bluuebunny/crossref_metadata_2025_split huggingface dataset:
Linking Magma Storage and Ascent to Eruption Volume and Composition at an Arc Caldera
Authors: Miller David , Bennington Ninfa , Haney Matthew , Bedrosian Paul , Key Kerry , Thurber Clifford , Hart Laney , Ohlendorf Summer 
Published: June 2020

AbstractConceptual models of magma storage and transport under calderas favor a connected system of sills and dikes. These features are individually below the resolution of standard seismic tomography, but radial seismic anisotropy can reveal where they exist in aggregate. We model radial anisotropy at Okmok caldera, Alaska, to demonstrate the presence of a caldera‐centered stacked sill complex and surrounding dike system. We show that ascending magma, inferred from seismicity, either intersects the sill complex, resulting in a larger volume eruption of evolved magma, or bypasses the overlying sill complex via dikes, resulting in a low‐volume mafic eruption. Our results exemplify how the locations of magma storage and paths of transport impact eruption size and composition. As this type of crustal storage is likely common to many calderas, this analysis offers a potential new framework for volcano observatories to forecast the size of impending eruptions.
A Shortening of the Life Cycle of Major Tropical Cyclones
Authors: Wang S. , Rashid T. , Throp H. , Toumi R. 
Published: June 2020

AbstractIn this study a comprehensive picture of the changing intensity life cycle of major (Category 3 and higher) tropical cyclones (TCs) is presented. Over the past decades, the lifetime maximum intensity has increased, but there has also been a significant decrease in duration of time spent at intensities greater than Category 1. These compensating effects have maintained a stable global mean‐accumulated cyclone energy of individual major TCs. The global mean duration of major TCs has shortened by about 1 day from 1982 to 2018. There has been both faster intensification (Categories 1 to 3) and weakening (Categories 3 to 1) by about 40%. The probabilities of rapid intensification and rapid weakening have both risen in the period 2000–2018 compared to 1982–1999. A statistically significant anticorrelation is found between the lifetime maximum intensity and the following duration of the final weakening. This suggests an element of self‐regulation of TC life cycles.
Synonymous GATA2 mutations result in selective loss of mutated RNA and are common in patients with GATA2 deficiency
Authors: Kozyra Emilia J. , Pastor Victor B. , Lefkopoulos Stylianos , Sahoo Sushree S. , Busch Hauke , Voss Rebecca K. , Erlacher Miriam , Lebrecht Dirk , Szvetnik Enikoe A. , Hirabayashi Shinsuke , Pasaulienė Ramunė , Pedace Lucia , Tartaglia Marco , Klemann Christian , Metzger Patrick , Boerries Melanie , Catala Albert , Hasle Henrik , de Haas Valerie , Kállay Krisztián , Masetti Riccardo , De Moerloose Barbara , Dworzak Michael , Schmugge Markus , Smith Owen , Starý Jan , Mejstrikova Ester , Ussowicz Marek , Morris Emma , Singh Preeti , Collin Matthew , Derecka Marta , Göhring Gudrun , Flotho Christian , Strahm Brigitte , Locatelli Franco , Niemeyer Charlotte M. , Trompouki Eirini , Wlodarski Marcin W. ,   European Working Group of MDS in Childhood (EWOG-MDS)
Published: June 2020

AbstractDeficiency of the transcription factor GATA2 is a highly penetrant genetic disorder predisposing to myelodysplastic syndromes (MDS) and immunodeficiency. It has been recognized as the most common cause underlying primary MDS in children. Triggered by the discovery of a recurrent synonymous GATA2 variant, we systematically investigated 911 patients with phenotype of pediatric MDS or cellular deficiencies for the presence of synonymous alterations in GATA2. In total, we identified nine individuals with five heterozygous synonymous mutations: c.351C>G, p.T117T (N = 4); c.649C>T, p.L217L; c.981G>A, p.G327G; c.1023C>T, p.A341A; and c.1416G>A, p.P472P (N = 2). They accounted for 8.2% (9/110) of cases with GATA2 deficiency in our cohort and resulted in selective loss of mutant RNA. While for the hotspot mutation (c.351C>G) a splicing error leading to RNA and protein reduction was identified, severe, likely late stage RNA loss without splicing disruption was found for other mutations. Finally, the synonymous mutations did not alter protein function or stability. In summary, synonymous GATA2 substitutions are a new common cause of GATA2 deficiency. These findings have broad implications for genetic counseling and pathogenic variant discovery in Mendelian disorders.
Distinct temporal trends in breast cancer incidence from 1997 to 2016 by molecular subtypes: a population-based study of Scottish cancer registry data
Authors: Mesa-Eguiagaray Ines , Wild Sarah H. , Rosenberg Philip S. , Bird Sheila M. , Brewster David H. , Hall Peter S. , Cameron David A. , Morrison David , Figueroa Jonine D. 
Published: June 2020

Abstract
Background
We describe temporal trends in breast cancer incidence by molecular subtypes in Scotland because public health prevention programmes, diagnostic and therapeutic services are shaped by differences in tumour biology.

