Microelectromechanical Systems (MEMS) Inertial Measurement Unit (IMU) containing a three-orthogonal gyroscope and three-orthogonal accelerometer has been widely utilized in position and navigation, due to gradually improved accuracy and its small size and low cost. However, the errors of a MEMS IMU based standalone Inertial Navigation System (INS) will diverge over time dramatically, since there are various and nonlinear errors contained in the MEMS IMU measurements. Therefore, MEMS INS is usually integrated with a Global Positioning System (GPS) for providing reliable navigation solutions. The GPS receiver is able to generate stable and precise position and time information in open sky environment. However, under signal challenging conditions, for instance dense forests, city canyons, or mountain valleys, if the GPS signal is weak and even is blocked, the GPS receiver will fail to output reliable positioning information, and the integration system will fade to an INS standalone system. A number of effects have been devoted to improving the accuracy of INS, and de-nosing or modelling the random errors contained in the MEMS IMU have been demonstrated to be an effective way of improving MEMS INS performance. In this paper, an Artificial Intelligence (AI) method was proposed to de-noise the MEMS IMU output signals, specifically, a popular variant of Recurrent Neural Network (RNN) Long Short Term Memory (LSTM) RNN was employed to filter the MEMS gyroscope outputs, in which the signals were treated as time series. A MEMS IMU (MSI3200, manufactured by MT Microsystems Company, Shijiazhuang, China) was employed to test the proposed method, a 2 min raw gyroscope data with 400 Hz sampling rate was collected and employed in this testing. The results show that the standard deviation (STD) of the gyroscope data decreased by 60.3%, 37%, and 44.6% respectively compared with raw signals, and on the other way, the three-axis attitude errors decreased by 15.8%, 18.3% and 51.3% individually. Further, compared with an Auto Regressive and Moving Average (ARMA) model with fixed parameters, the STD of the three-axis gyroscope outputs decreased by 42.4%, 21.4% and 21.4%, and the attitude errors decreased by 47.6%, 42.3% and 52.0%. The results indicated that the de-noising scheme was effective for improving MEMS INS accuracy, and the proposed LSTM-RNN method was more preferable in this application.
BackgroundBeta-blockers are antihypertensive drugs and have shown potential in cancer prognosis. However, this benefit has not been well defined due to inconsistent results from the published studies.MethodsTo investigate the association between administration of beta-blocker and cancer prognosis, we performed a meta-analysis. A literature search of PubMed, Embase, Cochrane Library, and Web of Science was conducted to identify all relevant studies published up to September 1, 2017. Thirty-six studies involving 319,006 patients were included. Hazard ratios were pooled using a random-effects model. Subgroup analyses were conducted by stratifying ethnicity, duration of drug use, cancer stage, sample size, beta-blocker type, chronological order of drug use, and different types of cancers.ResultsOverall, there was no evidence to suggest an association between beta-blocker use and overall survival (HR=0.94, 95% CI: 0.87–1.03), all-cause mortality (HR=0.99, 95% CI: 0.94–1.05), disease-free survival (HR=0.59, 95% CI: 0.30–1.17), progression-free survival (HR=0.90, 95% CI: 0.79–1.02), and recurrence-free survival (HR=0.99, 95% CI: 0.76–1.28), as well. In contrast, beta-blocker use was significantly associated with better cancer-specific survival (CSS) (HR=0.78, 95% CI: 0.65–0.95). Subgroup analysis generally supported main results. But there is still heterogeneity among cancer types that beta-blocker use is associated with improved survival among patients with ovarian cancer, pancreatic cancer, and melanoma.ConclusionThe present meta-analysis generally demonstrates no association between beta-blocker use and cancer prognosis except for CSS in all population groups examined. High-quality studies should be conducted to confirm this conclusion in future.
