bluuebunny/crossref_metadata_2025_split huggingface dataset:
On the determination of the temperature distribution within the color conversion elements of phosphor converted LEDs
Authors: Nemitz Wolfgang , Fulmek Paul , Nicolics Johann , Reil Frank , Wenzl Franz P. 
Published: August 2017

AbstractWe present an iterative optical and thermal simulation procedure which enables the determination of the temperature distribution in the phosphor layer of a phosphor converted LED with good accuracy. Using the simulation both the highest phosphor temperatures, which are mostly relevant to material degradation as well as the temperatures of those phosphor particles which mainly contribute to converted light emission can be determined. We compare the simulations with experimental studies on the phosphor temperature. While infrared thermography only gives information on the phosphor layer surface temperature, phosphor thermometry provides temperature data on the volume temperature of the phosphor layer relevant to color conversion.
Mastering the Wrinkling of Self-supported Graphene
Authors: Pacakova Barbara , Verhagen Tim , Bousa Milan , Hübner Uwe , Vejpravova Jana , Kalbac Martin , Frank Otakar 
Published: August 2017

AbstractWe present an approach that allows for the preparation of well-defined large arrays of graphene wrinkles with predictable geometry. Chemical vapor deposition grown graphene transferred onto hexagonal pillar arrays of SiO2 with sufficiently small interpillar distance forms a complex network of two main types of wrinkle arrangements. The first type is composed of arrays of aligned equidistantly separated parallel wrinkles propagating over large distances, and originates from line interfaces in the graphene, such as thin, long wrinkles and graphene grain boundaries. The second type of wrinkle arrangement is composed of non-aligned short wrinkles, formed in areas without line interfaces. Besides the presented hybrid graphene topography with distinct wrinkle geometries induced by the pre-patterned substrate, the graphene layers are suspended and self-supporting, exhibiting large surface area and negligible doping effects from the substrate. All these properties make this wrinkled graphene a promising candidate for a material with enhanced chemical reactivity useful in nanoelectronic applications.
Emergence of Alternative Structures in Amyloid Beta 1-42 Monomeric Landscape by N-terminal Hexapeptide Amyloid Inhibitors
Authors: Chakraborty Srirupa , Das Payel 
Published: August 2017

AbstractAlzheimer’s disease (AD) is characterized by deposition of amyloid beta (Aβ) peptides into senile plaques in the brain. While most familial mutations are associated with early-onset AD, recent studies report the AD-protective nature of two genetic human Aβ variants,i.e. A2T and A2V, in the heterozygous state. The mixture of A2V Aβ1-6 (Aβ6) hexapeptide and WT Aβ1–42 (Αβ42) is also found neuroprotective. Motivated by these findings, in this study we investigate the effects of WT, A2V, and A2T Aβ6hexapeptide binding on the monomeric WT Aβ42landscape. For this purpose, we have performed extensive atomistic Replica Exchange Molecular Dynamics simulations, elucidating preferential binding of Aβ42with the A2V and A2T hexapeptides compared to WT Aβ6. A notable reorganization of the Aβ42landscape is revealed due to hexapeptide association, as manifested by lowering of transient interactions between the central and C-terminal hydrophobic patches. Concurrently, Aβ6-bound Aβ42monomer exhibits alternative structural features that are strongly dependent on the hexapeptide sequence. For example, a central helix is more frequently populated within the A2T-bound monomer, while A2V-bound Aβ42is often enhanced in overall disorder. Taken together, the present simulations offer novel molecular insights onto the effect of the N-terminal hexapeptide binding on the Aβ42monomer structure, which might help in explaining their reported amyloid inhibition properties.
α-Synuclein Amyloids Hijack Prion Protein to Gain Cell Entry, Facilitate Cell-to-Cell Spreading and Block Prion Replication
Authors: Aulić Suzana , Masperone Lara , Narkiewicz Joanna , Isopi Elisa , Bistaffa Edoardo , Ambrosetti Elena , Pastore Beatrice , De Cecco Elena , Scaini Denis , Zago Paola , Moda Fabio , Tagliavini Fabrizio , Legname Giuseppe 
Published: August 2017

