Invisible surfaces enabled by the coalescence of anti-reflection and wavefront controllability in ultrathin metasurfaces

Though existing metamaterial antireflection coatings have been optimized in terms of thickness and functionality, these coatings do not provide phase control in the deep subwavelength scale. Here, the authors report multi-layered metasurfaces that provide both antireflection and phase control

A Low-Power Passive UHF Tag With High-Precision Temperature Sensor for Human Body Application

Radio frequency identification (RFID) tags are widely used in various electronic devices due to their low cost, simple structure, and convenient data reading. This topic aims to study the key technologies of ultra-high frequency (UHF) RFID tags and high-precision temperature sensors, and how to reduce the power consumption of the temperature sensor and the overall circuits while maintaining minimal loss of performance. Combined with the biomedicine, an innovative high-precision human UHF RFID chip for body temperature monitoring is designed. In this study, a ring oscillator whose output frequency is linearly related to temperature is designed and proposed as a temperature-sensing circuit by innovatively combining auxiliary calibration technology. Then, a binary counter is used to count the pulses, and the temperature is ultimately calculated. This topic designed a relaxation oscillator independent of voltage and current. The various types of resistors were used to offset the temperature deviation. A current mirror array calibration circuit is used to calibrate the process corner deviation of the clock circuit with a self-calibration algorithm. This study mainly contributes to reducing power consumption and improving accuracy. The total power consumption of the RF/analog front-end and temperature sensor is 7.65µW. The measurement error of the temperature sensor in the range of 0 to 60◦C is less than ±0.1%, and the accuracy of the output frequency of the clock circuit is ±2.5%

Distinct responses of niche and fitness differences to water availability underlie variable coexistence outcomes in semi-arid annual plant communities

Climate change is predicted to have profound consequences for multispecies coexistence, and thus, patterns of biological diversity. These consequences will be mediated by direct and indirect impacts of environmental change on species’ vital rates and interactions. While the impacts of environmental change on individual species has received much attention to date, the consequences for coexistence mediated by changes in the strength and direction of multispecies interactions are not as well understood. To investigate how coexistence dynamics may be sensitive to environmental change, we conducted a field experiment in a diverse semi-arid annual plant system. We imposed a water manipulation treatment in two sites that vary in aridity and associated rainfall. Focusing on four common annual plant species in these sites, we quantified the fecundity (seed production) of individuals in response to a gradient of intra- and interspecific competitor densities and aridity. We then used these fecundities to parameterize an annual plant population model and examine the influence of aridity and species identity on resultant coexistence dynamics (as a function of stabilizing niche differences and fitness inequalities). While the responses of some vital rates and competitive impacts to watering varied somewhat predictably across sites, coexistence metrics encapsulating changes in these vital rates and interaction strengths did not. Fitness inequalities among our focal species were driven largely by differences in sensitivity to competition, which were almost always much greater than the magnitude of stabilizing niche differences. These findings were surprising given observational evidence suggesting that these species do coexist at local scales in these natural communities. Synthesis. Our study is one of the first to explicitly consider the influence of environmental variation on the individual components of coexistence outcomes. We show that environmental change has the ability to influence coexistence not only through direct pathways (i.e., vital rates), but also indirect pathways (i.e., species interactions). Despite the consistency of many of the responses of these individual components to environmental variation, their combined influence on predictions of both current and future coexistence remains unclear

Evidence for Colour-Octet Mechanism from CERN LEP2 gamma gamma -> J/psi + X Data

We present theoretical predictions for the transverse-momentum distribution of J/psi mesons promptly produced in gamma gamma collisions within the factorization formalism of nonrelativistic quantum chromodynamics, including the contributions from both direct and resolved photons, and we perform a conservative error analysis. The fraction of J/psi mesons from decays of bottom-flavoured hadrons is estimated to be negligibly small. New data taken by the DELPHI Collaboration at LEP2 nicely confirm these predictions, while they disfavour those obtained within the traditional colour-singlet model.Comment: 11 pages (Latex), 3 figures (Postscript); updated experimental data included, references added, accepted for publication in Phys. Rev. Let

Distributed subgraph matching on timely dataflow

Recently there emerge many distributed algorithms that aim at solving subgraph matching at scale. Existing algorithm-level comparisons failed to provide a systematic view of distributed subgraph matching mainly due to the intertwining of strategy and optimization. In this paper, we identify four strategies and three general-purpose optimizations from representative state-of-the-art algorithms. We implement the four strategies with the optimizations based on the common Timely dataflow system for systematic strategy-level comparison. Our implementation covers all representative algorithms. We conduct extensive experiments for both un-labelled matching and labelled matching to analyze the performance of distributed subgraph matching under various settings, which is finally summarized as a practical guide

Emergence of the rtA181T/sW172* mutant increased the risk of hepatoma occurrence in patients with lamivudine-resistant chronic hepatitis B

