Performance Analysis and Optimization of Compressed Air Energy Storage Integrated with Latent Thermal Energy Storage

Recovering compression waste heat using latent thermal energy storage (LTES) is a promising method to enhance the round-trip efficiency of compressed air energy storage (CAES) systems. In this study, a systematic thermodynamic model coupled with a concentric diffusion heat transfer model of the cylindrical packed-bed LTES is established for a CAES system, and the numerical simulation model is validated by experimental data in the reference. Based on the numerical model, the charging–discharging performance of LTES and CAES systems is evaluated under different layouts of phase change materials (PCMs) in LTES, and the optimal layout of PCM is specified as a three-stage layout, since the exergy efficiency of LTES and round-trip efficiency are improved by 8.2% and 6.9% compared with a one-stage layout. Then, the proportion of three PCMs is optimized using response surface methods. The optimization results indicate that the exergy efficiency of LTES and round-trip efficiency of the CAES system are expected to be 80.9% and 73.3% under the PCM proportion of 0.48:0.3:0.22 for three stages, which are 7.0% and 13.1% higher than the original three-stage PCMs with equal proportions

Twins:Device-free Object Tracking using Passive Tags

Without requiring objects to carry any transceiver, device-free based object tracking provides a promising solution for many localization and tracking systems to monitor non-cooperative objects such as intruders. However, existing device-free solutions mainly use sensors and active RFID tags, which are much more expensive compared to passive tags. In this paper, we propose a novel motion detection and tracking method using passive RFID tags, named Twins. The method leverages a newly observed phenomenon called critical state caused by interference among passive tags. We contribute to both theory and practice of such phenomenon by presenting a new interference model that perfectly explains this phenomenon and using extensive experiments to validate it. We design a practical Twins based intrusion detection scheme and implement a real prototype with commercial off-the-shelf reader and tags. The results show that Twins is effective in detecting the moving object, with low location error of 0.75m in average

Antireflection self-reference method based on ultrathin metallic nanofilms for improving terahertz reflection spectroscopy

We present the potential of an antireflection self-reference method based on ultrathin tantalum nitride (TaN) nanofilms for improving terahertz (THz) reflection spectroscopy. The antireflection self-reference method is proposed to eliminate mutual interference caused by unwanted reflections, which significantly interferes with the important reflection from the actual sample in THz reflection measurement. The antireflection self-reference model was investigated using a wave-impedance matching approach, and the theoretical model was verified in experimental studies. We experimentally demonstrated this antireflection selfreference method can completely eliminate the effect of mutual interference, accurately recover the actual sample’s reflection and improve THz reflection spectroscopy. Our method paves the way to implement a straightforward, accurate and efficient approach to investigate THz properties of the liquids and biological samplesThe Fund from Hefei University of Technology (407-0371000019); Sichuan Province Science and Technology Support Program (No. 2016GZ0250); the Fundamental Research Funds for the Central Universities (Grant No. JD2017JGPY0006); National Natural Science Foundation of China (Grant No.51607050); MINECO (MAT2015–74381-JIN to B.P., RYC2014–16962 and CTQ2017-89588-R to P.dP.); Xunta de Galicia (Centro singular de investigación de Galicia accreditation 2016–2019, ED431G/09); European Union (European Regional Development Fund – ERDF)S

Scorpion Toxins from <em>Buthus martensii</em> Karsch (BmK) as Potential Therapeutic Agents for Neurological Disorders: State of the Art and Beyond

Scorpions are fascinating creatures which became residents of the planet well before human beings dwelled on Earth. Scorpions are always considered as a figure of fear, causing notable pain or mortality throughout the world. Their venoms are cocktails of bioactive molecules, called toxins, which are responsible for their toxicity. Fortunately, medical researchers have turned the life-threatening toxins into life-saving therapeutics. From Song Dynasty in ancient China, scorpions and their venoms have been applied in traditional medicine for treating neurological disorders, such as pain, stroke, and epilepsy. Neurotoxins purified from Chinese scorpion Buthus Martensii Karsch (BmK) are considered as the main active ingredients, which act on membrane ion channels. Long-chain toxins of BmK, composed of 58–76 amino acids, could specifically recognize voltage-gated sodium channels (VGSCs). Short-chain BmK toxins, containing 28–40 amino acids, are found to modulate the potassium or chloride channels. These components draw attention as useful scaffolds for drug-design in order to tackle the emerging global medical threats. In this chapter, we aim to summarize the most promising candidates that have been isolated from BmK venoms for drug development

