bluuebunny/crossref_metadata_2025_split huggingface dataset:
Relative Timing of Nightside and Dayside Plasmapause Motion: Two Events in June 2001
Authors: Goldstein J. , Sandel B. R. 
Published: December 2019

AbstractWe examine the relative timing of dayside and nightside plasmapause motion following southward interplanetary magnetic field turnings on 2 and 9 June 2001. For both events the delay between the dayside and nightside plasmapause response is less than the temporal resolution of Imager for Magnetopause‐to‐Aurora Global Exploration extreme ultraviolet observations (10 min). Our result thus establishes a possible upper limit (
10 min) on the day‐to‐night onset delay. From analysis of the extreme ultraviolet‐observed plasmapause motion we find on 2 June the time‐averaged plasmapause
field was (in mV/m) 0.61 near noon magnetic local time, 0.35 near midnight magnetic local time, and 0.44 overall. The normalized plasmapause speed data (both dayside and nightside) are fitted to the curve
, consistent with a spatially uniform and time‐constant dawn‐dusk penetration
field that is 9% of the solar wind field. On 9 June the time‐averaged
field values (mV/m) were 0.24 (dayside), 0.28 (nightside), and 0.26 (overall); the plasmapause motion was consistent with a penetration
field 10% of the solar wind field. Plasmasphere erosion is a fundamental element of the dynamic magnetospheric response to solar wind driving. This study yields an important observational constraint on the day‐to‐night timing of the plasmapause response. The result also has implications for the two main models for the cause of erosion (convection and interchange).
Evolution of a Long‐Duration Coronal Mass Ejection and Its Sheath Region Between Mercury and Earth on 9–14 July 2013
Authors: Lugaz N. , Winslow R. M. , Farrugia C. J. 
Published: December 2019

AbstractUsing in situ measurements and remote‐sensing observations, we study a coronal mass ejection (CME) that left the Sun on 9 July 2013 and impacted both Mercury and Earth while the planets were in radial alignment (within
). The CME had an initial speed as measured by coronagraphs of 580
20 km/s, an inferred speed at Mercury of 580
30 km/s, and a measured maximum speed at Earth of 530 km/s, indicating that it did not decelerate substantially in the inner heliosphere. The magnetic field measurements made by MESSENGER and Wind reveal a very similar magnetic ejecta at both planets. We consider the CME expansion as measured by the ejecta duration and the decrease of the magnetic field strength between Mercury and Earth and the velocity profile measured in situ by Wind. The long‐duration magnetic ejecta (20 and 42 hr at Mercury and Earth, respectively) is found to be associated with a relatively slowly expanding ejecta at 1 AU, revealing that the large size of the ejecta is due to the CME itself or its expansion in the corona or innermost heliosphere and not due to a rapid expansion between Mercury at 0.45 AU and Earth at 1 AU. We also find evidence that the CME sheath is composed of compressed material accumulated before the shock formed, as well as more recently shocked material.
Gemini-GRACES high-quality spectra of Kepler evolved stars with transiting planets
Authors: Jofré E. , Almenara J. M. , Petrucci R. , Díaz R. F. , Gómez Maqueo Chew Y. , Martioli E. , Ramírez I. , García L. , Saffe C. , Canul E. F. , Buccino A. , Gómez M. , Moreno Hilario E. 
Published: December 2019

