- Email: [email protected]
Plagiarism in an article: Is there any evidence?
Medical Hypotheses (2007) 69, 1154–1162
http://intl.elsevierhealth.com/journals/mehy
Correspondence
Plagiarism in an article: Is there any evidence? I have closely examined the article ‘‘Inflammation in variant angina: Is there any evidence?’’ in a recent issue of Medical Hypotheses. The article supports a concept that I promoted in a letter-tothe-editor that appeared in the 2005 volume of The American Journal of Cardiology [1,2]. Your ‘‘Guide for Authors’’ requests that submissions be ‘‘different from current thinking’’ – in other words, original. Li et al.’s article, however, is not original. Not only are its principal concepts outlined in earlier publications, but large portions of its text have been taken word for word from those sources. In regards to the central hypothesis itself, Dr. Li and his colleagues are not the first to suggest a role for inflammation in variant angina. I preceded them in uniting various pieces of evidence into a cohesive hypothesis about this role [2]. Remarkably, more than half of the sentences in my letter were transplanted verbatim, but with neither quotation marks nor even citation, to Li et al.’s text. Each of the authors’ major points is summarized using my exact words as enumerated below. 1. The concluding sentences of their abstract: ‘‘vasospastic coronary disease is at least partially driven by inflammation. [Although] much more research is obviously needed, [primary evidence] provide us with some direction for that research.’’ 2. The concluding sentences of their evidence section: ‘‘taken together, these observations hint that, as with atherosclerotic coronary disease, vasospastic coronary disease is at least partially driven by inflammation. [Recently,] the study by Hung et al. that correlated CRP protein levels to variant angina activity adds to the growing evidence that vasospastic coronary disease, like its atherosclerotic cousin, has a significant inflammatory component.’’ 3. The concluding sentences of their clinical implications section: ‘‘the therapeutic implication of
the premise is that anti-inflammatory, and perhaps antiallergy, medications offer potential benefit for this disorder. Statins, antihistamines, leukotriene inhibitors, and even rheumatologic drugs may join the limited therapeutic armamentarium for variant angina. Much more research is obviously needed, but at least studies [regarding inflammation and variant angina] provide us with some direction for that research.’’ Their heavy reliance upon my previous work is also reflected in the fact that they used 9 of the 10 references listed in my manuscript. Admittedly, Dr. Li and his colleagues do expand on my evidence but I strongly believe that the core of their argument is contained in my previous paper. Their solitary acknowledgment of my letter is buried in a sentence that notes that 17 published sources lend support to this hypothesis. In reviewing Li et al.’s prior publications, it is apparent that they have had an interest in the role of inflammation in atherosclerotic coronary disease but not in vasospastic coronary disease. Their review ‘‘Inflammation: an important mechanism for different clinical entities of coronary artery diseases’’ was published in the 2005 volume of the Chinese Medical Journal but contains no mention of variant angina [3]. Perhaps more significantly, their transgression was not limited to plagiarism of my work. Their most blatant violation of copyright is manifest in their two-page section ‘‘Evidence of inflammation in variant angina’’ in which they lay out the foundation for the hypothesis. This entire section is composed of abstracts taken verbatim from other authors’ publications. These abstracts are simply placed one after the next without quotation marks. It is for others to judge these authors on their intent. I can only provide the evidence that language and probably concepts were taken without acknowledgment. It is also not for me to decide
Correspondence on consequences for this behavior. In the very least, I believe that all authors, editors, and publishers affected by these copyright violations deserve notification. Future submissions by Dr. Li’s group should also receive closer scrutiny.
References [1] Li JJ, Nie S-P, Xu B, et al. Inflammation in variant angina: is there any evidence? Med Hypotheses 2007;68:635–40. [2] Rich MW. Is vasospastic angina an inflammatory disease? Am J Cardiol 2005;96:1612.
1155 [3] Li JJ. Inflammation: an important mechanism for different clinical entities of coronary artery disease. Chinese Med J 2005;118:1817–26.
