Researcher who stole manuscript during peer review earns second retraction

The researcher whose brazen theft of a manuscript he had reviewed prompted a “Dear plagiarist” letter from the aggrieved author once the deceit was discovered has lost a second paper for plagiarism.

International Scholarly Research Notices, a Hindawi publication, has retracted a 2012 study by Carmine Finelli and colleagues, citing widespread misuse of text from two previously published articles. The removal was prompted by the curiosity of a scientist in England who, on reading about Finelli’s first retraction, made the logical assumption: once a plagiarist, often a plagiarist.

The review article was titled “Physical Activity: An Important Adaptative Mechanism for Body-Weight Control.” The journal is not indexed by Clarivate Analytics’ Web of Science, but the paper has been cited seven times, according to Google Scholar. According to the retraction notice:

The article was found to contain a substantial amount of material from the following published articles: “Tappy, L., Binnert, C. and Schneiter, P. (2003) ‘Energy expenditure, physical activity and body-weight control’, Proceedings of the Nutrition Society, 62(3), pp. 663–666. doi: 10.1079/PNS2003280,” and “James A. Levine: Nonexercise activity thermogenesis (NEAT): environment and biology American Journal of Physiology – Endocrinology and Metabolism Published 1 May 2004 Vol. 286 no. 5, E675–E685 DOI: 10.1152/ajpendo.00562.2003.” The first author Carmine Finelli accepts responsibility for this and apologizes to Tappy et al. and Levine.

Finelli’s article does reference the Levine study, but not the Tappy paper — at least, not the one in the notice.

Finelli earned some infamy last December, when the Annals of Internal Medicine published a remarkable letter from a U.S. researcher, Michael Dansinger, of Tufts University. Dansinger accused an unnamed scientist of having pilfered his paper — after having reviewed it for the journal and recommending rejection. Finelli subsequently published a version of the article in EXCLI Journal, which has since retracted the paper. Although neither Dansinger’s letter nor an editorial accompanying the missive names Finelli, he took responsibility for the misconduct in the retraction notice and in an email exchange with us.

Tjibbe Donker, an expert in infectious diseases who holds at post at the University of Oxford, told us that he’d become curious about Fanelli last year after reading about the Italian researcher’s initial retraction. Speaking with a colleague, Donker said:

One of the questions we were left with was: Why would you think you could get away with almost literally copying a manuscript? And the obvious answer was: Because you got away with it before.

So I pulled a random paper from this author from Google Scholar, selected a random bit of text from the paper and put that back through Google again… And got a perfect hit with a paper by other authors on the first try.

After that, I informed the corresponding author of the original paper (Luc Tappy) and got in contact with the editors of the journal.

We’re guessing this retraction won’t be the last for Finelli. Commenters on PubPeer have raised concerns about at least 20 of his papers and book chapters.

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20 thoughts on “Researcher who stole manuscript during peer review earns second retraction”

  1. If Google Scholar can be used this way, can’t someone pretty easily write a script to do comparisons on a bulk basis?

  2. In fact the plagiarism in Finelli et al. goes further than the two sources cited in the retraction. The initial paragraphs are copied from Harrison & Day (2007), “Benefits of lifestyle modification in NAFLD” (Gut).

    Finelli et al.:
    1. Introduction
    Exercise physiology and the salutatory effects on weight loss, fat reduction, and insulin sensitivity have been described in great detail. These beneficial effects are now considered to reflect, at least in part, the effect of exercise on the activation of AMP-activated protein kinase (AMPK). In obese non-diabetics, exercise has been shown to reduce the risk of developing type 2 diabetes by up to 46% [1].

    Physical training, consisting of 20 min cycling or running, 20 min swimming at submaximal heart rate, followed by 20 min of warm up/cool down three times per week for 4 wk, resulted in a significant reduction in body weight and percentage body fat, and this was associated with improved whole-body glucose uptake, decreased fasting insulin concentrations, and increased circulating adiponectin and mRNA expression in muscle. Among patients with type 2 diabetes mellitus, increasing exercise led to a reduction in fasting plasma glucose [2].

