Magnetic structures of Mn3-xFexSn2: an experimental and theoretical study

We investigate the magnetic structure of Mn3-xFexSn2 using neutron powder diffraction experiments and electronic structure calculations. These alloys crystallize in the orthorhombic Ni3Sn2 type of structure (Pnma) and comprise two inequivalent sites for the transition metal atoms (4c and 8d) and two Sn sites (4c and 4c). The neutron data show that the substituting Fe atoms predominantly occupy the 4c transition metal site and carry a lower magnetic moment than Mn atoms. Four kinds of magnetic structures are encountered as a function of temperature and composition: two simple ferromagnetic structures (with the magnetic moments pointing along the b or c axis) and two canted ferromagnetic arrangements (with the ferromagnetic component pointing along the b or c axis). Electronic structure calculations results agree well with the low-temperature experimental magnetic moments and canting angles throughout the series. Comparisons between collinear and non-collinear computations show that the canted state is stabilized by a band mechanism through the opening of a hybridization gap. Synchrotron powder diffraction experiments on Mn3Sn2 reveal a weak monoclinic distortion at low temperature (90.08 deg at 175 K). This lowering of symmetry could explain the stabilization of the c-axis canted ferromagnetic structure, which mixes two orthorhombic magnetic space groups, a circumstance that would otherwise require unusually large high-order terms in the spin Hamiltonian.Comment: 11 pages, 13 figure

Direct observation of Fe spin reorientation in single crystalline YbFe6Ge6

We have grown single crystals of YbFe6Ge6 and LuFe6Ge6 and characterized their anisotropic behaviour through low field magnetic susceptibility, field-dependent magnetization, resistivity and heat capacity measurements. The Yb+3 valency is confirmed by LIII XANES measurements. YbFe6Ge6 crystals exhibit a field-dependent, sudden reorientation of the Fe spins at about 63 K, a unique effect in the RFe6Ge6 family (R = rare earths) where the Fe ions order anti-ferromagnetically with Neel temperatures above 450 K and the R ions' magnetism appears to behave independently. The possible origins of this unusual behaviour of the ordered Fe moments in this compound are discussed.Comment: 12 pages, 8 figures, accepted in J. Phys.: Cond. Matte

Banach Analytic Sets and a Non-Linear Version of the Levi Extension Theorem

We prove a certain non-linear version of the Levi extension theorem for meromorphic functions. This means that the meromorphic function in question is supposed to be extendable along a sequence of complex curves, which are arbitrary, not necessarily straight lines. Moreover, these curves are not supposed to belong to any finite dimensional analytic family. The conclusion of our theorem is that nevertheless the function in question meromorphically extends along an (infinite dimensional) analytic family of complex curves and its domain of existence is a pinched domain filled in by this analytic family.Comment: 19 pages, This is the final version with significant corrections and improvements. To appear in Arkiv f\"or matemati

Identification of the First Oomycete Mating-type Locus Sequence in the Grapevine Downy Mildew Pathogen, Plasmopara viticola

Mating types are self-incompatibility systems that promote outcrossing in plants, fungi, and oomycetes. Mating-type genes have been widely studied in plants and fungi but have yet to be identified in oomycetes, eukaryotic organisms closely related to brown algae that cause many destructive animal and plant diseases. We identified the mating-type locus of Plasmopara viticola, the oomycete responsible for grapevine downy mildew, one of the most damaging grapevine diseases worldwide. Using a genome-wide association approach, we identified a 570-kb repeat-rich non-recombining region controlling mating types, with two highly divergent alleles. We showed that one mating type was homozygous, whereas the other was heterozygous at this locus. The mating-type locus encompassed 40 genes, including one encoding a putative hormone receptor. Functional studies will, however, be required to validate the function of these genes and find the actual determinants of mating type. Our findings have fundamental implications for our understanding of the evolution of mating types, as they reveal a unique determinism involving an asymmetry of heterozygosity, as in sex chromosomes and unlike other mating-type systems. This identification of the mating-type locus in such an economically important crop pathogen also has applied implications, as outcrossing facilitates rapid evolution and resistance to harsh environmental conditions

Reliability of the CARE rule and the HEART score to rule out an acute coronary syndrome in non-traumatic chest pain patients

In patients consulting in the Emergency Department for chest pain, a HEART score ≤ 3 has been shown to rule out an acute coronary syndrome (ACS) with a low risk of major adverse cardiac event (MACE) occurrence. A negative CARE rule (≤ 1) that stands for the first four elements of the HEART score may have similar rule-out reliability without troponin assay requirement. We aim to prospectively assess the performance of the CARE rule and of the HEART score to predict MACE in a chest pain population. Prospective two-center non-interventional study. Patients admitted to the ED for non-traumatic chest pain were included, and followed-up at 6 weeks. The main study endpoint was the 6-week rate of MACE (myocardial infarction, coronary angioplasty, coronary bypass, and sudden unexplained death). 641 patients were included, of whom 9.5% presented a MACE at 6 weeks. The CARE rule was negative for 31.2% of patients, and none presented a MACE during follow-up [0, 95% confidence interval: (0.0–1.9)]. The HEART score was ≤ 3 for 63.0% of patients, and none presented a MACE during follow-up [0% (0.0–0.9)]. With an incidence below 2% in the negative group, the CARE rule seemed able to safely rule out a MACE without any biological test for one-third of patients with chest pain and the HEART score for another third with a single troponin assay

Interferon-γ couples CD8+ T cell avidity and differentiation during infection

Data availability: The mouse scRNAseq and scTCRseq data generated in this study have been deposited in the GEO database under accession code GSE244203 (https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE244203). Datasets reused in this study: EGAS00001005493 [44] (https://ega-archive.org/studies/EGAS00001005493). All data are included in the Supplementary Information or available from the authors upon reasonable requests, as are unique reagents used in this Article. The raw numbers for charts and graphs are available in the Source Data file whenever possible. Source data (https://www.nature.com/articles/s41467-023-42455-4#Sec26) are provided with this paper.Supplementary information is available online at: https://www.nature.com/articles/s41467-023-42455-4#Sec25 .Effective responses to intracellular pathogens are characterized by T cell clones with a broad affinity range for their cognate peptide and diverse functional phenotypes. How T cell clones are selected throughout the response to retain a breadth of avidities remains unclear. Here, we demonstrate that direct sensing of the cytokine IFN-γ by CD8+ T cells coordinates avidity and differentiation during infection. IFN-γ promotes the expansion of low-avidity T cells, allowing them to overcome the selective advantage of high-avidity T cells, whilst reinforcing high-avidity T cell entry into the memory pool, thus reducing the average avidity of the primary response and increasing that of the memory response. IFN-γ in this context is mainly provided by virtual memory T cells, an antigen-inexperienced subset with memory features. Overall, we propose that IFN-γ and virtual memory T cells fulfil a critical immunoregulatory role by enabling the coordination of T cell avidity and fate.This research was funded in whole, or in part, by the UKRI (BBSRC BB/R015651/1 to A.G.), Cancer Research UK (CR-UK) (C5255/A18085 through the Cancer Research UK Oxford Centre and 29549 to A.G); the Kennedy Trust for Rheumatology Research (KENN151607 and KENN202112 to A.G), John Fell Funds (0006162 to A.G), MLSTF funds (to A.G) and Kennedy Studentship (to L.F.K.U)