bluuebunny/crossref_metadata_2025_split huggingface dataset:
Statistical Study of the Properties of Magnetosheath Lion Roars
Authors: Giagkiozis Stefanos , Wilson Lynn B. , Burch James L. , Le Contel Olivier , Ergun Robert E. , Gershman Daniel J. , Lindqvist Per‐Arne , Mirioni Laurent , Moore Thomas E. , Strangeway Robert J. 
Published: June 2018

AbstractLion roars are narrowband whistler wave emissions that have been observed in several environments, such as planetary magnetosheaths, the Earth's magnetosphere, the solar wind, downstream of interplanetary shocks, and the cusp region. We present measurements of more than 30,000 such emissions observed by the Magnetospheric Multiscale spacecraft with high‐cadence (8,192 samples/s) search coil magnetometer data. A semiautomatic algorithm was used to identify the emissions, and an adaptive interval algorithm in conjunction with minimum variance analysis was used to determine their wave vector. The properties of the waves are determined in both the spacecraft and plasma rest frame. The mean wave normal angle, with respect to the background magnetic field (B0), plasma bulk flow velocity (Vb), and the coplanarity plane (Vb×B0) are 23°, 56°, and 0°, respectively. The average peak frequencies were ∼31% of the electron gyrofrequency (ωce) observed in the spacecraft frame and ∼18% of ωce in the plasma rest frame. In the spacecraft frame, ∼99% of the emissions had a frequency <ωce, while 98% had a peak frequency <0.72ωce in the plasma rest frame. None of the waves had frequencies lower than the lower hybrid frequency, ω. From the probability density function of the electron plasma βe, the ratio between the electron thermal and magnetic pressure, ∼99.6% of the waves were observed with βe<4 with a large narrow peak at 0.07 and two smaller, but wider, peaks at 1.26 and 2.28, while the average value was ∼1.25.
Caregiver Impressions of Clinical Effectiveness of an Intensive Behavioral Feeding Program
Authors: Begotka Andrea , Long Beth , Goday Praveen S. , Silverman Alan H. 
Published: June 2018

Intensive outpatient behavioral feeding programs are frequently used in the treatment of severe feeding disorders to decrease negative mealtime behaviors of affected children and improve caregiver-child mealtime interactions. Yet, there are few descriptions of these clinical practices and their clinical effectiveness. The purpose of this study is to describe an intensive outpatient feeding treatment protocol and to evaluate the clinical outcomes of the program. This study utilizes prepost treatment design studying patients completing a 5-day intensive outpatient parent training protocol. This study utilized caregiver completed measures including the Mealtime Behavior Questionnaire; the About Your Child’s Eating Questionnaire; the Feeding Strategies Questionnaire; and the Parent Stress Index. Findings showed pre-to-post improvements of interactions between caregivers and children within a mealtime context, decreased problematic mealtime behaviors, and improved caregiver use of effective mealtime strategies. Decreases in caregiver distress and caregiver perceptions of their child as “difficult” were also found. These findings support the use of intensive outpatient treatment programs to help caregivers learn to use effective strategies that facilitate appropriate interactions between themselves and their children within a feeding context. Implications for Impact Statement This study describes a brief intensive outpatient treatment program for feeding disorders of childhood. Based on caregiver impressions, this intervention improved mealtime interactions, child mealtime behaviors, caregiver use of effective mealtime strategies, while decreasing caregiver stress.
Temporal dynamics of microbiota before and after host death
Authors: Preiswerk David , Walser Jean-Claude , Ebert Dieter 
Published: June 2018

Abstract
The habitats that animals, humans and plants provide for microbial communities are inevitably transient, changing drastically when these hosts die. Because microbes associated with living hosts are ensured prime access to the deceased host’s organic matter, it is feasible that opportunistic, adaptable lifestyles are widespread among host-associated microbes. Here we investigate the temporal dynamics of microbiota by starving to death a host—the planktonic Crustacean Daphnia magna—and tracking the changes in its microbial community as it approaches death, dies and decomposes. Along with obligate host-associated microbes that vanished after the host’s death and decomposers that appeared after the host’s death, we also detected microbes with opportunistic lifestyles, seemingly capable of exploiting the host even before its death. We suggest that the period around host death plays an important role for host–microbiota ecology and for the evolution of hosts and their microbes.
A longitudinal study on deep brain stimulation of the medial forebrain bundle for treatment-resistant depression
Authors: Fenoy Albert J. , Schulz Paul E. , Selvaraj Sudhakar , Burrows Christina L. , Zunta-Soares Giovanna , Durkin Kathryn , Zanotti-Fregonara Paolo , Quevedo Joao , Soares Jair C. 
Published: June 2018