Methods
Population-based cancer registry data on 72,217 women diagnosed with incident primary breast cancer from 1997 to 2016 were analysed. Age-standardised rates (ASR) and age-specific incidence were estimated by tumour subtype after imputing the 8% of missing oestrogen receptor (ER) status. Joinpoint regression and age–period–cohort models were used to assess whether significant differences were observed in incidence trends by ER status.

Results
Overall, ER-positive tumour incidence increased by 0.4%/year (95% confidence interval (CI): −0.1, 1.0). Among routinely screened women aged 50–69 years, we observed an increase in ASR from 1997 to 2011 (1.6%/year, 95% CI: 1.2–2.1). ER-negative tumour incidence decreased among all ages by 2.5%/year (95% CI: −3.9 to −1.1%) over the study period. Compared with the 1941–1959 birth cohort, women born in 1912–1940 had lower incidence rate ratios (IRR) for ER+ tumours and women born in 1960–1986 had lower IRR for ER− tumours.

Conclusions
Future incidence and survival reporting should be monitored by molecular subtypes to inform clinical planning and cancer control programmes.
Bone marrow adipose tissue is a unique adipose subtype with distinct roles in glucose homeostasis
Authors: Suchacki Karla J. , Tavares Adriana A. S. , Mattiucci Domenico , Scheller Erica L. , Papanastasiou Giorgos , Gray Calum , Sinton Matthew C. , Ramage Lynne E. , McDougald Wendy A. , Lovdel Andrea , Sulston Richard J. , Thomas Benjamin J. , Nicholson Bonnie M. , Drake Amanda J. , Alcaide-Corral Carlos J. , Said Diana , Poloni Antonella , Cinti Saverio , Macpherson Gavin J. , Dweck Marc R. , Andrews Jack P. M. , Williams Michelle C. , Wallace Robert J. , van Beek Edwin J. R. , MacDougald Ormond A. , Morton Nicholas M. , Stimson Roland H. , Cawthorn William P. 
Published: June 2020

AbstractBone marrow adipose tissue (BMAT) comprises >10% of total adipose mass, yet unlike white or brown adipose tissues (WAT or BAT) its metabolic functions remain unclear. Herein, we address this critical gap in knowledge. Our transcriptomic analyses revealed that BMAT is distinct from WAT and BAT, with altered glucose metabolism and decreased insulin responsiveness. We therefore tested these functions in mice and humans using positron emission tomography-computed tomography (PET/CT) with18F-fluorodeoxyglucose. This revealed that BMAT resists insulin- and cold-stimulated glucose uptake, while further in vivo studies showed that, compared to WAT, BMAT resists insulin-stimulated Akt phosphorylation. Thus, BMAT is functionally distinct from WAT and BAT. However, in humans basal glucose uptake in BMAT is greater than in axial bones or subcutaneous WAT and can be greater than that in skeletal muscle, underscoring the potential of BMAT to influence systemic glucose homeostasis. These PET/CT studies characterise BMAT function in vivo, establish new methods for BMAT analysis, and identify BMAT as a distinct, major adipose tissue subtype.
Proline-rich protein PRR19 functions with cyclin-like CNTD1 to promote meiotic crossing over in mouse
Authors: Bondarieva Anastasiia , Raveendran Kavya , Telychko Vladyslav , Rao H. B. D. Prasada , Ravindranathan Ramya , Zorzompokou Chrysoula , Finsterbusch Friederike , Dereli Ihsan , Papanikos Frantzeskos , Tränkner Daniel , Schleiffer Alexander , Fei Ji-Feng , Klimova Anna , Ito Masaru , Kulkarni Dhananjaya S. , Roeder Ingo , Hunter Neil , Tóth Attila 
Published: June 2020

