Sound Attenuation by Trunks in the Ground with thick Snow

A main way for sound reduction by tree belts is to scatter sound waves by trunks while previous studies of sound absorption by trunks always contain the ground effects. This study aims to examine the difference of reverberation time in different kinds of tree belts through eliminating the influence from ground effect. In order to estimate the scattering of sound waves by trunks, this study investigates sound (Impulse sound) attenuation by three woodlands with same tree species and one woodland with mixed species in the ground with thick snow. The effect of receiver distance from the sound source was also investigated (5 m,10 m and 20m). The results showed that reverberation time can be used to describe the sound propagation over snow cover through tree belts. The reverberation time in different kinds of forests is different, but the variation shows a similar trend with the increase of frequency. The distance between the receiver and sound source affects the reverberation time. The species with higher ability of sound scattering can be used in urban green space to reduce urban noise

Strong spin-orbit interaction and magnetotransport in semiconductor Bi2_2O2_2Se nanoplates

Semiconductor Bi$_2$O$_2$Se nanolayers of high crystal quality have been realized via epitaxial growth. These two-dimensional (2D) materials possess excellent electron transport properties with potential application in nanoelectronics. It is also strongly expected that the 2D Bi$_2$O$_2$Se nanolayers could be of an excellent material platform for developing spintronic and topological quantum devices, if the presence of strong spin-orbit interaction in the 2D materials can be experimentally demonstrated. Here, we report on experimental determination of the strength of spin-orbit interaction in Bi$_2$O$_2$Se nanoplates through magnetotransport measurements. The nanoplates are epitaxially grown by chemical vapor deposition and the magnetotransport measurements are performed at low temperatures. The measured magnetoconductance exhibits a crossover behavior from weak antilocalization to weak localization at low magnetic fields with increasing temperature or decreasing back gate voltage. We have analyzed this transition behavior of the magnetoconductance based on an interference theory which describes the quantum correction to the magnetoconductance of a 2D system in the presence of spin-orbit interaction. Dephasing length and spin relaxation length are extracted from the magnetoconductance measurements. Comparing to other semiconductor nanostructures, the extracted relatively short spin relaxation length of ~150 nm indicates the existence of strong spin-orbit interaction in Bi$_2$O$_2$Se nanolayers.Comment: 14 pages, 4 figures, and 5 pages of Supplementary Material

Universal conductance fluctuations and phase-coherent transport in a semiconductor Bi2_2O2_2Se nanoplate with strong spin-orbit interaction

We report on phase-coherent transport studies of a Bi$_2$O$_2$Se nanoplate and on observation of universal conductance fluctuations and spin-orbit interaction induced reduction in fluctuation amplitude in the nanoplate. Thin-layered Bi$_2$O$_2$Se nanoplates are grown by chemical vapor deposition (CVD) and transport measurements are made on a Hall-bar device fabricated from a CVD-grown nanoplate. The measurements show weak antilocalization at low magnetic fields at low temperatures, as a result of spin-orbit interaction, and a crossover toward weak localization with increasing temperature. Temperature dependences of characteristic transport lengths, such as spin relaxation length, phase coherence length, and mean free path, are extracted from the low-field measurement data. Universal conductance fluctuations are visible in the low-temperature magnetoconductance over a large range of magnetic fields and the phase coherence length extracted from the autocorrelation function is in consistence with the result obtained from the weak localization analysis. More importantly, we find a strong reduction in amplitude of the universal conductance fluctuations and show that the results agree with the analysis assuming strong spin-orbit interaction in the Bi$_2$O$_2$Se nanoplate.Comment: 11 pages, 4 figures, supplementary material

Atrial cardiomyopathy: from cell to bedside

Atrial cardiomyopathy refers to structural and electrical remodelling of the atria, which can lead to impaired mechanical function. While historical studies have implicated atrial fibrillation as the leading cause of cardioembolic stroke, atrial cardiomyopathy may be an important, underestimated contributor. To date, the relationship between atrial cardiomyopathy, atrial fibrillation, and cardioembolic stroke remains obscure. This review summarizes the pathogenesis of atrial cardiomyopathy, with a special focus on neurohormonal and inflammatory mechanisms, as well as the role of adipose tissue, especially epicardial fat in atrial remodelling. It reviews the current evidence implicating atrial cardiomyopathy as a cause of embolic stroke, with atrial fibrillation as a lagging marker of an increased thrombogenic atrial substrate. Finally, it discusses the potential of antithrombotic therapy in embolic stroke with undetermined source and appraises the available diagnostic techniques for atrial cardiomyopathy, including imaging techniques such as echocardiography, computed tomography, and magnetic resonance imaging as well as electroanatomic mapping, electrocardiogram, biomarkers, and genetic testing. More prospective studies are needed to define the relationship between atrial cardiomyopathy, atrial fibrillation, and embolic stroke and to establish a prompt diagnosis and specific treatment strategies in these patients with atrial cardiomyopathy for the secondary and even primary prevention of embolic stroke

