[Federal Register Volume 73, Number 196 (Wednesday, October 8, 2008)]
[Notices]
[Pages 58967-58968]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: E8-23819]


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DEPARTMENT OF HEALTH AND HUMAN SERVICES

Office of the Secretary


Findings of Scientific Misconduct

AGENCY: Office of the Secretary, HHS.

ACTION: Notice.

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SUMMARY: Notice is hereby given that the Office of Research Integrity 
(ORI) and the Assistant Secretary for Health have taken final action in 
the following case:
    Peili Gu, PhD., Baylor College of Medicine: Based on the report of 
an investigation conducted by the Baylor College of Medicine (BCM) and 
an initial review conducted by the Office of Research Integrity (ORI), 
the U.S. Public Health Service (PHS) found that Dr. Peili Gu, former 
postdoctoral researcher, Department of Molecular and Cellular Biology, 
BCM, engaged in scientific misconduct in research supported by National 
Institute of Diabetes and Kidney Diseases (NIDDK), National Institutes 
of Health (NIH), grant R01 DK073524, National Institute of Child Health 
and Human Development (NICHD), NIH, grants T32 HD07165 and U54 HD07495, 
and National Institute of General Medical Sciences (NIGMS), NIH, grant 
R01 GM066099. ORI acknowledges Dr. Gu's full cooperation with the BCM 
misconduct proceedings.
    Specifically, PHS found that the Respondent committed misconduct in 
science with respect to reporting falsified data in the following three 
papers:
    1. Gu, P., LeMenuet, D., Chung, A., & Cooney, A.J. ``Differential 
Recruitment of Methylated CpG Binding Domains [MBDs] by the Orphan 
Receptor GCNF Initiates the Repression and Silencing of Oct4 
Expression.'' Mol. Cell. Biology 26(24):9471-9483, December 2006 
(hereafter referred to as the ``MBD paper''):

<bullet> Respondent falsified the relative expression level of Oct4 in 
differentiated P19 cells and embryonic stem cells treated with MBD2 and 
MBD3 small interfering RNA presented in Figures 5E and 6E, 
respectively.
<bullet> Respondent falsified Figure 6A depicting wild type and GCNF-/-
embryonic stem cells to compare the binding of GCNF, MBD2, and MBD3 to 
the Oct4 gene and the measurement of expression at the RNA and protein 
levels by deleting in photoshop the GCNF Western blot data in the GCNF-
/-cells (to match the lack of expression at the RNA level), and 
falsified the MBD 2 Western blot data in the GCNF-/-cells (or that 
depicted in Figure 7C, which shows the exact same data but reportedly 
from DNA methylation-deficient embryonic stem cells [Dnmt3A/Dnmt3B/ES 
cells]).
<bullet> Respondent falsified the MBD2 wild type and GCNF-/-chromatin 
Immunoprecipitation (ChIP) data in Figure 6B.

    2. Gu, P., Morgan, D.H., Sattar, M, Xu, X., Wagner, R., Raviscioni, 
M., Lichtarge, O., & Cooney, A.J. ``Evolutionary Trace-Based Peptides 
Identify a Novel Asymmetric Interaction that Mediates Oligomerization 
in Nuclear Receptors.'' Journal of Biological Chemistry 280(36):31818-
31829, September 2005:
<bullet> In Figures 3C and 3D, depicting transfected wild-type and 
mutated HA-GCNF expression levels in undifferentiated and 
differentiated P19 cells, Respondent planned not to show the data for 
the Asp307 mutant (the data for the Asp307 mutant were deleted in panel 
D); however, she falsified Figure 3C by deleting the least intensive 
band instead of the Asp307 mutant in order to make the overall data 
appear more consistent and support the claim that there were no 
significant differences in the expression levels between the GCNF 
mutants and the wild type HA-GCNF in P19 cells.
<bullet> In Figure 4A, where Respondent intended not to show the data 
for the Asp307 mutant, she falsified the reported results by deleting 
the least intensive band instead of the Asp307 mutant in order to make 
the overall data appear more consistent in support of the claim that 
all mutants were expressed at similar levels in COS1 cells and that the 
various point mutations had not altered the stability of the protein.
<bullet> Respondent falsified Figures 4C and 4D depicting supershift of 
HA-GCNF homodimers expressed in COS1 cells using anti-GCNF and anti-HA 
antibodies, respectively, by inserting non-specific bands in each of 
three lanes of each figure where non-specific bands were not visible in 
the original data.
<bullet> Respondent falsified Figure 5A, which reported the detection 
of HA-GCNF point mutant expression in retinoic acid-differentiated P19 
cells by Western blot with anti-HA antibody, by duplicating a series of 
lanes in the published figure: Lane 2 is the same as lane 4; lane 3 is 
the same as lanes 5, 7, and 9, and lane 6 is the same as lanes 8, 10, 
and 11.
<bullet> Respondent falsified Figure 6C, which reported on the 
dimerization abilities of various GCNF mutants, by cutting and pasting 
(in photoshop) bands into original lanes 7 and 8 to demonstrate the 
homodimer; certain of the comparisons reported in the text describing 
this figure do not appear to be confirmed in a repeat experiment.

    3. Gu, P., LeMenuet, D., Chung, A., Mancini, M., Wheeler, D., & 
Cooney, A.J. Orphan Nuclear Receptor GCNF Is Required for the 
Repression of Pluripotency Genes during Retinoic Acid-Induced Embryonic 
Stem Cell Differentiation.'' Mol. Cell. Biology 25(19):8507-8519, 
October 2005:


[[Page 58968]]


<bullet> Respondent falsified Figure 1A by cutting out lanes and 
relocating them, wild type GCNF lanes 7 and 8 of the original data 
becoming lanes 1 and 2 in the published figure; the effect of the 
falsification was to demonstrate the inverse correlation with 
expression of Oct4, which did not appear to be confirmed in a repeat of 
the experiment.
<bullet> Respondent falsified Figure 4A by switching the 6 hour and 12 
hour Oct4 expression data in the wild type embryonic stem cells (these 
falsified data also appear in Figure 5B).

Dr. Gu has entered into a Voluntary Settlement Agreement (Agreement) in 
which she has voluntarily agreed, for a period of three (3) years, 
beginning on September 12, 2008:

(1) To exclude herself from serving in any advisory capacity to PHS, 
including but not limited to service on any PHS advisory committee, 
board, and/or peer review committee, or as a consultant or contractor 
to PHS; and
(2) That any institution that submits an application for PHS support 
for a research project on which the Respondent's participation is 
proposed or that uses the Respondent in any capacity on PHS supported 
research, or that submits a report of PHS-funded research in which the 
Respondent is involved, must concurrently submit a plan for monitoring 
of the Respondent's research to the funding agency and ORI for 
approval. The monitoring plan must be designed to ensure the scientific 
integrity of the respondent's research contribution. Respondent agreed 
that she will not participate in any PHS-supported research until such 
a monitoring plan is submitted to ORI and the funding agency.

Dr. Gu also agreed that she would immediately cooperate with BCM 
officials to request retraction of the MBD paper. In the retraction 
letter, she will state that she alone was responsible for the 
falsification and fabrication of some of the data reported in the 
paper.

FOR FURTHER INFORMATION CONTACT: Director, Division of Investigative 
Oversight, Office of Research Integrity, 1101 Wootton Parkway, Suite 
750, Rockville, MD 20852, (240) 453-8800.

Chris B. Pascal,
Director, Office of Research Integrity.
[FR Doc. E8-23819 Filed 10-7-08; 8:45 am]
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