A microscopic model for a class of mixed-spin quantum antiferromagnets

We propose a microscopic model that describes the magnetic behavior of the mixed-spin quantum systems R$_2$BaNiO$_5$ (R= magnetic rare earth). An evaluation of the properties of this model by Quantum Monte Carlo simulations shows remarkable good agreement with the experimental data and provides new insight into the physics of mixed-spin quantum magnets.Comment: revised version to be published in Phys. Rev.

Signatures for Berezinskii Kosterlitz Thouless critical behavior in the planar antiferromagnet BaNi2V2O8

We investigate the critical properties of the spin 1 honeycomb antiferromagnet BaNi2V2O8, both below and above the ordering temperature TN using neutron diffraction and muon spin rotation measurements. Our results characterize BaNi2V2O8 as a two dimensional 2D antiferromagnet across the entire temperature range, displaying a series of crossovers from 2D Ising like to 2D XY and then to 2D Heisenberg behavior with increasing temperature. In particular, the extracted critical exponent of the order parameter reveals a narrow temperature regime close to TN , in which the system behaves as a 2D XY antiferromagnet. Above TN , evidence for Berezinsky Kosterlitz Thouless behavior driven by vortex excitations is obtained from the scaling of the correlation length. Our experimental results are in accord with classical and quantum Monte Carlo simulations performed for microscopic magnetic model Hamiltonians for BaNi2V2O

A Theory for High-TcT_c Superconductors Considering Inhomogeneous Charge Distribution

We propose a general theory for the critical $T_c$ and pseudogap $T^*$ temperature dependence on the doping concentration for high-$T_c$ oxides, taking into account the charge inhomogeneities in the $CuO_2$ planes. The well measured experimental inhomogeneous charge density in a given compound is assumed to produce a spatial distribution of local $\rho(r)$. These differences in the local charge concentration is assumed to yield insulator and metallic regions, possibly in a stripe morphology. In the metallic region, the inhomogeneous charge density yields also spatial distributions of superconducting critical temperatures $T_c(r)$ and zero temperature gap $\Delta_0(r)$. For a given sample, the measured onset of vanishing gap temperature is identified as the pseudogap temperature, that is, $T^*$, which is the maximum of all $T_c(r)$. Below $T^*$, due to the distribution of $T_c(r)$'s, there are some superconducting regions surrounded by insulator or metallic medium. The transition to a superconducting state corresponds to the percolation threshold among the superconducting regions with different $T_c(r)$'s. To model the charge inhomogeneities we use a double branched Poisson-Gaussian distribution. To make definite calculations and compare with the experimental results, we derive phase diagrams for the BSCO, LSCO and YBCO families, with a mean field theory for superconductivity using an extended Hubbard Hamiltonian. We show also that this novel approach provides new insights on several experimental features of high-$T_c$ oxides.Comment: 7 pages, 5 eps figures, corrected typo

Magnetic and electronic ordering phenomena in the Ru2O6 layer honeycomb lattice compound AgRuO3

The silver ruthenium oxide AgRuO3 consists of honeycomb Ru5 2O 6 layers and can be considered an analogue of SrRu2O6 with a different intercalation. We present measurements of magnetic susceptibility and specific heat on AgRuO3 single crystals, which reveal a sharp antiferromagnetic transition at 342 3 K. The electrical transport in single crystals of AgRuO3 is determined by a combination of activated conduction over an intrinsic semiconducting gap of almost equal to 100 meV and carriers trapped and thermally released from defects. From powder neutron diffraction data a N el type antiferromagnetic structure with the Ru moments along the c axis is derived. Raman spectroscopy on AgRuO3 single crystals and muon spin rotation spectroscopy on powder samples indicate a further weak phase transition or a crossover in the temperature range 125 200 K. The transition does not show up in the magnetic susceptibility, and its origin is argued to be related to defects but cannot be fully clarified. The experimental findings are complemented by density functional theory based electronic structure calculations. It is found that the magnetism in AgRuO3 is similar to that in SrRu2O6, however, with stronger intralayer and weaker interlayer magnetic exchange interaction

