bluuebunny/crossref_metadata_2025_split huggingface dataset:
Magnetospheric Dynamo Driving Large‐scale Birkeland Currents
Authors: Watanabe Masakazu , Tanaka Takashi , Fujita Shigeru 
Published: May 2019

AbstractBased upon recent global magnetohydrodynamic (MHD) simulations, we provide a theoretical foundation for magnetospheric dynamos driving large‐scale field‐aligned current (FAC) systems. In the framework of MHD, the dynamo is a process in which plasma thermal energy is converted to electromagnetic energy. Theoretical analysis using ideal MHD equations indicates the existence of two types of dynamos that allow this energy conversion. One is the expanding slow dynamo associated with flux tube expansion, and the other is the contracting slow dynamo associated with flux tube contraction. The expanding slow is a stationary dynamo without significant magnetic field curvature, with the field intensity gradient playing a central role. In contrast, the contracting slow is a dynamo with finite time variation and finite magnetic field curvature. A supplementary MHD simulation in this study, together with those in the past studies, indicates the existence of a general relation between the main voltage generator (i.e., dynamo) and the main FAC generator (i.e., divergence of FACs) that appears commonly for large‐scale FAC systems.. That is, the dynamo overlaps the FAC generator in a specific spatial configuration and that at the transition between compressible high beta plasma and incompressible low beta plasma. This overlap represents a coupling of slow mode and Alfvén mode disturbances. We performed linear analysis of that special configuration using ideal MHD equations and derived the general expression relating the voltage generator and the FAC generator.
Carbon Monoxide Cycle in the Bohai Sea and the Yellow Sea: Spatial Variability, Sea‐Air Exchange, and Biological Consumption in Autumn
Authors: Zhang Jing , Wang Jing , Zhuang Guang‐Chao , Yang Gui‐Peng 
Published: May 2019

AbstractAs an important trace gas, carbon monoxide (CO) is considered to be mainly released by the ocean into the atmosphere. To further understand the role of the marginal seas for marine CO emission, we investigated sea‐to‐air flux and spatial distribution as well as biological consumption of CO using the Yellow and Bohai Seas as research objects. In the surface water, CO concentrations varied largely between 0.109 and 6.26 nmol/L. Strong vertical and diurnal variabilities were also observed, which could be attributed to the sunlight‐induced photochemical production of CO at different sampling time and depth. The atmospheric CO mixing ratios generally decreased from the coast to the open ocean, possibly due to the influence of anthropogenic activity. Relative to atmospheric CO, the concentrations of CO were mostly supersaturated in the surface water, suggesting that both the Bohai and the Yellow Seas were significant CO source in the atmosphere. Average sea‐to‐air flux of CO was about 1.76 μmol · m‐2 · day‐1, which largely depended on the saturation factor and wind speed. As an important removal pathway, microbial consumption of CO exhibited the first order kinetics. The rapid turnover of CO (3.2−9.6 hr) indicated that microbial metabolism was the major CO consumer in the surface waters that could significantly regulate the emission of CO to the atmosphere. Overall, this study improved our understanding of the biogeochemical CO cycling in marginal seas as well as in coastal regions.
Fault Geometries and Structures Associated With the Rupture Endpoints of the 2008Mw7.9 Wenchuan Earthquake, Eastern Tibet Plateau, China
Authors: Li Chuanyou , Li Xinnan , Wei Zhanyu 
Published: May 2019

AbstractThe 2008 Wenchuan earthquake (Mw7.9) initiated at the southern part of the Yingxiu‐Beichuan fault of the Longmen Shan fault zone, eastern Tibet Plateau. The earthquake rupture propagated northeast for ~300 km, producing dextral‐thrust slip along the fault zone. Numerous studies have documented the characteristics of the rupture zone; however, the exact endpoints and the termination structures at both ends remain poorly constrained. On the northeasternmost rupture section, the aftershock distribution extends ~50 km along strike past the end of the observed surface rupture, suggesting that the rupture may extend northeastward at depth. Our field observations show that the aftershock zone follows a NE‐trending linear trace indicative of an active fault at the surface and confirm that the Qingchuan fault, which is one of the faults of the northeastern Longmen Shan fault zone and is reported to have ruptured during the 2008 earthquake by some studies, did not rupture during the Wenchuan earthquake. Detailed investigations show that the rupture terminated at an area between the Qingchuan and the Bahai‐Yuquanba faults where these two faults bound a 10‐ to 20‐km wide mountain block. To the southwest, the southwesternmost end of the Wenchuan earthquake rupture zone terminated south of Sanjiang, where a NE‐trending 50‐cm high fault scarp marks the endpoint of the surface rupture. Our study suggests that fault step overs at the northeastern and southwestern segments may have acted as a barrier to rupture propagation and thus play an important role in controlling the rupture propagation but were not critical in terminating the rupture, whereas the cross structures and/or stratigraphy (complex or massifs) in the northeastern and southwestern rupture endpoints area appear to have controlled the rupture termination.
Strain Diffusion from the 30 October 2016 Norcia (Central Italy) Earthquake
Authors: Viti Marcello 
Published: May 2019

