Strange Corrections in Early Human Development

Early Human Development, like some other journals, sometimes publishes conference proceedings.  In October 2009 a supplement was published with articles reflecting presentations made at a conference in Torino, in July 2010 another was published with articles written by presenters at a neonatal nutrition conference. The latest Early Human Development email, that I receive for new publications on-line, includes correction notices for 2 of those articles. This caught my eye as they are both about microbiome/probiotics in preterms, both co-authored by Maka Mshvildadze and Josef Neu. The correction notices both note that entire paragraphs had been copied from previous publications, and had not been appropriately acknowledged. The corrections suggest that they should have been enclosed in quotation marks, but I think honestly that they should not have been copied verbatim at all. 

In addition, with a bit of digging there are clearly other parts of the manuscripts which are also copied. Take this example, from the publication in EHD, (which is not listed in the correction statement as needing quotation marks)

Alterations in diet affect the composition and, more importantly, the collective metabolic output of the microbiota. Thus, deliberate dietary supplementation with bacterial fermentative substrates, usually complex carbohydrates can increase the growth of potentially beneficial microorganisms as well as the production of SCFAs, including butyrate, and indirectly modify immune function [47]. This approach is called “synbiotics.” Obviously, the emerging ability to couple metagenomics of bacterial populations with resultant metabolomics will facilitate rational attempts to manipulate endogenous gut microbiota by dietary changes

Compare this to an earlier article by Andrew Neish

Alterations in diet affect the composition and, more importantly, the collective metabolic output of the microbiota. Thus, deliberate dietary supplementation with bacterial fermentative substrates, usually complex carbohydrates (eg, inulin, oligofructose), can increase luminal concentrations of SCFAs, including butyrate, and indirectly modify immune function….  Prebiotic substrates could be administered with live bacteria most able to exploit that energy source, an approach called “synbiotics.” Obviously, the emerging ability to couple metagenomics of bacterial populations with resultant metabolomics will facilitate rational attempts to manipulate endogenous gut microbiota by dietary changes.

There is a reference to Neish’s article given, but no indication that large parts were directly copied. There are other large portions that are taken from Neu’s own previous work, which has sometimes been called “auto-plagiarism”. I am much more sanguine about that, it is hard to always find a new way to say the same thing, on the other hand the co-authors on the previous publications who actually produced the initial text have a right to be pissed that their work was not appropriately acknowledged. The text of the EHD article directly copies the results section of the abstract of another trial (Rinne M et al ) which is mentioned by name as Rinne et al, but doesn’t actually appear in the references, the reference number is to a different article altogether (that looks like its just a mistake, but the results are quoted verbatim):

Numbers of different types of stools, vomits and crying time were comparable between the groups during the 7th and the 12th weeks of life. Dominant microbiota consisted of bifidobacteria throughout the study. At 6 months, there were less clostridia in feces in the placebo compared with the probiotic group (P = 0.026), whereas after long-term follow-up at 2 years, there were less lactobacilli/enterococci and clostridia in feces in the probiotic group than in the placebo group (P = 0.011 and P = 0.032, respectively), reflecting the impact of clostridia as a marker of microbiota succession in healthy infants.  

Perhaps its not a big deal to directly quote factual information like that, but I have never done it in anything I have written, and the final phrase is clearly an opinion and should not be directly copied without attribution.

In the second of the two corrections a long paragraph lifted from an article in the PNEJM by James Madara is stated to need quotation marks. This is the EHD paragraph

“Components of bacteria provide chemical signals that are recognized by specific receptors – called toll-like receptors (TLRs) – of the innate immune system. The mechanisms of how microbes or their components interact with this system to provide innate immunity are still in the early phases of research. It is assumed that the healthy intestinal surface somehow defuses the threat of commensal bacteria to the lumen where they thus reside undetected. A study by Rakoff-nahoum et al provides insights on how this happens: commensal bacteria interact with the intestinal surface and to some degree trigger TLR-signaling. The authors used mice deficient in either TLR-2 or TLR-4 or a necessary downstream component of the TLR pathway (MyD88), to prevent TLR-signaling. Such mice were shown to have a profoundly exaggerated response to intestinal injury. This effect is not a consequence of acute inflammation or the unrestrained overgrowth of commensal bacteria; rather, it results from the loss of TLR-dependent conditioning that allows the intestinal surface to maintain its normally resistant homeostasis. Surprisingly this interaction is required to maintain the architectural integrity of the intestinal surface. Thus it seems that the epithelial and resident immune cells do not simply tolerate commensal bacteria but are dependent on them.” 

Bu this isn’t exactly a quotation, as the order of some parts have been re-arranged, and other sentences slightly edited, the original is:

 Like all bacteria, they release chemical signals with conserved patterns recognized by specific receptors ― called toll-like receptors (TLRs) ― of the innate immune system. It is therefore assumed that the healthy intestinal surface somehow defuses the threat of commensal bacteria to the lumen, where they thus reside undetected. A recent study by Rakoff-Nahoum and colleagues provides insight into how this happens: commensal bacteria interact with the intestinal surface and, to some degree, trigger TLR signaling…..

Surprisingly, this interaction is actually required to maintain the architectural integrity of the intestinal surface. Thus, it seems that the epithelium and resident immune cells do not simply tolerate commensal bacteria but are dependent on them….

The authors used mice deficient in a necessary downstream component of the TLR pathway, thereby preventing all TLR signaling. Such mice have a profoundly exaggerated response to intestinal injury. This effect is not a consequence of acute inflammation or the unrestrained overgrowth of commensal bacteria; rather, it results from the loss of TLR-dependent conditioning that allows the intestinal surface to maintain its normally resistant homeostasis.

I’m sorry but this is not unintentionally leaving off quotation marks, but this really looks like extensive plagiarism, and I think that just adding quotation marks is not sufficient, these articles should be retracted.

About keithbarrington

I am a neonatologist and clinical researcher at Sainte Justine University Health Center in Montréal
This entry was posted in Neonatal Research. Bookmark the permalink.

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