Contact homology of toric contact manifolds of Reeb type

We use contact homology to distinguish contact structures on various manifolds. We are primarily interested in contact manifolds which admit an action of Reeb type of a compact Lie group. In such situations it is well known that the contact manifold is then a circle orbi-bundle over a symplectic orbifold. With some extra conditions we are able to compute an invariant, cylindrical contact homology, of the contact structure in terms of some orbifold data, and the first Chern class of the tangent bundle of the base space. When these manifolds are obtained by contact reduction, then the grading of contact homology is given in terms of the weights of the moment map. In many cases, we are able to show that certain distinct toric contact structures are also non-contactomorphic. We also use some more general invariants by imposing extra constraints on moduli spaces of holomorphic curves to distinguish other manifolds in dimension $5.

On the Equivalence Problem for Toric Contact Structures on S^3-bundles over S^2$

We study the contact equivalence problem for toric contact structures on $S^3$-bundles over $S^2$. That is, given two toric contact structures, one can ask the question: when are they equivalent as contact structures while inequivalent as toric contact structures? In general this appears to be a difficult problem. To find inequivalent toric contact structures that are contact equivalent, we show that the corresponding 3-tori belong to distinct conjugacy classes in the contactomorphism group. To show that two toric contact structures with the same first Chern class are contact inequivalent, we use Morse-Bott contact homology. We treat a subclass of contact structures which include the Sasaki-Einstein contact structures $Y^{p,q}$ studied by physicists. In this subcase we give a complete solution to the contact equivalence problem by showing that $Y^{p,q}$ and $Y^{p'q'}$ are inequivalent as contact structures if and only if $p\neq p'$.Comment: 61 page

Caractérisation de Trypanosoma sp chez les animaux domestiques dans quatre foyers de la partie Ouest de la République Démocratique du Congo (RDC)

En vue d’identifier les trypanosomes circulants chez les animaux domestiques de Kinshasa, Mbanza-Ngungu, Masi-Manimba et Mushie et d’en déterminer les prévalences par PCR, une étude longitudinale a été menée. 1653 échantillons sanguins ont été prélevés chez les animaux domestiques dans les foyers de Kinshasa, Mbanza-Ngungu, Masi-Manimba et Mushie, dont 22 cas ont été positif au Trypanosoma congolense Forest, correspondant à une prévalence brute de 1,3%. Pour ce qui est des foyers, Kinshasa a eu une prévalence de 2,5%, Mbanza-Ngungu une prévalence de 2,4%, Masi-Manimba sans aucune prévalence et Mushie une prévalence de 1,3%. En rapport avec les saisons, la saison de pluie a eu une prévalence de 1,4%, alors que la saison sèche en a eu 1,3%. Concernant les espèces, les bovins ont eu une prévalence de 0,9%, les porcins une prévalence de 3,7%, les ovins une prévalence de 1,4% et les caprins une prévalence de 0,7%. Quant au sexe, les mâles ont eu une prévalence de 0,9%, alors que les femelles en ont eu 1,5%. Cette étude a montré que la Trypanosomiase Animale Africaine (TAA) serait en recul chez les animaux de ces quatre foyers. Ainsi, les cliniciens sur terrain devraient réorienter leur stratégie thérapeutique, en intégrant cette nouvelle donne. Mots clés: Trypanosoma sp, Animaux domestiques, Ouest RDCIn order to identify circulating trypanosomes in Kinshasa, Mbanza Ngungu, Masi Manimba and Mushie domestic animals and to determine their prevalence by PCR, a longitudinal study was conducted. 1653 blood samples were collected from domestic animals in the Kinshasa, Mbanza Ngungu, Masi Manimba and Mushie households, of which 22 were positive for Trypanosoma congolense Forest, corresponding to a gross prevalence of 1.3%. As for households, Kinshasa had a prevalence of 2.5%, Mbanza Ngungu a prevalence of 2.4%, Masi Manimba without any prevalence and Mushie a prevalence of 1.3%. In relation to the seasons, the rainy season had a prevalence of 1.4% while the dry season had a prevalence of 1.3%. Regarding species, cattle had a prevalence of 0.9%, pigs a prevalence of 3.7%, sheep a prevalence of 1.4% and goats a prevalence of 0.7%. As for sex, males had a prevalence of 0.9% while females had a prevalence of 1.5%. This study showed that African Animal Trypanosomiasis (AAT) is declining among animals in these four locations Thus, clinicians in the field should take into account this new situation in their therapeutic strategy. Keywords: Trypanosoma sp, Domestic animals, West DR

