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Ferroptosis is a type of non-apoptotic cell death, which demonstrates a definite iron-dependent expression pattern and is associated with lipid peroxidation. Glutathione peroxidase 4 (GPX4) is a key regulator of ferroptosis. Ferroptosis is involved in the development and progression of various diseases, such as cancer, tissue ischemia–reperfusion injury, neurological diseases, and respiratory diseases. It has been established previously that ferroptotic cells trigger the innate immune system by releasing inflammation-linked damage-related molecules, and immune cells stimulate the inflammatory response by recognizing the operational mechanism of ferroptosis. Some anti-inflammatory drugs have been shown to inhibit ferroptosis in certain cell models. Conversely, some ferroptosis inhibitors also exert anti-inflammatory effects in certain diseases. The present review evaluated the relationship between ferroptosis and inflammation, as well as the underlying internal mechanism, and provided valuable insights into developing novel treatment strategies for inflammatory diseases and cancer. [ABSTRACT FROM AUTHOR]

Gingival carcinoma is a common malignant tumor occurring in the anterior area of the mandible, which can be derived from the epithelium of gingival mucosa. Surgical extended resection is the main treatment of gingival cancer, which can lead to anterior mandibular defect including mouth floor and mandible and mucosa of lower lip. According to the size of the defect, the common repair method is free musculocutaneous flap with vascular pedicle or pedicle flap. We present a method of repairing mandibular anterior tooth defect with an island flap pedicled with the mental artery. [ABSTRACT FROM AUTHOR]

LncRNAs have recently emerged to influence the pathogenesis of fragile X syndrome (FXS), which is caused by the functional loss of fragile X mental retardation protein (FMRP). However, the interaction between FMRP and lncRNAs on regulating neuronal development remains elusive. Here, we reported that FMRP directly interacted with lncRNA TUG1, and decreased its stability. Furthermore, TUG1 bond to transcriptional regulator, SnoN, and negatively modulated SnoN-Ccd1 pathway to specifically control axonal development. These observations suggested interplay between FMRP and lncRNAs might contribute to the pathogenesis of FXS., (© The Author(s) 2017. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com.)