Editorial: No intelligence involved

You may have heard about the controversial movie “Expelled: No intelligence Allowed” by Ben Stein in which people behind the intelligent design movement whine about being suppressed the scientific community. The truth is obviously that intelligent design is not a falsifiable theory and hence simply does not qualify as science.

However, the movie is also controversial in other respects. To start with the producers conned both Richard Dawkins and fellow blogger PZ Myers into participating in the movie by interviewing them under false pretense.

Richard Dawkins and PZ Myers thus both registered for participating in a public screening of the movie. But while queuing up for the movie, PZ Myers was identified by security officers and told to leave the premises – immediately! Oh the irony, oh the double standard. They make a movie about suppression of views, they call it “Expelled”, and then they expel a person whom you conned into participating in the movie because you disagree with his views.

But it gets even better. The very same security officers were apparently oblivious to the fact that Richard Dawkins was standing right next to PZ Myers and thus let him enter to watch the movie. PZ Myers immediately wrote a blog post about it, while the movie was still being shown to the audience – including Richard Dawkins.

After the movie, Richard Dawkins (of course) stood up and asked why PZ Myers was not allowed to see the movie. The answer? Because he did not have a ticket and was thus a gate crasher! Very interesting explanation since it was not a ticket event – you simply had to register a seat, which PZ Myers had done.

The two gentlemen have now posted an interesting little discussion on YouTube in which they humorously describe the incident as well as just how bad the movie really is:

Richard Dawkins also reveals that Expelled includes one of the beautiful movies produced by the multimedia team at Harvard. You really have to wonder if they actually got permission for that, if they conned the people at Harvard as well, or if they just resorted to plain old plagiarism. In any case, this has to be one of the biggest PR disasters ever made by the intelligent design movement.

Expelled from Expelled: no intelligence involved.

Update: Warda and Han, one month after the storm

As most readers of this blog are probably aware, Mohammad Warda and Jin Han published a paper in Proteomics that contained several pages of text copied from unreferenced sources. Exactly one month ago it was thus retracted “due to a substantial overlap of the content of this article with previously published articles in other journals”.

Plagiarism is, however, not the main issue. The paper by Warda and Han also claimed to disprove the endosymbiotic origin of mitochondria, mentioned fingerprints of a mighty creator, and proposed mitochondria to be the missing link between the body and the preserved wisdom of the soul!

It remains a mystery how a manuscript with such unsubstantiated claims was accepted for publication in a respectable, peer-reviewed journal. The retraction notice by Proteomics made no attempt to explain this, and their approved draft press release merely states that it was due to “human error”. I would have been really worried if it could happen without human error being involved. Although this draft was approved a month ago, the final version is nowhere to be found on the internet, also not on the Proteomics website. I thus wonder if an official press release was ever published.

Attila Csordas, PZ Myers, Steven Salzberg, and I have decided to mark the one month anniversary of the retraction by pointing out the important questions that still remain to be answered by the Editor in Chief of Proteomics, Prof. Michael J. Dunn.

The manuscript contains four parts with unsupported claims that should have been caught by any peer reviewer or editor:

1. Title – “Mitochondria, the missing link between body and soul”.
2. Abstract – “These data are presented with novel proteomics evidence to disprove the endosymbiotic hypothesis of mitochondrial evolution that is replaced in this work by a more realistic alternative”.
3. Section 3.4 – “More logically, the points that show proteomics overlapping between different forms of life are more likely to be interpreted as a reflection of a single common fingerprint initiated by a mighty creator than relying on a single cell that is, in a doubtful way, surprisingly originating all other kinds of life”.
4. Conclusions – “We realize so far that the mitochondria could be the link between the body and this preserved wisdom of the soul devoted to guaranteeing life”.

My questions to Michael J. Dunn are when in the publication process these parts first appeared:

1. Were they already in the initial version that was submitted to Proteomics and sent out for peer review?
2. Did they appear in a revised version that was sent to the peer reviewers?
3. Were they introduced in a revised version that was accepted without sending it to the reviewers?
4. Or were they added at the copy editing stage, that is after the manuscript had formally been accepted?

I want to make explicit that the aim with these questions is not to place the blame but to elucidate what went wrong in the publication process. To prevent similar incidents inthe future, it is important to know whether the editor and the peer reviewers overlooked glaring flaws of the manuscript or if the flawed parts were introduced after peer review. It is not important who the editor and the peer reviewers are. I sincerely hope that Prof. Dunn will help improve the procedures for peer reviewed publication by answering the questions in this post and in the related posts on PIMM, Pharyngula, and Genomics, Evolution, and Pseudoscience.