    Harrison and Day:
    Effect of exercise alone on obesity, visceral fat and insulin resistance
    Exercise physiology and the salutatory effects on weight loss, fat reduction and insulin sensitivity have been described in great detail. These beneficial effects are now considered to reflect, at least in part, the effect of exercise on the activation of AMPK. In obese non‐diabetics, exercise has been shown to reduce the risk of developing diabetes mellitus by up to 46%.71 Physical training, consisting of 20 min cycling or running, 20 min swimming at submaximal heart rate, followed by 20 min of warm up/cool down three times per week for 4 weeks, resulted in a significant reduction in body weight and percentage body fat, and this was associated with improved whole‐body glucose uptake, decreased fasting insulin concentrations and increased circulating adiponectin and mRNA expression in muscle. Among patients with type 2 diabetes mellitus, increasing exercise led to a reduction in fasting plasma glucose.72

  3. Delving into the archives of Pubpeer, it appears that Finelli was quite impressed by the work of Harrison and Day (2007). Their malapropism about “the salutatory effects on weight loss” is copied verbatim into at least one other paper and a book chapter.

  4. This seems to be a treasure trove. I just did a most basic check for

    Finelli, C., & Tarantino, G. (2013). What is the role of adiponectin in obesity related non-alcoholic fatty liver disease?. World journal of gastroenterology: WJG, 19(6), 802.

    (cited 104 times on Google Scholar). Picking a phrase at random:
    “Insulin regulates the uptake, oxidation and storage of fuel within insulin-sensitive tissues including the liver, skeletal muscle and fat. Peripheral insulin resistance impairs glucose uptake from blood into skeletal muscle and adipose tissue; serum non-esterified fatty acid (NEFA) levels may also be elevated because of the failure of insulin to suppress lipolysis”

    I get two Hits. One is the paper and the other hit is:

    Wang, Y., Zhou, M., Lam, K. S., & Xu, A. (2009). Protective roles of adiponectin in obesity-related fatty liver diseases: mechanisms and therapeutic implications. Arquivos Brasileiros de Endocrinologia & Metabologia, 53(2), 201-212.

    (cited 79 times).
    http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0004-27302009000200012
    vs.
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3574877/

    The papers are virtual identical. Differences in the introduction amount to replacing “nowadays” by “current”. Some section headings have been modified by reordering the words, and the figures are reworked with different colors, but this is amazing….

    I recommend going ahead and taking all of the substantial number of publications…

    1. The papers are virtual identical. Differences in the introduction amount to replacing “nowadays” by “current”. Some section headings have been modified by reordering the words, and the figures are reworked with different colors, but this is amazing…

      There was another source. If I may plagiarise quote from the Pubpeer entry for the Adiponectin paper:
      ———————————————
      The Concluding Remarks include a paragraph copied from the Abstract of Robinson, Prins & Venkatesh (2001), “Clinical review: Adiponectin biology and its role in inflammation and critical illness” (BioMedCentral):
      https://ccforum.biomedcentral.com/articles/10.1186/cc10021

      Robinson &c:

      Abstract
      […] The role of adiponectin in systemic inflammation and critical illness is not well defined. Early data suggest that plasma levels of adiponectin are decreased in critical illness. Whether this is a result of the disease process itself or whether patients with lower levels of this hormone are more susceptible to developing a critical illness is not known. This observation of lower adiponectin levels then raises the possibility of therapeutic options to increase circulating adiponectin levels. The various options for modulation of serum adiponectin (recombinant adiponectin, thiazolidinediones) are discussed.

      Finelli & Tarantino:

      CONCLUDING REMARKS
      […] The role of adiponectin in systemic inflammation and critical illness is not well defined. Early data suggest that plasma levels of adiponectin are decreased in critical illness[143]. Whether this is a result of the disease process itself or whether patients with lower levels of this hormone are more susceptible to developing a critical illness is not known. This observation of lower adiponectin levels then raises the possibility of therapeutic options to increase circulating adiponectin levels[143]. The various options for modulation of serum adiponectin (recombinant adiponectin, thiazolidinediones) are discussed.

      1. I underestimated the “creativity”.

        Did you also find the link between:
        https://www.ncbi.nlm.nih.gov/pmc/articles/PMC406470/

        and

        https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3812473/

        Paterson, J. M., Morton, N. M., Fievet, C., Kenyon, C. J., Holmes, M. C., Staels, B., … Mullins, J. J. (2004). Metabolic syndrome without obesity: Hepatic overexpression of 11β-hydroxysteroid dehydrogenase type 1 in transgenic mice. Proceedings of the National Academy of Sciences of the United States of America, 101(18), 7088–7093. http://doi.org/10.1073/pnas.0305524101

        vs.

        Tarantino, G., & Finelli, C. (2013). Pathogenesis of hepatic steatosis: The link between hypercortisolism and non-alcoholic fatty liver disease. World Journal of Gastroenterology : WJG, 19(40), 6735–6743. http://doi.org/10.3748/wjg.v19.i40.6735

        Opening sentence:
        “In Cushing’s syndrome, high circulating glucocorticoid (GC) levels cause visceral obesity, insulin resistance, diabetes mellitus, dyslipidemia, hypertension, hepatic steatosis and an increased risk of coronary artery disease (CAD)[1,2]”

        vs.

