Covariant quantization of infinite spin particle models, and higher order gauge theories

Further properties of a recently proposed higher order infinite spin particle model are derived. Infinitely many classically equivalent but different Hamiltonian formulations are shown to exist. This leads to a condition of uniqueness in the quantization process. A consistent covariant quantization is shown to exist. Also a recently proposed supersymmetric version for half-odd integer spins is quantized. A general algorithm to derive gauge invariances of higher order Lagrangians is given and applied to the infinite spin particle model, and to a new higher order model for a spinning particle which is proposed here, as well as to a previously given higher order rigid particle model. The latter two models are also covariantly quantized.Comment: 38 pages, Late

Effects of Practice on Competency In Single-Rescuer Cardiopulmonary Resuscitation

This study demonstrated the effectiveness of brief practice on voice advisory manikins in improving skill retention by nursing students in single-rescuer cardiopulmonary resuscitation (CPR). Brief practice can assist nurses and other providers in maintaining their CPR skills and may lead to improved performance competency

Infinite spin particles

We show that Wigner's infinite spin particle classically is described by a reparametrization invariant higher order geometrical Lagrangian. The model exhibit unconventional features like tachyonic behaviour and momenta proportional to light-like accelerations. A simple higher order superversion for half-odd integer particles is also derived. Interaction with external vector fields and curved spacetimes are analyzed with negative results except for (anti)de Sitter spacetimes. We quantize the free theories covariantly and show that the resulting wave functions are fields containing arbitrary large spins. Closely related infinite spin particle models are also analyzed.Comment: 43 pages, Late

A Strategy For Identifying Putative Causes Of Gene Expression Variation In Human Cancer

There is often a need to predict the impact of alterations in one variable on another variable. This is especially the case in cancer research, where much effort has been made to carry out large-scale gene expression screening by microarray techniques. However, the causes of this variability from one cancer to another and from one gene to another often remain unknown. In this study we present a systematic procedure for finding genes whose expression is altered by an intrinsic or extrinsic explanatory phenomenon. The procedure has three stages: preprocessing, data integration and statistical analysis. We tested and verified the utility of this approach in a study, where expression and copy number of 13,824 genes were determined in 14 breast cancer samples. The expression of 270 genes could be explained by the variability of gene copy number. These genes may represent an important set of primary, genetically "damaged" genes that drive cancer progression

Topological Field Theories and Geometry of Batalin-Vilkovisky Algebras

The algebraic and geometric structures of deformations are analyzed concerning topological field theories of Schwarz type by means of the Batalin-Vilkovisky formalism. Deformations of the Chern-Simons-BF theory in three dimensions induces the Courant algebroid structure on the target space as a sigma model. Deformations of BF theories in $n$ dimensions are also analyzed. Two dimensional deformed BF theory induces the Poisson structure and three dimensional deformed BF theory induces the Courant algebroid structure on the target space as a sigma model. The deformations of BF theories in $n$ dimensions induce the structures of Batalin-Vilkovisky algebras on the target space.Comment: 25 page

