論文捏造

論文捏造・二重投稿・盗用の研究不正疑惑を追及。論文捏造反対!論文撤回、訂正も監視します。


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【6】 肺高血圧症と女性ホルモン

2012-02-01 | 千葉大学 呼吸器内科
さて、ここでもう一度、最初にとりあげた千葉大撤回論文に話を戻します。

We hereby retract this article for the following reasons: Due to negligence including a communication error between authors, the article contained a number of passages that were copied verbatim and close to verbatim from an excellent review in the field by Tim Lahm et al. in Critical Care Medicine (36: 2174 –2183, 2008).

上記の撤回理由によると、千葉大学の著者らはTim Lahm氏らの論文のみより文章を引用したかのように読み取れます。しかし、他の多くの論文からも文章を引用しているのが事実のようです。 

別の論文A2007年) 

It is apparent that preventing or reversing sustained constriction and neomuscularization of pulmonary arteries in these rodent models is not equivalent to "dissolving" obstructive neointimal and other complex vascular lesions that seemingly account for the high pulmonary vascular resistance (PVR) in PAH. Investigators evaluating new therapies for PAH should consider using more recent rodent models of neointimal lesion-associated pulmonary hypertension rather than the classic chronically hypoxic and monocrotaline-injected models.

千葉論文

Moreover, recent reports suggested that preventing or reversing sustained constriction and neomuscularization of pulmonary arteries in the classic chronically hypoxic and monocrotaline models is not equivalent to dissolving obstructive neointimal and other complex vascular lesions that seemingly account for the high pulmonary vascular resistance in PAH. The effects of estrogens should be evaluated by using more recent rodent models of neointimal lesion-associated PH rather than the classic rodent models. 

別の論文B2001年)

Pulmonary endothelial cells constitute a stable cell population with a very low turnover rate and, apparently, neither severe chronic hypoxia/hypoxemia nor monocrotaline pyrrole causes the emergence of a proliferative, dysfunctional endothelial cell phenotype. The defining pulmonary vascular alteration in both of these models, medial muscular thickening, is potentially reversible upon reexposure to normoxia or with the passage of time after monocrotaline injection. 

千葉論文

Pulmonary EC constitute a stable cell population with a very low turnover rate, and, apparently, neither severe chronic hypoxia/hypoxemia nor monocrotaline pyrrole causes the emergence of a proliferative, dysfunctional EC phenotype. The defining pulmonary vascular alteration in both of these models, namely, medial muscular thickening of proliferating SMC, is potentially reversible upon reexposure to normoxia or with the passage of time after monocrotaline injection. 

別の論文C2010年) 

Several significant factors generate confusion and opposite conclusions in evaluating the role of estrogens in inflammatory/immune diseases, including the relatively superficial translation done from the animal studies to the human condition, the different effects of estrogens on their different receptors or on different target cells, the different estrogen concentrations studied, and finally, the opposite effects (especially on cell proliferation/apoptosis) exerted by different peripheral estrogen metabolites. 

千葉論文

Several significant factors generate confusion and opposite conclusions in evaluating the role of estrogens in PAH. These factors include the several effects of estrogens on their different receptors and opposite effects (especially on cell proliferation) exerted by several peripheral estrogen metabolites.

 

論文の撤回理由を訂正した方がよいかも知れません。

千葉大学呼吸器内科を舞台とした「肺高血圧症と女性ホルモン」シリーズは今回で終了です。

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【5】 肺高血圧症と女性ホルモン

2012-02-01 | 千葉大学 呼吸器内科

【4】肺高血圧症と女性ホルモン からの続きです。

 

千葉大学医学部呼吸器内科のこの研究グループは、他の雑誌にも、さらにもう1編の総説論文を発表しています。ここまで書けば、あとは何について書かれるか想像がつくかとも思いますが、お付き合いください。

 

タイトルは

Vascular remodeling in pulmonary arterial hypertension: Multiple cancer-like pathways and possible treatment modalities

つい最近(2011年2月)の掲載です。

 

千葉論

Over 80 years ago, Otto Warburg first observed that tumor slices consume glucose at a higher rate than normal tissue. This high rate of aerobic glycolysis is now known as the Warburg effect. Warburg hypothesized that the increase in glycolysis under normal oxygen conditions arises from a deficiency in respiration. Since this seminal finding, many reports have documented the Warburg effect in a variety of different cancers. The clinical application of positron emission tomography (PET), which uses a glucose analogue to detect a significant increase in glucose uptake in tumors in comparison to other tissues, is based upon Warburg's initial observations.

