Mapping Attribution Metadata to the Open Provenance Model

A description of a data item's provenance can be provided in dierent forms, and which form is best depends on the intended use of that description. Because of this, dierent communities have made quite distinct underlying assumptions in their models for electronically representing provenance. Approaches deriving from the library and archiving communities emphasise agreed vocabulary by which resources can be described and, in particular, assert their attribution (who created the resource, who modied it, where it was stored etc.) The primary purpose here is to provide intuitive metadata by which users can search for and index resources. In comparison, models for representing the results of scientific workflows have been developed with the assumption that each event or piece of intermediary data in a process' execution can and should be documented, to give a full account of the experiment undertaken. These occurrences are connected together by stating where one derived from, triggered, or otherwise caused another, and so form a causal graph. Mapping between the two approaches would be benecial in integrating systems and exploiting the strengths of each. In this paper, we specify such a mapping between Dublin Core and the Open Provenance Model. We further explain the technical issues to overcome and the rationale behind the approach, to allow the same method to apply in mapping similar schemes.

Mapping of Diepoxybutane Damage in the Cytochrome b Domain of Mitochondrial DNA and the β-globin Domain of Nuclear Chicken DNA Using Quantitative PCR

Diepoxybutane (DEB), a known industrial carcinogen, reacts with DNA primarily at the N7 position of deoxyguanosine residues and creates interstrand cross-links at the sequence 5'-GNC. Since N7-N7 cross-links cause DNA to fragment upon heating, quantative polymerase chain reaction (QPCR) is being used in this experiment to measure the amount of DEB damage (lesion frequency) with three different targets-mitochondrial (unpackaged), open chromatin region, and closed chromatin region. Initial measurements of DEB damage within these three targets were not consistent because the template DNA was not the limiting reagent in the PCR. Follow-up PCR trials using a limiting amount of DNA are still in progress although initial experimentation looks promising. Sequencing of these three targets to confirm the primer targets has only been successfully performed for the closed chromatin target and does not match the sequence from NIH used to design that primer pair. Further sequencing trials need to be conducted on all three targets to assure that a mitochondrial, open chromatin, and closed chromatin region are actually being amplified in this experimental series.