bluuebunny/crossref_metadata_2025_split huggingface dataset:
The Planck Catalogue of Galactic Cold Clumps : PGCC
Authors: Montier L. 
Published: September 2016

AbstractThe Planck satellite has provided an unprecedented view of the submm sky, allowing us to search for the dust emission of Galactic cold sources. Combining Planck-HFI all-sky maps in the high frequency channels with the IRAS map at 100um, we built the Planck catalogue of Galactic Cold Clumps (PGCC, Planck 2015 results. XXVIII), counting 13188 sources distributed over the whole sky, and following mainly the Galactic structures at low and intermediate latitudes. This is the first all-sky catalogue of Galactic cold sources obtained with a single instrument at this resolution and sensitivity, which opens a new window on star-formation processes in our Galaxy.
Nobeyama 45m CO Galactic Plane Survey: Filament properties and star formation in M17
Authors: Nishimura Atsushi , Umemoto Tomofumi , Minamidani Tetsuhiro , Kuno Nario , Tosaki Tomoka , Fujita Shinji , Matsuo Mitsuhiro , Tsuda Yuya , Ohashi Satoshi ,   NRO-GPS team
Published: September 2016

AbstractWe present the 12CO J=1–0, 13CO J=1–0, and C18O J=1–0 maps of the M17 giant molecular clouds (GMCs) obtained as a part of the Nobeyama 45m CO Galactic Plane Survey. The observations cover the entire area of M17 SW and M17 N clouds at an angular resolution of ~ 15″ which corresponds to ~ 0.15 pc. We found that the N cloud consists of a couple of twisted filaments, they are extended in parallel toward the Hii region. The typicall width of the filaments is ~0.5 pc in 13CO intensity map. Most of young stellar objects (YSOs) are located on the filaments which have a bright rim structure in 8μm at the filament edge facing the Hii region. Furthermore, the time scale of the YSOs formation on the bright rim is comparable with that of NGC 6618 cluster which provides UV photons for the region. This fact indicates that the cluster triggered to form YSOs in N cloud. We also investigated the geometry of the Hii region and GMCs by comparing spatial distribution of 12CO velocity channel map and infrared dark cloud, and then found that NGC 6618 is possibly formed by the cloud cloud colision.
Massive pre-main sequence stars in M17
Authors: Ramirez-Tannus Maria C. , Kaper Lex , Ochsendorf Bram B. , Ellerbroek Lucas E. 
Published: September 2016

AbstractWe have obtained optical to near-infrared (300-2500 nm) VLT/X-shooter spectra of six candidate mYSOs, deeply embedded in the massive star forming region M17. These mYSO candidates have been identified based on their infrared excess and spectral features (double-peaked emission lines, CO band-head emission) indicating the presence of a disk (Hanson et al. 1997). In most cases, we detect a photospheric spectrum allowing us to measure the physical properties of the mYSOs and to confirm their PMS nature.
Mid-Infrared Enhanced Lenticulars caught in the dusty midst of transformation in the Coma Cluster
Authors: Riguccini Laurie , Temi Pasquale , Amblard Alexandre , Fanelli Michael 
Published: September 2016

AbstractWe explore the properties of early-type galaxies (ETGs) in rich environments such as clusters of galaxies. The L24/LK distribution of ETGs in both Virgo and Coma clusters shows that some lenticulars (S0, 10 in Coma and 3 in Virgo) have a much larger L24/LK ratio (0.5 to ~2 dex) than the bulk of the ETG population. We call these sources Mid-Infrared Enhanced Galaxies (MIEGs). In Coma, they are mostly located in the South-West part of the cluster where a substructure is falling onto the main cluster. MIEGs present lower g-r color than the rest of the ETGs, because of a blue continuum. We interpret the excess L24/LK ratio as evidence for an enhanced star-formation induced as a consequence of their infall into the main cluster.
SFR and Abundances of Nearby Galaxies
Authors: Takamiya Marianne , Berke Daniel , Bremer Forrest , Jones Casey , Poquet Guillaume 
Published: September 2016

AbstractWe present star formation rates and nebular abundances of 59 different star-forming regions in 16 nearby galaxies. The star-forming regions were selected to be bright in Hα and were observed with the SNIFS integral field spectrograph on the UH 2.2m telescope. The spectra span the wavelength range between 3200Å and 1μm. We find that the local star formation rates depend on the local abundances in that low SFRs show a dependence but high SFR appear insensitive to it.
Atlas of low-mass young stellar object disks from mid-infrared interferometry
Authors: Varga J. , Ábrahám P. , Ratzka Th. , Menu J. , Gabányi K. , Kóspál Á. , van Boekel R. , Mosoni L. , Henning Th. 
Published: September 2016

