Das Internet zwischen Regulierung und Selbstregulierung

Das Internet hat nicht nur eine kaum vorhersehbare Revolution in der Kommunikation hervorgerufen, sondern stellt auch vielfältige Herausforderungen an das Recht. Die besondere Problematik ist dabei, dass die handelnden Personen dies praktisch anonym tun können und dass das Internet auf Grund seiner Struktur inhaltsneutral ist. Daraus wurde in der öffentlichen Diskussion abgeleitet, dass das Internet ein rechtsfreier Raum sei, was aber nicht sein dürfe. Darauf reagiert in einigen Fällen der Gesetzgeber, weitaus häufiger wird die Entwicklung aber von der Rechtsprechung vorangetrieben. Ziel der Arbeit ist es, die spezifisch auf das Internet bezogenen rechtlichen Entwicklungen des Rechts darzustellen und ihre spezifische Problematik aufzuzeigen. Im Kontrast dazu werden die Mechanismen der Rechtsetzung der Organisationen beschrieben, die für die Entwicklung des Internets verantwortlich sind und deren Verfahren auch Vorbild für staatliche Rechtsetzung sein könnten.The Internet has not only caused a non foreseeable revolution in human communication, it also defies legislation and jurisprudence in many ways. Acting over the internet causes unknown problems as communication on the internet is due to its structure non discriminating regarding the content. Discussion in the public has therefore concluded, that the internet were a anarchic space, a state which could not persist. In many cases this has caused reactions by legislation, although most of the development is carried by jurisprudence. The target of this publication is to show the internet-specific legal developments in Germany and to show their specific problems. In contrast to the state law the mechanisms of standardization by the institutions developing the internet and its standards are described

SRP-27 is a novel component of the supramolecular signalling complex involved in skeletal muscle excitation-contraction coupling

SRP-27 (sarcoplasmic reticulum protein of 27 kDa) is a newly identified integral membrane protein constituent of the skeletal muscle SR (sarcoplasmic reticulum). We identified its primary structure from cDNA clones isolated from a mouse skeletal muscle cDNA library. ESTs (expressed sequence tags) of SRP-27 were found mainly in cDNA libraries from excitable tissues of mouse. Western blot analysis confirmed the expression of SRP-27 in skeletal muscle and, to a lower extent, in heart and brain. Mild trypsin proteolysis combined with primary-structure prediction analysis suggested that SRP-27 has four transmembrane-spanning alpha helices and its C-terminal domain faces the cytoplasmic side of the endo(sarco)plasmic reticulum. The expression of SRP-27 is higher in fast twitch skeletal muscles compared to slow twitch muscles and peaks during the first month of post-natal development. High-resolution immunohistochemistry and Western blot analysis of subcellular fractions indicated that SRP-27 is distributed in both longitudinal tubules and terminal cisternae of the SR, as well as in the perinuclear membrane systems and the nuclear envelope of myotubes and adult fibres. SRP-27 co-sediments with the RyR (ryanodine receptor) macromolecular complex in high-salt sucrose-gradient centrifugation, and is pulled-down by anti-RyR as well as by maurocalcin, a well characterized RyR modulator. Our results indicate that SRP-27 is part of a SR supramolecular complex, suggesting the involvement of SRP-27 in the structural organization or function of the molecular machinery underlying excitation-contraction coupling

Chlamydia pneumoniae infection acts as an endothelial stressor with the potential to initiate the earliest heat shock protein 60-dependent inflammatory stage of atherosclerosis

We identified increased expression and redistribution of the intracellular protein 60-kDa human heat shock protein (hHSP60) (HSPD1) to the cell surface in human endothelial cells subjected to classical atherosclerosis risk factors and subsequent immunologic cross-reactivity against this highly conserved molecule, as key events occurring early in the process of atherosclerosis. The present study aimed at investigating the role of infectious pathogens as stress factors for vascular endothelial cells and, as such, contributors to early atherosclerotic lesion formation. Using primary donor-matched arterial and venous human endothelial cells, we show that infection with Chlamydia pneumoniae leads to marked upregulation and surface expression of hHSP60 and adhesion molecules. Moreover, we provide evidence for an increased susceptibility of arterial endothelial cells for redistribution of hHSP60 to the cellular membrane in response to C. pneumoniae infection as compared to autologous venous endothelial cells. We also show that oxidative stress has a central role to play in endothelial cell activation in response to chlamydial infection. These data provide evidence for a role of C. pneumoniae as a potent primary endothelial stressor for arterial endothelial cells leading to enrichment of hHSP60 on the cellular membrane and, as such, a potential initiator of atherosclerosi