AbstractDeep brain stimulation (DBS) to the superolateral branch of the medial forebrain bundle (MFB) has been reported to lead to rapid antidepressant effects. In this longitudinal study, we expand upon the initial results we reported at 26 weeks (Fenoy et al., 2016), showing sustained antidepressant effects of MFB DBS on six patients with treatment-resistant depression (TRD) over 1 year. The Montgomery-Åsberg Depression Rating Scale (MADRS) was used as the primary assessment tool. Deterministic fiber tracking was used to individually map the target area; analysis was performed to compare modulated fiber tracts between patients. Intraoperatively, upon stimulation at target, responders reported immediate increases in energy and motivation. An insertional effect was seen during the 4-week sham stimulation phase from baseline (28% mean MADRS reduction,p = 0.02). However, after 1 week of initiating stimulation, three of six patients had a > 50% decrease in MADRS scores relative to baseline (43% mean MADRS reduction,p = 0.005). One patient withdrew from study participation. At 52 weeks, four of remaining five patients have > 70% decrease in MADRS scores relative to baseline (73% mean MADRS reduction,p = 0.007). Evaluation of modulated fiber tracts reveals significant common orbitofrontal connectivity to the target region in all responders. Neuropsychological testing and18F-fluoro-deoxyglucose-positron emission tomography cerebral metabolism evaluations performed at baseline and at 52 weeks showed minimal changes and verified safety. This longitudinal evaluation of MFB DBS demonstrated rapid antidepressant effects, as initially reported by Schlaepfer et al. (2013), and supports the use of DBS for TRD.
DDX39 promotes hepatocellular carcinoma growth and metastasis through activating Wnt/β-catenin pathway
Authors: Zhang Tong , Ma Zhenjiang , Liu Lijuan , Sun Jian , Tang Hui , Zhang Bing , Zou Ying , Li Heping 
Published: June 2018

AbstractHepatocellular carcinoma (HCC) is the third leading cause of cancer related death worldwide; however, the molecular mechanisms regulating HCC progression remain largely unknown. In this study, we determined the role of DDX39 which a DEAD-box RNA helicase in HCC progression, and found DDX39 was upregulated in HCC tissues and cells, DDX39 expression was positive correlated with advanced clinical stage, survival analysis showed patients with high-DDX39 levels had poor outcome, it was an independent prognostic factor. Functional analysis revealed that DDX39 overexpression promoted HCC cell migration, invasion, growth, and metastasis, DDX39 knockdown inhibited HCC cell migration, invasion, growth, and metastasis. Mechanism analysis suggested DDX39 overexpression increased β-catenin expression in nucleus and increased Wnt/β-catenin pathway target genes levels, while DDX39 knockdown reduced this effect. Knockdown of Wnt/β-catenin pathway co-activators TCF4 and LEF1 in DDX39 overexpressing HCC cells inhibited Wnt/β-catenin pathway target genes. The invasion ability was also reduced, confirming DDX39 regulates HCC progression by activating Wnt/β-catenin pathway. In conclusion, we found DDX39 is a target and prognostic factor for HCC, and promotes HCC migration, invasion, growth, and metastasis by activating Wnt/β-catenin pathway.
COMP-prohibitin 2 interaction maintains mitochondrial homeostasis and controls smooth muscle cell identity
Authors: Jia Yiting , Wang Meili , Mao Chenfeng , Yu Fang , Wang Yingbao , Xiao Rui , Jiang Changtao , Zheng Lemin , Xu Qingbo , Zheng Ming , Fu Yi , Hu Qinghua , Kong Wei 
Published: June 2018