AbstractWe present our approach of visibility modeling of disks around low-mass (< 2 M⊙) young stellar objects (YSOs). We compiled an atlas based on mid-infrared interferometric observations from the MIDI instrument at the VLTI. We use three different models to fit the data. These models allow us to determine overall sizes (and the extent of the inner gaps) of the modeled circumstellar disks.
Herschel Footprint Database and Service
Authors: Varga-Verebélyi E. , Dobos L. , Budavári T. , Kiss Cs. 
Published: September 2016

AbstractWe created the Herschel1 Footprint Database and web services for the Herschel Space Observatory imaging data. For this database we set up a unified data model for the PACS and SPIRE Herschel instruments, from the pointing and header information of each observation, generated and stored sky coverages (footprints) of the observations in their exact geometric form. With this tool we extend the capabilities of the Herschel Science Archive by providing an effective search tool that is able to find observations for selected sky locations (objects), or even in larger areas in the sky.
How surface density of galaxy disks affects metallicity? Outflow and Accretion
Authors: Wu Po-Feng , Kudritzki Rolf-Peter , Tully R. Brent , Neill J. D. 
Published: September 2016

AbstractIn this study, we examine the effect of surface density of disks on chemical evolution of galaxies. We find that, higher surface brightness galaxies on average possess higher gas-phase metallicity compared to lower surface brightness galaxies with the same stellar and gas mass. The surface brightness effect is more significant for low-mass galaxies. Using an analytical model of chemical evolution involving gas outflow and accretion, we find that the surface brightness dependence can be attributed to the strength of inflowing pristine gas. Galaxies with lower surface brightness experience stronger inflow than galaxies with a higher surface brightness of a similar mass.
Proteolytic inactivation of nuclear alarmin high-mobility group box 1 by complement protease C1s during apoptosis
Authors: Yeo J G , Leong J , Arkachaisri T , Cai Y , Teo B H D , Tan J H T , Das L , Lu J 
Published: September 2016

AbstractEffective clearance of apoptotic cells by phagocytes prevents the release of intracellular alarmins and manifestation of autoimmunity. This prompt efferocytosis is complemented by intracellular proteolytic degradation that occurs within the apoptotic cells and in the efferosome of the phagocytes. Although the role of extracellular proteases in apoptotic cells clearance is unknown, the strong association of congenital C1s deficiency with Systemic Lupus Erythematosus highlights the protective nature that this extracellular protease has against autoimmunity. The archetypical role of serine protease C1s as the catalytic arm of C1 complex (C1qC1r2C1s2) involve in the propagation of the classical complement pathway could not provide the biological basis for this association. However, a recent observation of the ability of C1 complex to cleave a spectrum of intracellular cryptic targets exposed during apoptosis provides a valuable insight to the underlying protective mechanism. High-mobility group box 1 (HMGB1), an intracellular alarmin that is capable of inducing the formation of antinuclear autoantibodies and causes lupus-like conditions in mice, is identified as a novel potential target by bioinformatics analysis. This is verified experimentally with C1s, both in its purified and physiological form as C1 complex, cleaving HMGB1 into defined fragments of 19 and 12 kDa. This cleavage diminishes HMGB1 ability to enhance lipopolysaccharide mediated pro-inflammatory cytokines production from monocytes, macrophages and dendritic cells. Further mass spectrometric analysis of the C1 complex treated apoptotic cellular proteins demonstrated additional C1s substrates and revealed the complementary role of C1s in apoptotic cells clearance through the proteolytic cleavage of intracellular alarmins and autoantigens. C1 complex may have evolved as, besides the bacteriolytic arm of antibodies in which it activates the complement cascade, a tissue renewal mechanism that reduces the immunogenicity of apoptotic tissue debris and decreases the likelihood of autoimmunity.
ZEB1 induces EPB41L5 in the cancer mesenchymal program that drives ARF6-based invasion, metastasis and drug resistance
Authors: Hashimoto A , Hashimoto S , Sugino H , Yoshikawa A , Onodera Y , Handa H , Oikawa T , Sabe H 
Published: September 2016

