bluuebunny/crossref_metadata_2025_split huggingface dataset:
Progress in satellite quantum key distribution
Authors: Bedington Robert , Arrazola Juan Miguel , Ling Alexander 
Published: August 2017

AbstractQuantum key distribution (QKD) is a family of protocols for growing a private encryption key between two parties. Despite much progress, all ground-based QKD approaches have a distance limit due to atmospheric losses or in-fibre attenuation. These limitations make purely ground-based systems impractical for a global distribution network. However, the range of communication may be extended by employing satellites equipped with high-quality optical links. This manuscript summarizes research and development which is beginning to enable QKD with satellites. It includes a discussion of protocols, infrastructure, and the technical challenges involved with implementing such systems, as well as a top level summary of on-going satellite QKD initiatives around the world.
Current limitations of global conservation to protect higher vulnerability and lower resilience fish species
Authors: Vasconcelos Rita P. , Batista Marisa I. , Henriques Sofia 
Published: August 2017

AbstractEstuaries are threatened by intense and continuously increasing human activities. Here we estimated the sensitivity of fish assemblages in a set of estuaries distributed worldwide (based on species vulnerability and resilience), and the exposure to cumulative stressors and coverage by protected areas in and around those estuaries (from marine, estuarine and freshwater ecosystems, due to their connectivity). Vulnerability and resilience of estuarine fish assemblages were not evenly distributed globally and were driven by environmental features. Exposure to pressures and extent of protection were also not evenly distributed worldwide. Assemblages with more vulnerable and less resilient species were associated with estuaries in higher latitudes (in particular Europe), and with higher connectivity with the marine ecosystem, moreover such estuaries were generally under high intensity of pressures but with no concomitant increase in protection. Current conservation schemes pay little attention to species traits, despite their role in maintaining ecosystem functioning and stability. Results emphasize that conservation is weakly related with the global distribution of sensitive fish species in sampled estuaries, and this shortcoming is aggravated by their association with highly pressured locations, which appeals for changes in the global conservation strategy (namely towards estuaries in temperate regions and highly connected with marine ecosystems).
Vitellogenin induction in caudal fin of guppy (Poecilia reticulata) as a less invasive and sensitive biomarker for environmental estrogens
Authors: Wang Jun , Ma Shuwei , Zhang Zhenzhong , Zheng Mingyi , Dong Yifei , Ru Shaoguo 
Published: August 2017

AbstractGuppy (Poecilia reticulata) is an ideal model for studying environmental estrogens, and its large caudal fin has a high capacity to regenerate. This study analyzed the feasibility of caudal fin for detecting vitellogenin (Vtg), the most commonly used biomarker of environmental estrogens. Firstly, a sandwich ELISA for guppy Vtg was developed using purified lipovitellin and its antibody and it had a working range of 7.8–1000 ng/mL and detection limit of 3.1 ng/mL. The ELISA was used to detect tissue distribution of Vtg. In male guppy exposed to 50 and 100 ng/L 17β-estradiol (E2), Vtg concentration in caudal fin was higher than that in whole fish, brain, eyes, gonad, and skin, and was close to that in the liver. Furthermore, male guppies were exposed to environmental concentrations of 17a-ethinylestradiol (EE2) and bisphenol S (BPS) to validate the utility of caudal fin Vtg for detecting estrogenic activities. The lowest observed effect concentration of EE2 and BPS were lower than 2 ng/L and 1 μg/L, which were below or equal to the values reported for other species, demonstrating that caudal fin Vtg was highly sensitive to estrogenic chemicals. Therefore, caudal fins of guppies are suggested as alternative samples for Vtg biomarker detection.
Lumican delays melanoma growth in mice and drives tumor molecular assembly as well as response to matrix-targeted TAX2 therapeutic peptide
Authors: Jeanne Albin , Untereiner Valérie , Perreau Corinne , Proult Isabelle , Gobinet Cyril , Boulagnon-Rombi Camille , Terryn Christine , Martiny Laurent , Brézillon Stéphane , Dedieu Stéphane 
Published: August 2017

