A Multi-Target Localization and Vital Sign Detection Method Using Ultra-Wide Band Radar.

Life detection technology using ultra-wideband (UWB) radar is a non-contact, active detection technology, which can be used to search for survivors in disaster rescues. The existing multi-target detection method based on UWB radar echo signals has low accuracy and has difficulty extracting breathing and heartbeat information at the same time. Therefore, this paper proposes a new multi-target localization and vital sign detection method using ultra-wide band radar. A target recognition and localization method based on permutation entropy (PE) and K means++ clustering is proposed to determine the number and position of targets in the environment. An adaptive denoising method for vital sign extraction based on ensemble empirical mode decomposition (EEMD) and wavelet analysis (WA) is proposed to reconstruct the breathing and heartbeat signals of human targets. A heartbeat frequency extraction method based on particle swarm optimization (PSO) and stochastic resonance (SR) is proposed to detect the heartbeat frequency of human targets. Experimental results show that the PE-K means++ method can successfully recognize and locate multiple human targets in the environment, and its average relative error is 1.83%. Using the EEMD-WA method can effectively filter the clutter signal, and the average relative error of the reconstructed respiratory signal frequency is 4.27%. The average relative error of heartbeat frequency detected by the PSO-SR method was 6.23%. The multi-target localization and vital sign detection method proposed in this paper can effectively recognize all human targets in the multi-target scene and provide their accurate location and vital signs information. This provides a theoretical basis for the technical system of emergency rescue and technical support for post-disaster rescue.

A Vital Signs Fast Detection and Extraction Method of UWB Impulse Radar Based on SVD.

The identification of weak vital signs has always been one of the difficulties in the field of life detection. In this paper, a novel vital sign detection and extraction method with high efficiency, high precision, high sensitivity and high signal-to-noise ratio is proposed. Based on the NVA6100 pulse radar system, the radar matrix which contains several radar pulse detection signals is received. According to the characteristics of vital signs and radar matrices, the Singular Value Decomposition (SVD) is adopted to perform signal denoising and decomposition after preprocessing, and the temporal and spatial eigenvectors of each principal component are obtained. Through the energy proportion screening, the Wavelet Transform decomposition and linear trend suppression, relatively pure vital signs in each principal component, are obtained. The human location is detected by the Energy Entropy of spatial eigenvectors, and the respiratory signal and heartbeat signal are restored through a Butterworth Filter and an MTI harmonic canceller. Finally, through an analysis of the performance of the algorithm, it is proved to have the properties of efficiency and accuracy.

The GLP-1/GIP dual-receptor agonist DA5-CH inhibits the NF-κB inflammatory pathway in the MPTP mouse model of Parkinson's disease more effectively than the GLP-1 single-receptor agonist NLY01.

The GLP-1 receptor agonist exendin-4 has recently shown good effects in a phase II clinical trial in Parkinson's disease (PD) patients. Here, a comparison of the new GLP-1/GIP dual receptor agonist DA5-CH and NLY01, a 40 kDa pegylated form of exendin-4, on motor impairments and reducing inflammation in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) PD mouse model is provided. The drug groups received either DA5-CH or NLY01 (25 nmol/kg) i.p. after daily MPTP intraperitoneal injection. Both drugs showed improvements in motor activity, open field experiments, rotarod tests, and gait analysis, but DA5-CH was more potent. Tyrosine hydroxylase expression in dopaminergic neurons was much reduced by MPTP and improved by DA5-CH, while NLY01 showed weak effects. When analyzing levels of α-synuclein (α-Syn), DA5-CH reduced levels effectively while NLY01 had no effect. When measuring the levels of the inflammation markers Toll-like receptor 4 (TLR4), specific markers of microglia activation (Iba-1), the marker of astrocyte activation glial fibrillary acidic protein (GFAP), nuclear factor-κB (NF-κB), tumor necrosis factor (TNF-α), and transforming growth factor ß1 (TGF-ß1), DA5-CH was very effective in reducing the chronic inflammation response, while NLY01 did not show significant effects. Levels of key growth factors such as Glial cell-derived neurotrophic factor (GDNF) and Brain-derived neurotrophic factor (BDNF) were much reduced by MPTP, and DA5-CH was able to normalize levels in the brain, while NLY01 showed little effect. The levels of pro-inflammatory cytokines (IL-6 and IL-Iß) were much reduced by DA5-CH, too, while NLY01 showed no effect. In a separate experiment, we tested the ability of the two drugs to cross the blood-brain barrier. After injecting fluorescin-labelled peptides peripherally, the fluorescence in brain tissue was measured. It was found that the pegylated NLY01 peptide did not cross the BBB in meaningful quantities while exendin-4 and the dual agonist DA5-CH did. The results show that DA5-CH shows promise as a therapeutic drug for PD.

Amifostine ameliorates cerebral ischaemia-reperfusion injury via p38-mediated oxidative stress and mitochondrial dysfunction.

Amifostine is a cytoprotective compound that is beneficial in ischaemic stroke cases. However, the neuroprotective effect of amifostine on ischaemia/reperfusion (I/R)-induced brain injury and its underlying mechanism are still poorly understood. Herein, we constructed an animal model of middle cerebral artery occlusion and reperfusion (MCAO/R) injury and an in vitro model of oxygen and glucose deprivation and reperfusion (OGD/R) injury. After administration of amifostine, we found significant improvements in neurological deficits, infarct size, and cerebral oedema. Moreover, amifostine alleviated histopathological alteration and increased the number of surviving neurons. Biochemical analysis showed that treatment with amifostine obviously improved the brain damage of MCAO/R mice, as manifested by a decrease in reactive oxygen species (ROS) and malondialdehyde (MDA) generation, and an increase in superoxide dismutase (SOD) activity. Moreover, amifostine decreased the mitochondrial membrane potential (m) loss, and cytochrome c escaping to cytoplasm, but increased the ATP level. In vitro, amifostine also showed an antioxidant effect, which was reflected by the reduced ROS generation, decreased mitochondrial superoxide generation, increased total SOD, SOD1 (Cu/Zn SOD, cytoplasmic SOD), and SOD2 (mitochondrial SOD) activities, and decreased m loss. Furthermore, amifostine suppressed neuronal apoptosis, accompanied by the reduction of Bax, cleaved caspase-9, cleaved caspase-3, and Bcl-2 upregulation. Amifostine also reduced the expression of p-p38 (Thr 180/Tyr 182) in vivo and in vitro. In short, amifostine exhibits a protective effect on cerebral I/R damage through modulating p38-related oxidative stress, mitochondrial dysfunction, and apoptosis.