AbstractOnset of the cancer mesenchymal program is closely associated with cancer malignancy and drug resistance. Among the different epithelial–mesenchymal transition (EMT)-associated transcriptional factors, ZEB1 has a key role in inducing the mesenchymal phenotypes and stem cell-like properties of different breast cancer cells. ARF6 and its effector AMAP1 are frequently overexpressed in breast cancer cells, and promote invasion, metastasis and drug resistance. EPB41L5 is induced during EMT, and mediates the disruption of E-cadherin-based cell–cell adhesion and the promotion of focal adhesion dynamics. Here we show that EPB41L5 is an integral component of the ARF6-based pathway, which is induced by ZEB1. We found that EPB41L5 is expressed at high levels in malignant breast cancer cells and binds to AMAP1. ZEB1 induced EPB41L5 both in cancer cells and normal cells. This relationship was recaptured with The Cancer Genome Atlas RNASeq data set, and correlated with the poor outcome of the patients. In contrast, diversified events, such as tumor growth factor β1 stimulation, expression of SNAI1 and TP53 mutation, can each cause the induction of ZEB1 and EPB41L5, depending on the cellular context. Our results demonstrated that the ZEB1-EPB41L5 axis is at the core of the cancer mesenchymal program that drives ARF6-based invasion, metastasis and drug resistance of significant populations of primary breast cancers, and is tightly correlated with the poor outcomes of patients.
Sequence variation between 462 human individuals fine-tunes functional sites of RNA processing
Authors: Ferreira Pedro G. , Oti Martin , Barann Matthias , Wieland Thomas , Ezquina Suzana , Friedländer Marc R. , Rivas Manuel A. , Esteve-Codina Anna ,   The GEUVADIS Consortium, Estivill Xavier , Guigó Roderic , Dermitzakis Emmanouil , Antonarakis Stylianos , Meitinger Thomas , Strom Tim M , Palotie Aarno , François Deleuze Jean , Sudbrak Ralf , Lerach Hans , Gut Ivo , Syvänen Ann-Christine , Gyllensten Ulf , Schreiber Stefan , Rosenstiel Philip , Brunner Han , Veltman Joris , Hoen Peter A.C.T , Jan van Ommen Gert , Carracedo Angel , Brazma Alvis , Flicek Paul , Cambon-Thomsen Anne , Mangion Jonathan , Bentley David , Hamosh Ada , Rosenstiel Philip , Strom Tim M , Lappalainen Tuuli , Guigó Roderic , Sammeth Michael 
Published: September 2016

AbstractRecent advances in the cost-efficiency of sequencing technologies enabled the combined DNA- and RNA-sequencing of human individuals at the population-scale, making genome-wide investigations of the inter-individual genetic impact on gene expression viable. Employing mRNA-sequencing data from the Geuvadis Project and genome sequencing data from the 1000 Genomes Project we show that the computational analysis of DNA sequences around splice sites and poly-A signals is able to explain several observations in the phenotype data. In contrast to widespread assessments of statistically significant associations between DNA polymorphisms and quantitative traits, we developed a computational tool to pinpoint the molecular mechanisms by which genetic markers drive variation in RNA-processing, cataloguing and classifying alleles that change the affinity of core RNA elements to their recognizing factors. The in silico models we employ further suggest RNA editing can moonlight as a splicing-modulator, albeit less frequently than genomic sequence diversity. Beyond existing annotations, we demonstrate that the ultra-high resolution of RNA-Seq combined from 462 individuals also provides evidence for thousands of bona fide novel elements of RNA processing—alternative splice sites, introns and cleavage sites—which are often rare and lowly expressed but in other characteristics similar to their annotated counterparts.
Local and Circulating Endothelial Cells Undergo Endothelial to Mesenchymal Transition (EndMT) in Response to Musculoskeletal Injury
Authors: Agarwal Shailesh , Loder Shawn , Cholok David , Peterson Joshua , Li John , Fireman David , Breuler Christopher , Hsieh Hsiao Sung , Ranganathan Kavitha , Hwang Charles , Drake James , Li Shuli , Chan Charles K. , Longaker Michael T. , Levi Benjamin 
Published: September 2016

