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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.

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