bluuebunny/crossref_metadata_2025_split huggingface dataset:
Infection by the semi-persistently transmitted Tomato chlorosis virus alters the biology and behaviour of Bemisia tabaci on two potato clones
Authors: Pereira L.S. , Lourenção A.L. , Salas F.J.S. , Bento J.M.S. , Rezende J.A.M. , Peñaflor M.F.G.V. 
Published: January 2019

AbstractInsect-borne plant viruses usually alter the interactions between host plant and insect vector in ways conducive to their transmission (‘host manipulation hypothesis’). Most studies have tested this hypothesis with persistently and non-persistently transmitted viruses, while few have examined semi-persistently transmitted viruses. The crinivirusTomato chlorosis virus(ToCV) is semi-persistently transmitted virus by whiteflies, and has been recently reported infecting potato plants in Brazil, whereBemisia tabaciMiddle East Asia Minor 1 (MEAM1) is a competent vector. We investigated how ToCV infection modifies the interaction between potato plants andB. tabaciin ways that increase the likelihood of ToCV transmission, in two clones, one susceptible (‘Agata’) and the other moderately resistant (Bach-4) toB. tabaci. Whiteflies alighted and laid more eggs on ToCV-infected plants than mock-inoculated plants of Bach-4. When non-viruliferous whiteflies were released on ToCV-infected plants near mock-inoculated plants, adults moved more intensely towards non-infected plants than in the reverse condition for both clones. Feeding on ToCV-infected plants reduced egg-incubation period in both clones, but the egg–adult cycle was similar for whiteflies fed on ToCV-infected and mock-inoculated plants. Our results demonstrated that ToCV infection in potato plants altersB. tabacibehaviour and development in distinct ways depending on the host clone, with potential implications for ToCV spread.
Temporal pathways of change in two randomized controlled trials for depression and harmful drinking in Goa, India
Authors: Singla Daisy R. , Hollon Steven D. , Velleman Richard , Weobong Benedict , Nadkarni Abhijit , Fairburn Christopher G. , Bhat Bhargav , Gurav Mahesh , Anand Arpita , McCambridge Jim , Dimidjian Sona , Patel Vikram 
Published: January 2019

AbstractBackgroundThe current study explored the temporal pathways of change within two treatments, the Healthy Activity Program (HAP) for depression and the Counselling for Alcohol Problems (CAP) Program for harmful drinking.MethodsThe study took place in the context of two parallel randomized controlled trials in Goa, India. N = 50 random participants who met a priori criteria were selected from each treatment trial and examined for potential direct and mediational pathways. In HAP, we examined the predictive roles of therapy quality and patient-reported activation, assessing whether activation mediated the effects of therapy quality on depression (Patient Health Questionnaire-9) outcomes. In CAP, we examined the predictive roles of therapy quality and patient change- and counter-change-talk, assessing whether change- or counter-change-talk mediated the effects of therapy quality on daily alcohol consumption.ResultsIn HAP, therapy quality (both general and treatment-specific skills) was associated with patient activation; patient activation but not therapy quality significantly predicted depression outcomes, and patient activation mediated the effects of higher general skills on subsequent clinical outcomes [a × b = −2.555, 95% confidence interval (CI) −5.811 to −0.142]. In CAP, higher treatment-specific skills, but not general skills, were directly associated with drinking outcomes, and reduced levels of counter-change talk both independently predicted, and mediated the effects of higher general skills on, reduced alcohol consumption (a × b = −24.515, 95% CI −41.190 to −11.060). Change talk did not predict alcohol consumption and was not correlated with counter-change talk.ConclusionThese findings suggest that therapy quality in early sessions operated through increased patient activation and reduced counter-change talk to reduce depression and harmful drinking respectively.
‘How one shall govern a city’: the polyphony of urban political thought in the fourteenth-century duchy of Brabant
Authors: DE BOODT MINNE 
Published: January 2019

ABSTRACT:This article examines late medieval urban political thought. By means of an intertextual methodology that combines the efforts of continental scholars and English literary historians, it provides new insights into the political ideas that circulated within the towns of the fourteenth-century duchy of Brabant. A qualitative analysis between different source types, that originated amongst socially diverse groups, will indicate that political ideas had a polyphonic character. Indeed, ideas were constantly reconstructed and reshaped by the social groups that used them and the context in which they were uttered. During the fourteenth century, the Brabantine citizenry was involved in an ideological battle that was fought with similar, but adaptable, weapons.
Fast modeling of electromagnetic scattering from 2D electrically large PEC objects using the complex line source type Green's function
Authors: Kutluay Deniz , Oğuzer Taner 
Published: January 2019

