bluuebunny/crossref_metadata_2025_split huggingface dataset:
The Mouse Intestinal Bacterial Collection (miBC) provides host-specific insight into cultured diversity and functional potential of the gut microbiota
Authors: Lagkouvardos Ilias , Pukall Rüdiger , Abt Birte , Foesel Bärbel U. , Meier-Kolthoff Jan P. , Kumar Neeraj , Bresciani Anne , Martínez Inés , Just Sarah , Ziegler Caroline , Brugiroux Sandrine , Garzetti Debora , Wenning Mareike , Bui Thi P. N. , Wang Jun , Hugenholtz Floor , Plugge Caroline M. , Peterson Daniel A. , Hornef Mathias W. , Baines John F. , Smidt Hauke , Walter Jens , Kristiansen Karsten , Nielsen Henrik B. , Haller Dirk , Overmann Jörg , Stecher Bärbel , Clavel Thomas 
Published: August 2016

AbstractIntestinal bacteria influence mammalian physiology, but many types of bacteria are still uncharacterized. Moreover, reference strains of mouse gut bacteria are not easily available, although mouse models are extensively used in medical research. These are major limitations for the investigation of intestinal microbiomes and their interactions with diet and host. It is thus important to study in detail the diversity and functions of gut microbiota members, including those colonizing the mouse intestine. To address these issues, we aimed at establishing the Mouse Intestinal Bacterial Collection (miBC), a public repository of bacterial strains and associated genomes from the mouse gut, and studied host-specificity of colonization and sequence-based relevance of the resource. The collection includes several strains representing novel species, genera and even one family. Genomic analyses showed that certain species are specific to the mouse intestine and that a minimal consortium of 18 strains covered 50–75% of the known functional potential of metagenomes. The present work will sustain future research on microbiota–host interactions in health and disease, as it will facilitate targeted colonization and molecular studies. The resource is available at www.dsmz.de/miBC.
Dynamic contrast-enhanced MRI detects acute radiotherapy-induced alterations in mandibular microvasculature: prospective assessment of imaging biomarkers of normal tissue injury
Authors:   Joint Head and Neck Radiotherapy-MRI Development Cooperative, Sandulache Vlad C. , Hobbs Brian P. , Mohamed Abdallah S.R. , Frank Steven J. , Song Juhee , Ding Yao , Ger Rachel , Court Laurence E. , Kalpathy-Cramer Jayashree , Hazle John D. , Wang Jihong , Awan Musaddiq J. , Rosenthal David I. , Garden Adam S. , Gunn G. Brandon , Colen Rivka R. , Elshafeey Nabil , Elbanan Mohamed , Hutcheson Katherine A. , Lewin Jan S. , Chambers Mark S. , Hofstede Theresa M. , Weber Randal S. , Lai Stephen Y. , Fuller Clifton D. 
Published: August 2016

AbstractNormal tissue toxicity is an important consideration in the continued development of more effective external beam radiotherapy (EBRT) regimens for head and neck tumors. The ability to detect EBRT-induced changes in mandibular bone vascularity represents a crucial step in decreasing potential toxicity. To date, no imaging modality has been shown to detect changes in bone vascularity in real time during treatment. Based on our institutional experience with multi-parametric MRI, we hypothesized that DCE-MRI can provide in-treatment information regarding EBRT-induced changes in mandibular vascularity. Thirty-two patients undergoing EBRT treatment for head and neck cancer were prospectively imaged prior to, mid-course and following treatment. DCE-MRI scans were co-registered to dosimetric maps to correlate EBRT dose and change in mandibular bone vascularity as measured by Ktrans and Ve. DCE-MRI was able to detect dose-dependent changes in both Ktrans and Ve in a subset of patients. One patient who developed ORN during the study period demonstrated decreases in Ktrans and Ve following treatment completion. We demonstrate, in a prospective imaging trial, that DCE-MRI can detect dose-dependent alterations in mandibular bone vascularity during chemoradiotherapy, providing biomarkers that are physiological correlates of acute of acute mandibular vascular injury and recovery temporal kinetics.
Imaging human teeth by phosphorus magnetic resonance with nuclear Overhauser enhancement
Authors: Sun Yi , Brauckmann Ole , Nixdorf Donald R. , Kentgens Arno , Garwood Michael , Idiyatullin Djaudat , Heerschap Arend 
Published: August 2016

