Personal comment from Dr. James Whitfield : Thank you for sending me this sad story ofa person being unable to repeata laboratory's improtant experiments. A person from my lab also once went to work in another lab and could not repeat their important published data, but unlike Dr Guo, hewisely left without making trouble. Surely this could, indeed should, should, now be resolved by doing exactly what Dr Chen has done. He appears to have found no or only a very low level of WTPC-2 in the cilia of his MDCK cells. This could mean that these cells don't concentrate normal PC2 in the cilium and that the PC2 that does get there eventually is a non-specific secondary intrusionand thatsome mutant PCs do somehow get in albeit slowly. But this seems to mean that the PC2 is not a normal cilial component. Thus, thekey fact from Dr Chen is that there is a problem here which must be resolved for the sake of those of us who have written about the calcium-mediated mechanodriven signaling from the kidney cell cilium. I am surprised that apparently the Harvard people did not take a little time andeffort to defuse this problem by carefully arranging an independently monitored set of experiments to verify or definitively refute Dr Guo's potentially serious observations. - Dr. James Whitfield Researcher Emeritus of the National Research Council of Canada
首先是郭磊教授。 郭磊的博客是非常有新闻价值的。郭也一直在请求新闻媒体的关注。哈佛医学院，再加耶鲁大学，自然等高端期刊论文，集体造假，N射线再现，诺奖可能竞争者出面，还有哈佛的打击报复，九阴真经，皇帝新装等等，这样的博客在科学网不火都难。郭又把这和正闹得沸沸扬扬的浙江大学学术造假相比较，进一步指出“美国哈佛等世界一流科研机构的那些造假的研究人员，才是真正的学术江洋大盗，才是现在学术腐败和科学造假的源头所在”。我倒是很诧异到现在居然没有新闻媒体满足郭的请求。有评论人说，郭以前就把相关博文发到海外的华人社区未名空间了。其实郭至少在半年前就在新浪开博宣传，只不过确实没几个人关注。郭是应该感谢科学网。 因为郭的博文涉及对同行评议机制的挑战，我就组织了对郭的博文及一篇有关论文的PPR后同行评议。一开始我就给郭发过短消息和电邮，请他推荐他认为合适的后评议人。我没收到郭就此发来的任何答复，却忽然看到了他给我的公开信，信里说已经提醒过我，希望我“能找几个有名的大范围的细胞生物学家来评论这些论文”。或许这中间有什么误会？请郭在此澄清一下。最好是明确指出在郭心目里谁是合适的评议人。 郭博客涉及两个方面的指控，一是以哈佛为首的PKD集体学术造假，二是哈佛就此对郭的打击报复。 我的上封公开信是发给PKD专家的。虽然同行评议本身有很多弊端，我还是认为应该首先尊重它，特别是因为我现在是开放获取的PPR，希望它能解开由郭博文引起的纷争。 请注意，“皇帝新装”指责不是，至少不仅仅是，造假的裁缝，更是对认可这新装的后来者。所以，PKD专家的必然反应，自然是，首先就用自己最熟悉的最有把握的工作来说话。也就是自己实验室的最近工作。这当然不是对裁缝造假指责的认可，而是对郭PKD集体造假的反驳。郭如果想把PPR的重点转移到以前发表的旧文，首先就要考虑一下是否应该撤销皇帝新装、N-Ray等集体造假指控。 很遗憾，郭磊教授对此很坚持，让我的PPR也无法深入下去。我将贴出更多专家对郭这一指控的答复。 如果郭磊教授具体推荐一些“大范围的细胞生物学家”来评论这一事件，我也会遵从。但是我不会自己去找这样的专家，因为当这样的专家出面后，一旦结论对郭不利，郭完全可以说他们不是PKD专家，没资格评论。我是分子束外延生长（MBE)专家。如果我要造假的话，我绝不会给大同行机会查出来。