The Mouse Phenome Database (MPD) provides access to primary experimental trait data, genotypic variation, protocols and analysis tools for mouse genetic studies. Data are contributed by investigators worldwide and represent a broad scope of phenotyping endpoints and disease-related traits in naïve mice and those exposed to drugs, environmental agents or other treatments. MPD ensures rigorous curation of phenotype data and supporting documentation using relevant ontologies and controlled vocabularies. As a repository of curated and integrated data, MPD provides a means to access/re-use baseline data, as well as allows users to identify sensitized backgrounds for making new mouse models with genome editing technologies, analyze trait co-inheritance, benchmark assays in their own laboratories, and many other research applications. MPD’s primary source of funding is NIDA. For this reason, a majority of MPD data is neuro- and behavior-related.
This presentation by the OHBM OpenScienceSIG covers common scenarios where Git can be extremely valuable. The essentials covered include cloning a repository and keeping it up to date, how to create and use your own repository, and how to contribute to other projects via forking and pull requests.
DataLad is a versatile data management and data publication multi-tool. In this session, you can learn the basic concepts and commands for version control and reproducible data analysis. You’ll get to see, create, and install DataLad datasets of many shapes and sizes, master local version workflows and provenance-captured analysis-execution, and you will get ideas for your next data analysis project.
This lecture focuses on how the immune system can target and attack the nervous system to produce autoimmune responses that may result in diseases such as multiple sclerosis, neuromyelitis, and lupus cerebritis manifested by motor, sensory, and cognitive impairments. Despite the fact that the brain is an immune-privileged site, autoreactive lymphocytes producing proinflammatory cytokines can cause active brain inflammation, leading to myelin and axonal loss.