Effect of symmetry breaking perturbations in the one-dimensional SU(4) spin-orbital model

We study the effect of symmetry breaking perturbations in the one-dimensional SU(4) spin-orbital model. We allow the exchange in spin ($J_1$) and orbital ($J_2$) channel to be different and thus reduce the symmetry to SU(2) $\otimes$ SU(2). A magnetic field $h$ along the $S^z$ direction is also applied. Using the formalism developped by Azaria et al we extend their analysis of the isotropic $J_1=J_2$, h=0 case and obtain the low-energy effective theory near the SU(4) point in the asymmetric case. An accurate analysis of the renormalization group flow is presented with a particular emphasis on the effect of the anisotropy. In zero magnetic field, we retrieve the same qualitative low-energy physics than in the isotropic case. In particular, the massless behavior found on the line $J_1=J_2>K/4$ extends in a large anisotropic region. We discover though that the anisotropy plays its trick in allowing non trivial scaling behaviors of the physical quantities. When a magnetic field is present the effect of the anisotropy is striking. In addition to the usual commensurate-incommensurate phase transition that occurs in the spin sector of the theory, we find that the field may induce a second transition of the KT type in the remaining degrees of freedom to which it does not couple directly. In this sector, we find that the effective theory is that of an SO(4) Gross-Neveu model with an h-dependent coupling that may change its sign as h varies.Comment: 14 pages, 5 Figs, added referenc

Form factors of integrable Heisenberg (higher) spin chains

We present determinant formulae for the form factors of spin operators of general integrable XXX Heisenberg spin chains for arbitrary (finite dimensional) spin representations. The results apply to any "mixed" spin chains, such as alternating spin chains, or to spin chains with magnetic impurities.Comment: 24 page

Multiple novel prostate cancer susceptibility signals identified by fine-mapping of known risk loci among Europeans

Genome-wide association studies (GWAS) have identified numerous common prostate cancer (PrCa) susceptibility loci. We have fine-mapped 64 GWAS regions known at the conclusion of the iCOGS study using large-scale genotyping and imputation in 25 723 PrCa cases and 26 274 controls of European ancestry. We detected evidence for multiple independent signals at 16 regions, 12 of which contained additional newly identified significant associations. A single signal comprising a spectrum of correlated variation was observed at 39 regions; 35 of which are now described by a novel more significantly associated lead SNP, while the originally reported variant remained as the lead SNP only in 4 regions. We also confirmed two association signals in Europeans that had been previously reported only in East-Asian GWAS. Based on statistical evidence and linkage disequilibrium (LD) structure, we have curated and narrowed down the list of the most likely candidate causal variants for each region. Functional annotation using data from ENCODE filtered for PrCa cell lines and eQTL analysis demonstrated significant enrichment for overlap with bio-features within this set. By incorporating the novel risk variants identified here alongside the refined data for existing association signals, we estimate that these loci now explain ∼38.9% of the familial relative risk of PrCa, an 8.9% improvement over the previously reported GWAS tag SNPs. This suggests that a significant fraction of the heritability of PrCa may have been hidden during the discovery phase of GWAS, in particular due to the presence of multiple independent signals within the same regio

The development and validation of a scoring tool to predict the operative duration of elective laparoscopic cholecystectomy