AbstractThree-dimensional phosphorus MR images (31P MRI) of teeth are obtained at a nominal resolution of 0.5 mm in less than 15 minutes using acquisition pulse sequences sensitive to ultra-short transversal relaxation times. The images directly reflect the spatially resolved phosphorus content of mineral tissue in dentin and enamel; they show a lack of signal from pulp tissue and reduced signal from de-mineralized carious lesions. We demonstrate for the first time that the signal in 31P MR images of mineralized tissue is enhanced by a 1H-31P nuclear Overhauser effect (NOE). Using teeth as a model for imaging mineralized human tissue, graded differences in signal enhancement are observed that correlate well with known mineral content. From solid-state NMR experiments we conclude that the NOE is facilitated by spin diffusion and that the NOE difference can be assigned to a higher water content and a different micro-structure of dentin. Thus, a novel method for imaging mineral content without ionizing radiation is proposed. This method has potential use in the assessment of de-mineralization states in humans, such as caries of teeth and osteoporosis of bones.
Serum metabolomic signatures discriminate early liver inflammation and fibrosis stages in patients with chronic hepatitis B
Authors: Huang Haijun , Sun Zeyu , Pan Hongying , Chen Meijuan , Tong Yongxi , Zhang Jiajie , Chen Deying , Su Xiaoling , Li Lanjuan 
Published: August 2016

AbstractChronic HBV (CHB) infected patients with intermediate necroinflammation and fibrosis are recommended to receive antiviral treatment. However, other than liver biopsy, there is a lack of sensitive and specific objective method to determine the necroinflammation and fibrosis stages in CHB patients. This study aims to identify unique serum metabolomic profile associated with histological progression in CHB patients and to develop novel metabolite biomarker panels for early CHB detection and stratification. A comprehensive metabolomic profiling method was established to compare serum samples collected from health donor (n = 67), patients with mild (G < 2 and S < 2, CHB1, n = 52) or intermediate (G ≥ 2 or S ≥ 2, CHB2, n = 36) necroinflammation and fibrosis. Multivariate models were developed to differentiate CHB1 and CHB2 from controls. A set of CHB-associated biomarkers was identified, including lysophosphatidylcholines, phosphatidylcholines, phosphatidylinositol, phosphatidylserine, and bile acid metabolism products. Stratification of CHB1 and CHB2 patients by a simple logistic index, the PIPSindex, based on phosphatidylinositol (PI) and phosphatidylserine (PS), was achieved with an AUC of 0.961, which outperformed all currently available markers. A panel of serum metabolites that differentiate health control, CHB1 and CHB2 patients has been identified. The proposed metabolomic biosignature has the potential to be used as indicator for antiviral treatment for CHB management.
Regulation of SLD5 gene expression by miR-370 during acute growth of cancer cells
Authors: Yamane Keitaro , Naito Hisamichi , Wakabayashi Taku , Yoshida Hironori , Muramatsu Fumitaka , Iba Tomohiro , Kidoya Hiroyasu , Takakura Nobuyuki 
Published: August 2016

AbstractSLD5 is a member of the GINS complex, essential for DNA replication in eukaryotes. It has been reported that SLD5 is involved in early embryogenesis in the mouse and cell cycle progression and genome integrity in Drosophila. SLD5 may be involved in malignant tumor progression, but its relevance in human cancer has not been determined. Here, we found strong SLD5 expression in both human bladder cancer tissues from patients and cell lines. Knockdown of SLD5 using small interfering RNA resulted in reduction of cell growth both in vitro and an in vivo xenograft model. Moreover, we found that high levels of SLD5 in bladder cancer cells result from downregulation of microRNA (miR)-370 that otherwise suppresses its expression. High level expression of DNA-methyltransferase (DNMT) 1 and IL-6 were also observed in bladder cancer cells. Knockdown of IL-6 led to downregulation of DNMT1 and SLD5 expression, suggesting that IL-6-induced overexpression of DNMT1 suppresses miR-370, resulting in high SLD5 expression. Our findings could contribute to understanding tumorigenic processes and progression of human bladder cancer, whereby inhibition of SLD5 could represent a novel strategy to prevent tumor growth.
Autophagy-associated alpha-arrestin signaling is required for conidiogenous cell development in Magnaporthe oryzae
Authors: Dong Bo , Xu Xiaojin , Chen Guoqing , Zhang Dandan , Tang Mingzhi , Xu Fei , Liu Xiaohong , Wang Hua , Zhou Bo 
Published: August 2016

