Meta-Research: Individual-level researcher data confirm the widening gender gap in publishing rates during COVID-19
- Aarhus University, Denmark
- University of Copenhagen, Denmark
- University of Michigan, United States
Abstract
Publishing is part and parcel of a successful academic career, and Covid-19 has amplified gender disparities in manuscript submissions and authorships. We used longitudinal publication data on 431,207 scientists in biology, chemistry, and clinical and basic medicine to quantify the differential impact of Covid-19 on women's and men's annual publishing rates. In a difference-in-differences analysis, we estimated that the average gender difference in publication productivity increased from -0.26 in 2019 (corresponding to a 17% lower output for women than men) to -0.35 in 2020 (corresponding to a 24% lower output for women than men). An age-group comparison showed a widening gender gap for both early career and mid-career scientists. The increasing gender gap was most pronounced among highly productive authors and scientists in clinical medicine and biology. Our study demonstrates the importance of reinforcing institutional commitments to diversity through policies that support the inclusion and retention of women researchers.
Data availability
The current manuscript is a computational study, so no data have been generated for this manuscript. Source data and code will be provided on git-hub for all tables and figures.
Article and author information
Author details
Emil Bargmann Madsen
Mathias Wullum Nielsen
Jens Peter Andersen
Funding
Samfund og Erhverv, Det Frie Forskningsråd (DFF-0133-00165B)
- Emil Bargmann Madsen
- Mathias Wullum Nielsen
- Josefine Bjørnholm
- Jens Peter Andersen
Aarhus Universitets Forskningsfond (AUFF-F-2018-7-5)
- Jens Peter Andersen
Independent Research Fund Denmark (9130-00029B)
- Mathias Wullum Nielsen
The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
Copyright
© 2022, Madsen 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
-
- 3,016
- views
-
- 270
- downloads
-
- 34
- 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)
Meta-Research: Individual-level researcher data confirm the widening gender gap in publishing rates during COVID-19
eLife 11:e76559.
https://doi.org/10.7554/eLife.76559
Further reading
-
eLife’s Executable Research Article lets authors include live code, data and interactive figures in their published paper.
-
- Cancer Biology
- Computational and Systems Biology
Effects from aging in single cells are heterogenous, whereas at the organ- and tissue-levels aging phenotypes tend to appear as stereotypical changes. The mammary epithelium is a bilayer of two major phenotypically and functionally distinct cell lineages: luminal epithelial and myoepithelial cells. Mammary luminal epithelia exhibit substantial stereotypical changes with age that merit attention because these cells are the putative cells-of-origin for breast cancers. We hypothesize that effects from aging that impinge upon maintenance of lineage fidelity increase susceptibility to cancer initiation. We generated and analyzed transcriptomes from primary luminal epithelial and myoepithelial cells from younger <30 (y)ears old and older >55 y women. In addition to age-dependent directional changes in gene expression, we observed increased transcriptional variance with age that contributed to genome-wide loss of lineage fidelity. Age-dependent variant responses were common to both lineages, whereas directional changes were almost exclusively detected in luminal epithelia and involved altered regulation of chromatin and genome organizers such as SATB1. Epithelial expression variance of gap junction protein GJB6 increased with age, and modulation of GJB6 expression in heterochronous co-cultures revealed that it provided a communication conduit from myoepithelial cells that drove directional change in luminal cells. Age-dependent luminal transcriptomes comprised a prominent signal that could be detected in bulk tissue during aging and transition into cancers. A machine learning classifier based on luminal-specific aging distinguished normal from cancer tissue and was highly predictive of breast cancer subtype. We speculate that luminal epithelia are the ultimate site of integration of the variant responses to aging in their surrounding tissue, and that their emergent phenotype both endows cells with the ability to become cancer-cells-of-origin and represents a biosensor that presages cancer susceptibility.