Intracerebral Hemorrhage among Blood Donors and Their Transfusion Recipients

Importance: Recent reports have suggested that cerebral amyloid angiopathy, a common cause of multiple spontaneous intracerebral hemorrhages (ICHs), may be transmissible through parenteral injection of contaminated cadaveric pituitary hormone in humans. Objective: To determine whether spontaneous ICH in blood donors after blood donation is associated with development of spontaneous ICH in transfusion recipients. Design, Setting, and Participants: Exploratory retrospective cohort study using nationwide blood bank and health register data from Sweden (main cohort) and Denmark (validation cohort) and including all 1089370 patients aged 5 to 80 years recorded to have received a red blood cell transfusion from January 1, 1970 (Sweden), or January 1, 1980 (Denmark), until December 31, 2017. Exposures: Receipt of red blood cell transfusions from blood donors who subsequently developed (1) a single spontaneous ICH, (2) multiple spontaneous ICHs, or (3) no spontaneous ICH. Main Outcomes and Measures: Spontaneous ICH in transfusion recipients; ischemic stroke was a negative control outcome. Results: A total of 759858 patients from Sweden (median age, 65 [IQR, 48-73] years; 59% female) and 329512 from Denmark (median age, 64 [IQR, 50-73] years; 58% female) were included, with a median follow-up of 5.8 (IQR, 1.4-12.5) years and 6.1 (IQR, 1.5-11.6) years, respectively. Patients who underwent transfusion with red blood cell units from donors who developed multiple spontaneous ICHs had a significantly higher risk of a single spontaneous ICH themselves, compared with patients receiving transfusions from donors who did not develop spontaneous ICH, in both the Swedish cohort (unadjusted incidence rate [IR], 3.16 vs 1.12 per 1000 person-years; adjusted hazard ratio [HR], 2.73; 95% CI, 1.72-4.35; P <.001) and the Danish cohort (unadjusted IR, 2.82 vs 1.09 per 1000 person-years; adjusted HR, 2.32; 95% CI, 1.04-5.19; P =.04). No significant difference was found for patients receiving transfusions from donors who developed a single spontaneous ICH in the Swedish cohort (unadjusted IR, 1.35 vs 1.12 per 1000 person-years; adjusted HR, 1.06; 95% CI, 0.84-1.36; P =.62) nor the Danish cohort (unadjusted IR, 1.36 vs 1.09 per 1000 person-years; adjusted HR, 1.06; 95% CI, 0.70-1.60; P =.73), nor for ischemic stroke as a negative control outcome. Conclusions and Relevance: In an exploratory analysis of patients who received red blood cell transfusions, patients who underwent transfusion with red blood cells from donors who later developed multiple spontaneous ICHs were at significantly increased risk of spontaneous ICH themselves. This may suggest a transfusion-transmissible agent associated with some types of spontaneous ICH, although the findings may be susceptible to selection bias and residual confounding, and further research is needed to investigate if transfusion transmission of cerebral amyloid angiopathy might explain this association.

Estimating heritability and genetic correlations from large health datasets in the absence of genetic data

Typically, estimating genetic parameters, such as disease heritability and between-disease genetic correlations, demands large datasets containing all relevant phenotypic measures and detailed knowledge of family relationships or, alternatively, genotypic and phenotypic data for numerous unrelated individuals. Here, we suggest an alternative, efficient estimation approach through the construction of two disease metrics from large health datasets: temporal disease prevalence curves and low-dimensional disease embeddings. We present eleven thousand heritability estimates corresponding to five study types: twins, traditional family studies, health records-based family studies, single nucleotide polymorphisms, and polygenic risk scores. We also compute over six hundred thousand estimates of genetic, environmental and phenotypic correlations. Furthermore, we find that: (1) disease curve shapes cluster into five general patterns; (2) early-onset diseases tend to have lower prevalence than late-onset diseases (Spearmans rho = 0.32, p amp;lt; 10(-16)); and (3) the disease onset age and heritability are negatively correlated (rho = -0.46, p amp;lt; 10(-16)).Funding Agencies|DARPA Big Mechanism program under ARO [W911NF1410333]; National Institutes of HealthUnited States Department of Health &amp; Human ServicesNational Institutes of Health (NIH) - USA [R01HL122712, 1P50MH094267, U01HL108634-01]; King Abdullah University of Science and Technology (KAUST)King Abdullah University of Science &amp; Technology [FCC/1/1976-18-01, FCC/1/1976-23-01, FCC/1/1976-25-01, FCC/1/1976-26-01, FCS/1/4102-02-01]</p

Estimating heritability and genetic correlations from large health datasets in the absence of genetic data.

Typically, estimating genetic parameters, such as disease heritability and between-disease genetic correlations, demands large datasets containing all relevant phenotypic measures and detailed knowledge of family relationships or, alternatively, genotypic and phenotypic data for numerous unrelated individuals. Here, we suggest an alternative, efficient estimation approach through the construction of two disease metrics from large health datasets: temporal disease prevalence curves and low-dimensional disease embeddings. We present eleven thousand heritability estimates corresponding to five study types: twins, traditional family studies, health records-based family studies, single nucleotide polymorphisms, and polygenic risk scores. We also compute over six hundred thousand estimates of genetic, environmental and phenotypic correlations. Furthermore, we find that: (1) disease curve shapes cluster into five general patterns; (2) early-onset diseases tend to have lower prevalence than late-onset diseases (Spearman\u27s ρ = 0.32, p \u3c 1