AbstractLumican is a small leucine-rich proteoglycan (SLRP) being known as a key regulator of collagen fibrillogenesis. However, little attention has been given so far in studying its influence on tumor-associated matrix architecture. Here, we investigate the role of host lumican on tumor matrix organization as well as on disease progression considering an immunocompetent model of melanoma implanted in Lum−/−vs. wild type syngeneic mice. Conjointly, lumican impact on tumor response to matrix-targeted therapy was evaluated considering a previously validated peptide, namely TAX2, that targets matricellular thrombospondin-1. Analysis of available genomics and proteomics databases for melanoma first established a correlation between lumican expression and patient outcome. In the B16 melanoma allograft model, endogenous lumican inhibits tumor growth and modulates response to TAX2 peptide. Indeed, IHC analyses revealed that lumican deficiency impacts intratumoral distribution of matricellular proteins, growth factor and stromal cells. Besides, innovative imaging approaches helped demonstrating that lumican host expression drives biochemical heterogeneity of s.c. tumors, while modulating intratumoral collagen deposition as well as organization. Altogether, the results obtained present lumican as a strong endogenous inhibitor of tumor growth, while identifying for the first time this proteoglycan as a major driver of tumor matrix coherent assembly.
TGFβ signaling is associated with changes in inflammatory gene expression and perineuronal net degradation around inhibitory neurons following various neurological insults
Authors: Kim Soo Young , Senatorov Vladimir V. , Morrissey Christapher S. , Lippmann Kristina , Vazquez Oscar , Milikovsky Dan Z. , Gu Feng , Parada Isabel , Prince David A. , Becker Albert J. , Heinemann Uwe , Friedman Alon , Kaufer Daniela 
Published: August 2017

AbstractBrain damage due to stroke or traumatic brain injury (TBI), both leading causes of serious long-term disability, often leads to the development of epilepsy. Patients who develop post-injury epilepsy tend to have poor functional outcomes. Emerging evidence highlights a potential role for blood-brain barrier (BBB) dysfunction in the development of post-injury epilepsy. However, common mechanisms underlying the pathological hyperexcitability are largely unknown. Here, we show that comparative transcriptome analyses predict remodeling of extracellular matrix (ECM) as a common response to different types of injuries. ECM-related transcriptional changes were induced by the serum protein albumin via TGFβ signaling in primary astrocytes. In accordance with transcriptional responses, we found persistent degradation of protective ECM structures called perineuronal nets (PNNs) around fast-spiking inhibitory interneurons, in a rat model of TBI as well as in brains of human epileptic patients. Exposure of a naïve brain to albumin was sufficient to induce the transcriptional and translational upregulation of molecules related to ECM remodeling and the persistent breakdown of PNNs around fast-spiking inhibitory interneurons, which was contingent on TGFβ signaling activation. Our findings provide insights on how albumin extravasation that occurs upon BBB dysfunction in various brain injuries can predispose neural circuitry to the development of chronic inhibition deficits.
Polymertropism of rod-shaped bacteria: movement along aligned polysaccharide fibers
Authors: Lemon David J. , Yang Xingbo , Srivastava Pragya , Luk Yan-Yeung , Garza Anthony G. 
Published: August 2017

AbstractIn nature, bacteria often live in surface-associated communities known as biofilms. Biofilm-forming bacteria typically deposit a layer of polysaccharide on the surfaces they inhabit; hence, polysaccharide is their immediate environment on many surfaces. In this study, we examined how the physical characteristics of polysaccharide substrates influence the behavior of the biofilm-forming bacterium Myxococcus xanthus. M. xanthus responds to the compression-induced deformation of polysaccharide substrates by preferentially spreading across the surface perpendicular to the axis of compression. Our results suggest that M. xanthus is not responding to the water that accumulates on the surface of the polysaccharide substrate after compression or to compression-induced changes in surface topography such as the formation of troughs. These directed surface movements do, however, consistently match the orientation of the long axes of aligned and tightly packed polysaccharide fibers in compressed substrates, as indicated by behavioral, birefringence and small angle X-ray scattering analyses. Therefore, we suggest that the directed movements are a response to the physical arrangement of the polymers in the substrate and refer to the directed movements as polymertropism. This behavior might be a common property of bacteria, as many biofilm-forming bacteria that are rod-shaped and motile on soft surfaces exhibit polymertropism.
Rapid decline in pH of coral calcification fluid due to incorporation of anthropogenic CO2
Authors: Kubota Kaoru , Yokoyama Yusuke , Ishikawa Tsuyoshi , Suzuki Atsushi , Ishii Masao 
Published: August 2017

