bluuebunny/crossref_metadata_2025_split huggingface dataset:
Geometric generalised Lagrangian-mean theories
Authors: Gilbert Andrew D. , Vanneste Jacques 
Published: January 2018

Many fluctuation-driven phenomena in fluids can be analysed effectively using the generalised Lagrangian-mean (GLM) theory of Andrews & McIntyre (J. Fluid Mech., vol. 89, 1978, pp. 609–646) This finite-amplitude theory relies on particle-following averaging to incorporate the constraints imposed by the material conservation of certain quantities in inviscid regimes. Its original formulation, in terms of Cartesian coordinates, relies implicitly on an assumed Euclidean structure; as a result, it does not have a geometrically intrinsic, coordinate-free interpretation on curved manifolds, and suffers from undesirable features. Motivated by this, we develop a geometric generalisation of GLM that we formulate intrinsically using coordinate-free notation. One benefit is that the theory applies to arbitrary Riemannian manifolds; another is that it establishes a clear distinction between results that stem directly from geometric consistency and those that depend on particular choices. Starting from a decomposition of an ensemble of flow maps into mean and perturbation, we define the Lagrangian-mean momentum as the average of the pull-back of the momentum one-form by the perturbation flow maps. We show that it obeys a simple equation which guarantees the conservation of Kelvin’s circulation, irrespective of the specific definition of the mean flow map. The Lagrangian-mean momentum is the integrand in Kelvin’s circulation and distinct from the mean velocity (the time derivative of the mean flow map) which advects the contour of integration. A pseudomomentum consistent with that in GLM can then be defined by subtracting the Lagrangian-mean momentum from the one-form obtained from the mean velocity using the manifold’s metric. The definition of the mean flow map is based on choices made for reasons of convenience or aesthetics. We discuss four possible definitions: a direct extension of standard GLM, a definition based on optimal transportation, a definition based on a geodesic distance in the group of volume-preserving diffeomorphisms, and the ‘glm’ definition proposed by Soward & Roberts (J. Fluid Mech., vol. 661, 2010, pp. 45–72). Assuming small-amplitude perturbations, we carry out order-by-order calculations to obtain explicit expressions for the mean velocity and Lagrangian-mean momentum at leading order. We also show how the wave-action conservation of GLM extends to the geometric setting. To make the paper self-contained, we introduce in some detail the tools of differential geometry and main ideas of geometric fluid dynamics on which we rely. These include variational formulations which we use for alternative derivations of some key results. We mostly focus on the Euler equations for incompressible inviscid fluids but sketch out extensions to the rotating–stratified Boussinesq, compressible Euler, and magnetohydrodynamic equations. We illustrate our results with an application to the interaction of inertia-gravity waves with balanced mean flows in rotating–stratified fluids.
The optimal kinematic dynamo driven by steady flows in a sphere
Authors: Chen L. , Herreman W. , Li K. , Livermore P. W. , Luo J. W. , Jackson A. 
Published: January 2018

We present a variational optimization method that can identify the most efficient kinematic dynamo in a sphere, where efficiency is based on the value of a magnetic Reynolds number that uses enstrophy to characterize the inductive effects of the fluid flow. In this large-scale optimization, we restrict the flow to be steady and incompressible, and the boundary of the sphere to be no-slip and electrically insulating. We impose these boundary conditions using a Galerkin method in terms of specifically designed vector field bases. We solve iteratively for the flow field and the accompanying magnetic eigenfunction in order to find the minimal critical magnetic Reynolds number $Rm_{c,min}$ for the onset of a dynamo. Although nonlinear, this iteration procedure converges to a single solution and there is no evidence that this is not a global optimum. We find that $Rm_{c,min}=64.45$ is at least three times lower than that of any published example of a spherical kinematic dynamo generated by steady flows, and our optimal dynamo clearly operates above the theoretical lower bounds for dynamo action. The corresponding optimal flow has a spatially localized helical structure in the centre of the sphere, and the dominant components are invariant under rotation by $\unicode[STIX]{x03C0}$.
The curvilinear relationship between career plateauing and organizational citizenship behavior
Authors: Song Gi R. , Kim Kyoung S. , Lee Min W. 
Published: January 2018