AbstractOrderly chromosome segregation is enabled by crossovers between homologous chromosomes in the first meiotic division. Crossovers arise from recombination-mediated repair of programmed DNA double-strand breaks (DSBs). Multiple DSBs initiate recombination, and most are repaired without crossover formation, although one or more generate crossovers on each chromosome. Although the underlying mechanisms are ill-defined, the differentiation and maturation of crossover-specific recombination intermediates requires the cyclin-like CNTD1. Here, we identify PRR19 as a partner of CNTD1. We find that, like CNTD1, PRR19 is required for timely DSB repair and the formation of crossover-specific recombination complexes. PRR19 and CNTD1 co-localise at crossover sites, physically interact, and are interdependent for accumulation, indicating a PRR19-CNTD1 partnership in crossing over. Further, we show that CNTD1 interacts with a cyclin-dependent kinase, CDK2, which also accumulates in crossover-specific recombination complexes. Thus, the PRR19-CNTD1 complex may enable crossover differentiation by regulating CDK2.
Phosphoregulated orthogonal signal transduction in mammalian cells
Authors: Scheller Leo , Schmollack Marc , Bertschi Adrian , Mansouri Maysam , Saxena Pratik , Fussenegger Martin 
Published: June 2020

AbstractOrthogonal tools for controlling protein function by post-translational modifications open up new possibilities for protein circuit engineering in synthetic biology. Phosphoregulation is a key mechanism of signal processing in all kingdoms of life, but tools to control the involved processes are very limited. Here, we repurpose components of bacterial two-component systems (TCSs) for chemically induced phosphotransfer in mammalian cells. TCSs are the most abundant multi-component signal-processing units in bacteria, but are not found in the animal kingdom. The presented phosphoregulated orthogonal signal transduction (POST) system uses induced nanobody dimerization to regulate the trans-autophosphorylation activity of engineered histidine kinases. Engineered response regulators use the phosphohistidine residue as a substrate to autophosphorylate an aspartate residue, inducing their own homodimerization. We verify this approach by demonstrating control of gene expression with engineered, dimerization-dependent transcription factors and propose a phosphoregulated relay system of protein dimerization as a basic building block for next-generation protein circuits.
Negative cooperativity upon hydrogen bond-stabilized O2 adsorption in a redox-active metal–organic framework
Authors: Oktawiec Julia , Jiang Henry Z. H. , Vitillo Jenny G. , Reed Douglas A. , Darago Lucy E. , Trump Benjamin A. , Bernales Varinia , Li Harriet , Colwell Kristen A. , Furukawa Hiroyasu , Brown Craig M. , Gagliardi Laura , Long Jeffrey R. 
Published: June 2020

AbstractThe design of stable adsorbents capable of selectively capturing dioxygen with a high reversible capacity is a crucial goal in functional materials development. Drawing inspiration from biological O2 carriers, we demonstrate that coupling metal-based electron transfer with secondary coordination sphere effects in the metal–organic framework Co2(OH)2(bbta) (H2bbta = 1H,5H-benzo(1,2-d:4,5-d′)bistriazole) leads to strong and reversible adsorption of O2. In particular, moderate-strength hydrogen bonding stabilizes a cobalt(III)-superoxo species formed upon O2 adsorption. Notably, O2-binding in this material weakens as a function of loading, as a result of negative cooperativity arising from electronic effects within the extended framework lattice. This unprecedented behavior extends the tunable properties that can be used to design metal–organic frameworks for adsorption-based applications.
High fat diet worsens Alzheimer’s disease-related behavioral abnormalities and neuropathology in APP/PS1 mice, but not by synergistically decreasing cerebral blood flow
Authors: Bracko Oliver , Vinarcsik Lindsay K. , Cruz Hernández Jean C. , Ruiz-Uribe Nancy E. , Haft-Javaherian Mohammad , Falkenhain Kaja , Ramanauskaite Egle M. , Ali Muhammad , Mohapatra Aditi , Swallow Madisen A. , Njiru Brendah N. , Muse Victorine , Michelucci Pietro E. , Nishimura Nozomi , Schaffer Chris B. 
Published: June 2020

