Glioma (GM) is an aggressive malignancy with high mortality rate across the world. Mounting studies demonstrates that abnormally expressed circular RNAs (circRNAs) act as important roles in tumor progression. In the current work, a novel circRNA, circ_0005198, was explored. Circ_0005198 level in GM tissue samples and cells was detected. The clinical implication of circ_0005198 was analyzed by Fisher's test and Kaplan‐Meier analysis. In vitro experiments were carried out to elucidate the influence of circ_0005198 on GM cell proliferation, apoptosis, and metastatic properties. Luciferase reporter and rescue experiments were conducted to clear the mechanism of circ_0005198. The expression of circ_0005198 was enhanced in GM tumors and cells. Its expression in tumor specimens was related to clinical severity and poor prognosis. Functionally, circ_0005198 could remarkably boost cell growth, clone‐forming ability, and metastatic properties and attenuate cell apoptosis in GM cells. What's more, circ_0005198 could directly sponge miR‐1294 to exert oncogenic functions. In summary, this study might provide an effective therapeutic target for GM.

Dysregulated circular RNAs (circRNAs) are involved in the carcinogenesis and progression of multiple human malignancies. Knowledge of circRNAs in glioma (GM) is limited and further study to uncover new therapeutic targets for GM is urgently required. The present study demonstrated that circ-TOP2A was elevated in GM tissue specimens and cells and that circ-TOP2A levels indicated an unfavorable clinical prognosis in GM. Functionally, circ-TOP2A knockdown reduced viability, migration and invasion and triggered apoptosis in LN229 cells. Ectopic expression of circ-TOP2A aggravated these malignant behaviors in U87MG cells. In terms of mechanism, RNA-seq was performed to discover the potential targets regulated by circ-TOP2A. Circ-TOP2A acted as a competing endogenous RNA to upregulate sushi domain-containing 2 (SUSD2) expression by sponging microRNA (miR) 346. Rescue assays revealed that the oncogenic function of circ-TOP2A was partially dependent on its regulation of the miR-346/SUSD2 axis. In conclusion, the present study identified that circ-TOP2A promoted GM proliferation and aggressiveness via miR-346/SUSD2 signaling, which is a potential prognostic biomarker and therapeutic target for GM.

Background: We explored the methylation modification in miR-205 promoter during the pathological changes of Parkinson's disease (PD) and its regulation on Leucine-Rich Repeat Kinase 2 (LRRK2), clarified the important role of methylation in miR-205 promoter region in PD, explained the role of miR-205 methylation in the pathological changes of PD, and looked for new targets for PD. Methods: Methylation of miR-205 promoter regions was determined by cell genomic DNA, with model bisulfite treatment, and the transcription of miR-205 and LRRK2 in PD model cells was determined by qPCR, and LRRK2 expression was determined by Western blot. The binding sites of miRNAs in the non-coding region of LRRK2 were analyzed by the targetscan database, and miR-205 expression in 293T cells was controlled. The correlation between miR-205 expression and LRRK2 was determined to clarify the regulation mode of miR-205 on LRRK2. Results: The level of miR-205 were reduced in the SH-SY5Y Parkinson model cells, and its promoter region was highly methylated, while LRRK2 expression decreased in the model cells after 5-Azacytidine inhibition of methylation in miR-205 promoter region. According to the target scan database analysis, LRRK2 non-coding region is a miR-205-specific binding site. After further miR-205 overexpression in 293T cells, the transcription and translation of LRRK2 decreased in cells, which increased after the treatment of miR-205 inhibitor on LRRK2. Conclusion: The methylation modification of miR-205 promoter region could regulate the transcription and translation of LRRK2 in dopaminergic neurons, so miR-205 methylation regulation can serve as a new potential target for the treatment of PD.

Underwater terrain-aided navigation (TAN) holds high potential for long-term underwater accurate navigation of autonomous underwater vehicles. TAN can locate a vehicle by calculating the similarity between an a priori map and a vehicle's real-time observation consisting of a set of bathymetric measurement points. However, the amount of measurement points in the real-time observation affects both positioning accuracy and computational consumption of the TAN system, making it challenging to calculate a suitable size of real-time observation in TAN. With a smooth seabed terrain, a small observation area leads to insufficient topographic features and finally an inaccurate matching result, while a large area with a mount of features results in high computational cost. This paper proposes a method to restrain the size of observation in TAN systems based on terrain entropy and difference of normals. Meanwhile, this paper implements the TAN algorithm into an embedded system architecture used by actual underwater vehicles that are already in service to reduce the power consumption of the TAN system. The effectiveness of the algorithm has been demonstrated through playback experiments based on a semi-physical simulation platform using a PC/104-embedded computer.

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