Deep Learning for Counting People from UWB Channel Impulse Response Signals.

The use of higher frequency bands compared to other wireless communication protocols enhances the capability of accurately determining locations from ultra-wideband (UWB) signals. It can also be used to estimate the number of people in a room based on the waveform of the channel impulse response (CIR) from UWB transceivers. In this paper, we apply deep neural networks to UWB CIR signals for the purpose of estimating the number of people in a room. We especially focus on empirically investigating the various network architectures for classification from single UWB CIR data, as well as from various ensemble configurations. We present our processes for acquiring and preprocessing CIR data, our designs of the different network architectures and ensembles that were applied, and the comparative experimental evaluations. We demonstrate that deep neural networks can accurately classify the number of people within a Line of Sight (LoS), thereby achieving an 99% performance and efficiency with respect to both memory size and FLOPs (Floating Point Operations Per Second).

Cdon ablation in motor neurons causes age-related motor neuron degeneration and impaired sciatic nerve repair.

BACKGROUND: The functional deterioration and loss of motor neurons are tightly associated with degenerative motor neuron diseases and aging-related muscle wasting. Motor neuron diseases or aging-related muscle wasting in turn contribute to increased risk of adverse health outcomes in the elderly. Cdon (cell adhesion molecule-downregulated oncogene) belongs to the immunoglobulin superfamily of cell adhesion molecule and plays essential roles in multiple signalling pathways, including sonic hedgehog (Shh), netrin, and cadherin-mediated signalling. Cdon as a Shh coreceptor plays a critical role in motor neuron specification during embryonic development. However, its role in adult motor neuron function is unknown. METHODS: Hb9-Cre recombinase-driven motor neuron-specific Cdon deficient mice (mnKO) and a compound mutant mice (mnKO::SOD1G93A ) were generated to investigate the role of Cdon in motor neuron degeneration. Motor neuron regeneration was examined by using a sciatic nerve crush injury model. To investigate the phenotype, physical activity, compound muscle action potential, immunostaining, and transmission electron microscopy were carried out. In the mechanism study, RNA sequencing and RNA/protein analyses were employed. RESULTS: Mice lacking Cdon in motor neurons exhibited middle age onset lethality and aging-related decline in motor function. In the sciatic nerve crush injury model, mnKO mice exhibited an impairment in motor function recovery evident by prolonged compound muscle action potential duration (4.63 ± 0.35 vs. 3.93 ± 0.22 s for f/f, P < 0.01) and physical activity. Consistently, neuromuscular junctions of mnKO muscles were incompletely occupied (49.79 ± 5.74 vs. 79.39 ± 3.77% fully occupied neuromuscular junctions for f/f, P < 0.0001), suggesting an impaired reinnervation. The transmission electron microscopy analysis revealed that mnKO sciatic nerves had smaller axon diameter (0.88 ± 0.13 vs. 1.43 ± 0.48 µm for f/f, P < 0.0001) and myelination defects. RNA sequencing of mnKO lumbar spinal cords showed alteration in genes related to neurogenesis, inflammation and cell death. Among the altered genes, ErbB4 and FgfR expressions were significantly altered in mnKO as well as in Cdon-depleted NSC34 motor neuron cells. Consistently, Cdon-depleted NSC34 cells exhibited elevated levels of cleaved Caspase3 and γH2AX proteins, as well as Bax transcription. Cdon-depleted NSC34 cells also exhibited impaired activation of Akt in response to neuregulin-1 (NRG1) treatment. CONCLUSIONS: Our current data demonstrate the functional importance of Cdon in motor neuron function and nerve repair. Cdon ablation causes alterations in neurotrophin signalling that leads to motor neuron degeneration.

Comparison of National Dysphagia Diet and International Dysphasia Diet Standardization Initiative Levels for Thickened Drinks Prepared with a Commercial Xanthan Gum-Based Thickener Used for Patients with Dysphagia.