AbstractThis study introduces an alternative approach to the numerical solution of two-dimensional (2D) electromagnetic scattering problems by a numerical method of moments (MoM). The real source position vector is replaced by a complex quantity, then Green's function generates a complex source point beam, therefore the interactions between the far zone elements in the impedance matrix are neglected, except the basis functions near to the edges, strongly localizing the impedance matrix. The memory storage increases with the number of edges, but for a fixed number of the edges, it is linearly proportional with N, i.e. O(N). Consequently, the overall running time can be drastically reduced and the far zone scattering pattern and the near field can be found. The proposed procedure is first explained for the single perfectly electrically conducting (PEC) strip geometry, then extended to the scattering by 2D PEC objects with closed polygonal cross-sections. Numerical results are presented for a strip and a square cylinder in both polarizations. The relative errors are also compared with the standard MoM.
Draining and Upwelling of Greenland Sea Deep Waters
Authors: Somavilla R. 
Published: January 2019

AbstractSince the beginning of the 1980s, deep convection has ceased in the Greenland Sea. The effects of this halt on the intense warming and salinification of Greenland Sea deep waters and on the “dome collapse” (sinking of the dome) have been intensively studied. However, their causes and the potential outflow of Greenland Sea deep and bottom waters toward southern adjacent basins have remained less investigated and are the focus of this work. Combining oceanic and atmospheric in situ data, together with satellite and reanalysis data, it is found that there is not a unique factor responsible for the halt of deep convection in the Greenland Sea. Changes in the Ekman pumping seem to only explain one tenth of the observed deepening of isopycnals of 1,300 m in the central Greenland Sea (dome collapse). Since the early 1980s, in addition, a decrease in the mean net heat loss from the ocean to the atmosphere and in the intensity and number of intense heat loss events would have contributed to the decrease in both the intensity of convective mixing and the generation of dense deep waters. The generation of waters not sufficiently dense to contribute to the reservoir of water below the Greenland Sea dome would have led to its emptying and sinking. More importantly, it is found that in situ evidence of a sustained bottom‐water upwelling driven by a secondary circulation cell whose major role in ventilating and draining the Greenland Sea deep and bottom waters has been largely underestimated.
Satellite and Station Observations Demonstrate Water Availability's Effect on Continental‐Scale Evaporative and Photosynthetic Land Surface Dynamics
Authors: Short Gianotti Daniel J. , Rigden Angela J. , Salvucci Guido D. , Entekhabi Dara 
Published: January 2019

AbstractEvapotranspiration and photosynthetic carbon uptake are both constrained by water availability, with presumed water‐limited and water‐independent but energy‐limited regimes. We investigate water availability's relationships with evaporative fluxes and photosynthetic measures at continental scale using surface and satellite‐based observations. The observation‐driven approach is independent of prior model‐based estimates. We find water‐limited and water‐independent regimes for both energy and carbon cycle processes in spatial and temporal aggregate, differences in water‐limitation relationships across ecohydrological regions, and more consistent signs of water limitation in photosynthetic than evaporative processes. Ecosystem water use efficiency's response to water availability changes in sign with aridity state across time and space generally but shows negative correlations in temporal anomalies.
The cirrhotic liver is depleted of docosahexaenoic acid (DHA), a key modulator of NF-κB and TGFβ pathways in hepatic stellate cells
Authors: Enguita Mónica , Razquin Nerea , Pamplona Reinald , Quiroga Jorge , Prieto Jesús , Fortes Puri 
Published: January 2019

