eSciDoc – a Scholarly Information and Communication Platform for the Max Planck Society

eSciDoc is as a joint project of the Max Planck Society and FIZ Karlsruhe, funded by the Federal Ministry of Education and Research (BMBF), with the aim to realize a next-generation platform for com-munication and publication in research organizations. The result of the entire eSciDoc project is intended to ensure open and persistent access to the research results and materials of the Max Planck Society and to integrate these materials in an emerging e-Science network, to increase the accountability of research and to improve the visibility of the Max Planck Society. At the same time, the project aims to provide effective and comprehensive access to information for Max Planck re-searchers and their work groups. Additionally, eSciDoc will support scientific collaboration and interdisciplinary research in future e-Science scenarios and optimize the exploitation of information avail-able through an interconnected global scientific knowledge space

eSciDoc – a Scholarly Information and Communication Platform for the Max Planck Society

eSciDoc is as a joint project of the Max Planck Society and FIZ Karlsruhe, funded by the Federal Ministry of Education and Research (BMBF), with the aim to realize a next-generation platform for com-munication and publication in research organizations. The result of the entire eSciDoc project is intended to ensure open and persistent access to the research results and materials of the Max Planck Society and to integrate these materials in an emerging e-Science network, to increase the accountability of research and to improve the visibility of the Max Planck Society. At the same time, the project aims to provide effective and comprehensive access to information for Max Planck re-searchers and their work groups. Additionally, eSciDoc will support scientific collaboration and interdisciplinary research in future e-Science scenarios and optimize the exploitation of information avail-able through an interconnected global scientific knowledge space

Digital Scrapbook – can we enable interlinked and recursive knowledge equilibrium?

We investigate possible tools and approaches to develop a Digital Scrapbook, a virtual research environment inspired by the recursive nature of research for scholars where they can combine web and own resources into a new scholarly edition readily enabled for Open Access. Web resources are interlinked in the digital scrapbook by content capture and detail selection, rather than sole bookmark or link to resource URL, along with necessary accompanying metadata. We analyse several open source and commercial tools, with special focus on a Scrapbook-X Firefox Add-On, in order to match to desired Digital Scrapbook features. We further address the wider requirement context for development of such Digital Scrapbook environment, discussing both technical and user experience dimensions. We conclude with a recommendation on how to approach the development and operation of a Digital Scrapbook environment

Ischemia-Reperfusion Injury and Pregnancy Initiate Time-Dependent and Robust Signs of Up-Regulation of Cardiac Progenitor Cells

To explore how cardiac regeneration and cell turnover adapts to disease, different forms of stress were studied for their effects on the cardiac progenitor cell markers c-Kit and Isl1, the early cardiomyocyte marker Nkx2.5, and mast cells. Adult female rats were examined during pregnancy, after myocardial infarction and ischemia-reperfusion injury with/out insulin like growth factor-1(IGF-1) and hepatocyte growth factor (HGF). Different cardiac sub-domains were analyzed at one and two weeks post-intervention, both at the mRNA and protein levels. While pregnancy and myocardial infarction up-regulated Nkx2.5 and c-Kit (adjusted for mast cell activation), ischemia-reperfusion injury induced the strongest up-regulation which occurred globally throughout the entire heart and not just around the site of injury. This response seems to be partly mediated by increased endogenous production of IGF-1 and HGF. Contrary to c-Kit, Isl1 was not up-regulated by pregnancy or myocardial infarction while ischemia-reperfusion injury induced not a global but a focal up-regulation in the outflow tract and also in the peri-ischemic region, correlating with the up-regulation of endogenous IGF-1. The addition of IGF-1 and HGF did boost the endogenous expression of IGF and HGF correlating to focal up-regulation of Isl1. c-Kit expression was not further influenced by the exogenous growth factors. This indicates that there is a spatial mismatch between on one hand c-Kit and Nkx2.5 expression and on the other hand Isl1 expression. In conclusion, ischemia-reperfusion injury was the strongest stimulus with both global and focal cardiomyocyte progenitor cell marker up-regulations, correlating to the endogenous up-regulation of the growth factors IGF-1 and HGF. Also pregnancy induced a general up-regulation of c-Kit and early Nkx2.5+ cardiomyocytes throughout the heart. Utilization of these pathways could provide new strategies for the treatment of cardiac disease