BMC research notes
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To analyse retraction notices from 2016 and compare their quality to the 2008 notices. ⋯ From 146 retractions retrieved, only 123 were included, of which, a clear reason for retraction was available for 122 (99.2%) and no reason was given for one (0.8%). The main reasons for retraction were mistakes 26.0% (n = 32), fraud 26.0% (n = 32), plagiarism 20.3% (n = 25), and overlap 8.1% (n = 10). In 100 (81.3%) cases, a mention of retraction was available on the original paper, in 15 (12.2%) there was no mention of retraction, and 8 (6.5%) papers were deleted. Compared to the previous cohorts, management of retraction has improved because 99.2% provided a clear reason, and 81.3% of original articles were available with a mention of the retraction.
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Earlier studies from our group using hypoxia-inducible factor 3α knockout mice showed impairments in lung remodeling and lung endothelial cells. Another research from our group demonstrated that impaired expression of hypoxia-inducible factor 2α induced compensatory expression of hypoxia-inducible factor 1α in hypoxia-inducible factor 2α knockdown mice. The present study uncovers more insights by extending the investigation, utilizing mice with both hypoxia-inducible factor 3α knockout and hypoxia-inducible factor 2α knockdown. ⋯ No mice with both hypoxia-inducible factor 3α knockout and hypoxia-inducible factor 2α knockdown died immediately after birth. The mice with both hypoxia-inducible factor 3α knockout and hypoxia-inducible factor 2α knockdown exhibited impaired alveolar sacs and lung alveolar structure and decreased endothelial cell numbers. Analysis of relative mRNA expression revealed depressed expressions of hypoxia-inducible factor 1α, vascular cell adhesion molecule 1, vascular endothelial cadherin, angiopoietin 2, Tie-2, and vascular endothelial growth factor in the lungs of mice with both hypoxia-inducible factor 3α knockout and hypoxia-inducible factor 2α knockdown compared to that in wild-type mice. Further analysis is needed to elucidate the impaired development occurred in the lung endothelial cells.