This paper presents a novel broadband rectenna for ambient wireless energy harvesting over the frequency band from 1.8 to 2.5 GHz. First of all, the characteristics of the ambient radio-frequency energy are studied. The results are then used to aid the design of a new rectenna. A novel two-branch impedance matching circuit is introduced to enhance the performance and efficiency of the rectenna at a relatively low ambient input power level. A novel broadband dual-polarized cross-dipole antenna is proposed which has embedded harmonic rejection property and can reject the 2 nd and 3 rd harmonics to further improve the rectenna efficiency. The measured power sensitivity of this design is down to -35 dBm and the conversion efficiency reaches 55% when the input power to the rectifier is -10 dBm. It is demonstrated that the output power from the proposed rectenna is higher than the other published designs with a similar antenna size under the same ambient condition. The proposed broadband rectenna could be used to power many low-power electronic devices and sensors and found a range of potential applications.
Purpose To quantitatively map cerebral metabolic rate of oxygen (CMRO2) and oxygen extraction fraction (OEF) in human brains using quantitative susceptibility mapping (QSM) and arterial spin labeling measured cerebral blood flow (CBF) before and after caffeine vasoconstriction. Methods Using the multiecho 3D gradient echo sequence and an oral bolus of 200 mg caffeine, whole brain CMRO2 and OEF were mapped at 3mm isotropic resolution on 13 healthy subjects. The QSM based CMRO2 was compared with an R2* based CMRO2 to analyze the regional consistency within cortical gray matter (CGM) with the scaling in the R2* method set to provide same total CMRO2 as the QSM method for each subject. Results Compared to pre-caffeine, susceptibility increased (5.1±1.1ppb, p<0.01) and CBF decreased (−23.6±6.7ml/100g/min, p<0.01) at 25min post-caffeine in CGM. This corresponded to a CMRO2 of 153.0±26.4µmol/100g/min with an OEF of 33.9±9.6% and 54.5±13.2% (p<0.01) pre- and post- caffeine respectively at CGM, and a CMRO2 of 58.0±26.6µmol/100g/min at white matter. CMRO2 from both QSM and R2* based methods showed good regional consistency (p>0.05), but quantitation of R2* based CMRO2 required an additional scaling factor. Conclusion QSM can be used with perfusion measurements pre- and post- caffeine vascoconstriction to map CMRO2 and OEF.
Background: Deregulated circular RNAs (circRNAs) are associated with the development of cancer and therapy resistance. However, functional research of circRNAs mostly focus on potential miRNA or protein binding and more potential regulation of circRNA on host gene DNA in cancers are yet to be inspected. Method: We performed total RNA sequencing on clinical breast cancer samples and identified the expression patterns of circRNAs and corresponding host genes in patient blood, tumor and adjacent normal tissues. qPCR, northern blot and in situ hybridization were used to validate the dysregulation of circRNA circSMARCA5. A series of procedures including R-loop dot-blotting, DNA-RNA immunoprecipitation and mass spectrum, etc. were conducted to explore the regulation of circSMARCA5 on the transcription of exon 15 of SMARCA5. Moreover, immunofluorescence and in vivo experiments were executed to investigate the overexpression of circSMARCA5 with drug sensitivities. Results: We found that circRNAs has average higher expression over its host linear genes in peripheral blood. Compared to adjacent normal tissues, circSMARCA5 is decreased in breast cancer tissues, contrary to host gene SMARCA5. The enforced expression of circSMARCA5 induced drug sensitivity of breast cancer cell lines in vitro and in vivo. Furthermore, we demonstrated that circSMARCA5 can bind to its parent gene locus, forming an R-loop, which results in transcriptional pausing at exon 15 of SMARCA5. CircSMARCA5 expression resulted in the downregulation of SMARCA5 and the production of a truncated nonfunctional protein, and the overexpression of circSMARCA5 was sufficient to improve sensitivity to cytotoxic drugs. Conclusion: Our results revealed a new regulatory mechanism for circRNA on its host gene and provided evidence that circSMARCA5 may serve as a therapeutic target for drug-resistant breast cancer patients.
In this paper we consider the problem of robot navigation in simple maze-like environments where the robot has to rely on its onboard sensors to perform the navigation task. In particular, we are interested in solutions to this problem that do not require localization, mapping or planning. Additionally, we require that our solution can quickly adapt to new situations (e.g., changing navigation goals and environments). To meet these criteria we frame this problem as a sequence of related reinforcement learning tasks. We propose a successor-feature-based deep reinforcement learning algorithm that can learn to transfer knowledge from previously mastered navigation tasks to new problem instances. Our algorithm substantially decreases the required learning time after the first task instance has been solved, which makes it easily adaptable to changing environments. We validate our method in both simulated and real robot experiments with a Robotino and compare it to a set of baseline methods including classical planning-based navigation.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.