AbstractConidiation patterning is evolutionarily complex and mechanism concerning conidiogenous cell differentiation remains largely unknown. Magnaporthe oryzae conidiates in a sympodial way and uses its conidia to infect host and disseminate blast disease. Arrestins are multifunctional proteins that modulate receptor down-regulation and scaffold components of intracellular trafficking routes. We here report an alpha-arrestin that regulates patterns of conidiation and contributes to pathogenicity in M. oryzae. We show that disruption of ARRDC1 generates mutants which produce conidia in an acropetal array and ARRDC1 significantly affects expression profile of CCA1, a virulence-related transcription factor required for conidiogenous cell differentiation. Although germ tubes normally develop appressoria, penetration peg formation is dramatically impaired and Δarrdc1 mutants are mostly nonpathogenic. Fluorescent analysis indicates that EGFP-ARRDC1 puncta are well colocalized with DsRed2-Atg8, and this distribution profile could not be altered in Δatg9 mutants, suggesting ARRDC1 enters into autophagic flux before autophagosome maturation. We propose that M. oryzae employs ARRDC1 to regulate specific receptors in response to conidiation-related signals for conidiogenous cell differentiation and utilize autophagosomes for desensitization of conidiogenous receptor, which transmits extracellular signal to the downstream elements of transcription factors. Our investigation extends novel significance of autophagy-associated alpha-arrestin signaling to fungal parasites.
Fibroblast growth factor 21 deficiency exacerbates chronic alcohol-induced hepatic steatosis and injury
Authors: Liu Yanlong , Zhao Cuiqing , Xiao Jian , Liu Liming , Zhang Min , Wang Cuiling , Wu Guicheng , Zheng Ming-Hua , Xu Lan-Man , Chen Yong-Ping , Mohammadi Moosa , Chen Shao-Yu , Cave Matthew , McClain Craig , Li Xiaokun , Feng Wenke 
Published: August 2016

AbstractFibroblast growth factor 21 (FGF21) is a hepatokine that regulates glucose and lipid metabolism in the liver. We sought to determine the role of FGF21 in hepatic steatosis in mice exposed to chronic alcohol treatment and to discern underlying mechanisms. Male FGF21 knockout (FGF21 KO) and control (WT) mice were divided into groups that were fed either the Lieber DeCarli diet containing 5% alcohol or an isocaloric (control) diet for 4 weeks. One group of WT mice exposed to alcohol received recombinant human FGF21 (rhFGF21) in the last 5 days. Liver steatosis and inflammation were assessed. Primary mouse hepatocytes and AML-12 cells were incubated with metformin or rhFGF21. Hepatic genes and the products involved in in situ lipogenesis and fatty acid β-oxidation were analyzed. Alcohol exposure increased circulating levels and hepatic expression of FGF21. FGF21 depletion exacerbated alcohol-induced hepatic steatosis and liver injury, which was associated with increased activation of genes involved in lipogenesis mediated by SREBP1c and decreased expression of genes involved in fatty acid β-oxidation mediated by PGC1α. rhFGF21 administration reduced alcohol-induced hepatic steatosis and inflammation in WT mice. These results reveal that alcohol-induced FGF21 expression is a hepatic adaptive response to lipid dysregulation. Targeting FGF21 signaling could be a novel treatment approach for alcoholic steatohepatitis.
Atomistic clustering-ordering and high-strain deformation of an Al0.1CrCoFeNi high-entropy alloy
Authors: Sharma Aayush , Singh Prashant , Johnson Duane D. , Liaw Peter K. , Balasubramanian Ganesh 
Published: August 2016