別の論文A2009年) 

Over 80 years ago, Otto Warburg first observed that tumor slices consume glucose at a higher rate than normal tissue. This high rate of aerobic glycolysis is now known as the “Warburg effect.” Warburg hypothesized that the increase in glycolysis under normal oxygen conditions arose from a deficiency in respiration. Since this seminal finding, many reports have documented the Warburg effect in a variety of different tumors. In fact, the clinical application of positron emission tomography (PET), which uses a glucose analogue to detect a significant increase in glucose uptake in tumors as compared to other tissue, is based upon Warburg’s initial observation. 

千葉論文

Additionally, sorafenib prevents pulmonary remodeling and improves cardiac and pulmonary function in experimental pulmonary hypertension. Sorafenib exerts direct myocardial antihypertrophic effects, which appear to be mediated via inhibition of the Raf kinase pathway.

別の論文B2008年)

The multikinase inhibitor sorafenib prevents pulmonary remodeling and improves cardiac and pulmonary function in experimental pulmonary hypertension. Sorafenib exerts direct myocardial antihypertrophic effects, which appear to be mediated via inhibition of the Raf kinase pathway. 

千葉論文

Mitochondrial metabolism and redox signaling are reversibly disordered in PAH and cancer, creating a pseudohypoxic redox state characterized by normoxic decreases in reactive oxygen species (ROS), a shift from oxidative to glycolytic metabolism and hypoxia inducible factor (HIF)-1α activation. These effects togethersuppress voltage-sensitive potassium channel (Kv) 1.5 expression, leading to membrane depolarization and an elevation of cytosolic K+ and Ca2+, and in an apoptosis-resistant phenotype in both PAH pulmonary artery SMCs and cancer cells.

別の論文C2008年)

In PAH and cancer, mitochondrial metabolism and redox signaling are reversibly disordered, creating a pseudohypoxic redox state characterized by normoxic decreases in ROS, a shift from oxidative to glycolytic metabolism and HIF-1α activation. .…..This metabolic shift suppresses Kv1.5 expression, leading to membrane depolarization and an elevation of cytosolic K+ and Ca2+. In both PAH PASMC and cancer cell lines, this creates a proliferative, apoptosis-resistant phenotype.

 

今回の千葉論文の著者は2名のみです。やはり、筆頭著者は責任著者も兼ねています。

研究のサポートは

This work was supported by the Research Grants for the Respiratory Failure Research Group and the Cardiovascular Diseases (2233) from the Ministry of Health, Labor and Welfare, Japan and the Grant-in-Aid for Scientific Research (Category C 22590851) from the Japanese Ministry of Education.

と記載されています。

最後に重要なことが宣言されています。

The authors of this manuscript have certified that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology.

 

Principles of Ethical Publishing in the International Journal of Cardiologyの4項目に

That the material in the manuscript has been acquired according to modern ethical standards and does not contain material copied from anyone else without their written permission.

とあります。 

 

この論文も今のところ撤回されていません。

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【4】 肺高血圧症と女性ホルモン

2012-02-01 | 千葉大学 呼吸器内科

【3】肺高血圧症と女性ホルモンからの続きです。

 

千葉大学医学部呼吸器内科のこの研究グループは、他の雑誌にも総説論文を発表しています。

 

Reversible or Irreversible Remodeling in Pulmonary Arterial Hypertension

というタイトルの論文で、2010年12月の雑誌掲載です。

内容はというと、別の研究者の書いた論文中の文章を写しているような箇所が数多く見られます。

千葉論文

In contrast to the human disease, both classical rodent models of mild to moderate pulmonary hypertension—the chronic hypoxia and monocrotaline models—lack clustered proliferated EC in the lumen of pulmonary arteries.

別の論文A2001年)

In contrast to the human disease, both classical rodent models of mild to moderate pulmonary hypertension—the chronic hypoxia and the alkaloid monocrotaline models—lack clustered proliferated endothelial cells in the lumen of pulmonary arteries.

千葉論

Neointimal pulmonary vascular occlusive lesions that consist of proliferating SMC are found in rats after the combination of pneumonectomy with monocrotaline injection. A combination of compensatory lung growth after a pneumonectomy, hemodynamic factors, and endothelial injury by monocrotaline pyrrole may combine to produce this neointimal pulmonary vascular disease.

