New Magnetic Anomaly Map of the Antarctic

The second generation Antarctic magnetic anomaly compilation for the region south of 60 degrees S includes some 3.5 million line-km of aeromagnetic and marine magnetic data that more than doubles the initial map's near-surface database. For the new compilation, the magnetic data sets were corrected for the International Geomagnetic Reference Field, diurnal effects, and high-frequency errors and leveled, gridded, and stitched together. The new magnetic data further constrain the crustal architecture and geological evolution of the Antarctic Peninsula and the West Antarctic Rift System in West Antarctica, as well as Dronning Maud Land, the Gamburtsev Subglacial Mountains, the Prince Charles Mountains, Princess Elizabeth Land, and Wilkes Land in East Antarctica and the circumjacent oceanic margins. Overall, the magnetic anomaly compilation helps unify disparate regional geologic and geophysical studies by providing new constraints on major tectonic and magmatic processes that affected the Antarctic from Precambrian to Cenozoic times.Korea Polar Research Institute (KOPRI) programs, PM15040 and PE17050Germany's AWI/Helmholtz Center for Polar and Marine ResearchFederal Institute for Geosciences and Natural ResourcesBritish Antarctic Survey/Natural Environmental Research CouncilItalian Antarctic Research ProgrammeRussian Ministry of Natural ResourcesU.S. National Science Foundation and National Space and Aeronautics AdministrationAustralian Antarctic Division and Antarctic Climate & Ecosystem Cooperative Research CentreFrench Polar InstituteGlobal geomagnetic observatories network (INTERMAGNET

Single-cell analysis shows that adipose tissue of persons with both HIV and diabetes is enriched for clonal, cytotoxic, and CMV-specific CD4+ T cells

Persons with HIV are at increased risk for diabetes mellitus compared with individuals without HIV. Adipose tissue is an important regulator of glucose and lipid metabolism, and adipose tissue T cells modulate local inflammatory responses and, by extension, adipocyte function. Persons with HIV and diabetes have a high proportion of CX3CR1+ GPR56+ CD57+ (C-G-C+) CD4+ T cells in adipose tissue, a subset of which are cytomegalovirus specific, whereas individuals with diabetes but without HIV have predominantly CD69+ CD4+ T cells. Adipose tissue CD69+ and C-G-C+ CD4+ T cell subsets demonstrate higher receptor clonality compared with the same cells in blood, potentially reflecting antigen-driven expansion, but C-G-C+ CD4+ T cells have a more inflammatory and cytotoxic RNA transcriptome. Future studies will explore whether viral antigens have a role in recruitment and proliferation of pro-inflammatory C-G-C+ CD4+ T cells in adipose tissue of persons with HIV

Quasielastic axial-vector mass from experiments on neutrino-nucleus scattering

We analyze available experimental data on the total and differential charged-current cross sections for quasielastic neutrino and antineutrino scattering off nucleons, measured with a variety of nuclear targets in the accelerator experiments at ANL, BNL, FNAL, CERN, and IHEP, dating from the end of sixties to the present day. The data are used to adjust the poorly known value of the axial-vector mass of the nucleon.Comment: 27 pages, 19 figures. Typos corrected; tables, figures and references added, discussion extended; matches published versio

Plane-wave impulse approximation extraction of the neutron magnetic form factor from quasielastic 3He(e,e′) at Q2=0.3 to 0.6 (GeV/c)2

A high precision measurement of the transverse spin-dependent asymmetry AT′ in 3He(e,e′) quasielastic scattering was performed in Hall A at Jefferson Lab at values of the squared four-momentum transfer, Q2, between 0.1 and 0.6 (GeV/c)2. AT′ is sensitive to the neutron magnetic form factor, GMn. Values of GMn at Q2=0.1 and 0.2 (GeV/c)2, extracted using Faddeev calculations, were reported previously. Here, we report the extraction of GMn for the remaining Q2 values in the range from 0.3 to 0.6 (GeV/c)2 using a plane-wave impulse approximation calculation. The results are in good agreement with recent precision data from experiments using a deuterium target

Plane-wave impulse approximation extraction of the neutron magnetic form factor from quasielastic 3He(e,e′) at Q2=0.3 to 0.6 (GeV/c)2