AbstractThe precise molecular mechanism of how misfolded α-synuclein (α-Syn) accumulates and spreads in synucleinopathies is still unknown. Here, we show the role of the cellular prion protein (PrPC) in mediating the uptake and the spread of recombinant α-Syn amyloids. The in vitro data revealed that the presence of PrPC fosters the higher uptake of α-Syn amyloid fibrils, which was also confirmed in vivo in wild type (Prnp+/+) compared to PrP knock-out (Prnp−/−) mice. Additionally, the presence of α-Syn amyloids blocked the replication of scrapie prions (PrPSc) in vitro and ex vivo, indicating a link between the two proteins. Indeed, whilst PrPC is mediating the internalization of α-Syn amyloids, PrPSc is not able to replicate in their presence. This observation has pathological relevance, since several reported case studies show that the accumulation of α-Syn amyloid deposits in Creutzfeldt-Jakob disease patients is accompanied by a longer disease course.
Electronic Metamaterials with Tunable Second-order Optical Nonlinearities
Authors: Lin Hung-Hsi , Vallini Felipe , Yang Mu-Han , Sharma Rajat , Puckett Matthew W. , Montoya Sergio , Wurm Christian D. , Fullerton Eric E. , Fainman Yeshaiahu 
Published: August 2017

AbstractThe ability to engineer metamaterials with tunable nonlinear optical properties is crucial for nonlinear optics. Traditionally, metals have been employed to enhance nonlinear optical interactions through field localization. Here, inspired by the electronic properties of materials, we introduce and demonstrate experimentally an asymmetric metal-semiconductor-metal (MSM) metamaterial that exhibits a large and electronically tunable effective second-order optical susceptibility (χ(2)). The induced χ(2) originates from the interaction between the third-order optical susceptibility of the semiconductor (χ(3)) with the engineered internal electric field resulting from the two metals possessing dissimilar work function at its interfaces. We demonstrate a five times larger second-harmonic intensity from the MSM metamaterial, compared to contributions from its constituents with electrically tunable nonlinear coefficient ranging from 2.8 to 15.6 pm/V. Spatial patterning of one of the metals on the semiconductor demonstrates tunable nonlinear diffraction, paving the way for all-optical spatial signal processing with space-invariant and -variant nonlinear impulse response.
Co-encapsulation and co-transplantation of mesenchymal stem cells reduces pericapsular fibrosis and improves encapsulated islet survival and function when allografted
Authors: Vaithilingam Vijayaganapathy , Evans Margaret D. M. , Lewy Denise M. , Bean Penelope A. , Bal Sumeet , Tuch Bernard E. 
Published: August 2017

AbstractPericapsular fibrotic overgrowth (PFO) is associated with poor survival of encapsulated islets. A strategy to combat PFO is the use of mesenchymal stem cells (MSC). MSC have anti-inflammatory properties and their potential can be enhanced by stimulation with proinflammatory cytokines. This study investigated whether co-encapsulation or co-transplantation of MSC with encapsulated islets would reduce PFO and improve graft survival. Stimulating MSC with a cytokine cocktail of IFN-γ and TNF-α enhanced their immunosuppressive potential by increasing nitric oxide production and secreting higher levels of immunomodulatory cytokines. In vitro, co-encapsulation with MSC did not affect islet viability but significantly enhanced glucose-induced insulin secretion. In vivo, normoglycemia was achieved in 100% mice receiving islets co-encapsulated with stimulated MSC as opposed to 71.4% receiving unstimulated MSC and only 9.1% receiving encapsulated islets alone. Microcapsules retrieved from both unstimulated and stimulated MSC groups had significantly less PFO with improved islet viability and function compared to encapsulated islets alone. Levels of peritoneal immunomodulatory cytokines IL-4, IL-6, IL-10 and G-CSF were significantly higher in MSC co-encapsulated groups. Similar results were obtained when encapsulated islets and MSC were co-transplanted. In summary, co-encapsulation or co-transplantation of MSC with encapsulated islets reduced PFO and improved the functional outcome of allotransplants.
Hydrological legacy determines the type of enzyme inhibition in a peatlands chronosequence
Authors: Bonnett Samuel Alexander Festing , Maltby Edward , Freeman Chris 
Published: August 2017

