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。

【デコイ】 が 反発

2012-02-01 | 阪大デコイ : 論文撤回Watch

【デコイ】 が 反発

Retraction Watch / 2011.01.24 00:14 / 推薦数 : 6

論文掲載が発表されると、その論文内容に関連した会社の株価が上昇することがあります。

阪大デコイグループより発表された論文の影響を受けて、ある会社の株価が上昇しました。

 

...が4日ぶりに反発した。4日に大阪大学医学部附属病院で実施されたHGF遺伝子治療臨床研究の長期成績が、末梢血管疾患など血管疾患分野の著名な専門誌に掲載されたと発表したことが買い材料となった。

 

発表された論文はこれです。内容を見てみますと、これも盗作論文ということがわかります。主に雑誌Circulation (1998;97:1114-1123) に掲載されたこの論文から盗用しています。

 

阪大デコイ論文 

The natural history of critical limb ischemia has been well documented to have an inexorable downhill course.  The inclusion criteria for this study were drafted to restrict treatment to patients in whom the natural history of critical limb ischemia was previously established

 

雑誌Circulation

The natural history of critical limb ischemia has been well documented to have an inexorable downhill course.  The inclusion criteria for this study were drafted to restrict treatment to patients in whom the natural history of critical limb ischemia had been establishedpreviously. 

 

阪大デコイ論文

Given the poor prognosis for patients with chronic critical limb ischemia, in whom the possibility of spontaneous improvement is remote, the outcome in this cohort is encouraging. 

 

雑誌Circulation

Given the poor prognosis for patients with chronic critical limb ischemia, in whom the possibility of spontaneous improvement is remotethe outcome in this initial cohort is thus encouraging.

 

阪大デコイ論文

...after the second transfection. Nevertheless, these findings are preliminary and do not establish the long-term safety of HGF.  

 

雑誌Circulation

...gene transfer. Nevertheless, these findings are preliminary and do not establish the long-term safety of VEGF, ...

 

株価の上昇した会社が実際にどの会社かは、論文撤回Watchの読者なら簡単にわかると思います。 さらに論文の筆頭著者と会社のかかわりについても、ここで説明する必要はないでしょう。

 

英文盗用で塗り固まれた論文。データだけには不正はないように願いたいものです。


【デコイ】 で どっこい

2012-02-01 | 阪大デコイ : 論文撤回Watch

【デコイ】 で どっこい

Retraction Watch / 2011.01.23 00:55 / 推薦数 : 2

編集委員や査読者が、特にインパクトのある論文に対してコメントを寄せることがあります。

大阪大学臨床遺伝子治療学に所属する2名の著者が、ある論文に対して次のようなコメントを雑誌Hypertension Researchに寄せたところ、掲載されました。 

内容はパクリです。すなわち盗作。

Murine Sall1 has a role in maintaining cellular pluripotency and proliferation. Thus, renal primordial cells in the ureteric bud epithelium and metanephric mesenchyme are able to produce nephrons and collecting ducts when induced from pluripotent embryonic stem cells. Only cells expressing high levels of Sall1 can reconstitute a three-dimensional kidney structure in an organ culture setting, indicating that renal progenitors with multipotent capacity require Sall1. In these cells, Sall1 is not required for the generation or differentiation of renal progenitors, but for their proliferation or survival.

全く同じ文章がこの論文に過去に掲載されています。

 

さらに別の論文からもそのままかっさらっています。

The homeotic spalt gene of Drosophila melanogaster determines the identity of the anterior head and the posterior tail regions during early development. At later stages, spalt is involved in the development of the wing disk, trachea and sensory organs. Humans and mice have four functional spalt-related genes, SALL1 to SALL4 (Sall1 to Sall4 in mice). The human SALL1 gene encodes transcription factors with a characteristic structure of evenly distributed zinc-finger domains. Human SALL1 has been described as a transcriptional repressor in a number of experimental settings, most of them involving the regulation of heterologous promoters fused to reporter genes.10 SALL1 gene expression is related to some human congenital diseases11,12,15,17–19 (Figure 2). In particular, mutations in SALL1 result in Townes–Brocks syndrome, a rare autosomal-dominant malformation syndrome characterized by dysplastic ears, pre-axial polydactyly and/or triphalangeal thumbs, imperforate anus, renal malformations and cardiac anomalies.

 

盗作してまで、コメントを寄稿したいのか!!!

と言いたいです。世迷い独り言でした。


【デコイ】 で どすこい

2012-02-01 | 阪大デコイ : 論文撤回Watch

【デコイ】 で どすこい

Retraction Watch / 2011.01.22 00:04 / 推薦数 : 2

過去に自分で創作した表現を別の論文にも使うことは、特に総説論文ではよく見られます。しかし、時にはSelf Plagiarism 自己盗作や自己剽窃と呼ばれる場合もあります。どの程度の再利用なら許容されるのでしょうか?

大阪大学老年内科から発表された2編の総説論文を紹介します。

1編目は1998年にここに掲載されており(以下98論文)、5年後の2003に掲載されたのが、これです(以下03論文)。

長くなりますが、2つの論文の記載内容のほんの一部をみてみましょう。

まずは抄録から

03論文

 

Molecular therapy is emerging as a potential strategy for the treatment of cardiovascular disease such as restenosis after angioplasty, vascular bypass graft occlusion, transplant coronary vasculopathy, homozygous familial hypercholesterolemia and cystic fibrosis, for which no known effective therapy exists. Molecular biology and pathophysiology of the cardiovascular system have started to emerge, and the time is ripe for the introduction of gene therapy to the management of cardiovascular disorders. In this review, we have focused on the future potential of oligonucleotide-based gene therapy for restenosis after angioplasty, which still remains an issue in the field of cardiovascular disease.