小同行想要发掘出来，有可能，但也很难。 实际上，郭磊教授对PKD集体造假的指控对自己非常不利。哈佛大学也就可以因此对他的指控不予理睬。因为按照郭的指控，没有专家有资格对此评论。就像按照郭的意见我无法进行PPR一样，哈佛也就无法继续进行调查。 所以，我对郭磊教授的建议是：写一份英文公开信，正式撤销皇帝新装或N-Ray等形式的集体作假指控，把学术作假指控局限于有限的几篇文章，最好是只有一篇，让PKD专家对此深入地进行PPR后评议。 我到目前为止，只选择一篇旧文PPR，就是要重点突破。只要一篇学术作假成立，自然会引起连锁反应。所以，我也很不认可郭在评论里提议我PPR更多文章的建议。 郭不断扩大战区的做法对谁有利呢？那就是真正的作假者。 哈佛大学方面的直接当事人以Jing ZHOU教授为首。 同样，在刚开始就此PPR时，我就向ZHUO发出了电邮。ZHUO答复了，但两份电邮都是说因为我的博客是中文的，要我翻译成英文以后她才看。即使我解释了我的相关博文是英文的以后，她也如此坚持，令我很诧异。好几位不懂中文的西方专家都可以来看并答复我的博客，反而懂中文的ZHUO却看不了评不了。到底有什么难言之隐呢？更多的人关注郭指控，也就更对哈佛方面不利。而且，我上面也指出，郭扩大战区的做法虽然会得到更多道义支持，但实际对他非常不利。这样下去只会对真正的学术造假者有利。或许他们会选择沉默。郭对哈佛的直接指控，只有哈佛出面，让大家看到双方面的意见，才有可能了解真相。 正如James Whitfield博士指出的，“I am surprised that apparently the Harvard people did not take a little time and effort to defuse this problem by carefully arranging an independently monitored set of experiments to verify or definitively refute Dr Guo's potentially serious observations.” 在哈佛保持沉默的情况下，我们至少可以认为ZHOU就本事件发展到如此地步有不可推卸的责任，我们也可以进一步推论至少ZHOU的实验室重复不了本实验室以前的报道。 科学研究出问题并不可怕，特别是无心之错，并非故意造假。像PKD这样一个炙手可热的研究领域，当年开创性的报告在今天受到挑战几乎是必然的。即使没错，也会被发现有需要改进的地方。如果仅仅是如此的错误，希望ZHOU勇于出面澄清事实。如果真如郭指控的那样是学术造假，澄清事实也比为掩盖事实而打击报复，错上加错要好。 因为Jing ZHOU教授有可能不看我的博客，我这封公开信的链接将随后以电邮的形式发给她。 请注意，我不欢迎看热闹和爱热闹式评论。希望我们共同努力，在科学网就此事找出真相。
PKD on cilia/flagella Reviewer： Joel Rosenbaum My lab is one of the originators of the ciliary hypothesis of PKD and was an author on the initial Pazour et al paper in Current Biology. Our recent work circumvents any problem anyone might have using immunofluorescence, as in the initial reports by Pazour, and then by Yoder, because we isolate cilia, and then the ciliary membranes, and show by Western Blots the presence of PKD2. I don't think that anyone believes that the total PKD2 of the cell is on the cilium, because it certainly is not....it is also on vesicles in the cytoplasm, we have isolated them, and believe they are being targeted to the cilium because other ciliary proteins are also present on these vesicles. PKD2 is also known to be at points of cell:cell interaction in the kidney. But some is, indeed, on the cilium, and when the ciliary dev is interrupted by use of IFT knockdowns/outs, PKD results. That's a fact, whether Li believes it or not. Joel Rosenbaum Porfessor, MCDB, Yale University ==== FYI, the laboratory homepage of Prof. Rosenbaum is http://www.yale.edu/rosenbaum/ .