The qualitative transparency deliberations: insights and implications

In recent years, a variety of efforts have been made in political science to enable, encourage, or require scholars to be more open and explicit about the bases of their empirical claims and, in turn, make those claims more readily evaluable by others. While qualitative scholars have long taken an interest in making their research open, reflexive, and systematic, the recent push for overarching transparency norms and requirements has provoked serious concern within qualitative research communities and raised fundamental questions about the meaning, value, costs, and intellectual relevance of transparency for qualitative inquiry. In this Perspectives Reflection, we crystallize the central findings of a three-year deliberative process—the Qualitative Transparency Deliberations (QTD)—involving hundreds of political scientists in a broad discussion of these issues. Following an overview of the process and the key insights that emerged, we present summaries of the QTD Working Groups’ final reports. Drawing on a series of public, online conversations that unfolded at www.qualtd.net, the reports unpack transparency’s promise, practicalities, risks, and limitations in relation to different qualitative methodologies, forms of evidence, and research contexts. Taken as a whole, these reports—the full versions of which can be found in the Supplementary Materials—offer practical guidance to scholars designing and implementing qualitative research, and to editors, reviewers, and funders seeking to develop criteria of evaluation that are appropriate—as understood by relevant research communities—to the forms of inquiry being assessed. We dedicate this Reflection to the memory of our coauthor and QTD working group leader Kendra Koivu

Spatial, temporal, and demographic patterns in prevalence of smoking tobacco use and attributable disease burden in 204 countries and territories, 1990-2019 : a systematic analysis from the Global Burden of Disease Study 2019

Background Ending the global tobacco epidemic is a defining challenge in global health. Timely and comprehensive estimates of the prevalence of smoking tobacco use and attributable disease burden are needed to guide tobacco control efforts nationally and globally. Methods We estimated the prevalence of smoking tobacco use and attributable disease burden for 204 countries and territories, by age and sex, from 1990 to 2019 as part of the Global Burden of Diseases, Injuries, and Risk Factors Study. We modelled multiple smoking-related indicators from 3625 nationally representative surveys. We completed systematic reviews and did Bayesian meta-regressions for 36 causally linked health outcomes to estimate non-linear dose-response risk curves for current and former smokers. We used a direct estimation approach to estimate attributable burden, providing more comprehensive estimates of the health effects of smoking than previously available. Findings Globally in 2019, 1.14 billion (95% uncertainty interval 1.13-1.16) individuals were current smokers, who consumed 7.41 trillion (7.11-7.74) cigarette-equivalents of tobacco in 2019. Although prevalence of smoking had decreased significantly since 1990 among both males (27.5% [26. 5-28.5] reduction) and females (37.7% [35.4-39.9] reduction) aged 15 years and older, population growth has led to a significant increase in the total number of smokers from 0.99 billion (0.98-1.00) in 1990. Globally in 2019, smoking tobacco use accounted for 7.69 million (7.16-8.20) deaths and 200 million (185-214) disability-adjusted life-years, and was the leading risk factor for death among males (20.2% [19.3-21.1] of male deaths). 6.68 million [86.9%] of 7.69 million deaths attributable to smoking tobacco use were among current smokers. Interpretation In the absence of intervention, the annual toll of 7.69 million deaths and 200 million disability-adjusted life-years attributable to smoking will increase over the coming decades. Substantial progress in reducing the prevalence of smoking tobacco use has been observed in countries from all regions and at all stages of development, but a large implementation gap remains for tobacco control. Countries have a dear and urgent opportunity to pass strong, evidence-based policies to accelerate reductions in the prevalence of smoking and reap massive health benefits for their citizens. Copyright (C) 2021 The Author(s). Published by Elsevier Ltd.Peer reviewe

Comparative cellular analysis of motor cortex in human, marmoset and mouse

The primary motor cortex (M1) is essential for voluntary fine-motor control and is functionally conserved across mammals(1). Here, using high-throughput transcriptomic and epigenomic profiling of more than 450,000 single nuclei in humans, marmoset monkeys and mice, we demonstrate a broadly conserved cellular makeup of this region, with similarities that mirror evolutionary distance and are consistent between the transcriptome and epigenome. The core conserved molecular identities of neuronal and non-neuronal cell types allow us to generate a cross-species consensus classification of cell types, and to infer conserved properties of cell types across species. Despite the overall conservation, however, many species-dependent specializations are apparent, including differences in cell-type proportions, gene expression, DNA methylation and chromatin state. Few cell-type marker genes are conserved across species, revealing a short list of candidate genes and regulatory mechanisms that are responsible for conserved features of homologous cell types, such as the GABAergic chandelier cells. This consensus transcriptomic classification allows us to use patch-seq (a combination of whole-cell patch-clamp recordings, RNA sequencing and morphological characterization) to identify corticospinal Betz cells from layer 5 in non-human primates and humans, and to characterize their highly specialized physiology and anatomy. These findings highlight the robust molecular underpinnings of cell-type diversity in M1 across mammals, and point to the genes and regulatory pathways responsible for the functional identity of cell types and their species-specific adaptations.Cardiovascular Aspects of Radiolog

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease