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Background and Aim: Single‐nucleotide polymorphisms (SNPs) in long non‐coding RNAs (lncRNAs) are potential biomarkers for cancer risk, but their association with hepatocellular carcinoma (HCC) is unclear. We examined the association of lncRNA‐related SNPs with HCC susceptibility and explored the optimal genetic models for SNPs. Methods: Five candidate SNPs linked with digestive tumors were first genotyped in a screening population of 700 HCC and 2800 control cases. The association between each SNP and HCC risk was estimated by multivariate logistic regression adjusted by sex and age and recorded as odds ratio (OR) with 95% confidence interval. Significant associations were further tested in a validation population with 1140 HCC and 5115 control cases. Finally, the most appropriate genetic models for HCC‐associated SNPs were identified using pairwise allele differences; the overall gene effects of each SNP were further evaluated based on optimal genetic models. Results: Three candidate SNPs, rs7315438, rs6983267, and rs10795668, showed statistical connections with HCC risk in the discovery stage. Among these, rs7315438 remained steadily significant in the validation stage; rs7315438 and rs10795668 both reached statistical threshold in the combined analysis of both stages. SNP rs7315438 (TC vs TT/CC, OR = 1.410, P < 0.001) was associated with increased risk of HCC in a complete overdominant model, whereas rs10795668 (AG vs AA/GG, OR = 0.892, P = 0.035) exerted a protective effect on HCC risk in a complete overdominant model. Conclusions: Long non‐coding RNA‐related SNPs rs7315438 and rs10795668 are potential biomarkers for HCC susceptibility, especially when evaluated based on their optimal genetic models. [ABSTRACT FROM AUTHOR]

Neuropathic pain (NP) is directly caused by an injury or disease of the somatosensory nervous system. It is a serious type of chronic pain that is a burden to the economy and public health. Although recent studies have improved our understanding of NP, its pathogenesis has not been fully elucidated. Noncoding RNAs, including lncRNAs, circRNAs, and miRNAs, are involved in the pathological development of NP through many mechanisms. In addition, extensive evidence suggests that novel regulatory mechanisms among lncRNAs/circRNAs, miRNAs, and mRNAs play a crucial role in the pathophysiological process of NP. In this review, we comprehensively summarize the regulatory relationship among lncRNAs/circRNAs, miRNAs, and mRNAs and emphasize the important role of the lncRNA/circRNA–miRNA–mRNA axis in NP. [ABSTRACT FROM AUTHOR]

Objective: Right aortic arch (RAA) can be associated with chromosomal anomalies. However, the incidence of chromosomal anomalies when RAA is isolated (iRAA), ie, not associated with intracardiac anomalies, varies between different studies (0%-28.5%). We have performed a meta-analysis to allow a more accurate prenatal counselling.Methods: We searched PubMed, Embase, and Web of Science for articles related to chromosomal anomalies among iRAA fetuses until April 2019. A total of 22 relevant studies, including 670 fetuses, were selected in the final meta-analysis.Results: The results revealed that the overall rates of chromosomal anomalies and 22q11.2 deletion in iRAA fetuses were 7.5% (95% confidence interval [CI], 4.7%-10.8%) and 4.3% (95% CI, 2.6%-6.4%), respectively, while the rates were lower in iRAA without extracardiac anomalies, 4.7% (95% CI, 1.1%-10.8%) and 2.4% (95% CI, 0.5%-5.7%). The rate of chromosomal or copy number variants including 22q11.2 deletion identified by chromosomal microarray analysis (CMA) in iRAA fetuses was 8.2% (95% CI, 5.0%-12.1%) and 3.7% (95% CI, 1.7%-6.6%), respectively, compared with 5.1% (95% CI, 2.5%-8.4%) and 2.4% (95% CI, 0.7%-5.1%) identified by traditional karyotyping.Conclusions: A considerable proportion of iRAA cases have associated chromosomal anomalies and prevalence of associated 22q11.2 deletion, and CMA is recommended if invasive prenatal testing is performed. [ABSTRACT FROM AUTHOR]