Michael W. Rich Summa Health System, Department of Medicine, 55 Arch Street, Suite 1A, Akron, OH 44304, USA Tel.: +1 330 375 3010 E-mail address: [email protected]
doi:10.1016/j.mehy.2007.05.039
Inflammation in variant angina: An old topic or novel finding? Dear Editor, I deeply apologized for the letter from Dr. Rich concerning our recent article published in Medical Hypotheses [1]. And also, I would like to make an apology again for insufficient attribution of Dr. Rich’s paper published in American Journal of Cardiology in our recent article [2]. We are in agreement with Dr. Rich’s comment regarding our article in which support the concept that variant angina is related to inflammation. Dr. Rich’s paper has been cited in our article [1], but careless insufficient. This was our biggest mistake in the article. The full understanding of citation model as well as language problem (English is not native language) for us may also be principle reasons for those mistakes. Therefore, we firstly apologized for those mistakes to Dr. Rich formally. We also understand that it may make Dr. Rich uncomfortable. However, we have really no intent to take up concept from Dr Rich’ paper. We completely agree with Dr Rich’s statement in that we are not the first to suggest a role of inflammation in variant angina, he preceded us in uniting various pieces of evidence into a cohesive hypothesis about this role. We have no intention to cover this fact because we have already incited his paper in our article [2]. This is the evidence. Inflammation in variant angina is not a novel finding but an old topic in cardiovascular medicine, the relating articles have already been published several years ago [4–6]. As early as 1978 Dr Lewis
JR, et al. reported a case with variant angina, and their autopsy data showed that normal coronary arteries and acute pericarditis, then they postulated that pericardial inflammation elicited severe spasm of the subjacent right coronary artery, resulting in spasm [3]. Data from Buffon et al. [4], Terashima et al. [5], Hung et al. [6], have already indicated role of inflammation in variant angina several years ago. Therefore, it is evidence that we are not original, and also have not taken this concept from Dr. Rich’s paper. In addition, our group has focused inflammation in coronary artery disease for many years, and published several original articles in peer-view international as well as Chinese Journals although the levels are very, very lower. Therefore, our attentions on relationship between variant angina and inflammation are reasonable. In the article we have just provided more evidence regarding inflammation in variant angina, accent on the importance for further attention. The fact that word count of our paper is more than 3800 is of evidence. Moreover, the clinical evidence study concerning inflammation in variant angina has been primarily performed in our group (Data not shown, Submitted to publication). Finally, the evidence regarding inflammation in variant angina is not either a novel finding or great discovery, but an old topic. This concept is indeed not worth taking up from the others. Therefore, we deeply express regret over Dr Rich’ statement ‘‘It is for others to judge these authors on their intent’’.
http://intl.elsevierhealth.com/journals/mehy
Correspondence
Plagiarism in an article: Is there any evidence? I have closely examined the article ‘‘Inflammation in variant angina: Is there any evidence?’’ in a recent issue of Medical Hypotheses. The article supports a concept that I promoted in a letter-tothe-editor that appeared in the 2005 volume of The American Journal of Cardiology [1,2]. Your ‘‘Guide for Authors’’ requests that submissions be ‘‘different from current thinking’’ – in other words, original. Li et al.’s article, however, is not original. Not only are its principal concepts outlined in earlier publications, but large portions of its text have been taken word for word from those sources. In regards to the central hypothesis itself, Dr. Li and his colleagues are not the first to suggest a role for inflammation in variant angina. I preceded them in uniting various pieces of evidence into a cohesive hypothesis about this role [2]. Remarkably, more than half of the sentences in my letter were transplanted verbatim, but with neither quotation marks nor even citation, to Li et al.’s text. Each of the authors’ major points is summarized using my exact words as enumerated below. 1. The concluding sentences of their abstract: ‘‘vasospastic coronary disease is at least partially driven by inflammation. [Although] much more research is obviously needed, [primary evidence] provide us with some direction for that research.’’ 2. The concluding sentences of their evidence section: ‘‘taken together, these observations hint that, as with atherosclerotic coronary disease, vasospastic coronary disease is at least partially driven by inflammation. [Recently,] the study by Hung et al. that correlated CRP protein levels to variant angina activity adds to the growing evidence that vasospastic coronary disease, like its atherosclerotic cousin, has a significant inflammatory component.’’ 3. The concluding sentences of their clinical implications section: ‘‘the therapeutic implication of
the premise is that anti-inflammatory, and perhaps antiallergy, medications offer potential benefit for this disorder. Statins, antihistamines, leukotriene inhibitors, and even rheumatologic drugs may join the limited therapeutic armamentarium for variant angina. Much more research is obviously needed, but at least studies [regarding inflammation and variant angina] provide us with some direction for that research.’’ Their heavy reliance upon my previous work is also reflected in the fact that they used 9 of the 10 references listed in my manuscript. Admittedly, Dr. Li and his colleagues do expand on my evidence but I strongly believe that the core of their argument is contained in my previous paper. Their solitary acknowledgment of my letter is buried in a sentence that notes that 17 published sources lend support to this hypothesis. In reviewing Li et al.’s prior publications, it is apparent that they have had an interest in the role of inflammation in atherosclerotic coronary disease but not in vasospastic coronary disease. Their review ‘‘Inflammation: an important mechanism for different clinical entities of coronary artery diseases’’ was published in the 2005 volume of the Chinese Medical Journal but contains no mention of variant angina [3]. Perhaps more significantly, their transgression was not limited to plagiarism of my work. Their most blatant violation of copyright is manifest in their two-page section ‘‘Evidence of inflammation in variant angina’’ in which they lay out the foundation for the hypothesis. This entire section is composed of abstracts taken verbatim from other authors’ publications. These abstracts are simply placed one after the next without quotation marks. It is for others to judge these authors on their intent. I can only provide the evidence that language and probably concepts were taken without acknowledgment. It is also not for me to decide
Correspondence on consequences for this behavior. In the very least, I believe that all authors, editors, and publishers affected by these copyright violations deserve notification. Future submissions by Dr. Li’s group should also receive closer scrutiny.
