An experimental test of the effects of redacting grant applicant identifiers on peer review outcomes
- Retired, United States
- NIH/Center for Scientific Review, United States
- National Institutes of Health, United States
- Evaluact, Inc, United States
Abstract
Background: Blinding reviewers to applicant identity has been proposed to reduce bias in peer review.
Methods: This experimental test used 1200 NIH grant applications, 400 from Black investigators, 400 matched applications from White investigators, and 400 randomly selected applications from White investigators. Applications were reviewed by mail in standard and redacted formats.
Results: Redaction reduced, but did not eliminate, reviewers' ability to correctly guess features of identity. The primary, pre-registered analysis hypothesized a differential effect of redaction according to investigator race in the matched applications. A set of secondary analyses (not pre-registered) used the randomly selected applications from White scientists and tested the same interaction. Both analyses revealed similar effects: Standard format applications from White investigators scored better than those from Black investigators. Redaction cut the size of the difference by about half (e.g. from a Cohen's d of 0.20 to 0.10 in matched applications); redaction caused applications from White scientists to score worse but had no effect on scores for Black applications.
Conclusions: Grant-writing considerations and halo effects are discussed as competing explanations for this pattern. The findings support further evaluation of peer review models that diminish the influence of applicant identity.
Funding: Funding was provided by the NIH.
Data availability
All data analyzed for the findings presented in this manuscript are included in the supporting files
Article and author information
Author details
Mark D Lindner PhD
Funding
National Institutes of Health (none)
- Richard Nakamura
Employees of the NIH were involved in study design, in data analysis, data interpretation and manuscript writing. Data were collected, and major data analysis completed, by a contract research organization.
Ethics
Human subjects: All participants gave informed consent to participate in this study in accordance with a protocol that was approved on March 27, 2017 by the Social Solutions, Inc. IRB, (FWA 00008632), protocol #47.
Copyright
This is an open-access article, free of all copyright, and may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose. The work is made available under the Creative Commons CC0 public domain dedication.
Metrics
-
- 4,790
- views
-
- 577
- downloads
-
- 23
- 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)
An experimental test of the effects of redacting grant applicant identifiers on peer review outcomes
eLife 10:e71368.
https://doi.org/10.7554/eLife.71368
Further reading
-
The study of science itself is a growing field of research.
-
- Cell Biology
Prostaglandin E2 (PGE2) is an endogenous inhibitor of glucose-stimulated insulin secretion (GSIS) and plays an important role in pancreatic β-cell dysfunction in type 2 diabetes mellitus (T2DM). This study aimed to explore the underlying mechanism by which PGE2 inhibits GSIS. Our results showed that PGE2 inhibited Kv2.2 channels via increasing PKA activity in HEK293T cells overexpressed with Kv2.2 channels. Point mutation analysis demonstrated that S448 residue was responsible for the PKA-dependent modulation of Kv2.2. Furthermore, the inhibitory effect of PGE2 on Kv2.2 was blocked by EP2/4 receptor antagonists, while mimicked by EP2/4 receptor agonists. The immune fluorescence results showed that EP1–4 receptors are expressed in both mouse and human β-cells. In INS-1(832/13) β-cells, PGE2 inhibited voltage-gated potassium currents and electrical activity through EP2/4 receptors and Kv2.2 channels. Knockdown of Kcnb2 reduced the action potential firing frequency and alleviated the inhibition of PGE2 on GSIS in INS-1(832/13) β-cells. PGE2 impaired glucose tolerance in wild-type mice but did not alter glucose tolerance in Kcnb2 knockout mice. Knockout of Kcnb2 reduced electrical activity, GSIS and abrogated the inhibition of PGE2 on GSIS in mouse islets. In conclusion, we have demonstrated that PGE2 inhibits GSIS in pancreatic β-cells through the EP2/4-Kv2.2 signaling pathway. The findings highlight the significant role of Kv2.2 channels in the regulation of β-cell repetitive firing and insulin secretion, and contribute to the understanding of the molecular basis of β-cell dysfunction in diabetes.