AbstractEndothelial-to-mesenchymal transition (EndMT) has been implicated in a variety of aberrant wound healing conditions. However, unambiguous evidence of EndMT has been elusive due to limitations of in vitro experimental designs and animal models. In vitro experiments cannot account for the myriad ligands and cells which regulate differentiation and in vivo tissue injury models may induce lineage-independent endothelial marker expression in mesenchymal cells. By using an inducible Cre model to mark mesenchymal cells (Scx-creERT/tdTomato + ) prior to injury, we demonstrate that musculoskeletal injury induces expression of CD31, VeCadherin, or Tie2 in mesenchymal cells. VeCadherin and Tie2 were expressed in non-endothelial cells (CD31−) present in marrow from uninjured adult mice, thereby limiting the specificity of these markers in inducible models (e.g. VeCadherin- or Tie2-creERT). However, cell transplantation assays confirmed that endothelial cells (ΔVeCadherin/CD31+/CD45−) isolated from uninjured hindlimb muscle tissue undergo in vivo EndMT when transplanted directly into the wound without intervening cell culture using PDGFRα, Osterix (OSX), SOX9 and Aggrecan (ACAN) as mesenchymal markers. These in vivo findings support EndMT in the presence of myriad ligands and cell types, using cell transplantation assays which can be applied for other pathologies implicated in EndMT including tissue fibrosis and atherosclerosis. Additionally, endothelial cell recruitment and trafficking are potential therapeutic targets to prevent EndMT.
Common variants of HTR3 genes are associated with obsessive-compulsive disorder and its phenotypic expression
Authors: Kim Hae Won , Kang Jee In , Lee Sang-Hyuk , An Suk Kyoon , Sohn Sung Yun , Hwang Eun Hee , Lee Su Young , Kim Se Joo 
Published: September 2016

AbstractEvidence from literature supports the existence of associations between serotonin-related genetic variants and obsessive-compulsive disorder (OCD), but few studies have explored the involvement of serotonin receptor type 3 genes (HTR3) in OCD. To identify whetherHTR3variability affects an individual’s susceptibility to OCD, we examined 10HTR3variants in 596 individuals with OCD and 599 controls. A significant difference existed in the genotypic distribution of theHTR3Bvariant rs1176744 between individuals with OCD and controls (odds ratio [OR] = 0.74, 95% confidence interval [CI] = 0.60–0.91,P = 0.0043). A protective haplotype inHTR3Bwas also associated with OCD (OR = 0.77, CI = 0.63–0.95, permutatedP = 0.0179). Analyses of OCD sub-phenotypes demonstrated significant associations between rs3758987 and early onset OCD in male subjects (OR = 0.49, CI = 0.31–0.79,P = 0.0031) and among rs6766410, rs6443930, and the cleaning dimension in female subjects (OR = 0.36, CI = 0.18–0.69,P = 0.0016 and OR = 0.47, CI = 0.29–0.79,P = 0.0030, respectively). Additionally, rs6766410 was related to contamination-based disgust in OCD (P = 0.0044). These results support that commonHTR3variants are involved in OCD and some of its clinical phenotypes.
Optimal search patterns in honeybee orientation flights are robust against emerging infectious diseases
Authors: Wolf Stephan , Nicholls Elizabeth , Reynolds Andrew M. , Wells Patricia , Lim Ka S. , Paxton Robert J. , Osborne Juliet L. 
Published: September 2016

AbstractLévy flights are scale-free (fractal) search patterns found in a wide range of animals. They can be an advantageous strategy promoting high encounter rates with rare cues that may indicate prey items, mating partners or navigational landmarks. The robustness of this behavioural strategy to ubiquitous threats to animal performance, such as pathogens, remains poorly understood. Using honeybees radar-tracked during their orientation flights in a novel landscape, we assess for the first time how two emerging infectious diseases (Nosema sp. and the Varroa-associated Deformed wing virus (DWV)) affect bees’ behavioural performance and search strategy. Nosema infection, unlike DWV, affected the spatial scale of orientation flights, causing significantly shorter and more compact flights. However, in stark contrast to disease-dependent temporal fractals, we find the same prevalence of optimal Lévy flight characteristics (μ ≈ 2) in both healthy and infected bees. We discuss the ecological and evolutionary implications of these surprising insights, arguing that Lévy search patterns are an emergent property of fundamental characteristics of neuronal and sensory components of the decision-making process, making them robust against diverse physiological effects of pathogen infection and possibly other stressors.
Sustained elevation of NF-κB activity sensitizes offspring of maternal inflammation to hypertension via impairing PGC-1α recovery
Authors: Deng Yafei , Zhang Qi , Luo Hongqin , Chen Xianhua , Han Qi , Wang Fangjie , Huang Pei , Lai Wenjing , Guan Xiao , Pan Xiaodong , Ji Yan , Guo Wei , Che Ling , Tang Yuan , Gu Liangqi , Yu Jianhua , Namaka Michael , Deng Youcai , Li Xiaohui 
Published: September 2016