AbstractVascular smooth muscle cells (VSMCs) are highly phenotypically plastic, and loss of the contractile phenotype in VSMCs has been recognized at the early onset of the pathology of a variety of vascular diseases. However, the endogenous regulatory mechanism to maintain contractile phenotype in VSMCs remains elusive. Moreover, little has been known about the role of the mitochondrial bioenergetics in terms of VSMC homeostasis. Herein, we asked if glycoprotein COMP (Cartilage oligomeric matrix protein) is involved in mitochondrial bioenergetics and therefore regulates VSMCs homeostasis. By using fluorescence assay, subcellular western blot and liquid chromatography tandem mass spectrometry analysis, we found that extracellular matrix protein COMP unexpectedly localized within mitochondria. Further mitochondrial transplantation revealed that both mitochondrial and non-mitochondrial COMP maintained VSMC identity. Moreover, microarray analysis revealed that COMP deficiency impaired mitochondrial oxidative phosphorylation in VSMCs. Further study confirmed that COMP deficiency caused mitochondrial oxidative phosphorylation dysfunction accompanied by morphological abnormality. Moreover, the interactome of mitochondrial COMP revealed that COMP interacted with prohibitin 2, and COMP–prohibitin 2 interaction maintained mitochondrial homeostasis. Additionally, disruption of COMP–prohibitin 2 interaction caused VSMC dedifferentiation in vitro and enhanced the neointima formation post rat carotid artery injury in vivo. In conclusion, COMP–prohibitin 2 interaction in mitochondria plays an important role in maintaining the contractile phenotype of VSMCs by regulating mitochondrial oxidative phosphorylation. Maintaining the homeostasis of mitochondrial respiration through COMP–prohibitin 2 interaction may shed light on prevention of vascular disease.
Sorting nexin 10 controls mTOR activation through regulating amino-acid metabolism in colorectal cancer
Authors: Le Yunchen , Zhang Sulin , Ni Jiahui , You Yan , Luo Kejing , Yu Yunqiu , Shen Xiaoyan 
Published: June 2018

AbstractAmino-acid metabolism plays a vital role in mammalian target of rapamycin (mTOR) signaling, which is the pivot in colorectal cancer (CRC). Upregulated chaperone-mediated autophagy (CMA) activity contributes to the regulation of metabolism in cancer cells. Previously, we found that sorting nexin 10 (SNX10) is a critical regulator in CMA activation. Here we investigated the role of SNX10 in regulating amino-acid metabolism and mTOR signaling pathway activation, as well as the impact on the tumor progression of mouse CRC. Our results showed that SNX10 deficiency promoted colorectal tumorigenesis in male FVB mice and CRC cell proliferation and survival. Metabolic pathway analysis of gas chromatography–mass spectrometry (GC-MS) data revealed unique changes of amino-acid metabolism by SNX10 deficiency. In HCT116 cells, SNX10 knockout resulted in the increase of CMA and mTOR activation, which could be abolished by chloroquine treatment or reversed by SNX10 overexpression. By small RNA interference (siRNA), we found that the activation of mTOR was dependent on lysosomal-associated membrane protein type-2A (LAMP-2A), which is a limiting factor of CMA. Similar results were also found in Caco-2 and SW480 cells. Ultra-high-performance liquid chromatography–quadrupole time of flight (UHPLC-QTOF) and GC-MS-based untargeted metabolomics revealed that 10 amino-acid metabolism in SNX10-deficient cells were significantly upregulated, which could be restored by LAMP-2A siRNA. All of these amino acids were previously reported to be involved in mTOR activation. In conclusion, this work revealed that SNX10 controls mTOR activation through regulating CMA-dependent amino-acid metabolism, which provides potential target and strategy for treating CRC.
Humanized mice reveal an essential role for human hepatocytes in the development of the liver immune system
Authors: Guo Jinglong , Li Yang , Shan Yanhong , Shu Chang , Wang Feng , Wang Xue , Zheng Ge , He Jin , Hu Zheng , Yang Yong-Guang 
Published: June 2018

AbstractThe liver is an immunological organ with a distinct immune cell profile. Although the composition and function of liver immune cells have been widely investigated, the mechanisms regulating the development and homeostasis of the specialized immune system, especially in humans, remain largely unknown. Herein, we address this question in humanized mice (hu-mice) that were constructed by transplantation of human fetal thymus and CD34+ hematopoietic stem/progenitor cells in immunodeficient mice with or without autologous human hepatocyte engraftment. Although the levels of human immune cell reconstitution in peripheral blood and spleen were comparable between hu-mice with and without human hepatocyte engraftment, the former group showed that human immune cell reconstitution in the liver was significantly improved. Notably, human immune cells, including Kupffer cells, dendritic cells and natural killer cells, were shown to be closely colocalized with human hepatocytes in the liver. Human hepatocytes engrafted in the mouse liver were found to produce IL-3, IL-15, GM-CSF, M-CSF, MCP-1, CXCL-1 and CXCL-10, which are known to be important for immune cell development, differentiation, tissue migration and retention, and have no or poor cross-reaction between humans and mice. Furthermore, human hepatocytes were able to support human immune cell survival and expansion in an in vitro co-culture assay. This study demonstrates an essential role for hepatocytes in the development and maintenance of the liver immune cell profile. The hu-mouse model with human autologous immune cell and hepatocyte reconstitution has potential for use in studies of the pathogenesis of liver immune disorders such as hepatotropic virus infections.
Macrophage migration inhibitory factor is required for NLRP3 inflammasome activation
Authors: Lang Tali , Lee Jacinta P. W. , Elgass Kirstin , Pinar Anita A. , Tate Michelle D. , Aitken Elizabeth H. , Fan Huapeng , Creed Sarah J. , Deen Nadia S. , Traore Daouda A. K. , Mueller Ivo , Stanisic Danielle , Baiwog Francesca S. , Skene Colin , Wilce Matthew C. J. , Mansell Ashley , Morand Eric F. , Harris James 
Published: June 2018