The association between serum uric acid and blood pressure in different age groups in a healthy Chinese cohort

High serum uric acid (sUA) has been reported to be a risk factor for hypertension however, whether this is the case for all age groups is not clear. We examined the association between sUA concentrations and systolic and diastolic blood pressure (SBP and DBP) in different age groups in a cohort of healthy Chinese participants. A total of 1082 healthy participants aged from 41 to 70 years were included. sUA concentration was measured by the uricaseperoxidase method. SBP and DBP were assessed using mercury sphygmomanometry. Hypertension was defined as SBP ≥140 mm Hg or DBP ≥90 mm Hg. Hyperuricemia (HUA) was defined as sUA concentration of >7mg/dL in men and >6mg/dL in women. The association between sUA concentration and SBP and DBP was examined using Pearson's correlation test, multivariate linear regression, and logistic regression analysis. The prevalence of hypertension and HUA increased with age (P<.001). Hypertension was more common in participants that had HUA than in those that did not (38.95% vs 30.16%, P=.02). Higher sUA was significantly associated with higher SBP and DBP in the 41- to 50-year-old participants (SBP, b=0.35, P<.001; DBP, b=.29, P<.001; after adjustment for age, sex, total cholesterol, estimated glomerular filtration rate, and fasting plasma glucose). HUA was also a risk factor for hypertension in this age group (odds ratio 1.425, 95% confidence interval, 1.217–1.668, P<.001). There was no association between sUA concentration and SBP and DBP in the other age groups. In this population of healthy Chinese participants, sUA concentration was positively associated with hypertension only in the 41- to 50-year-old group. Lowering uric acid in this age group may help to reduce the incidence of hypertension

A Consumer-tier based Visual-Brain Machine Interface for Augmented Reality Glasses Interactions

Objective.Visual-Brain Machine Interface(V-BMI) has provide a novel interaction technique for Augmented Reality (AR) industries. Several state-of-arts work has demonstates its high accuracy and real-time interaction capbilities. However, most of the studies employ EEGs devices that are rigid and difficult to apply in real-life AR glasseses application sceniraros. Here we develop a consumer-tier Visual-Brain Machine Inteface(V-BMI) system specialized for Augmented Reality(AR) glasses interactions. Approach. The developed system consists of a wearable hardware which takes advantages of fast set-up, reliable recording and comfortable wearable experience that specificized for AR glasses applications. Complementing this hardware, we have devised a software framework that facilitates real-time interactions within the system while accommodating a modular configuration to enhance scalability. Main results. The developed hardware is only 110g and 120x85x23 mm, which with 1 Tohm and peak to peak voltage is less than 1.5 uV, and a V-BMI based angry bird game and an Internet of Thing (IoT) AR applications are deisgned, we demonstrated such technology merits of intuitive experience and efficiency interaction. The real-time interaction accuracy is between 85 and 96 percentages in a commercial AR glasses (DTI is 2.24s and ITR 65 bits-min ). Significance. Our study indicates the developed system can provide an essential hardware-software framework for consumer based V-BMI AR glasses. Also, we derive several pivotal design factors for a consumer-grade V-BMI-based AR system: 1) Dynamic adaptation of stimulation patterns-classification methods via computer vision algorithms is necessary for AR glasses applications; and 2) Algorithmic localization to foster system stability and latency reduction.Comment: 15 pages,10 figure

Presenilin1 familial Alzheimer disease mutants inactivate EFNB1- and BDNF-dependent neuroprotection against excitotoxicity by affecting neuroprotective complexes of N-methyl-d-aspartate receptor