最近网上热议李连达院士课题组造假一事。在这场声讨李连达院士课题组造假的全民大运动中，我发现其中很多的文章充满了对国内现行学术打假制度缺失或执行不力的指责。他们每每行文，必称如在美国遇到此类事情，会如何如何。我读了以后，总觉得此类评论，像作者们坐井观天梦呓般之臆语，很是苍白无力得有点可笑。最近我在哈佛医学院揭露了一起学术造假，因而不幸亲历了美国调查和处理学术造假的过程。现将情况简介如下。希望大家能通过此文，多少明白我国当今在科学技术方面，特别是科研造假技术方面，和美国等发达国家的真实差距所在。国内造假后进们，实应好好学习，努力提高科研造假技术。千万不要再像李连达课题组一样低水平造假，以致被洋大人们轻易揭露，使我国科技界脸面尽失。 （以下是英文版故事，我在Nature，The Scientist等杂志的网上评论上发过，但马上就被删除了。在PKD的交流网上也发过，虽然不少人对我的故事表示相信，但他们也无能为力（他们知识有限，自身重病缠身）。我多次联系他们，最后他们把我介绍到PKD Foundation（多囊肾基金会）。PKD基金会刚开始根本没理会，后来可能在病人的强烈要求下，由一个病人的妈妈（也是PKD基金会的雇员）代表他们主席发个了语焉不详的并有虚假内容的statement，掩盖PKD界内如此重大的弄虚作假，以平息病人的怒气。并又把此事推给了哈佛医学院。我将在随后的时间里介绍PKD基因会主席的statement, 并分析她为什么伪造有虚假内容的statement。中文版请见博文发生在哈佛大学的一起严重学术造假。两个版本分别写成，内容互相补充。） Dear PKD community, I am writing to you to ask for assistance in fighting with massive and egregious PKD research misconduct and to uncover truth in PKD (Polycystic Kidney Diseases) research. I think the PKD community/families might be one of the groups who would be greatly concerned with massive falsification and fabrication in PKD research and might provide moral support to a whistle blower of PKD research misconduct. I was a biomedical scientist who complained about massive and egregious research misconduct in PKD research in Harvard Medical School (HMS) and was thus retaliated against for my whistle blowing by the institute. Harvard Medical Schoolis still on a track to try to cover up the egregious research misconduct and retaliation case. I am a biologist originally from China. I was a research fellow in PKD laboratory in Harvard Medical School and Brigham and Women's Hospital. As one of my major contributions, I identified and cloned multiple novel PKD gene homologues and created and characterized multiple novel PKD gene knockout models. In recent years, a major research breakthrough had been published in PKD field. That is, almost all PKD proteins were immunolocalized on primary cilia of kidney epithelial cells. In Human, mutation in either one of two PKD genes (PKD1 or PKD2) causes Autosomal Dominant Polycystic Kidney Disease (ADPKD). Both PKD1 and PKD2 proteins had been immunolocalized on primary cilia of the kidney epithelial cells. The first paper that claimed PKD2 immunolocalization on primary cilia was published in 2002 in Current Biology Journal. In 2003, a paper from Dr. Zhou's lab published in Nature Genetics. This paper confirmed both Pkd1 and Pkd2 proteins are localized on primary cilia and further develop the story by provided data showing ADPKD proteins function as mechanical sensor of fluid flow on primary cilia. The published data showed that, the deficiency of the function of PKD1 and/or PKD2 protein on the primary cilia would lead to the deficiency of mechanical sensation of primary cilia in kidney epithelia, eventually the epithelia of the kidney tubule start to grow and cysts is generated. As a research fellow working on PKD, I was asked by my principle investigator, Dr. Jing Zhou, to do PKD research on this direction of PKD research. In early 2006, after repetitive experiments, I started to see more and more evidences showing that immunolocalization of polycystin-1 and polycystin-2 on primary cilia on kidney cells might be false or fake. I first found the evidences showing that the polycystin-2 immunostaining on primary cilium of kidney epithelial cells might be caused by nonspecific binding of the primary antibodies and thus could be false. These results explained why many fellows experienced the difficulty in repeating the immunolocalization of polycystin-1 or -2 on the primary cilia of kidney cells. I reported the results in the laboratory several times since those irreproducible data severely hindered the progress of my research. I also made complaints that nonspecific binding of antibody caused artifact results several times to Dr. Jing Zhou. But Dr. Jing Zhou seemed not very concerned about my complaints. She cannot explain what I saw in the scientific experiments and ignored my complaint and pushed me to do research on the ciliary PKD story. According to my findings, I suspected that Drs. Li, Nauli and Zhou might be involved in fabrication or falsification by omitting these critical negative data or results. I felt it was not right to do that since falsification of scientific data about polycystic kidney diseases would directly and indirectly endanger the interests and safety of the PKD patients. During the daily interaction with my colleagues, I also found evidences that they were falsifying and fabricating scientific data.It was also scientifically obvious that, in some published papers, the cilia stories were flawed. For example, in one of the papers, the authors stated that in PKD knockout cells, the calcium wave response to fluid flow was abolished. However, according to my observation and findings, the truth is, calcium wave response was intact in either PKD1 