AbstractAccording to social exchange theory, the motivation for organizational citizenship behavior can be understood with the help of the frameworks of obligation to reciprocate and expected reciprocity. This study predicts that the true motivation for organizational citizenship behavior could be differentiated conditional on the career plateau. These relationships predict the existence of a U-shaped nonlinear relationship between the career plateau and organizational citizenship behavior. In addition to exploring this relationship, the study attempted to discover the effect of organizational commitment and job involvement on the relationship. As a result, a U-shaped curvilinear relationship is applied between career plateau and four dimensions of organizational citizenship behavior except civic virtue. Commitment and involvement show unexpected moderating effects on those curved relationships.
Partial melting of oceanic sediments in subduction zones and its contribution to the petrogenesis of peraluminous granites in the Chinese Altai
Authors: LUO QUN , ZHANG CHEN , JIANG SHU , LIU LUOFU , LIU DONGDONG , KONG XIANGYE , LIU XIAOYU , WANG XINPENG 
Published: January 2018

AbstractLate Carboniferous magmatism in the Chinese Altai provides an important view of geodynamic processes active during crustal growth in the Central Asian Orogenic Belt (CAOB). In this study, five representative peraluminous granite plutons from the Chinese Altai were selected for systematic geochronological, geochemical and Sr–Nd–Hf isotopic analyses (Table 1). These granites were emplaced between 449 and 327 Ma in an active subduction zone, and have moderate to high SiO2 (66.54–76.13 wt%), moderate Na2O+K2O (6.27–7.66 wt%), and high Al2O3 contents (12.43–16.18 wt%). All granite samples in this study showed significant decoupling of the Nd and Hf isotope systems. Results show negative εNd(t) values (−3.3 to −0.9), and predominantly positive εHf(t) values (+0.24 to +8.01, n=57) except for a few negative εHf(t) values (−7.44 to −0.03, n=9), high Mg# values (28.69–53.33), high Nd/Hf ratios (4.26–43.57), and enrichment of large-ion lithophile elements (LILEs; e.g. Pb, Th, and U), suggesting that the granites were derived from the partial melting of oceanic sediments and the associated mantle wedge, with fractionation of plagioclase, K-feldspar and biotite. In situ zircon Hf isotopic analyses yield negative εHf(t) values from −30.6 to −13.7 for the zircon xenocrysts. The U–Pb ages and Hf isotopic ratios of these zircon xenocrysts were probably inherited from oceanic sediments. Zircon saturation temperatures suggest that these peraluminous granites were emplaced at 537–765°C. We propose that: (1) the Nd isotopic system more faithfully reflects the source of peraluminous magmas in the Chinese Altai than the Hf isotopic system, and (2) the oceanic sediment recycling was an important process during continental growth in the CAOB.
Spatially localized particle energization by Landau damping in current sheets produced by strong Alfvén wave collisions
Authors: Howes Gregory G. , McCubbin Andrew J. , Klein Kristopher G. 
Published: January 2018

Understanding the removal of energy from turbulent fluctuations in a magnetized plasma and the consequent energization of the constituent plasma particles is a major goal of heliophysics and astrophysics. Previous work has shown that nonlinear interactions among counterpropagating Alfvén waves – or Alfvén wave collisions – are the fundamental building block of astrophysical plasma turbulence and naturally generate current sheets in the strongly nonlinear limit. A nonlinear gyrokinetic simulation of a strong Alfvén wave collision is used to examine the damping of the electromagnetic fluctuations and the associated energization of particles that occurs in self-consistently generated current sheets. A simple model explains the flow of energy due to the collisionless damping and the associated particle energization, as well as the subsequent thermalization of the particle energy by collisions. The net particle energization by the parallel electric field is shown to be spatially localized, and the nonlinear evolution is essential in enabling spatial non-uniformity. Using the recently developed field–particle correlation technique, we show that particles resonant with the Alfvén waves in the simulation dominate the energy transfer, demonstrating conclusively that Landau damping plays a key role in the spatially localized damping of the electromagnetic fluctuations and consequent energization of the particles in this strongly nonlinear simulation.
Efficient acceleration of a dense plasma projectile to hyper velocities in the laser-induced cavity pressure acceleration scheme
Authors: Badziak J. , Krousky E. , Marczak J. , Parys P. , Pisarczyk T. , Rosiński M. , Sarzynski A. , Chodukowski T. , Dostal J. , Dudzak R. , Kalinowska Z. , Kucharik M. , Liska R. , Pfeifer M. , Ullschmied J. , Zaraś-Szydłowska A. 
Published: January 2018