AbstractLiver cirrhosis results from chronic hepatic damage and is characterized by derangement of the organ architecture with increased liver fibrogenesis and defective hepatocellular function. It frequently evolves into progressive hepatic insufficiency associated with high mortality unless liver transplantation is performed. We have hypothesized that the deficiency of critical nutrients such as essential omega-3 fatty acids might play a role in the progression of liver cirrhosis. Here we evaluated by LC-MS/MS the liver content of omega-3 docosahexaenoic fatty acid (DHA) in cirrhotic patients and investigated the effect of DHA in a murine model of liver injury and in the response of hepatic stellate cells (HSCs) (the main producers of collagen in the liver) to pro-fibrogenic stimuli. We found that cirrhotic livers exhibit a marked depletion of DHA and that this alteration correlates with the progression of the disease. Administration of DHA exerts potent anti-fibrogenic effects in an acute model of liver damage. Studies with HSCs show that DHA inhibits fibrogenesis more intensely than other omega-3 fatty acids. Data from expression arrays revealed that DHA blocks TGFβ and NF-κB pathways. Mechanistically, DHA decreases late, but not early, SMAD3 nuclear accumulation and inhibits p65/RelA-S536 phosphorylation, which is required for HSC survival. Notably, DHA increases ADRP expression, leading to the formation of typical quiescence-associated perinuclear lipid droplets. In conclusion, a marked depletion of DHA is present in the liver of patients with advanced cirrhosis. DHA displays anti-fibrogenic activities on HSCs targeting NF-κB and TGFβ pathways and inducing ADPR expression and quiescence in these cells.
Wnt3a disrupts GR-TEAD4-PPARγ2 positive circuits and cytoskeletal rearrangement in a β-catenin-dependent manner during early adipogenesis
Authors: Park Bongju , Chang Soojeong , Lee Gwan-Jun , Kang Byeongsoo , Kim Jong Kyoung , Park Hyunsung 
Published: January 2019

AbstractAdipogenesis is a process which induces or represses many genes in a way to drive irreversible changes of cell phenotypes; lipid accumulation, round cell-shape, secreting many adipokines. As a master transcription factor (TF), PPARγ2 induces several target genes to orchestrate these adipogenic changes. Thus induction of Pparg2 gene is tightly regulated by many adipogenic and also anti-adipogenic factors. Four hours after the treatment of adipogenic hormones, more than fifteen TFs including glucocorticoid receptor (GR), C/EBPβ and AP-1 cooperatively bind the promoter of Pparg2 gene covering 400 bps, termed “hotspot”. In this study, we show that TEA domain family transcription factor (TEAD)4 reinforces occupancy of both GR and C/EBPβ on the hotspot of Pparg2 during early adipogenesis. Our findings that TEAD4 requires GR for its expression and for the ability to bind its own promoter and the hotspot region of Pparg2 gene indicate that GR is a common component of two positive circuits, which regulates the expression of both Tead4 and Pparg2. Wnt3a disrupts these mutually related positive circuits by limiting the nuclear location of GR in a β-catenin dependent manner. The antagonistic effects of β-catenin extend to cytoskeletal remodeling during the early phase of adipogenesis. GR is necessary for the rearrangements of both cytoskeleton and chromatin of Pparg2, whereas Wnt3a inhibits both processes in a β-catenin-dependent manner. Our results suggest that hotspot formation during early adipogenesis is related to cytoskeletal remodeling, which is regulated by the antagonistic action of GR and β-catenin, and that Wnt3a reinforces β-catenin function.
Molecular mechanisms in the pathogenesis of N-nitrosodimethylamine induced hepatic fibrosis
Authors: George Joseph , Tsuchishima Mutsumi , Tsutsumi Mikihiro 
Published: January 2019

AbstractHepatic fibrosis is marked by excessive synthesis and deposition of connective tissue proteins, especially interstitial collagens in the extracellular matrix of the liver. It is a result of an abnormal wound healing in response to chronic liver injury from various causes such as ethanol, viruses, toxins, drugs, or cholestasis. The chronic stimuli involved in the initiation of fibrosis leads to oxidative stress and generation of reactive oxygen species that serve as mediators of molecular events involved in the pathogenesis of hepatic fibrosis. These processes lead to cellular injury and initiate inflammatory responses releasing a variety of cytokines and growth factors that trigger activation and transformation of resting hepatic stellate cells into myofibroblast like cells, which in turn start excessive synthesis of connective tissue proteins, especially collagens. Uncontrolled and extensive fibrosis results in distortion of lobular architecture of the liver leading to nodular formation and cirrhosis. The perpetual injury and regeneration process could also results in genomic aberrations and mutations that lead to the development of hepatocellular carcinoma. This review covers most aspects of the molecular mechanisms involved in the pathogenesis of hepatic fibrosis with special emphasize on N-Nitrosodimethylamine (NDMA; Dimethylnitorsmaine, DMN) as the inducing agent.
Depletion of RIPK1 in hepatocytes exacerbates liver damage in fulminant viral hepatitis
Authors: Farooq Muhammad , Filliol Aveline , Simoes Eugénio Mélanie , Piquet-Pellorce Claire , Dion Sarah , Raguenes-Nicol Céline , Jan Aurélien , Dimanche-Boitrel Marie-Thérèse , Le Seyec Jacques , Samson Michel 
Published: January 2019