AbstractPeatland ecosystems contain one-third of the world’s soil carbon store and many have been exposed to drought leading to a loss of carbon. Understanding biogeochemical mechanisms affecting decomposition in peatlands is essential for improving resilience of ecosystem function to predicted climate change. We investigated biogeochemical changes along a chronosequence of hydrological restoration (dry eroded gully, drain-blocked <2 years, drain blocked <7 years and wet pristine site), and examined whether hydrological legacy alters the response of β-glucosidase kinetics (i.e. type of inhibition) to short-term drying and waterlogging. In the dry eroded gully at depth, low phenolic concentrations were associated with enhanced β-glucosidase enzyme activities (V
max
) but short-term drying and waterlogging caused a significant increase of dissolved organic carbon (DOC) and phenolics associated with increases in V
max
(enzyme production) and K
m
(indicative of competitive inhibition). Inhibition within the drain blocked and pristine sites at depth exhibited non-competitive inhibition (decreased Vmax), whilst uncompetitive inhibition (decreased V
max
and K
m
) occurred in surface peat explained by variation in humic substances and phenolics. These results suggest that loss of carbon by short-term drought or rewetting may occur from sites with a legacy of drought due to the release of non-inhibitory phenolics that permits enhanced enzyme activity.
Immune activated monocyte exosomes alter microRNAs in brain endothelial cells and initiate an inflammatory response through the TLR4/MyD88 pathway
Authors: Dalvi Pranjali , Sun Bing , Tang Norina , Pulliam Lynn 
Published: August 2017

AbstractThe host immune response is critical for homeostasis; however, when chronic low level activation of the immune response with or without the driver continues, a cascade of events can trigger immunological dysfunction. Monocytes are key peripheral sensors of the immune response and their activation is instrumental in the development of cognitive impairment. Here, we show that monocytes activated by interferon alpha, lipopolysaccharide or a combination of both generate exosomes carrying significantly altered microRNA profiles compared to non-activated monocytes. These exosomes alone can activate human brain microvascular endothelial cells to stimulate adhesion molecules, CCL2, ICAM1, VCAM1 and cytokines, IL1β and IL6. This activation is through the toll like receptor 4 (TLR4)/myeloid differentiation primary response gene 88 (MyD88) pathway that activates nuclear factor-κB and increases monocyte chemotaxis. Inhibition of monocyte exosome release reverses endothelial cell activation and monocyte chemotaxis. Our study suggests that activated monocytes have an impact on brain vascular function through intercellular exosome signaling.
Massive transcriptome sequencing of human spinal cord tissues provides new insights into motor neuron degeneration in ALS
Authors: D’Erchia Anna Maria , Gallo Angela , Manzari Caterina , Raho Susanna , Horner David S. , Chiara Matteo , Valletti Alessio , Aiello Italia , Mastropasqua Francesca , Ciaccia Loredana , Locatelli Franco , Pisani Francesco , Nicchia Grazia Paola , Svelto Maria , Pesole Graziano , Picardi Ernesto 
Published: August 2017

AbstractALS is a devastating and debilitating human disease characterized by the progressive death of upper and lower motor neurons. Although much effort has been made to elucidate molecular determinants underlying the onset and progression of the disorder, the causes of ALS remain largely unknown. In the present work, we have deeply sequenced whole transcriptome from spinal cord ventral horns of post-mortem ALS human donors affected by the sporadic form of the disease (which comprises ~90% of the cases but which is less investigated than the inherited form of the disease). We observe 1160 deregulated genes including 18 miRNAs and show that down regulated genes are mainly of neuronal derivation while up regulated genes have glial origin and tend to be involved in neuroinflammation or cell death. Remarkably, we find strong deregulation of SNAP25 and STX1B at both mRNA and protein levels suggesting impaired synaptic function through SNAP25 reduction as a possible cause of calcium elevation and glutamate excitotoxicity. We also note aberrant alternative splicing but not disrupted RNA editing.
Functional proteomics outlines the complexity of breast cancer molecular subtypes
Authors: Gámez-Pozo Angelo , Trilla-Fuertes Lucía , Berges-Soria Julia , Selevsek Nathalie , López-Vacas Rocío , Díaz-Almirón Mariana , Nanni Paolo , Arevalillo Jorge M. , Navarro Hilario , Grossmann Jonas , Gayá Moreno Francisco , Gómez Rioja Rubén , Prado-Vázquez Guillermo , Zapater-Moros Andrea , Main Paloma , Feliú Jaime , Martínez del Prado Purificación , Zamora Pilar , Ciruelos Eva , Espinosa Enrique , Fresno Vara Juan Ángel 
Published: August 2017

