Search

Real-world robotic operations often face uncertainties that can impede accurate control of manipulators. This study proposes a recurrent neural network (RNN) combining kinematic and dynamic models to address this issue. Assuming an unknown mass matrix, the proposed method enables effective trajectory tracking for manipulators. In detail, a kinematic controller is designed to determine the desired joint acceleration for a given task with error feedback. Subsequently, integrated with the kinematics controller, the RNN is proposed to combine the robot's dynamic model and a mass matrix estimator. This integration allows the manipulator system to handle uncertainties and synchronously achieve trajectory tracking effectively. Theoretical analysis demonstrates the learning and control capabilities of the RNN. Simulative experiments conducted on a Franka Emika Panda manipulator, and comparisons validate the effectiveness and superiority of the proposed method.

Mendelian randomization methods are prone to produce false positive results when assumptions are violated. Here, the authors propose a statistical model that offers good power to detect causation between traits while controlling the false positive rate.

BackgroundHirschsprung's disease (HSCR) is currently considered to be a congenital gastrointestinal malformation caused mainly by genetic factors. Endothelin Converting Enzyme-1 (ECE1) has been reported to be associated with HSCR. However, the relationship between ECE1 single nucleotide polymorphism (SNP) rs169884 and HSCR in the southern Chinese population remains unknown.Methods1,470 HSCR patients and 1,473 controls from a southern Chinese population were recruited. The intronic SNP rs169884 in ECE1 was genotyped in all samples. We tested the association between rs169884 and HSCR under various genetic models. We also evaluated the effect of rs169884 on HSCR subtypes, including short-segment HSCR (S-HSCR), long-segment HSCR (L-HSCR) and total colonic aganglionosis (TCA). External epigenetic data were integrated to investigate the potential biological function of rs169884.ResultsChromatin states data from derived neuron cells or fetal colon tissue revealed that rs169884 might control ECE1 expression through regulating its enhancer function. We did not find a significant association between rs169884 and HSCR. For HSCR subtypes, although no significant associations were detected between rs169884 and S-HSCR (OR = 1.00, 95% CI: 0.89∼1.12, Padj = 0.77) or TCA (OR = 1.00, 95% CI: 0.72∼1.38, Padj = 0.94), we found that rs169884 could increase the risk of L-HSCR (OR = 1.23, 95% CI 1.02∼1.45, Padj = 0.024).ConclusionThese results suggested that rs169884 might play a regulatory role for ECE1 expression and increase susceptibility of L-HSCR in southern Chinese children.

Power calculation is a necessary step when planning genome-wide association studies (GWAS) to ensure meaningful findings. Statistical power of GWAS depends on the genetic architecture of phenotype, sample size, and study design. While several computer programs have been developed to perform power calculation for single SNP association testing, it might be more appropriate for GWAS power calculation to address the probability of detecting any number of associated SNPs. In this paper, we derive the statistical power distribution across causal SNPs under the assumption of a point-normal effect size distribution. We demonstrate how key outcome indices of GWAS are related to the genetic architecture (heritability and polygenicity) of the phenotype through the power distribution. We also provide a fast, flexible and interactive power calculation tool which generates predictions for key GWAS outcomes including the number of independent significant SNPs, the phenotypic variance explained by these SNPs, and the predictive accuracy of resulting polygenic scores. These results could also be used to explore the future behaviour of GWAS as sample sizes increase further. Moreover, we present results from simulation studies to validate our derivation and evaluate the agreement between our predictions and reported GWAS results.

Sleep quality and duration are critical indicators of individual health. Traditional methods of monitoring them either were limited to the application environment or resulted in discomfort. To overcome these existing limitations, we propose a noncontact sleep monitoring system placed under the mattress, named SleepMatrix, to provide users with a comprehensive picture of their real-time to long-term health status. SleepMatrix is a sleep monitoring system that consists of two parts: a front-end sensor array and a cloud-edge data processing system. The data-driven system, based on the Internet of Things, can be flexibly deployed in environments from homes to transportation, and a variety of centralized control and monitoring functions can be flexibly deployed under different application scenarios. At the same time, users can view real-time and historical data through supporting applications and understand the sleep monitoring results. SleepMatrix is a complete and systematic sleep monitoring tool that can help people understand their health status and its evolution from a new perspective and therefore may contribute greatly to informing users of potential illnesses.