AbstractWe have modeled the propagation of the perturbation induced by the 30 October 2016 Norcia (Central Italy) earthquake by a two‐dimensional finite element procedure based on strain diffusion in the crust‐mantle system. This approach simulates the excitation of an elastic‐viscous medium by the coseismic slip related to the above seismic event. We have analyzed the temporal evolution of the expected planar strain and strain rate at selected points of the model, located near active fault systems of the Central and Northern Apennines. Moreover, the strain style (i.e., the ratio of the principal axes of the planar strain tensor) computed at each selected point is compared with available tectonic and seismological information concerning the active strain regime. Finally, we discuss the possible influence of postseismic strain perturbation on major fault systems of the Central and Northern Apennines.
Interplanetary Magnetic Field Control of Polar Ionospheric Equivalent Current System Modes
Authors: Shore R. M. , Freeman M. P. , Gjerloev J. W. 
Published: May 2019

AbstractWe analyze the response of different ionospheric equivalent current modes to variations in the interplanetary magnetic field (IMF) componentsByandBz. Each mode comprises a fixed spatial pattern whose amplitude varies in time, identified by a month‐by‐month empirical orthogonal function separation of surface measured magnetic field variance. Here we focus on four sets of modes that have been previously identified as DPY, DP2, NBZ, and DP1. We derive the cross‐correlation function of each mode set with either IMFByorBzfor lags ranging from −10 to +600 mins with respect to the IMF state at the bow shock nose. For all four sets of modes, the average correlation can be reproduced by a sum of up to three linear responses to the IMF component, each centered on a different lag. These are interpreted as the statistical ionospheric responses to magnetopause merging (15‐ to 20‐min lag) and magnetotail reconnection (60‐min lag) and to IMF persistence. Of the mode sets, NBZ and DPY are the most predictable from a given IMF component, with DP1 (the substorm component) the least predictable. The proportion of mode variability explained by the IMF increases for the longer lags, thought to indicate conductivity feedbacks from substorms. In summary, we confirm the postulated physical basis of these modes and quantify their multiple reconfiguration timescales.
Inhibition of BRD4 suppresses the malignancy of breast cancer cells via regulation of Snail
Authors: Lu Linlin , Chen Zhuojia , Lin Xinyao , Tian Lin , Su Qiao , An Panpan , Li Wuguo , Wu Yingmin , Du Jun , Shan Hong , Chiang Cheng-Ming , Wang Hongsheng 
Published: May 2019

Abstract
The mechanistic action of bromodomain-containing protein 4 (BRD4) in cancer motility, including epithelial-mesenchymal transition (EMT), remains largely undefined. We found that targeted inhibition of BRD4 reduces migration, invasion, in vivo growth of patient-derived xenograft (PDX), and lung colonization of breast cancer (BC) cells. Inhibition of BRD4 rapidly decreases the expression of Snail, a powerful EMT transcription factor (EMT-TF), via diminishing its protein stability and transcription. Protein kinase D1 (PRKD1) is responsible for BRD4-regulated Snail protein stability by triggering phosphorylation at Ser11 of Snail and then inducing proteasome-mediated degradation. BRD4 inhibition also suppresses the expression of Gli1, a key transductor of Hedgehog (Hh) required to activate the transcription of SNAI1, in BC cells. The GACCACC sequence (−341 to −333) in the SNAI1 promoter is responsible for Gli1-induced transcription of SNAI1. Clinically, BRD4 and Snail levels are increased in lung-metastasized, estrogen receptor-negative (ER-), and progesterone receptor-negative (PR-) breast cancers and correlate with the expression of mesenchymal markers. Collectively, BRD4 can regulate malignancy of breast cancer cells via both transcriptional and post-translational regulation of Snail.
Silver nanoparticles selectively induce human oncogenic γ-herpesvirus-related cancer cell death through reactivating viral lytic replication
Authors: Wan Chunlei , Tai Jiahui , Zhang Jie , Guo Yi , Zhu Qing , Ling Ding , Gu Feng , Gan Jin , Zhu Caixia , Wang Yuyan , Liu Sijin , Wei Fang , Cai Qiliang 
Published: May 2019