AbstractGrowing evidence has demonstrated that maternal detrimental factors, including inflammation, contribute to the development of hypertension in the offspring. The current study found that offspring subjected to prenatal exposure of inflammation by lipopolysaccharide (LPS) challenge during the second semester showed significantly increased systolic blood pressure. In addition, these offspring also displayed augmented vascular damage and reactive oxygen species (ROS) levels in thoracic aortas when challenged with deoxycorticosterone acetate and high-salt diet (DOCA-salt). Interestingly, the antioxidant N-acetyl-L-cysteine markedly reversed these changes. Mechanistically, prenatal LPS exposure led to pre-existing elevated peroxisome proliferators-activated receptor-γ co-activator (PGC)-1α, a critical master of ROS metabolism, which up-regulated the ROS defense capacity and maintained the balance of ROS generation and elimination under resting state. However, continued elevation of NF-κB activity significantly suppressed the rapid recovery of PGC-1α expression response to DOCA-salt challenge in offspring that underwent prenatal inflammatory stimulation. This was further confirmed by using a NF-κB inhibitor (N-p-Tosyl-L-phenylalanine chloromethyl ketone) that restored PGC-1α recovery and prevented blood pressure elevation induced by DOCA-salt. Our results suggest that maternal inflammation programmed proneness to NF-κB over-activation which impaired PGC-1α-mediated anti-oxidant capacity resulting in the increased sensitivity of offspring to hypertensive damage.
Interaction between isoprene and ozone fluxes in a poplar plantation and its impact on air quality at the European level
Authors: Zenone Terenzio , Hendriks Carlijn , Brilli Federico , Fransen Erik , Gioli Beniamio , Portillo-Estrada Miguel , Schaap Martijn , Ceulemans Reinhart 
Published: September 2016

AbstractThe emission of isoprene and other biogenic volatile organic compounds from vegetation plays an important role in tropospheric ozone (O3) formation. The potentially large expansion of isoprene emitting species (e.g., poplars) for bioenergy production might, therefore, impact tropospheric O3 formation. Using the eddy covariance technique we have simultaneously measured fluxes isoprene, O3 and of CO2 from a poplar (Populus) plantation grown for bioenergy production. We used the chemistry transport model LOTOS-EUROS to scale-up the isoprene emissions associated with the existing poplar plantations in Europe, and we assessed the impact of isoprene fluxes on ground level O3 concentrations. Our findings suggest that isoprene emissions from existing poplar-for-bioenergy plantations do not significantly affect the ground level of O3 concentration. Indeed the overall land in Europe covered with poplar plantations has not significantly changed over the last two decades despite policy incentives to produce bioenergy crops. The current surface area of isoprene emitting poplars-for-bioenergy remains too limited to significantly enhance O3 concentrations and thus to be considered a potential threat for air quality and human health.
Delayed Propionibacterium acnes surgical site infections occur only in the presence of an implant
Authors: Shiono Yuta , Ishii Ken , Nagai Shigenori , Kakinuma Hiroaki , Sasaki Aya , Funao Haruki , Kuramoto Tetsuya , Yoshioka Kenji , Ishihama Hiroko , Isogai Norihiro , Takeshima Kenichiro , Tsuji Takashi , Okada Yasunori , Koyasu Shigeo , Nakamura Masaya , Toyama Yoshiaki , Aizawa Mamoru , Matsumoto Morio 
Published: September 2016

AbstractWhether Propionibacterium acnes (P. acnes) causes surgical-site infections (SSI) after orthopedic surgery is controversial. We previously reported that we frequently find P. acnes in intraoperative specimens, yet none of the patients have clinically apparent infections. Here, we tracked P. acnes for 6 months in a mouse osteomyelitis model. We inoculated P. acnes with an implant into the mouse femur in the implant group; the control group was treated with the bacteria but no implant. We then observed over a 6-month period using optical imaging system. During the first 2 weeks, bacterial signals were detected in the femur in the both groups. The bacterial signal completely disappeared in the control group within 28 days. Interestingly, in the implant group, bacterial signals were still present 6 months after inoculation. Histological and scanning electron-microscope analyses confirmed that P. acnes was absent from the control group 6 months after inoculation, but in the implant group, the bacteria had survived in a biofilm around the implant. PCR analysis also identified P. acnes in the purulent effusion from the infected femurs in the implant group. To our knowledge, this is the first report showing that P. acnes causes SSI only in the presence of an implant.