Research software has become a central asset in academic research. It optimizes existing and enables new research methods, implements and embeds research knowledge, and constitutes an essential research product in itself. Research software must be sustainable in order to understand, replicate, reproduce, and build upon existing research or conduct new research effectively. In other words, software must be available, discoverable, usable, and adaptable to new needs, both now and in the future. Research software therefore requires an environment that supports sustainability. Hence, a change is needed in the way research software development and maintenance are currently motivated, incentivized, funded, structurally and infrastructurally supported, and legally treated. Failing to do so will threaten the quality and validity of research. In this paper, we identify challenges for research software sustainability in Germany and beyond, in terms of motivation, selection, research software engineering personnel, funding, infrastructure, and legal aspects. Besides researchers, we specifically address political and academic decision-makers to increase awareness of the importance and needs of sustainable research software practices. In particular, we recommend strategies and measures to create an environment for sustainable research software, with the ultimate goal to ensure that software-driven research is valid, reproducible and sustainable, and that software is recognized as a first class citizen in research. This paper is the outcome of two workshops run in Germany in 2019, at deRSE19 - the first International Conference of Research Software Engineers in Germany - and a dedicated DFG-supported follow-up workshop in Berlin.
Student Theses (1)
S. Appel. Parameteroptimierung zur Regulierung der calciumabhängigen Kraftentwicklung in Herzmuskelzellen. Institut für Biomedizinische Technik, Karlsruher Institut für Technologie (KIT). Bachelorarbeit. 2020
As direct activators of the contractile apparatus of cardiac myocytes, calcium ions have a strong impact on the tension development of the heart. Therefore, the standard procedure for modelling the electromechanical coupling is based on the transfer of the calcium transient from the cell model to the force model. As a consequence, the coupling of various models can lead to significantly different trajectories of active tension due to diverging implementations of calcium dynamics. As this phenomenon is not to be expected in a healthy human heart, the aim of this thesis was to generate standardized tension development in coupled force- and cell models for atria and ventricles. The ventricular cell models according to O’Hara et al. , Tomek et al.  and Ten Tusscher and Panfilov  as well as the atrial models following Courtemanche et al. , Koivumäki et al.  and Maleckar et al.  were considered. The calcium sensitivity of the parameters of the force models according to Land et al. [7, 8] were evaluated by means of a sensitivity analysis and categorized by their influence on the active tension. Based on the findings obtained, a parameter optimization of the Land models was developed. The results obtained showed that standardized tension developments could only be achieved when coupling selected models. For the cell model according to Courtemanche et al. and all considered cell models of the ventricle the optimization using constant stretches in the interval λ = [0.85, 1.2] gave convincing results with an error ≤ 50 %. The error refers to the average relative error of each considered characteristic of the active tension. With the use of time-variable stretches, the optimization did not yield satisfactory results so far, because only Courtemanche et al. was found to be robust to changes in stretch with an error of 40.4 %. It could also be concluded that calcium transients with unusual behavior hamper the parameter optimization. The limitations of the optimization were confirmed by tissue simulations. With the simu- lations an alternative method for the re-parameterization of the force models was also investigated. However, the considered scaling of the parameter Tref showed a second contrac- tion in the atrium and a maximum force of ≈ 320 kPa in the ventricle. Thus, the optimization based on single cells was still the better method for generating physiologically justified tension development. Furthermore, the implementations of the cell models according to Courtemanche et al. and O’Hara et al. were adapted to take into account the sarcomere length dependent calcium binding to Troponin C (TnC) described in Land et al. To re-determine the calciumsensitive parameters, parameter estimation methods were developed based on the previously designed optimization. It was shown that the simulated intracellular calcium concentration of the rescaled feedback systems, regarding varying sarcomere lengths, partly behave in reverse to experimental findings. This might be explained by the insufficiently detailed implementation of the cell models with respect to the calcium handling.