AbstractMarine calcifying organisms, such as stony corals, are under threat by rapid ocean acidification (OA) arising from the oceanic uptake of anthropogenic CO2. To better understand how organisms and ecosystems will adapt to or be damaged by the resulting environmental changes, field observations are crucial. Here, we show clear evidence, based on boron isotopic ratio (δ11B) measurements, that OA is affecting the pH of the calcification fluid (pHCF) in Porites corals within the western North Pacific Subtropical Gyre at two separate locations, Chichijima Island (Ogasawara Archipelago) and Kikaijima Island. Corals from each location have displayed a rapid decline in δ11B since 1960. A comparison with the pH of the ambient seawater (pHSW) near these islands, estimated from a large number of shipboard measurements of seawater CO2 chemistry and atmospheric CO2, indicates that pHCF is sensitive to changes in pHSW. This suggests that the calcification fluid of corals will become less supersaturated with respect to aragonite by the middle of this century (pHCF = ~8.3 when pHSW = ~8.0 in 2050), earlier than previously expected, despite the pHCF-upregulating mechanism of corals.
A pooled mutational analysis identifies ionizing radiation-associated mutational signatures conserved between mouse and human malignancies
Authors: Davidson Philip R. , Sherborne Amy L. , Taylor Barry , Nakamura Alice O. , Nakamura Jean L. 
Published: August 2017

AbstractSingle nucleotide variants (SNVs) identified in cancer genomes can be de-convolved using non-negative matrix factorization (NMF) into discrete trinucleotide-based mutational signatures indicative of specific cancer-causing processes. The stability of NMF-generated mutational signatures depends upon the numbers of variants available for analysis. In this work, we sought to assess whether data from well-controlled mouse models can compensate for scarce human data for some cancer types. High quality sequencing data from radiotherapy-induced cancers is particularly scarce and the mutational processes defining ionizing radiation (IR)-induced mutagenesis in vivo are poorly defined. Here, we combine sequencing data from mouse models of IR-induced malignancies and human IR-induced malignancies. To determine whether the signatures identified from IR-exposed subjects can be differentiated from other mutagenic signatures, we included data from an ultraviolet radiation (UV)-induced human skin cancer and from a mouse model of urethane-induced cancers. NMF distinguished all three mutagens and in the pooled analysis IR was associated with mutational signatures common to both species. These findings illustrate the utility of pooled analysis of mouse and human sequencing data.
Impaired lymphocyte trafficking in mice deficient in the kinase activity of PKN1
Authors: Mashud Rana , Nomachi Akira , Hayakawa Akihide , Kubouchi Koji , Danno Sally , Hirata Takako , Matsuo Kazuhiko , Nakayama Takashi , Satoh Ryosuke , Sugiura Reiko , Abe Manabu , Sakimura Kenji , Wakana Shigeharu , Ohsaki Hiroyuki , Kamoshida Shingo , Mukai Hideyuki 
Published: August 2017

AbstractKnock-in mice lacking PKN1 kinase activity were generated by introducing a T778A point mutation in the catalytic domain. PKN1[T778A] mutant mice developed to adulthood without apparent external abnormalities, but exhibited lower T and B lymphocyte counts in the peripheral blood than those of wild-type (WT) mice. T and B cell development proceeded in an apparently normal fashion in bone marrow and thymus of PKN1[T778A] mice, however, the number of T and B cell counts were significantly higher in the lymph nodes and spleen of mutant mice in those of WT mice. After transfusion into WT recipients, EGFP-labelled PKN1[T778A] donor lymphocytes were significantly less abundant in the peripheral circulation and more abundant in the spleen and lymph nodes of recipient mice compared with EGFP-labelled WT donor lymphocytes, likely reflecting lymphocyte sequestration in the spleen and lymph nodes in a cell-autonomous fashion. PKN1[T778A] lymphocytes showed significantly lower chemotaxis towards chemokines and sphingosine 1-phosphate (S1P) than WT cellsin vitro. The biggest migration defect was observed in response to S1P, which is essential for lymphocyte egress from secondary lymphoid organs. These results reveal a novel role of PKN1 in lymphocyte migration and localization.
External amplitude and frequency modulation of a terahertz quantum cascade laser using metamaterial/graphene devices
Authors: Kindness S. J. , Jessop D. S. , Wei B. , Wallis R. , Kamboj V. S. , Xiao L. , Ren Y. , Braeuninger-Weimer P. , Aria A. I. , Hofmann S. , Beere H. E. , Ritchie D. A. , Degl’Innocenti R. 
Published: August 2017

