well studied, yet, the extent by which environmental perturbations influence Cul1 rubylation/derubylation cycles per se is still unclear. In this study, we show that the level of cellular oxidation serves as a molecular switch, determining Cullin1 rubylation/derubylation ratio. We describe a mutant of the proteasome lid subunit, Rpn11 that exhibits accumulated levels of Cullin1-Rub1 conjugates, a characteristic phenotype of csn mutants. By dissecting between distinct phenotypes of rpn11 mutants, proteasome and mitochondria dysfunction, we were able to recognize the high reactive oxygen species (ROS) production during the transition of cells into mitochondrial respiration, as a checkpoint of Cullin1 rubylation in a reversible manner. Thus, the study adds the rubylation cascade to the list of cellular pathways regulated by redox homeostasis

How to Choose a Champion

League competition is investigated using random processes and scaling techniques. In our model, a weak team can upset a strong team with a fixed probability. Teams play an equal number of head-to-head matches and the team with the largest number of wins is declared to be the champion. The total number of games needed for the best team to win the championship with high certainty, T, grows as the cube of the number of teams, N, i.e., T ~ N^3. This number can be substantially reduced using preliminary rounds where teams play a small number of games and subsequently, only the top teams advance to the next round. When there are k rounds, the total number of games needed for the best team to emerge as champion, T_k, scales as follows, T_k ~N^(\gamma_k) with gamma_k=1/[1-(2/3)^(k+1)]. For example, gamma_k=9/5,27/19,81/65 for k=1,2,3. These results suggest an algorithm for how to infer the best team using a schedule that is linear in N. We conclude that league format is an ineffective method of determining the best team, and that sequential elimination from the bottom up is fair and efficient.Comment: 6 pages, 3 figure

A network-based dynamical ranking system for competitive sports

From the viewpoint of networks, a ranking system for players or teams in sports is equivalent to a centrality measure for sports networks, whereby a directed link represents the result of a single game. Previously proposed network-based ranking systems are derived from static networks, i.e., aggregation of the results of games over time. However, the score of a player (or team) fluctuates over time. Defeating a renowned player in the peak performance is intuitively more rewarding than defeating the same player in other periods. To account for this factor, we propose a dynamic variant of such a network-based ranking system and apply it to professional men's tennis data. We derive a set of linear online update equations for the score of each player. The proposed ranking system predicts the outcome of the future games with a higher accuracy than the static counterparts.Comment: 6 figure

Fission yeast 26S proteasome mutants are multi-drug resistant due to stabilization of the pap1 transcription factor

Here we report the result of a genetic screen for mutants resistant to the microtubule poison methyl benzimidazol-2-yl carbamate (MBC) that were also temperature sensitive for growth. In total the isolated mutants were distributed in ten complementation groups. Cloning experiments revealed that most of the mutants were in essential genes encoding various 26S proteasome subunits. We found that the proteasome mutants are multi-drug resistant due to stabilization of the stress-activated transcription factor Pap1. We show that the ubiquitylation and ultimately the degradation of Pap1 depend on the Rhp6/Ubc2 E2 ubiquitin conjugating enzyme and the Ubr1 E3 ubiquitin-protein ligase. Accordingly, mutants lacking Rhp6 or Ubr1 display drug-resistant phenotypes

Structure of the mirror nuclei 9^9Be and 9^9B in a microscopic cluster model

The structure of the mirror nuclei $^9$Be and $^9$B is studied in a microscopic $\alpha+ \alpha+ n$ and $\alpha+ \alpha+ p$ three-cluster model using a fully antisymmetrized 9-nucleon wave function. The two-nucleon interaction includes central and spin-orbit components and the Coulomb potential. The ground state of $^9$Be is obtained accurately with the stochastic variational method, while several particle-unbound states of both $^9$Be and $^9$B are investigated with the complex scaling method.The calculation for $^9$Be supports the recent identification for the existence of two broad states around 6.5 MeV, and predicts the $\frac{3}{2}^{-}_2$ and $\frac{5}{2}^{-}_2$ states at about 4.5 MeV and 8 MeV, respectively. The similarity of the calculated spectra of $^9$Be and $^9$B enables one to identify unknown spins and parities of the $^9$B states. Available data on electromagnetic moments and elastic electron scatterings are reproduced very well. The enhancement of the $E$1 transition of the first excited state in $^9$Be is well accounted for. The calculated density of $^9$Be is found to reproduce the reaction cross section on a Carbon target. The analysis of the beta decay of $^9$Li to $^9$Be clearly shows that the wave function of $^9$Be must contain a small component that cannot be described by the simple $\alpha+ \alpha+ n$ model. This small component can be well accounted for by extending a configuration space to include the distortion of the $\alpha$-particle to $t+p$ and $h+n$ partitions.Comment: 24 page

A Conditional Yeast E1 Mutant Blocks the Ubiquitin–Proteasome Pathway and Reveals a Role for Ubiquitin Conjugates in Targeting Rad23 to the Proteasome

E1 ubiquitin activating enzyme catalyzes the initial step in all ubiquitin-dependent processes. We report the isolation of uba1-204, a temperature-sensitive allele of the essential Saccharomyces cerevisiae E1 gene, UBA1. Uba1-204 cells exhibit dramatic inhibition of the ubiquitin–proteasome system, resulting in rapid depletion of cellular ubiquitin conjugates and stabilization of multiple substrates. We have employed the tight phenotype of this mutant to investigate the role ubiquitin conjugates play in the dynamic interaction of the UbL/UBA adaptor proteins Rad23 and Dsk2 with the proteasome. Although proteasomes purified from mutant cells are intact and proteolytically active, they are depleted of ubiquitin conjugates, Rad23, and Dsk2. Binding of Rad23 to these proteasomes in vitro is enhanced by addition of either free or substrate-linked ubiquitin chains. Moreover, association of Rad23 with proteasomes in mutant and wild-type cells is improved upon stabilizing ubiquitin conjugates with proteasome inhibitor. We propose that recognition of polyubiquitin chains by Rad23 promotes its shuttling to the proteasome in vivo

Trim17, novel E3 ubiquitin-ligase, initiates neuronal apoptosis

Accumulating data indicate that the ubiquitin-proteasome system controls apoptosis by regulating the level and the function of key regulatory proteins. In this study, we identified Trim17, a member of the TRIM/RBCC protein family, as one of the critical E3 ubiquitin ligases involved in the control of neuronal apoptosis upstream of mitochondria. We show that expression of Trim17 is increased both at the mRNA and protein level in several in vitro models of transcription-dependent neuronal apoptosis. Expression of Trim17 is controlled by the PI3K/Akt/GSK3 pathway in cerebellar granule neurons (CGN). Moreover, the Trim17 protein is expressed in vivo, in apoptotic neurons that naturally die during post-natal cerebellar development. Overexpression of active Trim17 in primary CGN was sufficient to induce the intrinsic pathway of apoptosis in survival conditions. This pro-apoptotic effect was abolished in Bax(-/-) neurons and depended on the E3 activity of Trim17 conferred by its RING domain. Furthermore, knock-down of endogenous Trim17 and overexpression of dominant-negative mutants of Trim17 blocked trophic factor withdrawal-induced apoptosis both in CGN and in sympathetic neurons. Collectively, our data are the first to assign a cellular function to Trim17 by showing that its E3 activity is both necessary and sufficient for the initiation of neuronal apoptosis. Cell Death and Differentiation (2010) 17, 1928-1941; doi: 10.1038/cdd.2010.73; published online 18 June 201