Excitotoxicity is thought to play key roles in brain neurodegeneration and stroke. Here we show that neuroprotection against excitotoxicity by trophic factors EFNB1 and brain-derived neurotrophic factor (called here factors) requires de novo formation of 'survival complexes' which are factor-stimulated complexes of N-methyl-D-aspartate receptor with factor receptor and presenilin 1. Absence of presenilin 1 reduces the formation of survival complexes and abolishes neuroprotection. EPH receptor B2- and N-methyl-D-aspartate receptor-derived peptides designed to disrupt formation of survival complexes also decrease the factor-stimulated neuroprotection. Strikingly, factor-dependent neuroprotection and levels of the de novo factor-stimulated survival complexes decrease dramatically in neurons expressing presenilin 1 familial Alzheimer disease mutants. Mouse neurons and brains expressing presenilin 1 familial Alzheimer disease mutants contain increased amounts of constitutive presenilin 1-N-methyl-D-aspartate receptor complexes unresponsive to factors. Interestingly, the stability of the familial Alzheimer disease presenilin 1-N-methyl-D-aspartate receptor complexes differs from that of wild type complexes and neurons of mutant-expressing brains are more vulnerable to cerebral ischaemia than neurons of wild type brains. Furthermore, N-methyl-D-aspartate receptor-mediated excitatory post-synaptic currents at CA1 synapses are altered by presenilin 1 familial Alzheimer disease mutants. Importantly, high levels of presenilin 1-N-methyl-D-aspartate receptor complexes are also found in post-mortem brains of Alzheimer disease patients expressing presenilin 1 familial Alzheimer disease mutants. Together, our data identify a novel presenilin 1-dependent neuroprotective mechanism against excitotoxicity and indicate a pathway by which presenilin 1 familial Alzheimer disease mutants decrease factor-depended neuroprotection against excitotoxicity and ischaemia in the absence of Alzheimer disease neuropathological hallmarks which may form downstream of neuronal damage. These findings have implications for the pathogenic effects of familial Alzheimer disease mutants and therapeutic strategies.This work was supported by National Institutes of Health grants 2RF1AG008200-29; 2R01-NS047229; P50AG05138; and by Grant AARF-17-531426 of the Alzheimer's Association

Promoter Hypermethylation Mediated Downregulation of FBP1 in Human Hepatocellular Carcinoma and Colon Cancer

FBP1, fructose-1,6-bisphosphatase-1, a gluconeogenesis regulatory enzyme, catalyzes the hydrolysis of fructose 1,6-bisphosphate to fructose 6-phosphate and inorganic phosphate. The mechanism that it functions to antagonize glycolysis and was epigenetically inactivated through NF-kappaB pathway in gastric cancer has been reported. However, its role in the liver carcinogenesis still remains unknown. Here, we investigated the expression and DNA methylation of FBP1 in primary HCC and colon tumor. FBP1 was lowly expressed in 80% (8/10) human hepatocellular carcinoma, 66.7% (6/9) liver cancer cell lines and 100% (6/6) colon cancer cell lines, but was higher in paired adjacent non-tumor tissues and immortalized normal cell lines, which was well correlated with its promoter methylation status. Methylation was further detected in primary HCCs, gastric and colon tumor tissues, but none or occasionally in paired adjacent non-tumor tissues. Detailed methylation analysis of 29 CpG sites at a 327-bp promoter region by bisulfite genomic sequencing confirmed its methylation. FBP1 silencing could be reversed by chemical demethylation treatment with 5-aza-2′-deoxycytidine (Aza), indicating direct epigenetic silencing. Restoring FBP1 expression in low expressed cells significantly inhibited cell growth and colony formation ability through the induction of G2-M phase cell cycle arrest. Moreover, the observed effects coincided with an increase in reactive oxygen species (ROS) generation. In summary, epigenetic inactivation of FBP1 is also common in human liver and colon cancer. FBP1 appears to be a functional tumor suppressor involved in the liver and colon carcinogenesis

Presenilin1 familial Alzheimer disease mutants inactivate EFNB1- and BDNF-dependent neuroprotection against excitotoxicity by affecting neuroprotective complexes of N-methyl-d-aspartate receptor

