Visual Aid for the Learning of Tree-based Data Structures

Computer Science

CRONOS: Colorization and Contrastive Learning for Device-Free NLoS Human Presence Detection using Wi-Fi CSI

In recent years, the demand for pervasive smart services and applications has increased rapidly. Device-free human detection through sensors or cameras has been widely adopted, but it comes with privacy issues as well as misdetection for motionless people. To address these drawbacks, channel state information (CSI) captured from commercialized Wi-Fi devices provides rich signal features for accurate detection. However, existing systems suffer from inaccurate classification under a non-line-of-sight (NLoS) and stationary scenario, such as when a person is standing still in a room corner. In this work, we propose a system called CRONOS (Colorization and Contrastive Learning Enhanced NLoS Human Presence Detection), which generates dynamic recurrence plots (RPs) and color-coded CSI ratios to distinguish mobile people from vacancy in a room, respectively. We also incorporate supervised contrastive learning to retrieve substantial representations, where consultation loss is formulated to differentiate the representative distances between dynamic and stationary cases. Furthermore, we propose a self-switched static feature enhanced classifier (S3FEC) to determine the utilization of either RPs or color-coded CSI ratios. Our comprehensive experimental results show that CRONOS outperforms existing systems that apply machine learning, non-learning based methods, as well as non-CSI based features in open literature. CRONOS achieves the highest presence detection accuracy in vacancy, mobility, line-of-sight (LoS), and NLoS scenarios

Src-homology 2 domain-containing tyrosine phosphatase 2 promotes oral cancer invasion and metastasis

BACKGROUND: Tumor invasion and metastasis represent a major unsolved problem in cancer pathogenesis. Recent studies have indicated the involvement of Src-homology 2 domain-containing tyrosine phosphatase 2 (SHP2) in multiple malignancies; however, the role of SHP2 in oral cancer progression has yet to be elucidated. We propose that SHP2 is involved in the progression of oral cancer toward metastasis. METHODS: SHP2 expression was evaluated in paired oral cancer tissues by using immunohistochemical staining and real-time reverse transcription polymerase chain reaction. Isogenic highly invasive oral cancer cell lines from their respective low invasive parental lines were established using a Boyden chamber assay, and changes in the hallmarks of the epithelial-mesenchymal transition (EMT) were assessed to evaluate SHP2 function. SHP2 activity in oral cancer cells was reduced using si-RNA knockdown or enforced expression of a catalytically deficient mutant to analyze migratory and invasive ability in vitro and metastasis toward the lung in mice in vivo. RESULTS: We observed the significant upregulation of SHP2 in oral cancer tissues and cell lines. Following SHP2 knockdown, the oral cancer cells markedly attenuated migratory and invasion ability. We observed similar results in phosphatase-dead SHP2 C459S mutant expressing cells. Enhanced invasiveness was associated with significant upregulation of E-cadherin, vimentin, Snail/Twist1, and matrix metalloproteinase-2 in the highly invasive clones. In addition, we determined that SHP2 activity is required for the downregulation of phosphorylated ERK1/2, which modulates the downstream effectors, Snail and Twist1 at a transcript level. In lung tissue sections of mice, we observed that HSC3 tumors with SHP2 deletion exhibited significantly reduced metastatic capacity, compared with tumors administered control si-RNA. CONCLUSIONS: Our data suggest that SHP2 promotes the invasion and metastasis of oral cancer cells. These results provide a rationale for further investigating the effects of small-molecule SHP2 inhibitors on the progression of oral cancer, and indicate a previously unrecognized SHP2-ERK1/2-Snail/Twist1 pathway that is likely to play a crucial role in oral cancer invasion and metastasis

Attention-based Learning for Sleep Apnea and Limb Movement Detection using Wi-Fi CSI Signals

