17 research outputs found
Collisional decoherence reexamined
We re-derive the quantum master equation for the decoherence of a massive
Brownian particle due to collisions with the lighter particles from a thermal
environment. Our careful treatment avoids the occurrence of squares of Dirac
delta functions. It leads to a decoherence rate which is smaller by a factor of
2 pi compared to previous findings. This result, which is in agreement with
recent experiments, is confirmed by both a physical analysis of the problem and
by a perturbative calculation in the weak coupling limit.Comment: 33 pages, 4 figure
On the Asymptotic Dynamics of a Quantum System Composed by Heavy and Light Particles
We consider a non relativistic quantum system consisting of heavy and
light particles in dimension three, where each heavy particle interacts with
the light ones via a two-body potential . No interaction is assumed
among particles of the same kind. Choosing an initial state in a product form
and assuming sufficiently small we characterize the asymptotic
dynamics of the system in the limit of small mass ratio, with an explicit
control of the error. In the case K=1 the result is extended to arbitrary
. The proof relies on a perturbative analysis and exploits a
generalized version of the standard dispersive estimates for the
Schr\"{o}dinger group. Exploiting the asymptotic formula, it is also outlined
an application to the problem of the decoherence effect produced on a heavy
particle by the interaction with the light ones.Comment: 38 page
A ballistic motion disrupted by quantum reflections
I study a Lindblad dynamics modeling a quantum test particle in a Dirac comb
that collides with particles from a background gas. The main result is a
homogenization theorem in an adiabatic limiting regime involving large initial
momentum for the test particle. Over the time interval considered, the particle
would exhibit essentially ballistic motion if either the singular periodic
potential or the kicks from the gas were removed. However, the particle behaves
diffusively when both sources of forcing are present. The conversion of the
motion from ballistic to diffusive is generated by occasional quantum
reflections that result when the test particle's momentum is driven through a
collision near to an element of the half-spaced reciprocal lattice of the Dirac
comb.Comment: 54 pages. I rewrote the introduction and simplified some of the
presentatio
Diffusive limit for a quantum linear Boltzmann dynamics
In this article, I study the diffusive behavior for a quantum test particle
interacting with a dilute background gas. The model I begin with is a reduced
picture for the test particle dynamics given by a quantum linear Boltzmann
equation in which the gas particle scattering is assumed to occur through a
hard-sphere interaction. The state of the particle is represented by a density
matrix that evolves according to a translation-covariant Lindblad equation. The
main result is a proof that the particle's position distribution converges to a
Gaussian under diffusive rescaling.Comment: 51 pages. I have restructured Sections 2-4 from the previous version
and corrected an error in the proof of Proposition 7.
Global, regional, and national comparative risk assessment of 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks, 1990-2015: A systematic analysis for the Global Burden of Disease Study 2015
Background: The Global Burden of Diseases, Injuries, and Risk Factors Study 2015 provides an up-to-date synthesis of the evidence for risk factor exposure and the attributable burden of disease. By providing national and subnational assessments spanning the past 25 years, this study can inform debates on the importance of addressing risks in context.
Methods: We used the comparative risk assessment framework developed for previous iterations of the Global Burden of Disease Study to estimate attributable deaths, disability-adjusted life-years (DALYs), and trends in exposure by age group, sex, year, and geography for 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks from 1990 to 2015. This study included 388 risk-outcome pairs that met World Cancer Research Fund-defined criteria for convincing or probable evidence. We extracted relative risk and exposure estimates from randomised controlled trials, cohorts, pooled cohorts, household surveys, census data, satellite data, and other sources. We used statistical models to pool data, adjust for bias, and incorporate covariates. We developed a metric that allows comparisons of exposure across risk factors—the summary exposure value. Using the counterfactual scenario of theoretical minimum risk level, we estimated the portion of deaths and DALYs that could be attributed to a given risk. We decomposed trends in attributable burden into contributions from population growth, population age structure, risk exposure, and risk-deleted cause-specific DALY rates. We characterised risk exposure in relation to a Socio-demographic Index (SDI).
