bluuebunny/crossref_metadata_2025_split huggingface dataset:
Environmental conditions regulate the impact of plants on cloud formation
Authors: Zhao D. F. , Buchholz A. , Tillmann R. , Kleist E. , Wu C. , Rubach F. , Kiendler-Scharr A. , Rudich Y. , Wildt J. , Mentel Th. F. 
Published: February 2017

AbstractThe terrestrial vegetation emits large amounts of volatile organic compounds (VOC) into the atmosphere, which on oxidation produce secondary organic aerosol (SOA). By acting as cloud condensation nuclei (CCN), SOA influences cloud formation and climate. In a warming climate, changes in environmental factors can cause stresses to plants, inducing changes of the emitted VOC. These can modify particle size and composition. Here we report how induced emissions eventually affect CCN activity of SOA, a key parameter in cloud formation. For boreal forest tree species, insect infestation by aphids causes additional VOC emissions which modifies SOA composition thus hygroscopicity and CCN activity. Moderate heat increases the total amount of constitutive VOC, which has a minor effect on hygroscopicity, but affects CCN activity by increasing the particles’ size. The coupling of plant stresses, VOC composition and CCN activity points to an important impact of induced plant emissions on cloud formation and climate.
Protein disulfide isomerase secretion following vascular injury initiates a regulatory pathway for thrombus formation
Authors: Bowley Sheryl R. , Fang Chao , Merrill-Skoloff Glenn , Furie Barbara C. , Furie Bruce 
Published: February 2017

AbstractProtein disulfide isomerase (PDI), secreted by platelets and endothelial cells on vascular injury, is required for thrombus formation. Using PDI variants that form mixed disulfide complexes with their substrates, we identify by kinetic trapping multiple substrate proteins, including vitronectin. Plasma vitronectin does not bind to αvβ3 or αIIbβ3 integrins on endothelial cells and platelets. The released PDI reduces disulfide bonds on plasma vitronectin, enabling vitronectin to bind to αVβ3 and αIIbβ3.In vivostudies of thrombus generation in mice demonstrate that vitronectin rapidly accumulates on the endothelium and the platelet thrombus following injury. This process requires PDI activity and promotes platelet accumulation and fibrin generation. We hypothesize that under physiologic conditions in the absence of secreted PDI, thrombus formation is suppressed and maintains a quiescent, patent vasculature. The release of PDI during vascular injury may serve as a regulatory switch that allows activation of proteins, among them vitronectin, critical for thrombus formation.
Iron isotopic fractionation between silicate mantle and metallic core at high pressure
Authors: Liu Jin , Dauphas Nicolas , Roskosz Mathieu , Hu Michael Y. , Yang Hong , Bi Wenli , Zhao Jiyong , Alp Esen E. , Hu Justin Y. , Lin Jung-Fu 
Published: February 2017

AbstractThe +0.1‰ elevated 56Fe/54Fe ratio of terrestrial basalts relative to chondrites was proposed to be a fingerprint of core-mantle segregation. However, the extent of iron isotopic fractionation between molten metal and silicate under high pressure–temperature conditions is poorly known. Here we show that iron forms chemical bonds of similar strengths in basaltic glasses and iron-rich alloys, even at high pressure. From the measured mean force constants of iron bonds, we calculate an equilibrium iron isotope fractionation between silicate and iron under core formation conditions in Earth of ∼0–0.02‰, which is small relative to the +0.1‰ shift of terrestrial basalts. This result is unaffected by small amounts of nickel and candidate core-forming light elements, as the isotopic shifts associated with such alloying are small. This study suggests that the variability in iron isotopic composition in planetary objects cannot be due to core formation.
Liquid-like cationic sub-lattice in copper selenide clusters
Authors: White Sarah L. , Banerjee Progna , Jain Prashant K. 
Published: February 2017

