bluuebunny/crossref_metadata_2025_split huggingface dataset:
Confirmation of monoperiodicity above 20 s for two blue large-amplitude pulsators
Authors: McWhirter Paul Ross , Lam Marco C , Steele Iain A 
Published: June 2020

ABSTRACT
Blue large-amplitude pulsators (BLAPs) are a new class of pulsating variable stars. They are located close to the hot subdwarf branch in the Hertzsprung–Russell diagram and have spectral classes of late O or early B. Stellar evolution models indicate that these stars are likely radially pulsating, driven by iron group opacity in their interiors. A number of variable stars with a similar driving mechanism exist near the hot subdwarf branch with multiperiodic oscillations caused by either pressure (p) or gravity (g) modes. No multiperiodic signals were detected in the OGLE (Optical Gravitational Lensing Experiment) discovery light curves since it would be difficult to detect short-period signals associated with higher order p modes with the OGLE cadence. Using the RISE instrument on the Liverpool Telescope, we produced high-cadence light curves of two BLAPs, OGLE-BLAP-009 (mv = 15.65 mag) and OGLE-BLAP-014 (mv = 16.79 mag), using a 720 nm longpass filter. Frequency analysis of these light curves identifies a primary oscillation with a period of 31.935 ± 0.0098 min and an amplitude from a Fourier series fit of 0.236 mag for BLAP-009. The analysis of BLAP-014 identifies a period of 33.625 ± 0.0214 min and an amplitude of 0.225 mag. Analysis of the residual light curves reveals no additional short-period variability down to an amplitude of 15.20 ± 0.26 mmag for BLAP-009 and 58.60 ± 3.44 mmag for BLAP-014 for minimum periods of 20 and 60 s, respectively. These results further confirm that the BLAPs are monoperiodic.
Cold molecular gas and free–free emission from hot, dust-obscured galaxies at z ∼ 3
Authors: Penney J I , Blain A W , Assef R J , Diaz-Santos T , González-López J , Tsai C-W , Aravena M , Eisenhardt P R M , Jones S F , Jun H D , Kim M , Stern D , Wu J 
Published: June 2020

ABSTRACT
We report on observations of redshifted CO(1–0) line emission and observed-frame $\rm \sim 30\,$GHz radio continuum emission from five ultra-luminous, mid-IR selected hot, Dust-Obscured Galaxies (Hot DOGs) at $z\rm \gtrsim 3$ using the Karl G. Jansky Very Large Array. We detect CO(1–0) line emission in all five Hot DOGs, with one of them at high signal-to-noise ratio. We analyse FIR-radio spectral energy distributions, including dust, free–free, and synchrotron emission for the galaxies. We find that most of the $\rm 115\,$ GHz rest-frame continuum is mostly due to synchrotron or free–free emission, with only a potentially small contribution from thermal emission. We see a deficit in the rest-frame $\rm 115\,$ GHz continuum emission compared to dusty star-forming galaxies and sub-millimetre galaxies (SMGs) at high redshift, suggesting that Hot DOGs do not have similar cold gas reserves compared with star-forming galaxies. One target, W2305−0039, is detected in the FIRST $\rm 1.4\, GHz$ survey, and is likely to possess compact radio jets. We compare to the FIR–radio correlation, and find that at least half of the Hot DOGs in our sample are radio-quiet with respect to normal galaxies. These findings suggest that Hot DOGs have comparably less cold molecular gas than star-forming galaxies at lower, $z\rm \sim 2$ redshifts, and are dominated by powerful, yet radio-quiet AGN.
Polycyclic aromatic hydrocarbon excitation in nearby spiral galaxies
Authors: Bendo G J , Lu N , Zijlstra A 
Published: June 2020

