bluuebunny/crossref_metadata_2025_split huggingface dataset:
Improvement of Surface Properties of Nickel-Based Superalloys Grade Haynes 214 by Pack Aluminizing
Authors: Keeratimas Pasuta , Visuttipitukul Patama , Wangyao Panyawat 
Published: December 2013

Abstract
This research studied mechanical properties and oxidation resistance of Haynes 214 after pack aluminizing. The Haynes 214 samples were heat treated at various temperatures (973 K, 1073 K and 1173 K) for 1, 1.25, 4 and 6.25 hours, respectively. After aluminizing, there were two layers at the surface: the inner layer (Ni2Al3) located adjacent to Haynes 214 substrate and the outer layer (Ni2Al3 and NiAl3) at the surface. After aluminizing, surface hardness significantly increases from about 250 HV of substrate to more than 570 HV. With increasing hardness, wear resistance of aluminized samples can also be improved as can be seen from decreasing the specific wear rate from 2.24 × 10−6 g N−1m−1 to 7.6 × 10−7 g N−1m−1 after aluminizing. Cyclic oxidation tests of Haynes 214 with and without aluminizing show that both of them have good oxidation resistance due to slow growth rate of oxide film.
Hazard assessment of glacial lake outburst floods from Kyagar glacier, Karakoram mountains, China
Authors: Haemmig Christoph , Huss Matthias , Keusen Hansrudolf , Hess Josef , Wegmüller Urs , Ao Zhigang , Kulubayi Wubuli 
Published: December 2013

AbstractKyagar glacier is located in the Chinese Karakoram mountains. The glacier tongue entirely blocks the riverbed in the upper Shaksgam valley and impounds a glacial lake, which was the source of several violent and disastrous glacial lake outburst floods (GLOFs). A GLOF early warning system was implemented between 2011 and 2013. We present an integrative analysis of the hazard potential of Kyagar lake, taking into account the ice flow dynamics of Kyagar glacier as well as the recent surface mass-balance response to climate change. Comparison of two high-resolution digital elevation models (DEMs) for the ice dam shows surface lowering rates of >5ma– 1 between 2002 and 2011, leading to a significant reduction in the maximum potential lake volume. However, two DEMs covering the entire glacier for the period 2000–10 indicate mass gains in its central part, and flow speed measurements show an acceleration in this region. This pattern of local ice-thickness changes combined with varying ice flow velocities is typical for surge-type glaciers. The velocity of the glacier surface and of the ice dam between 2011 and 2012 are analyzed at high temporal and spatial resolution, based on feature tracking of synthetic aperture radar (SAR) images.
Future fluctuations of Mer de Glace, French Alps, assessed using a parameterized model calibrated with past thickness changes
Authors: Vincent C. , Harter M. , Gilbert A. , Berthier E. , SIX D. 
Published: December 2013

AbstractSimulations of glacier evolution are needed to assess future changes in the runoff regime of mountain catchments. A simplified parameterized model is applied here to simulate future thickness changes and glacier retreat of Mer de Glace, French Alps. A normalized thickness change function describing the spatial distribution of surface-elevation changes as a function of elevation has been determined. The model reveals that under present climatic conditions Mer de Glace will continue to shrink dramatically in the coming decades, retreating by 1200 m between now and 2040. The method has certain limitations related to the uncertainties of the normalized function based on thickness change data. An error of 10% in the normalized function leads to uncertainties of 46%, 30% and 18% in Mer de Glace front, surface area and glacier-wide mass-balance changes respectively in 2040. Because the difference of the normalized function largely exceeds 10% from one glacier to another, even within a given glacier size class and elevation range, it would be very risky to extrapolate the normalized function to unmeasured glaciers. Consequently, the method is applicable only on glaciers where past surface elevation changes are well constrained.
The Great British Music Hall: Its Importance to British Culture and ‘The Trivial’
Authors: Gerrard Steven 
Published: December 2013

