Approaches and experiences implementing remote, electronic consent at the Leeds Clinical Trials Research Unit.

BACKGROUND: Use of electronic methods to support informed consent ('eConsent') is increasingly popular in clinical research. This commentary reports the approach taken to implement electronic consent methods and subsequent experiences from a range of studies at the Leeds Clinical Trials Research Unit (CTRU), a large clinical trials unit in the UK. MAIN TEXT: We implemented a remote eConsent process using the REDCap platform. The process can be used in trials of investigational medicinal products and other intervention types or research designs. Our standard eConsent system focuses on documenting informed consent, with other aspects of consent (e.g. providing information to potential participants and a recruiter discussing the study with each potential participant) occurring outside the system, though trial teams can use electronic methods for these activities where they have ethical approval. Our overall process includes a verbal consent step prior to confidential information being entered onto REDCap and an identity verification step in line with regulator guidance. We considered the regulatory requirements around the system's generation of source documents, how to ensure data protection standards were upheld and how to monitor informed consent within the system. We present four eConsent case studies from the CTRU: two randomised clinical trials and two other health research studies. These illustrate the ways eConsent can be implemented, and lessons learned, including about differences in uptake. CONCLUSIONS: We successfully implemented a remote eConsent process at the CTRU across multiple studies. Our case studies highlight benefits of study participants being able to give consent without having to be present at the study site. This may better align with patient preferences and trial site needs and therefore improve recruitment and resilience against external shocks (such as pandemics). Variation in uptake of eConsent may be influenced more by site-level factors than patient preferences, which may not align well with the aspiration towards patient-centred research. Our current process has some limitations, including the provision of all consent-related text in more than one language, and scalability of implementing more than one consent form version at a time. We consider how enhancements in CTRU processes, or external developments, might affect our approach.

Quinoxyfen perturbs signal transduction in barley powdery mildew (Blumeria graminis f.sp. hordei).

SUMMARY Quinoxyfen is a protectant fungicide which controls powdery mildew diseases by interfering with germination and/or appressorium formation. Mutants of barley powdery mildew, Blumeria graminis f.sp. hordei, which are resistant to quinoxyfen produce fewer conidia, which germinate and form appressoria more promiscuously than do the prolific numbers of wild-type spores. This suggests that resistance bypasses host recognition signals. RT-PCR profiles of signal transduction genes, recorded during wild-type germling morphogenesis, reveals that quinoxyfen alters the accumulation of Protein Kinase C (pkc), pkc-like and catalytic subunit of Protein Kinase A (cpka) transcripts. Differential display-reverse transcription PCR identified a gene transcript in wild-type conidia that was absent, or much less abundant, in conidia from quinoxyfen-resistant mutants. This mRNA was not detectable 24 h after wild-type conidia were inoculated on to barley. It encodes a GTPase activating protein (GAP), which may interact with a small molecular weight Ras-type GTP binding protein. In the presence of quinoxyfen, the gap mRNA remains throughout germling morphogenesis. The involvement of GAP in resistance suggests that quinoxyfen inhibits mildew infection by disrupting early cell signalling events.