TECHNOLOGY ENHANCED LEARNING

Abstract: Recently companies discover their employees knowledge as one of the major critical resources they need to have for successful business. Advances in technology enhanced learning provide the necessary means by which companies and employers are able to maintain and grow their knowledge assets. This being recognized by the EU several main objectives have been identified and will be tackled in the network of Excellence in Professional Learning proposed in the 6 th EU framework programme. The objectives are critical for advancing the state-of-the-art and ensuring the European leadership in technology enhanced learning thus will be pursued by integrating European research in the Network of Excellence

Virtuelle Bildungsnetzwerke: Struktur- und Betreibermodelle am Beispiel WINFOLine

Dieser Beitrag beschäftigt sich mit Struktur- und Betreibermodellen virtueller Bildungsnetzwerke. Er verdeutlicht Potenziale und Anforderungen beim Aufbau entsprechender Strukturen und betrachtet allgemein den Wertschöpfungsprozess von Bildungsnetzwerken, aus dem spezifische Betreibermodelle abgeleitet werden können. Dabei spielt die Betrachtung einzelner Partner von Bildungsnetzwerken und ihrer spezifischen Aufgaben innerhalb von Verbünden eine ebenso wichtige Rolle wie die Betrachtung potenzieller Abnehmer von Bildungsangeboten. Vertiefend werden in diesem Beitrag Ansätze der traditionellen Hochschulen diskutiert

Virtuelle Bildungsnetzwerke: Struktur- und Betreibermodelle am Beispiel WINFOLine

Dieser Beitrag beschäftigt sich mit Struktur- und Betreibermodellen virtueller Bildungsnetzwerke. Er verdeutlicht Potenziale und Anforderungen beim Aufbau entsprechender Strukturen und betrachtet allgemein den Wertschöpfungsprozess von Bildungsnetzwerken, aus dem spezifische Betreibermodelle abgeleitet werden können. Dabei spielt die Betrachtung einzelner Partner von Bildungsnetzwerken und ihrer spezifischen Aufgaben innerhalb von Verbünden eine ebenso wichtige Rolle wie die Betrachtung potenzieller Abnehmer von Bildungsangeboten. Vertiefend werden in diesem Beitrag Ansätze der traditionellen Hochschulen diskutiert

What is the optimal number of implants for fixed reconstructions: a systematic review

To assess the 5-year and 10-year survival and complication rates of implant-supported fixed reconstructions in partially and totally edentulous patients with regard to the optimal number and distribution of dental implants

Cytotoxicity of tumor antigen specific human T cells is unimpaired by arginine depletion.

Tumor-growth is often associated with the expansion of myeloid derived suppressor cells that lead to local or systemic arginine depletion via the enzyme arginase. It is generally assumed that this arginine deficiency induces a global shut-down of T cell activation with ensuing tumor immune escape. While the impact of arginine depletion on polyclonal T cell proliferation and cytokine secretion is well documented, its influence on chemotaxis, cytotoxicity and antigen specific activation of human T cells has not been demonstrated so far. We show here that chemotaxis and early calcium signaling of human T cells are unimpaired in the absence of arginine. We then analyzed CD8(+) T cell activation in a tumor peptide as well as a viral peptide antigen specific system: (i) CD8(+) T cells with specificity against the MART-1aa26-35*A27L tumor antigen expanded with in vitro generated dendritic cells, and (ii) clonal CMV pp65aa495-503 specific T cells and T cells retrovirally transduced with a CMV pp65aa495-503 specific T cell receptor were analyzed. Our data demonstrate that human CD8(+) T cell antigen specific cytotoxicity and perforin secretion are completely preserved in the absence of arginine, while antigen specific proliferation as well as IFN-γ and granzyme B secretion are severely compromised. These novel results highlight the complexity of antigen specific T cell activation and demonstrate that human T cells can preserve important activation-induced effector functions in the context of arginine deficiency

Arginine deficiency leads to impaired cofilin dephosphorylation in activated human T lymphocytes.

The amino acid arginine is fundamentally involved in the regulation of the immune response during infection, inflammatory diseases and tumor growth. Arginine deficiency (e.g. due to the myeloid cell enzyme arginase) inhibits proliferation and effector functions of activated T lymphocytes. Here, we studied intracellular mechanisms mediating this suppression of human T lymphocytes. Our proteomic analysis revealed an impaired dephosphorylation of the actin-binding protein cofilin upon T-cell activation in the absence of arginine. We show that this correlates with alteration of actin polymerization and impaired accumulation of CD2 and CD3 in the evolving immunological synapse in T cell-antigen presenting cells conjugates. In contrast, T-cell cytokine synthesis is differentially regulated in human T lymphocytes in the absence of arginine. While the production of certain cytokines (e.g. IFN-γ) is severely reduced, T lymphocytes produce other cytokines (e.g. IL-2) independent of extracellular arginine. MEK and PI3K activity are reciprocally regulated in association with impaired cofilin dephosphorylation. Finally, we show that impaired cofilin dephosphorylation is also detectable in human T cells activated in a granulocyte-dominated purulent micromilieu due to arginase-mediated arginine depletion. Our novel results identify cofilin as a potential regulator of human T-cell activation under conditions of inflammatory arginine deficiency