Federal Register / Vol. 73, No. 196 / Wednesday, October 8, 2008 / Notices 58967 

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 

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 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: 


jlentini on PROD1PC65 with NOTICES
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. 

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 

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: 

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 

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 


jlentini on PROD1PC65 with NOTICES