bluuebunny/crossref_metadata_2025_split huggingface dataset:
Mineralogy and Origin of Aerosol From an Arc Basaltic Eruption: Case Study of Tolbachik Volcano, Kamchatka
Authors: Zelenski M. , Kamenetsky V. S. , Taran Yu. , Kovalskii A. M. 
Published: February 2020

AbstractIntense emission of volcanic aerosol accompanied the 2012–2013 basaltic effusive eruption of Tolbachik volcano, Kamchatka. The aerosols sampled contain sulfuric acid droplets, glassy particles, and 70 mineral phases. All aerosol particles may be classified by their origin. The fragmentation aerosol includes magma fragments: silicate glass clasts, silicate microspheres, and small phenocrysts (olivine, pyroxene, and magnetite). The alteration aerosol comprises particles of quenched silicate melt covered with secondary minerals (fluorides, sulfates, and oxides/hydroxides of rock‐forming elements) and fragments of altered rocks composed solely of secondary minerals. The condensation aerosol dominated the mass during the later stages of the eruption when the explosive activity had ceased, and was characterized by the greatest variety of particle compositions. Na‐K sulfate and Fe (III) oxide comprised more than 95% of the solid fraction of the condensation aerosol. The remaining 5% was represented by native elements (Au, Ag‐Pt alloy, and Pt); sulfides of Fe, Cu, Ag, and Re; oxides and hydroxides of Al, Fe, Cu, Zn, Mo, W, Ta, and Zr; halides of Al, Mg, Na, K, Ca, Cd, Pb, Ag, and Tl; and sulfates of Na, K, Pb, Ca, and Ba; the only silicate was As‐bearing orthoclase. Droplets of H2SO4 formed the liquid phase of the condensation aerosol. Some of the aerosol components, such as magnetite spherules or phosphate‐carbonate‐fluorite association, likely had a nonvolcanic origin (country rocks and wood fly ash). The volcanic aerosols and their contained minerals, discharged at Tolbachik and elsewhere, result in a physical and chemical effect on the environment in the region of such volcanoes.
On Energetic Electron Dynamics During Geomagnetic Quiet Times in Earth's Inner Radiation Belt due to Atmospheric Collisional Loss and CRAND as a Source
Authors: Xiang Zheng , Li Xinlin , Temerin M. A. , Ni Binbin , Zhao Hong , Zhang Kun , Khoo Leng Ying 
Published: February 2020

AbstractTo investigate the role of atmospheric collisions and cosmic ray albedo neutron decay (CRAND) in the dynamics of energetic electrons in the Earth's inner radiation belt during geomagnetic quiet times, a drift‐collision‐source model that includes azimuthal drift, pitch angle diffusion from elastic collision, energy loss from inelastic collision, and a CRAND source is developed. In the model, the bounce‐averaged pitch angle diffusion coefficients and energy loss rates are calculated based on scattering of electrons with neutrals given by the NRLMSISE‐00 model and with ions and electrons given by International Reference Ionosphere (IRI) 2012 model. The electron source rate from CRAND follows the recently developed drift‐source model in Xiang et al. (2019). For 304‐keV quasi‐trapped electrons at L = 1.25, simulation results with CRAND show good agreement with Detection of Electro‐Magnetic Emissions Transmitted from Earthquake Regions satellite observations, confirming that CRAND is the main source for these quasi‐trapped electrons, in contrast to the previous understanding that these quasi‐trapped electrons were formed by wide‐angle scattering of the trapped populations. For trapped electrons, 153, 304, and 509 keV at L < 1.3, the simulation results with only azimuthal drift and atmospheric collisions show a much quicker decrease than observations, while simulation results including a CRAND source are generally comparable to the observations, suggesting that CRAND is an important source of trapped hundreds of kiloelectron‐volt electrons at L < 1.3 during quiet times and provides a baseline for the electron flux even during active times as well. Furthermore, these results suggest that actual radial diffusion rates in the inner belt are lower than previous estimates in which CRAND contributions were not considered.
Preeruptive P‐T Conditions and H2O Concentration of the Aso‐4 Silicic End‐Member Magma Based on High‐Pressure Experiments
Authors: Ushioda Masashi , Miyagi Isoji , Suzuki Toshihiro , Takahashi Eiichi , Hoshizumi Hideo 
Published: February 2020