Findings: Between 1990 and 2015, global exposure to unsafe sanitation, household air pollution, childhood underweight, childhood stunting, and smoking each decreased by more than 25%. Global exposure for several occupational risks, high body-mass index (BMI), and drug use increased by more than 25% over the same period. All risks jointly evaluated in 2015 accounted for 57·8% (95% CI 56·6–58·8) of global deaths and 41·2% (39·8–42·8) of DALYs. In 2015, the ten largest contributors to global DALYs among Level 3 risks were high systolic blood pressure (211·8 million [192·7 million to 231·1 million] global DALYs), smoking (148·6 million [134·2 million to 163·1 million]), high fasting plasma glucose (143·1 million [125·1 million to 163·5 million]), high BMI (120·1 million [83·8 million to 158·4 million]), childhood undernutrition (113·3 million [103·9 million to 123·4 million]), ambient particulate matter (103·1 million [90·8 million to 115·1 million]), high total cholesterol (88·7 million [74·6 million to 105·7 million]), household air pollution (85·6 million [66·7 million to 106·1 million]), alcohol use (85·0 million [77·2 million to 93·0 million]), and diets high in sodium (83·0 million [49·3 million to 127·5 million]). From 1990 to 2015, attributable DALYs declined for micronutrient deficiencies, childhood undernutrition, unsafe sanitation and water, and household air pollution; reductions in risk-deleted DALY rates rather than reductions in exposure drove these declines. Rising exposure contributed to notable increases in attributable DALYs from high BMI, high fasting plasma glucose, occupational carcinogens, and drug use. Environmental risks and childhood undernutrition declined steadily with SDI; low physical activity, high BMI, and high fasting plasma glucose increased with SDI. In 119 countries, metabolic risks, such as high BMI and fasting plasma glucose, contributed the most attributable DALYs in 2015. Regionally, smoking still ranked among the leading five risk factors for attributable DALYs in 109 countries; childhood underweight and unsafe sex remained primary drivers of early death and disability in much of sub-Saharan Africa.
Interpretation: Declines in some key environmental risks have contributed to declines in critical infectious diseases. Some risks appear to be invariant to SDI. Increasing risks, including high BMI, high fasting plasma glucose, drug use, and some occupational exposures, contribute to rising burden from some conditions, but also provide opportunities for intervention. Some highly preventable risks, such as smoking, remain major causes of attributable DALYs, even as exposure is declining. Public policy makers need to pay attention to the risks that are increasingly major contributors to global burden.
Funding: Bill & Melinda Gates Foundation
The LHCb upgrade I
The LHCb upgrade represents a major change of the experiment. The detectors have been almost completely renewed to allow running at an instantaneous luminosity five times larger than that of the previous running periods. Readout of all detectors into an all-software trigger is central to the new design, facilitating the reconstruction of events at the maximum LHC interaction rate, and their selection in real time. The experiment's tracking system has been completely upgraded with a new pixel vertex detector, a silicon tracker upstream of the dipole magnet and three scintillating fibre tracking stations downstream of the magnet. The whole photon detection system of the RICH detectors has been renewed and the readout electronics of the calorimeter and muon systems have been fully overhauled. The first stage of the all-software trigger is implemented on a GPU farm. The output of the trigger provides a combination of totally reconstructed physics objects, such as tracks and vertices, ready for final analysis, and of entire events which need further offline reprocessing. This scheme required a complete revision of the computing model and rewriting of the experiment's software
Analysis of EphB receptors and their ligands in the developing retinocollicular system of the wallaby reveals dynamic patterns of expression in the retina
Gene expression profiling reveals multiple novel intrinsic and extrinsic factors associated with axonal regeneration failure
In contrast to the regeneration-competent peripheral nervous system (PNS), lesions of nerve tracts within the central nervous system (CNS) lead to chronically impaired neuronal connections. We have analysed changes in gene expression patterns occurring as a consequence of postcommissural fornix transection at a time when spontaneous axonal growth has ceased at the lesion site. This was done in order to describe both extrinsic and intrinsic determinants of regeneration failure. Using a genomic approach we have identified a number of so far undetected factors such as bamacan and semaphorin 6B, which relate to chronic axonal growth arrest and therefore are promising candidates for lesion-induced axonal growth inhibitors. In addition, we observed that within the subiculum, where the fornix axons originate, neuronal Oct-6 was induced and NG2 was down-regulated, indicating that axotomized neurons as well as glial cells react at the level of gene expression to remote axotom