The thickness levels of fluids for patients with dysphagia are established according to the guidelines of the National Dysphagia Diet (NDD) and International Dysphagia Diet Standardization Initiative (IDDSI). The nectar- (level 2), honey- (level 3), and pudding-like (level 4) fluids in NDD are consistent with the mildly (level 2), moderately (level 3), and extremely (level 4) thick fluids in IDDSI, respectively. In this study, NDD levels were compared with IDDSI levels by estimating both the apparent viscosity (ηa,50) and the residual volume (mL) in the IDDSI syringe flow test of thickened drinks prepared with a commercial xanthan gum-based thickener at different concentrations (0.1∼3.1%, w/w). The concentration range of the thickener in thickened drinks at each IDDSI and NDD level increased in the following order: water> orange juice> milk. A small difference was noted in the range of thickener concentration in the same NDD and IDDSI levels for thickened milk when compared with other thickened drinks. These results indicate that the thickener concentration ranges of thickened drinks for the classification of NDD levels differed from those of IDDSI levels, and they appeared to be greatly influenced by the type of drink. These findings could provide useful information for practically indi-cating the reliable thickness levels by the IDDSI flow test in clinical practice.

Correction: Lee et al. Protein Arginine Methyltransferases in Neuromuscular Function and Diseases. Cells 2022, 11, 364.

The authors wish to make the following corrections to this paper [...].

Protein Arginine Methyltransferases in Neuromuscular Function and Diseases.

Neuromuscular diseases (NMDs) are characterized by progressive loss of muscle mass and strength that leads to impaired body movement. It not only severely diminishes the quality of life of the patients, but also subjects them to increased risk of secondary medical conditions such as fall-induced injuries and various chronic diseases. However, no effective treatment is currently available to prevent or reverse the disease progression. Protein arginine methyltransferases (PRMTs) are emerging as a potential therapeutic target for diverse diseases, such as cancer and cardiovascular diseases. Their expression levels are altered in the patients and molecular mechanisms underlying the association between PRMTs and the diseases are being investigated. PRMTs have been shown to regulate development, homeostasis, and regeneration of both muscle and neurons, and their association to NMDs are emerging as well. Through inhibition of PRMT activities, a few studies have reported suppression of cytotoxic phenotypes observed in NMDs. Here, we review our current understanding of PRMTs' involvement in the pathophysiology of NMDs and potential therapeutic strategies targeting PRMTs to address the unmet medical need.

PRMT7 ablation in cardiomyocytes causes cardiac hypertrophy and fibrosis through ß-catenin dysregulation.

Angiotensin II (AngII) has potent cardiac hypertrophic effects mediated through activation of hypertrophic signaling like Wnt/ß-Catenin signaling. In the current study, we examined the role of protein arginine methyltransferase 7 (PRMT7) in cardiac function. PRMT7 was greatly decreased in hypertrophic hearts chronically infused with AngII and cardiomyocytes treated with AngII. PRMT7 depletion in rat cardiomyocytes resulted in hypertrophic responses. Consistently, mice lacking PRMT7 exhibited the cardiac hypertrophy and fibrosis. PRMT7 overexpression abrogated the cellular hypertrophy elicited by AngII, while PRMT7 depletion exacerbated the hypertrophic response caused by AngII. Similar with AngII treatment, the cardiac transcriptome analysis of PRMT7-deficient hearts revealed the alteration in gene expression profile related to Wnt signaling pathway. Inhibition of PRMT7 by gene deletion or an inhibitor treatment enhanced the activity of ß-catenin. PRMT7 deficiency decreases symmetric dimethylation of ß-catenin. Mechanistic studies reveal that methylation of arginine residue 93 in ß-catenin decreases the activity of ß-catenin. Taken together, our data suggest that PRMT7 is important for normal cardiac function through suppression of ß-catenin activity.

BST204 Protects Dexamethasone-Induced Myotube Atrophy through the Upregulation of Myotube Formation and Mitochondrial Function.