AbstractActive control of the amplitude and frequency of terahertz sources is an essential prerequisite for exploiting a myriad of terahertz applications in imaging, spectroscopy, and communications. Here we present a optoelectronic, external modulation technique applied to a terahertz quantum cascade laser which holds the promise of addressing a number of important challenges in this research area. A hybrid metamaterial/graphene device is implemented into an external cavity set-up allowing for optoelectronic tuning of feedback into a quantum cascade laser. We demonstrate powerful, all-electronic, control over the amplitude and frequency of the laser output. Full laser switching is performed by electrostatic gating of the metamaterial/graphene device, demonstrating a modulation depth of 100%. External control of the emission spectrum is also achieved, highlighting the flexibility of this feedback method. By taking advantage of the frequency dispersive reflectivity of the metamaterial array, different modes of the QCL output are selectively suppressed using lithographic tuning and single mode operation of the multi-mode laser is enforced. Side mode suppression is electrically modulated from ~6 dB to ~21 dB, demonstrating active, optoelectronic modulation of the laser frequency content between multi-mode and single mode operation.
Up-regulation of BRCA1-associated RING Domain 1 Promotes Hepatocellular Carcinoma Progression by Targeting Akt Signaling
Authors: Liao Yan , Yuan Shengguang , Chen Xinhuang , Zhu Pengpeng , Li Jun , Qin Liling , Liao Weijia 
Published: August 2017

AbstractThe present study was designed to investigate the potential clinical, pathological, prognostic value, role and mechanism of BRCA1-associated RING Domain 1 (BARD1) in Hepatocellular carcinoma (HCC). Quantitative real-time PCR and immunohistochemistry were performed to evaluate the expression of BARD1 mRNA and protein. The expression of BARD1 in the HCC tissue samples was markedly higher than that in the adjacent noncancerous liver tissues. Elevated BARD1 expression was positively correlated with tumor-node-metastasis stage, Barcelona-Clinic Liver Cancer stage, hepatitis B surface antigen, large tumor size, serum alpha-fetoprotein levels, and serum aspartate aminotransferase levels. Univariate and multivariate analyses revealed the BARD1 was an independent predictor for decreased progression-free survival and overall survival in HCC. In vitro experiments demonstrated that knocking down BARD1 significantly inhibited the proliferation, invasion and migration of HCC cells. Moreover, silencing BARD1 inhibit the signaling pathway via decreased the levels of Akt, mTOR, and MMP-9 and inhibited the phosphorylation of Akt (Ser473) and mTOR (Ser2248). Collectively, our findings suggest that BARD1 may be a novel diagnostic and prognostic biomarker of HCC, and up-regulation of BARD1 can contribute to HCC progression by targeting Akt signaling.
Influence of Latent Heating over the Asian and Western Pacific Monsoon Region on Sahel Summer Rainfall
Authors: He Shan , Yang Song , Li Zhenning 
Published: August 2017

AbstractThere has been an interdecadal shift towards a less humid state in Sahel summer rainfall since the 1960s. The decreased Sahel summer rainfall was associated with enhanced summer latent heating over the South Asian and western Pacific summer monsoon region and anomalous zonal-vertical cell of the Asian summer monsoon circulation, indicating that the latent heating plays a significant role in the change in Sahel rainfall. The effects of the latent heating over different monsoon domains on the Sahel rainfall are investigated through several model experiments. Results show that the remote monsoon heating mainly affects Sahel rainfall by generating changes in the zonal-vertical atmospheric circulation.
The miR-183 family cluster alters zinc homeostasis in benign prostate cells, organoids and prostate cancer xenografts
Authors: Dambal Shweta , Baumann Bethany , McCray Tara , Williams LaTanya , Richards Zachary , Deaton Ryan , Prins Gail S. , Nonn Larisa 
Published: August 2017