Aims. Kepler-278 and Kepler-391 are two of the three evolved stars known to date on the red giant branch (RGB) to host multiple short-period transiting planets. Moreover, the planets orbiting Kepler-278 and Kepler-391 are among the smallest discovered around RGB stars. Here we present a detailed stellar and planetary characterization of these remarkable systems.
Methods. Based on high-quality spectra from Gemini-GRACES for Kepler-278 and Kepler-391, we obtained refined stellar parameters and precise chemical abundances for 25 elements. Nine of these elements and the carbon isotopic ratios, 12C∕13C, had not previously been measured. Also, combining our new stellar parameters with a photodynamical analysis of the Kepler light curves, we determined accurate planetary properties of both systems.
Results. Our revised stellar parameters agree reasonably well with most of the previous results, although we find that Kepler-278 is ~15% less massive than previously reported. The abundances of C, N, O, Na, Mg, Al, Si, S, Ca, Sc, Ti, V, Cr, Mn, Co, Ni, Cu, Zn, Sr, Y, Zr, Ba, and Ce, in both stars, are consistent with those of nearby evolved thin disk stars. Kepler-391 presents a relatively high abundance of lithium (A(Li)NLTE = 1.29 ± 0.09 dex), which is likely a remnant from the main-sequence phase. The precise spectroscopic parameters of Kepler-278 and Kepler-391, along with their high 12C∕13C ratios, show that both stars are just starting their ascent on the RGB. The planets Kepler-278b, Kepler-278c, and Kepler-391c are warm sub-Neptunes, whilst Kepler-391b is a hot sub-Neptune that falls in the hot super-Earth desert and, therefore, it might be undergoing photoevaporation of its outer envelope. The high-precision obtained in the transit times allowed us not only to confirm Kepler-278c’s TTV signal, but also to find evidence of a previously undetected TTV signal for the inner planet Kepler-278b. From the presence of gravitational interaction between these bodies we constrain, for the first time, the mass of Kepler-278b (Mp = 56 −13+37 M⊕) and Kepler-278c (Mp = 35 −21+9.9 M⊕). The mass limits, coupled with our precise determinations of the planetary radii, suggest that their bulk compositions are consistent with a significant amount of water content and the presence of H2 gaseous envelopes. Finally, our photodynamical analysis also shows that the orbits of both planets around Kepler-278 are highly eccentric (e ~ 0.7) and, surprisingly, coplanar. Further observations (e.g., precise radial velocities) of this system are needed to confirm the eccentricity values presented here.
Exploring the latitude and depth dependence of solar Rossby waves using ring-diagram analysis
Authors: Proxauf B. , Gizon L. , Löptien B. , Schou J. , Birch A. C. , Bogart R. S. 
Published: December 2019

Context. Global-scale equatorial Rossby waves have recently been unambiguously identified on the Sun. Like solar acoustic modes, Rossby waves are probes of the solar interior.
Aims. We study the latitude and depth dependence of the Rossby wave eigenfunctions.
Methods. By applying helioseismic ring-diagram analysis and granulation tracking to observations by HMI aboard SDO, we computed maps of the radial vorticity of flows in the upper solar convection zone (down to depths of more than 16 Mm). The horizontal sampling of the ring-diagram maps is approximately 90 Mm (∼7.5°) and the temporal sampling is roughly 27 hr. We used a Fourier transform in longitude to separate the different azimuthal orders m in the range 3 ≤ m ≤ 15. At each m we obtained the phase and amplitude of the Rossby waves as functions of depth using the helioseismic data. At each m we also measured the latitude dependence of the eigenfunctions by calculating the covariance between the equator and other latitudes.
Results. We conducted a study of the horizontal and radial dependences of the radial vorticity eigenfunctions. The horizontal eigenfunctions are complex. As observed previously, the real part peaks at the equator and switches sign near ±30°, thus the eigenfunctions show significant non-sectoral contributions. The imaginary part is smaller than the real part. The phase of the radial eigenfunctions varies by only ±5° over the top 15 Mm. The amplitude of the radial eigenfunctions decreases by about 10% from the surface down to 8 Mm (the region in which ring-diagram analysis is most reliable, as seen by comparing with the rotation rate measured by global-mode seismology).
Conclusions. The radial dependence of the radial vorticity eigenfunctions deduced from ring-diagram analysis is consistent with a power law down to 8 Mm and is unreliable at larger depths. However, the observations provide only weak constraints on the power-law exponents. For the real part, the latitude dependence of the eigenfunctions is consistent with previous work (using granulation tracking). The imaginary part is smaller than the real part but significantly nonzero.
Distinct responses of neurons and astrocytes to TDP-43 proteinopathy in amyotrophic lateral sclerosis
Authors: Smethurst Phillip , Risse Emmanuel , Tyzack Giulia E , Mitchell Jamie S , Taha Doaa M , Chen Yun-Ru , Newcombe Jia , Collinge John , Sidle Katie , Patani Rickie 
Published: December 2019

