Constraints on the quantum gravity scale from kappa - Minkowski spacetime

We compare two versions of deformed dispersion relations (energy vs momenta and momenta vs energy) and the corresponding time delay up to the second order accuracy in the quantum gravity scale (deformation parameter). A general framework describing modified dispersion relations and time delay with respect to different noncommutative kappa -Minkowski spacetime realizations is firstly proposed here and it covers all the cases introduced in the literature. It is shown that some of the realizations provide certain bounds on quadratic corrections, i.e. on quantum gravity scale, but it is not excluded in our framework that quantum gravity scale is the Planck scale. We also show how the coefficients in the dispersion relations can be obtained through a multiparameter fit of the gamma ray burst (GRB) data.Comment: 9 pages, final published version, revised abstract, introduction and conclusion, to make it clear to general reade

The Ups and Downs in Women's Employment: Shifting Composition or Behavior from 1970 to 2010?

This paper tracks factors contributing to the ups and downs in women’s employment from 1970 to 2010 using regression decompositions focusing on whether changes are due to shifts in the means (composition of women) or due to shifts in coefficients (inclinations of women to work for pay). Compositional shifts in education exerted a positive effect on women’s employment across all decades, while shifts in the composition of other family income, particularly at the highest deciles, depressed married women’s employment over the 1990s contributing to the slowdown in this decade. A positive coefficient effect of education was found in all decades, except the 1990s, when the effect was negative, depressing women’s employment. Further, positive coefficient results for other family income at the highest deciles bolstered married women’s employment over the 1990s. Models are run separately for married and single women demonstrating the varying results of other family income by marital status. This research was supported in part by an Upjohn Institute Early Career Research Award

The dominant Anopheles vectors of human malaria in Africa, Europe and the Middle East: occurrence data, distribution maps and bionomic précis

<p>Abstract</p> <p>Background</p> <p>This is the second in a series of three articles documenting the geographical distribution of 41 dominant vector species (DVS) of human malaria. The first paper addressed the DVS of the Americas and the third will consider those of the Asian Pacific Region. Here, the DVS of Africa, Europe and the Middle East are discussed. The continent of Africa experiences the bulk of the global malaria burden due in part to the presence of the <it>An. gambiae </it>complex. <it>Anopheles gambiae </it>is one of four DVS within the <it>An. gambiae </it>complex, the others being <it>An. arabiensis </it>and the coastal <it>An. merus </it>and <it>An. melas</it>. There are a further three, highly anthropophilic DVS in Africa, <it>An. funestus</it>, <it>An. moucheti </it>and <it>An. nili</it>. Conversely, across Europe and the Middle East, malaria transmission is low and frequently absent, despite the presence of six DVS. To help control malaria in Africa and the Middle East, or to identify the risk of its re-emergence in Europe, the contemporary distribution and bionomics of the relevant DVS are needed.</p> <p>Results</p> <p>A contemporary database of occurrence data, compiled from the formal literature and other relevant resources, resulted in the collation of information for seven DVS from 44 countries in Africa containing 4234 geo-referenced, independent sites. In Europe and the Middle East, six DVS were identified from 2784 geo-referenced sites across 49 countries. These occurrence data were combined with expert opinion ranges and a suite of environmental and climatic variables of relevance to anopheline ecology to produce predictive distribution maps using the Boosted Regression Tree (BRT) method.</p> <p>Conclusions</p> <p>The predicted geographic extent for the following DVS (or species/suspected species complex*) is provided for Africa: <it>Anopheles </it>(<it>Cellia</it>) <it>arabiensis</it>, <it>An. </it>(<it>Cel.</it>) <it>funestus*</it>, <it>An. </it>(<it>Cel.</it>) <it>gambiae</it>, <it>An. </it>(<it>Cel.</it>) <it>melas</it>, <it>An. </it>(<it>Cel.</it>) <it>merus</it>, <it>An. </it>(<it>Cel.</it>) <it>moucheti </it>and <it>An. </it>(<it>Cel.</it>) <it>nili*</it>, and in the European and Middle Eastern Region: <it>An. </it>(<it>Anopheles</it>) <it>atroparvus</it>, <it>An. </it>(<it>Ano.</it>) <it>labranchiae</it>, <it>An. </it>(<it>Ano.</it>) <it>messeae</it>, <it>An. </it>(<it>Ano.</it>) <it>sacharovi</it>, <it>An. </it>(<it>Cel.</it>) <it>sergentii </it>and <it>An. </it>(<it>Cel.</it>) <it>superpictus*</it>. These maps are presented alongside a bionomics summary for each species relevant to its control.</p