        “In Cushing’s syndrome, high circulating glucocorticoid (GC) levels cause visceral obesity, insulin resistance, diabetes mellitus, dyslipidemia, hypertension, and an increased risk of cardiovascular disease (1, 2). ”

        Note that there are round parantheses in the second one. I wil nto say which sentence is from which source… sigh…and it goes on…

        1. And I checked a third paper from the publication list:

          Compare:
          Finelli, Carmine, et al. “Should visceral fat be reduced to increase longevity?.” Ageing research reviews 12.4 (2013): 996-1004.

          https://www.researchgate.net/profile/Carmine_Finelli/publication/239063853_Should_visceral_fat_be_reduced_to_increase_longevity/links/55356f4a0cf268fd0015db1d.pdf

          with

          Huffman, D. M., & Barzilai, N. (2009). Role of Visceral Adipose Tissue in Aging. Biochimica et Biophysica Acta, 1790(10), 1117–1123. http://doi.org/10.1016/j.bbagen.2009.01.008

          “The prevalence of overweight (body mass index > 25) and obesity
          (body mass index > 30) has reached epidemic proportions in
          most of the developed world.”

          vs.

          “The prevalence of overweight (body mass index>25) and obesity (body mass index>30) now effects nearly two thirds of Americans and has reached epidemic proportions in most of the developed world. ”

          (some words have been eliminated, but the”parallelism” goes on and on…)

          This case is beyond ridiculous.

          1. An anonymous Pubpeer contributor noted the extensive parallelism with Huffman & Barzilai (2009):
            https://pubpeer.com/publications/73E9D9E3336C0F5B7CBF89873D53CC

            Other paragraphs and a Table were traced to Wolin, Carson and Colditz (2010), “Obesity and Cancer” (Oncologist).
            https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3227989/

            The main editorial contribution of Finelli et al. was to go through the citations within the borrowed paragraphs, replacing the recognition of original researchers with links to previous papers by Finelli et al.

    1. Which appears to contain plenty of copy-paste, too – including from Wikipedia. I also wonder whether the figure was reproduced with permission…

      1. First paragraph was Zivkovic et al (2007), and recycled here for what may be the 6th or 7th time… I lost track. Google the phrase “This constellation is also recognized as the metabolic syndrome and is characterized by underlying” and an entire Finelli oeuvre appears!

        As you say, there is a lot of Wikipedia in the 2nd, 4th, 5th and penultimate paragraphs.

        Antepenultimate paragraph is from Zelber-Saki et al. (2011). The phrase “an environment that encourages automobile use rather than walking (like lack of sidewalks)” is another productive search target.

        The diagram and the words “Following a Mediterranean diet has many benefits, but there are still a lot of misconceptions on exactly how to take advantage of the lifestyle to lead a healthier, longer life” may both have come from the same source.

  5. What always gets me about plagiarists is how…well .. lazy they are.

    For example “In Cushing’s syndrome, high circulating glucocorticoid (GC) levels cause visceral obesity, insulin resistance, diabetes mellitus, dyslipidemia, hypertension, hepatic steatosis and an increased risk of coronary artery disease ”

    It is literally the work of several minutes to write:
    “There are a number of factors in Cushing’s syndrome, such as diabetes mellitus and associated insulin resistance, hypertension, obesity and an increased risk of coronary artery disease which are all associated with the high levels of circulating GC levels”.

    La! First time I’ve heard of this syndrome and I am now an expert! True I did not mention the dyslipidemia or steatosis but we can’t all be perfect (also no idea what they are and to lazy to find out).

    1. A cursory glance of Finelli’s latest work reveals it to be an extended version of Finelli et al. (2014) (EXCLI J),
      https://pubpeer.com/publications/06B692A6508328B51152F2115BF1F8
      which was itself a verbatim copy of Finelli et al. (2013) (OMICS),
      https://pubpeer.com/publications/D74E3C650B9791806D0CF5525AE375
      apart from a slightly different list of et al.s in those two earlier appearances.

      Those earlier versions were collages of paragraphs and sentences copied from various sources, some of them cited in the References; they lacked quotation marks or original sentences. Reprinted as a chapter, the text acquired various typos and three new sections / paragraphs, but it lost six co-authors, leaving one to wonder what they originally contributed.

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