Transdisziplinäre Forschung weiterentwicklen: Eine Synthese mit 15 Empfehlungen

Inter- und Transdisziplinarität erfährt in Lehre und Forschung heutzutage eine vielversprechende Entwicklung, nicht nur im Schweizer Hochschulsystem, sondern auch auf europäischer und globaler Ebene. Sollen die Probleme unserer Zeit adäquat verstanden, analysiert und schliesslich gelöst werden, ist es unabdingbar, die disziplinären Kompetenzen in einen konstruktiven Austauschprozess und Dialog zu bringen. Die Behandlung unserer komplexen, menschlichen, sozialen, politischen und die Umwelt betreffenden Probleme drängt zunehmend auf die Durchlässigkeit des disziplinären Wissens und Wissenssystems. Dieses Buch richtet sich an all jene, die sich in ihrer täglichen Arbeit in Lehre, Forschung oder Studium mit komplexen Fragenstellungen beschäftigen und sich dabei nicht auf die Reduktion auf eine einzelne Disziplin beschränken können. Es zeigt den aktuellen Stand der inter- und transdisziplinären Lehre und Forschung in der Schweiz auf. Schwerpunkt liegt bei der Präsentation von erfolgreichen Projekten, ihren konzeptuellen, theoretischen und methodologischen Grundlagen sowie den daraus gewonnenen Erfahrungen.

Model-Centric, Context-Aware Software Adaptation

Software must be constantly adapted to changing requirements. The time scale, abstraction level and granularity of adaptations may vary from short-term, fine-grained adaptation to long-term, coarse-grained evolution. Fine-grained, dynamic and context-dependent adaptations can be particularly difficult to realize in long-lived, large-scale software systems. We argue that, in order to effectively and efficiently deploy such changes, adaptive applications must be built on an infrastructure that is not just model-driven, but is both model-centric and context-aware. Specifically, this means that high-level, causally-connected models of the application and the software infrastructure itself should be available at run-time, and that changes may need to be scoped to the run-time execution context. We first review the dimensions of software adaptation and evolution, and then we show how model-centric design can address the adaptation needs of a variety of applications that span these dimensions. We demonstrate through concrete examples how model-centric and context-aware designs work at the level of application interface, programming language and runtime. We then propose a research agenda for a model-centric development environment that supports dynamic software adaptation and evolution.

A comparison of the strength of biodiversity effects across multiple functions

In order to predict which ecosystem functions are most at risk from biodiversity loss, meta-analyses have generalised results from biodiversity experiments over different sites and ecosystem types. In contrast, comparing the strength of biodiversity effects across a large number of ecosystem processes measured in a single experiment permits more direct comparisons. Here, we present an analysis of 418 separate measures of 38 ecosystem processes. Overall, 45 % of processes were significantly affected by plant species richness, suggesting that, while diversity affects a large number of processes not all respond to biodiversity. We therefore compared the strength of plant diversity effects between different categories of ecosystem processes, grouping processes according to the year of measurement, their biogeochemical cycle, trophic level and compartment (above- or belowground) and according to whether they were measures of biodiversity or other ecosystem processes, biotic or abiotic and static or dynamic. Overall, and for several individual processes, we found that biodiversity effects became stronger over time. Measures of the carbon cycle were also affected more strongly by plant species richness than were the measures associated with the nitrogen cycle. Further, we found greater plant species richness effects on measures of biodiversity than on other processes. The differential effects of plant diversity on the various types of ecosystem processes indicate that future research and political effort should shift from a general debate about whether biodiversity loss impairs ecosystem functions to focussing on the specific functions of interest and ways to preserve them individually or in combination.

Mutations in SDHD lead to autosomal recessive encephalomyopathy and isolated mitochondrial complex II deficiency

BACKGROUND Defects of the mitochondrial respiratory chain complex II (succinate dehydrogenase (SDH) complex) are extremely rare. Of the four nuclear encoded proteins composing complex II, only mutations in the 70 kDa flavoprotein (SDHA) and the recently identified complex II assembly factor (SDHAF1) have been found to be causative for mitochondrial respiratory chain diseases. Mutations in the other three subunits (SDHB, SDHC, SDHD) and the second assembly factor (SDHAF2) have so far only been associated with hereditary paragangliomas and phaeochromocytomas. Recessive germline mutations in SDHB have recently been associated with complex II deficiency and leukodystrophy in one patient. METHODS AND RESULTS We present the clinical and molecular investigations of the first patient with biochemical evidence of a severe isolated complex II deficiency due to compound heterozygous SDHD gene mutations. The patient presented with early progressive encephalomyopathy due to compound heterozygous p.E69 K and p.*164Lext*3 SDHD mutations. Native polyacrylamide gel electrophoresis and western blotting demonstrated an impaired complex II assembly. Complementation of a patient cell line additionally supported the pathogenicity of the novel identified mutations in SDHD. CONCLUSIONS This report describes the first case of isolated complex II deficiency due to recessive SDHD germline mutations. We therefore recommend screening for all SDH genes in isolated complex II deficiencies. It further emphasises the importance of appropriate genetic counselling to the family with regard to SDHD mutations and their role in tumorigenesis.

Stimulation of MMP-1 and CCL2 by NAMPT in PDL cells

Periodontitis is an inflammatory disease caused by pathogenic microorganisms and characterized by the destruction of the periodontium. Obese individuals have an increased risk of periodontitis, and elevated circulating levels of adipokines, such as nicotinamide phosphoribosyltransferase (NAMPT), may be a pathomechanistic link between both diseases. The aim of this in vitro study was to examine the regulation of periodontal ligament (PDL) cells by NAMPT and its production under inflammatory and infectious conditions. NAMPT caused a significant upregulation of 9 genes and downregulation of 3 genes, as analyzed by microarray analysis. Eight of these genes could be confirmed by real-time PCR: NAMPT induced a significant upregulation of EGR1, MMP-1, SYT7, ITPKA, CCL2, NTM, IGF2BP3, and NRP1. NAMPT also increased significantly the MMP-1 and CCL2 protein synthesis. NAMPT was significantly induced by interleukin-1 β and the periodontal microorganism P. gingivalis. NAMPT may contribute to periodontitis through upregulation of MMP-1 and CCL2 in PDL cells. Increased NAMPT levels, as found in obesity, may therefore represent a mechanism whereby obesity could confer an increased risk of periodontitis. Furthermore, microbial and inflammatory signals may enhance the NAMPT synthesis in PDL cells and thereby contribute to the increased gingival and serum levels of this adipokine, as found in periodontitis.