AbstractThe protein kinase RIPK1 plays a crucial role at the crossroad of stress-induced signaling pathways that affects cell’s decision to live or die. The present study aimed to define the role of RIPK1 in hepatocytes during fulminant viral hepatitis, a worldwide syndrome mainly observed in hepatitis B virus (HBV) infected patients. Mice deficient for RIPK1, specifically in liver parenchymal cells (Ripk1LPC-KO) and their wild-type littermates (Ripk1fl/fl), were challenged by either the murine hepatitis virus type 3 (MHV3) or poly I:C, a synthetic analog of double-stranded RNA mimicking viral pathogen-associated molecular pattern. Ripk1LPC-KO mice developed more severe symptoms at early stage of the MHV3-induced fulminant hepatitis. Similarly, administration of poly I:C only triggered increase of systemic transaminases in Ripk1LPC-KO mice, reflecting liver damage through induced apoptosis as illustrated by cleaved-caspase 3 labeling of liver tissue sections. Neutralization of TNF-α or prior depletion of macrophages were able to prevent the appearance of apoptosis of hepatocytes in poly I:C-challenged Ripk1LPC-KO mice. Moreover, poly I:C never induced direct hepatocyte death in primary culture whatever the murine genotype, while it always stimulated an anti-viral response. Our investigations demonstrated that RIPK1 protects hepatocytes from TNF-α secreted from macrophages during viral induced fulminant hepatitis. These data emphasize the potential worsening risks of an HBV infection in people with polymorphism or homozygous amorphic mutations already described for the RIPK1 gene.
Rapid determination of quaternary protein structures in complex biological samples
Authors: Hauri Simon , Khakzad Hamed , Happonen Lotta , Teleman Johan , Malmström Johan , Malmström Lars 
Published: January 2019

AbstractThe understanding of complex biological systems is still hampered by limited knowledge of biologically relevant quaternary protein structures. Here, we demonstrate quaternary structure determination in biological samples using a combination of chemical cross-linking, high-resolution mass spectrometry and high-accuracy protein structure modeling. This approach, termed targeted cross-linking mass spectrometry (TX-MS), relies on computational structural models to score sets of targeted cross-linked peptide signals acquired using a combination of mass spectrometry acquisition techniques. We demonstrate the utility of TX-MS by creating a high-resolution quaternary model of a 1.8 MDa protein complex composed of a pathogen surface protein and ten human plasma proteins. The model is based on a dense network of cross-link distance constraints obtained directly in a mixture of human plasma and live bacteria. These results demonstrate that TX-MS can increase the applicability of flexible backbone docking algorithms to large protein complexes by providing rich cross-link distance information from complex biological samples.
Dinitroimidazoles as bifunctional bioconjugation reagents for protein functionalization and peptide macrocyclization
Authors: Luo Qunfeng , Tao Youqi , Sheng Wangjian , Lu Jingxia , Wang Huan 
Published: January 2019

AbstractEfficient and site-specific chemical modification of proteins under physiological conditions remains a challenge. Here we report that 1,4-dinitroimidazoles are highly efficient bifunctional bioconjugation reagents for protein functionalization and peptide macrocyclization. Under acidic to neutral aqueous conditions, 1,4-dinitroimidazoles react specifically with cysteines via a cine-substitution mechanism, providing rapid, stable and chemoselective protein bioconjugation. On the other hand, although unreactive towards amine groups under neutral aqueous conditions, 1,4-dinitroimidazoles react with lysines in organic solvents in the presence of base through a ring-opening & ring-close mechanism. The resulting cysteine- and lysine-(4-nitroimidazole) linkages exhibit stability superior to that of commonly employed maleimide-thiol conjugates. We demonstrate that 1,4-dinitroimidazoles can be applied in site-specific protein bioconjugation with functionalities such as fluorophores and bioactive peptides. Furthermore, a bisfunctional 1,4-dinitroimidazole derivative provides facile access to peptide macrocycles by crosslinking a pair of cysteine or lysine residues, including bicyclic peptides of complex architectures through highly controlled consecutive peptide macrocyclization.
Promoted cobalt metal catalysts suitable for the production of lower olefins from natural gas
Authors: Xie Jingxiu , Paalanen Pasi P. , van Deelen Tom W. , Weckhuysen Bert M. , Louwerse Manuel J. , de Jong Krijn P. 
Published: January 2019

