Large-step neural network for learning the symplectic evolution from partitioned data

In this study, we focus on learning Hamiltonian systems, which involves predicting the coordinate (q) and momentum (p) variables generated by a symplectic mapping. Based on Chen & Tao (2021), the symplectic mapping is represented by a generating function. To extend the prediction time period, we develop a new learning scheme by splitting the time series (q_i, p_i) into several partitions. We then train a large-step neural network (LSNN) to approximate the generating function between the first partition (i.e. the initial condition) and each one of the remaining partitions. This partition approach makes our LSNN effectively suppress the accumulative error when predicting the system evolution. Then we train the LSNN to learn the motions of the 2:3 resonant Kuiper belt objects for a long time period of 25000 yr. The results show that there are two significant improvements over the neural network constructed in our previous work (Li et al. 2022): (1) the conservation of the Jacobi integral, and (2) the highly accurate predictions of the orbital evolution. Overall, we propose that the designed LSNN has the potential to considerably improve predictions of the long-term evolution of more general Hamiltonian systems.Comment: 13 pages, 7 figures, accepted for publication in MNRA

Smooth and Stepwise Self-Distillation for Object Detection

Distilling the structured information captured in feature maps has contributed to improved results for object detection tasks, but requires careful selection of baseline architectures and substantial pre-training. Self-distillation addresses these limitations and has recently achieved state-of-the-art performance for object detection despite making several simplifying architectural assumptions. Building on this work, we propose Smooth and Stepwise Self-Distillation (SSSD) for object detection. Our SSSD architecture forms an implicit teacher from object labels and a feature pyramid network backbone to distill label-annotated feature maps using Jensen-Shannon distance, which is smoother than distillation losses used in prior work. We additionally add a distillation coefficient that is adaptively configured based on the learning rate. We extensively benchmark SSSD against a baseline and two state-of-the-art object detector architectures on the COCO dataset by varying the coefficients and backbone and detector networks. We demonstrate that SSSD achieves higher average precision in most experimental settings, is robust to a wide range of coefficients, and benefits from our stepwise distillation procedure.Comment: Accepted by International Conference on Image Processing (ICIP) 202

Asymmetry in the number of L4 and L5 Jupiter Trojans driven by jumping Jupiter

Context. More than 10000 Jupiter Trojans have been detected so far. They are moving around the L4 and L5 triangular Lagrangian points of the Sun-Jupiter system and their distributions can provide important clues to the early evolution of the Solar System. Aims. The number asymmetry of the L4 and L5 Jupiter Trojans is a longstanding problem. We aim to test a new mechanism in order to explain this anomalous feature by invoking the jumping-Jupiter scenario. Methods. First, we introduce the orbital evolution of Jupiter caused by the giant planet instability in the early Solar System. In this scenario, Jupiter could undergo an outward migration at a very high speed. We then investigate how such a jump changes the numbers of the L4 (N4) and L5 (N5) Trojans. Results. The outward migration of Jupiter can distort the co-orbital orbits near the Lagrangian points, resulting in L4 Trojans being more stable than the L5 ones. We find that, this mechanism could potentially explain the unbiased number asymmetry of N4/N5~1.6 for the known Jupiter Trojans. The uncertainties of the system parameters, e.g. Jupiter's eccentricity and inclination, the inclination distribution of Jupiter Trojans, are also taken into account and our results about the L4/L5 asymmetry have been further validated. However, the resonant amplitudes of the simulated Trojans are excited to higher values compared to the current population. A possible solution is that collisions among the Trojans may reduce their resonant amplitudes.Comment: 11 pages, 5 figures, accepted for publication in A&

Signal Processing for Digital Beamforming FMCW SAR

According to the limitations of single channel Frequency Modulation Continuous Wave (FMCW) Synthetic Aperture Radar (SAR), Digital Beamforming (DBF) technology is introduced to improve system performance. Combined with multiple receive apertures, DBF FMCW SAR can obtain high resolution in low pulse repetition frequency, which can increase the processing gain and decrease the sampling frequency. The received signal model of DBF FMCW SAR is derived. The continuous antenna motion which is the main characteristic of FMCW SAR received signal is taken into account in the whole signal processing. The detailed imaging diagram of DBF FMCW SAR is given. A reference system is also demonstrated in the paper by comparing with a single channel FMCW SAR. The validity of the presented diagram is demonstrated with a point target simulation results