Quantum Spacetime Phenomenology

I review the current status of phenomenological programs inspired by quantum-spacetime research. I stress in particular the significance of results establishing that certain data analyses provide sensitivity to effects introduced genuinely at the Planck scale. And my main focus is on phenomenological programs that managed to affect the directions taken by studies of quantum-spacetime theories.Comment: 125 pages, LaTex. This V2 is updated and more detailed than the V1, particularly for quantum-spacetime phenomenology. The main text of this V2 is about 25% more than the main text of the V1. Reference list roughly double

How Heme Oxygenase-1 Prevents Heme-Induced Cell Death.

Earlier observations indicate that free heme is selectively toxic to cells lacking heme oxygenase-1 (HO-1) but how this enzyme prevents heme toxicity remains unexplained. Here, using A549 (human lung cancer) and immortalized human bronchial epithelial cells incubated with exogenous heme, we find knock-down of HO-1 using siRNA does promote the accumulation of cell-associated heme and heme-induced cell death. However, it appears that the toxic effects of heme are exerted by "loose" (probably intralysosomal) iron because cytotoxic effects of heme are lessened by pre-incubation of HO-1 deficient cells with desferrioxamine (which localizes preferentially in the lysosomal compartment). Desferrioxamine also decreases lysosomal rupture promoted by intracellularly generated hydrogen peroxide. Supporting the importance of endogenous oxidant production, both chemical and siRNA inhibition of catalase activity predisposes HO-1 deficient cells to heme-mediated killing. Importantly, it appears that HO-1 deficiency somehow blocks the induction of ferritin; control cells exposed to heme show ~10-fold increases in ferritin heavy chain expression whereas in heme-exposed HO-1 deficient cells ferritin expression is unchanged. Finally, overexpression of ferritin H chain in HO-1 deficient cells completely prevents heme-induced cytotoxicity. Although two other products of HO-1 activity--CO and bilirubin--have been invoked to explain HO-1-mediated cytoprotection, we conclude that, at least in this experimental system, HO-1 activity triggers the induction of ferritin and the latter is actually responsible for the cytoprotective effects of HO-1 activity

HO-1KO in A549 cells sensitizes the cells to heme-mediated cytotoxicity.

<p><b>(A)</b> A549 cells were transfected with the indicated HO-1 siRNA for 24 hours, then treated with or without 100 μM heme for 36 hours. Western blot shows substantial reduction in HO-1 mRNA expression in cells transfected with HO-1 siRNA. <b>(B)</b> Cells were exposed to 100 μM heme for 36 hours and viability was assessed with Alamar blue reduction. Data are means ± SEM of 6 independent experiments. *p≤0.01. <b>(C)</b> Human bronchial epithelial cells (HBEC) were transfected with the indicated HO-1 siRNA for 24 hours, and HO-1 expression was measured by western blot. <b>(D)</b> HBEC were transfected with the indicated HO-1 siRNA for 24 hours, then treated with or without 25 μM heme for 24 hours. Cell viability was measured by Alamar blue reduction.</p

Heme exposure of HO-1KO A549 cells leads to lysosomal rupture and loss of viability which is prevented by pre-incubation with DFO.

<p>A549 cells were challenged with 100 μM heme for 24 hours and then stained with 5 μg/ml AO. <b>(A)</b> A549 cells deficient in intact lysosomes (‘pale’ cells) were measured by flow cytometry. <b>(B)</b> The summary of data shown in (A). Data are means ± SEM of 3 independent experiments. *p≤0.01. <b>(C)</b> A549 cells were pre-treated with 1 mM DFO for 2 hours and then challenged with 100 μM heme for 24 hours. Cell viability was measured using alamar blue. Data are means ± SEM of 3 independent experiments. *p≤0.05.</p

Chemical and siRNA-mediated inhibition of catalase activity in A549 cells enhances the cytotoxic effects of heme.

<p><b>(A)</b> A549 cells were pre-treated with 5 mM 3-AT for 2 hours and then challenged with 100 μM heme for 36 hours. Cell viability was measured by alamar blue. <b>(B)</b> A549 cells were transfected with both 10 nM HO-1 and human catalase siRNAs for 24 hours and then challenged with 100 μM heme for 36 hours. Cell viability was measured by alamar blue. In both cases, data are means ± SEM of 3 independent experiments. *p≤0.05.</p