PUSHing Core-Collapse Supernovae to Explosions in Spherical Symmetry: Nucleosynthesis Yields

Core-collapse supernovae (CCSNe) are the extremely energetic deaths of massive stars. They play a vital role in the synthesis and dissemination of many heavy elements in the universe. In the past, CCSN nucleosynthesis calculations have relied on artificial explosion methods that do not adequately capture the physics of the innermost layers of the star. The PUSH method, calibrated against SN1987A, utilizes the energy of heavy-flavor neutrinos emitted by the proto-neutron star (PNS) to trigger parametrized explosions. This makes it possible to follow the consistent evolution of the PNS and to ensure a more accurate treatment of the electron fraction of the ejecta. Here, we present the Iron group nucleosynthesis results for core-collapse supernovae, exploded with PUSH, for two different progenitor series. Comparisons of the calculated yields to observational metal-poor star data are also presented. Nucleosynthesis yields will be calculated for all elements and over a wide range of progenitor masses. These yields can be immensely useful for models of galactic chemical evolution.Comment: 3 pages, 3 figures, poster presentation to appear in the proceedings of the 14th International Symposium on Nuclei in the Cosmos (NIC-XIV), Ed. S. Kubono, JPS (Japan Physical Society

Explosion Dynamics of Parametrized Spherically Symmetric Core-Collapse Supernova Simulations

We report on a method, PUSH, for triggering core-collapse supernova (CCSN) explosions of massive stars in spherical symmetry. This method provides a framework to study many important aspects of core collapse supernovae: the effects of the shock passage through the star, explosive supernova nucleosynthesis and the progenitor-remnant connection. Here we give an overview of the method, compare the results to multi-dimensional simulations and investigate the effects of the progenitor and the equation of state on black hole formation.Comment: Proceedings for Nuclei in the Cosmos XIV, Niigata, Japan (2016

AQP1 Is Not Only a Water Channel: It Contributes to Cell Migration through Lin7/Beta-Catenin

Background: AQP1 belongs to aquaporins family, water-specific, membrane-channel proteins expressed in diverse tissues. Recent papers showed that during angiogenesis, AQP1 is expressed preferentially by microvessels, favoring angiogenesis via the increase of permeability In particular, in AQP1 null mice, endothelial cell migration is impaired without altering their proliferation or adhesion. Therefore, AQP1 has been proposed as a novel promoter of tumor angiogenesis. Methods/Findings: Using targeted silencing of AQP1 gene expression, an impairment in the organization of F-actin and a reduced migration capacity was demonstrated in human endothelial and melanoma cell lines. Interestingly, we showed, for the first time, that AQP1 co-immunoprecipitated with Lin-7. Lin7-GFP experiments confirmed co-immunoprecipitation. In addition, the knock down of AQP1 decreased the level of expression of Lin-7 and b-catenin and the inhibition of proteasome contrasted partially such a decrease. Conclusions/Significance: All together, our findings show that AQP1 plays a role inside the cells through Lin-7/b-catenin interaction. Such a role of AQP1 is the same in human melanoma and endothelial cells, suggesting that AQP1 plays a global physiological role. A model is presented

Autoantibodies against the glial glutamate transporter GLT1/EAAT2 in Type 1 diabetes mellitus-Clues to novel immunological and non-immunological therapies