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Commentary: We apologize

Attila Chordash over at “PIMM – Partial immortalization” discovered that Proteomics have now changed the abstract of the infamous paper by Warda and Han to be an apology to their readership:

While I am pleased to see this public apology from the publisher, the retraction is still only based on “a substantial overlap of the content of this article with previously published articles in other journals”. That is a euphemism for “the authors copied four entire pages of text from sources that were not cited”. However, I am concerned that this apology – like the press release from Proteomics – ignores the central question: how did the manuscript make it through peer review?

I was a bit surprised to see an apology being published via PubMed, but a quick search revealed that Proteomics is far from the only journal to apologize to their readers in this way. In fact, a systematic count of the abstracts mentioning the words “apologise(s)” or “apologize(s)” has increased exponentially over the past decade (note the logarithmic scale):

The number shown for 2008 is an extrapolation based on the first six weeks; if the apologies keep coming at the current rate, there will be 32 by the end of the year. The line shows an exponential fit of the data points from 1999 to 2007. The doubling time for the number of apologies is just 3 years whereas the number of papers doubles only every 22 years. If these trends continue, there will be more apologies than papers published from the year 2067 and onwards. I apologize for the extrapolation.

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Update: Not treasure but buried

There is good news regarding the Warda and Han scandal. After numerous researchers including myself emailed the Editor in Chief of Proteomics, Michael J. Dunn, the paper is now listed as retracted. I am pleased to see that the editorial team of Proteomics has acted swiftly against plagiarism.

Edit: The last author of the paper, Jin Han, has written a reply to PZ Myers. According to the email, he has himself contacted the editorial office and requested that the paper be retracted. I am still looking forward to hearing an official explanation from Proteomics of how this paper got accepted in the first place.

Edit: Michael J. Dunn has emailed me a copy of the approved press release from Proteomics that announces the retraction of the paper by Warda and Han. The only explanation offered is that the paper made it through peer review due to “human error” – or in other words “someone did something wrong”. I would have been truly worried if a paper like this had been accepted without human error being involved. I hope that Proteomics will provide the scientific community with more details when they have completed the internal investigation of the incident.

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Commentary: Neither buried nor treasure

This post might be considered off topic since it is about a paper that is unfortunately neither buried nor treasure. I would rather describe it as “organic fertilizer that has come into contact with a rotary air-circulation device”.

The paper that I will dissect is “Mitochondria, the missing link between body and soul: Proteomic prospective evidence” by Mohamad Warda and Jin Han. This review is at the time of writing published in electronic form by the journal Proteomics (ISI impact factor 5.735). It was aptly described as “A baffling failure of peer review” by PZ Myers on his blog Pharyngula, which led to a flash mob of researchers (including me) quickly identifying several flaws, any one of which should in my view be sufficient to cause the journal to retract the paper:

• Warda and Han twice suggest that mitochondria provide a link between body and soul, but they never provide any argument for this.
• They claim to present data that disproves the accepted endosymbiotic theory for the origin of mitochondria. But in reality they present no such evidence.
• They promise to replace this theory by “a more realistic alternative”. The alternative turns out to be “a mighty creator”, or in other words Intelligent Design.
• To support these truly remarkable claims, the authors misrepresent the results of cited references. Some of these references are even completely unrelated to the topic at hand.
• Entire sections or paragraphs of the paper are plagiarism of other researcher’s papers and from the website of another group. Not only is this material not presented as quotations, the sources are not even cited.
• Finally, numerous sentences have been copied verbatim from the cited sources. This may be partly excused by the authors borrowing better English, but I nonetheless consider it an unacceptable practice especially in reviews.

Note how I use block quotations below to show which parts are not my own words. That is what Warda and Han should have done to avoid their biggest problem: being accused of plagiarism. Let us start by looking at the first sentence of the abstract:

Mitochondria are the gatekeepers of the life and death of most cells that regulate signaling, metabolism, and energy production needed for cellular function.

This sentence is identical to the first sentence on the webpage of a competing group, namely the Mitochondrial Research & Innovation Group at University of Rochester Medical Center. The rest of the paragraph from the webpage can be found later in the paper by Warda and Han:

Recent scientific studies show that mitochondrial dysfunction is more commonplace than previously thought and that substantial mitochondrial involvement is present in many acute and chronic diseases. Mitochondrial dysfunction is now implicated in a range of human diseases, including aging, diabetes, atherosclerosis, heart failure, myocardial infarction, stroke and other ischemic-reperfusion injuries, neurodegenerative diseases including Alzhiemer’s and Parkinson’s diseases; cancer, HIV; sepsis and trauma with multiorgan dysfunction or failure. Some rare mitochondria diseases (e.g., MELAS, Kearns-Sayre) are associated with large deletions in the mitochondrial genome. More recently, the so-called OXPHOS diseases that reflect a limited capacity to produce the energy needed to respond to normal stress conditions.