The pulmonary fibrosis could be caused by long-term inhalation of carbon black (CB) particles. Studies on the mechanisms of pulmonary fibrosis induced by CB are required to develop the stratagem of prevention and treatment on fibrosis. The RNA-binding protein DiGeorge syndrome critical region gene 8 (DGCR8)-dependent pri-miRNAs processing is regulated by N6-methyladenosine (m6A) modification, which targets the downstream signal pathway. However, its role in pulmonary fibrosis has not been known clearly. In the present study, rats inhaled CB at dose of 0, 5 or 30 mg/m3 for 28 days, 6 h/day, respectively. The rats inhaled CB at dose of 0 or 30 mg/m3 for 14 days, 28 days and 90 days, respectively. In vitro experiments, the normal human bronchial epithelial cell line (16HBE) was treated with CB (0, 50, 100 and 200 μg/mL) for 24 h. In vitro and vivo study, the levels of fibrosis indicators including α-SMA, vimentin, collagen-I and hydroxyproline in CB treatment groups statistically increased in dose- or time- dependent manners compared with the control. After CB treatment, PI3K-AKT-mTOR pathway was activated and regulated by miRNA-126. We found that both of m6A modifications of pri-miRNA-126 and its binding with DGCR8 were decreased after CB treatment, which resulted in the reduction of mature miRNA-126 accompanied by accumulation of unprocessed pri-miRNA-126. This work demonstrated that m6A modification of pri-miRNA-126 and its binding with DGCR8 decreases blocked miRNA-126 maturation, and then activated the PI3K/AKT/mTOR pathway, which drove the fibro genesis in the lung after CB exposure. [ABSTRACT FROM AUTHOR]

Few tropical marine sites have been thoroughly characterised for their animal species, even though they constitute the largest proportion of multicellular diversity. A number of focused biodiversity sampling programmes have amassed immense collections to address this shortfall, but obstacles remain due to the lack of identification tools and large proportion of undescribed species globally. These problems can be partially addressed with DNA barcodes ("biocodes"), which have the potential to facilitate the estimation of species diversity and identify animals to named species via barcode databases. Here, we present the first results of what is intended to be a sustained, systematic study of the marine fauna of Singapore's first marine park, reporting more than 365 animal species, determined based on DNA barcodes and/or morphology represented by 931 specimens (367 zooplankton, 564 macrofauna including 36 fish). Due to the lack of morphological and molecular identification tools, only a small proportion could be identified to species solely based on either morphology (24.5%) or barcodes (24.6%). Estimation of species numbers for some taxa was difficult because of the lack of sufficiently clear barcoding gaps. The specimens were imaged and added to "Biodiversity of Singapore" (http://singapore.biodiversity.online), which now contains images for > 13,000 species occurring in the country. [ABSTRACT FROM AUTHOR]

Myocardial ischemia/reperfusion (MI/R) causes loss of cardiomyocytes via oxidative stress-induced cardiomyocyte apoptosis. miR322, orthologous to human miR-424, was identified as an ischemia-induced angiogenic miRNA, but its cellular source and function in the setting of acute MI/R remains largely unknown. Using LacZ-tagged miR322 cluster reporter mice, we observed that vascular endothelial cells are the major cellular source of the miR322 cluster in adult hearts. Moreover, miR322 levels were significantly reduced in the heart at 24 h after MI/R injury. Intramyocardial injection of mimic-miR322 significantly diminished cardiac apoptosis (as determined by expression levels of active caspase 3 by Western blot analysis and immunostaining for TUNEL) and reduced infarct size by about 40%, in association with reduced FBXW7 and increased active Notch 1 levels in the ischemic hearts. FBXW7, which is an ubiquitin ligase that is crucial for activated Notch1 turnover, was identified as a direct target of miR322 via FBXW7 3'UTR reporter assay. Co-injection of FBXW7 plasmid with mimic-miR322 in ischemic hearts abolished the effect of mimic-miR322 to reduce apoptosis and infarct size in MI/R hearts. These data identify FBXW7 as a direct target of miR322 and suggest that miR322 could have potential therapeutic application for cardioprotection against ischemia/reperfusion-induced injury. [ABSTRACT FROM AUTHOR]