BackgroundAccumulating evidence has highlighted the potential role of RNA binding proteins (RBPs) in the biological behaviors of glioblastoma cells. Herein, the expression and function of RNA binding proteins FXR1 were investigated in human glioma cells.MethodsQuantitative real-time PCR were conducted to evaluate the expression of MIR17HG and miR-346, miRNA-425-5p in glioma tissues and cells. Western blot were used to explore the expression of FXR1, TAL1 and DEC1 in glioma tissues and cells. Stable knockdown of FXR1 and MIR17HG in glioma cells were established to explore the function of FXR1, MIR17HG in glioma cells. Further, RIP and RNA pull-down assays were used to investigate the correlation between FXR1 and MIR17HG. Cell Counting Kit-8, transwell assays, and flow cytometry were used to investigate the function of FXR1 and MIR17HG in malignant biological behaviors of glioma cells. ChIP assays were employed to ascertain the correlations between TAL1 and MIR17HG.ResultsFXR1and MIR17HG were upregulated in glioma tissues and cell lines. Downregulation of FXR1 or MIR17HG resulted in inhibition of glioma cells progression. We also found that FXR1 regulates the biological behavior of glioma cells via stabilizing MIR17HG. In addition, downregulated MIR17HG increased miR-346/miR-425-5p expression and MIR17HG acted as ceRNA to sponge miR-346/miR-425-5p. TAL1 was a direct target of miR-346/miR-425-5p, and played oncogenic role in glioma cells. More importantly, TAL1 activated MIR17HG promoter and upregulated its expression, forming a feedback loop. Remarkably, FXR1 knockdown combined with inhibition of MIR17HG resulted in the smallest tumor volumes and the longest survivals of nude mice in vivo.ConclusionsFXR1/MIR17HG/miR-346(miR-425-5p)/TAL1/DEC1 axis plays a novel role in regulating the malignant behavior of glioma cells, which may be a new potential therapeutic strategy for glioma therapy.Electronic supplementary materialThe online version of this article (10.1186/s13046-018-0991-0) contains supplementary material, which is available to authorized users.
Aqueous rechargeable zinc-ion batteries (ARZIBs) are widely supposed to be a prospect energy storage substance because of their low toxicity, low cost and environmentally friendliness. Recent studies prove that hydrated...
Phytochrome A (phyA) is the primary plant photoreceptor responsible for perceiving and mediating various responses to farred (FR) light and is essential for survival in canopy shade. In this study, we identified two Arabidopsis thaliana mutants that grew longer hypocotyls in FR light. Genetic analyses showed that they were allelic and their FR phenotypes were caused by mutations in the gene named TANDEM ZINC-FINGER/PLUS3 (TZP), previously shown to encode a nuclear protein involved in blue light signaling and phyB-dependent regulation of photoperiodic flowering. We show that the expression of TZP is dramatically induced by light and that TZP proteins are differentially modified in different light conditions. Furthermore, we show that TZP interacts with both phyA and FAR-RED ELONGATED HYPOCOTYL1 (FHY1) and regulates the abundance of phyA, FHY1, and ELONGATED HYPOCOTYL5 proteins in FR light. Moreover, our data indicate that TZP is required for the formation of a phosphorylated form of phyA in the nucleus in FR light. Together, our results identify TZP as a positive regulator of phyA signaling required for phosphorylation of the phyA photoreceptor, thus suggesting an important role of phosphorylated phyA in inducing the FR light response.
Dysregulation of miR-488 has been implicated in several human cancers. In this study, we aim to explore its expression and biological function in ovarian cancers. We found miR-488 expression was downregulated in ovarian cancer tissues. Using CCK8 and colony formation assay showed that miR-488 inhibited SKOV3 cell proliferation and colony formation, with downregulation of cyclin D1 and cyclin E protein. While miR-488 inhibitor promoted OVCAR3 cell growth and colony formation. Cell viability and Annexin V/PI staining showed that miR-488 downregulated cell survival and increased apoptosis rate when treated with cisplatin and paclitaxel. Further experiments using MitoTracker and JC-1 staining indicated that miR-488 regulated mitochondrial fission/fusion balance and inhibited mitochondrial membrane potential, with p-Drp1, Drp1 and Fis1 downregulation. Luciferase reporter assay showed that Six1 is a target of miR-488. We also found a negative association between Six1 and miR-488 in ovarian cancer tissues. In addition, Six1 overexpression induced mitochondrial fission and increased mitochondrial potential, with upregulation of Drp1 signaling. Six1 depletion showed the opposite effects. Restoration of Six1 in SKOV3 cells rescued decreased p-Drp1 and Drp1 expression induced by miR-488 mimic. Six1 plasmid also reversed the effects of miR-488 on chemoresistance and apoptosis. Taken together, the present study showed that, by targeting Six1, miR-488 inhibits chemoresistance of ovarian cancer cells through regulation of mitochondrial function.
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