However, most of the plagiarized material is not from webpages; it is from peer-reviewed papers of other researchers. For example, the two paragraph below appear to originate from the paper “Peroxisome Proliferator-Activated Receptor gamma Coactivator-1 (PGC-1) Regulatory Cascade in Cardiac Physiology and Disease” published by Brian N. Finck and Daniel P. Kelly in the journal Circulation:

Emerging evidence supports the notion that derangements in mitochondrial energy metabolism contribute to cardiac dysfunction [186]. For example, human mitochondrial DNA mutations resulting in global impairment in mitochondrial respiratory function cause hypertrophic or dilated cardiomyopathy and cardiac conduction defects [187, 188]. Mutations in nuclear genes encoding mitochondrial fatty acid oxidation enzymes may also manifest as cardiomyopathy [189, 190]. Interestingly, cardiomyopathies resulting from inborn errors in mitochondrial fatty acid oxidation enzymes are often provoked by physiological or pathophysiological conditions that increase dependence on fat oxidation for myocardial ATP production such as prolonged exercise or fasting associated with infectious illness [190,191].

A causal relationship between mitochondrial dysfunction and cardiomyopathy is also evidenced by several genetically engineered mouse models. Targeted deletion of the adenine nucleotide translocator 1, which transports mitochondrially generated ATP to the cytosol, leads to mitochondrial dysfunction and cardiomyopathy [192]. Mice with cardiac-specific deletion of the transcription factor of activated mitochondria, which controls transcription and replication of the mitochondrial genome, also exhibit marked impairments in mitochondrial metabolism, severe cardiomyopathy, and premature mortality [193]. Cardiomyopathy and/or conduction defects are also observed in several mouse models with targeted deletion of specific fatty acid oxidation enzymes [194, 195].

I discovered these plagiarized sections myself, but they only scratch the surface and pale in comparison to the amount of copied material identified by others. I should make clear that I do not blame the reviewers for not discovering this; their job is to check the scientific quality of the material presented, not to detect fraudulent or plagiarized material.

The editor and the reviewers are not off the hook, though. Interspersed between the sensible review material, much of which has been copied from elsewhere, there are a few sections that are “a mélange of truths, half-truths, quarter-truths, falsehoods, non sequiturs, and syntactically correct sentences that have no meaning whatsoever” (to use the words of Alan Sokal).

The first of these is the following sentence from the abstract:

These data are presented with other novel proteomics evidence to disprove the endosymbiotic hypothesis of mitochondrial evolution that is replaced in this work by a more realistic alternative.

Clearly the editors and the reviewers should have examined the evidence for such an exceptional claim. The “evidence” that supposedly disproves the serial endosymbiotic theory (SET) of mitochondrial evolution is presented in section 3.4, which after explaining the theory makes the following baffling statement:

The proof of SET was based on the parallel connection between plant mitochondrial and phage T4 genome replication [107, 108] …

This is simply not true. First, the scientific method can never prove a theory. Second, the similarity between the replication of mitochondrial and phage T4 genomes is completely irrelevant with respect to the endosymbiotic origin of mitochondria. Third, reference 108 is about chloroplasts and not mitochondria.

Next, the authors try to convince the reader that people are still debating the validity of the endosymbiotic theory:

Therefore, the debates concerning the mitochondrial endosymbiotic hypothesis recently terminated with many questions still left unanswered [111].

Reference 111 is a paper in Cellular Immunology by Gray and coworkers with the title “Modulation of CD8+ T cell avidity by increasing the turnover of viral antigen during infection”. It has nothing to do with the evolution of mitochondria.

The authors go on to recite the well known facts that the vast majority of mitochondrial proteins are encoded by nuclear genes and that most bacterial genes do not match within the mitochondrial DNA. They then give a long description of how tightly integrated mitochondria are with the rest of the cell and use the tired old argument of irreducible complexity to dismiss the endosymbiotic theory. Needless to say, the authors have what they consider to be a more realistic explanation:

Alternatively, instead of sinking in a swamp of endless debates about the evolution of mitochondria, it is better to come up with a unified assumption that all living cells undergo a certain degree of convergence or divergence to or from each other to meet their survival in specific habitats. Proteomics data greatly assist this realistic assumption that connects all kinds of life. More logically, the points that show proteomics overlapping between different forms of life are more likely to be interpreted as a reflection of a single common fingerprint initiated by a mighty creator than relying on a single cell that is, in a doubtful way, surprisingly originating all other kinds of life.

In other words: “God did it”. If I can read correctly, the authors here reject not only the endosymbiotic origin of mitochondria but also the common ancestry of eukaryotes. And as if this was not enough, the authors end the paper with the following bold conclusion that also explains the mysterious title of the paper:

We realize so far that mitochondria could be the link between the body and this preserved wisdom of the soul devoted to guaranteeing life.

I am speechless. As anyone who knows me can attest, that very rarely happens.

Edit: The paper has now been retracted, but there are still many open questions as to how it got accepted in the first place.

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