                         ˿µϣ20060329գ

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2006.3.26. 

й걨2006.3.29

(XYS20060329)

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йҽѧԺָԵԺ

ߣPaul Mooney
ߵȽ±2006329

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Chinese Medical School Fires Assistant Dean Who Was Accused of Plagiarism

The Chronicle of Higher Education
Wednesday, March 29, 2006

By PAUL MOONEY

Beijing

China's Tsinghua University has fired the assistant dean of its  
School of Medicine following accusations that the professor  
plagiarized an article from an American medical journal, and may have  
fabricated work experience listed on his resume.

The accusations first surfaced last November on a blog set up by a  
local scholar, Fang Zhouzhi, that is devoted to exposing cases of  
plagiarism and academic corruption.

Mr. Fang accused the medical-school official, Liu Hui, of having  
plagiarized a scholarly work by another Chinese doctor in the United  
States that was published in the Journal of General Virology. Mr.  
Fang also raised doubts about Dr. Liu's claim on his resume which  
was posted on a university Web site, that he had worked at the New  
York University Medical Center from 1994 to 2004, including a stint  
as the director of a surgery-research institute. Tsinghua University  
has since deleted Dr. Liu's page from its Web site.

A spokesman for the New York University School of Medicine, which is  
part of the medical center, confirmed that no one by the name Liu Hui  
had worked at the center during the period listed on the resume.

Tsinghua University, which dismissed Dr. Liu on March 10, did not  
respond to requests for information. However, in an official  
statement, the university said that after carrying out an  
investigation, it had discovered "serious inaccuracies" and "improper  
actions" in the materials submitted to the university in Dr. Liu's  
employment application and on his personal Web site, and had decided  
to cancel his contract.

Dr. Liu could not be reached for an interview and did not reply to an  
e-mail message requesting information. However, the newspaper Beijing  
Youth Daily reported last week that Dr. Liu had sent an e-mail  
message to Tsinghua administrators vigorously denying plagiarizing  
the article. According to the newspaper, Dr. Liu argued that the  
paper had mistakenly appeared on his list of research papers because  
of a data-collection error by a library data-retrieval system. Dr.  
Liu said that the actual author of the article shared the same  
surname and first initial, Liu, H.

Mr. Fang alleges that Dr. Liu was actually working in a surgical  
laboratory at the Mount Sinai School of Medicine, also in New York,  
during part of the period that he claimed to be working at New York  
University.

The Ministry of Education made a public statement confirming the  
dismissal of Dr. Liu, adding that it was planning to set up a special  
commission to monitor what critics say is a rapid increase in  
academic corruption and plagiarism in China.

Mr. Fang, however, attributed the growing problem to scholars  
"seeking power and profit without morality" and to the lack of a free  
media to report such incidents. "China does not have an official  
channel to report, investigate, and punish scientific misconduct," he  
said. "Therefore, cheaters don't have to worry that they will some  
day be caught and punished."

The biologist, who now works as a freelance writer, said that he had  
exposed more than 500 cases of "scientific misconduct" since August  
2000, but that most of the cases were ignored by the government. He  
said Liu's dismissal was "an exception."

The popular magazine China Newsweek ran a 12-page cover story last  
week on academic misconduct here titled "The Abnormal Corruption of  
Higher Education."

(XYS20060329)

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ԡȻҽѧת˾ĵһλشԭģ

We would like to thank Dr. Si for his interest in our work. His first 
concern is related to whole cell as antigens. To our knowledge, there 
is no published evidence to support his statement that As all of 
these proteins can be immunogens, the immunized animals should produce 
the antibodies against, if not all, at least most of proteins. By 
contrast, in accordance with our observations, it has been reported by 
others1-5 that only some or even a few proteins in a cell, not most of 
proteins, may be responsible for the generation of the antibodies 
against xenogeneic whole cells, including the use of the xenograft of 
organs or tissues1, 2, xenogeneic endothelial cells3 and the other 
xenogeneic agents such as Schistosoma mansoni4 and Dirofilaria immitis 
larva5, etc. In addition, the other whole cancer cell vaccines 
elicited antibody against only one antigen6, 7. Thus, whether or not 
the molecules in whole cells can be found by the antibodies induced 
with the whole cells as antigens may be dependent on a variety of 
factors, including cell types (antigens types), the level of their 
expression, intact cells or cell lysates adjuvant, and route of the 
vaccination, as well as the methods of the identification of the 
antigens, etc.  