By 1960, Britain’s once-thriving Music Hall industry was virtually dead. Theatres with their faded notions of Empire gave way to Cinema and the threat of Television. Where thousands once linked arms singing popular songs, watch acrobatics, see feats of strength, and listen to risqué jokes, now the echoes of those acts lay as whispers amongst the stalls’ threadbare seats.
The Halls flourished in the 19th Century, but had their origins in the taverns of the 16th and 17th Centuries. Minstrels plied their trade egged on by drunken crowds. As time passed, the notoriety of the Music Hall acts and camaraderie produced grew. Entrepreneurial businessman tapped into this commerciality and had purpose-built status symbol theatres to provide a ‘home’ for acts and punters. With names like The Apollo giving gravitas approaching Olympian ideals, so the owners basked in wealth and glory.
The Music Hall became the mass populist entertainment for the population. Every town had one, where everyone could be entertained by variety acts showing off the performers’ skills. The acts varied from singers, joke-tellers, comics, acrobats, to dancers. They all aimed to entertain. They enabled audiences to share a symbiotic relationship with one another; became recruitment officers for the Army; inspired War Poets; showed short films; and they and the halls reflected both the ideals and foibles of their era.
By using Raymond Williams’ structures of feeling as its cornerstone, the article will give a brief history of the halls, whilst providing analysis into how they grew into mass populist entertainment that represented British culture. Case studies of famous artistes are given, plus an insight into how Music Hall segued into radio, film and television.
IL-32 Promotes Angiogenesis
Authors: Nold-Petry Claudia A. , Rudloff Ina , Baumer Yvonne , Ruvo Menotti , Marasco Daniela , Botti Paolo , Farkas Laszlo , Cho Steven X. , Zepp Jarod A. , Azam Tania , Dinkel Hannah , Palmer Brent E. , Boisvert William A. , Cool Carlyne D. , Taraseviciene-Stewart Laima , Heinhuis Bas , Joosten Leo A. B. , Dinarello Charles A. , Voelkel Norbert F. , Nold Marcel F. 
Published: December 2013

Abstract
IL-32 is a multifaceted cytokine with a role in infections, autoimmune diseases, and cancer, and it exerts diverse functions, including aggravation of inflammation and inhibition of virus propagation. We previously identified IL-32 as a critical regulator of endothelial cell (EC) functions, and we now reveal that IL-32 also possesses angiogenic properties. The hyperproliferative ECs of human pulmonary arterial hypertension and glioblastoma multiforme exhibited a markedly increased abundance of IL-32, and, significantly, the cytokine colocalized with integrin αVβ3. Vascular endothelial growth factor (VEGF) receptor blockade, which resulted in EC hyperproliferation, increased IL-32 three-fold. Small interfering RNA–mediated silencing of IL-32 negated the 58% proliferation of ECs that occurred within 24 h in scrambled-transfected controls. Reduction of IL-32 neither affected apoptosis (insignificant changes in Bak-1, Bcl-2, Bcl-xL, lactate dehydrogenase, annexin V, and propidium iodide) nor VEGF or TGF-β levels, but siIL-32–transfected adult and neonatal ECs produced up to 61% less NO, IL-8, and matrix metalloproteinase-9, and up to 3-fold more activin A and endostatin. In coculture-based angiogenesis assays, IL-32γ dose-dependently increased tube formation up to 3-fold; an αVβ3 inhibitor prevented this activity and reduced IL-32γ–induced IL-8 by 85%. In matrigel plugs loaded with IL-32γ, VEGF, or vehicle and injected into live mice, we observed the anticipated VEGF-induced increase in neocapillarization (8-fold versus vehicle), but unexpectedly, IL-32γ was equally angiogenic. A second signal such as IFN-γ was required to render cells responsive to exogenous IL-32γ; importantly, this was confirmed using a completely synthetic preparation of IL-32γ. In summary, we add angiogenic properties that are mediated by integrin αVβ3 but VEGF-independent to the portfolio of IL-32, implicating a role for this versatile cytokine in pulmonary arterial hypertension and neoplastic diseases.
IL-27, a Cytokine, and IFN-λ1, a Type III IFN, Are Coordinated To Regulate Virus Replication through Type I IFN
Authors: Cao Yanhua , Zhang Rui , Zhang Wei , Zhu Chengliang , Yu Yi , Song Yu , Wang Qing , Bai Lan , Liu Yingle , Wu Kailang , Wu Jianguo 
Published: December 2013