AbstractThe experimental study of the plasma projectile acceleration in the laser-induced cavity pressure acceleration (LICPA) scheme is reported. In the experiment performed at the kilojoule PALS laser facility, the parameters of the projectile were measured using interferometry, a streak camera and ion diagnostics, and the measurements were supported by two-dimensional hydrodynamic simulations. It is shown that in the LICPA accelerator with a 200-J laser driver, a 4-μg gold plasma projectile is accelerated to the velocity of 140 km/s with the energetic acceleration efficiency of 15–19% which is significantly higher than those achieved with the commonly used ablative acceleration and the highest among the ones measured so far for any projectiles accelerated to the velocities ≥100 km/s. This achievement opens the possibility of creation and investigation of high-energy-density matter states with the use of moderate-energy lasers and may also have an impact on the development of the impact ignition approach to inertial confinement fusion.
MODELLING HYDROGEN CLEARANCE FROM THE RETINA
Authors: FARROW D. E. , HOCKING G. C. , CRINGLE S. J. , YU D.-Y. 
Published: January 2018

The human retina is supplied by two vascular systems: the highly vascular choroidal, situated behind the retina; and the retinal, which is dependent on the restriction that the light path must be minimally disrupted. Between these two circulations, the avascular retinal layers depend on diffusion of metabolites through the tissue. Oxygen supply to these layers may be threatened by diseases affecting microvasculature, for example diabetes and hypertension, which may ultimately cause loss of sight.An accurate model of retinal blood flow will therefore facilitate the study of retinal oxygen supply and, hence, the complications caused by systemic vascular disease. Here, two simple models of the blood flow and exchange of hydrogen with the retina are presented and compared qualitatively with data obtained from experimental measurements. The models capture some interesting features of the exchange and highlight effects that will need to be considered in a more sophisticated model and in the interpretation of experimental results.
The consequences of niche and physiological differentiation of archaeal and bacterial ammonia oxidisers for nitrous oxide emissions
Authors: Hink Linda , Gubry-Rangin Cécile , Nicol Graeme W , Prosser James I 
Published: January 2018

Abstract
High and low rates of ammonium supply are believed to favour ammonia-oxidising bacteria (AOB) and archaea (AOA), respectively. Although their contrasting affinities for ammonium are suggested to account for these differences, the influence of ammonia concentration on AOA and AOB has not been tested under environmental conditions. In addition, while both AOB and AOA contribute to nitrous oxide (N2O) emissions from soil, N2O yields (N2O–N produced per NO2−–N generated from ammonia oxidation) of AOA are lower, suggesting lower emissions when AOA dominate ammonia oxidation. This study tested the hypothesis that ammonium supplied continuously at low rates is preferentially oxidised by AOA, with lower N2O yield than expected for AOB-dominated processes. Soil microcosms were supplied with water, urea or a slow release, urea-based fertiliser and 1-octyne (inhibiting only AOB) was applied to distinguish AOA and AOB activity and associated N2O production. Low ammonium supply, from mineralisation of organic matter, or of the fertiliser, led to growth, ammonia oxidation and N2O production by AOA only, with low N2O yield. High ammonium supply, from free urea within the fertiliser or after urea addition, led to growth of both groups, but AOB-dominated ammonia oxidation was associated with twofold greater N2O yield than that dominated by AOA. This study therefore demonstrates growth of both AOA and AOB at high ammonium concentration, confirms AOA dominance during low ammonium supply and suggests that slow release or organic fertilisers potentially mitigate N2O emissions through differences in niche specialisation and N2O production mechanisms in AOA and AOB.
Cell death-based approaches in treatment of the urinary tract-associated diseases: a fight for survival in the killing fields
Authors: Martin-Sanchez Diego , Fontecha-Barriuso Miguel , Sanchez-Niño Maria Dolores , Ramos Adrian M. , Cabello Ramiro , Gonzalez-Enguita Carmen , Linkermann Andreas , Sanz Ana Belén , Ortiz Alberto 
Published: January 2018