His second question is related to the potential side effect by the 
adoptive transfer of the antibody against VEGFR-2 or alpha-v integrin. 
His statement the cancer patients treated with several angiogenesis 
inhibitors, including anti-VEGFRII antibody, were reported to 
experience thrombosis, hypertension and proteinuria, implying the 
involvement of platelets and kidney is incorrect. In fact, there is 
no report about the side effect, such as thrombosis, hypertension and 
proteinuria, in the cancer patients treated with anti-VEGFRII (VEGFR-2). 
It has been reported that these side effects are related to the 
antibody against VEGF, not to antibody against VEGFR-2, seeing the 
number 2 of his references, and the side effects of the antibody 
against VEGF are also only modest. Although VEGFR-2 or alpha-v 
integrin may express at lower level in some normal tissues, it has not 
been reported to show disastrous sequelae by targeting to VEGFR-2 
or alpha-v integrin with the different strategies including the 
vaccines based on VEGFR-2 (Ref. 8, 9) or adoptive transfer of antibody 
against VEGFR-2 (Ref. 10, 11) or against alpha-v integrin12,13 in mice 
models. In accordance with our observations, these treatments was also 
well tolerated in mice and no apparent adverse consequences were 
observed, and histological examination also appeared normal in mice 
treated by the anti-VEGFR-2 mAb or by the vaccine based on VEGFR-2 (Ref. 
8-12). Clinical trial with antibody against alpha-v beta-3 also 
resulted in little or no toxicity14. Thus, based on the findings 
mentioned above, the lack of major toxicity in the targeting of 
VEGFR-2 or alpha-v integrin support the view that the sensitivity of 
the vascular endothelium in some normal tissues may be different from 
that in malignant tumor to inhibition of angiogenesis8-12. This view 
is also supported by the findings that VEGFR-2 and alpa-v beta 3 
integrin is expressed in normal vascular endothelium in lower levels, 
compared with that in tumor vasculature15,16. In addition, there were 
no positive staining found in the glomerular capillaries of the 
immunized mice. 

Thirdly, his concern is about the mechanism by which our antibody 
against alpha v integrin subunit worked. Although our antibody against 
alpha-v integrin was not a conformation-specific antibody and 
interacts with alpha-chain, it showed the antitumor activity. In 
accordance with our observations, the others have also demonstrated 
that the antibody against alpha-v integrin subunit alone showed the 
inhibition of angiogenesis or adhesion and migration of cancer cell12, 
13, suggesting the important roles of alpha-v integrin subunit alone 
in the function of the cells. It has been also known that some 
antibodies against non-binding domain can block the function of the 
integrin allosterically as well17, as we have discussed previously18. 
As mentioned above, the antibody against VEGFR-2 or against alpha-v 
integrin alone or the vaccine based on VEGFR-2 alone had already 
showed the potent anti-angiogenesis and antitumor effect8-12. Thus, 
the high potency of the polyclonal serum isolated from xenogeneic 
endothelial cells in our study may result from the blockade of some 
important angiogenesis-associated molecules such as alpha-v integrin 
and VEGFR-2 as well as other unidentified molecules and may involve 
targeting to multiple sites18, as angiogenesis is a complex process 
involving in many molecules on new vessels. This suggestion is also 
supported by the recent findings by the others that the polyclonal 
antibodies obtained with the vaccination of xenogeneic endothelial 
cells showed the potent inhibition of endothelial cells and induction 
of apoptosis of endothelial cells as well as the abrogation of tumor 
growth without major toxicity3. In addition, whether or not these 
polyclonal antibodies obtained by the immunization with xenogeneic 
endothelial cells also showed the antitumor activity in vivo by 
complement-mediated cytotoxicity or by antibody-dependent 
cell-mediated cytotoxicity against the endothelial cells is an 
intriguing question to be further explored.

Finally, the tumor size in two perpendicular diameters was measured 
with calipers. Tumor size can be expressed in diameter, as also 
reported by the others19, 20.  

References: 

1.	Brouard, S, et al. Induction of anti-Forssman antibodies in 
the hamster-to-rat xenotransplantation model. Transplantation. 69, 
1193-201 (2000).

2.	Chong, A. S. et al. Modification of humoral responses by the 
combination of leflunomide and cyclosporine in Lewis rats transplanted 
with hamster hearts. Transplantation. 64, 1650-7 (1997) 

3.	Scappaticci, F.A. et al. Polyclonal antibodies to xenogeneic 
endothelial cells induce apoptosis and block support of tumor growth 
in mice. Vaccine, 21, 2667-2677 (2003). 

4.	James, S. L., Pearce, E. J and Sher, A. Induction of 
protective immunity against Schistosoma mansoni by a non living vaccine. 
The Journal of Immunology, 134, 3432-3438 (1985). 

5.	Grieve, R. B. et al. Identification of Dirofilaria immitis 
larval antigens with immunoprophylactic potential using sera from 
immune dogs. The Journal of Immunology, 148, 2511-2515 (1992). 

6.	Chung, M. H. et al. Humoral immune response to a therapeutic 
polyvalent cancer vaccine after complete resection of thick primary 
melanoma and sentinel lymphadenectomy. J Clin Oncol. 21, 313-9 (2003)

7.	Hoon, D. S., et al. Melanoma patients immunized with melanoma 
cell vaccine induce antibody responses to recombinant MAGE-1 antigen. 
The Journal of Immunology, 154, 730-737 (1995). 

8.	Niethammer, A. G, et al. A DNA vaccine against VEGF receptor 2 
prevents effective angiogenesis and inhibits tumor growth. Nat Med. 
2002;8:1369-1375.