References [1] Li JJ, Nie S-P, Xu B, et al. Inflammation in variant angina: is there any evidence? Med Hypotheses 2007;68:635–40. [2] Rich MW. Is vasospastic angina an inflammatory disease? Am J Cardiol 2005;96:1612.
1155 [3] Li JJ. Inflammation: an important mechanism for different clinical entities of coronary artery disease. Chinese Med J 2005;118:1817–26.
Michael W. Rich Summa Health System, Department of Medicine, 55 Arch Street, Suite 1A, Akron, OH 44304, USA Tel.: +1 330 375 3010 E-mail address: [email protected]
doi:10.1016/j.mehy.2007.05.039
Inflammation in variant angina: An old topic or novel finding? Dear Editor, I deeply apologized for the letter from Dr. Rich concerning our recent article published in Medical Hypotheses [1]. And also, I would like to make an apology again for insufficient attribution of Dr. Rich’s paper published in American Journal of Cardiology in our recent article [2]. We are in agreement with Dr. Rich’s comment regarding our article in which support the concept that variant angina is related to inflammation. Dr. Rich’s paper has been cited in our article [1], but careless insufficient. This was our biggest mistake in the article. The full understanding of citation model as well as language problem (English is not native language) for us may also be principle reasons for those mistakes. Therefore, we firstly apologized for those mistakes to Dr. Rich formally. We also understand that it may make Dr. Rich uncomfortable. However, we have really no intent to take up concept from Dr Rich’ paper. We completely agree with Dr Rich’s statement in that we are not the first to suggest a role of inflammation in variant angina, he preceded us in uniting various pieces of evidence into a cohesive hypothesis about this role. We have no intention to cover this fact because we have already incited his paper in our article [2]. This is the evidence. Inflammation in variant angina is not a novel finding but an old topic in cardiovascular medicine, the relating articles have already been published several years ago [4–6]. As early as 1978 Dr Lewis
JR, et al. reported a case with variant angina, and their autopsy data showed that normal coronary arteries and acute pericarditis, then they postulated that pericardial inflammation elicited severe spasm of the subjacent right coronary artery, resulting in spasm [3]. Data from Buffon et al. [4], Terashima et al. [5], Hung et al. [6], have already indicated role of inflammation in variant angina several years ago. Therefore, it is evidence that we are not original, and also have not taken this concept from Dr. Rich’s paper. In addition, our group has focused inflammation in coronary artery disease for many years, and published several original articles in peer-view international as well as Chinese Journals although the levels are very, very lower. Therefore, our attentions on relationship between variant angina and inflammation are reasonable. In the article we have just provided more evidence regarding inflammation in variant angina, accent on the importance for further attention. The fact that word count of our paper is more than 3800 is of evidence. Moreover, the clinical evidence study concerning inflammation in variant angina has been primarily performed in our group (Data not shown, Submitted to publication). Finally, the evidence regarding inflammation in variant angina is not either a novel finding or great discovery, but an old topic. This concept is indeed not worth taking up from the others. Therefore, we deeply express regret over Dr Rich’ statement ‘‘It is for others to judge these authors on their intent’’.