1,471 research outputs found
Is Schr\"{o}dinger's Conjecture for the Hydrogen Atom Coherent States Attainable
We construct the most general SO(4,2) hydrogen atom coherent states which are
the counterpart of Schr\"{o}dinger's harmonic oscillator coherent states. We
show that these states cannot be localized and cannot follow the classical
orbits. Thus, Schr\"{o}dinger's conjecture for the hydrogen atom coherent
states is unattainable.Comment: 10 pages, report
Complete genome sequences of 15 chikungunya virus isolates from Puerto Rico
Here, we report the complete genome sequences of 15 chikungunya virus strains isolated from human plasma from infected patients in Puerto Rico. The results show that currently circulating chikungunya strains in Puerto Rico are closely related
Willing and able: action-state orientation and the relation between procedural justice and employee cooperation
Existing justice theory explains why fair procedures motivate employees to adopt cooperative goals, but it fails to explain how employees strive towards these goals. We study self-regulatory abilities that underlie goal striving; abilities that should thus affect employees’ display of cooperative behavior in response to procedural justice. Building on action control theory, we argue that employees who display effective self-regulatory strategies (action oriented employees) display relatively strong cooperative behavioral responses to fair procedures. A multisource field study and a laboratory experiment support this prediction. A subsequent experiment addresses the process underlying this effect by explicitly showing that action orientation facilitates attainment of the cooperative goals that people adopt in response to fair procedures, thus facilitating the display of actual cooperative behavior. This goal striving approach better integrates research on the relationship between procedural justice and employee cooperation in the self-regulation and the work motivation literature. It also offers organizations a new perspective on making procedural justice effective in stimulating employee cooperation by suggesting factors that help employees reach their adopted goals
Non-steroidal anti-inflammatory drug use, hormone receptor status, and breast cancer-specific mortality in the Carolina Breast Cancer Study
Epidemiologic studies report a protective association between non-steroidal anti-inflammatory drug (NSAID) use and hormone receptor-positive breast cancer risk, a finding consistent with NSAID-mediated suppression of aromatase-driven estrogen biosynthesis. However, the association between NSAID use and breast cancer-specific mortality is uncertain and it is unknown whether this relationship differs by hormone receptor status. This study comprised 935 invasive breast cancer cases, of which 490 were estrogen receptor (ER)-positive, enrolled between 1996 and 2001 in the Carolina Breast Cancer Study. Self-reported NSAID use in the decade prior to diagnosis was categorized by duration and regularity of use. Differences in tumor size, stage, node, and receptor status by NSAID use were examined using Chi-square tests. Associations between NSAID use and breast cancer-specific mortality were examined using age- and race-adjusted Cox proportional hazards analysis. Tumor characteristics did not differ by NSAID use. Increased duration and regularity of NSAID use was associated with reduced breast cancer-specific mortality in women with ER-positive tumors (long-term regular use (≥8 days/month for ≥ 3 - years) versus no use; hazard ratio (HR) 0.48; 95 % confidence interval (CI) 0.23–0.98), with a statistically significant trend with increasing duration and regularity (p-trend = 0.036). There was no association for ER-negative cases (HR 1.19; 95 %CI 0.50–2.81; p-trend = 0.891). Long-term, regular NSAID use in the decade prior to breast cancer diagnosis was associated with reduced breast cancer-specific mortality in ER-positive cases. If confirmed, these findings support the hypothesis that potential chemopreventive properties of NSAIDs are mediated, at least in part, through suppression of estrogen biosynthesis
Ross Gyre variability modulates oceanic heat supply toward the West Antarctic continental shelf
C.J.P., G.A.M., M.R.M., L.D.T., and S.T.G. were supported by NSF PLR-1425989 and OPP-1936222 (Southern Ocean Carbon and Climate Observations and Modeling project). C.J.P. received additional support from a NOAA Climate & Global Change Postdoctoral Fellowship. G.A.M. received additional support from UKRI Grant Ref. MR/W013835/1. G.E.M. was supported by NSF OPP-2220969. R.Q.P. was supported by the High Meadows Environmental Institute Internship Program. R.M. was supported by the General Sir John Monash Foundation. A.F.T. was supported by NSF OPP-1644172 and NASA grant 80NSSC21K0916. M.R.M. also acknowledges funding from NSF awards OCE-1924388 and OPP-2319829 and NASA awards 80NSSC22K0387 and 80NSSC20K1076.West Antarctic Ice Sheet mass loss is a major source of uncertainty in sea level projections. The primary driver of this melting is oceanic heat from Circumpolar Deep Water originating offshore in the Antarctic Circumpolar Current. Yet, in assessing melt variability, open ocean processes have received considerably less attention than those governing cross-shelf exchange. Here, we use Lagrangian particle release experiments in an ocean model to investigate the pathways by which Circumpolar Deep Water moves toward the continental shelf across the Pacific sector of the Southern Ocean. We show that Ross Gyre expansion, linked to wind and sea ice variability, increases poleward heat transport along the gyre’s eastern limb and the relative fraction of transport toward the Amundsen Sea. Ross Gyre variability, therefore, influences oceanic heat supply toward the West Antarctic continental slope. Understanding remote controls on basal melt is necessary to predict the ice sheet response to anthropogenic forcing.Publisher PDFPeer reviewe
Development of the Pulmonary Vein and the Systemic Venous Sinus: An Interactive 3D Overview