AbstractAmyotrophic lateral sclerosis (ALS) is a fatal and incurable neurodegenerative disease caused by motor neuron loss, resulting in muscle wasting, paralysis and eventual death. A key pathological feature of ALS is cytoplasmically mislocalized and aggregated TDP-43 protein in &gt;95% of cases, which is considered to have prion-like properties. Historical studies have predominantly focused on genetic forms of ALS, which represent ∼10% of cases, leaving the remaining 90% of sporadic ALS relatively understudied. Additionally, the role of astrocytes in ALS and their relationship with TDP-43 pathology is also not currently well understood. We have therefore used highly enriched human induced pluripotent stem cell (iPSC)-derived motor neurons and astrocytes to model early cell type-specific features of sporadic ALS. We first demonstrate seeded aggregation of TDP-43 by exposing human iPSC-derived motor neurons to serially passaged sporadic ALS post-mortem tissue (spALS) extracts. Next, we show that human iPSC-derived motor neurons are more vulnerable to TDP-43 aggregation and toxicity compared with their astrocyte counterparts. We demonstrate that these TDP-43 aggregates can more readily propagate from motor neurons into astrocytes in co-culture paradigms. We next found that astrocytes are neuroprotective to seeded aggregation within motor neurons by reducing (mislocalized) cytoplasmic TDP-43, TDP-43 aggregation and cell toxicity. Furthermore, we detected TDP-43 oligomers in these spALS spinal cord extracts, and as such demonstrated that highly purified recombinant TDP-43 oligomers can reproduce this observed cell-type specific toxicity, providing further support to a protein oligomer-mediated toxicity hypothesis in ALS. In summary, we have developed a human, clinically relevant, and cell-type specific modelling platform that recapitulates key aspects of sporadic ALS and uncovers both an initial neuroprotective role for astrocytes and the cell type-specific toxic effect of TDP-43 oligomers.
Cooperation in the Face of Transboundary Crisis: A Framework for Analysis
Authors: Blondin Donald , Boin Arjen 
Published: December 2019

AbstractThe nation state is discovering the limits of its crisis management capacities. The Ebola and Zika outbreaks, the financial crisis, the downing of flight MH17 over Ukraine, sinking ships overfilled with refugees, cyber-attacks, urban terrorism and existential environmental threats serve as strong reminders of the complex origins and transboundary dimensions of many contemporary crises and disasters. As these transboundary aspects of modern crises become increasingly manifest, the need for international, collaborative responses appears ever clearer. But that collaboration does not always emerge in time (or at all). Even in the European Union, which has various transboundary crisis management mechanisms in place, the willingness to initiate joint crisis responses varies. This observation prompted our research question: Why do states collaborate in response to some transboundary crises but not others? We bring together the crisis and collective action literatures to formulate a theoretical framework that can help answer this question. This article identifies crucial factors that facilitate a possible pathway toward a joint response.
The null identities for boundary operators in the (2, 2p + 1) minimal gravity
Authors: Ishiki Goro , Muraki Hisayoshi , Rim Chaiho 
Published: December 2019

Abstract
By using the matrix model representation, we show that correlation numbers of boundary-changing operators (BCOs) in $(2,2p+1)$ minimal Liouville gravity satisfy some identities, which we call the null identities. These identities enable us to express the correlation numbers of BCOs in terms of those of boundary-preserving operators. We also discuss a physical implication of the null identities as the manifestation of the boundary interaction.
Comment on ‘Optimal Policy for Multi-Alternative Decisions’
Authors: Marshall James A. R. 
Published: December 2019

