Autonomic Management of Large Clusters and Their Integration into the Grid

We present a framework for the co-ordinated, autonomic management of multiple clusters in a compute center and their integration into a Grid environment. Site autonomy and the automation of administrative tasks are prime aspects in this framework. The system behavior is continuously monitored in a steering cycle and appropriate actions are taken to resolve any problems. All presented components have been implemented in the course of the EU project DataGrid: The Lemon monitoring components, the FT fault-tolerance mechanism, the quattor system for software installation and configuration, the RMS job and resource management system, and the Gridification scheme that integrates clusters into the Grid

Towards automation of computing fabrics using tools from the fabric management workpackage of the EU DataGrid project

This article describes the architecture behind the designed fabric management system and the status of the different developments. It also covers the experience with an existing tool for automated configuration and installation that have been adapted and used from the beginning to manage the EU DataGrid testbed, which is now used for LHC data challenge

Stimulating healthy tissue regeneration by targeting the 5-HT(2B) receptor in chronic liver disease

LettersTissue homeostasis requires an effective, limited wound-healing response to injury. In chronic disease, failure to regenerate parenchymal tissue leads to the replacement of lost cellular mass with a fibrotic matrix. The mechanisms that dictate the balance of cell regeneration and fibrogenesis are not well understood1. Here we report that fibrogenic hepatic stellate cells (HSCs) in the liver are negative regulators of hepatocyte regeneration. This negative regulatory function requires stimulation of the 5-hydroxytryptamine 2B receptor (5-HT2B) on HSCs by serotonin, which activates expression of transforming growth factor β1 (TGF-β1), a powerful suppressor of hepatocyte proliferation, through signaling by mitogen-activated protein kinase 1 (ERK) and the transcription factor JunD. Selective antagonism of 5-HT2B enhanced hepatocyte growth in models of acute and chronic liver injury. We also observed similar effects in mice lacking 5-HT2B or JunD or upon selective depletion of HSCs in wild-type mice. Antagonism of 5-HT2B attenuated fibrogenesis and improved liver function in disease models in which fibrosis was pre-established and progressive. Pharmacological targeting of 5-HT2B is clinically safe in humans and may be therapeutic in chronic liver disease.Mohammad R Ebrahimkhani, Fiona Oakley, Lindsay B Murphy, Jelena Mann, Anna Moles, Maria J Perugorria, Elizabeth Ellis, Anne F Lakey, Alastair D Burt, Angela Douglass, Matthew C Wright, Steven A White, Fabrice Jaffré, Luc Maroteaux & Derek A Man