Crystallographic and magnetic identification of secondary phase in orientated Bi5Fe0.5Co0.5Ti3O15 ceramics

Oxide materials which exhibit both ferroelectricity and ferromagnetism are of great interest for sensors and memory applications. Layered bismuth titanates with an Aurivillius structure, (BiFeO3)nBi4Ti3O12, can possess ferroelectric and ferromagnetic order parameters simultaneously. It has recently been demonstrated that one such example, Bi5Fe0.5Co0.5Ti3O15,where n = 1 with half the Fe3+ sites substituted by Co3+ ions, exhibits both ferroelectric and ferromagnetic properties at room temperature. Here we report the fabrication of highly-oriented polycrystalline ceramics of this material, prepared via molten salt synthesis and uniaxial pressing of high aspect ratio platelets. Electron backscatter images showed that there is a secondary phase within the ceramic matrix which is rich in cobalt and iron, hence this secondary phase could contribute in the main phase ferromagnetic property. The concentration of the secondary phase obtained from secondary electron microscopy is estimated at less than 2.5 %, below the detection limit of XRD. TEM was used to identify the crystallographic structure of the secondary phase, which was shown to be cobalt ferrite, CoFe2O4. It is inferred from the data that the resultant ferromagnetic response identified using VSM measurements was due to the presence of the minor secondary phase. The Remanent magnetization at room temperature was Mr ≈ 76 memu/g which dropped down to almost zero (Mr ≈ 0.8 memu/g) at 460 oC, far lower than the anticipated for CoFe2O4

Estimating the Effect of Liver and Pancreas Volume and Fat Content on Risk of Diabetes: A Mendelian Randomization Study

Fat content and volume of liver and pancreas are associated with risk of diabetes in observational studies; whether these associations are causal is unknown. We conducted a Mendelian randomization (MR) study to examine causality of such associations. We used genetic variants associated (P < 5 × 10-8) with the exposures (liver and pancreas volume and fat content) using MRI scans of UK Biobank participants (n = 32,859). We obtained summary-level data for risk of type 1 (9,358 cases) and type 2 (55,005 cases) diabetes from the largest available genome-wide association studies. We performed inverse-variance weighted MR as main analysis and several sensitivity analyses to assess pleiotropy and to exclude variants with potential pleiotropic effects. Observationally, liver fat and volume were associated with type 2 diabetes (odds ratio per 1 SD higher exposure 2.16 [2.02, 2.31] and 2.11 [1.96, 2.27], respectively). Pancreatic fat was associated with type 2 diabetes (1.42 [1.34, 1.51]) but not type 1 diabetes, and pancreas volume was negatively associated with type 1 diabetes (0.42 [0.36, 0.48]) and type 2 diabetes (0.73 [0.68, 0.78]). MR analysis provided evidence only for a causal role of liver fat and pancreas volume in risk of type 2 diabetes (1.27 [1.08, 1.49] or 27% increased risk and 0.76 [0.62, 0.94] or 24% decreased risk per 1SD, respectively) and no causal associations with type 1 diabetes. Our findings assist in understanding the causal role of ectopic fat in the liver and pancreas and of organ volume in the pathophysiology of type 1 and 2 diabetes. [Abstract copyright: © 2022 by the American Diabetes Association.

On a Dynamical Mordell-Lang Conjecture for Coherent Sheaves

We introduce a dynamical Mordell-Lang-type conjecture for coherent sheaves. When the sheaves are structure sheaves of closed subschemes, our conjecture becomes a statement about unlikely intersections. We prove an analogue of this conjecture for affinoid spaces, which we then use to prove our conjecture in the case of surfaces. These results rely on a module-theoretic variant of Strassman's theorem that we prove in the appendix.Comment: Minor changes from previous version; to appear in the Journal of the London Mathematial Societ

Potential Impact of Amantadine on Aggression in Chronic Traumatic Brain Injury

Objective: To assess the effects of amantadine on anger and aggression among individuals with a chronic traumatic brain injury (TBI). Methods: A cohort of 118 persons with chronic TBI (>6 months postinjury) and moderate-severe aggression selected from a larger cohort of 168 participants enrolled in a parallel-group, randomized, double-blind, placebo-controlled trial of amantadine 100 mg twice daily (n = 82) versus placebo (n = 86) for treatment of irritability were studied. Anger and aggression were measured at treatment days 0, 28, and 60 using observer-rated and participant-rated State-Trait Anger Expression Inventory-2 (STAXI-2) and Neuropsychiatric Inventory-Agitation/Aggression domain (NPI-A) Most Problematic and Distress scores. Results: Participant-rated day 60 NPI-A Most Problematic (adjusted P = .0118) and NPI-A Distress (adjusted P = .0118) were statistically significant between the 2 groups, but STAXI-2 differences were not significant after adjustment for multiple comparisons. Substantial improvements were noted in both amantadine and placebo groups (70% vs 56% improving at least 3 points on day 60 Observer NPI-A; P = .11). Conclusion: Amantadine 100 mg twice daily in this population with chronic TBI appears to be beneficial in decreasing aggression from the perspective of the individual with TBI. No beneficial impact on anger was found