: Islet cell surface autoantibodies were previously found in subjects with type 1 diabetes mellitus (T1DM), but their target antigens and pathogenic mechanisms remain elusive. The glutamate transporter solute carrier family 1, member 2 (GLT1/EAAT2) is expressed on the membrane of pancreatic β-cells and physiologically controls extracellular glutamate concentrations thus preventing glutamate-induced β-cell death. We hypothesized that GLT1 could be an immunological target in T1DM and that autoantibodies against GLT1 could be pathogenic. Immunoprecipitation and ELISA experiments showed that sera from T1DM subjects recognized GLT1 expressed in brain, pancreatic islets, and GLT1-transfected COS7-cell extracts. We validated these findings in two cohorts of T1DM patients by quantitative immunofluorescence assays. Analysis of the combined data sets indicated the presence of autoantibodies against GLT1 in 32 of the 87 (37%) T1DM subjects and in none of healthy controls (n = 64) (p < 0.0001). Exposure of pancreatic βTC3 cells and human islets to purified IgGs from anti-GLT1 positive sera supplemented with complement resulted in plasma membrane ruffling, cell lysis and death. The cytotoxic effect was prevented when sera were depleted from IgGs. Furthermore, in the absence of complement, 6 out of 16 (37%) anti-GLT1 positive sera markedly reduced GLT1 transport activity in βTC3 cells by inducing GLT1 internalization, also resulting in β-cell death. In conclusion, we provide evidence that GLT1 is a novel T1DM autoantigen and that anti-GLT1 autoantibodies cause β-cell death through complement-dependent and independent mechanisms. GLT1 seems an attractive novel therapeutic target for the prevention of β-cell death in individuals with diabetes and prediabetes

Trafficking of the glutamate transporter is impaired in LRRK2-related Parkinson's disease

The Excitatory Amino Acid Transporter 2 (EAAT2) accounts for 80% of brain glutamate clearance and is mainly expressed in astrocytic perisynaptic processes. EAAT2 function is finely regulated by endocytic events, recycling to the plasma membrane and degradation. Noteworthy, deficits in EAAT2 have been associated with neuronal excitotoxicity and neurodegeneration. In this study, we show that EAAT2 trafficking is impaired by the leucine-rich repeat kinase 2 (LRRK2) pathogenic variant G2019S, a common cause of late-onset familial Parkinson’s disease (PD). In LRRK2 G2019S human brains and experimental animal models, EAAT2 protein levels are significantly decreased, which is associated with elevated gliosis. The decreased expression of the transporter correlates with its reduced functionality in mouse LRRK2 G2019S purified astrocytic terminals and in Xenopus laevis oocytes expressing human LRRK2 G2019S. In LRRK2 G2019S knock-in mouse brain, the correct surface localization of the endogenous transporter is impaired, resulting in its interaction with a plethora of endo-vesicular proteins. Mechanistically, we report that pathogenic LRRK2 kinase activity delays the recycling of the transporter to the plasma membrane via Rabs inactivation, causing its intracellular re-localization and degradation. Taken together, our results demonstrate that pathogenic LRRK2 interferes with the physiology of EAAT2, pointing to extracellular glutamate overload as a possible contributor to neurodegeneration in PD

Catching Element Formation In The Act

Gamma-ray astronomy explores the most energetic photons in nature to address some of the most pressing puzzles in contemporary astrophysics. It encompasses a wide range of objects and phenomena: stars, supernovae, novae, neutron stars, stellar-mass black holes, nucleosynthesis, the interstellar medium, cosmic rays and relativistic-particle acceleration, and the evolution of galaxies. MeV gamma-rays provide a unique probe of nuclear processes in astronomy, directly measuring radioactive decay, nuclear de-excitation, and positron annihilation. The substantial information carried by gamma-ray photons allows us to see deeper into these objects, the bulk of the power is often emitted at gamma-ray energies, and radioactivity provides a natural physical clock that adds unique information. New science will be driven by time-domain population studies at gamma-ray energies. This science is enabled by next-generation gamma-ray instruments with one to two orders of magnitude better sensitivity, larger sky coverage, and faster cadence than all previous gamma-ray instruments. This transformative capability permits: (a) the accurate identification of the gamma-ray emitting objects and correlations with observations taken at other wavelengths and with other messengers; (b) construction of new gamma-ray maps of the Milky Way and other nearby galaxies where extended regions are distinguished from point sources; and (c) considerable serendipitous science of scarce events -- nearby neutron star mergers, for example. Advances in technology push the performance of new gamma-ray instruments to address a wide set of astrophysical questions.Comment: 14 pages including 3 figure

Altered Insulin Receptor Signalling and β-Cell Cycle Dynamics in Type 2 Diabetes Mellitus

