Background: When researchers' careers are disrupted by life events-such as illness or childbirth-they often need to take extended time off. This creates a gap in their research output that can reduce their chances of winning funding. In Australia, applicants can disclose their career disruptions and peer reviewers are instructed to make appropriate adjustments. However, it is not clear if and how applicants use career disruption sections or how reviewers adjust and if they do it consistently.
Methods: To examine career disruption, we used surveys of the Australian health and medical research community. We used both a random sample of Australian authors on PubMed and a non-random convenience sample.
Results: Respondents expressed concerns that sharing information on career disruption would harm their chances of being funded, with 13% saying they have medical or social circumstances but would not include it in their application, with concerns about appearing 'weak'. Women were more reluctant to include disruption. There was inconsistency in how disruption was adjusted for, with less time given for those with depression compared with caring responsibilities, and less time given for those who did not provide medical details of their disruption.
Conclusions: The current system is likely not adequately adjusting for career disruption and this may help explain the ongoing funding gap for senior women in Australia.
Funding: National Health and Medical Research Council Senior Research Fellowship (Barnett).
All data and code are openly available here https://github.com/agbarnett/career_disruption
Survey of career disruptionGithub.
- Adrian Barnett
- Susanna Cramb
The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
Human subjects: Ethics approval was obtained from the Queensland University of Technology human research ethics committee. All participants provided informed consent before completing the survey.
- Ilse S Daehn, Icahn School of Medicine at Mount Sinai, United States
© 2022, Barnett et al.
This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.
Background: Compelling evidence has accumulated on the role of oxidative stress on the endothelial cell (EC) dysfunction underlying acute coronary syndrome. However, unveiling the underlying metabolic determinants has been hampered by the scarcity of appropriate cell models to address cell-autonomous mechanisms of ED dysfunction.
Methods: We have generated endothelial cells derived from thrombectomy specimens from patients affected with acute myocardial infarction (AMI) and conducted phenotypical and metabolic characterization, focused on central carbon metabolism.
Results: AMI-derived endothelial cells (AMIECs), but not control healthy coronary endothelial cells, display impaired growth, migration and tubulogenesis. Metabolically, AMIECs displayed augmented reactive oxygen species (ROS) and glutathione intracellular content, along with a diminished glucose consumption coupled to high lactate production. Consistent with diminished glycolysis in AMIECs, the protein levels of 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase type 3, PFKFB3, were downregulated. In contrast, PFKFB4 levels were upregulated, suggesting a shunting of glycolysis towards the pentose phosphate pathway (PPP), supported by upregulation in AMIECs of G6PD, the key enzyme in the oxidative branch of the PPP. Further, the glutaminolytic enzyme GLS was upregulated in AMIECs, providing a mechanistic explanation for the observed increase in glutathione content. Finally, AMIECs displayed a significantly higher mitochondrial membrane potential than control ECs, which, together with high ROS levels, suggest a highly coupled mitochondrial activity in patient ECs.
Conclusions: We suggest high mitochondrial proton coupling underlies the abnormally high production of ROS, balanced by PPP- and glutaminolysis-driven synthesis of glutathione, as a primary, cell-autonomous abnormality driving EC dysfunction in AMI.
Funding: European Commission Horizon 2020; CIBER- Carlos III National Institute of Health, Spain; Ministerio de Economia y Competitividad (MINECO) and Ministerio de Ciencia e Innovación, Spain; Generalitat de Catalunya-AGAUR, Catalonia; Plataforma Temática Interdisciplinar Salud Global (PTI-SG), Spain; British Heart Foundation, UK.
Reproducible research and open science practices have the potential to accelerate scientific progress by allowing others to reuse research outputs, and by promoting rigorous research that is more likely to yield trustworthy results. However, these practices are uncommon in many fields, so there is a clear need for training that helps and encourages researchers to integrate reproducible research and open science practices into their daily work. Here, we outline eleven strategies for making training in these practices the norm at research institutions. The strategies, which emerged from a virtual brainstorming event organized in collaboration with the German Reproducibility Network, are concentrated in three areas: (i) adapting research assessment criteria and program requirements; (ii) training; (iii) building communities. We provide a brief overview of each strategy, offer tips for implementation, and provide links to resources. We also highlight the importance of allocating resources and monitoring impact. Our goal is to encourage researchers – in their roles as scientists, supervisors, mentors, instructors, and members of curriculum, hiring or evaluation committees – to think creatively about the many ways they can promote reproducible research and open science practices in their institutions.