AbstractObesity is linked to increased risk for and severity of Alzheimer’s disease (AD). Cerebral blood flow (CBF) reductions are an early feature of AD and are also linked to obesity. We recently showed that non-flowing capillaries, caused by adhered neutrophils, contribute to CBF reduction in mouse models of AD. Because obesity could exacerbate the vascular inflammation likely underlying this neutrophil adhesion, we tested links between obesity and AD by feeding APP/PS1 mice a high fat diet (Hfd) and evaluating behavioral, physiological, and pathological changes. We found trends toward poorer memory performance in APP/PS1 mice fed a Hfd, impaired social interactions with either APP/PS1 genotype or a Hfd, and synergistic impairment of sensory-motor function in APP/PS1 mice fed a Hfd. The Hfd led to increases in amyloid-beta monomers and plaques in APP/PS1 mice, as well as increased brain inflammation. These results agree with previous reports showing obesity exacerbates AD-related pathology and symptoms in mice. We used a crowd-sourced, citizen science approach to analyze imaging data to determine the impact of the APP/PS1 genotype and a Hfd on capillary stalling and CBF. Surprisingly, we did not see an increase in the number of non-flowing capillaries or a worsening of the CBF deficit in APP/PS1 mice fed a Hfd as compared to controls, suggesting that capillary stalling is not a mechanistic link between a Hfd and increased severity of AD in mice. Reducing capillary stalling by blocking neutrophil adhesion improved CBF and short-term memory function in APP/PS1 mice, even when fed a Hfd.
Genetic variants associated with alcohol dependence co-ordinate regulation of ADH genes in gastrointestinal and adipose tissues
Authors: Hibberd Rebecca , Golovina Evgeniia , Farrow Sophie , O’Sullivan Justin M. 
Published: June 2020

AbstractGWAS studies have identified genetic variants associated with Alcohol Dependence (AD), but how they link to genes, their regulation and disease traits, remains largely unexplored. Here we integrated information on the 3D genome organization with expression quantitative loci (eQTLs) analysis, using CoDeS3D, to identify the functional impacts of single nucleotide polymorphisms associated with AD (p < 1 × 10−6). We report that 42% of the 285 significant tissue-specific regulatory interactions we identify were associated with four genes encoding Alcohol Dehydrogenase - ADH1A, ADH1B, ADH1C and ADH4. Identified eQTLs produced a co-ordinated regulatory action between ADH genes, especially between ADH1A and ADH1C within the subcutaneous adipose and gastrointestinal tissues. Five eQTLs were associated with regulatory motif alterations and tissue-specific histone marks consistent with these variants falling in enhancer and promoter regions. By contrast, few regulatory connections were identified in the stomach and liver. This suggests that changes in gene regulation associated with AD are linked to changes in tissues other than the primary sites of alcohol absorption and metabolism. Future work to functionally characterise the putative regulatory regions we have identified and their links to metabolic and regulatory changes in genes will improve our mechanistic understanding of AD disease development and progression.
Evidence of radial Weibel instability in relativistic intensity laser-plasma interactions inside a sub-micron thick liquid target
Authors: Ngirmang Gregory K. , Morrison John T. , George Kevin M. , Smith Joseph R. , Frische Kyle D. , Orban Chris , Chowdhury Enam A. , Roquemore W. Mel 
Published: June 2020

AbstractSuper-intense laser plasma interaction has shown great promise as a platform for next generation particle accelerators and sources for electron, x-rays, ions and neutrons. In particular, when a relativistic intense laser focus interacts with a thin solid density target, ionized electrons are accelerated to near the speed of light (c) within an optical cycle and are pushed in the forward and transverse directions away from focus, carrying a significant portion of the laser energy. These relativistic electrons are effectively collisionless, and their interactions with the ions and surrounding cold electrons are predominantly mediated by collective electromagnetic effects of the resulting currents and charge separation. Thus, a deeper understanding of subsequent high energy ions generated from various mechanisms and their optimization requires knowledge of the relativistic electron dynamics and the fields they produce. In addition to producing MV/m quasi-static fields, accelerating the ions and confining the majority of the electrons near the bulk of the laser target, these relativistic electron currents are subject to plasma instabilities like the Weibel instability as they propagate through the thermal population in the bulk target. In this work, we present high temporal (100 fs) and spatial (1 μm) resolution shadowgraphy video capturing relativistic radial ionization front expansion and the appearance of filamentation radiating from the laser spot within a sub-micron thick liquid sheet target. Filamentation within the region persists for several picoseconds and seeds the eventual recombination and heating dynamics on the nanosecond timescale. A large scale three-dimensional particle-in-cell (PIC) simulation of the interaction revealed the presence of strong magnetic fields characteristic of Weibel Instability, and corroborated the relativistic radial expansion of the ionization front, whose speed was determined to be 0.77c. Both the experimental and simulation results strongly point towards the target field ionization and the outward expanding hot electron current as the cause of the radial expansion.
Crystal and Magnetic Structures of Double Hexagonal Close-Packed Iron Deuteride
Authors: Saitoh Hiroyuki , Machida Akihiko , Iizuka-Oku Riko , Hattori Takanori , Sano-Furukawa Asami , Funakoshi Ken-ichi , Sato Toyoto , Orimo Shin-ichi , Aoki Katsutoshi 
Published: June 2020