AbstractSuper-ionic solids, which exhibit ion mobilities as high as those in liquids or molten salts, have been employed as solid-state electrolytes in batteries, improved thermoelectrics and fast-ion conductors in super-capacitors and fuel cells. Fast-ion transport in many of these solids is supported by a disordered, ‘liquid-like’ sub-lattice of cations mobile within a rigid anionic sub-lattice, often achieved at high temperatures or pressures via a phase transition. Here we show that ultrasmall clusters of copper selenide exhibit a disordered cationic sub-lattice under ambient conditions unlike larger nanocrystals, where Cu+ ions and vacancies form an ordered super-structure similar to the bulk solid. The clusters exhibit an unusual cationic sub-lattice arrangement wherein octahedral sites, which serve as bridges for cation migration, are stabilized by compressive strain. The room-temperature liquid-like nature of the Cu+ sub-lattice combined with the actively tunable plasmonic properties of the Cu2Se clusters make them suitable as fast electro-optic switches.
Room temperature organic magnets derived from sp3 functionalized graphene
Authors: Tuček Jiří , Holá Kateřina , Bourlinos Athanasios B. , Błoński Piotr , Bakandritsos Aristides , Ugolotti Juri , Dubecký Matúš , Karlický František , Ranc Václav , Čépe Klára , Otyepka Michal , Zbořil Radek 
Published: February 2017

AbstractMaterials based on metallic elements that have d orbitals and exhibit room temperature magnetism have been known for centuries and applied in a huge range of technologies. Development of room temperature carbon magnets containing exclusively sp orbitals is viewed as great challenge in chemistry, physics, spintronics and materials science. Here we describe a series of room temperature organic magnets prepared by a simple and controllable route based on the substitution of fluorine atoms in fluorographene with hydroxyl groups. Depending on the chemical composition (an F/OH ratio) and sp3 coverage, these new graphene derivatives show room temperature antiferromagnetic ordering, which has never been observed for any sp-based materials. Such 2D magnets undergo a transition to a ferromagnetic state at low temperatures, showing an extraordinarily high magnetic moment. The developed theoretical model addresses the origin of the room temperature magnetism in terms of sp2-conjugated diradical motifs embedded in an sp3 matrix and superexchange interactions via –OH functionalization.
SMURF2 regulates bone homeostasis by disrupting SMAD3 interaction with vitamin D receptor in osteoblasts
Authors: Xu Zhan , Greenblatt Matthew B. , Yan Guang , Feng Heng , Sun Jun , Lotinun Sutada , Brady Nicholas , Baron Roland , Glimcher Laurie H. , Zou Weiguo 
Published: February 2017

AbstractCoordination between osteoblasts and osteoclasts is required for bone health and homeostasis. Here we show that mice deficient in SMURF2 have severe osteoporosis in vivo. This low bone mass phenotype is accompanied by a pronounced increase in osteoclast numbers, although Smurf2-deficient osteoclasts have no intrinsic alterations in activity. Smurf2-deficient osteoblasts display increased expression of RANKL, the central osteoclastogenic cytokine. Mechanistically, SMURF2 regulates RANKL expression by disrupting the interaction between SMAD3 and vitamin D receptor by altering SMAD3 ubiquitination. Selective deletion of Smurf2 in the osteoblast lineage recapitulates the phenotype of germline Smurf2-deficient mice, indicating that SMURF2 regulates osteoblast-dependent osteoclast activity rather than directly affecting the osteoclast. Our results reveal SMURF2 as an important regulator of the critical communication between osteoblasts and osteoclasts. Furthermore, the bone mass phenotype in Smurf2- and Smurf1-deficient mice is opposite, indicating that SMURF2 has a non-overlapping and, in some respects, opposite function to SMURF1.
Aurora kinase A regulates Survivin stability through targeting FBXL7 in gastric cancer drug resistance and prognosis
Authors: Kamran M , Long Z-J , Xu D , Lv S-S , Liu B , Wang C-L , Xu J , Lam E W-F , Liu Q 
Published: February 2017