AbstractDue to the surge of natural gas production, feedstocks for chemicals shift towards lighter hydrocarbons, particularly methane. The success of a Gas-to-Chemicals process via synthesis gas (CO and H2) depends on the ability of catalysts to suppress methane and carbon dioxide formation. We designed a Co/Mn/Na/S catalyst, which gives rise to negligible Water-Gas-Shift activity and a hydrocarbon product spectrum deviating from the Anderson–Schulz–Flory distribution. At 240 °C and 1 bar, it shows a C2-C4olefins selectivity of 54%. At 10 bar, it displays 30% and 59% selectivities towards lower olefins and fuels, respectively. The spent catalyst consists of 10 nm Co nanoparticles with hcp Co metal phase. We propose a synergistic effect of Na plus S, which act as electronic promoters on the Co surface, thus improving selectivities towards lower olefins and fuels while largely reducing methane and carbon dioxide formation.
Estrogen signaling in arcuate Kiss1 neurons suppresses a sex-dependent female circuit promoting dense strong bones
Authors: Herber Candice B. , Krause William C. , Wang Liping , Bayrer James R. , Li Alfred , Schmitz Matthew , Fields Aaron , Ford Breanna , Zhang Zhi , Reid Michelle S. , Nomura Daniel K. , Nissenson Robert A. , Correa Stephanie M. , Ingraham Holly A. 
Published: January 2019

AbstractCentral estrogen signaling coordinates energy expenditure, reproduction, and in concert with peripheral estrogen impacts skeletal homeostasis in females. Here, we ablate estrogen receptor alpha (ERα) in the medial basal hypothalamus and find a robust bone phenotype only in female mice that results in exceptionally strong trabecular and cortical bones, whose density surpasses other reported mouse models. Stereotaxic guided deletion of ERα in the arcuate nucleus increases bone mass in intact and ovariectomized females, confirming the central role of estrogen signaling in this sex-dependent bone phenotype. Loss of ERα in kisspeptin (Kiss1)-expressing cells is sufficient to recapitulate the bone phenotype, identifying Kiss1 neurons as a critical node in this powerful neuroskeletal circuit. We propose that this newly-identified female brain-to-bone pathway exists as a homeostatic regulator diverting calcium and energy stores from bone building when energetic demands are high. Our work reveals a previously unknown target for treatment of age-related bone disease.
The splicing factor RBM25 controls MYC activity in acute myeloid leukemia
Authors: Ge Ying , Schuster Mikkel Bruhn , Pundhir Sachin , Rapin Nicolas , Bagger Frederik Otzen , Sidiropoulos Nikos , Hashem Nadia , Porse Bo Torben 
Published: January 2019

AbstractCancer sequencing studies have implicated regulators of pre-mRNA splicing as important disease determinants in acute myeloid leukemia (AML), but the underlying mechanisms have remained elusive. We hypothesized that “non-mutated” splicing regulators may also play a role in AML biology and therefore conducted an in vivo shRNA screen in a mouse model of CEBPA mutant AML. This has led to the identification of the splicing regulator RBM25 as a novel tumor suppressor. In multiple human leukemic cell lines, knockdown of RBM25 promotes proliferation and decreases apoptosis. Mechanistically, we show that RBM25 controls the splicing of key genes, including those encoding the apoptotic regulator BCL-X and the MYC inhibitor BIN1. This mechanism is also operative in human AML patients where low RBM25 levels are associated with high MYC activity and poor outcome. Thus, we demonstrate that RBM25 acts as a regulator of MYC activity and sensitizes cells to increased MYC levels.