1,391 research outputs found

    The Decay of the Inflaton in No-scale Supergravity

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    We study the decay of the inflaton in no-scale supergravity and show that decay due to the gravitational interactions through supergravity effects is highly suppressed relative to the case in minimal supergravity or models with a generic Kahler potential. We also show that decay to gravitinos is suppressed. We demonstrate that decay and sufficient reheating are possible with the introduction of a non-trivial gauge kinetic term. This channel may be dominant in no-scale supergravity, yet yields a re-heating temperature which is low enough to avoid the gravitino problem while high enough for Big Bang Nucleosynthesis and baryogenesis.Comment: Added the footnote in the conclusion section which discusses the constrains on the explicit inflaton couplings to the matter fields via non-renormalizable operators. To appear in JCA

    Synthesis of magnesium ZIF-8 from Mg(BH₄)₂.

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    Porous Mg(2-methyl imidazolate)2 (Mg-ZIF-8) was synthesised from Mg(BH4)2 as a precursor under an Ar atmosphere. It possesses an uncommon tetrahedral Mg(2+)-N coordination geometry that is stabilised by the formation of a framework, and it exhibits a Brunauer-Emmett-Teller surface area greater than 1800 m(2) g(-1)

    The Earliest Optical Observations of GRB 030329

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    We present the earliest optical imaging observations of GRB 030329 related to SN 2003dh. The burst was detected by the HETE-2 satellite at 2003 March 29, 11:37:14.67 UT. Our wide-field monitoring started 97 minutes before the trigger and the burst position was continuously observed. We found no precursor or contemporaneous flare brighter than V=5.1V=5.1 (V=5.5V=5.5) in 32 s (64 s) timescale between 10:00 and 13:00 UT. Follow-up time series photometries started at 12:51:39 UT (75 s after position notice through the GCN) and continued for more than 5 hours. The afterglow was Rc=12.35±0.07Rc= 12.35\pm0.07 at t=74t=74 min after burst. Its fading between 1.2 and 6.3 hours is well characterized by a single power-law of the form f(mJy)=(1.99±0.02(statistic)±0.14(systematic))×(t/1day)0.890±0.006(statistic)±0.010(systematic)f{\rm(mJy)} = (1.99\pm0.02{\rm (statistic)}\pm0.14{\rm (systematic)}) \times (t/1 {\rm day})^{-0.890\pm 0.006 {\rm (statistic)}\pm 0.010 {\rm (systematic)}} in RcRc-band. No significant flux variation was detected and upper limits are derived as (Δf/f)RMS=35(\Delta f/f)_{\rm RMS} = 3-5% in minutes to hours timescales and (Δf/f)RMS=355(\Delta f/f)_{\rm RMS} = 35-5% in seconds to minutes timescales. Such a featureless lightcurve is explained by the smooth distribution of circumburst medium. Another explanation is that the optical band was above the synchrotron cooling frequency where emergent flux is insensitive to the ambient density contrasts. Extrapolation of the afterglow lightcurve to the burst epoch excludes the presence of an additional flare component at t<10t<10 minutes as seen in GRB 990123 and GRB 021211.Comment: ApJL, in pres

    Chondrosarcoma and Peroxisome Proliferator-Activated Receptor

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    Induction of differentiation and apoptosis in cancer cells by ligands of PPARγ is a novel therapeutic approach to malignant tumors. Chondrosarcoma (malignant cartilage tumor) and OUMS-27 cells (cell line established from grade III human chondrosarcoma) express PPARγ. PPARγ ligands inhibited cell proliferation in a dose-dependent manner, and induced apoptosis of OUMS-27. The higher-grade chondrosarcoma expressed a higher amount of antiapoptotic Bcl-xL in vivo. The treatment of OUMS-27 by 15d-PGJ2, the most potent endogenous ligand for PPARγ, downregulated expression of Bcl-xL and induced transient upregulation of proapoptotic Bax, which could accelerate cytochrome c release from mitochondria to the cytosol, followed by induction of caspase-dependent apoptosis. 15d-PGJ2 induced the expression of CDK inhibitor p21 protein in human chondrosarcoma cells, which appears to be involved in the mechanism of inhibition of cell proliferation. These findings suggest that targeted therapy with PPARγ ligands could be a novel strategy against chondrosarcoma
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