AbstractAurora kinase A (AURKA) has been implicated in the regulation of cell cycle progression, mitosis and a key number of oncogenic signaling pathways in various malignancies. However, little is known about its role in gastric cancer prognosis and genotoxic resistance. Here we found that AURKA was highly overexpressed in gastric cancer and inversely correlated with disease prognosis. Overexpression of AURKA exacerbated gastric cancer drug resistance through upregulating the expression of the anti-apoptotic protein Survivin. Conversely, we demonstrated that AURKA depletion caused a decrease in Survivin protein levels by increasing its ubiquitylation and degradation. Mass spectrometric analysis revealed that upon AURKA depletion, Survivin bound to the FBXL7 E3 ubiquitin ligase, which induced ubiquitin-proteasome degradation of Survivin. In addition, we showed that AURKA regulated FBXL7 both at the levels of transcription and translation. Moreover, proteomic analysis of nuclear AURKA-interacting proteins identified Forkhead box protein P1 (FOXP1). We next showed that AURKA was required for FBXL7 transcription and that AURKA negatively regulated FOXP1-mediated FBXL7 expression. The physiological relevance of the regulation of Survivin by AURKA through the FOXP1–FBXL7 axis was further underscored by the significant positive correlations between AURKA and Survivin expression in gastric cancer patient samples. Moreover, the AURKA depletion or kinase inhibition-induced apoptotic cell death could be reversed by Survivin ectopic overexpression, further supporting that AURKA regulated Survivin to enhance drug resistance. In agreement, inhibition of AURKA synergistically enhanced the cytotoxic effect of DNA-damaging agents in cancer cells by suppressing Survivin expression. Taken together, our data suggest that AURKA restricts Survivin ubiquitylation and degradation in gastric cancer to promote drug resistance and hence the AURKA–Survivin axis can be targeted to promote the efficacy of DNA-damaging agents in gastric cancer.
Computational modeling sheds light on structural evolution in metallic glasses and supercooled liquids
Authors: Ding Jun , Ma En 
Published: February 2017

AbstractThis article presents an overview of three challenging issues that are currently being debated in the community researching on the evolution of amorphous structures in metallic glasses and their parent supercooled liquids. Our emphasis is on the valuable insights acquired in recent computational analyses that have supplemented experimental investigations. The first idea is to use the local structural order developed, and in particular its evolution during undercooling, as a signature indicator to rationalize the experimentally observed temperature-dependence of viscosity, hence suggesting a possible structural origin of liquid fragility. The second issue concerns with the claim that the average nearest-neighbor distance in metallic melts contracts rather than expands upon heating, concurrent with a reduced coordination number. This postulate is, however, based on the shift of the first peak maximum in the pair distribution function and an average bond length determined from nearest neighbors designated using a distance cutoff. These can instead be a result of increasing skewness of the broad first peak, upon thermally exacerbated asymmetric distribution of neighboring atoms activated to shorter and longer distances under the anharmonic interatomic interaction potential. The third topic deals with crystal-like peak positions in the pair distribution function of metallic glasses. These peak locations can be explained using various connection schemes of coordination polyhedra, and found to be present already in high-temperature liquids without hidden crystal order. We also present an outlook to invite more in-depth computational research to fully settle these issues in future, and to establish more robust structure-property relations in amorphous alloys.
Seismic Hazards Implications of Uplifted Pleistocene Coral Terraces in the Gulf of Aqaba
Authors: Bosworth W. , Montagna P. , Pons-Branchu E. , Rasul N. , Taviani M. 
Published: February 2017

AbstractThe Gulf of Aqaba transform plate boundary is a source of destructive teleseismic earthquakes. Seismicity is concentrated in the central sub-basin and decreases to both the north and south. Although principally a strike-slip plate boundary, the faulted margins of the Gulf display largely dip-slip extensional movement and accompanying footwall uplift. We have constrained rates of this uplift by measurements of elevated Pleistocene coral terraces. In particular the terrace that formed during the last interglacial (~125 ka) is found discontinuously along the length of the Gulf at elevations of 3 to 26 m. Global sea level was ~7 m higher than today at 125 ka indicating net maximum tectonic uplift of ~19 m with an average rate of ~0.015 cm/yr. Uplift has been greatest adjacent to the central sub-basin and like the seismicity decreases to the north and south. We suggest that the present pattern of a seismically active central region linked to more aseismic areas in the north and south has therefore persisted for at least the past 125 kyr. Consequently the potential for future destructive earthquakes in the central Gulf is greater than in the sub-basins to the north and south.
Roles of Serum Calcium, Phosphorus, PTH and ALP on Mortality in Peritoneal Dialysis Patients: A Nationwide, Population-based Longitudinal Study Using TWRDS 2005–2012
Authors: Liu Chung-Te , Lin Yen-Chung , Lin Yi-Chun , Kao Chih-Chin , Chen Hsi-Hsien , Hsu Chih-Cheng , Wu Mai-Szu 
Published: February 2017

