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Quality teaching in higher education (HE) is gaining increasing international attention and pedagogical innovation is seen as an important construct of quality teaching. The drivers for pedagogical innovation include the need for 21st century skills and understandings, student demographics and empowerment, technological advances, and a turn to teaching in HE. Defining innovative pedagogies is a recurring challenge in the literature and a key focus of this article. Using an investigation into innovative approaches to teaching and learning at one New Zealand university, prevailing themes of newness, benefit, and student outcomes are discussed to develop a working definition. What is missing from the discourses and definitions is specific consideration of the influence of context on what counts as pedagogical innovation. In light of this, the authors offer an emergent definition of pedagogical innovation in higher education.

Recent large-scale surveys of appendix samples estimate that as many as 1 in 2000 people in the UK have abnormal accumulation of disease-associated PrP, suggesting that they may be subclinically infected with variant Creutzfeldt-Jakob disease (vCJD) [1]. If these individuals are infectious, they pose a potential risk to others through blood and organ donation, or contamination of surgical instruments. Indeed, several cases of vCJD have been attributed to receiving blood products from individuals who donated blood during the preclinical stage of the disease [2]. Thus, a robust diagnostic test for vCJD is urgently required to detect these ‘silent’ (preclinical/subclinical) infections, in order to protect the UK blood supply.Efforts to develop such a test are complicated by the extremely low concentrations of PrPSc present in readily accessible biological samples, such as blood, and this value is likely to be even lower in preclinical samples. Recently, several platforms have been developed which may be sensitive enough to overcome this challenge. One such technique, an ultrasensitive in vitro prion amplification assay, termed ‘real-time quaking induced conversion’ (RT-QuIC), has already proven to be a highly effective tool in the diagnosis of sporadic Creutzfeldt-Jakob disease (sCJD), when applied to samples of cerebrospinal fluid. [3] However, attempts to develop RT-QuIC into a blood-based diagnostic test for vCJD have been less successful.Here we present a novel version of the RT-QuIC reaction, using a previously untested recombinant prion protein (recPrP) substrate. Due to a paucity of suitable human samples (which are necessary to optimize the platform and evaluate its performance in detecting preclinical infection), we have optimized our assay using an animal model of vCJD infection – sheep that have been experimentally infected with BSE. We show that our version of the RT-QuIC assay gives positive amplification results when applied to whole blood samples spiked with BSE-infected sheep brain homogenate. Positive samples are amplified within 20–40 h, with a high degree of analytical sensitivity, equivalent to a 10−6 dilution of BSE-infected brain homogenate. We then assess the performance of the assay on ‘endogenously’ infected whole blood samples, collected from BSE-infected sheep at regular time points, from the time of infection to the onset of clinical signs. If this version of the RT-QuIC reaction demonstrates high levels of sensitivity and specificity in identifying blood samples from pre-clinically infected individuals, it could then be adapted for use in humans.

It is now 18 years since the first identification of a case of vCJD in the UK. Since that time, there has been much speculation over how vCJD might impact human health. To date there have been 177 case reports in the UK and a further 51 cases worldwide in 11 different countries. Since establishing that BSE and vCJD are of the same strain of agent, we have also shown that there is broad similarity between UK and non-UK vCJD cases on first passage to mice. Transgenic mouse studies have indicated that all codon 129 genotypes are susceptible to vCJD and that genotype may influence whether disease appears in a clinical or asymptomatic form, supported by the appearance of the first case of potential asymptomatic vCJD infection in a PRNP 129MV patient. Following evidence of blood transfusion as a route of transmission, we have ascertained that all blood components and leucoreduced blood in a sheep model of vCJD have the ability to transmit disease. Importantly, we recently established that a PRNP 129MV patient blood recipient with an asymptomatic infection and limited PrP(Sc) deposition in the spleen could readily transmit disease into mice, demonstrating the potential for peripheral infection in the absence of clinical disease. This, along with the recent appendix survey which identified 16 positive appendices in a study of 32,441 cases, underlines the importance of continued CJD surveillance and maintaining control measures already in place to protect human health.