別の論文B2003年)

Neointimal pulmonary vascular occlusive lesions, consisting of proliferating smooth muscle cells and bearing similarities to the pathological lesions in human PPH, are evident in rats after the combination of pneumonectomy with monocrotaline injection. We hypothesize that a combination of compensatory lung growth after pneumonectomy, hemodynamic factors, and endothelial injury by monocrotaline pyrrole combine to produce this neointimal pulmonary vascular disease.

千葉論

Although less well studied, the shift of vascular SMC, whereby proliferative adult vascular SMC convert back to a nonproliferative state, is an important observation.This particular phenotype switch is essential for limiting SMC accumulation and for the termination of vascular remodeling. The regulatory factors that drive proliferative SMC into a nonproliferative state, and hold them in that state, are critical for effective vascular remodeling and for limiting vascular disease.

別の論文C2006年)

Although less well studied, an equally important manifestation of SMC plasticity is the reverse shift, whereby proliferative adult SMCs convert back to a nonproliferative state. This particular phenotype switch is essential for limiting SMC accumulation and for terminating vascular remodeling. As such, the regulatory factors that drive proliferative SMCs into a nonproliferative state, and hold them in that state, are critical for effective vascular remodeling and for limiting vascular disease.

 

まだありますが、これくらい示しておけば十分でしょう。

なお、 著者は3人で、2人は千葉大学、1人は米国の研究者です。筆頭著者は責任著者でもあります。

 

研究サポート資金は以下のとおり:

This study was supported by National Institutes of Health (NIH) Grant 5P01
HL66254–03 PI; an NIH Program Project Grant (to N.F.V.); Research Grants for the
Respiratory Failure Research Group from the Ministry of Health, Labor and Welfare,
Japan; and Chiba foundation for health promotion and disease prevention. 

 

この論文は今のところ撤回されていません。
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【3】 肺高血圧症と女性ホルモン

2012-02-01 | 千葉大学 呼吸器内科

復活後の第一弾は、千葉大学の肺高血圧症と女性ホルモン【2】 からの続きです。

Retraction Watchによると、

 

And what about the other “negligences” not covered by communication error? Those go unenumerated, unfortunately. We emailed the first author of the paper, Seiichiro Sakao, for comment but haven’t received a reply. 

 

というわけで、Retraction Watchは筆頭著者かつ責任著者である人物にメールをして詳しい説明を求めていますが、 今のところ、返事はない、ということです。

 

さらに、この総説論文の最後に 

This study was supported by Research Grants for the Respiratory Failure
Research Group and Cardiovascular Diseases (19-9, 22-33) from the Ministry
of Health, Labor, and Welfare, Japan, the Grant-in-Aid for Scientific Research
(Category C 22590851) from the Japanese Ministry of Education and Science,
and Chiba Foundation for Health Promotion and Disease Prevention

とあり、この総説論文・研究はいくつかの公的研究資金を受けていることが明記されています。 

 

【4】 肺高血圧症と女性ホルモン

に続きます。

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肺高血圧症と女性ホルモン 【2】

2012-02-01 | 千葉大学 呼吸器内科

肺高血圧症と女性ホルモン【1】からの続きです。

実際の撤回アナウンスは下記のとおりです。

 

We hereby retract this article for the following reasons: Due to negligence including a communication error between authors, the article contained a number of passages that were copied verbatim and close to verbatim from an excellent review in the field by Tim Lahm et al. in Critical Care Medicine (36: 2174–2183, 2008). We also did not reference the source of these passages.

We offer our formal apologies for this error and for any inconvenience associated with the publication of the article. The paper is therefore being retracted by the American Physiological Society at the request of Dr. Sakao and with the approval of the coauthors.

 

撤回の理由は盗作以外に、もうひとつあり、

negligence including a communication error between authors

とあります。

ここでAuthorsというのは千葉大学医学部呼吸器内科に所属する3人のことです。筆頭著者は責任著者でもあります。


この3人の著者の間で、論文投稿にあたって合意がなされていなかったということでしょうか?この3人のうち誰かひとりが勝手にこの論文を投稿した。よって他の2人の著者は盗作については知らなかった、というこを訴えたかったのでしょうか?

ところが、撤回された論文の最後には
ACKNOWLEDGMENTS
All authors read and approved the final manuscript.
と、あります。

 

さらによくわからないのは、

We offer our formal apologies for this error and for any inconvenience associated with the publication of the article.

となるくだりです。


this errorとは何をさすのでしょうか?コピーした文の出典先を示さなかったことをさしているのでしょうか?

はっきりと this misconduct (研究不正)あるいは this plagiarism(盗作)と表記しないのは、なぜでしょう?

 

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