<p>Abstract</p> <p>Background</p> <p>Development of the hepatitis B virus (HBV) rtA181T/sW172* mutant could occur during prolonged lamivudine (LAM) therapy, conferring cross resistance to adefovir. Recent studies demonstrated an increased oncogenic potential of this mutant in NIH3T3 cells. In this study, we aimed to investigate the clinical significance of this finding.</p> <p>Methods</p> <p>Serum samples from 123 LAM-resistant chronic hepatitis B patients were submitted for virological assays. A highly sensitive amplification created restriction enzyme site (ACRES) method was devised to detect small amounts of the rtA181T mutant in the serum. Virological factors including HBV-DNA level, genotype, precore G1896A, BCP A1762T/G1764A, rtM204I/V, rtA181T and pre-S internal deletion mutations as well as clinical variables including subsequent use of rescue drugs were submitted for outcome analysis.</p> <p>Results</p> <p>By use of the highly sensitive ACRES method, the rtA181T mutant was detectable in 10 of the 123 LAM-resistant patients. During the mean follow-up period of 26.2 ± 16.4 months (range 2 to 108 months), 3 of the 10 (30.0%) rtA181T-positive patients and 2 of the 113 (1.8%) rtA181T-negative patients developed hepatocellular carcinoma (HCC). Kaplan-Meier analysis indicated that the presence of rtA181T mutation (P < 0.001), age > 50 years (P = 0.001), and liver cirrhosis (P < 0.001) were significantly associated with subsequent occurrence of HCC. All 5 HCC patients belonged to the older age and cirrhosis groups.</p> <p>Conclusions</p> <p>Emergence of the rtA181T/sW172* mutant in LAM-resistant patients increased the risk of HCC development in the subsequent courses of antiviral therapy.</p

Estimation of Parent Specific DNA Copy Number in Tumors using High-Density Genotyping Arrays

Chromosomal gains and losses comprise an important type of genetic change in tumors, and can now be assayed using microarray hybridization-based experiments. Most current statistical models for DNA copy number estimate total copy number, which do not distinguish between the underlying quantities of the two inherited chromosomes. This latter information, sometimes called parent specific copy number, is important for identifying allele-specific amplifications and deletions, for quantifying normal cell contamination, and for giving a more complete molecular portrait of the tumor. We propose a stochastic segmentation model for parent-specific DNA copy number in tumor samples, and give an estimation procedure that is computationally efficient and can be applied to data from the current high density genotyping platforms. The proposed method does not require matched normal samples, and can estimate the unknown genotypes simultaneously with the parent specific copy number. The new method is used to analyze 223 glioblastoma samples from the Cancer Genome Atlas (TCGA) project, giving a more comprehensive summary of the copy number events in these samples. Detailed case studies on these samples reveal the additional insights that can be gained from an allele-specific copy number analysis, such as the quantification of fractional gains and losses, the identification of copy neutral loss of heterozygosity, and the characterization of regions of simultaneous changes of both inherited chromosomes

NLRP3 inflammasome assembly in neutrophils is supported by PAD4 and promotes NETosis under sterile conditions

© The Author(s), 2021. This article is distributed under the terms of the Creative Commons Attribution License. The definitive version was published in Muenzer, P., Negro, R., Fukui, S., di Meglio, L., Aymonnier, K., Chu, L., Cherpokova, D., Gutch, S., Sorvillo, N., Shi, L., Magupalli, V. G., Weber, A. N. R., Scharf, R. E., Waterman, C. M., Wu, H., & Wagner, D. D. NLRP3 inflammasome assembly in neutrophils is supported by PAD4 and promotes NETosis under sterile conditions. Frontiers in Immunology, 12, (2021): 683803, https://doi.org/10.3389/fimmu.2021.683803.Neutrophil extracellular trap formation (NETosis) and the NLR family pyrin domain containing 3 (NLRP3) inflammasome assembly are associated with a similar spectrum of human disorders. While NETosis is known to be regulated by peptidylarginine deiminase 4 (PAD4), the role of the NLRP3 inflammasome in NETosis was not addressed. Here, we establish that under sterile conditions the cannonical NLRP3 inflammasome participates in NETosis. We show apoptosis-associated speck-like protein containing a CARD (ASC) speck assembly and caspase-1 cleavage in stimulated mouse neutrophils without LPS priming. PAD4 was needed for optimal NLRP3 inflammasome assembly by regulating NLRP3 and ASC protein levels post-transcriptionally. Genetic ablation of NLRP3 signaling resulted in impaired NET formation, because NLRP3 supported both nuclear envelope and plasma membrane rupture. Pharmacological inhibition of NLRP3 in either mouse or human neutrophils also diminished NETosis. Finally, NLRP3 deficiency resulted in a lower density of NETs in thrombi produced by a stenosis-induced mouse model of deep vein thrombosis. Altogether, our results indicate a PAD4-dependent formation of the NLRP3 inflammasome in neutrophils and implicate NLRP3 in NETosis under noninfectious conditions in vitro and in vivo.This work was supported by a grant from National Heart, Lung, and Blood Institute of the National Institutes of Health (grant R35 HL135765) and a Steven Berzin family support to DDW, an Individual Erwin Deutsch fellowship by the German, Austrian and Swiss Society of Thrombosis and Hemostasis Research to RES, a Whitman fellowship (MBL) to DDW, and an Individual Marie Skłodowska-Curie Actions fellowship by the European Commission (796365 - COAGULANT) to PM. ANRW was funded by the Deutsche Forschungsgemeinschaft (TRR156/2 –246807620) and a research grant (We-4195/15-19). CMW was supported by the Division of Intramural Research, NHLBI, NIH