Characterization of a p75NTR Apoptotic Signaling Pathway Using a Novel Cellular Model

The p75 neurotrophin receptor (p75(NTR)) belongs to the tumor necrosis factor receptor/nerve growth factor receptor superfamily. In some cells derived from neuronal tissues it causes cell death through a poorly characterized pathway. We developed a neuronal system using conditionally immortalized striatal neurons, in which the expression of p75(NTR) is inducibly controlled by the ecdysone receptor. In these cells p75(NTR) induces apoptosis through its death domain in a nerve growth factor-independent manner. Caspases 9, 6, and 3 are activated by receptor expression indicating the activation of the common effector pathway of apoptosis. Cell death is blocked by a dominant negative form of caspase 9 and Bcl-X(L) consistent with a pathway that involves mitochondria. Significantly, the viral flice inhibitory protein E8 protects from p75(NTR)-induced cell death indicating that death effector domains are involved. A p75(NTR) construct with a deleted death domain dominantly interferes with p75(NTR) signaling, implying that receptor multimerization is required. However, in contrast to the other receptors of the family, p75(NTR)-mediated apoptosis does not involve the adaptor proteins Fas-associated death domain protein or tumor necrosis factor-associated death domain protein, and the apical caspase 8 is not activated. We conclude that p75(NTR) signals apoptosis by similar mechanisms as other death receptors but uses different adaptors and apical caspases

Electrochemical Sensing in Paper-Based Microfluidic Devices

This paper describes the fabrication and the performance of microfluidic paper-based electrochemical sensing devices (we call the microfluidic paper-based electrochemical devices, μPEDs). The μPEDs comprise paper-based microfluidic channels patterned by photolithography or wax printing, and electrodes screen-printed from conducting inks (e.g., carbon or Ag/AgCl). We demonstrated that the μPEDs are capable of quantifying the concentrations of various analytes (e.g., heavy-metal ions and glucose) in aqueous solutions. This low-cost analytical device should be useful for applications in public health, environmental monitoring, and the developing world

Adverse Effects of Simulated Hyper- and Hypo-Phosphatemia on Endothelial Cell Function and Viability

Dysregulation of phosphate homeostasis as occurs in chronic kidney disease is associated with cardiovascular complications. It has been suggested that both hyperphosphatemia and hypophosphatemia can cause cardiovascular disease. The molecular mechanisms by which high or low serum phosphate levels adversely affect cardiovascular function are poorly understood. The purpose of this study was to explore the mechanisms of endothelial dysfunction in the presence of non-physiologic phosphate levels.We studied the effects of simulated hyper- and hypophosphatemia in human umbilical vein endothelial cells in vitro. We found both simulated hyperphosphatemia and hypophosphatemia decrease eNOS expression and NO production. This was associated with reduced intracellular calcium, increased protein kinase C β2 (PKCβ2), reduced cell viability, and increased apoptosis. While simulated hyperphosphatemia was associated with decreased Akt/p-Akt, Bcl-xl/Bax ratios, NFkB-p65 and p-Erk abundance, simulated hypophosphatemia was associated with increased Akt/p-Akt and Bcl-xl/Bax ratios and p-Mek, p38, and p-p38 abundance.This is the first demonstration of endothelial dysfunction with hypophosphatemia. Our data suggests that both hyperphosphatemia and hypophosphatemia decrease eNOS activity via reduced intracellular calcium and increased PKCβ2. Hyperphosphatemia also appears to reduce eNOS transcription via reduced signaling through PI3K/Akt/NF-kB and MAPK/NF-kB pathways. On the other hand, hypophosphatemia appears to activate these pathways. Our data provides the basis for further studies to elucidate the relationship between altered phosphate homeostasis and cardiovascular disease. As a corollary, our data suggests that the level of phosphate in the culture media, if not in the physiologic range, may inadvertently affect experimental results