AbstractUrinary tract-associated diseases comprise a complex set of disorders with a variety of etiologic agents and therapeutic approaches and a huge global burden of disease, estimated at around 1 million deaths per year. These diseases include cancer (mainly prostate, renal, and bladder), urinary tract infections, and urolithiasis. Cell death plays a key role in the pathogenesis and therapy of these conditions. During urinary tract infections, invading bacteria may either promote or prevent host cell death by interfering with cell death pathways. This has been studied in detail for uropathogenic E. coli (UPEC). Inhibition of host cell death may allow intracellular persistence of live bacteria, while promoting host cell death causes tissue damage and releases the microbes. Both crystals and urinary tract obstruction lead to tubular cell death and kidney injury. Among the pathomechanisms, apoptosis, necroptosis, and autophagy represent key processes. With respect to malignant disorders, traditional therapeutic efforts have focused on directly promoting cancer cell death. This may exploit tumor-specific characteristics, such as targeting Vascular Endothelial Growth Factor (VEGF) signaling and mammalian Target of Rapamycin (mTOR) activity in renal cancer and inducing survival factor deprivation by targeting androgen signaling in prostate cancer. An area of intense research is the use of immune checkpoint inhibitors, aiming at unleashing the full potential of immune cells to kill cancer cells. In the future, this may be combined with additional approaches exploiting intrinsic sensitivities to specific modes of cell death such as necroptosis and ferroptosis. Here, we review the contribution of diverse cell death mechanisms to the pathogenesis of urinary tract-associated diseases as well as the potential for novel therapeutic approaches based on an improved molecular understanding of these mechanisms.
Necroptosis and neutrophil-associated disorders
Authors: Wang Xiaoliang , Yousefi Shida , Simon Hans-Uwe 
Published: January 2018

AbstractNecroptosis is a form of regulated necrosis and is dependent on a signaling pathway involving receptor interacting protein kinase-3 (RIPK3) and mixed lineage kinase domain-like protein (MLKL). Necroptosis is considered to have important functions in inflammation and, based on studies with animal disease models, is believed likely to be involved in the pathogenesis of many human inflammatory diseases. In neutrophils, necroptosis has recently been reported to be triggered by tumor necrosis factor (TNF) stimulation, ligation of adhesion receptors, exposure to monosodium urate (MSU) crystals, or phagocytosis of Staphylococcus aureus (S. aureus). Because neutrophils are involved in many kinds of tissue inflammation and disease, neutrophil necroptosis probably plays a vital role in such processes. Dissecting the signaling pathway of neutrophil necroptotic death may help to identify novel drug targets for inflammatory or autoimmune diseases. In this review, we discuss different mechanisms which regulate neutrophil necroptosis and are thus potentially important in neutrophil-associated disorders.
Cell death-based treatments of melanoma:conventional treatments and new therapeutic strategies
Authors: Mattia Gianfranco , Puglisi Rossella , Ascione Barbara , Malorni Walter , Carè Alessandra , Matarrese Paola 
Published: January 2018

AbstractThe incidence of malignant melanoma has continued to rise during the past decades. However, in the last few years, treatment protocols have significantly been improved thanks to a better understanding of the key oncogenes and signaling pathways involved in its pathogenesis and progression. Anticancer therapy would either kill tumor cells by triggering apoptosis or permanently arrest them in the G1 phase of the cell cycle. Unfortunately, melanoma is often refractory to commonly used anticancer drugs. More recently, however, some new anticancer strategies have been developed that are “external” to cancer cells, for example stimulating the immune system’s response or inhibiting angiogenesis. In fact, the increasing knowledge of melanoma pathogenetic mechanisms, in particular the discovery of genetic mutations activating specific oncogenes, stimulated the development of molecularly targeted therapies, a form of treatment in which a drug (chemical or biological) is developed with the goal of exclusively destroying cancer cells by interfering with specific molecules that drive growth and spreading of the tumor. Again, after the initial exciting results associated with targeted therapy, tumor resistance and/or relapse of the melanoma lesion have been observed. Hence, very recently, new therapeutic strategies based on the modulation of the immune system function have been developed. Since cancer cells are known to be capable of evading immune-mediated surveillance, i.e., to block the immune system cell activity, a series of molecular strategies, including monoclonal antibodies, have been developed in order to “release the brakes” on the immune system igniting immune reactivation and hindering metastatic melanoma cell growth. In this review we analyze the various biological strategies underlying conventional chemotherapy as well as the most recently developed targeted therapies and immunotherapies, pointing at the molecular mechanisms of cell injury and death engaged by the different classes of therapeutic agents.
MIF inhibits the formation and toxicity of misfolded SOD1 amyloid aggregates: implications for familial ALS
Authors: Shvil Neta , Banerjee Victor , Zoltsman Guy , Shani Tom , Kahn Joy , Abu-Hamad Salah , Papo Niv , Engel Stanislav , Bernhagen Jurgen , Israelson Adrian 
Published: January 2018