ABSTRACT
We have examined polycyclic aromatic hydrocarbon (PAH) excitation in a sample of 25 nearby face-on spiral galaxies using the ratio of mid-infrared PAH emission to dust mass. Within 11 of the galaxies, we found that the PAH excitation was straightforwardly linked to ultraviolet (UV) or mid-infrared star formation tracers, which, along with other results studying the relation of PAH emission to star formation, indicates that the PAHs are most strongly excited in dusty shells around the star-forming (SF) regions. Within another five galaxies, the PAH emission is enhanced around SF regions only at specific galactocentric radii. In six more galaxies, PAH excitation is more strongly correlated with the evolved stellar populations as traced by 3.6 μm emission. The results for the remaining three galaxies were ambiguous. The radial gradients of the PAH/dust ratios were generally not linked to log(O/H) gradients except when the log(O/H) gradients were relatively steep. Galaxies in which PAHs were excited by evolved stars had relatively high far-UV to mid-infrared ratios, implying that variations in the link between PAH excitation and different stellar populations are connected to changes in dust attenuation within galaxies. Alternately, differences in morphology could make it more likely that PAHs are excited by evolved stars, as five of the six galaxies where this occurs are late-type flocculent spiral galaxies. These heterogeneous results demonstrate the complexity of describing PAH excitation and have broad implications for using PAH emission as a star formation tracer as well as for modelling dust emission and radiative transfer.
Planet migration in self-gravitating discs: survival of planets
Authors: Rowther Sahl , Meru Farzana 
Published: June 2020

ABSTRACT
We carry out three-dimensional smoothed particle hydrodynamics simulations to study whether planets can survive in self-gravitating protoplanetary discs. The discs modelled here use a cooling prescription that mimics a real disc, which is only gravitationally unstable in the outer regions. We do this by modelling the cooling using a simplified method such that the cooling time in the outer parts of the disc is shorter than in the inner regions, as expected in real discs. We find that both giant (&gt;MSat) and low-mass (&lt;MNep) planets initially migrate inwards very rapidly, but are able to slow down in the inner gravitationally stable regions of the disc without needing to open up a gap. This is in contrast to previous studies where the cooling was modelled in a more simplified manner where, regardless of mass, the planets were unable to slow down their inward migration. This shows the important effect the thermodynamics has on planet migration. In a broader context, these results show that planets that form in the early stages of the discs’ evolution, when they are still quite massive and self-gravitating, can survive.
Flyby encounters between two planetary systems II: exploring the interactions of diverse planetary system architectures
Authors: Li Daohai , Mustill Alexander J , Davies Melvyn B 
Published: June 2020

ABSTRACT
Planetary systems formed in clusters may be subject to stellar encounter flybys. Here, we create a diverse range of representative planetary systems with different orbital scales and planets’ masses and examine encounters between them in a typical open cluster. We first explore the close-in multisuper Earth systems ≲0.1 au. They are resistant to flybys in that only ones inside a few au can destabilize a planet or break the resonance between such planets. But these systems may capture giant planets on to wide orbits from the intruding star during distant flybys. If so, the original close-in small planets’ orbits may be tilted together through Kozai–Lidov mechanism, forming a ‘cold’ system that is significantly inclined against the equator of the central host. Moving to the intermediately placed planets around solar-like stars, we find that the planets’ mass gradient governs the systems’ long-term evolution post-encounter: more massive planets have better chances to survive. Also, a system’s angular momentum deficit, a quantity describing how eccentric/inclined the orbits are, measured immediately after the encounter, closely relates to the longevity of the systems – whether or not and when the systems turn unstable in the ensuing evolution millions of years post-encounter. We compare the orbits of the surviving planets in the unstable systems through (1) the immediate consequence of the stellar fly or (2) internal interplanetary scattering long post-encounter and find that those for the former are systematically colder. Finally, we show that massive wide-orbit multiplanet systems like that of HR 8799 can be easily disrupted and encounters at a few hundreds of au suffice.
Pathological mutations in PNKP trigger defects in DNA single-strand break repair but not DNA double-strand break repair
Authors: Kalasova Ilona , Hailstone Richard , Bublitz Janin , Bogantes Jovel , Hofmann Winfried , Leal Alejandro , Hanzlikova Hana , Caldecott Keith W 
Published: June 2020

AbstractHereditary mutations in polynucleotide kinase-phosphatase (PNKP) result in a spectrum of neurological pathologies ranging from neurodevelopmental dysfunction in microcephaly with early onset seizures (MCSZ) to neurodegeneration in ataxia oculomotor apraxia-4 (AOA4) and Charcot-Marie-Tooth disease (CMT2B2). Consistent with this, PNKP is implicated in the repair of both DNA single-strand breaks (SSBs) and DNA double-strand breaks (DSBs); lesions that can trigger neurodegeneration and neurodevelopmental dysfunction, respectively. Surprisingly, however, we did not detect a significant defect in DSB repair (DSBR) in primary fibroblasts from PNKP patients spanning the spectrum of PNKP-mutated pathologies. In contrast, the rate of SSB repair (SSBR) is markedly reduced. Moreover, we show that the restoration of SSBR in patient fibroblasts collectively requires both the DNA kinase and DNA phosphatase activities of PNKP, and the fork-head associated (FHA) domain that interacts with the SSBR protein, XRCC1. Notably, however, the two enzymatic activities of PNKP appear to affect different aspects of disease pathology, with reduced DNA phosphatase activity correlating with neurodevelopmental dysfunction and reduced DNA kinase activity correlating with neurodegeneration. In summary, these data implicate reduced rates of SSBR, not DSBR, as the source of both neurodevelopmental and neurodegenerative pathology in PNKP-mutated disease, and the extent and nature of this reduction as the primary determinant of disease severity.
Antisense oligonucleotide-mediated correction of CFTR splicing improves chloride secretion in cystic fibrosis patient-derived bronchial epithelial cells
Authors: Michaels Wren E , Bridges Robert J , Hastings Michelle L 
Published: June 2020