or PKD2 knockout cells. In the papers, the authors obviously chose a portion of negative result to represent the PKD1/PKD2 knockout cells. This kind of research conduct, if done intentionally, was definitely scientific misconduct. In May and June, 2006, I started to report to Dr. Joseph Bonventre, the director of renal division that there might be egregious research misconduct occurred in the lab. Soon after that, I was threatened by Dr. Jing Zhou several times that I would lose my position if I still stick to my scientific opinion. Dr. Bonventre seemed reluctant to pursue the scientific misconduct and just tell Dr. Jing Zhou. He was one of the principle investigators in an NIH-funded grant lead by Dr. Jing Zhou. Afterwards, as I continued working on the projects, I found more evidences that previous publications in the field might contain false or even falsified or fabricated data. On March 27, 2007, I sent an email to Dr. Margaret L. Dale, the officer of research integrity of Harvard Medical School raising the issues of research misconducts and authorship argument in the laboratory. I also sent an email to Dr. Bonventre stating the same issues. On April 12, 2007, I met with Dr. Dale and Partners attorney Chris Clark to raise the issues of falsifications and/or fabrications in the laboratory and the related authorship issues. I didn't receive any following-up message until May 8, I sent an email to Dr. Dale to inquire the consequence of their investigation. On the same day, Dr. Dale replied to me saying that she was still contactingDr. Bonventre to set up a time to talk about this issue. On May 14, 2007, I received an email from Dr. Jing Zhou asking me leave my position. The email was also sent to Dr. Bonventre. I immediately responded to her email to say her email was not right and not appropriate. I felt I was under retaliatory action. I wrote emails to Dr. Dale to make the allegation that I was retaliated against by Dr. Jing Zhou because of my reporting of research misconduct of her laboratory. On June 21, 2007, Dr. Bonventre, Dr. Dale and I met in Dr. Bonventre's office. I was told by Dr. Bonventre that I had to leave on a designated date. I said I still felt that forcing me leave on a designated date was retaliatory action to my reporting of research misconducts in the laboratory. To obtain more time to protect my visa status and to accomplish more research, I had to agree to sign the letter. I then had to write to Dr. Dale to ask for immediate protection from the retaliatory action taken against me after I complained about the research misconduct. Dr. Dale replied to me that it was not retaliation because my complaint on April 12, 2007 was not formal allegation. I was shocked by her words. I suffered severe emotional distress in those days. But I still stuck to my scientific opinion that PKD cilia connection was false. I continue making research misconduct complaints to numerous officials in the institute. On Oct 17th, Dr. Jing Zhou came to me and asked me to go to her office. She threatened me by saying that everything going upper level would come back to her. I had to leave her office in order not to hear more threats from her. As arranged, on Oct 26, Dr. Handin, the vice chair of department of Medicine of BWH, Dr Zhou, and I met in his office. Dr. Handin first said that he thought there was no research misconduct and there was no retaliation against me and I had to leave in Feb, 2008. During the meeting, He kept persuading me to drop my allegations by saying that Can you put this in your CV even if you can prove there is research misconduct? and threatened me by saying How will you pay bills after March 1st, 2008, etc. He also said to me with scornful tone, You told so many people, nobody thought there was falsification or fabrication. Are you crazy? I thought the meeting was not fair to me and refused to withdraw the allegations. On Nov 14, 2007, I reported the research misconduct and the retaliation against me to office of research integrity (ORI) at Department of Health and Human Services (DHHS), USA. However, ORI, knowing that I was complaining to be retaliated against by Harvard Medical School/Brigham and Women's Hospital, just request HMS/BWH to conduct self investigation. On Jan 5, 2008, the vice president of BWH sent me a mail. In the mail, she said that they would start to investigate the research misconduct and retaliation issues. Before investigation, Dr. Bierer, vice president of BWH, asserted the research misconduct and the retaliation were two separate things thus should be investigated separately. I raised the concerns about the fairness of the inside panels and the procedure of the investigations. She also threatened me that I would have to leave my position before any investigation started. On Feb 11, 2008, due to the tremendous pressure from