9.	Li Y, et al. Active immunization against the vascular 
endothelial growth factor receptor flk1 inhibits tumor angiogenesis 
and metastasis. J Exp Med. 195, 1575-84 (2002)

10.	Prewett M, et al. Antivascular endothelial growth factor 
receptor (Fetal Liver Kinase 1) monoclonal antibody inhibits tumor 
angiogenesis and growth of several mouse and human tumors. Cancer Res. 
59, 5209-5218 (1999). 

11.	Kunkel P, et al. Inhibition of glioma angiogenesis and growth 
in vivo by systemic treatment with a monoclonal antibody against 
vascular endothelial growth factor receptor-2. Cancer Res. 61, 
6624-6628 (2001).

12.	Deryugina, E. I. et al. A novel monoclonal antibody, L1A3, is 
directed to the functional site of the alpha v integrin subunit. 
Hybridoma. 15: 279-88 (1996). 

13.	Jang, Y. C. et al. Role of alpha(v) integrins and angiogenesis 
during wound repair. Wound Repair Regen. 7, 375-80 (1999).

14.	Posey JA, et al. A pilot trial of Vitaxin, a humanized 
anti-vitronectin receptor (anti alpha v beta 3) antibody in patients 
with metastatic cancer. Cancer Biother Radiopharm. 16,125-32 (2001). 
Grieve, R.B. et al. 

15.	Eliceiri, B.P. and Cheresh, D.A. The Role of integrins during 
angiogenesis: insights into potential mechanisms of action and 
clinical development. J. Clin. Invest. 103, 1227-1230 (1999) 

16.	Brown, L.F. et al. Expression of vascular permeability factor 
(vascular endothelial growth factor) and its receptors in breast cancer. 
Hum. Pathol. 26:86C91 (1995)

17.	Lin, E. C. et al: A series of function blocking antibodies 
against the avb3 integrin binding allosteric to the ligand binding 
site and induce ligand dissociation. Cell adhes. Commun. 6, 451-464 
(1998).  

18.	Wei, Y, et al. Immunotherapy of tumors with xenogeneic 
endothelial cells as a vaccine. Nature Medicine, 6, 1160-1166 (2000). 

19.	Lu, W. et al. Eradication of primary murine fibrosarcomas and 
induction of systemic immunity by adenovirus-mediated interferon-beta 
gene therapy. Cancer Research 59, 5202-5208 (1999)

20.	Jagat R. et al. Vascular attack by 
5,6-Dimethylxanthenone-4-acetic acid combined with B7.1 
(CD80)-mediated immunotherapy overcomes immune resistance and leads to 
the eradication of large tumors and multiple tumor Foci. Cancer 
Research 61, 1948-1956 (2001).

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µġĴѧbbsκȫ¼Ĺ Ȼơ־༭ 
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Leedsѧйѧߵ

ߣContiConti

ӢLeedsѧвйѧʦѧԺһйѧDr. 
Ping Zheng⡣

ȹڵıѧλ(Hons)һ˵ӢӢ
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1, 20063 Leedsѧĸ˽ܣ
http://lubswww.leeds.ac.uk/lubs/index.php?id=113&backPID=81&tx_staffde
tails_staff=196

Dr Ping Zheng

BA (Hons) Economics, China
2002 - 2004: Part-time lecturer, University of Abertay Dundee (UAD)

22005ҳ

http://72.14.203.104/u/abertay?q=cache:VpkUJmxEIP4J:www.abertay.ac.uk/
Schools/DBS/staff.cfm%3Fprinter%3DTRUE%26Key%3D001.003.003+zheng+ping&
hl=en&ct=clnk&cd=1&ie=UTF-8

Ping Zheng
Part-time Language Tutor (Chinese) Dundee Business School

ȷԼĲˣλ֪

(XYS20060329)

˿(www.xys.org)(xys.dxiong.com)(xys.3322.org)(xys.xlogit.com)

ԡʨԺʿһͶ¼Ŀ

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3006-3-30

(XYS20060329)

˿(www.xys.org)(xys.dxiong.com)(xys.3322.org)(xys.xlogit.com)

֮ǴĿģ

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˵զ죿LNCS帺Alfred Hofmannʼ
Alfred.Hofmann@springer-sbm.deҪˣԵйﶷ

(XYS20060329)

˿(www.xys.org)(xys.dxiong.com)(xys.3322.org)(xys.xlogit.com)

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ɣһĹϵ

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̫ȱپĿɲԣ˵Ƿɹ涨취ضҪ
ٱ˻֤˵ְȫΣϹأ
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˵2001꣬ȫ˴ʼо֤޸ġϷ͡
о漰֤˺;ٱ˱ƶȣ2007̨μҺ
μ̡֤

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ߣ仰˵ٱ˾ٱʵǲʵģҲӦܵ


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˵2004625գƱָ788ҵ˰
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ձԺ͹ԣʵٱϵ˶Ϊٱð´
踵£ʵҾǺģȴ߲ǰ̨Ҳ⣬
˵ﻰġ

ߣľٱԺΧձĿǾ̫ɵ ̫
ֵˡ

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