AbstractThe miR-183 cluster, which is comprised of paralogous miRs-183, -96 and -182, is overexpressed in many cancers, including prostate adenocarcinoma (PCa). Prior studies showed that overexpression of individual pre-miRs-182, -96 and -183 in prostate cells decreased zinc import, which is a characteristic feature of PCa tumours. Zinc is concentrated in healthy prostate 10-fold higher than any other tissue, and an >80% decrease in zinc is observed in PCa specimens. Here, we studied the effect of overexpression of the entire 4.8 kb miR-183 family cluster, including the intergenic region which contains highly conserved genomic regions, in prostate cells. This resulted in overexpression of mature miR-183 family miRs at levels that mimic cancer-related changes. Overexpression of the miR-183 cluster reduced zinc transporter and intracellular zinc levels in benign prostate cells, PCa xenografts and fresh prostate epithelial organoids. Microarray analysis of miR-183 family cluster overexpression in prostate cells showed an enrichment for cancer-related pathways including adhesion, migration and wound healing. An active secondary transcription start site was identified within the intergenic region of the miR-183 cluster, which may regulate expression of miR-182. Taken together, this study shows that physiologically relevant expression of the miR-183 family regulates zinc levels and carcinogenic pathways in prostate cells.
Proximity-effect-induced Superconducting Gap in Topological Surface States – A Point Contact Spectroscopy Study of NbSe2/Bi2Se3 Superconductor-Topological Insulator Heterostructures
Authors: Dai Wenqing , Richardella Anthony , Du Renzhong , Zhao Weiwei , Liu Xin , Liu C. X. , Huang Song-Hsun , Sankar Raman , Chou Fangcheng , Samarth Nitin , Li Qi 
Published: August 2017

AbstractProximity-effect-induced superconductivity was studied in epitaxial topological insulator Bi2Se3 thin films grown on superconducting NbSe2 single crystals. A point contact spectroscopy (PCS) method was used at low temperatures down to 40 mK. An induced superconducting gap in Bi2Se3 was observed in the spectra, which decreased with increasing Bi2Se3 layer thickness, consistent with the proximity effect in the bulk states of Bi2Se3 induced by NbSe2. At very low temperatures, an extra point contact feature which may correspond to a second energy gap appeared in the spectrum. For a 16 quintuple layer Bi2Se3 on NbSe2 sample, the bulk state gap value near the top surface is ~159 μeV, while the second gap value is ~120 μeV at 40 mK. The second gap value decreased with increasing Bi2Se3 layer thickness, but the ratio between the second gap and the bulk state gap remained about the same for different Bi2Se3 thicknesses. It is plausible that this is due to superconductivity in Bi2Se3 topological surface states induced through the bulk states. The two induced gaps in the PCS measurement are consistent with the three-dimensional bulk state and the two-dimensional surface state superconducting gaps observed in the angle-resolved photoemission spectroscopy (ARPES) measurement.
Transmission is a Noticeable Cause of Resistance Among Treated Tuberculosis Patients in Shanghai, China
Authors: Nsofor Chijioke A. , Jiang Qi , Wu Jie , Gan Mingyu , Liu Qingyun , Zuo Tianyu , Zhu Guofeng , Gao Qian 
Published: August 2017

AbstractIt is generally believed that drug resistance among treated tuberculosis (TB) patients is as a result of acquired drug resistance due to inappropriate treatment. Previous studies have shown that primary drug resistance caused by transmission also plays a role among treated cases. Differentiating the two types of drug resistance will help in developing appropriate strategies for control of drug resistant tuberculosis. In this study, we tested the hypothesis that drug resistance among treated TB patients is mainly caused by primary resistance rather than acquired resistance. Defining resistance profiles by molecular drug susceptibility test, we used Unit Variable Number Tandem Repeats (VNTR) to genotype and Whole Genome Sequencing (WGS) to confirm the accordance of the first and last Mycobacterium tuberculosis isolates from treated pulmonary TB patients in Shanghai from 2009–2015. Among 81 patients with increasing drug resistance, out of 390 patients enrolled, paired isolates from 59.3% (48/81) had different VNTR patterns indicating primary drug resistance. Our results have demonstrated that primary resistance due to exogenous reinfection is the major cause of drug resistance among treated TB patients in Shanghai; thus, strategies aimed at preventing and interrupting transmission are urgently needed to effectively reduce the epidemic of drug resistant tuberculosis.