Doping effect on magnetic properties of high-temperature multiferroic compound YBaCuFeO5

We have investigated the impurity effects on magnetic properties for the oxygen-deficiency ordered perovskite YBaCuFeO5, which has multiferroic phenomenon at TN2 = 319 K. The measurements of the magnetic susceptibility χ have been carried out for the polycrystalline samples of YBaCu1-xMxFeO5 (M = Ni, Mn, and Zn), where the Cu2+ spins (S = 1/2) are partially substituted by the nonmagnetic and magnetic ions. From anomalies of the temperature dependence of χ, the doping concentration dependences of the magnetic transition temperatures such as TN1 and TN2, were determined. With increasing the doping concentration for YBaCu1-xMxFeO5 (M = Ni, Mn, and Zn), the value of TN1 decreases, and that of TN2 increases, and two magnetic transitions become one at x = xc. In the doping region of x > xc, the magnetic behaviors of the magnetic ions doped systems are different from that of the nonmagnetic one. In particular, we found that two magnetic transitions newly appear for the Ni- and Mn-doped systems in the region of x > xc. Based on the obtained results, we discussed the physics of impurity effects on the magnetic transitions for the high-temperature multiferroic compound YBaCuFeO5

Bob1 maintains T follicular helper cells for long-term humoral immunity

Abstract Humoral immunity is vital for host protection, yet aberrant antibody responses can trigger harmful inflammation and immune-related disorders. T follicular helper (Tfh) cells, central to humoral immunity, have garnered significant attention for unraveling immune mechanisms. This study shows the role of B-cell Oct-binding protein 1 (Bob1), a transcriptional coactivator, in Tfh cell regulation. Our investigation, utilizing conditional Bob1-deficient mice, suggests that Bob1 plays a critical role in modulating inducible T-cell costimulator expression and cellular respiration in Tfh cells. This regulation maintains the long-term functionality of Tfh cells, enabling their reactivation from central memory T cells to produce antibodies during recall responses. In a bronchial asthma model induced by house dust mite (HDM) inhalation, Bob1 is observed to enhance HDM-specific antibodies, including IgE, highlighting its pivotal function in Tfh cell regulation. Further exploration of Bob1-dependent mechanisms in Tfh cells holds promise for governing protective immunity and addressing immune-related disorders

Pressure Induced Amorphization of Pb²⁺ and Pb⁴⁺ in Perovskite PbFeO₃

Perovskite-type oxides have been the subject of intense research due to their various fascinating physical properties stemming from their charge degree of freedom. PbFeO3 has an unusual Pb2+0.5Pb4+0.5Fe3+O3 charge distribution with a long-ranged ordering of Pb2+ and Pb4+ and two inequivalent Fe3+ sites in a perovskite structure. Combined synchrotron X-ray diffraction and Mössbauer spectroscopy revealed a change to an orthorhombic GdFeO3 structure with a unique Fe3+ site and randomly distributed Pb2+ and Pb4+ at 29.0 GPa, namely, pressure-induced amorphization of Pb2+ and Pb4+. The absence of a charge transfer transition to the Pb2+Fe4+O3 phase, which was expected from the comparison with PbCrO3 and PbCoO3, was verified using ab initio density functional theory calculations in the range of 0–70 GPa

Mst1 inhibits autophagy by promoting the interaction between beclin1 and Bcl-2

Here we show that Mst1, a proapoptotic kinase, impairs protein quality control mechanisms in the heart through inhibition of autophagy. Stress-induced activation of Mst1 in cardiomyocytes promoted accumulation of p62 and aggresome formation, accompanied by the disappearance of autophagosomes. Mst1 phosphorylated the Thr108 residue in the BH3 domain of Beclin1, which enhanced the interaction between Beclin1 and Bcl-2 and/or Bcl-xL, stabilized the Beclin1 homodimer, inhibited the phosphatidylinositide 3-kinase activity of the Atg14L-Beclin1-Vps34 complex and suppressed autophagy. Furthermore, Mst1-induced sequestration of Bcl-2 and Bcl-xL by Beclin1 allows Bax to become active, thereby stimulating apoptosis. Mst1 promoted cardiac dysfunction in mice subjected to myocardial infarction by inhibiting autophagy, associated with increased levels of Thr108-phosphorylated Beclin1. Moreover, dilated cardiomyopathy in humans was associated with increased levels of Thr108-phosphorylated Beclin1 and signs of autophagic suppression. These results suggest that Mst1 coordinately regulates autophagy and apoptosis by phosphorylating Beclin1 and consequently modulating a three-way interaction among Bcl-2 proteins, Beclin1 and Bax