the officials from BWH/HMS, I suffered from severe illness, so I sent Dr. Bierer an email to tell her that I was ill. After knowing my illness, Dr. Bierer pressed me again by sending me an email to say that my administrative leave date would be moved up. Since then, I had to see doctors for several times to prevent my illness worsening. I received the inside panel's investigation report on June 27, 2008. The report contained some false statements, ignored some important facts. It is an extremely unfair, unjust and biased report. The facts I discovered that the PKD proteins on primary cilia were false were of significant interests to PKD and field and patients. In recent years, National Institutes of Health had invested millions of money in the research along the direction of PKD and cilia connection. PKD foundation also invested tens of thousands of US dollar in this direction. Everyone (including patients and scientists) was expecting breakthrough on pathogenesis and therapy of PKD by pursuing this direction. Many thought this could be the right direction to cure the PKD, provided the PKD and cilia connection were true. However, if the allegation I made be confirmed, the event might be one of the most egregious, notorious and massive research misconducts that involving multiple previously very prestigious institutions. However, as the whistle blower in PKD field, I had been fighting with extreme difficulties. From what they had acted, it was easy to tell that they knew clearly there was egregious and mass research misconduct in the PKD field as I reported. But Harvard Medical School chose to cover up the mass research misconduct, ignoring all of the normal procedure in protecting the whistle blower's legal right. Harvard Medical School/Brigham and Women's Hospital also got involved in imposing severe retaliation and threats against a good-faith whistle blower. I reported the research misconduct to Harvard Medical School on April 2007. I had seen Harvard Medical School was slow in trying to investigate the research misconduct. On the contrary, Harvard Medical School was extremely speedy in retaliation against a whistle blower. Officials in Harvard Medical School/Brigham and Women's Hospital started to seek to terminate me in a matter of days after I made the misconduct complaints with the internal officer of research integrity, Dr. Dale on April 12, 2007. The investigation panel to research misconduct had their first meeting on June, 2008, 4 months later after the job of whistle blower was terminated by Dr. Bierer, the vice president of BWH. After my job was terminated, they started to investigate into the research misconduct allegation I raised, asking me providing related information which would be only available to me when I was at work. Obviously, the inside panel was intentionally set up to cover up this egregious and massive research misconduct and retaliation case. To help yourself understand the essence of this PKD research misconduct, you should also consult your doctors, or other scientists/professors in the biomedical field.
Dear Dr. Wang, Regarding whether polycystin-2 (PC2) localizes to primary cilia, it's possible that PC2 antibodies non-specifically bind cilia. However, so far, there seems to be no sufficient evidence to conclude that all reported or unreported PC2 cilia localization data are due to non-specific binding. In contrast, I would like to see that some specifically designed experiments can prove that PC2 can target to cilia in some types of epithelial cells under specific conditions. My laboratory has made several C-terminal truncation mutants of PC2, all tagged with GFP. We then examined their localization to MDCK cell primary cilia. The following is our finding: No WT PC2 (monitored by green fluorescence) was found in MDCK primary cilia up to two weeks after confluency and only a low proportion (5%) of cilia were green fluorescent at weeks 3-4. Similarly, no cilium staining was seen for up to two weeks for mutants R872X and E837X and for EGFP (as the control). In contrast, fluorescence of mutants E813X, T771X, R742X and S689X was observed in cilia 3-7 days after cilium growth (or 4-8 days after confluency) I attached a figure (Word file) to show the cilia localization of mutant S689X. These data did not use an antibody and thus have no concern of non-specific binding. Conclusion: at least some PC2 mutants can easily go to primary cilia. Hope this provides data somehow relevant to the discussion. Best Regards, Xing-Zhen Xing-Zhen Chen, Ph.D. Associate Professor AHFMR Senior Scholar Membrane Protein Research Group Department of Physiology Faculty of Medicine and Dentistry University of Alberta 7-29 Medical Sciences Building Edmonton, Alberta, T6G 2H7, CANADA Lab web: http://www.physiology.ualberta.ca/Home/People/Academic/chen.cfm Department web: http://www.physiology.ualberta.ca MPRG web: http://www.mprg.med.ualberta.ca