AbstractMutations in superoxide dismutase (SOD1) cause amyotrophic lateral sclerosis (ALS), a fatal neurodegenerative disease caused by the progressive loss of motor neurons in the brain and spinal cord. It has been suggested that toxicity of mutant SOD1 results from its misfolding, however, it is yet unclear why misfolded SOD1 accumulates specifically within motor neurons. We recently demonstrated that macrophage migration inhibitory factor (MIF)—a multifunctional protein with cytokine/chemokine activity and cytosolic chaperone-like properties—inhibits the accumulation of misfolded SOD1. Here, we show that MIF inhibits mutant SOD1 nuclear clearance when overexpressed in motor neuron-like NSC-34 cells. In addition, MIF alters the typical SOD1 amyloid aggregation pathway in vitro, and, instead, promotes the formation of disordered aggregates, as measured by Thioflavin T (ThT) assay and transmission electron microscopy (TEM) imaging. Moreover, we report that MIF reduces the toxicity of misfolded SOD1 by directly interacting with it, and that the chaperone function and protective effect of MIF in neuronal cultures do not require its intrinsic catalytic activities. Importantly, we report that the locked-trimeric MIFN110C mutant, which exhibits strongly impaired CD74-mediated cytokine functions, has strong chaperone activity, dissociating, for the first time, these two cellular functions. Altogether, our study implicates MIF as a potential therapeutic candidate in the treatment of ALS.
Cellular death, reactive oxygen species (ROS) and diabetic complications
Authors: Volpe Caroline Maria Oliveira , Villar-Delfino Pedro Henrique , dos Anjos Paula Martins Ferreira , Nogueira-Machado José Augusto 
Published: January 2018

AbstractChronic or intermittent hyperglycemia is associated with the development of diabetic complications. Several signaling pathways can be altered by having hyperglycemia in different tissues, producing oxidative stress, the formation of advanced glycation end products (AGEs), as well as the secretion of the pro-inflammatory cytokines and cellular death (pathological autophagy and/or apoptosis). However, the signaling pathways that are directly triggered by hyperglycemia appear to have a pivotal role in diabetic complications due to the production of reactive oxygen species (ROS), oxidative stress, and cellular death. The present review will discuss the role of cellular death in diabetic complications, and it will suggest the cause and the consequences between the hyperglycemia-induced signaling pathways and cell death. The signaling pathways discussed in this review are to be described step-by-step, together with their respective inhibitors. They involve diacylglycerol, the activation of protein kinase C (PKC) and NADPH-oxidase system, and the consequent production of ROS. This was initially entitled the “dangerous metabolic route in diabetes”. The historical usages and the recent advancement of new drugs in controlling possible therapeutical targets have been highlighted, in order to evaluate the evolution of knowledge in this sensitive area. It has recently been shown that the metabolic responses to stimuli (i.e., hyperglycemia) involve an integrated network of signaling pathways, in order to define the exact responses. Certain new drugs have been experimentally tested—or suggested and proposed—for their ability to modulate the possible biochemical therapeutical targets for the downregulation of retinopathy, nephropathy, neuropathy, heart disease, angiogenesis, oxidative stress, and cellular death. The aim of this study was to critically and didactically evaluate the exact steps of these signaling pathways and hence mark the indicated sites for the actions of such drugs and their possible consequences. This review will emphasize, besides others, the therapeutical targets for controlling the signaling pathways, when aimed at the downregulation of ROS generation, oxidative stress, and, consequently, cellular death—with all of these conditions being a problem in diabetes.