Mass Bounds on a Very Light Neutralino

Within the Minimal Supersymmetric Standard Model (MSSM) we systematically investigate the bounds on the mass of the lightest neutralino. We allow for non-universal gaugino masses and thus even consider massless neutralinos, while assuming in general that R-parity is conserved. Our main focus are laboratory constraints. We consider collider data, precision observables, and also rare meson decays to very light neutralinos. We then discuss the astrophysical and cosmological implications. We find that a massless neutralino is allowed by all existing experimental data and astrophysical and cosmological observations.Comment: 36 pages, 13 figures, minor modification in astro-physical bounds. EPJC versio

Numerical hydrodynamics in general relativity

The current status of numerical solutions for the equations of ideal general relativistic hydrodynamics is reviewed. With respect to an earlier version of the article the present update provides additional information on numerical schemes and extends the discussion of astrophysical simulations in general relativistic hydrodynamics. Different formulations of the equations are presented, with special mention of conservative and hyperbolic formulations well-adapted to advanced numerical methods. A large sample of available numerical schemes is discussed, paying particular attention to solution procedures based on schemes exploiting the characteristic structure of the equations through linearized Riemann solvers. A comprehensive summary of astrophysical simulations in strong gravitational fields is presented. These include gravitational collapse, accretion onto black holes and hydrodynamical evolutions of neutron stars. The material contained in these sections highlights the numerical challenges of various representative simulations. It also follows, to some extent, the chronological development of the field, concerning advances on the formulation of the gravitational field and hydrodynamic equations and the numerical methodology designed to solve them.Comment: 105 pages, 12 figures. The full online-readable version of this article, including several animations, will be published in Living Reviews in Relativity at http://www.livingreviews.or

G6PD deficiency in Latin America: systematic review on prevalence and variants

Plasmodium vivax radical cure requires the use of primaquine (PQ), a drug that induces haemolysis in glucose-6-phosphate dehydrogenase deficient (G6PDd) individuals, which further hampers malaria control efforts. The aim of this work was to study the G6PDd prevalence and variants in Latin America (LA) and the Caribbean region. A systematic search of the published literature was undertaken in August 2013. Bibliographies of manuscripts were also searched and additional references were identified. Low prevalence rates of G6PDd were documented in Argentina, Bolivia, Mexico, Peru and Uruguay, but studies from Curaçao, Ecuador, Jamaica, Saint Lucia, Suriname and Trinidad, as well as some surveys carried out in areas of Brazil, Colombia and Cuba, have shown a high prevalence (> 10%) of G6PDd. The G6PD A-202A mutation was the variant most broadly distributed across LA and was identified in 81.1% of the deficient individuals surveyed. G6PDd is a frequent phenomenon in LA, although certain Amerindian populations may not be affected, suggesting that PQ could be safely used in these specific populations. Population-wide use of PQ as part of malaria elimination strategies in LA cannot be supported unless a rapid, accurate and field-deployable G6PDd diagnostic test is made available

Knockdown of SCF^Skp2 Function Causes Double-Parked Accumulation in the Nucleus and DNA Re-Replication in <i>Drosophila</i> Plasmatocytes

<div><p>In <i>Drosophila</i>, circulating hemocytes are derived from the cephalic mesoderm during the embryonic wave of hematopoiesis. These cells are contributed to the larva and persist through metamorphosis into the adult. To analyze this population of hemocytes, we considered data from a previously published RNAi screen in the hematopoietic niche, which suggested several members of the SCF complex play a role in lymph gland development. <i>eater-Gal4</i>;<i>UAS-GFP</i> flies were crossed to <i>UAS-RNAi</i> lines to knockdown the function of all known SCF complex members in a plasmatocyte-specific fashion, in order to identify which members are novel regulators of plasmatocytes. This specific SCF complex contains five core members: Lin-19-like, SkpA, Skp2, Roc1a and complex activator Nedd8. The complex was identified by its very distinctive large cell phenotype. Furthermore, these large cells stained for anti-P1, a plasmatocyte-specific antibody. It was also noted that the DNA in these cells appeared to be over-replicated. Gamma-tubulin and DAPI staining suggest the cells are undergoing re-replication as they had multiple centrioles and excessive DNA content. Further experimentation determined enlarged cells were BrdU-positive indicating they have progressed through S-phase. To determine how these cells become enlarged and undergo re-replication, cell cycle proteins were analyzed by immunofluorescence. This analysis identified three proteins that had altered subcellular localization in these enlarged cells: Cyclin E, Geminin and Double-parked. Previous research has shown that Double-parked must be degraded to exit S-phase, otherwise the DNA will undergo re-replication. When Double-parked was titrated from the nucleus by an excess of its inhibitor, geminin, the enlarged cells and aberrant protein localization phenotypes were partially rescued. The data in this report suggests that the SCF^Skp2 complex is necessary to ubiquitinate Double-parked during plasmatocyte cell division, ensuring proper cell cycle progression and the generation of a normal population of this essential blood cell type.</p> </div

Enlarged cells elicited by functional knockdown of <i>lin19</i> exhibit increased nuclear BrdU staining.

<p>(A,B) <i>PxnGal4>w</i>^<i>1118</i> wild-type animals were fed BrdU during larval stages resulting in slight incorporation into the DNA as visualized by anti-BrdU and DAPI staining. (C,D) <i>pxnGal4>lin19 </i><i>RNAi</i>^{<i>HM05197</i>} were fed BrdU during laval stages resulting in a distinct nuclear BrdU staining in the nucleus when observed with DAPI staining. Scale bar = 20 μm.</p

Overexpression of Gem elicits a partial rescue of SCF knockdown plasmatocyte phenotypes.

<p>(A-C) <i>pxnGal4>w</i>^<i>1118</i> control hemolymph samples stained with (A) α-Cyclin E, (B) α-Gem, and (C) α-Dup and (D-F) DAPI. (G-I) <i>pxnGal4>UAS-lin19 </i><i>RNAi</i>^{<i>HM05197</i>} hemocytes stained with (G) α-Cyclin E, (H) α-Gem, and (I) α-Dup and (J-L) DAPI. (M-O) <i>pxnGal4> UAS-Gem</i>^<i>43</i><i>; UAS-lin19 </i><i>RNAi</i>^{<i>HM05197</i>} hemocytes stained with (M) α-Cyclin E, (N) α-Gem, and (O) α-Dup and (P-R) DAPI. (S) Graph indicating the number of cells that fall into specific size categories for <i>pxnGal4>w</i>^<i>1118</i>, <i>pxnGal4>UAS-Gem</i>⁴³, <i>pxnGal4>UAS-lin19 </i><i>RNAi</i>^{<i>HM05197</i>}, and <i>pxnGal4>UAS-Gem</i>^<i>43</i><i>; UAS-lin19 </i><i>RNAi</i>^{<i>HM05197</i>} genotypes. As indicated by the graph, overexpression of Gem in the SCF knockdown background causes a great reduction in the number of giant cells when compared to knockdown of the SCF complex only. Nuclear stained cells indicated by white filled arrows, cytoplasmic stained cells indicated by outlined arrows. Scale bar = 20 μm.</p