Insulin resistance, reduced β-cell mass, and hyperglucagonemia are consistent features in type 2 diabetes mellitus (T2DM). We used pancreas and islets from humans with T2DM to examine the regulation of insulin signaling and cell-cycle control of islet cells. We observed reduced β-cell mass and increased α-cell mass in the Type 2 diabetic pancreas. Confocal microscopy, real-time PCR and western blotting analyses revealed increased expression of PCNA and down-regulation of p27-Kip1 and altered expression of insulin receptors, insulin receptor substrate-2 and phosphorylated BAD. To investigate the mechanisms underlying these findings, we examined a mouse model of insulin resistance in β-cells – which also exhibits reduced β-cell mass, the β-cell-specific insulin receptor knockout (βIRKO). Freshly isolated islets and β-cell lines derived from βIRKO mice exhibited poor cell-cycle progression, nuclear restriction of FoxO1 and reduced expression of cell-cycle proteins favoring growth arrest. Re-expression of insulin receptors in βIRKO β-cells reversed the defects and promoted cell cycle progression and proliferation implying a role for insulin-signaling in β-cell growth. These data provide evidence that human β- and α-cells can enter the cell-cycle, but proliferation of β-cells in T2DM fails due to G1-to-S phase arrest secondary to defective insulin signaling. Activation of insulin signaling, FoxO1 and proteins in β-cell-cycle progression are attractive therapeutic targets to enhance β-cell regeneration in the treatment of T2DM

Spotlights on Contemporary Family Life

Spotlights on Contemporary Family Life covers four issues of cross-cutting importance to families Structures and forms of families: issues relating to a diversification of families away from the ‘traditional nuclear family form’ are relatively uncontroversial from an academic perspective, but much more so for policy makers and family associations. Chapter 1 provides a thorough overview of the state of contemporary European families. Solidarities in families: too often the issue of an ‘ageing society’ is simply reduced to the problem of over-burdening social care systems, but longevity also represents opportunities for new kinds of solidarities inside families and family networks, and new relations between family members – not to mention the satisfaction felt by people who can continue to live fulfilling and rewarding lives long after they’re considered ‘elderly’. Chapter 2 gives voice to authors who identify these new opportunities and challenges. Demographic change: women are having fewer children and having them later in life. Having children is now a conscious decision and fertility rates have declined below the level required to sustain our current populations. At the same time we witness the ‘greying’ of Europe, which brings with it a whole host of opportunities and challenges. Chapter 3 raises important issues for policy makers today. Volunteering: inspired by family associations who could not survive without the support of volunteers, this chapter gives an overview of what’s known - and what isn’t - about volunteering. Coinciding with the European Year of Volunteering 2011, this chapter takes a timely look at the efforts that families put into volunteering across Europe and the important benefits that Europe gains from all of this combined voluntary effort. Linden Farrer and William Lay work for the Confederation of Family Organisations in the European Union (COFACE). This publication was produced by FAMILYPLATFORM, a project funded by the European Commission

Reconstructing Native American Population History

The peopling of the Americas has been the subject of extensive genetic, archaeological and linguistic research; however, central questions remain unresolved1–5. One contentious issue is whether the settlement occurred via a single6–8 or multiple streams of migration from Siberia9–15. The pattern of dispersals within the Americas is also poorly understood. To address these questions at higher resolution than was previously possible, we assembled data from 52 Native American and 17 Siberian groups genotyped at 364,470 single nucleotide polymorphisms. We show that Native Americans descend from at least three streams of Asian gene flow. Most descend entirely from a single ancestral population that we call “First American”. However, speakers of Eskimo-Aleut languages from the Arctic inherit almost half their ancestry from a second stream of Asian gene flow, and the Na-Dene-speaking Chipewyan from Canada inherit roughly one-tenth of their ancestry from a third stream. We show that the initial peopling followed a southward expansion facilitated by the coast, with sequential population splits and little gene flow after divergence, especially in South America. A major exception is in Chibchan-speakers on both sides of the Panama Isthmus, who have ancestry from both North and South America