BST204 is a purified ginseng dry extract that has an inhibitory effect on lipopolysaccharide-induced inflammatory responses, but its effect on muscle atrophy is yet to be investigated. In this study, C2C12 myoblasts were induced to differentiate for three days followed by the treatment of dexamethasone (DEX), a corticosteroid drug, with vehicle or BST204 for one day and subjected to immunoblotting, immunocytochemistry, qRT-PCR and biochemical analysis for mitochondrial function. BST204 alleviates the myotube atrophic effect mediated by DEX via the activation of protein kinase B/mammalian target of rapamycin (Akt/mTOR) signaling. Through this pathway, BST204 suppresses the expression of muscle-specific E3 ubiquitin ligases contributing to the enhanced myotube formation and enlarged myotube diameter in DEX-treated myotubes. In addition, BST204 treatment significantly decreases the mitochondrial reactive oxygen species production in DEX-treated myotubes. Furthermore, BST204 improves mitochondrial function by upregulating the expression of peroxisome proliferator-activated receptor-γ coactivator-1α (PGC1α) in DEX-induced myotube atrophy. This study provides a mechanistic insight into the effect of BST204 on DEX-induced myotube atrophy, suggesting that BST204 has protective effects against the toxicity of a corticosteroid drug in muscle and promising potential as a nutraceutical remedy for the treatment of muscle weakness and atrophy.

Emodin induces apoptosis of concanavalin A-stimulated murine splenocytes.

Emodin, one of the major compounds in the herb Reynoutria elliptica, is known to maintain immunosuppressive, anti-allergic, anti-cancer, and anti-inflammatory effects. In this study, we assessed the possibility of using emodin to induce apoptosis in stimulated immune cells in vitro. After treatment with emodin and concanavalin A (Con A), we observed DNA damage-induced apoptosis in splenocytes. Moreover, treatment with emodin and Con A increased the number of apoptotic splenocytes compared with untreated controls. Emodin also diminished the size of CD45R/B220+ cells, CD19+CD69+ cells, and cDC populations. These results indicate that emodin-induced apoptosis was involved in attenuating the immune activity promoted by DNA damage and in decreasing the number of CD45R/B220+ B cells and CD19+CD69+ activating B cells. This demonstration of emodin inducing apoptosis of Con A-stimulated immune cells indicates its potential utility as a therapy for diseases caused by abnormally activated immune cells.

Reduced graphene oxide/carbon double-coated 3-D porous ZnO aggregates as high-performance Li-ion anode materials.

The reduced graphene oxide (RGO)/carbon double-coated 3-D porous ZnO aggregates (RGO/C/ZnO) have been successfully synthesized as anode materials for Li-ion batteries with excellent cyclability and rate capability. The mesoporous ZnO aggregates prepared by a simple solvothermal method are sequentially modified through distinct carbon-based double coating. These novel architectures take unique advantages of mesopores acting as space to accommodate volume expansion during cycling, while the conformal carbon layer on each nanoparticle buffering volume changes, and conductive RGO sheets connect the aggregates to each other. Consequently, the RGO/C/ZnO exhibits superior electrochemical performance, including remarkably prolonged cycle life and excellent rate capability. Such improved performance of RGO/C/ZnO may be attributed to synergistic effects of both the 3-D porous nanostructures and RGO/C double coating.

Jeju ground water containing vanadium induced immune activation on splenocytes of low dose γ-rays-irradiated mice.

Vanadium, an essential micronutrient, has been implicated in controlling diabetes and carcinogenesis and in impeding reactive oxygen species (ROS) generation. γ-ray irradiation triggers DNA damage by inducing ROS production and causes diminution in radiosensitive immunocytes. In this study, we elucidate the immune activation capacities of Jeju water containing vanadium on immunosuppression caused by γ-ray irradiation, and identify its mechanism using various low doses of NaVO(3). We examined the intracellular ROS generation, DNA damage, cell proliferation, population of splenocytes, and cytokine/antibody profiles in irradiated mice drinking Jeju water for 180 days and in non-irradiated and in irradiated splenocytes both of which were treated with NaVO(3). Both Jeju water and 0.245 µM NaVO(3) attenuated the intracellular ROS generation and DNA damage in splenocytes against γ-ray irradiation. Splenocytes were significantly proliferated by the long-term intake of Jeju water and by 0.245 µM NaVO(3) treatment, and the expansion of B cells accounted for the increased number of splenocytes. Also, 0.245 µM NaVO(3) treatment showed the potency to amplify the production of IFN-γ and total IgG in irradiated splenocytes, which correlated with the expansion of B cells. Collectively, Jeju water containing vanadium possesses the immune activation property against damages caused by γ-irradiation.