Findings of Scientific Misconduct, 58967-58968 [E8-23819]
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Federal Register / Vol. 73, No. 196 / Wednesday, October 8, 2008 / Notices
concerning the final effect of the HHS
decision to designate a class of
employees at the Y–12 Plant in Oak
Ridge, Tennessee, as an addition to the
Special Exposure Cohort (SEC) under
the Energy Employees Occupational
Illness Compensation Program Act of
2000. On August 15, 2008, as provided
for under 42 U.S.C. 7384q(b), the
Secretary of HHS designated the
following class of employees as an
addition to the SEC:
All employees of the Department of Energy
(DOE), its predecessor agencies, and DOE
contractors or subcontractors who worked at
the Y–12 Plant in Oak Ridge, Tennessee from
March 1, 1943 through December 31, 1947 for
a number of work days aggregating at least
250 work days occurring either solely under
this employment or in combination with
work days within the parameters established
for one or more other classes of employees
in the Special Exposure Cohort.
This designation became effective on
September 14, 2008, as provided for
under 42 U.S.C. 7384l(14)(C). Hence,
beginning on September 14, 2008,
members of this class of employees,
defined as reported in this notice,
became members of the Special
Exposure Cohort.
FOR FURTHER INFORMATION CONTACT:
Larry Elliott, Director, Office of
Compensation Analysis and Support,
National Institute for Occupational
Safety and Health (NIOSH), 4676
Columbia Parkway, MS C–46,
Cincinnati, OH 45226, Telephone 513–
533–6800 (this is not a toll-free
number). Information requests can also
be submitted by e-mail to
OCAS@CDC.GOV.
Dated: September 22, 2008.
Christine M. Branche,
Acting Director, National Institute for
Occupational Safety and Health.
[FR Doc. E8–23894 Filed 10–7–08; 8:45 am]
BILLING CODE 4163–19–P
DEPARTMENT OF HEALTH AND
HUMAN SERVICES
Office of the Secretary
Findings of Scientific Misconduct
Office of the Secretary, HHS.
Notice.
AGENCY:
jlentini on PROD1PC65 with NOTICES
ACTION:
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
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19:10 Oct 07, 2008
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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’’):
• 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.
• 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]).
• 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:
PO 00000
Frm 00044
Fmt 4703
Sfmt 4703
58967
• 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.
• 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.
• 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 nonspecific bands were not visible in the
original data.
• 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.
• 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:
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58968
Federal Register / Vol. 73, No. 196 / Wednesday, October 8, 2008 / Notices
• 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.
• 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.
jlentini on PROD1PC65 with NOTICES
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]
BILLING CODE 4150–31–P
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DEPARTMENT OF HEALTH AND
HUMAN SERVICES
Office of the Secretary
Findings of Scientific Misconduct
Office of the Secretary, HHS.
Notice.
AGENCY:
ACTION:
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:
Kirk Sperber, M.D., Mount Sinai
School of Medicine: Based on the report
of an investigation conducted by the
Mount Sinai School of Medicine
(MSSM) and additional analysis
conducted by the Office of Research
Integrity (ORI) in its oversight review,
the U.S. Public Health Service (PHS)
found that Dr. Kirk Sperber, former
Associate Professor, Department of
Medicine, Division of Clinical
Immunology, MSSM, engaged in
scientific misconduct while supported
by National Institute of Allergy and
Infectious Diseases (NIAID), National
Institutes of Health (NIH), grants R01
AI45343 and P01 AI44236, and National
Cancer Institute, NIH, grant R29
CA256990.
PHS finds the Respondent engaged in
scientific misconduct by falsifying and
fabricating data that were included in
NIAID, NIH, grant applications R01
AI45343–01A1, R01 AI45343–04A2, and
P01 AI44236–05. Respondent’s
scientific misconduct occurred while he
was a faculty member at MSSM.
Respondent is no longer employed at
MSSM.
