Asymptotically anti-de Sitter space-times: symmetries and conservation laws revisited

In this short note, we verify explicitly in static coordinates that the non trivial asymptotic Killing vectors at spatial infinity for anti-de Sitter space-times correspond one to one to the conformal Killing vectors of the conformally flat metric induced on the boundary. The fall-off conditions for the metric perturbations that guarantee finiteness of the associated conserved charges are derived.Comment: 6 pages Latex file, Proceedings for the conference "Renormalization Group and Anomalies in Gravity and Cosmology", Ouro Preto, Brazil, 17 - 23 March, 200

Radio Emission and Particle Acceleration in SN 1993J

The radio light curves of SN 1993J are found to be well fit by a synchrotron spectrum, suppressed by external free-free absorption and synchrotron self-absorption. A standard r^-2 circumstellar medium is assumed, and found to be adequate. The magnetic field and number density of relativistic electrons behind the shock are determined. The strength of the magnetic field argues strongly for turbulent amplification behind the shock. The ratio of the magnetic and thermal energy density behind the shock is ~0.14. Synchrotron and Coulomb cooling dominate the losses of the electrons. The injected electron spectrum has a power law index -2.1, consistent with diffusive shock acceleration, and the number density scales with the thermal electron energy density. The total energy density of the relativistic electrons is, if extrapolated to gamma ~ 1, ~ 5x10^-4 of the thermal energy density. The free-free absorption required is consistent with previous calculations of the circumstellar temperature of SN 1993J, T_e ~ (2-10)x10^5 K. The relative importance of free-free absorption, Razin suppression, and the synchrotron self-absorption effect for other supernovae are briefly discussed. Guidelines for the modeling and interpretation of VLBI observations are given.Comment: accepted for Ap.

Integration of microRNA changes in vivo identifies novel molecular features of muscle insulin resistance in type 2 diabetes

Skeletal muscle insulin resistance (IR) is considered a critical component of type II diabetes, yet to date IR has evaded characterization at the global gene expression level in humans. MicroRNAs (miRNAs) are considered fine-scale rheostats of protein-coding gene product abundance. The relative importance and mode of action of miRNAs in human complex diseases remains to be fully elucidated. We produce a global map of coding and non-coding RNAs in human muscle IR with the aim of identifying novel disease biomarkers. We profiled >47,000 mRNA sequences and >500 human miRNAs using gene-chips and 118 subjects (n = 71 patients versus n = 47 controls). A tissue-specific gene-ranking system was developed to stratify thousands of miRNA target-genes, removing false positives, yielding a weighted inhibitor score, which integrated the net impact of both up- and down-regulated miRNAs. Both informatic and protein detection validation was used to verify the predictions of in vivo changes. The muscle mRNA transcriptome is invariant with respect to insulin or glucose homeostasis. In contrast, a third of miRNAs detected in muscle were altered in disease (n = 62), many changing prior to the onset of clinical diabetes. The novel ranking metric identified six canonical pathways with proven links to metabolic disease while the control data demonstrated no enrichment. The Benjamini-Hochberg adjusted Gene Ontology profile of the highest ranked targets was metabolic (P < 7.4 × 10-8), post-translational modification (P < 9.7 × 10-5) and developmental (P < 1.3 × 10-6) processes. Protein profiling of six development-related genes validated the predictions. Brain-derived neurotrophic factor protein was detectable only in muscle satellite cells and was increased in diabetes patients compared with controls, consistent with the observation that global miRNA changes were opposite from those found during myogenic differentiation. We provide evidence that IR in humans may be related to coordinated changes in multiple microRNAs, which act to target relevant signaling pathways. It would appear that miRNAs can produce marked changes in target protein abundance in vivo by working in a combinatorial manner. Thus, miRNA detection represents a new molecular biomarker strategy for insulin resistance, where micrograms of patient material is needed to monitor efficacy during drug or life-style interventions