AbstractComputational investigations of structural, chemical, and deformation behavior in high-entropy alloys (HEAs), which possess notable mechanical strength, have been limited due to the absence of applicable force fields. To extend investigations, we propose a set of intermolecular potential parameters for a quinary Al-Cr-Co-Fe-Ni alloy, using the available ternary Embedded Atom Method and Lennard-Jones potential in classical molecular-dynamics simulations. The simulation results are validated by a comparison to first-principles Korringa-Kohn-Rostoker (KKR) - Coherent Potential Approximation (CPA) [KKR-CPA] calculations for the HEA structural properties (lattice constants and bulk moduli), relative stability, pair probabilities, and high-temperature short-range ordering. The simulation (MD)-derived properties are in quantitative agreement with KKR-CPA calculations (first-principles) and experiments. We study AlxCrCoFeNi for Al ranging from 0 ≤ x ≤2 mole fractions, and find that the HEA shows large chemical clustering over a wide temperature range for x < 0.5. At various temperatures high-strain compression promotes atomistic rearrangements in Al0.1CrCoFeNi, resulting in a clustering-to-ordering transition that is absent for tensile loading. Large fluctuations under stress, and at higher temperatures, are attributed to the thermo-plastic instability in Al0.1CrCoFeNi.
Free-energy studies reveal a possible mechanism for oxidation-dependent inhibition of MGL
Authors: Scalvini Laura , Vacondio Federica , Bassi Michele , Pala Daniele , Lodola Alessio , Rivara Silvia , Jung Kwang-Mook , Piomelli Daniele , Mor Marco 
Published: August 2016

AbstractThe function of monoacylglycerol lipase (MGL), a key actor in the hydrolytic deactivation of the endocannabinoid 2-arachidonoyl-sn-glycerol (2AG), is tightly controlled by the cell’s redox state: oxidative signals such as hydrogen peroxide suppress MGL activity in a reversible manner through sulfenylation of the peroxidatic cysteines, C201 and C208. Here, using as a starting point the crystal structures of human MGL (hMGL), we present evidence from molecular dynamics and metadynamics simulations along with high-resolution mass spectrometry studies indicating that sulfenylation of C201 and C208 alters the conformational equilibrium of the membrane-associated lid domain of MGL to favour closed conformations of the enzyme that do not permit the entry of substrate into the active site.
Competing Orders and Anomalies
Authors: Moon Eun-Gook 
Published: August 2016

AbstractA conservation law is one of the most fundamental properties in nature, but a certain class of conservation “laws” could be spoiled by intrinsic quantum mechanical effects, so-called quantum anomalies. Profound properties of the anomalies have deepened our understanding in quantum many body systems. Here, we investigate quantum anomaly effects in quantum phase transitions between competing orders and striking consequences of their presence. We explicitly calculate topological nature of anomalies of non-linear sigma models (NLSMs) with the Wess-Zumino-Witten (WZW) terms. The non-perturbative nature is directly related with the ’t Hooft anomaly matching condition: anomalies are conserved in renormalization group flow. By applying the matching condition, we show massless excitations are enforced by the anomalies in a whole phase diagram in sharp contrast to the case of the Landau-Ginzburg-Wilson theory which only has massive excitations in symmetric phases. Furthermore, we find non-perturbative criteria to characterize quantum phase transitions between competing orders. For example, in 4D, we show the two competing order parameter theories, CP(1) and the NLSM with WZW, describe different universality class. Physical realizations and experimental implication of the anomalies are also discussed.
Isolation and Characterization of a Highly Mutated Chinese Isolate of Enterovirus B84 from a Patient with Acute Flaccid Paralysis
Authors: Zheng Huanying , Zhang Yong , Liu Leng , Lu Jing , Guo Xue , Li Hui , Zeng Hanri , Fang Ling , Xu Wenbo , Ke Changwen 
Published: August 2016

AbstractEnterovirus B84 (EV-B84) is a newly identified serotype within the species Enterovirus B (EV-B). To date, only ten nucleotide sequences of EV-B84 are published and only one full-length genome sequence (the prototype strain) is available in the GenBank database. Here, a highly mutated EV-B84 (strain AFP452/GD/CHN/2004) was recovered from a patient with acute flaccid paralysis in the Guangdong province of China in 2004 making this the first report of EV-B84 in China. Sequence comparison and phylogenetic dendrogram analysis revealed high variation from the global EV-B84 strains (African and Indian strains) and frequent intertypic recombination in the non-structural protein region, suggesting high genetic diversity in EV-B84. The Chinese EV-B84 strain, apparently evolving independently of the other ten strains, strongly suggests that the EV-B84 strain has been circulating for many years. However, the extremely low isolation rate suggests that it is not a prevalent EV serotype in China or worldwide. This study provides valuable information about the molecular epidemiology of EV-B84 in China, and will be helpful in future studies to understand the association of EV-B84 with neurological disorders; it also helps expand the number of whole virus genome sequences of EV-B84 in the GenBank database.
Heritability of fear of humans in urban and rural populations of a bird species
Authors: Carrete Martina , Martínez-Padilla Jesús , Rodríguez-Martínez Sol , Rebolo-Ifrán Natalia , Palma Antonio , Tella José L. 
Published: August 2016

