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Federal Register / Vol. 86, No. 158 / Thursday, August 19, 2021 / Notices
DEPARTMENT OF HEALTH AND
HUMAN SERVICES
Office of the Secretary Findings of Research Misconduct Office of the Secretary, HHS.
Notice.

AGENCY:

lotter on DSK11XQN23PROD with NOTICES1

ACTION:

SUMMARY: Findings of research misconduct have been made against Viravuth Yin, Ph.D. Respondent, former Associate Professor, Mount Desert Island Biological Laboratory MDIBL. Respondent engaged in research misconduct in research supported by U.S. Public Health Service PHS funds, specifically National Institute of General Medical Sciences NIGMS, National Institutes of Health NIH, grants P20 GM104318 and P20
GM103423. The administrative actions, including supervision for a period of two 2 years, were implemented beginning on August 2, 2021, and are detailed below.
FOR FURTHER INFORMATION CONTACT:
Wanda K. Jones, Dr.P.H., Acting Director, Office of Research Integrity, 1101 Wootton Parkway, Suite 240, Rockville, MD 20852, 240 4538200.
SUPPLEMENTARY INFORMATION: Notice is hereby given that the Office of Research Integrity ORI has taken final action in the following case:
Viravuth Yin, Ph.D., Mount Desert Island Biological Laboratory: Based on the report of an investigation conducted by MDIBL and analysis conducted by ORI in its oversight review, ORI found that Dr. Viravuth Yin, former Associate Professor, MDIBL, engaged in research misconduct in research supported by PHS funds, specifically NIGMS, NIH, grants P20 GM104318 and P20
GM103423.
Respondent neither admits nor denies ORIs findings of research misconduct.
The settlement is not an admission of liability on the part of the Respondent.
The parties entered into a Voluntary Settlement Agreement to conclude this matter without further expenditure of time, finances, or other resources.
ORI found that Respondent engaged in research misconduct by knowingly, intentionally, and/or recklessly falsifying and/or fabricating data included in the following three 3
published papers and two 2 submitted manuscripts:
Smith AM, Dykeman CA, King BL, Yin VP. Modulation of TNFa Activity by the microRNA Let-7 Coordinates Heart Regeneration. iScience 2019;15:1
15; doi: 10.1016/j.isci.2019.04.009
hereafter referred to as iScience 2019.

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Smith AM, Dykeman CA, King BL, Yin VP. Modulation of TNFa Activity by the microRNA Let-7 Coordinates Heart Regeneration. iScience 2019;17:22529; doi: 10.1016/
j.isci.2019.06.017 hereafter referred to as iScience Correction.
Beauchemin M, Smith A, Yin VP.
Dynamic microRNA101a and Fosab expression controls zebrafish heart regeneration. Development 2015;142:402637; doi: 10.1242/
dev.126649 hereafter referred to as Development 2015.
Smith AM, Dykeman CA, Yin VP.
Modulation of epicardial TNFa Activity by the microRNA Let-7 Coordinates the Zebrafish Heart Regeneration.
Manuscript submitted to iScience in 2018 hereafter referred to as iScience 2018 draft.
Smith AM, Dykeman CA, Yin VP.
Modulation of epicardial TNFa Activity by the microRNA let-7 coordinates the zebrafish heart regeneration. Manuscript submitted to PNAS in 2018 hereafter referred to as PNAS 2018 draft.
Specifically, Respondent intentionally, knowingly, and/or recklessly falsified and/or fabricated data by:
Reusing, relabeling, and reporting Phosphate Buffered Saline PBS
controls as scrambled antisense Locked Nucleic Acids LNAs in the following experimental results:
RT-qPCR data representing the knockdown of let7 expression in Figure 2B of PNAS 2018 draft, iScience 2018 draft, and iScience 2019
images of tcf21:Dsred expression in LNA-let-7 treated hearts at 3, 14, and 21 days postamputation dpa showing defects in wound closure in Figure 2C of PNAS 2018 draft, iScience 2018 draft, and iScience 2019
quantification of tcf21:Dsred expression within the resection wound in LNA-let-7 treated hearts in Figure 2D of iScience 2019
images exhibiting proliferating cardiac muscle CM in Figure 3A of PNAS 2018 draft, iScience 2018 draft, and iScience 2019
suppression of CM proliferation indices in LNA-let-7 hearts at 3 and 7 dpa in Figure 3B of PNAS 2018
draft, iScience 2018 draft, and iScience 2019
severity of the injured heart phenotype in Figure 3C of PNAS 2018
draft, iScience 2018 draft, and iScience 2019
quantification of the severity of the injury heart phenotype in Figure 3D
of iScience 2019

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electron microscopy images of remote and injury zones of resected 7-dpa hearts in Figure 4A of PNAS 2018
draft, iScience 2018 draft, iScience 2019, and iScience Correction images of Tggata4:GFP expression in the primordial heart muscle layer in Figure 4B of PNAS 2018 draft, iScience 2018 draft, iScience 2019, and iScience Correction quantification of gata4:GFP
expression in control and LNA-let-7
treated hearts in Figure 4C of iScience 2019 and iScience Correction RNA transcripts identifying differentially upregulated TNFa transcripts in Figure 5A of PNAS 2018
draft, iScience 2018 draft, iScience 2019, and their resultant qPCR results, which identified increased TNFa expression in Figure 5C of PNAS 2018
draft, Figure 5B of iScience 2018 draft, iScience 2019, and Table S1 of iScience 2019
CM proliferation analyses results in Figures S4B and S4C of PNAS 2018
draft and iScience 2018 draft, and Figures S5B and S5C of iScience 2019
images representing the function of let-7 in Figure 2C of iScience Correction and reusing and relabeling images from an unrelated experiment, such that let-7 function is not represented in the image images reporting the function of let-7
in Figure 3A of iScience Correction images representing differences in the effects of miR101a depletion on Met2 and PNA expression and the quantification of cardiomyocyte proliferation in uninjured control and Tghs:miR-101a-sp heat exposed hearts CM proliferation analysis in Figures 2A, 2B, 2C, and 2D, and results in Figure 2E of Development 2015
muscle, fibrin, and collagen staining images representing increased scar tissue presence in Tghs:miR-101a-sp heat-treated hearts, as compared to wild type hearts in Figures 3A, 3B, 3C, 3D, 3E, and 3F of Development 2015
scarring indices and the size of the injured area in wild type versus Tghs:miR-101a-sp heat-treated hearts in Figures 3G and 3H of Development 2015
differences in 1 the amount of scarring, as represented by AFOG
staining in control and Tg hs:miR101-a-sp ventricles from resected and heat-treated hearts in Figures 4B and 4C; 2 the amount of scar tissue in the presence of suppressed miR-101a expression in Tghs:miR-101a-sp hearts, compared to control hearts in Figures 4H and 4I; and 3 the quantification of the scarring indices
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