Re-branding Abu Dhabi: From oil giant to energy titan

This article presents a case study of Abu Dhabi\u27s \u27energy re-branding\u27 since 2005 when it declared its intention to transform itself from an oil exporter to a total energy giant that also embraces alternative (renewable and nuclear) energy. The first part of the article identifies the benefits of this policy for Abu Dhabi\u27s external diplomacy but argues that the real driver is the emirate\u27s domestic gas shortage and its effects on economic diversification and political legitimacy. The second part of the article discusses the motivations and interactions of local and foreign agents by focusing on the implementation of alternative energy platforms. It therefore provides a rare glimpse of the policy-making process in Abu Dhabi. The final part of the article examines the extent to which energy re-branding may be linked to a process by the government to reiterate, reinterpret and repudiate Emirati identity in order to enhance regime legitimacy in the twenty-first century. © 2012 Macmillan Publishers Ltd

The Arab Gulf States in the Shadow of the Iranian Nuclear Challenge

Emile El-Hokayem; Matteo Legrenz

Tracing Distributed Component-Based Systems, a Brief Overview

International audienceWe overview a framework for tracing asynchronous distributed component-based systems with multiparty interactions managed by distributed schedulers. Neither the global state nor the total ordering of the system events is available at runtime. We instrument the system to retrieve local events from the local traces of the schedulers. Local events are sent to a global observer which reconstructs on-the-fly the global traces that are compatible with the local traces, in a concurrency-preserving and communication-delay insensitive fashion. The global traces are represented as an original lattice over partial states, such that any path of the lattice projected on a scheduler represents the corresponding local partial trace according to that scheduler (soundness), and all possible global traces of the system are recorded (completeness)

Convergent Pathways in Idiopathic Autism Revealed by Time Course Transcriptomic Analysis of Patient-Derived Neurons

Potentially pathogenic alterations have been identified in individuals with autism spectrum disorders (ASDs) within a variety of key neurodevelopment genes. While this hints at a common ASD molecular etiology, gaps persist in our understanding of the neurodevelopmental mechanisms impacted by genetic variants enriched in ASD patients. Induced pluripotent stem cells (iPSCs) can model neurodevelopment in vitro, permitting the characterization of pathogenic mechanisms that manifest during corticogenesis. Taking this approach, we examined the transcriptional differences between iPSC-derived cortical neurons from patients with idiopathic ASD and unaffected controls over a 135-day course of neuronal differentiation. Our data show ASD-specific misregulation of genes involved in neuronal differentiation, axon guidance, cell migration, DNA and RNA metabolism, and neural region patterning. Furthermore, functional analysis revealed defects in neuronal migration and electrophysiological activity, providing compelling support for the transcriptome analysis data. This study reveals important and functionally validated insights into common processes altered in early neuronal development and corticogenesis and may contribute to ASD pathogenesis

E6-Associated Protein Dependent Estrogen Receptor Regulation of Protein Kinase A Regulatory Subunit R2A Expression in Neuroblastoma

E6ap is a known transcriptional coregulator for estrogen receptor alpha (Er, Erα) in the presence of estrogen. Protein kinase A (PKA) contains two regulatory subunits derived from four genes. Recent evidence demonstrates that PKA regulates E6ap activity. Data generated in our lab indicated estrogen dependent regulation of Pkar2a levels. Our project sets to investigate a possible feedback mechanism constituting of Erα and E6ap transcriptional regulation of Pkar2a expression. Western blot evaluated protein regulation correlations with E2 in mouse neuroblastoma lines. Bioinformatics detected estrogen response element (ERE) sequences. quantitative polymerase chain reaction (qPCR) validated the western blot results. ERE oligonucleotides were synthesized. Reporter gene transcriptional activity was evaluated via Luciferase assay output. Electromobility shift assay (EMSA) assessed direct binding between Erα relevant sequences. Chromatin immunoprecipitation (ChIP) and Re-ChIP were conducted in quantifying protein complex recruitment levels. Pkar2a protein expression directly correlated with E2, and four putative ERE sequences were identified. Pkar2a mRNA expression reverted to baseline with either E2 or E6ap absent. In the presence of E2, ERE-1 and ERE-4 possessed Luciferase reporter gene transcriptional capabilities. ERE-1 portrayed band shifts, representing direct binding to Erα with E2 supplementation. With E2, ERE-1 significantly enhanced Erα and E6ap recruitment levels to the Pkar2a promoter. Pkar2a is directly regulated by Erα and E6ap in the presence of estrogen stimulus. This work indicates a feedback mechanism in the interplay between PKA and E6ap, which may prove crucial for the role of both proteins in cancers and neurogenetic diseases like Angelman syndrome