AbstractTo constrain the preeruptive physical and chemical conditions (pressure, temperature, H2O content, and fO2) of the most recent and largest eruption (Aso‐4) of Aso volcano, Japan, we compared phase assemblages and chemical compositions of erupted material with those of experimentally determined run charges of the silicic end‐member magma of Aso‐4 (the KJ5665 pumice and MY5774 welded lens from the Aso‐4 pyroclastic flow deposit; SiO2 = 70.5 wt %). Experimental conditions were as follows: starting material = KJ5665 pumice, pressure = 100–700 MPa, temperature range = 810–950 °C, and injected H2O content = 2.9–6.7 wt %. The starting material comprised mainly rhyolitic glass with plagioclase, orthopyroxene, magnetite, and ilmenite phenocrysts. Hornblende phenocrysts are not found on cross sections of the KJ5665 pumice. Core compositions of these phenocrysts are unimodal. Using the magnetite‐ilmenite thermometer, the preeruptive magmatic temperature and fO2 of KJ5665 were estimated to be ~900 °C and Nickel‐Nickel oxide (NNO) +1.1 log units, respectively. Run products contain plagioclase (An20–48), orthopyroxene (Mg# = 53–72), magnetite, ilmenite, biotite, and K‐feldspar. Hornblende was not observed. Preeruptive conditions of the silicic end‐member magma of the Aso‐4 eruption are estimated to be ~900 °C, ≤ 300 MPa, and ≤ 3 wt % H2O.
Flexible and Modular Simultaneous Modeling of Flow and Reactive Transport in Rivers and Hyporheic Zones
Authors: Li Bing , Liu Xiaofeng , Kaufman Matthew H. , Turetcaia Anna , Chen Xingyuan , Cardenas M. Bayani 
Published: February 2020

AbstractInvestigations of coupled multiphysics processes in rivers and hyporheic zones have extensively used numerical models. Most existing models use a sequential, one‐way coupling between the surface and subsurface domains. Such one‐way coupling potentially introduces error. To overcome this, a fully coupled model, hyporheicFoam, was developed using the open‐source computational platform OpenFOAM. It captures the coupled flow and multicomponent reactive transport processes within both surface and subsurface domains and across their interface. The coupling between two domains is implemented by mapping conservative flux boundary conditions at the interface through an iterative algorithm. Reactive transport is enabled by specifying a reaction network. To start, we have implemented reaction kinetics following the double Monod‐type model with inhibition. The model capability is illustrated through modeling of both conservative and reactive hyporheic flow and transport through dune bedforms. With the novel coupled model, it is now possible to quantify reactions wherein the reactants and products are constantly exchanging between domains and have feedbacks. hyporheicFoam can simulate large, three‐dimensional cases owing to the computational flexibility and power offered by the code structure and parallel design of OpenFOAM.
Wnt signaling in cancer: therapeutic targeting of Wnt signaling beyond β-catenin and the destruction complex
Authors: Jung Youn-Sang , Park Jae-Il 
Published: February 2020

AbstractWnt/β-catenin signaling is implicated in many physiological processes, including development, tissue homeostasis, and tissue regeneration. In human cancers, Wnt/β-catenin signaling is highly activated, which has led to the development of various Wnt signaling inhibitors for cancer therapies. Nonetheless, the blockade of Wnt signaling causes side effects such as impairment of tissue homeostasis and regeneration. Recently, several studies have identified cancer-specific Wnt signaling regulators. In this review, we discuss the Wnt inhibitors currently being used in clinical trials and suggest how additional cancer-specific regulators could be utilized to treat Wnt signaling-associated cancer.
Carrier-assisted differential detection
Authors: Shieh William , Sun Chuanbowen , Ji Honglin 
Published: February 2020

AbstractTo overcome power fading induced by chromatic dispersion in optical fiber communications, optical field recovery is a promising solution for direct detection short-reach applications, such as fast-evolving data center interconnects (DCIs). To date, various direct detection schemes capable of optical field recovery have been proposed, including Kramers−Kronig (KK) and signal−signal beat interference (SSBI) iterative cancellation (IC) receivers. However, they are all restricted to the single sideband (SSB) modulation format, thus conspicuously losing half of the electrical spectral efficiency (SE) compared with double sideband (DSB) modulation. Additionally, SSB suffers from the noise folding issue, requiring a precise optical filter that complicates the receiver design. As such, it is highly desirable to investigate the field recovery of DSB signals via direct detection. In this paper, for the first time, we propose a novel receiver scheme called carrier-assisted differential detection (CADD) to realize optical field recovery of complex-valued DSB signals via direct detection. First, CADD doubles the electrical SE compared with the KK and SSBI IC receivers by adopting DSB modulation without sacrificing receiver sensitivities. Furthermore, by using direct detection without needing a precise receiver optical filter, CADD can employ cost-effective uncooled lasers as opposed to expensive temperature-controlled lasers in coherent systems. Our proposed receiver architecture opens a new class of direct detection schemes that are suitable for photonic integration analogous to homodyne receivers in coherent detection.
Electrogenic sulfide oxidation mediated by cable bacteria stimulates sulfate reduction in freshwater sediments
Authors: Sandfeld Tobias , Marzocchi Ugo , Petro Caitlin , Schramm Andreas , Risgaard-Petersen Nils 
Published: February 2020