AbstractSilver nanoparticle (nAg), which is one of the most common manufactured nanomaterials, has a wide range of biomedical applications. The human oncogenic γ-herpesviruses, Kaposi’s sarcoma-associated herpesvirus (KSHV) and Epstein–Barr Virus (EBV), are etiologically linked to many malignancies. Currently, there are no efficient or specific treatments for these types of tumors, and most patients die because of resistance to conventional cytotoxic chemotherapy. Despite nAg having antitumor and antiviral activities, its effects on oncogenic herpesvirus-related cancer cells remain largely unknown. Here, we reveal that nAg presents higher cytotoxicity against KSHV- or EBV-latently infected cells via reactivating viral lytic replication, which relies on the induction of reactive oxygen species (ROS) generation and autophagy. Moreover, nAg blocks KSHV primary infection by directly destroying virion particles, as well as effectively inhibits colony formation and moderately represses the growth of KSHV-associated tumors in xenograft mouse model. Taken together, these results demonstrate the therapeutic potential of nAg for use in the antiviral infection and treatment of oncogenic herpesvirus-related cancers.
XPO1 inhibitor KPT-330 synergizes with Bcl-xL inhibitor to induce cancer cell apoptosis by perturbing rRNA processing and Mcl-1 protein synthesis
Authors: Zhu Zhi-Chuan , Liu Ji-Wei , Yang Can , Zhao Miao , Xiong Zhi-Qi 
Published: May 2019

AbstractXPO1 (exportin1) mediates nuclear export of proteins and RNAs and is frequently overexpressed in cancers. In this study, we show that the orally bioavailable XPO1 inhibitor KPT-330 reduced Mcl-1 protein level, by which it synergized with Bcl-xL inhibitor A-1331852 to induce apoptosis in cancer cells. KPT-330/A-1331852 combination disrupted bindings of Mcl-1 and Bcl-xL to Bax, Bak, and/or Bim, elicited mitochondrial outer membrane permeabilization, and triggered apoptosis. KPT-330 generally mitigated mRNA expression and protein synthesis rather than mRNA nuclear export or protein stability of Mcl-1. KPT-330 inhibited mTORC1/4E-BP1 and Mnk1/eIF4E axes, which disrupted the eIF4F translation initiation complex but was dispensable for Mcl-1 reduction and KPT-330/A-1331852 combination-induced apoptosis. Mature rRNAs are integral components of the ribosome that determines protein synthesis ability. KPT-330 impeded nucleolar rRNA processing and reduced total levels of multiple mature rRNAs. Reconstitution of XPO1 by expressing degradation-resistant C528S mutant retained rRNA amount, Mcl-1 expression, and Bcl-xL inhibitor resistance upon KPT-330 treatment. KPT-330/A-1331852 combination suppressed growth and enhanced apoptosis of non-small cell lung cancer xenografts. Therefore, we clarify the reason of apoptosis resistance of cancer cells to XPO1 inhibition and develop a potential strategy for treating solid tumors.
MeHg-induced autophagy via JNK/Vps34 complex pathway promotes autophagosome accumulation and neuronal cell death
Authors: Lin Tianji , Ruan Shijuan , Huang Dingbang , Meng Xiaojing , Li Wenjun , Wang Bin , Zou Fei 
Published: May 2019