AbstractBreast cancer is a heterogeneous disease comprising a variety of entities with various genetic backgrounds. Estrogen receptor-positive, human epidermal growth factor receptor 2-negative tumors typically have a favorable outcome; however, some patients eventually relapse, which suggests some heterogeneity within this category. In the present study, we used proteomics and miRNA profiling techniques to characterize a set of 102 either estrogen receptor-positive (ER+)/progesterone receptor-positive (PR+) or triple-negative formalin-fixed, paraffin-embedded breast tumors. Protein expression-based probabilistic graphical models and flux balance analyses revealed that some ER+/PR+ samples had a protein expression profile similar to that of triple-negative samples and had a clinical outcome similar to those with triple-negative disease. This probabilistic graphical model-based classification had prognostic value in patients with luminal A breast cancer. This prognostic information was independent of that provided by standard genomic tests for breast cancer, such as MammaPrint, OncoType Dx and the 8-gene Score.
PPARα-dependent Insig2a overexpression inhibits SREBP-1c processing during fasting
Authors: Lee Jae-Ho , Kang Hye Suk , Park Hyeon Young , Moon Young-Ah , Kang Yu Na , Oh Byung-Chul , Song Dae-Kyu , Bae Jae-Hoon , Im Seung-Soon 
Published: August 2017

AbstractPeroxisome-proliferator-activated receptor alpha (PPARα) and sterol regulatory element-binding protein (SREBP) play a role in regulating cellular fatty acid and cholesterol homeostasis via fatty acid oxidation and lipogenesis. The control of SREBP processing is regulated by the insulin induced gene (INSIG)2a protein, which binds SREBP to prevent SREBP translocation to the Golgi apparatus during nutrient starvation in the liver. However, the regulation of SREBP-1c processing by INSIGs during fasting and the regulatory mechanisms of the mouse Insig2a gene expression have not been clearly addressed. In the present study, we found that Insig2a was upregulated by PPARα in mouse livers and primary hepatocytes during fasting, whereas Insig2a mRNA expression was decreased in the livers of refed mice. A PPAR-responsive element between −126 bp and −114 bp in the Insig2a promoter was identified by a transient transfection assay and a chromatin immunoprecipitation assay; its role in regulation by PPARα was characterised using Pparα-null mice. These results suggest that PPARα is a trans-acting factor that enhances Insig2a gene expression, thereby suppressing SREBP-1c processing during fasting.
PPARα activation protects against cholestatic liver injury
Authors: Zhao Qi , Yang Rui , Wang Jing , Hu Dan-Dan , Li Fei 
Published: August 2017

AbstractIntrahepatic cholestasis induced by drug toxicity, bile salt export pump (BSEP) deficiency, or pregnancy frequently causes cholestatic liver damage, which ultimately may lead to liver fibrosis and cirrhosis. Here, the preventive and therapeutic effects of peroxisome proliferator-activated receptor α (PPARα) signaling activated by fenofibrate was evaluated on cholestatic liver damage. Metabolomic analysis revealed that alpha-naphthyl isothiocyanate (ANIT)-induced intrahepatic cholestasis resulted in the accumulation of serum long-chain acylcarnitines and triglyceride, and the reduced expression of four fatty acid β-oxidation (β-FAO) relevant genes (Cpt1b, Cpt2, Mcad and Hadha), indicating the disruption of β-FAO. The increase of acylcarnitines in hepatic cell resulted in the enhanced expression of anti-oxidative genes glutathione S-transferases (Gsta2 and Gstm3) directly. As direct PPARα-regulated genes, Cpt1b, Cpt2, and Mcad were up-regulated after pretreatment with PPARα agonist, fenofibrate, indicating the improvement of β-FAO. In the end, the disrupted bile acid metabolism in the enterohepatic circulation and the enhanced oxidative stress and inflammation cytokines induced by ANIT exposure were significantly recovered with the improvement of β-FAO using fenofibrate treatment. These findings provide the rationale for the use of PPARα agonists as therapeutic alternatives for cholestatic liver damage.
The molecular basis of differential morphology and bleaching thresholds in two morphs of the coral Pocillopora acuta
Authors: Smith Hillary , Epstein Hannah , Torda Gergely 
Published: August 2017

AbstractProcesses of cnidarian evolution, including hybridization and phenotypic plasticity, have complicated the clear diagnosis of species boundaries within the phylum. Pocillopora acuta, a species of scleractinian coral that was recently split from the widespread Pocillopora damicornis species complex, occurs in at least two distinct morphs on the Great Barrier Reef. Contrasting morphology combined with evidence of differential bleaching thresholds among sympatrically distributed colonies suggest that the taxonomy of this recently described species is not fully resolved and may represent its own species complex. To examine the basis of sympatric differentiation between the two morphs, we combined analyses of micro- and macro-skeletal morphology with genome wide sequencing of the coral host, as well as ITS2 genotyping of the associated Symbiodinium communities. We found consistent differences between morphs on both the macro- and micro-skeletal scale. In addition, we identified 18 candidate functional genes that relate to skeletal formation and morphology that may explain how the two morphs regulate growth to achieve their distinct growth forms. With inconclusive results in endosymbiotic algal community diversity between the two morphs, we propose that colony morphology may be linked to bleaching susceptibility. We conclude that cryptic speciation may be in the early stages within the species P. acuta.
Detection of frequency-dependent endothelial response to oscillatory shear stress using a microfluidic transcellular monitor
Authors: Sei Yoshitaka J. , Ahn Song Ih , Virtue Theodore , Kim Taeyoung , Kim YongTae 
Published: August 2017