Wi-Fi channel state information (CSI) has become a promising solution for non-invasive breathing and body motion monitoring during sleep. Sleep disorders of apnea and periodic limb movement disorder (PLMD) are often unconscious and fatal. The existing researches detect abnormal sleep disorders in impractically controlled environments. Moreover, it leads to compelling challenges to classify complex macro- and micro-scales of sleep movements as well as entangled similar waveforms of cases of apnea and PLMD. In this paper, we propose the attention-based learning for sleep apnea and limb movement detection (ALESAL) system that can jointly detect sleep apnea and PLMD under different sleep postures across a variety of patients. ALESAL contains antenna-pair and time attention mechanisms for mitigating the impact of modest antenna pairs and emphasizing the duration of interest, respectively. Performance results show that our proposed ALESAL system can achieve a weighted F1-score of 84.33, outperforming the other existing non-attention based methods of support vector machine and deep multilayer perceptron

Cyclin D1 Restrains Oncogene-Induced Autophagy by Regulating the AMPK-LKB1 Signaling Axis.

Autophagy activated after DNA damage or other stresses mitigates cellular damage by removing damaged proteins, lipids, and organelles. Activation of the master metabolic kinase AMPK enhances autophagy. Here we report that cyclin D1 restrains autophagy by modulating the activation of AMPK. In cell models of human breast cancer or in a cyclin D1-deficient model, we observed a cyclin D1-mediated reduction in AMPK activation. Mechanistic investigations showed that cyclin D1 inhibited mitochondrial function, promoted glycolysis, and reduced activation of AMPK (pT172), possibly through a mechanism that involves cyclin D1-Cdk4/Cdk6 phosphorylation of LKB1. Our findings suggest how AMPK activation by cyclin D1 may couple cell proliferation to energy homeostasis

Dilated Dense U-Net for Infant Hippocampus Subfield Segmentation

Accurate and automatic segmentation of infant hippocampal subfields from magnetic resonance (MR) images is an important step for studying memory related infant neurological diseases. However, existing hippocampal subfield segmentation methods were generally designed based on adult subjects, and would compromise performance when applied to infant subjects due to insufficient tissue contrast and fast changing structural patterns of early hippocampal development. In this paper, we propose a new fully convolutional network (FCN) for infant hippocampal subfield segmentation by embedding the dilated dense network in the U-net, namely DUnet. The embedded dilated dense network can generate multi-scale features while keeping high spatial resolution, which is useful in fusing the low-level features in the contracting path with the high-level features in the expanding path. To further improve the performance, we group every pair of convolutional layers with one residual connection in the DUnet, and obtain the Residual DUnet (ResDUnet). Experimental results show that our proposed DUnet and ResDUnet improve the average Dice coefficient by 2.1 and 2.5% for infant hippocampal subfield segmentation, respectively, when compared with the classic 3D U-net. The results also demonstrate that our methods outperform other state-of-the-art methods

Associations between Tumor Vascularity, Vascular Endothelial Growth Factor Expression and PET/MRI Radiomic Signatures in Primary Clear-Cell–Renal-Cell-Carcinoma: Proof-of-Concept Study

Studies have shown that tumor angiogenesis is an essential process for tumor growth, proliferation and metastasis. Also, tumor angiogenesis is an important prognostic factor of clear cell renal cell carcinoma (ccRCC), as well as a factor in guiding treatment with antiangiogenic agents. Here, we attempted to find the associations between tumor angiogenesis and radiomic imaging features from PET/MRI. Specifically, sparse canonical correlation analysis was conducted on 3 feature datasets (i.e., radiomic imaging features, tumor microvascular density (MVD), and vascular endothelial growth factor (VEGF) expression) from 9 patients with primary ccRCC. In order to overcome the potential bias of intratumoral heterogeneity of angiogenesis, this study investigated the relationship between regional expressions of angiogenesis and VEGF, and localized radiomic features from different parts within the tumors. Our study highlighted the significant strong correlations between radiomic features and MVD, and also demonstrated that the spatiotemporal features extracted from DCE-MRI provided stronger radiomic correlation to MVD than the textural features extracted from Dixon sequences and FDG PET. Furthermore, PET/MRI, which takes advantage of the combined functional and structural information, had higher radiomics correlation to MVD than solely utilizing PET or MRI alone