98論文

Gene therapy is emerging as a potential strategy for the treatment of cardiovascular disease such as restenosis after angioplasty, vascular bypass graft occlusion, transplant coronary vasculopathy, homozygous familial hypercholesterolemia and cystic fibrosis, for which no known effective therapy exists.  Gene therapy requires efficient in vivo gene transfer technology. During the past decade, many gene transfer methods including viral transfer techniques have been developed, and some are being applied clinically in human gene therapy studies.  Molecular biology and pathophysiology of the cardiovascular system have started to emerge, and the time is ripe for the introduction of gene therapy to the management of cardiovascular disorders.  In this review, we have focused on the future potential of oligonucleotide-based gene therapy for the treatment of cardiovascular disease.

 

 

本文はどうでしょうか。

 

03論文

3. Decoy-Based Therapy

Transfection of cis-element double-stranded (ds) ODN (=decoy) has been reported as a powerful tool in a new class of anti-gene strategies for molecular therapy. Transfection of decoy ODN corresponding to the cis sequence will result in attenuation of authentic cis-traninteraction, leading to the removal of trans-factors from the endogenous cis-element with subsequent modulation of gene expression.  Therefore, the decoy approach may enable us to treat various diseases by modulation of endogenous transcriptional regulation. Previously, many researchers employed antisense technology as a “loss of function” approach at the transcriptional and translational levels [30, 31].  On the other hand, the cis-element decoy strategy is also applicable as a “loss of function” approach at the pre-transcriptional and transcriptional levels to study transcription factors.  Restenosis is also a major target disease of decoy-based molecular therapy, and more than a few researchers have evaluated its effect in animal models [32, 33].

98論文

2. Decoy-Based Gene Therapy

Transfection of cis-element double stranded (ds) ODN (= decoy) has also been reported as a powerful tool in a new class of anti-gene strategies for gene therapy and the study of transcriptional regulation (4, 20–27).  Transfection of ds ODN corresponding to the cis sequence will result in the attenuation of authentic cis-trans interaction, leading to the removal of trans-factors from the endogenous cis-element, with subsequent modulation of gene expression (Fig. 1). Therefore, the decoy approach may also enable us to treat disease by modulation of endogenous transcriptional regulation.  Currently, several studies have reported the application of the “decoy” ODN strategy as in vivo gene therapy (4, 21–25).  Previously, many researchers employed antisense technology as a “loss of function” approach at the transnational levels.  On the other hand, the cis-element decoy strategy is also applicable as a “loss of function” approach at the pre-transcriptional and transcriptional levels to study transcription factors (Tab. 1).

 

まだ続きます。

03論文

As discussed above, the process of VSMC proliferation is dependent on the coordinated activation of a series of cell cycle regulatory genes, which results in mitosis. A critical element of cell cycle progression regulation involves the complex formed by E2F, cyclin A and cdk 2 [34]. The dissociation of the transcription factor E2F from the retinoblastoma (Rb) gene product is proposed to play a pivotal role in the regulation of cell proliferation, by inducing coordinated transactivation of genes involved in cell cycle regulation including c-myc, c-myb, cdc 2, PCNA and thymidine kinase [34]. Accordingly, we hypothesized that transfection of VSMC with a sufficient quantity of decoy ODN containing the E2F cis element (consensus sequence “TTTTCGGCGC”) would effectively bind E2F, prevent it from transactivating the gene expression of essential cell cycle regulatory proteins, and thereby inhibit VSMC proliferation and neointimal formation (Fig. 2).

98論文

As discussed above, the process of VSMC proliferation is dependent on the coordinated activation of a series of cell cycle regulatory genes which results in mitosis. A critical element in regulation of cell cycle progression is the complex formed by E2F, cyclin A and cdk 2 (8, 9)Dissociation of the transcription factor E2F from the retinoblastoma (Rb) gene product is proposed to play a pivotal role in the regulation of cell proliferation by inducing a coordinated transactivation of genes involved in cell cycle regulation including c-myc, cmyb, cdc 2, PCNA and thymidine kinase (8, 9). Indeed, the antiproliferative effects of the retinoblastoma gene product appear to depend on its capacity to bind to E2F and thereby prevent this transcription factor from binding to the E2F cis-element within the promoters of these essential cell cycle regulatory genes.

 

これでおわりにします。

03論文

Synthesized 14-mer ds ODN containing the consensus sequence effectively competed with binding of E2F to its binding site, assessed by gel mobility shift assay. Transfection of E2F decoy ODN into rat balloon-injured carotid arteries using the HVJ-liposome method resulted in almost complete inhibition of neointimal formation at 2 weeks after balloon injury, accompanied by a reduction in mRNA of PCNA and cdc 2 kinase, but not b-actin, whereas mismatched ODN had no effect on neointimal hyperplasia [6]. Of importance, sustained inhibition of neointimal formation by a single administration of E2F decoy ODN was observed for at least 8 weeks after treatment.

98論文

Synthesized 14-mer ds ODN containing the consensus sequence effectively competed with binding of E2F to its binding site, assessed by gel mobility shift assay (21). Transfection of E2F decoy ODN into rat balloon-injured carotid arteries using HVJ-liposome method resulted in almost complete inhibition of neointimal formation at 2 weeks after balloon injury, accompanied by a reduction in mRNA of PCNA and cdc 2 kinase, but not b-actin, whereas mismatched ODN had no effect on neointimal hyperplasia (21). Of importance, sustained inhibition of neointimal formation by a single administration of E2F decoy ODN was observed at least up to 8 weeks after the treatment.

 

 

さて、どう思われますか?

Doctors Blog の読者なら、両論文に共通する著者の名前に聞き覚えがあるはずです。なお第3の総説論文としてこれもご覧になられるとことをお勧めします。