Abstract
IL-27, a member of the IL-12 family, plays a critical role in the control of innate and adaptive immune responses. IFN-λ1, a member of the type III IFN family, shows antiviral abilities. In this study, we investigated the effects of IL-27 and IFN-λ1 on the replication of hepatitis B virus (HBV), a major pathogen associated with a high risk for cirrhosis, liver failure, and hepatocellular carcinoma. We revealed that HBV infection activates IL-27 expression and IFN-λ1 production and demonstrated that viral-activated IL-27 and IFN-λ1 are coordinated to inhibit HBV replication. Initially, HBV infection upregulates IL-27 expression, which, in turn, stimulates IFN-λ1 production through regulating ERK1/2 signaling and by enhancing NF-κB nuclear translocation to bind to the IFN-λ1 promoter. Moreover, IL-27–activated IFN-λ1 upregulates IFN-λ1 receptor (IL-28R1 and IL-10Rβ) activity, resulting in the activation of the STAT1/2 pathway, which, in turn, induces the expression of IFN-stimulated genes, including IFN-inducible dsRNA-activated protein kinase, oligoadenylate synthetase 1, and IFN-induced GTP-binding protein 1 and, finally, inhibits HBV protein expression and viral capsid–associated DNA replication. More interestingly, we also revealed that type I IFN (IFN-α) is also involved in the downregulation of HBV replication mediated by IL-27. Thus, we identified a previously unknown mechanism by which IL-27 and IFN-λ1 are coordinated to regulate virus replication through type I IFN.
Killer Ig-like Receptor 2DL4 Does Not Mediate NK Cell IFN-γ Responses to Soluble HLA-G Preparations
Authors: Le Page Michael E. L. , Goodridge Jodie P. , John Elisabeth , Christiansen Frank T. , Witt Campbell S. 
Published: December 2013

Abstract
The MHC class Ib molecule HLA-G has previously been reported to be the ligand for the NK cell receptor killer Ig-like receptor (KIR)2DL4, but this remains controversial. In this study, we investigated IFN-γ production by freshly isolated NK cells in response to both soluble and solid-phase ligands, including anti-KIR2DL4 mAbs and rHLA-G. Although freshly isolated CD56bright NK cells produced IFN-γ in response to soluble HLA-G preparations, the response was found to be absolutely dependent on the presence of small numbers of contaminating CD56−, CD14−, CD11c+ myeloid dendritic cells (mDCs). HLA-G tetramers bound only to the contaminating mDCs in the NK preparations, and Abs to KIR2DL4 and HLA-G did not block NK cell IFN-γ production. NK cells did not respond to plate-bound HLA-G. Freshly isolated NK cells also produced IFN-γ in response to unpurified soluble anti-KIR2DL4 mAb but not to low endotoxin affinity–purified Ab. The data suggest that previous reports of functional interactions between KIR2DL4 and HLA-G may have resulted from the use of purified NK cells that were contaminated with mDCs and HLA-G preparations that were contaminated with material capable of stimulating mDCs to produce cytokines that stimulate NK cells to produce IFN-γ.
Novel Mechanisms Underlying the Immediate and Transient Global Tolerization of Splenic Dendritic Cells after Vaccination with a Self-Antigen
Authors: Farkas Adam M. , Finn Olivera J. 
Published: December 2013

Abstract
Dendritic cells (DCs) are important orchestrators of the immune response, ensuring that immunity against pathogens is generated, whereas immunity against healthy tissues is prevented. Using the tumor Ag MUC1, we previously showed that i.v. immunization of MUC1 transgenic mice, but not wild-type, with a MUC1 peptide resulted in transient tolerization of all splenic DCs. These DCs did not upregulate costimulatory molecules and induced regulatory T cells rather than effector T cells. They were characterized by suppressed expression of a cohort of pancreatic enzymes not previously reported in DCs, which were upregulated in DCs presenting the same MUC1 peptide as a foreign Ag. In this article, we examined the self-antigen–tolerized DC phenotype, function, and mechanisms responsible for inducing or maintaining their tolerized state. Tolerized DCs share some characteristics with immature DCs, such as a less inflammatory cytokine/chemokine profile, deficient activation of NF-κB, and sustained expression of zDC and CCR2. However, tolerized DCs demonstrated a novel inducible expression of aldehyde dehydrogenase 1/2 and phospho-STAT3. Suppressed expression of one of the pancreatic enzymes, trypsin, in these DC impeded their ability to degrade extracellular matrix, thus affecting their motility. Suppressed metallopeptidases, reflected in low expression of carboxypeptidase B1, prevented optimal Ag-specific CD4+ T cell proliferation suggesting their role in Ag processing. Tolerized DCs were not refractory to maturation after stimulation with a TLR3 agonist, demonstrating that this tolerized state is not terminally differentiated and that tolerized DCs can recover their ability to induce immunity to foreign Ags.
Oral Escherichia coli Colonization Factor Antigen I Fimbriae Ameliorate Arthritis via IL-35, Not IL-27
Authors: Kochetkova Irina , Thornburg Theresa , Callis Gayle , Holderness Kathryn , Maddaloni Massimo , Pascual David W. 
Published: December 2013

