Thermal equilibrium of a macroscopic quantum system in a pure state

We consider the notion of thermal equilibrium for an individual closed macroscopic quantum system in a pure state, i.e., described by a wave function. The macroscopic properties in thermal equilibrium of such a system, determined by its wave function, must be the same as those obtained from thermodynamics, e.g., spatial uniformity of temperature and chemical potential. When this is true we say that the system is in macroscopic thermal equilibrium (MATE). Such a system may however not be in microscopic thermal equilibrium (MITE). The latter requires that the reduced density matrices of small subsystems be close to those obtained from the microcanonical, equivalently the canonical, ensemble for the whole system. The distinction between MITE and MATE is particularly relevant for systems with many-body localization (MBL) for which the energy eigenfunctions fail to be in MITE while necessarily most of them, but not all, are in MATE. We note however that for generic macroscopic systems, including those with MBL, most wave functions in an energy shell are in both MATE and MITE. For a classical macroscopic system, MATE holds for most phase points on the energy surface, but MITE fails to hold for any phase point

Liver Transplantation to Provide Low-Density-Lipoprotein Receptors and Lower Plasma Cholesterol in a Child with Homozygous Familial Hypercholesterolemia

A six-year-old girl with severe hypercholesterolemia and atherosclerosis had two defective genes at the low-density-lipoprotein (LDL) receptor locus, as determined by biochemical studies of cultured fibroblasts. One gene, inherited from the mother, produced no LDL receptors; the other gene, inherited from the father, produced a receptor precursor that was not transported to the cell surface and was unable to bind LDL. The patient degraded intravenously administered 125I-LDL at an extremely low rate, indicating that her high plasma LDL-cholesterol level was caused by defective receptor-mediated removal of LDL from plasma. After transplantation of a liver and a heart from a normal donor, the patient's plasma LDL-cholesterol level declined by 81 per cent, from 988 to 184 mg per deciliter. The fractional catabolic rate for intravenously administered 125I-LDL, a measure of functional LDL receptors in vivo, increased by 2.5-fold. Thus, the transplanted liver, with its normal complement of LDL receptors, was able to remove LDL cholesterol from plasma at a nearly normal rate. We conclude that a genetically determined deficiency of LDL receptors can be largely reversed by liver transplantation. These data underscore the importance of hepatic LDL receptors in controlling the plasma level of LDL cholesterol in human beings. (N Engl J Med 1984; 311: 1658–64.). © 1984, Massachusetts Medical Society. All rights reserved

Creating a Simple Single Computational Approach to Modeling Rarefied and Continuum Flow About Aerospace Vehicles

We proposed to create a single computational code incorporating methods that can model both rarefied and continuum flow to enable the efficient simulation of flow about space craft and high altitude hypersonic aerospace vehicles. The code was to use a single grid structure that permits a smooth transition between the continuum and rarefied portions of the flow. Developing an appropriate computational boundary between the two regions represented a major challenge. The primary approach chosen involves coupling a four-speed Lattice Boltzmann model for the continuum flow with the DSMC method in the rarefied regime. We also explored the possibility of using a standard finite difference Navier Stokes solver for the continuum flow. With the resulting code we will ultimately investigate three-dimensional plume impingement effects, a subject of critical importance to NASA and related to the work of Drs. Forrest Lumpkin, Steve Fitzgerald and Jay Le Beau at Johnson Space Center. Below is a brief background on the project and a summary of the results as of the end of the grant

Acute kidney injury in critically ill newborns: What do we know? What do we need to learn?

Outcomes in critically ill neonates have improved over the past three decades, yet high residual mortality and morbidity rates exist. Acute kidney injury (AKI) is not just an innocent by-stander in the critically ill patient. Research on incidence and outcomes of AKI in the critically ill neonatal population is scarce. The objective of this publication is to (a) review original articles on the short- and long-term outcomes after neonatal AKI, (b) highlight key articles on adults and children with AKI in order to demonstrate how such insights might be applied to neonates, and (c) suggest clinical research studies to fill the gaps in our understanding of neonatal AKI. To date, observational studies suggest high rates of AKI and poor outcomes in critically ill neonates. Neonates with AKI are at risk of developing chronic kidney disease and hypertension. Large prospective studies are needed to test definitions and to better understand risk factors, incidence, independent outcomes, and mechanisms that lead to poor short- and long-term outcomes. Early biomarkers of AKI need to be explored in critically ill neonates. Infants with AKI need to be followed for sequelae after AKI