Knowledge of the normal formation of the heart is crucial for the understanding of cardiac pathologies and congenital malformations. The understanding of early cardiac development, however, is complicated because it is inseparably associated with other developmental processes such as embryonic folding, formation of the coelomic cavity, and vascular development. Because of this, it is necessary to integrate morphological and experimental analyses. Morphological insights, however, are limited by the difficulty in communication of complex 3D-processes. Most controversies, in consequence, result from differences in interpretation, rather than observation. An example of such a continuing debate is the development of the pulmonary vein and the systemic venous sinus, or “sinus venosus”. To facilitate understanding, we present a 3D study of the developing venous pole in the chicken embryo, showing our results in a novel interactive fashion, which permits the reader to form an independent opinion. We clarify how the pulmonary vein separates from a greater vascular plexus within the splanchnic mesoderm. The systemic venous sinus, in contrast, develops at the junction between the splanchnic and somatic mesoderm. We discuss our model with respect to normal formation of the heart, congenital cardiac malformations, and the phylogeny of the venous tributaries
Reversing Blood Flows Act through klf2a to Ensure Normal Valvulogenesis in the Developing Heart
Heart valve anomalies are some of the most common congenital heart defects, yet neither the genetic nor the epigenetic forces guiding heart valve development are well understood. When functioning normally, mature heart valves prevent intracardiac retrograde blood flow; before valves develop, there is considerable regurgitation, resulting in reversing (or oscillatory) flows between the atrium and ventricle. As reversing flows are particularly strong stimuli to endothelial cells in culture, an attractive hypothesis is that heart valves form as a developmental response to retrograde blood flows through the maturing heart. Here, we exploit the relationship between oscillatory flow and heart rate to manipulate the amount of retrograde flow in the atrioventricular (AV) canal before and during valvulogenesis, and find that this leads to arrested valve growth. Using this manipulation, we determined that klf2a is normally expressed in the valve precursors in response to reversing flows, and is dramatically reduced by treatments that decrease such flows. Experimentally knocking down the expression of this shear-responsive gene with morpholine antisense oligonucleotides (MOs) results in dysfunctional valves. Thus, klf2a expression appears to be necessary for normal valve formation. This, together with its dependence on intracardiac hemodynamic forces, makes klf2a expression an early and reliable indicator of proper valve development. Together, these results demonstrate a critical role for reversing flows during valvulogenesis and show how relatively subtle perturbations of normal hemodynamic patterns can lead to both major alterations in gene expression and severe valve dysgenesis
More than a decade of developmental gene expression atlases: where are we now?
To unravel regulatory networks of genes functioning during embryonic development, information on in situ gene expression is required. Enormous amounts of such data are available in literature, where each paper reports on a limited number of genes and developmental stages. The best way to make these data accessible is via spatio-temporal gene expression atlases. Eleven atlases, describing developing vertebrates and covering at least 100 genes, were reviewed. This review focuses on: (i) the used anatomical framework, (ii) the handling of input data and (iii) the retrieval of information. Our aim is to provide insights into both the possibilities of the atlases, as well as to describe what more than a decade of developmental gene expression atlases can teach us about the requirements of the design of the ‘ideal atlas’. This review shows that most ingredients needed to develop the ideal atlas are already applied to some extent in at least one of the discussed atlases. A review of these atlases shows that the ideal atlas should be based on a spatial framework, i.e. a series of 3D reference models, which is anatomically annotated using an ontology with sufficient resolution, both for relations as well as for anatomical terms
Association between DNA Damage Response and Repair Genes and Risk of Invasive Serous Ovarian Cancer
BACKGROUND: We analyzed the association between 53 genes related to DNA repair and p53-mediated damage response and serous ovarian cancer risk using case-control data from the North Carolina Ovarian Cancer Study (NCOCS), a population-based, case-control study. METHODS/PRINCIPAL FINDINGS: The analysis was restricted to 364 invasive serous ovarian cancer cases and 761 controls of white, non-Hispanic race. Statistical analysis was two staged: a screen using marginal Bayes factors (BFs) for 484 SNPs and a modeling stage in which we calculated multivariate adjusted posterior probabilities of association for 77 SNPs that passed the screen. These probabilities were conditional on subject age at diagnosis/interview, batch, a DNA quality metric and genotypes of other SNPs and allowed for uncertainty in the genetic parameterizations of the SNPs and number of associated SNPs. Six SNPs had Bayes factors greater than 10 in favor of an association with invasive serous ovarian cancer. These included rs5762746 (median OR(odds ratio)(per allele) = 0.66; 95% credible interval (CI) = 0.44-1.00) and rs6005835 (median OR(per allele) = 0.69; 95% CI = 0.53-0.91) in CHEK2, rs2078486 (median OR(per allele) = 1.65; 95% CI = 1.21-2.25) and rs12951053 (median OR(per allele) = 1.65; 95% CI = 1.20-2.26) in TP53, rs411697 (median OR (rare homozygote) = 0.53; 95% CI = 0.35 - 0.79) in BACH1 and rs10131 (median OR( rare homozygote) = not estimable) in LIG4. The six most highly associated SNPs are either predicted to be functionally significant or are in LD with such a variant. The variants in TP53 were confirmed to be associated in a large follow-up study. CONCLUSIONS/SIGNIFICANCE: Based on our findings, further follow-up of the DNA repair and response pathways in a larger dataset is warranted to confirm these results
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