AbstractCystic fibrosis (CF) is an autosomal recessive disorder caused by mutations in the CF transmembrane conductance regulator (CFTR) gene, encoding an anion channel that conducts chloride and bicarbonate across epithelial membranes. Mutations that disrupt pre-mRNA splicing occur in &gt;15% of CF cases. One common CFTR splicing mutation is CFTR c.3718-2477C&gt;T (3849+10 kb C&gt;T), which creates a new 5′ splice site, resulting in splicing to a cryptic exon with a premature termination codon. Splice-switching antisense oligonucleotides (ASOs) have emerged as an effective therapeutic strategy to block aberrant splicing. We test an ASO targeting the CFTR c.3718-2477C&gt;T mutation and show that it effectively blocks aberrant splicing in primary bronchial epithelial (hBE) cells from CF patients with the mutation. ASO treatment results in long-term improvement in CFTR activity in hBE cells, as demonstrated by a recovery of chloride secretion and apical membrane conductance. We also show that the ASO is more effective at recovering chloride secretion in our assay than ivacaftor, the potentiator treatment currently available to these patients. Our findings demonstrate the utility of ASOs in correcting CFTR expression and channel activity in a manner expected to be therapeutic in patients.
Intrinsic disorder is essential for Cas9 inhibition of anti-CRISPR AcrIIA5
Authors: An So Young , Ka Donghyun , Kim Iktae , Kim Eun-Hee , Kim Nak-Kyoon , Bae Euiyoung , Suh Jeong-Yong 
Published: June 2020

AbstractClustered regularly interspaced short palindromic repeats (CRISPRs) and CRISPR-associated (Cas) proteins provide adaptive immunity to prokaryotes against invading phages and plasmids. As a countermeasure, phages have evolved anti-CRISPR (Acr) proteins that neutralize the CRISPR immunity. AcrIIA5, isolated from a virulent phage of Streptococcus thermophilus, strongly inhibits diverse Cas9 homologs, but the molecular mechanism underlying the Cas9 inhibition remains unknown. Here, we report the solution structure of AcrIIA5, which features a novel α/β fold connected to an N-terminal intrinsically disordered region (IDR). Remarkably, truncation of the N-terminal IDR abrogates the inhibitory activity against Cas9, revealing that the IDR is essential for Cas9 inhibition by AcrIIA5. Progressive truncations and mutations of the IDR illustrate that the disordered region not only modulates the association between AcrIIA5 and Cas9–sgRNA, but also alters the catalytic efficiency of the inhibitory complex. The length of IDR is critical for the Cas9–sgRNA recognition by AcrIIA5, whereas the charge content of IDR dictates the inhibitory activity. Conformational plasticity of IDR may be linked to the broad-spectrum inhibition of Cas9 homologs by AcrIIA5. Identification of the IDR as the main determinant for Cas9 inhibition expands the inventory of phage anti-CRISPR mechanisms.
IncC conjugative plasmids and SXT/R391 elements repair double-strand breaks caused by CRISPR–Cas during conjugation
Authors: Roy David , Huguet Kevin T , Grenier Frédéric , Burrus Vincent 
Published: June 2020