The first and direct concerned publication: Nature Genetics 33 , 129 - 137 (2003) Published online: 6 January 2003; | doi:10.1038/ng1076 Polycystins 1 and 2 mediate mechanosensation in the primary cilium of kidney cells Surya M. Nauli 1, 4 , Francis J. Alenghat 2 , Ying Luo 1, 4 , Eric Williams 1 , Peter Vassilev 3 , Xiaogang Li 1 , Andrew E. H. Elia 1 , Weining Lu 1 , Edward M. Brown 3 , Stephen J. Quinn 3 , Donald E. Ingber 2 Jing Zhou 1 1 Renal Division, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, 4 Blackfan Circle, Boston, Massachusetts 02115, USA. 2 Vascular Biology Program, Departments of Pathology and Surgery, Children's Hospital and Harvard Medical School, Boston, Massachusetts, USA. 3 Endocrine-Hypertension Division, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA. 4 These authors contributed equally to this work. Correspondence should be addressed to Jing Zhou zhou@rics.bwh.harvard.edu Several proteins implicated in the pathogenesis of polycystic kidney disease (PKD) localize to cilia. Furthermore, cilia are malformed in mice with PKD with mutations in TgN737Rpw (encoding polaris). It is not known, however, whether ciliary dysfunction occurs or is relevant to cyst formation in PKD. Here, we show that polycystin-1 (PC1) and polycystin-2 (PC2), proteins respectively encoded by Pkd1 and Pkd2 , mouse orthologs of genes mutated in human autosomal dominant PKD, co-distribute in the primary cilia of kidney epithelium. Cells isolated from transgenic mice that lack functional PC1 formed cilia but did not increase Ca 2+ influx in response to physiological fluid flow. Blocking antibodies directed against PC2 similarly abolished the flow response in wild-type cells as did inhibitors of the ryanodine receptor, whereas inhibitors of G-proteins, phospholipase C and InsP 3 receptors had no effect. These data suggest that PC1 and PC2 contribute to fluid-flow sensation by the primary cilium in renal epithelium and that they both function in the same mechanotransduction pathway. Loss or dysfunction of PC1 or PC2 may therefore lead to PKD owing to the inability of cells to sense mechanical cues that normally regulate tissue morphogenesis.
English Version of Lei GUO's blog post (Comment #8): Dear PKD community, I am writing to you to ask for assistance in fighting with massive and egregious PKD research misconduct and to uncover truth in PKD (Polycystic Kidney Diseases) research. I think the PKD community/families might be one of the groups who would be greatly concerned with massive falsification and fabrication in PKD research and might provide moral support to a whistle blower of PKD research misconduct. I was a biomedical scientist who complained about massive and egregious research misconduct in PKD research in Harvard Medical School (HMS) and was thus retaliated against for my whistle blowing by the institute. Harvard Medical School was still on a track to try to cover up the egregious research misconduct and retaliation case. I am a biologist originally from China. I was a research fellow in Dr. Jing Zhou"s PKD laboratory in Harvard Medical School and Brigham and Women"s Hospital. As one of my major contributions, I identified and cloned multiple novel PKD gene homologues and created and characterized multiple novel PKD gene knockout models. In recent years, a major research "breakthrough" had been published in PKD field. That is, almost all PKD proteins were immunolocalized on primary cilia of kidney epithelial cells. In Human, mutation in either one of two PKD genes (PKD1 or PKD2) causes Autosomal Dominant Polycystic Kidney Disease (ADPKD). Both PKD1 and PKD2 proteins had been immunolocalized on primary cilia of the kidney epithelial cells. The first paper that claimed PKD2 immunolocalization on primary cilia was published in 2002 in Current Biology Journal. In 2003, a paper from Dr. Jing Zhou"s lab published in Nature Genetics. This paper "confirmed" both Pkd1 and Pkd2 proteins are localized on primary cilia and further develop the story by provided data showing ADPKD proteins function as mechanical sensor of fluid flow on primary cilia. The published data showed that, the deficiency of the function of PKD1 and/or PKD2 protein on the primary cilia would lead to the deficiency of mechanical sensation of primary cilia in kidney epithelia, eventually the epithelia of the kidney tubule start to grow and cysts is generated. As a research fellow working on PKD, I was asked by my principle investigator, Dr. Jing Zhou, to do PKD research on this direction of PKD research. In early 2006, after repetitive experiments, I started to see more and more evidences showing that immunolocalization of polycystin-1 and polycystin-2 on primary cilia on kidney cells might be false or fake. I first