Expansion of the Tetragonal Magnetic Phase with Pressure in the Iron Arsenide Superconductor Ba₁₋ₓKₓFe₂As₂

In the temperature-concentration phase diagram of most iron-based superconductors, antiferromagnetic order is gradually suppressed to zero at a critical point, and a dome of superconductivity forms around that point. The nature of the magnetic phase and its fluctuations is of fundamental importance for elucidating the pairing mechanism. In Ba1-xKxFe2As2 and Ba1-xNaxFe2As2, it has recently become clear that the usual stripelike magnetic phase, of orthorhombic symmetry, gives way to a second magnetic phase, of tetragonal symmetry, near the critical point, in the range from x = 0.24 to x=0.28 for Ba1-xKxFe2As2. In a prior study, an unidentified phase was discovered for x \u3c 0.24 but under applied pressure, whose onset was detected as a sharp anomaly in the resistivity. Here we report measurements of the electrical resistivity of Ba1-xKxFe2As2 under applied hydrostatic pressures up to 2.75 GPa, for x = 0.22, 0.24, and 0.28. The critical pressure above which the unidentified phase appears is seen to decrease with increasing x and vanish at x = 0.24, thereby linking the pressure-induced phase to the tetragonal magnetic phase observed at ambient pressure. In the temperature-concentration phase diagram of Ba1-xKxFe2As2, we find that pressure greatly expands the tetragonal magnetic phase, while the stripelike phase shrinks. This reveals that pressure may be a powerful tuning parameter with which to explore the interplay between magnetism and superconductivity in this material

VLTI-MATISSE chromatic aperture-synthesis imaging of η Carinae\u27s stellar wind across the Br α line: Periastron passage observations in February 2020

Context. Eta Carinae is a highly eccentric, massive binary system (semimajor axis ~15.5 au) with powerful stellar winds and a phase-dependent wind-wind collision (WWC) zone. The primary star, η Car A, is a luminous blue variable (LBV); the secondary, η Car B, is a Wolf-Rayet or O star with a faster but less dense wind. Aperture-synthesis imaging allows us to study the mass loss from the enigmatic LBV η Car. Understanding LBVs is a crucial step toward improving our knowledge about massive stars and their evolution. Aims. Our aim is to study the intensity distribution and kinematics of η Car\u27s WWC zone. Methods. Using the VLTI-MATISSE mid-infrared interferometry instrument, we perform Brα imaging of η Car\u27s distorted wind. Results. We present the first VLTI-MATISSE aperture-synthesis images of η Car A\u27s stellar windin several spectral channels distributed across the Brα 4.052 μm line (spectral resolving power R ~ 960). Our observations were performed close to periastron passage in February 2020 (orbital phase ~ 14.0022). The reconstructed iso-velocity images show the dependence of the primary stellar wind on wavelength or line-of-sight (LOS) velocity with a spatial resolution of 6 mas (~14 au). The radius of the faintest outer wind regions is ~26 mas (~60 au). At several negative LOS velocities, the primary stellar wind is less extended to the northwest than in other directions. This asymmetry is most likely caused by the WWC. Therefore, we see both the velocity field of the undisturbed primary wind and the WWC cavity. In continuum spectral channels, the primary star wind is more compact than in line channels. A fit of the observed continuum visibilities with the visibilities of a stellar wind CMFGEN model (CMFGEN is an atmosphere code developed to model the spectra of a variety of objects) provides a full width at half maximum fit diameter of the primary stellar wind of 2.84 ± 0.06 mas (6.54 ± 0.14 au). We comparethe derived intensity distributions with the CMFGEN stellar wind model and hydrodynamic WWC models

Neutrino masses: From fantasy to facts

Theory suggests the existence of neutrino masses, but little more. Facts are coming close to reveal our fantasy: solar and atmospheric neutrino data strongly indicate the need for neutrino conversions, while LSND provides an intriguing hint. The simplest ways to reconcile these data in terms of neutrino oscillations invoke a light sterile neutrino in addition to the three active ones. Out of the four neutrinos, two are maximally-mixed and lie at the LSND scale, while the others are at the solar mass scale. These schemes can be distinguished at neutral-current-sensitive solar & atmospheric neutrino experiments. I discuss the simplest theoretical scenarios, where the lightness of the sterile neutrino, the nearly maximal atmospheric neutrino mixing, and the generation of $\Delta {m^2}_\odot$ & $\Delta {m^2}_{atm}$ all follow naturally from the assumed lepton-number symmetry and its breaking. Although the most likely interpretation of the present data is in terms of neutrino-mass-induced oscillations, one still has room for alternative explanations, such as flavour changing neutrino interactions, with no need for neutrino mass or mixing. Such flavour violating transitions arise in theories with strictly massless neutrinos, and may lead to other sizeable flavour non-conservation effects, such as $\mu \to e + \gamma$, $\mu-e$ conversion in nuclei, unaccompanied by neutrino-less double beta decay.Comment: 33 pages, latex, 16 figures. Invited Talk at Ioannina Conference, Symmetries in Intermediate High Energy Physics and its Applications, Oct. 1998, to be published by Springer Tracts in Modern Physics. Festschrift in Honour of John Vergados' 60th Birthda