Emergence of Hemagglutinin Mutations during the Course of Influenza Infection

Influenza remains a significant cause of disease mortality. The ongoing threat of influenza infection is partly attributable to the emergence of new mutations in the influenza genome. Among the influenza viral gene products, the hemagglutinin (HA) glycoprotein plays a critical role in influenza pathogenesis, is the target for vaccines and accumulates new mutations that may alter the efficacy of immunization. To study the emergence of HA mutations during the course of infection, we employed a deep-targeted sequencing method. We used samples from 17 patients with active H1N1 or H3N2 influenza infections. These patients were not treated with antivirals. In addition, we had samples from five patients who were analyzed longitudinally. Thus, we determined the quantitative changes in the fractional representation of HA mutations during the course of infection. Across individuals in the study, a series of novel HA mutations directly altered the HA coding sequence were identified. Serial viral sampling revealed HA mutations that either were stable, expanded or were reduced in representation during the course of the infection. Overall, we demonstrated the emergence of unique mutations specific to an infected individual and temporal genetic variation during infection

Gas, Stars, and Star Formation in ALFALFA Dwarf Galaxies

We examine the global properties of the stellar and H I components of 229 low H_I mass dwarf galaxies extracted from the ALFALFA survey, including a complete sample of 176 galaxies with H_I masses <10^(7.7) M_☉ and H_I line widths <80 km s^(–1). Sloan Digital Sky Survey (SDSS) data are combined with photometric properties derived from Galaxy Evolution Explorer to derive stellar masses (M_*) and star formation rates (SFRs) by fitting their UV-optical spectral energy distributions (SEDs). In optical images, many of the ALFALFA dwarfs are faint and of low surface brightness; only 56% of those within the SDSS footprint have a counterpart in the SDSS spectroscopic survey. A large fraction of the dwarfs have high specific star formation rates (SSFRs), and estimates of their SFRs and M_* obtained by SED fitting are systematically smaller than ones derived via standard formulae assuming a constant SFR. The increased dispersion of the SSFR distribution at M_* ≲ 10^8 M_☉ is driven by a set of dwarf galaxies that have low gas fractions and SSFRs; some of these are dE/dSphs in the Virgo Cluster. The imposition of an upper H_I mass limit yields the selection of a sample with lower gas fractions for their M_* than found for the overall ALFALFA population. Many of the ALFALFA dwarfs, particularly the Virgo members, have H_I depletion timescales shorter than a Hubble time. An examination of the dwarf galaxies within the full ALFALFA population in the context of global star formation (SF) laws is consistent with the general assumptions that gas-rich galaxies have lower SF efficiencies than do optically selected populations and that H_I disks are more extended than stellar ones

Deficiency in origin licensing proteins impairs cilia formation: implications for the aetiology of meier-gorlin syndrome

Mutations in ORC1, ORC4, ORC6, CDT1, and CDC6, which encode proteins required for DNA replication origin licensing, cause Meier-Gorlin syndrome (MGS), a disorder conferring microcephaly, primordial dwarfism, underdeveloped ears, and skeletal abnormalities. Mutations in ATR, which also functions during replication, can cause Seckel syndrome, a clinically related disorder. These findings suggest that impaired DNA replication could underlie the developmental defects characteristic of these disorders. Here, we show that although origin licensing capacity is impaired in all patient cells with mutations in origin licensing component proteins, this does not correlate with the rate of progression through S phase. Thus, the replicative capacity in MGS patient cells does not correlate with clinical manifestation. However, ORC1-deficient cells from MGS patients and siRNA-mediated depletion of origin licensing proteins also have impaired centrosome and centriole copy number. As a novel and unexpected finding, we show that they also display a striking defect in the rate of formation of primary cilia. We demonstrate that this impacts sonic hedgehog signalling in ORC1-deficient primary fibroblasts. Additionally, reduced growth factor-dependent signaling via primary cilia affects the kinetics of cell cycle progression following cell cycle exit and re-entry, highlighting an unexpected mechanism whereby origin licensing components can influence cell cycle progression. Finally, using a cell-based model, we show that defects in cilia function impair chondroinduction. Our findings raise the possibility that a reduced efficiency in forming cilia could contribute to the clinical features of MGS, particularly the bone development abnormalities, and could provide a new dimension for considering developmental impacts of licensing deficiency