found the evidences showing that the polycystin-2 immunostaining on primary cilium of kidney epithelial cells might be caused by nonspecific binding of the primary antibodies and thus could be false. These results explained why many fellows experienced the difficulty in repeating the immunolocalization of polycystin-1 or -2 on the primary cilia of kidney cells. I reported the results in the laboratory several times since those irreproducible data severely hindered the progress of my research. I also made complaints that nonspecific binding of antibody caused artifact results several times to Dr. Jing Zhou. But Dr. Jing Zhou seemed not very concerned about my complaints. She cannot explain what I saw in the scientific experiments and ignored my complaint and pushed me to do research on the ciliary PKD story. According to my findings, I suspected that Drs. Li, Nauli and Zhou might be involved in fabrication or falsification by omitting these critical negative data or results. I felt it was not right to do that since falsification of scientific data about polycystic kidney diseases would directly and indirectly endanger the interests and safety of the PKD patients. During the daily interaction with my colleagues, I also found evidences that they were falsifying and fabricating scientific data. Also, it was also scientifically obvious that, in some published papers, the cilia stories were flawed. For example, in one of the papers, the authors stated that in PKD knockout cells, the calcium wave response to fluid flow was abolished. However, according to my observation and findings, the truth is, calcium wave response was intact in either PKD1 or PKD2 knockout cells. In the papers, the authors obviously chose a portion of negative result to represent the PKD1/PKD2 knockout cells. This kind of research conduct, if done intentionally, was definitely scientific misconduct. In May and June, 2006, I started to report to Dr. Joseph Bonventre, the director of renal division that there might be egregious research misconduct occurred in the lab. Soon after that, I was threatened by Dr. Jing Zhou several times that I would lose my position if I still stick to my scientific opinion. Dr. Bonventre seemed reluctant to pursue the scientific misconduct and just tell Dr. Jing Zhou. He was one of the principle investigators in an NIH-funded grant lead by Dr. Jing Zhou. Afterwards, as I continued working on the projects, I found more evidences that previous publications in the field might contain false or even falsified or fabricated data. On March 27, 2007, I sent an email to Dr. Margaret L. Dale, the officer of research integrity of Harvard Medical School raising the issues of research misconducts and authorship argument in the laboratory. I also sent an email to Dr. Bonventre stating the same issues. On April 12, 2007, I met with Dr. Dale and Partners attorney Chris Clark to raise the issues of falsifications and/or fabrications in the laboratory and the related authorship issues. I didn"t receive any following-up message until May 8, I sent an email to Dr. Dale to inquire the consequence of their investigation. On the same day, Dr. Dale replied to me saying that she was still contacting with Dr. Bonventre to set up a time to talk about this issue. On May 14, 2007, I received an email from Dr. Jing Zhou asking me leave my position. The email was also sent to Dr. Bonventre. I immediately responded to her email to say her email was not right and not appropriate. I felt I was under retaliatory action. I wrote emails to Dr. Dale to make the allegation that I was retaliated against by Dr. Jing Zhou because of my reporting of research misconduct of her laboratory. On June 21, 2007, Dr. Bonventre, Dr. Dale and I met in Dr. Bonventre"s office. I was told by Dr. Bonventre that I had to leave on a designated date. I said I still felt that forcing me leave on a designated date was retaliatory action to my reporting of research misconducts in the laboratory. To obtain more time to protect my visa status and to accomplish more research, I had to agree to sign the letter. I then had to write to Dr. Dale to ask for immediate protection from the retaliatory action taken against me after I complained about the research misconduct. Dr. Dale replied to me that it was not retaliation because my complaint on April 12, 2007 was not formal allegation. I was shocked by her words. I suffered severe emotional distress in those days. But I still stuck to my scientific opinion that PKD cilia connection was false. I continue making research misconduct complaints to numerous officials in the institute. On Oct 17th, Dr. Jing Zhou came to me and asked me to go to her office. She threatened me by saying that everything going upper level would come back to her. I had to leave her office in order not to hear more threats