AbstractNeutron powder diffraction profiles were collected for iron deuteride (FeDx) while the temperature decreased from 1023 to 300 K for a pressure range of 4–6 gigapascal (GPa). The ε′ deuteride with a double hexagonal close-packed (dhcp) structure, which coexisted with other stable or metastable deutrides at each temperature and pressure condition, formed solid solutions with a composition of FeD0.68(1) at 673 K and 6.1 GPa and FeD0.74(1) at 603 K and 4.8 GPa. Upon stepwise cooling to 300 K, the D-content x increased to a stoichiometric value of 1.0 to form monodeuteride FeD1.0. In the dhcp FeD1.0 at 300 K and 4.2 GPa, dissolved D atoms fully occupied the octahedral interstitial sites, slightly displaced from the octahedral centers in the dhcp metal lattice, and the dhcp sequence of close-packed Fe planes contained hcp-stacking faults at 12%. Magnetic moments with 2.11 ± 0.06 μB/Fe-atom aligned ferromagnetically in parallel on the Fe planes.
Amelioration of Physical Properties and Printability of Paper Coated with N-methylated Chitosan
Authors: Wu Meiyan , Xu Rui , Liu Chao , Li Bin , Long Zhu 
Published: June 2020

AbstractIn offset printing process, poor mechanical properties and printability of paper substrate usually result in printing problems, low quality of print and waste of paper materials. Therefore, many researches focus on the quality improvement of paper substrates using suitable additives. In this work, N-methylated chitosan, including N, N-dimethyl chitosan (DMC) and N, N, N-trimethyl chitosan (TMC), were prepared and employed as coating agents to ameliorate the mechanical properties and printability of paper sheets. Analysis results showed that the mechanical strength of coated papers with DMC and TMC were largely improved, because the fibers with negative charges were prone to form electrostatic bonding with the positively charged N-methylated chitosan, thus enhancing paper strength. Particularly, compared with chitosan and DMC, the TMC-coated paper exhibited better mechanical properties, printability and surface properties due to the high cationic charge density of TMC. Therefore, surface coating with TMC is of great benefit to decrease the printing problem of paper sheets and enhance the operation speed in offset printing. This work provides a valuable reference for the amelioration of the printability and physical properties of high-quality paper products for many promising applications.
Characterisation of iron oxide encrusted microbial fossils
Authors: Levett Alan , Gagen Emma J. , Rintoul Llew , Guagliardo Paul , Diao Hui , Vasconcelos Paulo M. , Southam Gordon 
Published: June 2020

AbstractRobust methods for the characterisation of microbial biosignatures in geological matrices is critical for developing mineralogical biosignatures. Studying microbial fossils is fundamental for our understanding of the role microorganisms have played in elemental cycling in modern and ancient environments on Earth and potentially Mars. Here, we aim to understand what promotes the fossilisation of microorganisms after the initial stages of biomineralisation, committing bacteriomorphic structures to the geological record within iron-rich environments. Mineral encrusted cell envelope structures were routinely identified within a goethite-rich vein that cross-cut the saprolite (iron ore) of a weathered banded iron formation (BIF) system in the Quadrilátero Ferrífero, Brazil. The preservation of potential organic and mineralogical biosignatures associated with these fossils was characterised using the following high-resolution analytical techniques: scanning and transmission electron microscopy, focused ion beam scanning electron microscopy, nanoscale secondary ion mass spectrometry, synchrotron-based Fourier transform infrared spectroscopy and Raman spectroscopy. Electron microscopy demonstrated that mineral nucleation associated with a range of cell envelope structures typically followed the extant cell templates. These biologically-influenced iron-rich minerals are microcrystalline with minimal secondary growth. In contrast, intracellular mineralisation formed larger minerals that grew inward from the cell membrane to infill intracellular voids after cell death. A three dimensional reconstruction of encrusted cell envelopes in a fossilised biofilm suggests that microorganisms may be able to replicate, during the initial stages of mineralisation. Carbon and nitrogen signatures are preserved associated with the cell envelope structures; however, there were no conclusive mineralogical biosignatures associated with the mineralised cell envelopes highlighting the classical importance of morphology and elemental biosignatures in determining the biogenicity of bacteriomorphic structures.