AbstractBacteria have evolved defence mechanisms against bacteriophages. Restriction-modification systems provide innate immunity by degrading invading DNAs that lack proper methylation. CRISPR–Cas systems provide adaptive immunity by sampling the genome of past invaders and cutting the DNA of closely related DNA molecules. These barriers also restrict horizontal gene transfer mediated by conjugative plasmids. IncC conjugative plasmids are important contributors to the global dissemination of multidrug resistance among pathogenic bacteria infecting animals and humans. Here, we show that IncC conjugative plasmids are highly resilient to host defence systems during entry into a new host by conjugation. Using a TnSeq strategy, we uncover a conserved operon containing five genes (vcrx089–vcrx093) that confer a novel host defence evasion (hde) phenotype. We show that vcrx089–vcrx090 promote resistance against type I restriction-modification, whereas vcrx091–vcxr093 promote CRISPR–Cas evasion by repairing double-strand DNA breaks via recombination between short sequence repeats. vcrx091, vcrx092 and vcrx093 encode a single-strand binding protein, and a single-strand annealing recombinase and double-strand exonuclease related to Redβ and λExo of bacteriophage λ, respectively. Homologous genes of the integrative and conjugative element R391 also provide CRISPR–Cas evasion. Hence, the conserved hde operon considerably broadens the host range of large families of mobile elements spreading multidrug resistance.
Temperature-dependent Rutile Solubility in Garnet and Clinopyroxene from Mantle Eclogite: Implications for Continental Crust Formation and V-based Oxybarometry
Authors: Aulbach Sonja 
Published: June 2020

Abstract
Despite its accessory mineral status in metabasaltic rocks, rutile controls the whole-rock Ti, Nb and Ta budget. These are key elements used to trace fluid- and melt-mediated mass transfer across the mantle–crust boundary. Rutile also contains significant amounts of the redox-sensitive element V, which is increasingly used to estimate oxygen fugacity. Kimberlite-borne mantle eclogite xenoliths, which are frequently rutile-bearing, have been interpreted as residues from the extraction of silicic partial melt similar in composition to the average continental crust. Published mineral compositions for eclogite xenoliths from various cratons combined with geothermobarometrical calculations show that TiO2 contents in garnet and clinopyroxene increase with increasing temperature of last residence in the lithospheric mantle, whereas apparent clinopyroxene–garnet distribution coefficients decrease. This implies that (1) increasing TiO2 contents in eclogitic garnet or clinopyroxene are not a signature of increasing metasomatism with depth, (2) whole-rock eclogites reconstructed without rutile will increasingly underestimate TiO2, Nb and Ta contents with decreasing temperature, and (3) low-temperature eclogites are more likely to contain free rutile. Only about a third of the ∼250 samples considered here would have whole-rock TiO2 contents (reconstructed with calculated rutile modes) required for rutile saturation during subduction and partial melting. If there is a role for subducting oceanic crust now sampled as mantle eclogite, the characteristic Ti–Nb–Ta depletion in continental crust may require fluid-dominated processes, where these elements are not efficiently mobilised. In garnet, Ti uptake on the octahedral site is accommodated primarily by coupled substitution with Na and subordinately with a divalent metal cation, and there is no evidence for substitution on the tetrahedral site. For samples equilibrated to the conductive geotherm, Ti in addition to Na enrichment may be indicative of equilibration in the diamond stability field. The jadeite component in clinopyroxene as a function of temperature is a good indicator of the geotherm to which the various samples equilibrated, and can be used to reveal samples within each suite that have been affected by isobaric heating. The distribution of V in eclogitic garnet, clinopyroxene and rutile is affected by bulk composition, temperature and oxygen fugacity. In carefully vetted, low-temperature samples with TiO2 contents &gt;0·8 wt%, V-based oxybarometry may monitor redox conditions prevailing during metamorphism of oceanic crust or, at lower TiO2, during (secular) cooling-related exsolution of rutile from garnet or clinopyroxene, whereas in higher-temperature ilmenite-bearing samples metasomatic conditions may be recorded.
Common Biological Modulators of Acute Pain: An Overview Within the AAAPT Project (ACTTION-APS-AAPM Acute Pain Taxonomy)
Authors: Curatolo Michele 
Published: June 2020