from her. As arranged, on Oct 26, Dr. Handin, the vice chair of department of Medicine of BWH, Dr Zhou, and I met in his office. Dr. Handin first said that he thought there was no research misconduct and there was no retaliation against me and I had to leave in Feb, 2008. During the meeting, He kept persuading me to drop my allegations by saying that "Can you put this in your CV even if you can prove there is research misconduct?" and threatened me by saying "How will you pay bills after March 1st, 2008", etc. He also said to me with scornful tone, "You told so many people, nobody thought there was falsification or fabrication (in Dr Zhou"s research). Are you crazy?" I thought the meeting was not fair to me and refused to withdraw the allegations. On Nov 14, 2007, I reported the research misconduct and the retaliation against me to office of research integrity (ORI) at Department of Health and Human Services (DHHS), USA. However, ORI, knowing that I was complaining to be retaliated against by Harvard Medical School/Brigham and Women"s Hospital, just request HMS/BWH to conduct self investigation. On Jan 5, 2008, the vice president of BWH sent me a mail. In the mail, she said that they would start to investigate the research misconduct and retaliation issues. Before investigation, Dr. Bierer, vice president of BWH, asserted the research misconduct and the retaliation were two separate things thus should be investigated separately. I raised the concerns about the fairness of the inside panels and the procedure of the investigations. She also threatened me that I would have to leave my position before any investigation started. On Feb 11, 2008, due to the tremendous pressure from the officials from BWH/HMS, I suffered from severe illness, so I sent Dr. Bierer an email to tell her that I was ill. After knowing my illness, Dr. Bierer pressed me again by sending me an email to say that my administrative leave date would be moved up. Since then, I had to see doctors for several times to prevent my illness worsening. I received the inside panel"s investigation report on June 27, 2008. The report contained some false statements, ignored some important facts. It is an extremely unfair, unjust and biased report. The facts I discovered that the PKD proteins on primary cilia were false were of significant interests to PKD and field and patients. In recent years, National Institutes of Health had invested millions of money in the research along the direction of PKD and cilia connection. PKD foundation also invested tens of thousands of US dollar in this direction. Everyone (including patients and scientists) was expecting breakthrough on parthenogenesis and therapy of PKD by pursuing this direction. Many thought this could be the right direction to cure the PKD, provided the PKD and cilia connection were true. However, if the allegation I made be confirmed, the event might be one of the most egregious, notorious and massive research misconduct that involving multiple previously very prestigious institutions. However, as the whistle blower in PKD field, I had been fighting with extreme difficulties. From what they had acted, it was easy to tell that they knew clearly there was egregious and mass research misconduct in the PKD field as I reported. But Harvard Medical School chose to cover up the massive research misconduct, ignoring all of the normal procedure in protecting the whistle blower"s legal right. Harvard Medical School/Brigham and Women"s Hospital also got involved in imposing severe retaliation and threats against a good-faith whistle blower. I reported the research misconduct to Harvard Medical School on April 2007. I had seen Harvard Medical School was slow in trying to investigate the research misconduct. On the contrary, Harvard Medical School was extremely speedy in retaliation against a whistle blower. Officials in Harvard Medical School/Brigham and Women"s Hospital started to seek to terminate me in a matter of days after I made the misconduct complaints with the internal officer of research integrity, Dr. Dale on April 12, 2007. The investigation panel to research misconduct had their first meeting on June, 2008, 4 months later after the job of whistle blower was terminated by Dr. Bierer, the vice president of BWH. After my job was terminated, they started to investigate into the research misconduct allegation I raised, asking me providing related information which would be only available to me when I was at work. Obviously, the inside panel was intentionally set up to cover up this egregious and massive research misconduct and retaliation case. To help yourself understand the essence of this PKD research misconduct, you should also consult your doctors, or other scientists/professors in the biomedical field. Linc
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