AbstractMacrophage migration inhibitory factor (MIF) exerts multiple effects on immune cells, as well as having functions outside the immune system. MIF can promote inflammation through the induction of other cytokines, including TNF, IL-6, and IL-1 family cytokines. Here, we show that inhibition of MIF regulates the release of IL-1α, IL-1β, and IL-18, not by affecting transcription or translation of these cytokines, but via activation of the NLRP3 inflammasome. MIF is required for the interaction between NLRP3 and the intermediate filament protein vimentin, which is critical for NLRP3 activation. Further, we demonstrate that MIF interacts with NLRP3, indicating a role for MIF in inflammasome activation independent of its role as a cytokine. These data advance our understanding of how MIF regulates inflammation and identify it as a factor critical for NLRP3 inflammasome activation.
Rapid and widespread white matter plasticity during an intensive reading intervention
Authors: Huber Elizabeth , Donnelly Patrick M. , Rokem Ariel , Yeatman Jason D. 
Published: June 2018

AbstractWhite matter tissue properties are known to correlate with performance across domains ranging from reading to math, to executive function. Here, we use a longitudinal intervention design to examine experience-dependent growth in reading skills and white matter in grade school-aged, struggling readers. Diffusion MRI data were collected at regular intervals during an 8-week, intensive reading intervention. These measurements reveal large-scale changes throughout a collection of white matter tracts, in concert with growth in reading skill. Additionally, we identify tracts whose properties predict reading skill but remain fixed throughout the intervention, suggesting that some anatomical properties stably predict the ease with which a child learns to read, while others dynamically reflect the effects of experience. These results underscore the importance of considering recent experience when interpreting cross-sectional anatomy–behavior correlations. Widespread changes throughout the white matter may be a hallmark of rapid plasticity associated with an intensive learning experience.
Dynamically prognosticating patients with hepatocellular carcinoma through survival paths mapping based on time-series data
Authors: Shen Lujun , Zeng Qi , Guo Pi , Huang Jingjun , Li Chaofeng , Pan Tao , Chang Boyang , Wu Nan , Yang Lewei , Chen Qifeng , Huang Tao , Li Wang , Wu Peihong 
Published: June 2018

AbstractPatients with hepatocellular carcinoma (HCC) always require routine surveillance and repeated treatment, which leads to accumulation of huge amount of clinical data. A predictive model utilizes the time-series data to facilitate dynamic prognosis prediction and treatment planning is warranted. Here we introduced an analytical approach, which converts the time-series data into a cascading survival map, in which each survival path bifurcates at fixed time interval depending on selected prognostic features by the Cox-based feature selection. We apply this approach in an intermediate-scale database of patients with BCLC stage B HCC and get a survival map consisting of 13 different survival paths, which is demonstrated to have superior or equal value than conventional staging systems in dynamic prognosis prediction from 3 to 12 months after initial diagnosis in derivation, internal testing, and multicentric testing cohorts. This methodology/model could facilitate dynamic prognosis prediction and treatment planning for patients with HCC in the future.
Interplay between spherical confinement and particle shape on the self-assembly of rounded cubes
Authors: Wang Da , Hermes Michiel , Kotni Ramakrishna , Wu Yaoting , Tasios Nikos , Liu Yang , de Nijs Bart , van der Wee Ernest B. , Murray Christopher B. , Dijkstra Marjolein , van Blaaderen Alfons 
Published: June 2018