AbstractBiomarkers of chronic kidney disease-mineral and bone disorder (CKD-MBD) correlate with morbidity and mortality in dialysis patients. However, the comparative roles of each CKD-MBD biomarker remained undetermined on long-term peritoneal dialysis (PD) patients. This retrospective study, employing a population-based database, aimed to evaluate the performance and provide the best evidence of each biomarker of CKD-MBD as predictor of all-cause mortality. Throughout the 8-year study period, total 12,116 PD patients were included in this study. Cox proportional regression and Kaplan-Meier method were used for survival analysis. For Cox regression model, baseline measurements and time-varying covariates were used for analysis. In Cox regression model using time-dependent covariates, serum calcium level of ≧9.5 mg/dL was associated with increased mortality. For phosphorus, serum levels of either ≧6.5 mg/dL or <3.5 mg/dL were associated with increased mortality. For parathyroid hormone (PTH), higher serum levels were not associated increased mortality. For alkaline phosphatase (ALP), mortality increased at levels ≧100 IU/L. Our findings suggested that the detrimental effect of ALP on survival was more consistent, while serum calcium, phosphorus and PTH may have a less prominent effect on mortality. This study provided additional information for manipulating CKD-MBD biomarkers in PD patients.
Plin5 alleviates myocardial ischaemia/reperfusion injury by reducing oxidative stress through inhibiting the lipolysis of lipid droplets
Authors: Zheng Pengfei , Xie Zhonglin , Yuan Yuan , Sui Wen , Wang Chao , Gao Xing , Zhao Yuanlin , Zhang Feng , Gu Yu , Hu Peizhen , Ye Jing , Feng Xuyang , Zhang Lijun 
Published: February 2017

AbstractMyocardial ischaemia-reperfusion (I/R) injury is a complex pathophysiological process. Current research has suggested that energy metabolism disorders, of which the abnormal consumption of fatty acids is closely related, compose the main pathological basis for myocardial I/R injury. Lipid droplets (LD) are critical regulators of lipid metabolism by LD-associated proteins. Among the lipid droplet proteins, the perilipin family members regulate lipolysis and lipogenesis through different mechanisms. Plin5, an important perilipin protein, promotes LD generation and lowers fatty acid oxidation, thus protecting the myocardium from lipotoxicity. This study investigated the protective effects of Plin5 in I/R myocardium. Our results indicated that Plin5 deficiency exacerbated the myocardial infarct area, aggravated left ventricular systolic dysfunction, reduced lipid storage, and elevated free fatty acids. Plin5-deficient myocardium exhibited severely damaged mitochondria, elevated reactive oxygen species (ROS) and malondialdehyde (MDA) levels, and decreased superoxide dismutase (SOD) activity. Furthermore, the decreased phosphorylation of PI3K/Akt in Plin5-null cardiomyocytes might contribute to I/R injury aggravation. In conclusion, Plin5, a new regulator of myocardial lipid metabolism, decreases free fatty acid peroxidation by inhibiting the lipolysis of intracellular lipid droplets, thus providing cardioprotection against I/R injury and shedding new light on therapeutic solutions for I/R diseases.
The interaction between the proliferating macroalga Asparagopsis taxiformis and the coral Astroides calycularis induces changes in microbiome and metabolomic fingerprints
Authors: Greff Stéphane , Aires Tânia , Serrão Ester A. , Engelen Aschwin H. , Thomas Olivier P. , Pérez Thierry 
Published: February 2017

AbstractMediterranean Sea ecosystems are considered as hotspots of biological introductions, exposed to possible negative effects of non–indigenous species. In such temperate marine ecosystems, macroalgae may be dominant, with a great percentage of their diversity represented by introduced species. Their interaction with temperate indigenous benthic organisms have been poorly investigated. To provide new insights, we performed an experimental study on the interaction between the introduced proliferative red alga Asparagopsis taxiformis and the indigenous Mediterranean coral Astroides calycularis. The biological response measurements included meta–barcoding of the associated microbial communities and metabolomic fingerprinting of both species. Significant changes were detected among both associated microbial communities, the interspecific differences decreasing with stronger host interaction. No short term effects of the macroalga on the coral health, neither on its polyp activity or its metabolism, were detected. In contrast, the contact interaction with the coral induced a change in the macroalgal metabolomic fingerprint with a significant increase of its bioactivity against the marine bacteria Aliivibrio fischeri. This induction was related to the expression of bioactive metabolites located on the macroalgal surface, a phenomenon which might represent an immediate defensive response of the macroalga or an allelopathic offense against coral.
Natural and laboratory mutations in kuzbanian are associated with zinc stress phenotypes in Drosophila melanogaster
Authors: Le Manh Hung , Guio Lain , Merenciano Miriam , Rovira Quirze , Barrón Maite G. , González Josefa 
Published: February 2017

