Meta-research: Justifying career disruption in funding applications, a survey of Australian researchers

  1. Adrian Barnett  Is a corresponding author
  2. Katie Page
  3. Carly Dyer
  4. Susanna Cramb
  1. Queensland University of Technology, Australia
  2. University of Technology Sydney, Australia
  3. Queensland University of Technology, Australia

Abstract

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).

Data availability

All data and code are openly available here https://github.com/agbarnett/career_disruption

The following data sets were generated

Article and author information

Author details

  1. Adrian Barnett

    School of Public Health and Social Work, Queensland University of Technology, Brisbane, Australia
    For correspondence
    a.barnett@qut.edu.au
    Competing interests
    Adrian Barnett, receives funding from the NHMRC and is a member of the NHMRC Research Committee..
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0001-6339-0374
  2. Katie Page

    Centre for Health Economics Research and Evaluation, University of Technology Sydney, Sydney, Australia
    Competing interests
    No competing interests declared.
  3. Carly Dyer

    Australian Centre for Health Services Innovation and Centre for Healthcare Transformation, Queensland University of Technology, Brisbane, Australia
    Competing interests
    No competing interests declared.
  4. Susanna Cramb

    Australian Centre for Health Services Innovation and Centre for Healthcare Transformation, Queensland University of Technology, Brisbane, Australia
    Competing interests
    Susanna Cramb, receives funding from the NHMRC.

Funding

National Health and Medical Research Council (APP1117784)

  • Adrian Barnett

National Health and Medical Research Council (APP2008313)

  • Susanna Cramb

The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.

Ethics

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.

Copyright

© 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.

Metrics

  • 1,704
    views
  • 155
    downloads
  • 6
    citations

Views, downloads and citations are aggregated across all versions of this paper published by eLife.

Download links

A two-part list of links to download the article, or parts of the article, in various formats.

Downloads (link to download the article as PDF)

Open citations (links to open the citations from this article in various online reference manager services)

Cite this article (links to download the citations from this article in formats compatible with various reference manager tools)

  1. Adrian Barnett
  2. Katie Page
  3. Carly Dyer
  4. Susanna Cramb
(2022)
Meta-research: Justifying career disruption in funding applications, a survey of Australian researchers
eLife 11:e76123.
https://doi.org/10.7554/eLife.76123

Share this article

https://doi.org/10.7554/eLife.76123

Further reading

    1. Cell Biology
    2. Medicine
    Shuo He, Lei Huang ... Jinlong He
    Research Article

    Disturbed shear stress-induced endothelial atherogenic responses are pivotal in the initiation and progression of atherosclerosis, contributing to the uneven distribution of atherosclerotic lesions. This study investigates the role of Aff3ir-ORF2, a novel nested gene variant, in disturbed flow-induced endothelial cell activation and atherosclerosis. We demonstrate that disturbed shear stress significantly reduces Aff3ir-ORF2 expression in athero-prone regions. Using three distinct mouse models with manipulated Aff3ir-ORF2 expression, we demonstrate that Aff3ir-ORF2 exerts potent anti-inflammatory and anti-atherosclerotic effects in Apoe-/- mice. RNA sequencing revealed that interferon regulatory factor 5 (Irf5), a key regulator of inflammatory processes, mediates inflammatory responses associated with Aff3ir-ORF2 deficiency. Aff3ir-ORF2 interacts with Irf5, promoting its retention in the cytoplasm, thereby inhibiting the Irf5-dependent inflammatory pathways. Notably, Irf5 knockdown in Aff3ir-ORF2 deficient mice almost completely rescues the aggravated atherosclerotic phenotype. Moreover, endothelial-specific Aff3ir-ORF2 supplementation using the CRISPR/Cas9 system significantly ameliorated endothelial activation and atherosclerosis. These findings elucidate a novel role for Aff3ir-ORF2 in mitigating endothelial inflammation and atherosclerosis by acting as an inhibitor of Irf5, highlighting its potential as a valuable therapeutic approach for treating atherosclerosis.

    1. Medicine
    2. Neuroscience
    Joanna Kosinska, Julian C Assmann ... Markus Schwaninger
    Research Article

    Monomethyl fumarate (MMF) and its prodrug dimethyl fumarate (DMF) are currently the most widely used agents for the treatment of multiple sclerosis (MS). However, not all patients benefit from DMF. We hypothesized that the variable response of patients may be due to their diet. In support of this hypothesis, mice subjected to experimental autoimmune encephalomyelitis (EAE), a model of MS, did not benefit from DMF treatment when fed a lauric acid-rich (LA) diet. Mice on normal chow (NC) diet, in contrast, and even more so mice on high-fiber (HFb) diet showed the expected protective DMF effect. DMF lacked efficacy in the LA diet-fed group despite similar resorption and preserved effects on plasma lipids. When mice were fed the permissive HFb diet, the protective effect of DMF treatment depended on hydroxycarboxylic receptor 2 (HCAR2) which is highly expressed in neutrophil granulocytes. Indeed, deletion of Hcar2 in neutrophils abrogated DMF protective effects in EAE. Diet had a profound effect on the transcriptional profile of neutrophils and modulated their response to MMF. In summary, DMF required HCAR2 on neutrophils as well as permissive dietary effects for its therapeutic action. Translating the dietary intervention into the clinic may improve MS therapy.