Proposing a 'Consent Commons' in open education - balancing the desire for openness with the rights of people to refuse or withdraw from participation

A new 'Consent Commons' licensing framework is proposed, complementing Creative Commons, to clarify the permissions given for using and reusing clinical and non-clinical digital recordings of people (patients and non-patients) for educational purposes. Consent Commons is a sophisticated expression of ethically based 'digital professionalism', which recognises the rights of patients, carers, their families, teachers, clinicians, students and members of the public to have some say in how their digital recordings are used (including refusing or withdrawing their consent), and is necessary in order to ensure the long term sustainability of teaching materials, including Open Educational Resources (OER). Consent Commons can ameliorate uncertainty about the status of educational resources depicting people, and protect institutions from legal risk by developing robust and sophisticated policies and promoting best practice in managing their information.

An Ontology for Open Rubric Exchange on the Web

While the Internet has given educators access to a steady supply of Open Educational Resources, the educational rubrics commonly shared on the Web are generally in the form of static, non-semantic presentational documents or in the proprietary data structures of commercial content and learning management systems.With the advent of Semantic Web Standards, producers of online resources have a new framework to support the open exchange of software-readable datasets. Despite these advances, the state of the art of digital representation of rubrics as sharable documents has not progressed.This paper proposes an ontological model for digital rubrics. This model is built upon the Semantic Web Standards of the World Wide Web Consortium (W3C), principally the Resource Description Framework (RDF) and Web Ontology Language (OWL).

Bradykinin, but not muscarinic, inhibition of M-current in rat sympathetic ganglion neurons involves phospholipase C-β4

Rat superior cervical ganglion (SCG) neurons express low-threshold noninactivating M-type potassium channels (I-K(M)), which can be inhibited by activation of M-1 muscarinic receptors (M-1 mAChR) and bradykinin (BK) B-2 receptors. Inhibition by the M1 mAChR agonist oxotremorine methiodide (Oxo-M) is mediated, at least in part, by the pertussis toxin-insensitive G-protein G alpha (q) (Caulfield et al., 1994; Haley et al., 1998a), whereas BK inhibition involves G alpha (q) and/or G alpha (11) (Jones et al., 1995). G alpha (q) and G alpha (11) can stimulate phospholipase C-beta (PLC-beta), raising the possibility that PLC is involved in I-K(M) inhibition by Oxo-M and BK. RT-PCR and antibody staining confirmed the presence of PLC-beta1, - beta2, - beta3, and - beta4 in rat SCG. We have tested the role of two PLC isoforms (PLC-beta1 and PLC-beta4) using antisense-expression constructs. Antisense constructs, consisting of the cytomegalovirus promoter driving antisense cRNA corresponding to the 3'-untranslated regions of PLC-beta1 and PLC-beta4, were injected into the nucleus of dissociated SCG neurons. Injected cells showed reduced antibody staining for the relevant PLC-beta isoform when compared to uninjected cells 48 hr later. BK inhibition of I-K(M) was significantly reduced 48 hr after injection of the PLC-beta4, but not the PLC-beta1, antisense-encoding plasmid. Neither PLC-beta antisense altered M-1 mAChR inhibition by Oxo-M. These data support the conclusion of Cruzblanca et al. (1998) that BK, but not M-1 mAChR, inhibition of I-K(M) involves PLC and extends this finding by indicating that PLC-beta4 is involved.