AbstractObjectiveThe ACTTION-APS-AAPM Acute Pain Taxonomy (AAAPT) project relies on the identification of modulators to improve characterization and classification of acute pain conditions. In the frame of the AAAPT effort, this paper presents an overview of common biological modulators of acute pain.MethodsNonsystematic overview.ResultsFemales may experience more acute pain than males, but the clinical significance may be modest. Increasing age is associated with decreasing analgesic requirement and decreasing pain intensity after surgery and with higher risk of acute low back pain. Racial and ethnic minorities have worse pain, function, and perceived well-being. Patients with preexisting chronic pain and opioid use are at higher risk of severe acute pain and high opioid consumption. The OPRM1 gene A118G polymorphism is associated with pain severity and opioid consumption, with modest quantitative impact. Most studies have found positive associations between pain sensitivity and intensity of acute clinical pain. However, the strength of the association is unclear. Surgical techniques, approaches, and complications influence postoperative pain.ConclusionsSex, age, race, ethnicity, preexisting chronic pain and opioid use, surgical approaches, genetic factors, and pain sensitivity are biological modulators of acute pain. Large studies with multisite replication will quantify accurately the association between modulators and acute pain and establish the value of modulators for characterization and classification of acute pain conditions, as well as their ability to identify patients at risk of uncontrolled pain. The development and validation of quick, bed-side pain sensitivity tests would allow their implementation as clinical screening tools. Acute nonsurgical pain requires more investigation.
Clonal haematopoiesis is increased in early onset in systemic sclerosis
Authors: Ricard Laure , Hirsch Pierre , Largeaud Laëtitia , Deswarte Caroline , Jachiet Vincent , Mohty Mohamad , Rivière Sébastien , Malard Florent , Tenon Maxime , de Vassoigne Frédéric , Fain Olivier , Gaugler Béatrice , Rossignol Julien , Delhommeau François , Mekinian Arsène ,   on behalf MINHEMON (French Network of dysimmune disorders associated with hemopathies)
Published: June 2020

Abstract

Objectives
SSc is an autoimmune disease characterized by fibrosis, microangiopathy and immune dysfunctions including dysregulation of proinflammatory cytokines. Clonal haematopoiesis of indeterminate potential (CHIP) is defined by the acquisition of somatic mutations in haematopoietic stem cells leading to detectable clones in the blood. Recent data have shown a higher risk of cardiovascular disease in patients with CHIP resulting from increased production of proinflammatory cytokines and accelerated atherosclerosis. Eventual links between CHIP and autoimmune diseases are undetermined. The aim of our study was to evaluate the prevalence of CHIP in SSc patients and its association with clinical phenotype.

Methods
Forty-one genes frequently mutated in myeloid malignancies were sequenced in peripheral blood mononuclear cells from 90 SSc patients and 44 healthy donors.

Results
A total of 15 somatic variants were detected in 13/90 SSc patients (14%) and four somatic variants in 4/44 (9%) healthy donors (HD) (P = 0.58). The prevalence of CHIP was significantly higher in younger SSc patients than in HD: 25% (6/24) vs 4% (1/26) (P = 0.045) under 50 years and 17% (7/42) vs 3% (1/38) (P = 0.065) under 60 years. The prevalence of CHIP in patients over 70 years was similar in SSc patients and healthy donors. The most common mutations occurred in DNMT3A (seven variants). No major clinical differences were observed between SSc patients with or without CHIP.

Conclusion
Whether CHIP increases the risk to develop SSc or is a consequence of a SSc-derived modified bone marrow micro-environment remains to be explored.
Pre-operative withholding of infliximab and the risk of infections after major surgery in patients with rheumatoid arthritis
Authors: Ward Michael M , Dasgupta Abhijit 
Published: June 2020

Abstract

Objectives
Withholding TNF inhibitors (TNFI) before surgery has been recommended due to concern for post-operative infection. We examined the risks of post-operative infections and mortality in patients with RA in relation to the pre-operative timing of infliximab infusion.

Methods
In this population-based retrospective cohort study, we used US Medicare claims data from 2007 to 2015 to identify patients with RA who underwent coronary artery bypass grafting (CABG), aortic or vascular surgery, or bowel resection, and who were treated with infliximab in the 90 days prior to surgery. We examined associations between the timing of infusion and infections and mortality in the 30 days after surgery. We adjusted for the predicted probability of post-operative infection or death, demographic characteristics, use of MTX, post-operative blood transfusion and hospital volume.

Results
We studied 712 patients with CABG, 244 patients with vascular surgery and 862 patients with bowel resections. Post-operative pneumonia occurred in 7.4–11.9%, urinary tract infection in 9.0–15.2%, surgical site infection in 3.2–18.9%, sepsis in 4.2–9.6% and death in 3.5–7.0% among surgery cohorts. There was no association between the time from last infliximab dose to surgery and the risk of post-operative infection or mortality in any surgical cohort. No subgroups were identified that had an increased risk of infection with more proximate use of infliximab.

Conclusion
Among elderly patients with RA, risks of infection and mortality after major surgery were not related to the pre-operative timing of infliximab infusion.