AbstractOptimality analysis has recently been proposed for value-based decision-making, in which decision agents are rewarded by the value of the selected option. This contrasts with psychophysics where decision agents are typically rewarded only if they choose the ‘correct’ or best option. The analysis of optimal policies for value-based decisions raises interesting and surprising parallels with decision rules proposed for accuracy-based decisions in binary and multi-alternative cases, and explains experimentally-observed deviations from rationality. However, the analysis assumes that decision agents should treat time as a linear cost, and thus optimise their Bayes Risk from decisions. A more naturalistic assumption is that future rewards are geometrically discounted, since they are less likely to be realised in an uncertain world. Changing the way in which time is costed leads to substantive changes in the resulting optimal policies, explains empirical data that previously could not be explained, and makes falsifiable predictions for future experiments.
Drumming motor sequence training induces apparent myelin remodelling in Huntington’s disease: a longitudinal diffusion MRI and quantitative magnetization transfer study
Authors: Casella Chiara , Bourbon-Teles Jose , Bells Sonya , Coulthard Elizabeth , Parker Greg D. , Rosser Anne , Jones Derek K. , Metzler-Baddeley Claudia 
Published: December 2019

1.AbstractBackgroundImpaired myelination may contribute to Huntington’s disease (HD) pathogenesis. This study assessed differences in white matter (WM) microstructure between HD patients and controls, and tested whether drumming training stimulates WM remodelling in HD. Furthermore, it examined whether training-induced microstructural changes are related to improvements in motor and cognitive function.MethodsParticipants undertook two months of drumming exercises. Working memory and executive function were assessed before and after training. Changes in WM microstructure were investigated with diffusion tensor magnetic resonance imaging (DT-MRI)-based metrics, the restricted diffusion signal fraction (Fr) from the composite hindered and restricted model of diffusion (CHARMED) and the macromolecular proton fraction (MPF) from quantitative magnetization transfer (qMT) imaging. WM pathways linking the putamen and the supplementary motor area (SMA-Putamen), and three segments of the corpus callosum (CCI, CCII, CCIII) were studied using deterministic tractography. Baseline MPF differences between patients and controls were assessed with tract-based spatial statistics (TBSS).ResultsMPF was reduced in HD patients compared to controls in the mid-section of the CC in HD subjects at baseline, while a significantly greater change in MPF was detected in HD patients relative to controls in the CCII, CCIII, and the right SMA-putamen post-training. Further, although patients improved their drumming and executive function performance, such improvements did not correlate with microstructural changes.ConclusionsIncreased MPF suggests training-induced myelin changes in HD. Tailored behavioural stimulation may lead to neural benefits in early HD that could be exploited for delaying disease progression.
FilterDCA: interpretable supervised contact prediction using inter-domain coevolution
Authors: Muscat Maureen , Croce Giancarlo , Sarti Edoardo , Weigt Martin 
Published: December 2019

AbstractPredicting three-dimensional protein structure and assembling protein complexes using sequence information belongs to the most prominent tasks in computational biology. Recently substantial progress has been obtained in the case of single proteins using a combination of unsupervised coevolutionary sequence analysis with structurally supervised deep learning. While reaching impressive accuracies in predicting residue-residue contacts, deep learning has a number of disadvantages. The need for large structural training sets limits the applicability to multi-protein complexes; and their deep architecture makes the interpretability of the convolutional neural networks intrinsically hard. Here we introduce FilterDCA, a simpler supervised predictor for inter-domain and inter-protein contacts. It is based on the fact that contact maps of proteins show typical contact patterns, which results from secondary structure and are reflected by patterns in coevolutionary analysis. We explicitly integrate averaged contacts patterns with coevolutionary scores derived by Direct Coupling Analysis, reaching results comparable to more complex deep-learning approaches, while remaining fully transparent and interpretable. The FilterDCA code is available athttp://gitlab.lcqb.upmc.fr/muscat/FilterDCA.Author summaryThede novoprediction of tertiary and quaternary protein structures has recently seen important advances, by combining unsupervised, purely sequence-based coevolutionary analyses with structure-based supervision using deep learning for contact-map prediction. While showing impressive performance, deep-learning methods require large training sets and pose severe obstacles for their interpretability. Here we construct a simple, transparent and therefore fully interpretable inter-domain contact predictor, which uses the results of coevolutionary Direct Coupling Analysis in combination with explicitly constructed filters reflecting typical contact patterns in a training set of known protein structures, and which improves the accuracy of predicted contacts significantly. Our approach thereby sheds light on the question how contact information is encoded in coevolutionary signals.
Mapping the coevolution, leadership and financing of research on viral vectors, RNAi, CRSPR/Cas9 and other genomic editing technologies
Authors: Ortiz David Fajardo , Shattuck Annie , Hornbostel Stefan 
Published: December 2019