Void Structures in Regularly Patterned ZnO Nanorods Grown with the Hydrothermal Method

The void structures and related optical properties after thermal annealing with ambient oxygen in regularly patterned ZnO nanrorod (NR) arrays grown with the hydrothermal method are studied. In increasing the thermal annealing temperature, void distribution starts from the bottom and extends to the top of an NR in the vertical (c-axis) growth region. When the annealing temperature is higher than 400°C, void distribution spreads into the lateral (m-axis) growth region. Photoluminescence measurement shows that the ZnO band-edge emission, in contrast to defect emission in the yellow-red range, is the strongest under the n-ZnO NR process conditions of 0.003 M in Ga-doping concentration and 300°C in thermal annealing temperature with ambient oxygen. Energy dispersive X-ray spectroscopy data indicate that the concentration of hydroxyl groups in the vertical growth region is significantly higher than that in the lateral growth region. During thermal annealing, hydroxyl groups are desorbed from the NR leaving anion vacancies for reacting with cation vacancies to form voids

Elevated expression of TDP-43 in the forebrain of mice is sufficient to cause neurological and pathological phenotypes mimicking FTLD-U

TDP-43 is a multifunctional DNA/RNA-binding factor that has been implicated in the regulation of neuronal plasticity. TDP-43 has also been identified as the major constituent of the neuronal cytoplasmic inclusions (NCIs) that are characteristic of a range of neurodegenerative diseases, including the frontotemporal lobar degeneration with ubiquitin+ inclusions (FTLD-U) and amyotrophic lateral sclerosis (ALS). We have generated a FTLD-U mouse model (CaMKII-TDP-43 Tg) in which TDP-43 is transgenically overexpressed in the forebrain resulting in phenotypic characteristics mimicking those of FTLD-U. In particular, the transgenic (Tg) mice exhibit impaired learning/memory, progressive motor dysfunction, and hippocampal atrophy. The cognitive and motor impairments are accompanied by reduced levels of the neuronal regulators phospho–extracellular signal-regulated kinase and phosphorylated cAMP response element-binding protein and increased levels of gliosis in the brains of the Tg mice. Moreover, cells with TDP-43+, ubiquitin+ NCIs and TDP-43–deleted nuclei appear in the Tg mouse brains in an age-dependent manner. Our data provide direct evidence that increased levels of TDP-43 protein in the forebrain is sufficient to lead to the formation of TDP-43+, ubiquitin+ NCIs and neurodegeneration. This FTLD-U mouse model should be valuable for the mechanistic analysis of the role of TDP-43 in the pathogenesis of FTLD-U and for the design of effective therapeutic approaches of the disease

Human Mesenchymal Stem Cells Prolong Survival and Ameliorate Motor Deficit through Trophic Support in Huntington's Disease Mouse Models

We investigated the therapeutic potential of human bone marrow-derived mesenchymal stem cells (hBM-MSCs) in Huntington's disease (HD) mouse models. Ten weeks after intrastriatal injection of quinolinic acid (QA), mice that received hBM-MSC transplantation showed a significant reduction in motor function impairment and increased survival rate. Transplanted hBM-MSCs were capable of survival, and inducing neural proliferation and differentiation in the QA-lesioned striatum. In addition, the transplanted hBM-MSCs induced microglia, neuroblasts and bone marrow-derived cells to migrate into the QA-lesioned region. Similar results were obtained in R6/2-J2, a genetically-modified animal model of HD, except for the improvement of motor function. After hBM-MSC transplantation, the transplanted hBM-MSCs may integrate with the host cells and increase the levels of laminin, Von Willebrand Factor (VWF), stromal cell-derived factor-1 (SDF-1), and the SDF-1 receptor Cxcr4. The p-Erk1/2 expression was increased while Bax and caspase-3 levels were decreased after hBM-MSC transplantation suggesting that the reduced level of apoptosis after hBM-MSC transplantation was of benefit to the QA-lesioned mice. Our data suggest that hBM-MSCs have neural differentiation improvement potential, neurotrophic support capability and an anti-apoptotic effect, and may be a feasible candidate for HD therapy