AbstractSelf-assembly of nanoparticles (NPs) inside drying emulsion droplets provides a general strategy for hierarchical structuring of matter at different length scales. The local orientation of neighboring crystalline NPs can be crucial to optimize for instance the optical and electronic properties of the self-assembled superstructures. By integrating experiments and computer simulations, we demonstrate that the orientational correlations of cubic NPs inside drying emulsion droplets are significantly determined by their flat faces. We analyze the rich interplay of positional and orientational order as the particle shape changes from a sharp cube to a rounded cube. Sharp cubes strongly align to form simple-cubic superstructures whereas rounded cubes assemble into icosahedral clusters with additionally strong local orientational correlations. This demonstrates that the interplay between packing, confinement and shape can be utilized to develop new materials with novel properties.
Dephosphorylation of the HIV-1 restriction factor SAMHD1 is mediated by PP2A-B55α holoenzymes during mitotic exit
Authors: Schott Kerstin , Fuchs Nina V. , Derua Rita , Mahboubi Bijan , Schnellbächer Esther , Seifried Janna , Tondera Christiane , Schmitz Heike , Shepard Caitlin , Brandariz-Nuñez Alberto , Diaz-Griffero Felipe , Reuter Andreas , Kim Baek , Janssens Veerle , König Renate 
Published: June 2018

AbstractSAMHD1 is a critical restriction factor for HIV-1 in non-cycling cells and its antiviral activity is regulated by T592 phosphorylation. Here, we show that SAMHD1 dephosphorylation at T592 is controlled during the cell cycle, occurring during M/G1 transition in proliferating cells. Using several complementary proteomics and biochemical approaches, we identify the phosphatase PP2A-B55α responsible for rendering SAMHD1 antivirally active. SAMHD1 is specifically targeted by PP2A-B55α holoenzymes during mitotic exit, in line with observations that PP2A-B55α is a key mitotic exit phosphatase in mammalian cells. Strikingly, as HeLa or activated primary CD4+ T cells enter the G1 phase, pronounced reduction of RT products is observed upon HIV-1 infection dependent on the presence of dephosphorylated SAMHD1. Moreover, PP2A controls SAMHD1 pT592 level in non-cycling monocyte-derived macrophages (MDMs). Thus, the PP2A-B55α holoenzyme is a key regulator to switch on the antiviral activity of SAMHD1.
Mitochondrial reactive oxygen species regulate the induction of CD8+ T cells by plasmacytoid dendritic cells
Authors: Oberkampf Marine , Guillerey Camille , Mouriès Juliette , Rosenbaum Pierre , Fayolle Catherine , Bobard Alexandre , Savina Ariel , Ogier-Denis Eric , Enninga Jost , Amigorena Sebastian , Leclerc Claude , Dadaglio Gilles 
Published: June 2018

AbstractCross-presentation allows exogenous antigen presentation in association with major histocompatibility complex class I molecules, a process crucial for the priming of CD8+ T-cell responses against viruses and tumors. By contrast to conventional dendritic cells (cDC), which cross-present antigens in the steady state, plasmacytoid dendritic cells (pDC) acquire this ability only after stimulation by Toll-like receptor (TLR) ligands. The intracellular pathways accounting for this functional difference are still unknown. Here we show that the induction of cross-presentation by pDCs is regulated by mitochondria through a reactive oxygen species (ROS)-dependent mechanism, involving pH alkalization and antigen protection. The reduction of mitochondrial ROS production dramatically decreases the cross-presentation capacity of pDCs, leading to a strong reduction of their capacity to trigger CD8+ T-cell responses. Our results demonstrate the importance of mitochondrial metabolism in pDC biology, particularly for the induction of adaptive immune responses.
The Roles of Attentional Shifts and Attentional Reengagement in Resolving The Spatial Compatibility Effect in Tactile Simon-like Tasks
Authors: Zheng Wanting , Chen Lihan 
Published: June 2018

AbstractThe Simon effect refers to the acceleration of choice responses when the target position and response location are consistent compared with scenarios in which they are inconsistent, even if the target position is not relevant to the response. Here, we provide the first demonstration that the tactile Simon-like effect operates in an attention-shifting manner. In unimodal scenarios (Experiments 1–4), for the tactile direction task, the spatial compatibility effect was absent in the focused-attention condition but maintained in the divided-attention condition. For the tactile localization task, this pattern was reversed: the spatial compatibility effect occurred for the focused-attention condition but was reduced/absent in the divided-attention condition. In the audiotactile interaction scenario (Experiment 5), the reaction times (RTs) for discriminating the tactile motion direction were prolonged; however, a spatial compatibility effect was not observed. We propose that the temporal course of resolving conflicts between spatial codes during attentional shifts, including attentional reengagement, may account for the tactile Simon-like effect.