Abstract
Cable bacteria are filamentous members of the Desulfobulbaceae family that oxidize sulfide with oxygen or nitrate by transferring electrons over centimeter distances in sediments. Recent studies show that freshwater sediments can support populations of cable bacteria at densities comparable to those found in marine environments. This is surprising since sulfide availability is presumably low in freshwater sediments due to sulfate limitation of sulfate reduction. Here we show that cable bacteria stimulate sulfate reduction in freshwater sediment through promotion of sulfate availability. Comparing experimental freshwater sediments with and without active cable bacteria, we observed a three- to tenfold increase in sulfate concentrations and a 4.5-fold increase in sulfate reduction rates when cable bacteria were present, while abundance and community composition of sulfate-reducing microorganisms (SRM) were unaffected. Correlation and ANCOVA analysis supported the hypothesis that the stimulation of sulfate reduction activity was due to relieve of the kinetic limitations of the SRM community through the elevated sulfate concentrations in sediments with cable bacteria activity. The elevated sulfate concentration was caused by cable bacteria-driven sulfide oxidation, by sulfate production from an indigenous sulfide pool, likely through cable bacteria-mediated dissolution and oxidation of iron sulfides, and by enhanced retention of sulfate, triggered by an electric field generated by the cable bacteria. Cable bacteria in freshwater sediments may thus be an integral component of a cryptic sulfur cycle and provide a mechanism for recycling of the scarce resource sulfate, stimulating sulfate reduction. It is possible that this stimulation has implication for methanogenesis and greenhouse gas emissions.
Effects of tetrahedral framework nucleic acid/wogonin complexes on osteoarthritis
Authors: Sirong Shi , Yang Chen , Taoran Tian , Songhang Li , Shiyu Lin , Yuxin Zhang , Xiaoru Shao , Tao Zhang , Yunfeng Lin , Xiaoxiao Cai 
Published: February 2020

AbstractOsteoarthritis, a disorder characterized by articular cartilage deterioration, varying degrees of inflammation, and chondrocyte apoptosis, is the most common chronic joint disease. To slow or reverse its progression, inflammation should be inhibited, and chondrocyte proliferation should be promoted. Tetrahedral framework nucleic acids can be internalized by chondrocytes (even inflammatory chondrocytes) and can enhance their proliferation and migration. Wogonin, a naturally occurring flavonoid, suppresses oxidative stress and inhibits inflammation. In this study, tetrahedral framework nucleic acids were successfully self-assembled and used to load wogonin. We confirmed the effective formation of tetrahedral framework nucleic acid/wogonin complexes by dynamic light scattering, zeta potential analysis, transmission electron microscopy, and fluorescence spectrophotometry. Tetrahedral framework nucleic acids, wogonin, and especially tetrahedral framework nucleic acid/wogonin complexes effectively alleviated inflammation in vitro and in vivo and prevented cartilage destruction. In addition, these materials remarkably downregulated the expression of inflammatory mediators and matrix metalloproteinases, upregulated chondrogenic markers, and promoted tissue inhibitor of metalloproteinase 1 and B-cell lymphoma 2 expression. In vivo, after treatment with tetrahedral framework nucleic acid/wogonin complexes, the bone mineral density in regenerated tissues was much higher than that found in the untreated groups. Histologically, the complexes enhanced new tissue regeneration, significantly suppressed chondrocyte apoptosis, and promoted chondrogenic marker expression. They also inhibited cell apoptosis, increased chondrogenic marker expression, and suppressed the expression of inflammatory mediators in osteoarthritis. Therefore, we believe that tetrahedral framework nucleic acid/wogonin complexes can be used as an injectable form of therapy for osteoarthritis.
IgSF11 regulates osteoclast differentiation through association with the scaffold protein PSD-95
Authors: Kim Hyunsoo , Takegahara Noriko , Walsh Matthew C. , Middleton Sarah A. , Yu Jiyeon , Shirakawa Jumpei , Ueda Jun , Fujihara Yoshitaka , Ikawa Masahito , Ishii Masaru , Kim Junhyong , Choi Yongwon 
Published: February 2020

