Detection of plagiarism among rhinology scientific journals.

Automated plagiarism-checking software can be a valuable tool for detecting plagiarism in manuscripts. Twenty-five of 60 articles (42%) had at least one incidence of plagiarism, predominately text recycling. A "similarity score" ranging from 22% to 35% could be a potential cut-off value when screening submitted manuscripts.

The molecular link between obesity and genomic instability in cancer development.

Obesity has been known to be a major risk factor for various types of cancers for several decades. More recently, the relationship between dysregulated adipokines and cancer development has been the focus of much research. Adipose tissue is an important endocrine organ that secretes adipokines that affect both autocrine and paracrine signaling.

OBIF: an omics-based interaction framework to reveal molecular drivers of synergy.

Bioactive molecule library screening may empirically identify effective combination therapies, but molecular mechanisms underlying favorable drug-drug interactions often remain unclear, precluding further rational design. In the absence of an accepted systems theory to interrogate synergistic responses, we introduce Omics-Based Interaction Framework (OBIF) to reveal molecular drivers of synergy through integration of statistical and biological interactions in synergistic biological responses. OBIF performs full factorial analysis of feature expression data from single versus dual exposures to identify molecular clusters that reveal synergy-mediating pathways, functions and regulators.

Incidental finding of mandibular ossifying fibroma with parasymphyseal mandibular fracture.

We present an interesting case of a young male with incidental finding of a mandibular ossifying fibroma. The patient sustained direct trauma to the mandible which prompted a computer tomography (CT) scan evaluation of the facial bones. The CT scan showed bilateral mandibular fractures with one of the fractures extending through an incidental finding of a 2.

Mitochondrial dysfunction triggers a catabolic response in chondrocytes via ROS-mediated activation of the JNK/AP1 pathway.

Mitochondrial function is impaired in osteoarthritis (OA) but its impact on cartilage catabolism is not fully understood. Here, we investigated the molecular mechanism of mitochondrial dysfunction-induced activation of the catabolic response in chondrocytes. Using cartilage slices from normal and OA cartilage, we showed that mitochondrial membrane potential was lower in OA cartilage, and that this was associated with increased production of mitochondrial superoxide and catabolic genes [interleukin 6 (IL-6), COX-2 (also known as PTGS2), MMP-3, -9, -13 and ADAMTS5].