AbstractFlight initiation distance (FID), a measure of an animal’s tolerance to human disturbance and a descriptor of its fear of humans, is increasingly employed for conservation purposes and to predict the response of species to urbanization. However, most work devoted to understanding variability in FID has been conducted at the population level and little is still known about inter-individual variability in this behaviour. We estimated the heritability of FID, a factor fundamental to understanding the strength and evolutionary consequences of selection of particular phenotypes associated with human disturbances. We used a population of burrowing owls (Athene cunicularia) monitored long-term and for which FID was previously shown to be highly consistent across an individual’s lifespan. Heritability estimates varied between 0.37 and 0.80, depending on the habitat considered (urban-rural) and method used (parent-offspring regressions or animal models). These values are unusually high compared with those previously reported for other behavioural traits. Although more research is needed to fully understand the underlying causes of this resemblance between relatives, selection pressures acting on this behaviour should be seriously considered as an important evolutionary force in animal populations increasingly exposed to human disturbance worldwide.
Suppression of superconductivity and structural phase transitions under pressure in tetragonal FeS
Authors: Lai Xiaofang , Liu Ying , Lü Xujie , Zhang Sijia , Bu Kejun , Jin Changqing , Zhang Hui , Lin Jianhua , Huang Fuqiang 
Published: August 2016

AbstractPressure is a powerful tool to study iron-based superconductors. Here, we report systematic high-pressure transport and structural characterizations of the newly discovered superconductor FeS. It is found that superconductor FeS (tetragonal) partly transforms to a hexagonal structure at 0.4 GPa and then completely transforms to an orthorhombic phase at 7.4 GPa and finally to a monoclinic phase above 9.0 GPa. The superconducting transition temperature of tetragonal FeS was gradually depressed by pressure, different from the case in tetragonal FeSe. With pressure increasing, the S-Fe-S angles only slightly change but the anion height deviates farther from 1.38 Å. This change of anion height, together with the structural instability under pressure, should be closely related to the suppression of superconductivity. We also observed an anomalous metal-semiconductor transition at 6.0 GPa and an unusual increased resistance with further compression above 9.6 GPa. The former can be ascribed to the tetragonal-orthorhombic structural phase transition and the latter to the electronic structure changes of the high-pressure monoclinic phase. Finally, a phase diagram of tetragonal FeS as functions of pressure and temperature was mapped out for the first time, which will shed new light on understanding of the structure and physics of the superconducting FeS.
Requirement of HDAC6 for activation of Notch1 by TGF-β1
Authors: Deskin Brian , Lasky Joseph , Zhuang Yan , Shan Bin 
Published: August 2016

AbstractTGF-β1 is enriched in the tumor microenvironment and acts as a key inducer of epithelial to mesenchymal transition (EMT) in lung cancer. The NOTCH signaling pathway is conserved across species and is an essential pathway for development, cell differentiation and cancer biology. Dysregulation of Notch signaling is a common feature of non-small cell lung cancer (NSCLC) and is correlated with poor prognosis. Crosstalk exists between the NOTCH and TGF-β signaling pathways in EMT. Herein we report that histone deacetylase 6 (HDAC6) modulates TGF-β1-mediated activation of the Notch pathway. HDAC6, a primarily cytoplasmic deacetylase, mediates TGF-β1-induced EMT in human lung cancer cells. Inhibition of HDAC6 with a small molecule inhibitor, namely tubacin or with siRNA attenuated TGF-β1-induced Notch-1 signaling. We show that TGFβ-1-induced EMT is accompanied by rapid HDAC6-dependent deacetylation of heat shock protein 90 (HSP90). Consistently, inhibition of HSP90 with its small molecule inhibitor 17AAG attenuated expression of TGF-β1-induced Notch-1 target genes, HEY-1 and HES-1. These findings reveal a novel function of HDAC6 in EMT via mediating the TGF-β-Notch signaling cascade and support HDAC6 as a key regulator of TGFβ-induced EMT in NSCLC. This work suggests that HDAC6 may be an attractive therapeutic target against tumor progression and metastasis.