Marine transportation and operations have attracted the attention of more and more countries and scholars in recent years. A full-state finite time feedback control scheme is designed for the model parameters uncertainty, unknown ocean environment disturbances, and unmeasured system states in the underactuated Unmanned Surface Vessel (USV) trajectory tracking control. The external wind, wave and current environmental disturbances and model parameters perturbation are extended by Nonlinear Extended State Observer (NESO) to the state of the system, namely complex disturbances. The complex disturbances, positions and velocities of USV can be observed by NESO and feedback to USV control system. Next, the underactuated USV error model is obtained by operating the obtained feedback information and the virtual ship model. According to the error model, a Nonsingular Fast Terminal Sliding Model surface (NFTSM) is constructed to realize finite-time control. The control law is deduced through the Lyapunov stability theory to ensure the stability of the system. The results of MATLAB numerical simulations under different disturbances show that the trajectory tracking algorithm has fast responses, and a good convergence of the errors is observed, which verifies the effectiveness of the designed scheme.

There are currently increasingly concerns over DNA damage related to free radicals due to their vital roles in human health, especially high-performance detection method. Herein, we report an ultra- sensitive monitoring of DNA damage associated with free radicals exposure using interdigitated electrode (IDE) array for the first time. The proposed IDE array was equipped with DNA-wrapped carbon nanotube-based bridges, which utilized the DNA damage mechanism due to the free radicals’ attack and the efficient electrical detection nature of the interdigitated electrode. Experiments have been performed, and the results showed the device’s capability for detecting DNA damage induced by multiple free radicals generated from different sources, including the Fenton reaction, UV radiation and cigarette smoke, showing the promising ability for DNA damage detection. In addition, the carbon nanotubes bridge-based interdigitated electrode sensor enabled different levels of sensing of DNA damage with great sensitivity and a wide detection range. It was illustrated that the ultrasensitive detection of free radicals generated from ultraviolet radiation (15 min – 125 min), cigarette smoke tar (1 μg/mL to 10 μg/mL) and Fenton reaction under different concentration of H2O2 (2.5 pM – 100 pM), have been detected successfully. Typically, the IDE array supports further performance improvement for the electrochemical detection in an ultrasensitive and high throughput route.

An underactuated unmanned surface vessel (USV) is a nonholonomic system, in which trajectory tracking is a challenging problem that has drawn more and more attention from researchers recently. The control of trajectory tracking is of critical importance since it determines whether the task can be carried out successfully. In this paper, a non-singular terminal sliding model (NTSM) controller is proposed for the trajectory tracking control of the underactuated USV, with a nonlinear disturbance observer which is designed to measure complex environmental disturbances such as wind, waves, and currents. Exploratory simulations were carried out and the results show that the proposed controller is effective and robust for the trajectory tracking of underactuated USVs in the presence of environmental disturbances.

The disulfide bonds and sulfhydryl in gluten were evaluated to investigate the effects of structural characteristics on the quality of white noodles. The free sulfhydryl concentration increased significantly, but disulphide bonds decreased initially, and then became stable with increasing sodium sulfite concentration. With a decrease in disulfide bond concentration from 56.78 μmol/g to 20.01 μmol/g in gluten added to noodles, microstructural graphs verified that the cross-section and surface of noodles became rougher and looser with more holes generated; optimal cooking time decreased from 4.4 min to 3.3 min for fresh noodles and from 10.11 min to 9.19 min for dried samples; water absorption and cooking loss increased from 159% to 203% and from 5.26% to 9.06%, respectively. A decreasing trend and marked differences were observed for hardness, springiness, chewiness as well as resilience of fresh and cooked noodles, but the cohesiveness of fresh noodles exhibited no significant changes (P < 0.05).

Abstract This paper presents a novel integrated framework for simulating the charging load of an electric vehicle charging station. The framework is built based on the cellular automaton model, including five modules: vehicle generation, charging station, lane change, speed update and boundary clear. The proposed framework can effectively stimulate the system dynamics of the traffic system and charging power process in a charging station. Case studies have verified its feasibility and effectiveness.

Motivation: Prediction and prioritization of human non-coding regulatory variants is critical for understanding the regulatory mechanisms of disease pathogenesis and promoting personalized medicine. Existing tools utilize functional genomics data and evolutionary information to evaluate the pathogenicity or regulatory functions of non-coding variants. However, different algorithms lead to inconsistent and even conflicting predictions. Combining multiple methods may increase accuracy in regulatory variant prediction. Results: Here, we compiled an integrative resource for predictions from eight different tools on functional annotation of non-coding variants. We further developed a composite strategy to integrate multiple predictions and computed the composite likelihood of a given variant being regulatory variant. Benchmarked by multiple independent causal variants datasets, we demonstrated that our composite model significantly improves the prediction performance. [ABSTRACT FROM AUTHOR]