Serum N‐glycans outperform CA19‐9 in diagnosis of extrahepatic cholangiocarcinoma

Extensive efforts have been devoted to improve the diagnosis of extrahepatic cholangiocarcinoma (ECCA) due to its silent clinical character and lack of effective diagnostic biomarkers. Specific alterations in N‐glycosylation of glycoproteins are considered a key component in cancer progression, which can serve as a distinct molecular signature for cancer detection. This study aims to find potential serum N‐glycan markers for ECCA. In total, 255 serum samples from patients with ECCA (n = 106), benign bile tract disease (BBD, n = 60) and healthy controls (HC, n = 89) were recruited. Only 2 μL of serum from individual patients was used in this assay where the N‐glycome of serum glycoproteins was profiled by DNA sequencer‐assisted fluorophore‐assisted capillary electrophoresis (DSA‐FACE) technology. Multi‐parameter models were constructed by combining the N‐glycans and carbohydrate antigen 19‐9 (CA19‐9) which is currently used clinically. Quantitative analyses showed that among 13 N‐glycan structures, the bifucosylated triantennary N‐glycan (peak10, NA3F2) presented the best diagnostic performance for distinguishing ECCA from BBD and HC. Two diagnostic models (Glycotest1 and Glycotest2) performed better than single N‐glycan or CA19‐9. Additionally, two N‐glycan structures (peak9, NA3Fb; peak12, NA4Fb) were tightly related to lymph node metastasis in ECCA patients. In conclusion, sera of ECCA showed relatively specific N‐glycome profiling patterns. Serum N‐glycan markers and models are novel, valuable and noninvasive alternatives in ECCA diagnosis and progression monitoring.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/139072/1/elps6272.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/139072/2/elps6272_am.pd

Spatiotemporal patterns and spatial risk factors for visceral leishmaniasis from 2007 to 2017 in Western and Central China: a modelling analysis

Visceral leishmaniasis (VL) is a neglected disease caused by trypanosomatid protozoa in the genus Leishmania, which is transmitted by phlebotomine sandflies. Although this vector-borne disease has been eliminated in several regions of China during the last century, the reported human VL cases have rebounded in Western and Central China in recent decades. However, understanding of the spatial epidemiology of the disease remains vague, as the spatial risk factors driving the spatial heterogeneity of VL. In this study, we analyzed the spatiotemporal patterns of annual human VL cases in Western and Central China from 2007 to 2017. Based on the related spatial maps, the boosted regression tree (BRT) model was adopted to explore the relationships between VL and spatial correlates as well as predicting both the existing and potential infection risk zones of VL in Western and Central China. The mined links reveal that elevation, minimum temperature, relative humidity, and annual accumulated precipitation make great contributions to the spatial heterogeneity of VL. The maps show that Xinjiang Uygur Autonomous Region, Gansu, western Inner Mongolia Autonomous Region, and Sichuan are predicted to fall in the highest infection risk zones of VL. Approximately 61.60 million resident populations lived in the high-risk regions of VL in Western and Central China. Our results provide a better understanding of how spatial risk factors driving VL spread as well as identifying the potential endemic risk region of VL, thereby enhancing the biosurveillance capacity of public health authorities

Integrated gene-based and pathway analyses using UK Biobank data identify novel genes for chronic respiratory diseases

