Injection of iodine to the stratosphere

We report a new estimation of the injection of iodine into the stratosphere based on novel daytime (solar zenith angle < 45°) aircraft observations in the tropical tropopause layer and a global atmospheric model with the most recent knowledge about iodine photochemistry. The results indicate that significant levels of total reactive iodine (0.25-0.7 parts per trillion by volume), between 2 and 5 times larger than the accepted upper limits, can be injected into the stratosphere via tropical convective outflow. At these iodine levels, modeled iodine catalytic cycles account for up to 30% of the contemporary ozone loss in the tropical lower stratosphere and can exert a stratospheric ozone depletion potential equivalent to, or even larger than, that of very short-lived bromocarbons. Therefore, we suggest that iodine sources and chemistry need to be considered in assessments of the historical and future evolution of the stratospheric ozone layer.Fil: Saiz López, Alfonso. Consejo Superior de Investigaciones Científicas. Instituto de Química Física; España. National Center For Atmospheric Research. Amospheric Chemistry División; Estados Unidos. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Baidar, S.. Cooperative Institute For Research In Environmental Science; Estados Unidos. State University of Colorado at Boulder; Estados UnidosFil: Cuevas, Carlos Alberto. Consejo Superior de Investigaciones Científicas. Instituto de Química Física; EspañaFil: Koening, T. K.. State University of Colorado at Boulder; Estados UnidosFil: Fernandez, Rafael Pedro. Consejo Superior de Investigaciones Científicas. Instituto de Química Física; España. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Dix, Barbara. State University of Colorado at Boulder; Estados UnidosFil: Douglas E. KINNISON. National Center For Atmospheric Research. Amospheric Chemistry División; Estados UnidosFil: Jean-Francoise LAMARQUE. National Center For Atmospheric Research. Amospheric Chemistry División; Estados UnidosFil: Xavier Rodriguez-Lloeveras. Consejo Superior de Investigaciones Científicas. Instituto de Química Física; EspañaFil: Campos, T.L.. National Center For Atmospheric Research. Amospheric Chemistry División; Estados UnidosFil: Volkamer, Rainer. Cooperative Institute For Research In Environmental Science; Estados Unidos. State University of Colorado at Boulder; Estados Unido

Raman spectroscopy of graphene and bilayer under biaxial strain: bubbles and balloons

In this letter we use graphene bubbles to study the Raman spectrum of graphene under biaxial (e.g. isotropic) strain. Our Gruneisen parameters are in excellent agreement with the theoretical values. Discrepancy in the previously reported values is attributed to the interaction of graphene with the substrate. Bilayer balloons (intentionally pressurized membranes) have been used to avoid the effect of the substrate and to study the dependence of strain on the inter-layer interactions.Comment: 14 pages, 4 figure

Medium effects in high energy heavy-ion collisions

The change of hadron properties in dense matter based on various theoretical approaches are reviewed. Incorporating these medium effects in the relativistic transport model, which treats consistently the change of hadron masses and energies in dense matter via the scalar and vector fields, heavy-ion collisions at energies available from SIS/GSI, AGS/BNL, and SPS/CERN are studied. This model is seen to provide satisfactory explanations for the observed enhancement of kaon, antikaon, and antiproton yields as well as soft pions in the transverse direction from the SIS experiments. In the AGS heavy-ion experiments, it can account for the enhanced $K^+/\pi^+$ ratio, the difference in the slope parameters of the $K^+$ and $K^-$ transverse kinetic energy spectra, and the lower apparent temperature of antiprotons than that of protons. This model also provides possible explanations for the observed enhancement of low-mass dileptons, phi mesons, and antilambdas in heavy-ion collisions at SPS energies. Furthermore, the change of hadron properties in hot dense matter leads to new signatures of the quark-gluon plasma to hadronic matter transition in future ultrarelativistic heavy-ion collisions at RHIC/BNL.Comment: RevTeX, 65 pages, including 25 postscript figures, invited topical review for Journal of Physics G: Nuclear and Particle Physic

Tumor Necrosis Factor α Inhibits Expression of the Iron Regulating Hormone Hepcidin in Murine Models of Innate Colitis

Background: Abnormal expression of the liver peptide hormone hepcidin, a key regulator of iron homeostasis, contributes to the pathogenesis of anemia in conditions such as inflammatory bowel disease (IBD). Since little is known about the mechanisms that control hepcidin expression during states of intestinal inflammation, we sought to shed light on this issue using mouse models. Methodology/Principal Findings: Hepcidin expression was evaluated in two types of intestinal inflammation caused by innate immune activation—dextran sulfate sodium (DSS)-induced colitis in wild-type mice and the spontaneous colitis occurring in T-bet/Rag2-deficient (TRUC) mice. The role of tumor necrosis factor (TNF) $\alpha$ was investigated by in vivo neutralization, and by treatment of a hepatocyte cell line, as well as mice, with the recombinant cytokine. Expression and activation of Smad1, a positive regulator of hepcidin transcription, were assessed during colitis and following administration or neutralization of TNF$\alpha$. Hepcidin expression progressively decreased with time during DSS colitis, correlating with changes in systemic iron distribution. TNF$\alpha$ inhibited hepcidin expression in cultured hepatocytes and non-colitic mice, while TNF$\alpha$ neutralization during DSS colitis increased it. Similar results were obtained in TRUC mice. These effects involved a TNF$\alpha$-dependent decrease in Smad1 protein but not mRNA. Conclusions/Significance: TNF$\alpha$ inhibits hepcidin expression in two distinct types of innate colitis, with down-regulation of Smad1 protein playing an important role in this process. This inhibitory effect of TNF$\alpha$ may be superseded by other factors in the context of T cell-mediated colitis given that in the latter form of intestinal inflammation hepcidin is usually up-regulated