A high precision measurement of the transverse spin-dependent asymmetry AT′ in 3He(e,e′) quasielastic scattering was performed in Hall A at Jefferson Lab at values of the squared four-momentum transfer, Q2, between 0.1 and 0.6 (GeV/c)2. AT′ is sensitive to the neutron magnetic form factor, GMn. Values of GMn at Q2=0.1 and 0.2 (GeV/c)2, extracted using Faddeev calculations, were reported previously. Here, we report the extraction of GMn for the remaining Q2 values in the range from 0.3 to 0.6 (GeV/c)2 using a plane-wave impulse approximation calculation. The results are in good agreement with recent precision data from experiments using a deuterium target

In Vitro Identification of Novel Plasminogen-Binding Receptors of the Pathogen Leptospira interrogans

Background: Leptospirosis is a multisystem disease caused by pathogenic strains of the genus Leptospira. We have reported that Leptospira are able to bind plasminogen (PLG), to generate active plasmin in the presence of activator, and to degrade purified extracellular matrix fibronectin. Methodology/Principal Findings: We have now cloned, expressed and purified 14 leptospiral recombinant proteins. The proteins were confirmed to be surface exposed by immunofluorescence microscopy and were evaluated for their ability to bind plasminogen (PLG). We identified eight as PLG-binding proteins, including the major outer membrane protein LipL32, the previously published rLIC12730, rLIC10494, Lp29, Lp49, LipL40 and MPL36, and one novel leptospiral protein, rLIC12238. Bound PLG could be converted to plasmin by the addition of urokinase-type PLG activator (uPA), showing specific proteolytic activity, as assessed by its reaction with the chromogenic plasmin substrate, D-Val-Leu-Lys 4-nitroanilide dihydrochloride. The addition of the lysine analog 6-aminocaproic acid (ACA) inhibited the protein-PLG interaction, thus strongly suggesting the involvement of lysine residues in plasminogen binding. The binding of leptospiral surface proteins to PLG was specific, dose-dependent and saturable. PLG and collagen type IV competed with LipL32 protein for the same binding site, whereas separate binding sites were observed for plasma fibronectin. Conclusions/Significance: PLG-binding/activation through the proteins/receptors on the surface of Leptospira could help the bacteria to specifically overcome tissue barriers, facilitating its spread throughout the host.FAPESP (Fundacao de Amparo a Pesquisa do Estado de Sao Paulo)CNPq (Conselho Nacional de Desenvolvimento Cientifico e Tecnologico)Fundacao Butantan, BrazilFAPESP (Brazil

Extraction of the Neutron Magnetic Form Factor from Quasi-Elastic 3He(pol)(e(pol),e') at Q^2 = 0.1 - 0.6 (GeV/c)^2

We have measured the spin-dependent transverse asymmetry, A_T', in quasi-elastic inclusive electron scattering from polarized 3He with high precision at Q^2 = 0.1 to 0.6 (GeV/c)^2. The neutron magnetic form factor, GMn, was extracted at Q^2 = 0.1 and 0.2 (GeV/c)^2 using a non-relativistic Faddeev calculation that includes both final-state interactions (FSI) and meson-exchange currents (MEC). In addition, GMn was extracted at Q^2 = 0.3 to 0.6 (GeV/c)^2 using a Plane Wave Impulse Approximation calculation. The accuracy of the modeling of FSI and MEC effects was tested and confirmed with a precision measurement of the spin-dependent asymmetry in the breakup threshold region of the 3He(pol)(e(pol),e') reaction. The total relative uncertainty of the extracted GMn data is approximately 3%. Close agreement was found with other recent high-precision GMn data in this Q^2 range.Comment: Archival paper, 17 pages, 10 figures, 5 tables, submitted to Physical Review C. v2: shortened considerably, updated comparison to theor

Stress testing and non-invasive coronary angiography in patients with suspected coronary artery disease: time for a new paradigm

Diagnosis and management of coronary artery disease represents major challenges to our health care system, affecting millions of patients each year. Until recently, the diagnosis of coronary artery disease was possible only through cardiac catheterization and invasive coronary angiography. To avoid the risks of an invasive procedure, stress testing is often employed for an initial assessment of patients with suspected coronary artery disease, serving as a gatekeeper for cardiac catheterization. With the emergence of non-invasive coronary angiography, the question arises if such a strategy is still sensible, particularly, in view of only a modest agreement between stress testing results and the presence of coronary artery disease established by cardiac catheterization. Much data in support of the diagnostic accuracy and prognostic value of non-invasive coronary angiography by computed tomography have emerged within the last few years. These data challenge the role of stress testing as the initial imaging modality in patients with suspected coronary artery disease. This article reviews the clinical utility, limitations, as well as the hazards of stress testing compared with non-invasive coronary artery imaging by computed tomography. Finally, the implications of this review are discussed in relation to clinical practice

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