RESUMO
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.
RESUMO
BACKGROUND: Drug resistance is a considerable challenge for chemotherapy in non-small cell lung cancer (NSCLC). Propofol, a commonly used intravenous anesthetics, has been reported to suppress the malignancy of various cancers. However, the effects of propofol on cisplatin (DDP) sensitivity in NSCLC and its molecular mechanisms have not been clearly clarified yet, and the present study aimed to resolve this problem. METHODS: NSCLC cells were co-treated with propofol and DDP, Cell Counting kit-8 assay, colony formation assay and flow cytometry were conducted to test the role of propofol in regulating DDP-resistance in NSCLC. Next, through conducting quantitative real-time polymerase chain reaction, dual-luciferase gene reporter system and western blot, the responsible molecular axis in propofol regulating the DDP sensitivity in NSCLC was uncovered, and the function verification experiments were performed by transfection with the inhibitors or small interfering RNAs of those molecules. RESULTS: Propofol suppressed cell viability, colony formation ability, tumorigenesis, and promoted cell apoptosis to enhance DDP-sensitivity in NSCLC in vitro and in vivo. Propofol increased miR-486-5p level in NSCLC cells and xenograft tumors tissues in a N6-methyladenosine (m6A)-dependent manner, thus inactivating the Ras-associated protein1 (RAP1)-NF-kappaB (NF-κB) axis. Propofol regulated the miR-486-5p/RAP1-NF-κB axis to improve DDP-sensitivity in NSCLC. CONCLUSIONS: Taken together, this study firstly investigates the detailed molecular mechanisms by which propofol enhanced DDP-sensitivity in NSCLC cells, and a novel m6A-dependent miR-486-5p/RAP1-NF-κB axis is identified to be closely associated with the process.