Abstract
A Salmonella therapeutic expressing enterotoxigenic Escherichia coli colonization factor Ag I (CFA/I) fimbriae protects against collagen-induced arthritis (CIA) by eliciting two regulatory T cell (Treg) subsets: TGF-β–producing Foxp3−CD39+CD4+ T cells and IL-10–producing Foxp3+CD39+CD4+ T cells. However, it is unclear whether CFA/I fimbriae alone are protective and whether other regulatory cytokines are involved, especially in the context for the EBI3-sharing cytokines, Treg-derived IL-35 and APC-derived IL-27, both capable of suppressing Th17 cells and regulating autoimmune diseases. Subsequent evaluation revealed that a single oral dose of purified, soluble CFA/I fimbriae protected against CIA as effectively as did Salmonella-CFA/I and found that Foxp3+CD39+CD4+ T cells were the source of secreted IL-35, whereas IL-27 production by CD11c+ cells was inhibited. Inquiring into their relevance, CFA/I fimbriae–treated IL-27R–deficient (WSX-1−/−) mice were equally protected against CIA as were wild-type mice, suggesting a limited role for IL-27. In contrast, CFA/I fimbriae–mediated protection was abated in EBI3−/− mice, accompanied by the loss of TGF-β– and IL-10–producing Tregs. Adoptive transfer of C57BL/6 CD39+CD4+ T cells to EBI3−/− mice with concurrent CFA/I plus IL-35 treatment effectively stimulated Tregs suppressing proinflammatory collagen II–specific Th cells. In contrast, recipients cotransferred with C57BL/6 and EBI3−/− CD39+CD4+ T cells and treated with CFA/I plus IL-35 were not protected, implicating the importance of endogenous IL-35 for conferring CFA/I-mediated protection. Thus, CFA/I fimbriae stimulate IL-35 required for the coinduction of TGF-β and IL-10.
Effector-Memory T Cells Develop in Islets and Report Islet Pathology in Type 1 Diabetes
Authors: Chee Jonathan , Ko Hyun-Ja , Skowera Ania , Jhala Gaurang , Catterall Tara , Graham Kate L. , Sutherland Robyn M. , Thomas Helen E. , Lew Andrew M. , Peakman Mark , Kay Thomas W. H. , Krishnamurthy Balasubramanian 
Published: December 2013

Abstract
CD8+ T cells are critical in human type 1 diabetes and in the NOD mouse. In this study, we elucidated the natural history of islet-specific glucose-6-phosphatase catalytic subunit-related protein (IGRP)-specific CD8+ T cells in NOD diabetes using MHC-tetramer technology. IGRP206–214-specific T cells in the peripheral lymphoid tissue increased with age, and their numbers correlated with insulitis progression. IGRP206–214-specific T cells in the peripheral lymphoid tissue expressed markers of chronic Ag stimulation, and their numbers were stable after diagnosis of diabetes, consistent with their memory phenotype. IGRP206–214-specific T cells in NOD mice expand, acquire the phenotype of effector-memory T cells in the islets, and emigrate to the peripheral lymphoid tissue. Our observations suggest that enumeration of effector-memory T cells of multiple autoantigen specificities in the periphery of type 1 diabetic subjects could be a reliable reporter for progression of islet pathology.
TNFR-Associated Factor 6 and TGF-β–Activated Kinase 1 Control Signals for a Senescence Response by an Endosomal NK Cell Receptor
Authors: Rajagopalan Sumati , Lee Elizabeth C. , DuPrie Matthew L. , Long Eric O. 
Published: December 2013

Abstract
The endosomal innate receptor CD158d (killer cell Ig-like receptor 2DL4) induces cellular senescence in human NK cells in response to soluble ligand (HLA-G or agonist Ab). These senescent NK cells display a senescence-associated secretory phenotype, and their secretome promotes vascular remodeling and angiogenesis. To understand how CD158d initiates signaling for a senescence response, we mapped the region in its cytoplasmic tail that controls signaling. We identified a conserved TNFR-associated factor 6 (TRAF6) binding motif, which was required for CD158d-induced NF-κB activation and IL-8 secretion, TRAF6 association with CD158d, and TRAF6 recruitment to CD158d+ endosomes in transfected cells. The adaptor TRAF6 is known to couple proximal signals from receptors such as endosomal TLRs and CD40 through the kinase TGF-β–activated kinase 1 (TAK1) for NF-κB–dependent proinflammatory responses. Small interfering RNA–mediated silencing of TRAF6 and TAK1, and inhibition of TAK1 blocked CD158d-dependent IL-8 secretion. Stimulation of primary, resting NK cells with soluble Ab to CD158d induced TRAF6 association with CD158d, induced TAK1 phosphorylation, and inhibition of TAK1 blocked the CD158d-dependent reprogramming of NK cells that produces the senescence-associated secretory phenotype signature. Our results reveal that a prototypic TLR and TNFR signaling pathway is used by a killer cell Ig-like receptor that promotes secretion of proinflammatory and proangiogenic mediators as part of a unique senescence phenotype in NK cells.
Foliar Consumption across a Sudden Oak Death Chronosequence in Laboratory Fires
Authors: Kuljian Howard , Varner J. Morgan 
Published: December 2013