AbstractIn the present investigation, we set out to determine and compare the evolution of the research on viral vectors, RNAi and genomic editing platforms as well as determine the profile of the main research institutions and funding agencies. A search of papers on viral vectors RNAi, CRISPR/Cas, TALENs, ZFNs and meganucleases was carried out in the Web of Science. A citation network of 16,746 papers was constructed. An analysis of network clustering combined with text mining was performed. In the case of viral vectors a long term process of incremental innovation in which the clusters of papers are organized around specific improvements of clinical relevance was identified. The most influential investigations on viral vectors were conducted in the United States and the European Union where the main funders were government agencies. The trajectory of RNAi research included clusters related to the study of RNAi as a biological phenomenon and its use in functional genomics, biomedicine and pest control. A British philanthropic organization and a US pharmaceutical company played a key role in the development of basic RNAi research and clinical application respectively, in addition to government agencies and academic institutions. In the case of CRISPR/Cas research, basic science discoveries led to the development of technical improvements, and these two in turn provided the information required for the development of biomedical, agricultural, livestock and industrial applications. The trajectory of CRISPR/Cas research exhibits a geopolitical division of the investigation efforts between the US, as the main producer of basic research and technical improvements, and China increasingly leading the applied research. A set of philanthropic foundations played a key role in specific stages of the CRISPR/Cas research. Our results reflect a change in the model in the financing of science and the emergence of China as a scientific superpower, with implications for the trajectory of development for applications of genomic technologies.
EGFR exon 19‐deletion aberrantly regulate ERCC1 expression that may partly impaired DNA damage repair ability in non‐small cell lung cancer
Authors: Zhang Linlin , Pradhan Barun , Guo Lili , Meng Fanlu , Zhong Diansheng 
Published: December 2019

AbstractBackgroundEpidermal growth factor receptor (EGFR) activating mutations are usually associated with DNA damage repair (DDR) deficiency. However, the precise mechanism has remained elusive. In this study, we aimed to investigate whether EGFR exon 19 deletion mutation downstream signals contributed to DDR deficiency by downregulation of excision repair cross‐complementation group‐1 (ERCC1), a key factor in DDR, expression and function.MethodsWe first measured cell survival, DNA damage (γ‐H2AX foci formation) and damage repair (ERCC1 and RAD51 foci formation) ability in response to DNA cross‐linking drug in EGFR exon 19 deletion and EGFR wild‐type cells separately. We then investigated the involvement of EGFR downstream signals in regulating ERCC1 expression and function in EGFR exon 19 deletion cells as compared with EGFR wild‐type ones.ResultsWe observed increased γ‐H2AX, but impaired ERCC1 and RAD51 nuclear foci formation in EGFR exon 19 deletion cells as compared with EGFR wild‐type ones treated with DNA cross‐linker. In addition, we identified that inhibition of EGFR exon 19 deletion signals increased ERCC1 expression, whereas blocked wild‐type EGFR signals decreased ERCC1 expression, on both mRNA and protein levels. Furthermore, EGFR exon 19 deletion downstream signals not only inhibited ERCC1 expression but also influenced ERCC1 foci formation in response to DNA cross‐linker.ConclusionOur findings indicated that the aberrant EGFR exon 19 deletion signals were not only associated with decreased expression of ERCC1 but were also involved in impaired ERCC1 recruitment in response to DNA cross‐link damage, thereby providing us with more evidence for exploring the mechanism of DDR deficiency in EGFR mutant NSCLC.