AbstractOsteoclasts are multinucleated, giant cells derived from myeloid progenitors. While receptor activator of NF-κB ligand (RANKL) stimulation is the primary driver of osteoclast differentiation, additional signaling further contributes to osteoclast maturation. Here, we demonstrate that immunoglobulin superfamily member 11 (IgSF11), whose expression increases during osteoclast differentiation, regulates osteoclast differentiation through interaction with postsynaptic density protein 95 (PSD-95), a scaffold protein with multiple protein interaction domains. IgSF11 deficiency in vivo results in impaired osteoclast differentiation and bone resorption but no observed defect in bone formation. Consequently, IgSF11-deficient mice exhibit increased bone mass. Using in vitro osteoclast culture systems, we show that IgSF11 functions through homophilic interactions. Additionally, we demonstrate that impaired osteoclast differentiation in IgSF11-deficient cells is rescued by full-length IgSF11 and that the IgSF11-PSD-95 interaction requires the 75 C-terminal amino acids of IgSF11. Our findings reveal a critical role for IgSF11 during osteoclast differentiation and suggest a role for IgSF11 in a receptor- and signal transduction molecule-containing protein complex.
Errors in determination of net survival: cause-specific and relative survival settings
Authors: Bright Chloe J. , Brentnall Adam R. , Wooldrage Kate , Myles Jonathon , Sasieni Peter , Duffy Stephen W. 
Published: February 2020

Abstract
Background
Cause-specific and relative survival estimates differ. We aimed to examine these differences in common cancers where by possible identifying the most plausible sources of error in each estimate.

Methods
Ten-year cause-specific and relative survival were estimated for lung, breast, prostate, ovary, oesophagus and colorectal cancers. The cause-specific survival was corrected for misclassification of cause of death. The Pohar-Perme relative survival estimator was modified by (1) correcting for differences in deaths from ischaemic heart disease (IHD) between cancers and general population; or (2) correcting the population hazard for smoking (lung cancer only).

Results
For all cancers except breast and prostate, relative survival was lower than cause-specific. Correction for published error rates in cause of death gave implausible results. Correction for rates of IHD death gave slightly different relative survival estimates for lung, oesophagus and colorectal cancers. For lung cancer, when the population hazard was inflated for smoking, survival estimates were increased.

Conclusion
Results agreed with the consensus that relative survival is usually preferable. However, for some cancers, relative survival might be inaccurate (e.g. lung and prostate). Likely solutions include enhancing life tables to include other demographic variables than age and sex, and to stratify relative survival calculation by cause of death.
Combined lifestyle factors, incident cancer, and cancer mortality: a systematic review and meta-analysis of prospective cohort studies
Authors: Zhang Yan-Bo , Pan Xiong-Fei , Chen Junxiang , Cao Anlan , Zhang Yu-Ge , Xia Lu , Wang Jing , Li Huiqi , Liu Gang , Pan An 
Published: February 2020

AbstractBackgroundCancer poses a huge disease burden, which could be reduced by adopting healthy lifestyles mainly composed of healthy diet, body weight, physical activity, limited alcohol consumption, and avoidance of smoking. However, no systematic review has summarised the relations of combined lifestyle factors with cancer morbidity and mortality.MethodsEMBASE and PubMed were searched up to April 2019. Cohort studies investigating the association of combined lifestyle factors with risks of incident cancer and cancer mortality were selected. Summary hazard ratios (HRs) and 95% confidence intervals (CIs) were calculated using random-effects models. Heterogeneity and publication bias tests were conducted.ResultsThe HRs (95% CIs) comparing individuals with the healthiest versus the least healthy lifestyles were 0.71 (0.66–0.76; 16 studies with 1.9 million participants) for incident cancer and 0.48 (0.42–0.54; 30 studies with 1.8 million participants) for cancer mortality. Adopting the healthiest lifestyles was also associated with 17 to 58% lower risks of bladder, breast, colon, endometrial, oesophageal, kidney, liver, lung, rectal, and gastric cancer. The relations were largely consistent and significant among participants with different characteristics in the subgroup analyses.ConclusionsAdopting healthy lifestyles is associated with substantial risk reduction in cancer morbidity and mortality, and thus should be given priority for cancer prevention.
Development of prediction models for lymph node metastasis in endometrioid endometrial carcinoma
Authors: Berg Hege F. , Ju Zhenlin , Myrvold Madeleine , Fasmer Kristine E. , Halle Mari K. , Hoivik Erling A. , Westin Shannon N. , Trovik Jone , Haldorsen Ingfrid S. , Mills Gordon B. , Krakstad Camilla , Werner Henrica M. J. 
Published: February 2020