Background: The ability to accurately predict operative duration has the potential to optimise theatre efficiency and utilisation, thus reducing costs and increasing staff and patient satisfaction. With laparoscopic cholecystectomy being one of the most commonly performed procedures worldwide, a tool to predict operative duration could be extremely beneficial to healthcare organisations. Methods: Data collected from the CholeS study on patients undergoing cholecystectomy in UK and Irish hospitals between 04/2014 and 05/2014 were used to study operative duration. A multivariable binary logistic regression model was produced in order to identify significant independent predictors of long (> 90 min) operations. The resulting model was converted to a risk score, which was subsequently validated on second cohort of patients using ROC curves. Results: After exclusions, data were available for 7227 patients in the derivation (CholeS) cohort. The median operative duration was 60 min (interquartile range 45–85), with 17.7% of operations lasting longer than 90 min. Ten factors were found to be significant independent predictors of operative durations > 90 min, including ASA, age, previous surgical admissions, BMI, gallbladder wall thickness and CBD diameter. A risk score was then produced from these factors, and applied to a cohort of 2405 patients from a tertiary centre for external validation. This returned an area under the ROC curve of 0.708 (SE = 0.013, p  90 min increasing more than eightfold from 5.1 to 41.8% in the extremes of the score. Conclusion: The scoring tool produced in this study was found to be significantly predictive of long operative durations on validation in an external cohort. As such, the tool may have the potential to enable organisations to better organise theatre lists and deliver greater efficiencies in care

Global injury morbidity and mortality from 1990 to 2017 : results from the Global Burden of Disease Study 2017

Correction:Background Past research in population health trends has shown that injuries form a substantial burden of population health loss. Regular updates to injury burden assessments are critical. We report Global Burden of Disease (GBD) 2017 Study estimates on morbidity and mortality for all injuries. Methods We reviewed results for injuries from the GBD 2017 study. GBD 2017 measured injury-specific mortality and years of life lost (YLLs) using the Cause of Death Ensemble model. To measure non-fatal injuries, GBD 2017 modelled injury-specific incidence and converted this to prevalence and years lived with disability (YLDs). YLLs and YLDs were summed to calculate disability-adjusted life years (DALYs). Findings In 1990, there were 4 260 493 (4 085 700 to 4 396 138) injury deaths, which increased to 4 484 722 (4 332 010 to 4 585 554) deaths in 2017, while age-standardised mortality decreased from 1079 (1073 to 1086) to 738 (730 to 745) per 100 000. In 1990, there were 354 064 302 (95% uncertainty interval: 338 174 876 to 371 610 802) new cases of injury globally, which increased to 520 710 288 (493 430 247 to 547 988 635) new cases in 2017. During this time, age-standardised incidence decreased non-significantly from 6824 (6534 to 7147) to 6763 (6412 to 7118) per 100 000. Between 1990 and 2017, age-standardised DALYs decreased from 4947 (4655 to 5233) per 100 000 to 3267 (3058 to 3505). Interpretation Injuries are an important cause of health loss globally, though mortality has declined between 1990 and 2017. Future research in injury burden should focus on prevention in high-burden populations, improving data collection and ensuring access to medical care.Peer reviewe

Global, regional, and national age-sex-specific mortality for 282 causes of death in 195 countries and territories, 1980-2017 : a systematic analysis for the Global Burden of Disease Study 2017

