PaaS-IaaS Inter-Layer Adaptation in an Energy-Aware Cloud Environment

Cloud computing providers resort to a variety of techniques to improve energy consumption at each level of the cloud computing stack. Most of these techniques consider resource-level energy optimization at IaaS layer. This paper argues energy gains can be obtained by creating a cooperation between the PaaS layer (in charge of hosting the application/service) and the IaaS layer (in charge of handling the computing resources). It presents a novel method based on steering information and decision taking to trigger the PaaS and IaaS layers to adapt their energy mode in service operation, therefore enabling the Cloud stack to actively adapt to changing situations. Experimental results demonstrate such adaptation achieves dynamic energy management in each of the PaaS and IaaS cloud layers

Nuclear Fusion Programme: Annual Report of the Association Karlsruhe Institute of Technology (KIT)/EURATOM ; January 2010 - December 2010 (KIT Scientific Reports ; 7592)

The Karlsruhe Institute of Technology (KIT) is working in the framework of the European Fusion Programme on key technologies in the areas of superconducting magnets, microwave heating systems (Electron-Cyclotron-Resonance-Heating, ECRH), the deuterium-tritium fuel cycle, He-cooled breeding blankets, a He-cooled divertor and structural materials, as well as refractory metals for high heat flux applications including a major participation in the preparation of the international IFMIF project

Nuclear fusion programme annual report of the association Forschungszentrum Karlsruhe/EURATOM, January 2007 - December 2007

BIBLIOTHE

Investigating protein- protein interactions in order to develop novel therapeutics for the treatment of Alzheimer’s disease

Alzheimer’s disease (AD) accounts for around two thirds of all dementia cases and an increase in life expectancy of the population has resulted in a substantial increase in dementia cases and with that a rise in AD. AD is a debilitating and ultimately fatal neurodegenerative disorder of the elderly, and despite being identified over a century ago, the current treatments do not treat the underlying causes behind the disease, instead they help to mask the symptoms of the disease and prolong the brain’s remaining function. It is therefore vital that an effective, disease modifying treatment for this disease is established as soon as possible. Soluble intracellular forms of amyloid β (peptide Aβ), a hallmark of AD have been identified and intracellular targets of Aβ are being investigated as potential drug targets for the disease. Two key intracellular, mitochondrial proteins investigated as potential drug targets: amyloid binding alcohol dehydrogenase (ABAD) and cyclophilin D (CypD) are the focus of the work reported in this thesis. To begin identifying potential inhibitors of the ABAD-Aβ interaction, a two-pronged approach was taken. Firstly, a series of analogues based on a known inhibitor of the interaction were tested using a variety of biophysical assays, for their therapeutic affect on the interaction, and secondly a fragment based screening approach was used to identify new small molecule binding partners of ABAD which could potentially be modified to produced inhibitors of the ABAD-Aβ interaction. Three different CypD constructs have been successfully expressed and purified, and taken into crystal trials. It is hoped that these constructs can be used to significantly aid the progress of identifying any potential inhibitors and binding partners of CypD that may produce therapeutic effects, and in the future could lead to the identification of an effective disease modifying drug in the treatment of AD. The work reported in this thesis has built upon previously reported findings and the groundwork has also been established for several in vitro biophysical assays, these include for example: measuring ABAD enzyme activity, and the novel morphology specific Aβ aggregation assay, which can be used as screening tools to help identify potential inhibitors of these interactions. Both the ABAD-Aβ interaction, and the blockade of CypD are known to be drug targets in the treatment of AD, and by elucidating the molecular mechanisms behind these interactions, through implementing biophysical assays, this will help in the identification and design of potential new therapeutic agents for the treatment of AD