Signal transducer and activator of transcription 3 (STAT3) activation is key for ischemic postconditioning (IPo) to attenuate myocardial ischemia-reperfusion injury (MIRI), but IPo loses cardioprotection in diabetes in which cardiac STAT3 activation is impaired and adiponectin (APN) reduced. We found that IPo increased postischemic cardiomyocyte-derived APN, activated mitochondrial STAT3 (mitoSTAT3), improved mitochondrial function, and attenuated MIRI in wild-type but not in APN knockout (Adipo(-/-)) mice subjected to 30 min coronary occlusion, followed by 2 or 24 h of reperfusion. Hypoxic postconditioning-induced protection against hypoxia/reoxygenation injury was lost in Adipo(-/-) cardiomyocytes but restored by recombinant APN, but this APN beneficial effect was abolished by specific STAT3 or APN receptor 1 (AdipoR1) gene knockdown, or caveolin-3 (Cav3) disruption. APN activated cardiac STAT3 and restored IPo cardioprotection in 4-week diabetic rats where AdipoR1 and Cav3 were functionally interactive but not in 8-week diabetic rats whose cardiac Cav3 was severely reduced and AdipoR1/Cav3 signaling impaired. We concluded that IPo activates mitoSTAT3 through APN/AdipoR1/Cav3 pathway to confer cardioprotection, whereas in diabetes, IPo loses cardioprotection due to impaired APN/AdipoR1/Cav3 signaling. Therefore, effective means that may concomitantly activate APN and repair APN signaling (i.e., AdipoR1/Cav3) in diabetes may represent promising avenues in the treatment of MIRI in diabetes. [ABSTRACT FROM AUTHOR]

Background: Large body of evidences accumulated in clinical and epidemiological studies indicate that hearts of diabetic subjects are more sensitive to ischemia reperfusion injury (IRI), which results in a higher rate of mortality at post-operation than that of non-diabetes. However, experimental results are equivocal and point to either increased or decreased susceptibility of the diabetic hearts to IRI, especially at the early stage of the disease. The present study was designed to test the hypothesis that the duration/severity of the indexed ischemia is a major determinant of the vulnerability to myocardial IRI at early stage of diabetes. Methods: Four weeks streptozotocin (STZ)-induced diabetic (D) and non-diabetic (C) Sprague-Dawley rats were randomly assigned to receive 30 or 45 min of left anterior descending artery ligation followed by 2 or 3 hours of reperfusion, respectively. Cardiac function was recorded by using Pressure-Volume (PV) conduction system. Myocardial infarct size was determined with triphenyltetrazolium chloride staining. Plasma Creatine kinase-MB (CK-MB), Lactate dehydrogenase (LDH) release, myocardial nitric oxide(NO) content and nitrotyrosine formation, 15-F2t-Isoprostane and plasma superoxide dismutase (SOD) were measured with colorimetric assays. Cardiomyocyte apoptosis was assessed by TUNEL staining. Myocardial TNFα, Caspase-3, STAT3, Akt, and GSK-3β were determined by Western blotting. Results: Prolongation of ischemia but not reperfusion from 30 min to 45 min significantly increased infarct size in D compared to C rats (P < 0.05), accompanied with significantly increased plasma CK-MB (P < 0.05). Prolongation of the duration of either ischemia or reperfusion significantly increased plasma LDH release and myocardial 15-F2t-Isoprostane and reduced plasma SOD activity, with concomitant reduction of myocardial NO and increase of nitrotyrosine formation in D relative to C (P < 0.05). Prolongation of ischemia and reperfusion significantly reduced left ventricular ejection fraction and increased the peak rate of pressure, accompanied with increased end systolic pressure in D relative to C rats (P < 0.05) but reduced phosphorylations of myocardial STAT3 at site Ser727 and Akt at site Ser473 as well as GSK-3β at Ser 9 (P < 0.05). Conclusions: Diabetic hearts, even at early stage of the disease are more sensitive to IRI, and this increased severity of post-ischemic myocardial injury depends more on the duration of ischemia than that of reperfusion. [ABSTRACT FROM AUTHOR]

The article discusses the study of the support of genetic evidence for cardiovascular risk induced by antineoplastic drugs. Topics discusses include Cardiovascular dysfunction is one of the most common complications of long-term cancer treatment. Growing evidence has shown that antineoplastic drugs can increase cardiovascular risk during cancer therapy, seriously affecting patient survival; and results establish a link between the causal allele of cardiovascular disease genes.