Background Global development goals increasingly rely on country-specific estimates for benchmarking a nation's progress. To meet this need, the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2016 estimated global, regional, national, and, for selected locations, subnational cause-specific mortality beginning in the year 1980. Here we report an update to that study, making use of newly available data and improved methods. GBD 2017 provides a comprehensive assessment of cause-specific mortality for 282 causes in 195 countries and territories from 1980 to 2017. Methods The causes of death database is composed of vital registration (VR), verbal autopsy (VA), registry, survey, police, and surveillance data. GBD 2017 added ten VA studies, 127 country-years of VR data, 502 cancer-registry country-years, and an additional surveillance country-year. Expansions of the GBD cause of death hierarchy resulted in 18 additional causes estimated for GBD 2017. Newly available data led to subnational estimates for five additional countries Ethiopia, Iran, New Zealand, Norway, and Russia. Deaths assigned International Classification of Diseases (ICD) codes for non-specific, implausible, or intermediate causes of death were reassigned to underlying causes by redistribution algorithms that were incorporated into uncertainty estimation. We used statistical modelling tools developed for GBD, including the Cause of Death Ensemble model (CODErn), to generate cause fractions and cause specific death rates for each location, year, age, and sex. Instead of using UN estimates as in previous versions, GBD 2017 independently estimated population size and fertility rate for all locations. Years of life lost (YLLs) were then calculated as the sum of each death multiplied by the standard life expectancy at each age. All rates reported here are age-standardised. Findings At the broadest grouping of causes of death (Level 1), non-communicable diseases (NC Ds) comprised the greatest fraction of deaths, contributing to 73.4% (95% uncertainty interval [UI] 72.5-74.1) of total deaths in 2017, while communicable, maternal, neonatal, and nutritional (CMNN) causes accounted for 186% (17.9-19.6), and injuries 8.0% (7.7-8.2). Total numbers of deaths from NCD causes increased from 2007 to 2017 by 22.7% (21.5-23.9), representing an additional 7.61 million (7. 20-8.01) deaths estimated in 2017 versus 2007. The death rate from NCDs decreased globally by 7.9% (7.08.8). The number of deaths for CMNN causes decreased by 222% (20.0-24.0) and the death rate by 31.8% (30.1-33.3). Total deaths from injuries increased by 2.3% (0-5-4-0) between 2007 and 2017, and the death rate from injuries decreased by 13.7% (12.2-15.1) to 57.9 deaths (55.9-59.2) per 100 000 in 2017. Deaths from substance use disorders also increased, rising from 284 000 deaths (268 000-289 000) globally in 2007 to 352 000 (334 000-363 000) in 2017. Between 2007 and 2017, total deaths from conflict and terrorism increased by 118.0% (88.8-148.6). A greater reduction in total deaths and death rates was observed for some CMNN causes among children younger than 5 years than for older adults, such as a 36.4% (32.2-40.6) reduction in deaths from lower respiratory infections for children younger than 5 years compared with a 33.6% (31.2-36.1) increase in adults older than 70 years. Globally, the number of deaths was greater for men than for women at most ages in 2017, except at ages older than 85 years. Trends in global YLLs reflect an epidemiological transition, with decreases in total YLLs from enteric infections, respirator}, infections and tuberculosis, and maternal and neonatal disorders between 1990 and 2017; these were generally greater in magnitude at the lowest levels of the Socio-demographic Index (SDI). At the same time, there were large increases in YLLs from neoplasms and cardiovascular diseases. YLL rates decreased across the five leading Level 2 causes in all SDI quintiles. The leading causes of YLLs in 1990 neonatal disorders, lower respiratory infections, and diarrhoeal diseases were ranked second, fourth, and fifth, in 2017. Meanwhile, estimated YLLs increased for ischaemic heart disease (ranked first in 2017) and stroke (ranked third), even though YLL rates decreased. Population growth contributed to increased total deaths across the 20 leading Level 2 causes of mortality between 2007 and 2017. Decreases in the cause-specific mortality rate reduced the effect of population growth for all but three causes: substance use disorders, neurological disorders, and skin and subcutaneous diseases. Interpretation Improvements in global health have been unevenly distributed among populations. Deaths due to injuries, substance use disorders, armed conflict and terrorism, neoplasms, and cardiovascular disease are expanding threats to global health. For causes of death such as lower respiratory and enteric infections, more rapid progress occurred for children than for the oldest adults, and there is continuing disparity in mortality rates by sex across age groups. Reductions in the death rate of some common diseases are themselves slowing or have ceased, primarily for NCDs, and the death rate for selected causes has increased in the past decade. Copyright (C) 2018 The Author(s). Published by Elsevier Ltd.Peer reviewe