Stellar Dynamics of Extreme-Mass-Ratio Inspirals

Inspiral of compact stellar remnants into massive black holes (MBHs) is accompanied by the emission of gravitational waves at frequencies that are potentially detectable by space-based interferometers. Event rates computed from statistical (Fokker-Planck, Monte-Carlo) approaches span a wide range due to uncertaintities about the rate coefficients. Here we present results from direct integration of the post-Newtonian N-body equations of motion descrbing dense clusters of compact stars around Schwarzschild MBHs. These simulations embody an essentially exact (at the post-Newtonian level) treatment of the interplay between stellar dynamical relaxation, relativistic precession, and gravitational-wave energy loss. The rate of capture of stars by the MBH is found to be greatly reduced by relativistic precession, which limits the ability of torques from the stellar potential to change orbital angular momenta. Penetration of this "Schwarzschild barrier" does occasionally occur, resulting in capture of stars onto orbits that gradually inspiral due to gravitational wave emission; we discuss two mechanisms for barrier penetration and find evidence for both in the simulations. We derive an approximate formula for the capture rate, which predicts that captures would be strongly disfavored from orbits with semi-major axes below a certain value; this prediction, as well as the predicted rate, are verified in the N-body integrations. We discuss the implications of our results for the detection of extreme-mass-ratio inspirals from galactic nuclei with a range of physical properties.Comment: 28 pages, 16 figures. Version 2 is significantly revised to reflect new insights into J and Q effects, to be published late

Axonal stress kinase activation and tau misbehavior induced by kinesin-1 transport defects

Many neurodegenerative diseases exhibit axonal pathology, transport defects, and aberrant phosphorylation and aggregation of the microtubule binding protein tau. While mutant tau protein in frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP17) causes aberrant microtubule binding and assembly of tau into filaments, the pathways leading to tau-mediated neurotoxicity in Alzheimer's disease and other neurodegenerative disorders in which tau protein is not genetically modified remain unknown. To test the hypothesis that axonal transport defects alone can cause pathological abnormalities in tau protein and neurodegeneration in the absence of mutant tau or amyloid β deposits, we induced transport defects by deletion of the kinesin light chain 1 (KLC1) subunit of the anterograde motor kinesin-1. We found that upon aging, early selective axonal transport defects in mice lacking the KLC1 protein (KLC1-/-) led to axonopathies with cytoskeletal disorganization and abnormal cargo accumulation. In addition, increased c-jun N-terminal stress kinase activation colocalized with aberrant tau in dystrophic axons. Surprisingly, swollen dystrophic axons exhibited abnormal tau hyperphosphorylation and accumulation. Thus, directly interfering with axonal transport is sufficient to activate stress kinase pathways initiating a biochemical cascade that drives normal tau protein into a pathological state found in a variety of neurodegenerative disorders including Alzheimer's disease.Fil: Falzone, Tomas Luis. Howard Hughes Medical Institute; Estados Unidos. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; ArgentinaFil: Stokin, Gorazd B.. University Psychiatric Hospital; EsloveniaFil: Lillo, Concepción. University of California at San Diego; Estados UnidosFil: Rodrigues, Elizabeth M.. Howard Hughes Medical Institute; Estados UnidosFil: Westerman, Eileen L.. Howard Hughes Medical Institute; Estados UnidosFil: Williams, David S.. University of California at San Diego; Estados UnidosFil: Goldstein, Lawrence S. B.. Howard Hughes Medical Institute; Estados Unido

Mandated Leave Policies in the Context of Student Mental Health Challenges at Canadian Universities: A Framework Analysis

Although there is increased attention to the mental health needs of university students, far less attention has been given to mental health-related university policies. Many Canadian public universities have mandated leave policies that specify the conditions under which a student may be required to take a leave of absence from university. The purpose of the current study was to conduct an in-depth analysis of current mandated leave policies in public Canadian English-speaking universities. Applied framework analysis methodology was used to examine the approaches to balancing the needs of students experiencing mental health challenges and providing a safe environment on campus. Three primary themes regarding mandated leave policies were identified, including (a) approaches for addressing mental health concerns, (b) balancing the needs of the student with the needs of the institution, and (c) guidelines, standards, and quality assurance. Implications for mandated leave policies and approaches to students experiencing mental health challenges are discussed.Bien que l’on s’intéresse de plus en plus aux besoins des étudiants universitaires en matière de santé mentale, on a accordé moins d’attention aux politiques universitaires relatives à la santé mentale. De nombreuses universités publiques canadiennes ont des politiques de congé obligatoire qui précisent les conditions dans lesquelles un étudiant doit prendre un congé de l’université. L’ob-jectif de la présente étude est d’analyser les politiques actuelles de congé obligatoire dans les universités publiques canadiennes anglophones. Une méthodologie d’analyse de cadre appliquée a été utilisée pour examiner les approches visant à trouver un équilibre entre les besoins des étudiants ayant des problèmes de santé mentale et la nécessité de fournir un environnement sûr sur le campus. Trois thèmes principaux ressortent concernant les politiques en matière de congés obligatoires, soit (a) les approches pour répondre aux problèmes de santé mentale, (b) l’équilibre entre les besoins de l’étudiant et les besoins de l’université, et (c) les lignes directrices, les normes et l’assurance de la qualité. Les implications pour les politiques de congé obligatoire et les approches auprès des étudiants ayant des problèmes de santé mentale sont discutées