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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【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。

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