AbstractThe recent introduction and spread of sudden oak death (SOD; caused byPhytopthora ramorum) has caused heavy mortality in native tanoak (Notholithocarpus densiflorus[Hook. & Arn.] Manoset al.=Lithocarpus densiflorus[Hook. & Arn.] Rehder) forests in California and Oregon, USA. Following tree death, killed tanoaks retain their dead foliage, resulting in a 1 to 3 year period of extremely low foliar moisture and increased probability of crown ignition. We compared foliage ignition and consumption in a laboratory experiment at simulated crown heights from 0.5 m to 1.5 m across a range of representative foliar moistures (80 %, 70 %, 9 %, and 5 %) found in affected regional forests. Results revealed differences in live and dead foliage consumption. All foliage categories were consumed at the lowest crown base heights; consumption of live foliage declined quickly with increasing height, with minimal consumption occurring above 1 m. Consumption of dead foliage also declined with increasing heights, but some consumption (∼25 %) still occurred up to 1.25 m. These data inform the mechanism for patterns of individual tree torching and firebrand generation reported in wildfires in SOD-infected forests and woodlands.
Short-Term Effects of Repeated Wildfires in Oak-Juniper Woodlands
Authors: Reemts Charlotte M. , Hansen Laura L. 
Published: December 2013

AbstractFire can shape both the structure and composition of vegetation communities, especially those dominated by species with different regeneration strategies. The dominant species of oak-juniper communities in central Texas include resprouters (oaks [Quercus spp.]) and a reseeder (Ashe juniper [Juniperus ashei Buchholz]). We studied the effects of two overlapping wildfires (1996 and 2009) on oak-juniper woodlands on Fort Hood Military Reservation, Texas, USA. We estimated burn severity and measured vegetation regeneration along permanent transects in once-burned, twice-burned, and nonburned areas. Burn severity was highly variable, but was higher in 1996 than in 2009. In the first growing season after the second fire (2009), understory stem density was 3 to 4 times higher than in 1996, but that difference had disappeared by the third growing season. Overstory density did not differ after the two fires, but density on slopes was 3 to 10 times higher than on mesas. Overall species composition was similar after the two fires, but differed from nonburned areas due to the absence of Ashe juniper. Ashe juniper was still absent from twice-burned areas in 2011, whereas small numbers of junipers (21 ± 34 stems ha−1) had colonized the once-burned areas within three years. Our data suggest that wildfires controlled the historical distribution of Ashe juniper, but not of resprouting species, in the Edwards Plateau, and that long intervals between wildfires are required for Ashe juniper to become a canopy dominant in these woodlands.
First simultaneous space measurements of atmospheric pollutants in the boundary layer from IASI: A case study in the North China Plain
Authors: Boynard Anne , Clerbaux Cathy , Clarisse Lieven , Safieddine Sarah , Pommier Matthieu , Van Damme Martin , Bauduin Sophie , Oudot Charlotte , Hadji‐Lazaro Juliette , Hurtmans Daniel , Coheur Pierre‐Francois 
Published: December 2013

AbstractIn this paper we investigate a severe pollution episode that occurred in Beijing, Tianjin, and the Hebei province in January 2013. The episode was caused by the combination of anthropogenic emissions and a high‐pressure system that trapped pollutants in the boundary layer. Using IASI (Infrared Atmospheric Sounding Interferometer) satellite measurements, high concentrations of key trace gases such as carbon monoxide (CO), sulfur dioxide (SO2), and ammonia (NH3) along with ammonium sulfate aerosol ((NH4)2SO4) are found. We show that IASI is able to detect boundary layer pollution in case of large negative thermal contrast combined with high levels of pollution. Our findings demonstrate that anthropogenic key pollutants, such as CO and SO2, can be monitored by IASI in the North China Plain during wintertime in support of air quality evaluation and management.