Conformational changes in α7 acetylcholine receptors underlying allosteric modulation by divalent cations

Allosteric modulation of membrane receptors is a widespread mechanism by which endogenous and exogenous agents regulate receptor function. For example, several members of the nicotinic receptor family are modulated by physiological concentrations of extracellular calcium ions. In this paper, we examined conformational changes underlying this modulation and compare these with changes evoked by ACh. Two sets of residues in the α7 acetylcholine receptor extracellular domain were mutated to cysteine and analyzed by measuring the rates of modification by the thiol-specific reagent 2-aminoethylmethane thiosulfonate. Using Ba2+ as a surrogate for Ca2+, we found a divalent-dependent decrease the modification rates of cysteine substitutions at M37 and M40, residues at which rates were also slowed by ACh. In contrast, Ba2+ had no significant effect at N52C, a residue where ACh increased the rate of modification. Thus divalent modulators cause some but not all of the conformational effects elicited by agonist. Cysteine substitution of either of two glutamates (E44 or E172), thought to participate in the divalent cation binding site, caused a loss of allosteric modulation, yet Ba2+ still had a significant effect on modification rates of these residues. In addition, the effect of Ba2+ at these residues did not appear to be due to direct occlusion. Our data demonstrate that modulation by divalent cations involves substantial conformational changes in the receptor extracellular domain. Our evidence also suggests the modulation occurs via a binding site distinct from one which includes either (or both) of the conserved glutamates at E44 or E172

Mitochondrial dysfunction and biogenesis: do ICU patients die from mitochondrial failure?

Mitochondrial functions include production of energy, activation of programmed cell death, and a number of cell specific tasks, e.g., cell signaling, control of Ca2+ metabolism, and synthesis of a number of important biomolecules. As proper mitochondrial function is critical for normal performance and survival of cells, mitochondrial dysfunction often leads to pathological conditions resulting in various human diseases. Recently mitochondrial dysfunction has been linked to multiple organ failure (MOF) often leading to the death of critical care patients. However, there are two main reasons why this insight did not generate an adequate resonance in clinical settings. First, most data regarding mitochondrial dysfunction in organs susceptible to failure in critical care diseases (liver, kidney, heart, lung, intestine, brain) were collected using animal models. Second, there is no clear therapeutic strategy how acquired mitochondrial dysfunction can be improved. Only the benefit of such therapies will confirm the critical role of mitochondrial dysfunction in clinical settings. Here we summarized data on mitochondrial dysfunction obtained in diverse experimental systems, which are related to conditions seen in intensive care unit (ICU) patients. Particular attention is given to mechanisms that cause cell death and organ dysfunction and to prospective therapeutic strategies, directed to recover mitochondrial function. Collectively the data discussed in this review suggest that appropriate diagnosis and specific treatment of mitochondrial dysfunction in ICU patients may significantly improve the clinical outcome

Parallels between Pathogens and Gluten Peptides in Celiac Sprue

Pathogens are exogenous agents capable of causing disease in susceptible organisms. In celiac sprue, a disease triggered by partially hydrolyzed gluten peptides in the small intestine, the offending immunotoxins cannot replicate, but otherwise have many hallmarks of classical pathogens. First, dietary gluten and its peptide metabolites are ubiquitous components of the modern diet, yet only a small, genetically susceptible fraction of the human population contracts celiac sprue. Second, immunotoxic gluten peptides have certain unusual structural features that allow them to survive the harsh proteolytic conditions of the gastrointestinal tract and thereby interact extensively with the mucosal lining of the small intestine. Third, they invade across epithelial barriers intact to access the underlying gut-associated lymphoid tissue. Fourth, they possess recognition sequences for selective modification by an endogenous enzyme, transglutaminase 2, allowing for in situ activation to a more immunotoxic form via host subversion. Fifth, they precipitate a T cell–mediated immune reaction comprising both innate and adaptive responses that causes chronic inflammation of the small intestine. Sixth, complete elimination of immunotoxic gluten peptides from the celiac diet results in remission, whereas reintroduction of gluten in the diet causes relapse. Therefore, in analogy with antibiotics, orally administered proteases that reduce the host's exposure to the immunotoxin by accelerating gluten peptide destruction have considerable therapeutic potential. Last but not least, notwithstanding the power of in vitro methods to reconstitute the essence of the immune response to gluten in a celiac patient, animal models for the disease, while elusive, are likely to yield fundamentally new systems-level insights