AbstractMethylmercury (MeHg), an environmental toxin, may specifically cause neurological disorders. Recent studies have reported that autophagy can be induced by metals and be involved in metal cytotoxicity. However, the role of autophagy in MeHg-induced neurotoxicity remains unknown. Here, we demonstrate that MeHg induces mTOR-independent autophagy through JNK/Vps34 complex pathway, which further promotes autophagosome accumulation and neuronal cell death. In addition to cell death, MeHg increased LC3-II expression in a concentration- and time-dependent manner in neuronal cells; furthermore, western blot analysis of LC3-II expression under baf A1-treated condition indicates that MeHg activates autophagy induction. However, we found lysosomal degradative function was impaired by MeHg. Under this condition, MeHg-activated autophagy induction would elicit autophagosome accumulation and cell death. Consistent with this inference, the autophagy inhibitor decreased the MeHg-induced autophagosome accumulation and neuronal cells death, whereas the autophagy inducers further augmented MeHg cytotoxicity. Then, the mechanism of autophagy induction is investigated. We show that MeHg-induced autophagy is mTOR-independent. Vacuolar protein sorting 34 (Vps34) complex is critical for mTOR-independent autophagy. MeHg induced the interaction between Beclin1 and Vps34 to form Vps34 complex. Importantly, knockdown of Vps34 inhibited autophagy induction by MeHg. Furthermore, we found that JNK, but not p38 or ERK, promoted the formation of Vps34 complex and autophagy induction. Finally, inhibition of JNK or downregulation of Vps34 decreased autophagosome accumulation and alleviated MeHg-induced neuronal cell death. The present study implies that inhibiting JNK/Vps34 complex autophagy induction pathway may be a novel therapeutic approach for the treatment of MeHg-induced neurotoxicity.
CTL-mediated immunotherapy can suppress SHIV rebound in ART-free macaques
Authors: Fan Jin , Liang Hua , Ji Xiaolin , Wang Shuo , Xue Jing , Li Dan , Peng Hong , Qin Chuan , Yee Cassian , Shao Yiming 
Published: May 2019

AbstractA major barrier to human immunodeficiency virus (HIV) cure is the existence of viral reservoirs that lead to viral rebound following discontinuation of antiretroviral therapy (ART). We postulate that enhancing cytotoxic T lymphocytes (CTL) targeting conserved envelope (Env) regions can eliminate HIV infected cells in latency. Here, we evaluate the use of adoptively transferred HIV vaccine-induced subtype C Env-specific CTLs in a macaque subtype B simian-human immunodeficiency virus (SHIV) model to determine whether plasma viremia can be controlled after ART interruption. We demonstrate that adoptive cellular therapy (ACT) using autologous Env-specific T cells augmented by therapeutic vaccination can suppress ART-free viral rebound in the SHIV model. Furthermore, phenotypic and functional characterization of adoptively transferred cells in ACT-responsive and nonresponsive animals support a critical role for cross-reactive central memory T cells in viremia control. Our study offers an approach to potentiate immunological suppression of HIV in the absence of antiviral drugs.
Excitatory rubral cells encode the acquisition of novel complex motor tasks
Authors: Rizzi Giorgio , Coban Mustafa , Tan Kelly R. 
Published: May 2019

AbstractThe red nucleus (RN) is required for limb control, specifically fine motor coordination. There is some evidence for a role of the RN in reaching and grasping, mainly from lesion studies, but results so far have been inconsistent. In addition, the role of RN neurons in such learned motor functions at the level of synaptic transmission has been largely neglected. Here, we show that Vglut2-expressing RN neurons undergo plastic events and encode the optimization of fine movements. RN light-ablation severely impairs reaching and grasping functions while sparing general locomotion. We identify a neuronal population co-expressing Vglut2, PV and C1QL2, which specifically undergoes training-dependent plasticity. Selective chemo-genetic inhibition of these neurons perturbs reaching and grasping skills. Our study highlights the role of the Vglut2-positive rubral population in complex fine motor tasks, with its related plasticity representing an important starting point for the investigation of mechanistic substrates of fine motor coordination training.
Aptasensor for multiplex detection of antibiotics based on FRET strategy combined with aptamer/graphene oxide complex
Authors: Youn Hyungjun , Lee Kwanghyun , Her Jin , Jeon Jinseong , Mok Jihyun , So Jae-in , Shin Sangeon , Ban Changill 
Published: May 2019