AbstractThe endothelial microenvironment is critical in maintaining the health and function of the intimal layer in vasculature. In the context of cardiovascular disease (CVD), the vascular endothelium is the layer of initiation for the progression of atherosclerosis. While laminar blood flows are known to maintain endothelial homeostasis, disturbed flow conditions including those the endothelium experiences in the carotid artery are responsible for determining the fate of CVD progression. We present a microfluidic device designed to monitor the endothelium on two fronts: the real-time monitoring of the endothelial permeability using integrated electrodes and the end-point characterization of the endothelium through immunostaining. Our key findings demonstrate endothelial monolayer permeability and adhesion protein expression change in response to oscillatory shear stress frequency. These changes were found to be significant at certain frequencies, suggesting that a frequency threshold is needed to elicit an endothelial response. Our device made possible the real-time monitoring of changes in the endothelial monolayer and its end-point inspection through a design previously absent from the literature. This system may serve as a reliable research platform to investigate the mechanisms of various inflammatory complications of endothelial disorders and screen their possible therapeutics in a mechanistic and high-throughput manner.
Collagen Complexity Spatially Defines Microregions of Total Tissue Pressure in Pancreatic Cancer
Authors: Nieskoski Michael D. , Marra Kayla , Gunn Jason R. , Hoopes P. Jack , Doyley Marvin M. , Hasan Tayyaba , Trembly B. Stuart , Pogue Brian W. 
Published: August 2017

AbstractThe poor efficacy of systemic cancer therapeutics in pancreatic ductal adenocarcinoma (PDAC) is partly attributed to deposition of collagen and hyaluronan, leading to interstitial hypertension collapsing blood and lymphatic vessels, limiting drug delivery. The intrinsic micro﻿-regional﻿ interactions between hyaluronic acid (HA), collagen and the spatial origins of mechanical stresses that close off blood vessels was investigated here. Multiple localized pressure measurements were analyzed with spatially-matched histochemical images of HA, collagen and vessel perfusion. HA is known to swell, fitting a linear elastic model with total tissue pressure (TTP) increasing above interstitial fluid pressure (IFP) directly with collagen content. However, local TTP appears to originate from collagen area fraction, as well as increased its entropy and fractal dimension, and morphologically appears to be maximized when HA regions are encapsulated by collagen. TTP was inversely correlated with vascular patency and verteporfin uptake, suggesting interstitial hypertension results in vascular compression and decreased molecular delivery in PDAC. Collagenase injection led to acute decreases in total tissue pressure and increased drug perfusion. Large microscopic variations in collagen distributions within PDAC leads to microregional TPP values that vary on the hundred micron distance scale, causing micro-heterogeneous limitations in molecular perfusion, and narrows viable treatment regimes for systemically delivered therapeutics.
Role of 2D and 3D defects on the reduction of LaNiO3 nanoparticles for catalysis
Authors: Singh Sarika , Prestat Eric , Huang Liang-Feng , Rondinelli James M. , Haigh Sarah J. , Rosen Brian A. 
Published: August 2017

AbstractSolid phase crystallization offers an attractive route to synthesize Ni nanoparticles on a La2O3 support. These materials have shown great promise as catalysts for methane oxidation and similar reactions. Synthesis is achieved by the reduction of a LaNiO3 (LNO) precursor at high temperatures, but the reduction pathway can follow a variety of routes. Optimization of catalytic properties such as the long-term stability has been held back by a lack of understanding of the factors impacting the reduction pathway, and its strong influence on the structure of the resulting Ni/La2O3 catalyst. Here we show the first evidence of the importance of extended structural defects in the LNO precursor material (2D stacking faults and 3D inclusions) for determining the reaction pathway and therefore the properties of the final catalyst. Here we compare the crystallization of LNO nanoparticles via two different pathways using in-situ STEM, in-situ synchrotron XRD, and DFT electronic structure calculations. Control of extended defects is shown to be a key microstructure component for improving catalyst lifetimes.