Specifically, PHS found that
Respondent engaged in scientific
misconduct by falsifying and fabricating
data in the following publications:
1. In multiple figures reported in
Sperber, K., Beuria, P., Singha, N.,
Gelman, I., Cortes, P., Chen, H., & Kraus,
T. ‘‘Induction of apoptosis by HIV–1–
infected monocytic cells.’’ Journal of
Immunology 170:1566–1578, 2003
(‘‘2003 J. Immunol. paper’’) (Retracted
in December 2005); by duplicating and
reusing panels of FACS data in Figures
1A, 2, 4A, 4B, and 7; by duplicating and
reusing lanes of polyacrylamide gels in
Figure 3, of Western blot analyses in
Figures 5A, 5C, 6C, and 9, and of
agarose gels in PCR analyses in Figure
5B; and by duplicating and reusing laser
confocal micrographs in Figures 10 and
11. Respondent’s claims that Figures
1A, 2, 4A, and 7 were representative of
experiments repeated five times and
that Figures 3, 4B, 5A, 6C, and 9 were
representative of experiments repeated
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Fmt 4703
Sfmt 4703
three times constitute additional
falsifications. The effect of these
misrepresentations was to falsely
demonstrate the proapoptotic activity of
a protein from a novel cDNA clone
isolated from an HIV-infected human
macrophage cell line and to falsify its
presence in brain and lymphoid tissue
from patients with HIV-associated
dementia.
2. In Figure 10 reported in RakoffNahoum, S., Chen, H., Kraus, T., George,
I., Oei, E., Tyorlin, M., Salik, E., Beuria,
P., & Sperber, K. ‘‘Regulation of Class II
Expression in Monocytic Cells after
HIV–1 Infection.’’ J. Immunol.
167:2331–2342, 2001 (Retracted in
November 2006), by duplicating and
reusing four confocal micrographs to
misrepresent different panels for the
Cath D, 43pol and CD–63, 43neve data;
for the Cath D, 43gag and Cath D, 43nef
data; for the DAMP, 43 nef and M6PR,
43nef data; and for the M6PR, 43gag and
the CD–63, 43gag data. Respondent’s
reported claim that the results were
representative of an experiment
repeated five times constitutes an
additional falsification.
3. In Figures 3B, 4B, and 6B reporting
flow cytometry analyses (FACS) in
Chen, H., Yip, Y.K., George, I., Tyorkin,
M., Salik, E., & Sperber, K. ‘‘Chronically
HIV–1–Infected Monocytic Cells Induce
Apoptosis in Cocultured T Cells.’’ J.
Immunol. 161:4257–4267, 1998
(Retracted in November 2006); by
reusing two FACS histograms, each to
represent 2 different experiments in
Figure 3B; by reusing the same FACS
histogram as the negative control for
CD–4 cells and for the CD–8 cells in
Figure 4B; and by duplications of the
top two panels, the middle two panels,
and the bottom two panels of data as
graded dilutions of different fractions in
Figure 6B to falsely show that a soluble
factor from 43HIV cells induced
apoptosis. Figure 6B was also presented
in grant application AI45343–01A1 as
Figure 5B. Respondent’s reported claims
that the results in Figures 3B, 4B, and
6B were each representative of
experiments that were repeated three
times constitute additional
falsifications.
PHS also finds that Respondent
engaged in scientific misconduct by
falsifying and fabricating the following
data in NIAID, NIH, research
applications R01 AI45343–04A2 and
P01 AI44236–05:
4. The results of Figures 1, 6C, 7, 9,
10 and 11 from the 2003 J. Immunology
paper were reported in NIAID, NIH,
grant application R01 AI45343–04A2;
nearly all of the figures in the paper
were falsified, so that the claims in the
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]]>Agencies
[Federal Register Volume 73, Number 196 (Wednesday, October 8, 2008)]
[Notices]
[Pages 58967-58968]
From the Federal Register Online via the Government Printing Office [www.gpo.gov]
[FR Doc No: E8-23819]
-----------------------------------------------------------------------
DEPARTMENT OF HEALTH AND HUMAN SERVICES
Office of the Secretary
Findings of Scientific Misconduct
AGENCY: Office of the Secretary, HHS.
ACTION: Notice.
-----------------------------------------------------------------------
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''):
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.
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]).
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:
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.
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.
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.
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.
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]]
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.
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]
BILLING CODE 4150-31-P
