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Objective. To observe the morphological changes of corneal endothelial cells in healthy Chinese children and youngsters and analyze the sensitive and specificity of the endothelial assessments. Methods. 14,670 Chinese healthy volunteers enrolled were examined by specular microscopy, and the endothelial descriptive indexes: the central corneal thickness (CCT), endothelial cell density (ECD), coefficient of variation in average cell size (CV), the percentage of regular hexagonal cells (hexagonality, HEX), cell size of minimal cell ( S min ), cell size of maximal cell ( S max ), average cell size ( S avg ), and size of standard deviation of cell area ( S sd ) as well as sex and age were analyzed. Results. The average age of this study is 17.36 ± 7.58 (4–30) years. There is no sex predominance: 7,260 male (49.5%) and 7,410 female (50.5%). The mean CCT, ECD, CV, HEX, S min / max , S avg , and S sd are 529.94 ± 31.53 (437–644) μm, 3,051.28 ± 375.49 (2,031–4,074) cells/mm2, 28.34 ± 4.36 (18–40) %, 61.21 ± 10.29 (17–89) %, ( 147.79 ± 21.94 to 678.29 ± 120.96 ) μm2, 332.74 ± 44.62 μm2, and 95.02 ± 23.17 μm2, respectively. The CCTs keep consistency. The ECD decreased rate is 1.02%/year. The curve of ECD and hexagonality expresses the same linear tender. The CCT and endothelial evaluation indexes have no sex predominant ( p > 0.05 ); the quantitative indicators: CCT, ECD, and HEX are significant negative associated with age ( p = 0.001 or p < 0.001 ); the variability indexes: the CV, S min , S max , S avg , and S sd are positive correlation ( p < 0.001 ). The coefficients of CCT, HE, and S min are -0.35, -0.59, and 1.17, respectively. Conclusions. The ECD decrease rate is 1.02%/year of the normal Chinese Han childhood to the earlier adulthood. The ages 4 to 12, 13 to 20, and 21 to 30 can be named as the childhood, puberty and adulthood from endothelial biologic identity. The HEX is the sensitivity marks for the polymorphisms while the S min is the specificity indicator CVs upon the Topcon Noncon Specular microscopy results.

The hairless (HR) gene encodes a transcription factor with histone demethylase activity that is essential for development and tissue homeostasis. Previous studies suggest that mutational inactivation of HR promotes tumorigenesis. To investigate HR mutations in breast cancer, we performed targeted next-gen sequencing using DNA isolated from primary breast cancer tissues. We identified HR somatic mutations in approximately 15% of the patient cohort (n=85), compared to 23% for BRCA2, 13% for GATA3, 7% for BRCA1, and 3% for PTEN in the same patient cohort. We also found an average 23% HR copy number loss in breast cancers. In support of HR’s antitumor functions, HR reconstitution in HR-deficient human breast cancer cells significantly suppressed tumor growth in orthotopic xenograft mouse models. We further demonstrated that HR’s antitumor activity was at least partly mediated by transcriptional activation of CELF2, a tumor suppressor with RNA-binding activity. Consistent with HR’s histone demethylase activity, pharmacologic inhibition of histone methylation suppressed HR-deficient breast cancer cell proliferation, migration and tumor growth. Taken together, we identified HR as a novel tumor suppressor that is frequently mutated in breast cancer. We also showed that pharmacologic inhibition of histone methylation is effective in suppressing HR-deficient breast tumor growth and progression.

Scar formation after filtration surgery of glaucoma is mainly caused by excessive synthesis of new extracellular matrix (ECM) and contraction of subconjunctival tissue mediated by human Tenon fibroblasts (HTFs) and the transforming growth factor (TGF-β1). Montelukast, a potent and specific cysteinyl leukotriene receptor 1 (cysLT1R) antagonist, is a licensed drug clinically used for the treatment of bronchial asthma. In this study, we investigated the effects of montelukast on the contractility of HTFs cultured in a three-dimensional collagen gel. We found that cysLT1R was expressed in HTFs. Interestingly, the expression of cysLT1R was increased in response to TGF-β1 in a dose dependent manner, suggesting its potential role in TGF-β1 induced fibrosis. Importantly, we found that montelukast inhibited TGF-β1-induced collagen gel contraction mediated by HTFs in a concentration- and time-dependent manner. In addition, TGF-β1-induced expression of MMP-1 and MMP-3, generation of fibronectin and type I collagen production, focal adhesion kinase (FAK) and paxillin phosphorylation in HTFs were also ameliorated by montelukast in a dose dependent manner. These results suggested that montelukast might provide therapeutic possibilities for inhibition of scar formation after such surgery.

The 18th World Conference on Lung Cancer (WCLC) organized by the International Association for the Study of Lung Cancer (IASLC) was held in Yokohama, Japan from 14–18 October, 2017. As the world’s largest multidisciplinary oncology conference on lung cancer, it gathered more than 7,000 key opinion leaders, professionals and researchers from over 100 countries, who came together to unfold a series of in-depth academic exchanges and collaborations. In the meantime, AME seized the opportunity to conduct interviews with a number of experts.

Dr. Kian Fan Chung ( Figure 1 ) is Professor of Respiratory Medicine and Head of Experimental Studies Medicine at National Heart & Lung Institute, Imperial College London, and is consultant physician at the Royal Brompton & Harefield NHS Trust, London, UK.