AbstractThe development of a multiplexed sensing platform is necessary for highly selective, sensitive, and rapid screening of specific antibiotics. In this study, we designed a novel multiplex aptasensor for antibiotics by fluorescence resonance energy transfer (FRET) strategy using DNase I-assisted cyclic enzymatic signal amplification (CESA) method combined with aptamer/graphene oxide complex. The aptamers specific for sulfadimethoxine, kanamycin, and ampicillin were conjugated with Cyanine 3 (Cy3), 6-Carboxyfluorescein (FAM), and Cyanine 5 (Cy5), respectively, and graphene oxide (GO) was adopted to quench the fluorescence of the three different fluorophores with the efficiencies of 94.36%, 93.94%, and 96.97% for Cy3, FAM, and Cy5, respectively. CESA method was used for sensitive detection, resulting in a 2.1-fold increased signal compared to those of unamplified method. The aptasensor rapidly detected antibiotics in solution with limit of detection of 1.997, 2.664, and 2.337 ng/mL for sulfadimethoxine, kanamycin, and ampicillin, respectively. In addition, antibiotics dissolved in milk were efficiently detected with similar sensitivities. Multiplexed detection test proved that the fluorescently modified aptamers could work separately from each other. The results indicate that the aptasensor offers high specificity for each antibiotic and enables simultaneous and multicolor sensing for rapid screening of multiple antibiotics at the same time.
High-throughput targeted gene deletion in the model mushroom Schizophyllum commune using pre-assembled Cas9 ribonucleoproteins
Authors: Jan Vonk Peter , Escobar Natalia , Wösten Han A. B. , Lugones Luis G. , Ohm Robin A. 
Published: May 2019

AbstractEfficient gene deletion methods are essential for the high-throughput study of gene function. Compared to most ascomycete model systems, gene deletion is more laborious in mushroom-forming basidiomycetes due to the relatively low incidence of homologous recombination (HR) and relatively high incidence of non-homologous end-joining (NHEJ). Here, we describe the use of pre-assembled Cas9-sgRNA ribonucleoproteins (RNPs) to efficiently delete the homeodomain transcription factor gene hom2 in the mushroom-forming basidiomycete Schizophyllum commune by replacing it with a selectable marker. All components (Cas9 protein, sgRNA, and repair template with selectable marker) were supplied to wild type protoplasts by PEG-mediated transformation, abolishing the need to optimize the expression of cas9 and sgRNAs. A Δku80 background further increased the efficiency of gene deletion. A repair template with homology arms of 250 bp was sufficient to efficiently induce homologous recombination. This is the first report of the use of pre-assembled Cas9 RNPs in a mushroom-forming basidiomycete and this approach may also improve the genetic accessibility of non-model species.
Role of the membrane potential in mitochondrial protein unfolding and import
Authors: Sato Takehiro K. , Kawano Shin , Endo Toshiya 
Published: May 2019

AbstractNewly synthesized mitochondrial precursor proteins have to become unfolded to cross the mitochondrial membranes. This unfolding is achieved primarily by mitochondrial Hsp70 (mtHsp70) for presequence-containing precursor proteins. However, the membrane potential across the inner membrane (ΔΨ) could also contribute to unfolding of short-presequence containing mitochondrial precursor proteins. Here we investigated the role of ΔΨ in mitochondrial protein unfolding and import. We found that the effects of mutations in the presequence on import rates are correlated well with the hydrophobicity or ability to interact with import motor components including mtHsp70, but not with ΔΨ (negative inside). A spontaneously unfolded precursor protein with a short presequence is therefore trapped by motor components including mtHsp70, but not ΔΨ, which could cause global unfolding of the precursor protein. Instead, ΔΨ may contribute the precursor unfolding by holding the presequence at the inner membrane for trapping of the unfolded species by the import motor system.
Complex networks from classical to quantum
Authors: Biamonte Jacob , Faccin Mauro , De Domenico Manlio 
Published: May 2019

AbstractRecent progress in applying complex network theory to problems in quantum information has resulted in a beneficial cross-over. Complex network methods have successfully been applied to transport and entanglement models while information physics is setting the stage for a theory of complex systems with quantum information-inspired methods. Novel quantum induced effects have been predicted in random graphs—where edges represent entangled links—and quantum computer algorithms have been proposed to offer enhancement for several network problems. Here we review the results at the cutting edge, pinpointing the similarities and the differences found at the intersection of these two fields.