AbstractOrganisms must cope with altered environmental conditions such as high concentrations of heavy metals. Stress response to heavy metals is mediated by the metal-responsive transcription factor 1 (MTF-1), which is conserved from Drosophila to humans. MTF-1 binds to metal response elements (MREs) and changes the expression of target genes.kuzbanian (kuz), a metalloendopeptidase that activates the evolutionary conservedNotchsignaling pathway, has been identified as an MTF-1 target gene. We have previously identified a putatively adaptive transposable element in theDrosophila melanogastergenome, namedFBti0019170,inserted in akuzintron. In this work, we investigated whether a laboratory mutant stock overexpressingkuzis associated with zinc stress phenotypes. We found that both embryos and adult flies overexpressingkuzare more tolerant to zinc compared with wild-type flies. On the other hand, we found that the effect ofFBti0019170on zinc stress tolerance depends on developmental stage and genetic background. Moreover, in the majority of the genetic backgrounds analyzed,FBti0019170has a deleterious effect in unpolluted environments in pre-adult stages. These results highlight the complexity of natural mutations and suggest that besides laboratory mutations, natural mutations should be studied in order to accurately characterize gene function and evolution.
Ubiquitination and dynactin regulate TMEPAI lysosomal trafficking
Authors: Luo Shenheng , Jing Lei , Zhao Tian , Li Yuyin , Liu Zhenxing , Diao Aipo 
Published: February 2017

AbstractThe transmembrane prostate androgen-induced protein (TMEPAI) has been reported to be elevated in various tumor cells, is localized to the lysosome and promotes lysosome stability. The molecular mechanism of TMEPAI trafficking however to the lysosome is unknown. Here we report that clathrin and CI-M6PR mediate TMEPAI transport from the Golgi directly into the endo-lysosomal pathway. TMEPAI is ubiquitinated at its C-terminal region and ubiquitination modification of TMEPAI is a signal for its lysosomal trafficking. Moreover, TMEPAI binds the ubiquitin binding proteins Hrs and STAM which is required for its lysosomal transport. In addition, TMEPAI interacts with the dynactin pointed-end complex subunits dynactin 5 and dynactin 6. The aa 132–155 domain is essential for specific TMEPAI binding and deletion of this binding site leads to mis-trafficking of TMEPAI to the plasma membrane. These results reveal the pathway and mechanism regulating transport of TMEPAI to the lysosome, which helps to further understand the role of TMEPAI in tumorigenesis.
miR-203 enhances let-7 biogenesis by targeting LIN28B to suppress tumor growth in lung cancer
Authors: Zhou Yong , Liang Hongwei , Liao Zhicong , Wang Yanbo , Hu Xiuting , Chen Xi , Xu Lin , Hu Zhibin 
Published: February 2017

AbstractHuman cancers often exhibit increased microRNA (miRNA) biogenesis and global aberrant expression of miRNAs; thus, targeting the miRNA biogenesis pathway represents a novel strategy for cancer therapy. Here, we report that miR-203 enhances the biogenesis of tumor suppressor let-7 in lung cancer by directly targeting LIN28B. Specially, we found that the LIN28B protein levels were dramatically increased in lung cancer tissues, but its mRNA levels did not differ significantly, suggesting that a post-transcriptional mechanism is involved in LIN28B regulation. Interestingly, miR-203 overexpression was accompanied by massive upregulation of a group of miRNAs, especially let-7, and the let-7 expression level was concordant with the miR-203 expression in lung cancer tissues, implying its biological relevance. Furthermore, we showed that miR-203 played a critical role in inhibiting the proliferation and promoting the apoptosis of lung cancer cells by suppressing LIN28B and enhancing let-7 biogenesis. In summary, our results establish a novel mechanism by which miR-203, LIN28B and let-7 are tightly linked to form a regulatory network in lung cancer cells. The findings shed light on the role of a specific miRNA as a modulator of miRNA biogenesis and provide basis for developing new strategies for lung cancer therapy.