Disordered mesoscopic systems with interactions: induced two-body ensembles and the Hartree-Fock approach

We introduce a generic approach to study interaction effects in diffusive or chaotic quantum dots in the Coulomb blockade regime. The randomness of the single-particle wave functions induces randomness in the two-body interaction matrix elements. We classify the possible induced two-body ensembles, both in the presence and absence of spin degrees of freedom. The ensembles depend on the underlying space-time symmetries as well as on features of the two-body interaction. Confining ourselves to spinless electrons, we then use the Hartree-Fock (HF) approximation to calculate HF single-particle energies and HF wave functions for many realizations of the ensemble. We study the statistical properties of the resulting one-body HF ensemble for a fixed number of electrons. In particular, we determine the statistics of the interaction matrix elements in the HF basis, of the HF single-particle energies (including the HF gap between the last occupied and the first empty HF level), and of the HF single-particle wave functions. We also study the addition of electrons, and in particular the distribution of the distance between successive conductance peaks and of the conductance peak heights.Comment: 25 pages, 16 figure

Indicators for managing human centred manufacturing

Establishing indicators for managing human factors (HF) aspects in the design of production systems remains a challenge. We address the problem in two dimensions – firstly, what aspects of HF are to be considered, and secondly, where in the development process HF is to be measured. In these dimensions a large number of HF metrics are possible in the perceptual, cognitive, physical and psychosocial domains of HF. The relevance of these measures to injury, productivity, quality and organizational strategy continue to be poorly understood. From this perspective we make propositions on the need for: 1) strategic HF metrics selection, 2) metrics application throughout the development process, 3) predictive ‘virtual’ HF metrics approaches, 4) metrics based design guidelines, 5) connecting metrics with design choices and strategies, 6) integrating HF metrics within existing approaches, 7) continuous improvement of the metrics system, and 8) the need to evaluate metrics system quality

Influence of Sacubitril/Valsartan (LCZ696) on 30-day readmission after heart failure hospitalization

Background: Patients with heart failure (HF) are at high risk for hospital readmission in the first 30 days following HF hospitalization. Objectives: This study sought to determine if treatment with sacubitril/valsartan (LCZ696) reduces rates of hospital readmission at 30-days following HF hospitalization compared with enalapril. Methods: We assessed the risk of 30-day readmission for any cause following investigator-reported hospitalizations for HF in the PARADIGM-HF trial, which randomized 8,399 participants with HF and reduced ejection fraction to treatment with LCZ696 or enalapril. Results: Accounting for multiple hospitalizations per patient, there were 2,383 investigator-reported HF hospitalizations, of which 1,076 (45.2%) occurred in subjects assigned to LCZ696 and 1,307 (54.8%) occurred in subjects assigned to enalapril. Rates of readmission for any cause at 30 days were 17.8% in LCZ696-assigned subjects and 21.0% in enalapril-assigned subjects (odds ratio: 0.74; 95% confidence interval: 0.56 to 0.97; p = 0.031). Rates of readmission for HF at 30-days were also lower in subjects assigned to LCZ696 (9.7% vs. 13.4%; odds ratio: 0.62; 95% confidence interval: 0.45 to 0.87; p = 0.006). The reduction in both all-cause and HF readmissions with LCZ696 was maintained when the time window from discharge was extended to 60 days and in sensitivity analyses restricted to adjudicated HF hospitalizations. Conclusions: Compared with enalapril, treatment with LCZ696 reduces 30-day readmissions for any cause following discharge from HF hospitalization

Hydrogen Fluoride in High-Mass Star-forming Regions

Hydrogen fluoride has been established to be an excellent tracer of molecular hydrogen in diffuse clouds. In denser environments, however, the HF abundance has been shown to be approximately two orders of magnitude lower. We present Herschel/HIFI observations of HF J=1-0 toward two high-mass star formation sites, NGC6334 I and AFGL 2591. In NGC6334 I the HF line is seen in absorption in foreground clouds and the source itself, while in AFGL 2591 HF is partially in emission. We find an HF abundance with respect to H2 of 1.5e-8 in the diffuse foreground clouds, whereas in the denser parts of NGC6334 I, we derive a lower limit on the HF abundance of 5e-10. Lower HF abundances in dense clouds are most likely caused by freeze out of HF molecules onto dust grains in high-density gas. In AFGL 2591, the view of the hot core is obstructed by absorption in the massive outflow, in which HF is also very abundant 3.6e-8) due to the desorption by sputtering. These observations provide further evidence that the chemistry of interstellar fluorine is controlled by freeze out onto gas grains.Comment: accepted in Ap

Examining mortality among formerly homeless adults enrolled in Housing First: An observational study

