Room temperature ferromagnetic-like behavior in Mn-implanted and post-annealed InAs layers deposited by Molecular Beam Epitaxy

We report on the magnetic and structural properties of Ar and Mn implanted InAs epitaxial films grown on GaAs (100) by Molecular Beam Epitaxy (MBE) and the effect of Rapid Thermal Annealing (RTA) for 30 seconds at 750C. Channeling Particle Induced X- ray Emission (PIXE) experiments reveal that after Mn implantation almost all Mn atoms are subsbtitutional in the In-site of the InAs lattice, like in a diluted magnetic semiconductor (DMS). All of these samples show diamagnetic behavior. But, after RTA treatment the Mn-InAs films exhibit room-temperature magnetism. According to PIXE measurements the Mn atoms are no longer substitutional. When the same set of experiments were performed with As as implantation ion all of the layers present diamagnetism without exception. This indicates that the appearance of room-temperature ferromagnetic-like behavior in the Mn-InAs-RTA layer is not related to lattice disorder produce during implantation, but to a Mn reaction produced after a short thermal treatment. X-ray diffraction patterns (XRD) and Rutherford Back Scattering (RBS) measurements evidence the segregation of an oxygen deficient-MnO2 phase (nominally MnO1.94) in the Mn-InAs-RTA epitaxial layers which might be on the origin of room temperature ferromagnetic-like response observed.Comment: 16 pages, 5 figures. Acepted in J. Appl. Phy

Influence of Radiation on the Properties and the Stability of Hybrid Perovskites

Organic inorganic perovskites are well suited for optoelectronic applications. In particular, perovskite single and perovskite tandem solar cells with silicon are close to their market entry. Despite their swift rise in efficiency to more than 21 , solar cell lifetimes are way below the needed 25 years. In fact, comparison of the time when the device performance has degraded to 80 of its initial value T80 lifetime of numerous solar cells throughout literature reveals a strongly reduced stability under illumination. The various detrimental effects are discussed. Most notably, moisture and heat related degradation can be mitigated easily by now. Recently however, several photo induced degradation mechanisms have been observed. Under illumination alloyed perovskites tend to phase segregate, while further, oxygen catalyzes deprotonation of the organic cations. Additionally, during illumination photo generated charge can be trapped in the N H antibonding orbitals causing the dissociation of the organic cation. On the other hand, organic inorganic perovskites exhibit a high radiation hardness that is superior to crystalline silicon. This progress report thoroughly reviews proposed degradation mechanisms reported in literature and discusses the microscopic mechanisms and their implications for solar cell

Status report on the Los Alamos National Laboratory Ion Beam Facility

The Ion Beam Facility operated for 6000 machine hours last year, ranging in energy from 300 Kev to 24 Mev. Improvements include cryopumps replacing diffusion pumps, a rebuilding of the tandem chopper electronics and the vertical's corona charging system. Methane molecules were successfully accelerated by the vertical in quantities of hundreds of nanoamperes. Two replacement magnet power supplies on the tandem and a completely new capacitor shell regulator on the vertical are soon to be installed

Evolution of a Signaling Nexus Constrained by Protein Interfaces and Conformational States

Heterotrimeric G proteins act as the physical nexus between numerous receptors that respond to extracellular signals and proteins that drive the cytoplasmic response. The Gα subunit of the G protein, in particular, is highly constrained due to its many interactions with proteins that control or react to its conformational state. Various organisms contain differing sets of Gα-interacting proteins, clearly indicating that shifts in sequence and associated Gα functionality were acquired over time. These numerous interactions constrained much of Gα evolution; yet Gα has diversified, through poorly understood processes, into several functionally specialized classes, each with a unique set of interacting proteins. Applying a synthetic sequence-based approach to mammalian Gα subunits, we established a set of seventy-five evolutionarily important class-distinctive residues, sites where a single Gα class is differentiated from the three other classes. We tested the hypothesis that shifts at these sites are important for class-specific functionality. Importantly, we mapped known and well-studied class-specific functionalities from all four mammalian classes to sixteen of our class-distinctive sites, validating the hypothesis. Our results show how unique functionality can evolve through the recruitment of residues that were ancestrally functional. We also studied acquisition of functionalities by following these evolutionarily important sites in non-mammalian organisms. Our results suggest that many class-distinctive sites were established early on in eukaryotic diversification and were critical for the establishment of new Gα classes, whereas others arose in punctuated bursts throughout metazoan evolution. These Gα class-distinctive residues are rational targets for future structural and functional studies

Ferromagnetism in cobalt doped n-GaN

Ferromagnetic ordering is reported in the post-annealed samples of Co doped n-GaN formed by Co+ implantation. A maximum Curie temperature ~ 250K is recorded for the sample with 8 atomic percent Co. Particle induced x-ray emission-channeling study confirmed the substitutional Co in Ga lattice site. Local atomic arrangement around magnetic impurities is also analyzed using Raman study. A disordered model with carrier mediated coupling of localized magnetic moments is made responsible for the observed ferromagnetic ordering.Comment: 11 pages, 3 figures, Journa