AbstractBackgroundIn endometrioid endometrial cancer (EEC), current clinical algorithms do not accurately predict patients with lymph node metastasis (LNM), leading to both under- and over-treatment. We aimed to develop models that integrate protein data with clinical information to identify patients requiring more aggressive surgery, including lymphadenectomy.MethodsProtein expression profiles were generated for 399 patients using reverse-phase protein array. Three generalised linear models were built on proteins and clinical information (model 1), also with magnetic resonance imaging included (model 2), and on proteins only (model 3), using a training set, and tested in independent sets. Gene expression data from the tumours were used for confirmatory testing.ResultsLNM was predicted with area under the curve 0.72–0.89 and cyclin D1; fibronectin and grade were identified as important markers. High levels of fibronectin and cyclin D1 were associated with poor survival (p = 0.018), and with markers of tumour aggressiveness. Upregulation of bothFN1andCCND1messenger RNA was related to cancer invasion and mesenchymal phenotype.ConclusionsWe demonstrate that data-driven prediction models, adding protein markers to clinical information, have potential to significantly improve preoperative identification of patients with LNM in EEC.
Metformin reduces HGF-induced resistance to alectinib via the inhibition of Gab1
Authors: Chen Hengyi , Lin Caiyu , Peng Tao , Hu Cheng , Lu Conghua , Li Li , Wang Yubo , Han Rui , Feng Mingxia , Sun FenFen , He Yong 
Published: February 2020

AbstractAlectinib is a second-generation anaplastic lymphoma kinase (ALK) inhibitor that has sufficient clinical efficacy and satisfactory safety in ALK-positive non-small cell lung cancer (NSCLC) patients with or without brain metastasis. Alectinib has now become an important drug in the first-line treatment of advanced ALK-positive NSCLC; however, resistance is almost inevitable. The increased expression of hepatocyte growth factor (HGF) and its physiological receptor tyrosine kinase MET have been shown to be linked to acquired resistance to various tyrosine kinase inhibitors (TKIs), and this phenomenon has been observed in some ALK-positive NSCLC tumour tissues. In this study, we found that HGF levels in the culture supernatant of an ALK-positive cell line tended to increase with time and could be further increased by alectinib in a time-dependent manner. Exogenous or endogenous HGF did not cause resistance to the ALK/MET double-targeted small molecule inhibitor crizotinib, but it was an important cause of alectinib resistance. Furthermore, Gab1 was a key effector in the HGF/MET signal transduction pathway that mediated alectinib resistance. The antidiabetic drug metformin combined with alectinib overcame alectinib resistance triggered by HGF/MET through disrupting the complex between MET and Gab1, thereby inhibiting Gab1 phosphorylation and the activation of downstream signal transduction pathways. These results suggest that metformin combined with alectinib may be useful for overcoming alectinib resistance induced by the activation of the HGF/MET signalling pathway and improving the efficacy of alectinib.
PALB2 chromatin recruitment restores homologous recombination in BRCA1-deficient cells depleted of 53BP1
Authors: Belotserkovskaya Rimma , Raga Gil Elisenda , Lawrence Nicola , Butler Richard , Clifford Gillian , Wilson Marcus D. , Jackson Stephen P. 
Published: February 2020

AbstractLoss of functional BRCA1 protein leads to defects in DNA double-strand break (DSB) repair by homologous recombination (HR) and renders cells hypersensitive to poly (ADP-ribose) polymerase (PARP) inhibitors used to treat BRCA1/2-deficient cancers. However, upon chronic treatment of BRCA1-mutant cells with PARP inhibitors, resistant clones can arise via several mechanisms, including loss of 53BP1 or its downstream co-factors. Defects in the 53BP1 axis partially restore the ability of a BRCA1-deficient cell to form RAD51 filaments at resected DSBs in a PALB2- and BRCA2-dependent manner, and thereby repair DSBs by HR. Here we show that depleting 53BP1 in BRCA1-null cells restores PALB2 accrual at resected DSBs. Moreover, we demonstrate that PALB2 DSB recruitment in BRCA1/53BP1-deficient cells is mediated by an interaction between PALB2’s chromatin associated motif (ChAM) and the nucleosome acidic patch region, which in 53BP1-expressing cells is bound by 53BP1’s ubiquitin-directed recruitment (UDR) domain.