BackgroundChronic respiratory diseases have become a non-negligible cause of death globally. Although smoking and environmental exposures are primary risk factors for chronic respiratory diseases, genetic factors also play an important role in determining individual’s susceptibility to diseases. Here we performed integrated gene-based and pathway analyses to systematically illuminate the heritable characteristics of chronic respiratory diseases.MethodsUK (United Kingdom) Biobank is a very large, population-based prospective study with over 500,000 participants, established to allow detailed investigations of the genetic and nongenetic determinants of the diseases. Utilizing the GWAS-summarized data downloaded from UK Biobank, we conducted gene-based analysis to obtain associations of susceptibility genes with asthma, chronic obstructive pulmonary disease (COPD) and pneumonia using FUSION and MAGMA software. Across the identified susceptibility regions, functional annotation integrating multiple functional data sources was performed to explore potential regulatory mechanisms with INQUISIT algorithm. To further detect the biological process involved in the development of chronic respiratory diseases, we undertook pathway enrichment analysis with the R package (clusterProfiler).ResultsA total of 195 susceptibility genes were identified significantly associated with chronic respiratory diseases (Pbonferroni < 0.05), and 24/195 located out of known susceptibility regions (e.g. WDPCP in 2p15). Within the identified susceptibility regions, functional annotation revealed an aggregation of credible variants in promoter-like and enhancer-like histone modification regions and such regulatory mechanisms were specific to lung tissues. Furthermore, 110 genes with INQUISIT score ≥1 may influence diseases susceptibility through exerting effects on coding sequences, proximal promoter and distal enhancer regulations. Pathway enrichment results showed that these genes were enriched in immune-related processes and nicotinic acetylcholine receptors pathways.ConclusionsThis study implemented an integrated gene-based and pathway strategy to explore the underlying biological mechanisms and our findings may serve as promising targets for future clinical treatments of chronic respiratory diseases

A new unconventional HLA-A2-restricted epitope from HBV core protein elicits antiviral cytotoxic T lymphocytes

Cytotoxic T cells (CTLs) play a key role in the control of Hepatitis B virus (HBV) infection and viral clearance. However, most of identified CTL epitopes are derived from HBV of genotypes A and D, and few have been defined in virus of genotypes B and C which are more prevalent in Asia. As HBV core protein (HBc) is the most conservative and immunogenic component, in this study we used an overlapping 9-mer peptide pool covering HBc to screen and identify specific CTL epitopes. An unconventional HLA-A2-restricted epitope HBc141–149 was discovered and structurally characterized by crystallization analysis. The immunogenicity and anti-HBV activity were further determined in HBV and HLA-A2 transgenic mice. Finally, we show that mutations in HBc141–149 epitope are associated with viral parameters and disease progression in HBV infected patients. Our data therefore provide insights into the structure characteristics of this unconventional epitope binding to MHC-I molecules, as well as epitope specific CTL activity that orchestrate T cell response and immune evasion in HBV infected patients

Cross-Cancer Pleiotropic Analysis Reveals Novel Susceptibility Loci for Lung Cancer

Genome-wide association studies (GWASs) have identified hundreds of single nucleotide polymorphisms (SNPs) associated with cancer risk, several of which have shown pleiotropic effects across cancers. Therefore, we performed a systematic cross-cancer pleiotropic analysis to detect the effects of GWAS-identified variants from non-lung cancers on lung cancer risk in 12,843 cases and 12,639 controls from four lung cancer GWASs. The overall association between variants in each cancer and risk of lung cancer was explored using sequential kernel association test (SKAT) analysis. For single variant analysis, we combined the result of specific study using fixed-effect meta-analysis. We performed functional exploration of significant associations based on features from public databases. To further detect the biological mechanism underlying identified observations, pathway enrichment analysis were conducted with R package “clusterProfiler.” SNP-set analysis revealed the overall associations between variants of 8 cancer types and lung cancer risk. Single variant analysis identified 6 novel SNPs related to lung cancer risk after multiple correction (Pfdr &lt; 0.10), including rs1707302 (1p34.1, OR = 0.93, 95% CI: 0.90–0.97, P = 7.60 × 10−4), rs2516448 (6p21.33, OR = 1.07, 95% CI: 1.03–1.11, P = 1.00 × 10−3), rs3869062 (6p22.1, OR = 0.91, 95% CI: 0.86–0.96, P = 7.10 × 10−4), rs174549 (11q12.2, OR = 0.90, 95% CI: 0.87–0.94, P = 1.00 × 10−7), rs7193541 (16q23.1, OR = 0.93, 95% CI: 0.90–0.96, P = 1.20 × 10−4), and rs8064454 (17q12, OR = 1.07, 95% CI: 1.03–1.11, P = 4.30 × 10−4). The eQTL analysis and functional annotation suggested that these variants might modify lung cancer susceptibility through regulating the expression of related genes. Pathway enrichment analysis showed that genes modulated by these variants play important roles in cancer carcinogenesis. Our findings demonstrate the pleiotropic associations between non-lung cancer susceptibility loci and lung cancer risk, providing important insights into the shared mechanisms of carcinogenesis across cancers.<br/