Bayesian framework for parametric bivariate accelerated lifetime modeling and its application to hospital acquired infections.

Infectious diseases that can be spread directly or indirectly from one person to another are caused by pathogenic microorganisms such as bacteria, viruses, parasites, or fungi. Infectious diseases remain one of the greatest threats to human health and the analysis of infectious disease data is among the most important application of statistics. In this article, we develop Bayesian methodology using parametric bivariate accelerated lifetime model to study dependency between the colonization and infection times for Acinetobacter baumannii bacteria which is leading cause of infection among the hospital infection agents. We also study their associations with covariates such as age, gender, apache score, antibiotics use 3 months before admission and invasive mechanical ventilation use. To account for singularity, we use Singular Bivariate Extreme Value distribution to model residuals in Bivariate Accelerated lifetime model under the fully Bayesian framework. We analyze a censored data related to the colonization and infection collected in five major hospitals in Turkey using our methodology. The data analysis done in this article is for illustration of our proposed method and can be applied to any situation that our model can be used.

Retracted: Postoperative pain after irrigation with Vibringe versus a conventional needle: a randomized controlled trial.

The following article from International Endodontic Journal, 'Postoperative pain after irrigation with Vibringe versus a conventional needle: a randomized controlled trial' by D. Bilgili, S. Yilmaz, A. Dumani & O. Yoldas, published online on 29 February 2016 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the authors, the Journal Editor in Chief, Prof. Paul Dummer, and John Wiley & Sons Ltd. The retraction has been agreed because the corresponding author did not contact the first author who carried out the work before alterations to the article were made prior to submission. This damages the integrity of the work and there are additional concerns over the number of patients and the accuracy of the results and conclusions.

Differential oncogenic potential of activated RAS isoforms in melanocytes.

RAS genes are mutated in approximately 30% of all human cancers. Interestingly, there exists a strong bias in favor of mutation of only one of the three major RAS genes in tumors of different cellular origins. NRAS mutations occur in approximately 20% of human melanomas, whereas HRAS and KRAS mutations are rare in this disease. To define the mechanism(s) responsible for this preference in melanocytes, we compared the transformation efficiencies of mutant NRAS and KRAS in immortal, non-transformed Ink4a/Arf-deficient melanocytes. NRAS mutation leads to increased cellular proliferation and is potently tumorigenic. In contrast, KRAS mutation does not enhance melanocyte proliferation and is only weakly tumorigenic on its own. Although both NRAS and KRAS activate mitogen-activated protein kinase signaling, only NRAS enhances MYC activity in these cells. Our data suggest that the activity of specific RAS isoforms is context-dependent and provide a possible explanation for the prevalence of NRAS mutations in melanoma. In addition, understanding this mechanism will have important implications for cancer therapies targeting RAS pathways.