BACKGROUND: Adults who experience prolonged homelessness have mortality rates 3 to 4 times that of the general population. Housing First (HF) is an evidence-based practice that effectively ends chronic homelessness, yet there has been virtually no research on premature mortality among HF enrollees. In the United States, this gap in the literature exists despite research that has suggested chronically homeless adults constitute an aging cohort, with nearly half aged 50 years old or older. METHODS: This observational study examined mortality among formerly homeless adults in an HF program. We examined death rates and causes of death among HF participants and assessed the timing and predictors of death among HF participants following entry into housing. We also compared mortality rates between HF participants and (a) members of the general population and (b) individuals experiencing homelessness. We supplemented these analyses with a comparison of the causes of death and characteristics of decedents in the HF program with a sample of adults identified as homeless in the same city at the time of death through a formal review process. RESULTS: The majority of decedents in both groups were between the ages of 45 and 64 at their time of death; the average age at death for HF participants was 57, compared to 53 for individuals in the homeless sample. Among those in the HF group, 72 % died from natural causes, compared to 49 % from the homeless group. This included 21 % of HF participants and 7 % from the homeless group who died from cancer. Among homeless adults, 40 % died from an accident, which was significantly more than the 14 % of HF participants who died from an accident. HIV or other infectious diseases contributed to 13 % of homeless deaths compared to only 2 % of HF participants. Hypothermia contributed to 6 % of homeless deaths, which was not a cause of death for HF participants. CONCLUSIONS: Results suggest HF participants face excess mortality in comparison to members of the general population and that mortality rates among HF participants are higher than among those reported among members of the general homeless population in prior studies. However, findings also suggest that causes of death may differ between HF participants and their homeless counterparts. Specifically, chronic diseases appear to be more prominent causes of death among HF participants, indicating the potential need for integrating medical support and end-of-life care in HF

A network analysis to identify pathophysiological pathways distinguishing ischaemic from non-ischaemic heart failure

Aims Heart failure (HF) is frequently caused by an ischaemic event (e.g. myocardial infarction) but might also be caused by a primary disease of the myocardium (cardiomyopathy). In order to identify targeted therapies specific for either ischaemic or non‐ischaemic HF, it is important to better understand differences in underlying molecular mechanisms. Methods and results We performed a biological physical protein–protein interaction network analysis to identify pathophysiological pathways distinguishing ischaemic from non‐ischaemic HF. First, differentially expressed plasma protein biomarkers were identified in 1160 patients enrolled in the BIOSTAT‐CHF study, 715 of whom had ischaemic HF and 445 had non‐ischaemic HF. Second, we constructed an enriched physical protein–protein interaction network, followed by a pathway over‐representation analysis. Finally, we identified key network proteins. Data were validated in an independent HF cohort comprised of 765 ischaemic and 100 non‐ischaemic HF patients. We found 21/92 proteins to be up‐regulated and 2/92 down‐regulated in ischaemic relative to non‐ischaemic HF patients. An enriched network of 18 proteins that were specific for ischaemic heart disease yielded six pathways, which are related to inflammation, endothelial dysfunction superoxide production, coagulation, and atherosclerosis. We identified five key network proteins: acid phosphatase 5, epidermal growth factor receptor, insulin‐like growth factor binding protein‐1, plasminogen activator urokinase receptor, and secreted phosphoprotein 1. Similar results were observed in the independent validation cohort. Conclusions Pathophysiological pathways distinguishing patients with ischaemic HF from those with non‐ischaemic HF were related to inflammation, endothelial dysfunction superoxide production, coagulation, and atherosclerosis. The five key pathway proteins identified are potential treatment targets specifically for patients with ischaemic HF

Rescue of Pressure Overload-Induced Heart Failure by Estrogen Therapy.

BackgroundEstrogen pretreatment has been shown to attenuate the development of heart hypertrophy, but it is not known whether estrogen could also rescue heart failure (HF). Furthermore, the heart has all the machinery to locally biosynthesize estrogen via aromatase, but the role of local cardiac estrogen synthesis in HF has not yet been studied. Here we hypothesized that cardiac estrogen is reduced in HF and examined whether exogenous estrogen therapy can rescue HF.Methods and resultsHF was induced by transaortic constriction in mice, and once mice reached an ejection fraction (EF) of ≈35%, they were treated with estrogen for 10 days. Cardiac structure and function, angiogenesis, and fibrosis were assessed, and estrogen was measured in plasma and in heart. Cardiac estrogen concentrations (6.18±1.12 pg/160 mg heart in HF versus 17.79±1.28 pg/mL in control) and aromatase transcripts (0.19±0.04, normalized to control, P<0.05) were significantly reduced in HF. Estrogen therapy increased cardiac estrogen 3-fold and restored aromatase transcripts. Estrogen also rescued HF by restoring ejection fraction to 53.1±1.3% (P<0.001) and improving cardiac hemodynamics both in male and female mice. Estrogen therapy stimulated angiogenesis as capillary density increased from 0.66±0.07 in HF to 2.83±0.14 (P<0.001, normalized to control) and reversed the fibrotic scarring observed in HF (45.5±2.8% in HF versus 5.3±1.0%, P<0.001). Stimulation of angiogenesis by estrogen seems to be one of the key mechanisms, since in the presence of an angiogenesis inhibitor estrogen failed to rescue HF (ejection fraction=29.3±2.1%, P<0.001 versus E2).ConclusionsEstrogen rescues pre-existing HF by restoring cardiac estrogen and aromatase, stimulating angiogenesis, and suppressing fibrosis