【6】 肺高血圧症と女性ホルモン
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。
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B（2001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.
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。