Lecithin : cholesterol acyltransferase: symposium on 50 years of biomedical research from its discovery to latest findings

LCAT converts free cholesterol to cholesteryl esters in the process of reverse cholesterol transport. Familial LCAT deficiency (FLD) is a genetic disease that was first described by Kaare R. Norum and Egil Gjone in 1967. This report is a summary from a 2017 symposium where Dr. Norum recounted the history of FLD and leading experts on LCAT shared their results. The Tesmer laboratory shared structural findings on LCAT and the close homolog, lysosomal phospholipase A2. Results from studies of FLD patients in Finland, Brazil, Norway, and Italy were presented, as well as the status of a patient registry. Drs. Kuivenhoven and Calabresi presented data from carriers of genetic mutations suggesting that FLD does not necessarily accelerate atherosclerosis. Dr. Ng shared that LCAT-null mice were protected from diet-induced obesity, insulin resistance, and nonalcoholic fatty liver disease. Dr. Zhou presented multiple innovations for increasing LCAT activity for therapeutic purposes, whereas Dr. Remaley showed results from treatment of an FLD patient with recombinant human LCAT (rhLCAT). Dr. Karathanasis showed that rhLCAT infusion in mice stimulates cholesterol efflux and suggested that it could also enhance cholesterol efflux from macrophages. While the role of LCAT in atherosclerosis remains elusive, the consensus is that a continued study of both the enzyme and disease will lead toward better treatments for patients with heart disease and FLD.Peer reviewe

Lecithin:cholesterol acyltransferase:symposium on 50 years of biomedical research from its discovery to latest findings

LCAT converts free cholesterol to cholesteryl esters in the process of reverse cholesterol transport. Familial LCAT deficiency (FLD) is a genetic disease that was first described by Kaare R. Norum and Egil Gjone in 1967. This report is a summary from a 2017 symposium where Dr. Norum recounted the history of FLD and leading experts on LCAT shared their results. The Tesmer laboratory shared structural findings on LCAT and the close homolog, lysosomal phospholipase A2. Results from studies of FLD patients in Finland, Brazil, Norway, and Italy were presented, as well as the status of a patient registry. Drs. Kuivenhoven and Calabresi presented data from carriers of genetic mutations suggesting that FLD does not necessarily accelerate atherosclerosis. Dr. Ng shared that LCAT-null mice were protected from diet-induced obesity, insulin resistance, and nonalcoholic fatty liver disease. Dr. Zhou presented multiple innovations for increasing LCAT activity for therapeutic purposes, whereas Dr. Remaley showed results from treatment of an FLD patient with recombinant human LCAT (rhLCAT). Dr. Karathanasis showed that rhLCAT infusion in mice stimulates cholesterol efflux and suggested that it could also enhance cholesterol efflux from macrophages. While the role of LCAT in atherosclerosis remains elusive, the consensus is that a continued study of both the enzyme and disease will lead toward better treatments for patients with heart disease and FLD.</p

IL-23 suppresses innate immune response independently of IL-17A during carcinogenesis and metastasis

IL-23 is an important molecular driver of Th17 cells and has strong tumor-promoting proinflammatory activity postulated to occur via adaptive immunity. Conversely, more recently it has been reported that IL-17A elicits a protective inflammation that promotes the activation of tumor-specific CD8(+) T cells. Here we show the much broader impact of IL-23 in antagonizing antitumor immune responses primarily mediated by innate immunity. Furthermore, the majority of this impact was independent of IL-17A, which did not appear critical for many host responses to tumor initiation or metastases. IL-23-deficient mice were resistant to experimental tumor metastases in three models where host NK cells controlled disease. Immunotherapy with IL-2 was more effective in mice lacking IL-23, and again the protection afforded was NK cell mediated and independent of IL-17A. Further investigation revealed that loss of IL-23 promoted perforin and IFN-gamma antitumor effector function in both metastasis models examined. IL-23-deficiency also strikingly protected mice from tumor formation in two distinct mouse models of carcinogenesis where the dependence on host IL-12p40 and IL-17A was quite different. Notably, in the 3'-methylcholanthrene (MCA) induction of fibrosarcoma model, this protection was completely lost in the absence of NK cells. Overall, these data indicate the general role that IL-23 plays in suppressing natural or cytokine-induced innate immunity, promoting tumor development and metastases independently of IL-17A

Nutrient Control of Yeast PKA Activity Involves Opposing Effects on Phosphorylation of the Bcy1 Regulatory Subunit

Kelch repeat proteins Gpb1 and Gpb2 control yeast PKA activity in response to nutrients by stimulating phosphorylation of the Bcy1 regulatory subunit. Gpb1 and Gpb2 function by blocking inhibition of Bcy1 phosphorylation by PKA catalytic subunits. Phosphorylated Bcy1 is more stable and is a more effective inhibitor of PKA activity