Excitotoxicity is thought to play key roles in brain neurodegeneration and stroke. Here we show that neuroprotection against excitotoxicity by trophic factors EFNB1 and brain-derived neurotrophic factor (called here factors) requires de novo formation of 'survival complexes' which are factor-stimulated complexes of N-methyl-d-aspartate receptor with factor receptor and presenilin 1. Absence of presenilin 1 reduces the formation of survival complexes and abolishes neuroprotection. EPH receptor B2- and N-methyl-d-aspartate receptor-derived peptides designed to disrupt formation of survival complexes also decrease the factor-stimulated neuroprotection. Strikingly, factor-dependent neuroprotection and levels of the de novo factor-stimulated survival complexes decrease dramatically in neurons expressing presenilin 1 familial Alzheimer disease mutants. Mouse neurons and brains expressing presenilin 1 familial Alzheimer disease mutants contain increased amounts of constitutive presenilin 1-N-methyl-d-aspartate receptor complexes unresponsive to factors. Interestingly, the stability of the familial Alzheimer disease presenilin 1-N-methyl-d-aspartate receptor complexes differs from that of wild type complexes and neurons of mutant-expressing brains are more vulnerable to cerebral ischaemia than neurons of wild type brains. Furthermore, N-methyl-d-aspartate receptor-mediated excitatory post-synaptic currents at CA1 synapses are altered by presenilin 1 familial Alzheimer disease mutants. Importantly, high levels of presenilin 1-N-methyl-d-aspartate receptor complexes are also found in post-mortem brains of Alzheimer disease patients expressing presenilin 1 familial Alzheimer disease mutants. Together, our data identify a novel presenilin 1-dependent neuroprotective mechanism against excitotoxicity and indicate a pathway by which presenilin 1 familial Alzheimer disease mutants decrease factor-depended neuroprotection against excitotoxicity and ischaemia in the absence of Alzheimer disease neuropathological hallmarks which may form downstream of neuronal damage. These findings have implications for the pathogenic effects of familial Alzheimer disease mutants and therapeutic strategies.This work was supported by National Institutes of Health grants 2RF1AG008200-29; 2R01-NS047229; P50AG05138; and by Grant AARF-17-531426 of the Alzheimer’s Association.Peer reviewe

Neutralization sites of human papillomavirus-6 relate to virus attachment and entry phase in viral infection.

Human papillomavirus type 6 (HPV6) is the major etiologic agent of genital warts and recurrent respiratory papillomatosis. Although the commercial HPV vaccines cover HPV6, the neutralization sites and mode for HPV6 are poorly understood. Here, we identify the HPV6 neutralization sites and discriminate the inhibition of virus attachment and entry by three potent neutralizing antibodies (nAbs), 5D3, 17D5, and 15F7. Mutagenesis assays showed that these nAbs predominantly target surface loops BC, DE, and FG of HPV6 L1. Cryo-EM structures of the HPV6 pseudovirus (PsV) and its immune complexes revealed three distinct binding modalities - full-occupation-bound to capsid, top-center-bound-, and top-rim-bound to pentamers - and illustrated a structural atlas for three classes of antibody-bound footprints that are located at center-distal ring, center, and center-proximal ring of pentamer surface for 5D3, 17D5, and 15F7, respectively. Two modes of neutralization were identified: mAb 5D3 and 17D5 block HPV PsV from attaching to the extracellular matrix (ECM) and the cell surface, whereas 15F7 allows PsV attachment but prohibits PsV from entering the cell. These findings highlight three neutralization sites of HPV6 L1 and outline two antibody-mediated neutralization mechanisms against HPV6, which will be relevant for HPV virology and antiviral inhibitor design. HighlightsMajor neutralization sites of HPV6 were mapped on the pseudovirus cryo-EM structuremAb 15F7 binds HPV6 capsid with a novel top-rim binding modality and confers a post-attachment neutralizationmAb 17D5 binds capsid in top-centre manner but unexpectedly prevents virus from attachment to cell surface