Objectives: To investigate the current prevalence of open access (OA) in the field of dentistry, the means used to provide OA, as well as the association between OA and citation counts.Methods: PubMed was searched for dental articles published in 2013. The OA status of each article was determined by manually checking Google, Google Scholar, PubMed and ResearchGate. Citation data were extracted from Google Scholar, Scopus and Web of Science. Chi-square tests were used to compare the OA prevalence by different subjects, study types, and continents of origin. The association between OA and citation count was studied with multivariable logistic regression analyses.Results: A random sample of 908 articles was deemed eligible and therefore included.Among these, 416 were found freely available online, indicating an overall OA rate of 45.8%. Significant difference in OA rate was detected among articles in different subjects (P<0.001) and among those from different continents (P<0.001). Of articles that were OA, 74.2% were available via self-archiving ('Green road' OA), 53.3% were available from publishers ('Gold road' OA). According to multivariable logistic regression analyses, OA status was not significantly associated with either the existence of citation (P=0.37) or the level of citation (P=0.52). Conclusions/Clinical Significance:In the field of dentistry, 54% of recent journal articles are behind the paywall (non-OA) one year after their publication dates. The 'Green road' of providing OA was more common than the 'Gold road'. No evidence suggested that OA articles received significantly more citations than non-OA articles.2

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Background:

Epithelial cells forming mammary gland ducts and alveoli require adhesion to the extracellular matrix for their function. Mammary epithelial cells need β1-integrins for normal cell cycle regulation. However, the role of β1-integrins in tumorigenesis has not been fully resolved. β1-integrin is necessary for tumour formation in transgenic mice expressing the Polyomavirus Middle T antigen, but it is dispensable in those overexpressing ErbB2. This suggests that some oncogenes can manage without β1-integrin to proliferate and form tumours, while others still require it. Here we have developed a model to test whether expression of an oncogene can surpass the need for β1-integrin to drive proliferation. We co-expressed the ErbB2 or Akt oncogenes with shRNA to target β1-integrin in mammary epithelial cells, and found that they show a differential dependence on β1-integrin for cell division. Moreover, we identified a key proliferative role of the Rac1-Pak axis downstream of β1-integrin signalling. Our data suggest that, in mammary epithelial cells, oncogenes with the ability to signal to Pak surpass the requirement of integrins for malignant transformation. This highlights the importance of using the correct combination therapy for breast cancer, depending on the oncogenes expressed in the tumour.