Potential Haptic Perceptual Dimensionality of Rendered Compliance.

Studies have proven that humans perceive haptic textures through different perceptual dimensions, such as rough/smooth and soft/hard, which provide useful guidance in the design of haptic devices. However, few of these have focused on the perception of compliance, which is another important perceptual property in haptic interfaces. This research was conducted to investigate the potential basic perceptual dimensions of the rendered compliance and quantify the effects of the simulation parameters. Two perceptual experiments were designed based on 27 stimuli samples generated by a 3-DOF haptic feedback device. Subjects were asked to describe these stimuli using adjectives, classify the samples, and rate them according to corresponding adjective labels. Multi-dimensional scaling (MDS) methods were then used to project adjective ratings into 2D and 3D perception spaces. According to the results, hardness and viscosity are considered two basic perceptual dimensions of the rendered compliance, while crispness can be regarded as a subsidiary perceptual dimension. Then, the relations between simulation parameters and perceptual feelings were analyzed by the regression analysis. This paper may provide a better understanding of the compliance perception mechanism and useful guidance for the improvement of rendering algorithms and devices for haptic human-computer interaction.

Hsa_circ_0069244 acts as the sponge of miR-346 to inhibit non-small cell lung cancer progression by regulating XPC expression.

Circular RNAs (circRNAs) play a significant role in the progression of diverse malignancies. Here, we aimed to probe the function and mechanism of circ_0069244 in non-small cell lung cancer (NSCLC). In the present study, circ_0069244 was selected from the circRNA microarray datasets (GSE112214). Quantitative real-time polymerase chain reaction (qRT-PCR) was applied to examine circ_0069244, miR-346 and XPC complex subunit, DNA damage recognition and repair factor (XPC) expression levels. Kaplan-Meier curve was employed to analyze the association between circ_0069244 expression and overall survival of NSCLC patients. Cell counting kit-8 (CCK-8) and 5-Bromo-2'-deoxyuridine (BrdU) experiments were utilized to examine the proliferation of NSCLC cells. Scratch healing and Transwell experiments were executed to examine the migration of NSCLC cells. Western blot was conducted to detect XPC expression at protein level in NSCLC cells. Bioinformatics analysis, dual-luciferase reporter gene and RNA immunoprecipitation (RIP) experiments predicted and validated the targeting relationships of circ_0069244 and miR-346, as well as miR-346 and 3'untranslated region (UTR) of XPC mRNA, respectively. We reported that circ_0069244 was remarkably down modulated in NSCLC and was linked to shorter survival and poor tumor histological grade in NSCLC patients. Functionally, circ_0069244 repressed NSCLC cell proliferation and migration. Furthermore, miR-346-5p was unveiled to be a downstream target of circ_0069244, and miR-346-5p specifically modulated XPC expression. Rescue experiments indicated that the inhibitory effect of circ_0069244 was abolished by co-expression of miR-346-5p mimics. Taken together, circ_0069244 restrained NSCLC progression by modulating the miR-346-5p/XPC axis.

MicroRNA-130a targeting hypoxia-inducible factor 1 alpha suppresses cell metastasis and Warburg effect of NSCLC cells under hypoxia.

MicroRNAs have been demonstrated to play critical role in the development of non-small cell lung cancer (NSCLC) and hypoxia is a common hallmark of NSCLC. MiRNA-130a-3p (miR-130a) is a well-known tumor suppressor, and we intended to explore the role and mechanism of miR-130a in NSCLC cells under hypoxia. We used real-time quantitative polymerase chain reaction method to measure miR-130a expression, and found that miR-130a was downregulated in human NSCLC tumors and cell lines (A549 and H1299), accompanied with upregulation of hypoxia-inducible factor 1 alpha (HIF1A), a marker of hypoxia. Besides, miR-130a low expression was associated with tumor burden and poor overall survival. Moreover, miR-130a expression was even downregulated in hypoxia-treated A549 and H1299 cells. Ectopic expression of miR-130a suppressed Warburg effect, migration and invasion in hypoxic A549 and H1299 cells, as evidenced by decreased glucose consumption, lactate production, hexokinase 2 expression, and numbers of migration cells and invasion cells analyzed by commercial glucose and lactate assay kits, western blotting and transwell assays. Furthermore, overexpression of miR-130a restrained xenograft tumor growth of A549 cells in mice. However, recovery of HIF1A could reverse the suppressive effect of miR-130a overexpression on cell migration, invasion and Warburg effect in hypoxic A549 and H1299 cells. Mechanically, dual-luciferase reporter assay, RNA immunoprecipitation and RNA pull-down assay confirmed a target relationship between miR-130a and HIF1A. Collectively, we demonstrated an anti-tumor role of miR-130a in NSCLC cells under hypoxia through targeting HIF1A, suggesting a potential target for the interfering of NSCLC.

Biocompatible ionic liquid [Betaine][H2PO4] as a reusable catalyst for the substitution of xanthen-9-ol under solvent-free conditions.

An ionic liquid, namely [Betaine][H2PO4], was found to be an efficient catalyst for the direct substitution reaction of xanthen-9-ol with different nucleophiles under solvent-free conditions. This catalytic system is easy to be operated and the following work-up procedure is simple, with the ionic liquid catalyst reusable for at least five cycles at a high catalytic activity level. In addition, the ionic liquid is easy to prepare and its raw materials are inexpensive and have good biocompatibility. Therefore, our study presents an intriguing and sustainable protocol for the direct substitution of alcohol.

Long non-coding RNA HOTTIP promotes hypoxia-induced glycolysis through targeting miR-615-3p/HMGB3 axis in non-small cell lung cancer cells.

Increased glycolysis under hypoxic stress is a fundamentally important feature of non-small cell lung cancer (NSCLC) cells, but molecular mechanisms of hypoxia on glycolysis remain elusive. Herein, we aimed to explore whether lncRNAs and miRNAs are involved in the glycolytic reprogramming under hypoxic conditions. The levels of HOXA transcript at the distal tip (HOTTIP), miR-615-3p and high mobility group box 3 (HMGB3) mRNA were assessed by qRT-PCR. Western blot was performed to determine the protein expression of hexokinase 2 (HK-2) and HMGB3. Glucose consumption and lactate production were analyzed using a respective assay kit. The targeted correlation between miR-615-3p and HOTTIP or HMGB3 was verified using dual-luciferase reporter and RNA immunoprecipition assays. Our data revealed that HOTTIP was upregulated and miR-615-3p was downregulated in NSCLC tissues and cells. Hypoxia induced glycolysis, increased HOTTIP and HMGB3 mRNA levels and repressed miR-615-3p expression in NSCLC cells. HOTTIP deficiency or miR-615-3p expression restoration repressed hypoxia-induced glycolysis. Moreover, HOTTIP acted as a molecular sponge for miR-615-3p and HMGB3 was a direct target of miR-615-3p. The inhibitory effect of HOTTIP deficiency on glycolysis under hypoxic exposure was reversed by miR-615-3p restoration. Additionally, HOTTIP regulated HMGB3 expression by acting as a molecular sponge of miR-615-3p in NSCLC cells. In conclusion, our study suggested that HOTTIP might promote glycolysis under hypoxic conditions at least partly through regulating miR-615-3p/HMGB3 axis in NSCLC cells. Targeting HOTTIP might be a promising therapeutic strategy for NSCLC treatment.