Long Noncoding RNA ACTA2-AS1 Inhibits Cell Growth and Facilitates Apoptosis in Gastric Cancer by Binding with miR-6720-5p to Regulate ESRRB.

Gastric cancer (GC) is a common malignant tumor, posing a great threat to human's health and life. Previous studies have suggested aberrant expression of long non-coding RNAs (lncRNAs) in GC. This study elucidated the effects of lncRNA ACTA2-AS1 on the biological characteristics of GC. Gene expression in stomach adenocarcinoma (STAD) samples compared with normal tissues and the correlation between gene expression and prognosis of STAD patients were analyzed using bioinformatic tools. Gene expression at protein and mRNA levels in GC and normal cells was tested by western blotting and RT-qPCR. The subcellular localization of ACTA2-AS1 in AGS and HGC27 cells was identified by nuclear-cytoplasmic fractionation and FISH assay. EdU, CCK-8, flow cytometry analysis, TUNEL staining assays were conducted to evaluate the role of ACTA2-AS1 and ESRRB on GC cellular behaviors. The binding relationship among ACTA2-AS1, miR-6720-5p and ESRRB was verified by RNA pulldown, luciferase reporter assay and RIP assay. LncRNA ACTA2-AS1 was underexpressed in GC tissues and cell lines. ACTA2-AS1 elevation suppressed GC cell proliferation and induced apoptosis. Mechanistically, ACTA2-AS1 directly bound to miR-6720-5p and subsequently promoted the expression of target gene ESRRB in GC cells. Furthermore, ESRRB knockdown reversed the influence of ACTA2-AS1 overexpression on GC proliferation and apoptosis. ACTA2-AS1 plays an antioncogenic role in GC via binding with miR-6720-5p to regulate ESRRB expression.

Strolling in Room-Scale VR: Hex-Core-MK1 Omnidirectional Treadmill.

The natural locomotion interface is critical to the development of many VR applications. For household VR applications, there are two basic requirements: natural immersive experience and minimized space occupation. The existing locomotion strategies generally do not simultaneously satisfy these two requirements well. This article presents a novel omnidirectional treadmill (ODT) system named Hex-Core-MK1 (HCMK1). By implementing two kinds of mirror-symmetrical spiral rollers to generate the omnidirectional velocity field, this proposed system is capable of providing real walking experiences with a full-degree of freedom in an area as small as 1.76 m 2, while delivering great advantages over several existing ODT systems in terms of weight, volume, latency and dynamic performance. Compared with the sizes of Infinadeck and HCP, the two best motor-driven ODTs so far, the 8 cm height of HCMK1 is only 20% of Infinadeck and 50% of HCP. In addition, HCMK1 is a lightweight device weighing only 110 kg, which provides possibilities for further expanding VR scenarios, such as terrain simulation. The system latency of HCMK1 is only 9ms. The experiments show that HCMK1 can deliver a starting acceleration of 16.00 m/s 2 and a braking acceleration of 30.00 m/s 2.

Simvastatin augments activation of liver regeneration through attenuating transforming growth factor-ß1 induced-apoptosis in obstructive jaundice rats.

Obstructive jaundice, owing to biliary obstruction, has been illustrated to trigger various biochemical, histological and immunological changes, leading to liver damage or even failure. The detailed molecular mechanism of simvastatin (Sim) involvement in liver regeneration during obstructive jaundice progression remains poorly elucidated. In the present study, an acute obstructive jaundice rat model was established by ligation and division of common bile duct, which was used to investigate the effects of Sim as a hepatoprotective treatment. Male Sprague-Dawley rats were randomly divided into four groups: Sham-operated, bile duct ligation (BDL) plus saline treatment [0.02 mg/kg/d, intraperitoneally (i.p.)], BDL plus low-dose Sim treatment (0.02 mg/kg, i.p.) and BDL plus high-dose Sim treatment (0.2 mg/kg, i.p.). During this experiment, the BDL+normal saline (NS) group demonstrated increased levels of transforming growth factor-ß1 (TGF-ß1) expression. Furthermore, Sim-treated animals demonstrated significantly downregulated TGF-ß1 expression and improved liver function vs. the BDL+NS group, indicating a TGF-ß1 antagonizing function. Additionally, Sim increased hepatocyte DNA synthesis in BDL rats compared to both the BDL+NS and Sham group. Apoptosis was increased in BDL+NS compared to the Sham group, and Sim markedly reduced hepatocyte apoptosis in the BDL group. Moreover, analysis of TGF-ß1 signaling pathways demonstrated that there was an increased hepatic TGF-ß1 and Smad3 expression in the BDL group, which was attenuated in the presence of Sim. In contrast to TGF-ß1, Sim induced the activity of the Smad7 (an inhibitor of TGF-ß1 signaling) mRNA and Smad7 protein expression. Sim displays hepatoprotective effects in liver cells via the upregulation of Smad7 expression and impaired TGF-ß signaling. Furthermore, the observations of the present study may provide evidence on the mechanism behind Sim blunting TGF-ß1 signaling, which is used to ameliorate the complication of liver damage and reduce the mortality rates associated with obstructive jaundice.