bluuebunny/crossref_metadata_2025_split huggingface dataset:
α1 adrenoceptor activation by norepinephrine inhibits LPS‐induced cardiomyocyte TNF‐α production via modulating ERK1/2 and NF‐κB pathway
Authors: Yu Xiaohui , Jia Baoyin , Wang Faqiang , Lv Xiuxiu , Peng Xuemei , Wang Yiyang , Li Hongmei , Wang Yanping , Lu Daxiang , Wang Huadong 
Published: December 2013

AbstractCardiomyocyte tumour necrosis factor α (TNF‐α) production contributes to myocardial depression during sepsis. This study was designed to observe the effect of norepinephrine (NE) on lipopolysaccharide (LPS)‐induced cardiomyocyte TNF‐α expression and to further investigate the underlying mechanisms in neonatal rat cardiomyocytes and endotoxaemic mice. In cultured neonatal rat cardiomyocytes, NE inhibited LPS‐induced TNF‐α production in a dose‐dependent manner. α1‐ adrenoceptor (AR) antagonist (prazosin), but neither β1‐ nor β2‐AR antagonist, abrogated the inhibitory effect of NE on LPS‐stimulated TNF‐α production. Furthermore, phenylephrine (PE), an α1‐AR agonist, also suppressed LPS‐induced TNF‐α production. NE inhibited p38 phosphorylation and NF‐κB activation, but enhanced extracellular signal‐regulated kinase 1/2 (ERK1/2) phosphorylation and c‐Fos expression in LPS‐treated cardiomyocytes, all of which were reversed by prazosin pre‐treatment. To determine whether ERK1/2 regulates c‐Fos expression, p38 phosphorylation, NF‐κB activation and TNF‐α production, cardiomyocytes were also treated with U0126, a selective ERK1/2 inhibitor. Treatment with U0126 reversed the effects of NE on c‐Fos expression, p38 mitogen‐activated protein kinase (MAPK) phosphorylation and TNF‐α production, but not NF‐κB activation in LPS‐challenged cardiomyocytes. In addition, pre‐treatment with SB202190, a p38 MAPK inhibitor, partly inhibited LPS‐induced TNF‐α production in cardiomyocytes. In endotoxaemic mice, PE promoted myocardial ERK1/2 phosphorylation and c‐Fos expression, inhibited p38 phosphorylation and IκBα degradation, reduced myocardial TNF‐α production and prevented LPS‐provoked cardiac dysfunction. Altogether, these findings indicate that activation of α1‐AR by NE suppresses LPS‐induced cardiomyocyte TNF‐α expression and improves cardiac dysfunction during endotoxaemia via promoting myocardial ERK phosphorylation and suppressing NF‐κB activation.
‘Thinking Before Acting’ or ‘Acting Before Thinking’: Antecedents of Individual Action Propensity in Work Situations
Authors: Vera Dusya , Crossan Mary , Rerup Claus , Werner Steve 
Published: December 2013

AbstractWe introduce the concept of ‘individual action propensity’ to examine the approach of individuals towards solving situations for which they lack knowledge and/or experience about what to do. We focus on a naturally contrasting pair of responses: ‘thinking before acting’ or ‘acting before thinking’, and associate low action propensity with thinking one's way into understanding how to act, and high action propensity with acting one's way into understanding such situations. We build on regulatory mode theory – with its dimensions of locomotion and assessment and the trade‐off between speed and accuracy – to examine individual characteristics as predictors of individual action propensity. We find that individual action propensity is associated with being a woman, having fewer years of formal education, not relying on help‐seeking behaviours, and having a positive attitude towards spontaneity. Our findings shed light on why individuals take action, or not, and provide implications for research on organizational action propensity.
Optimal Capital Taxation in a Neoclassical Growth Model
Authors: LU CHIA‐HUI , CHEN BEEN‐LON 
Published: December 2013

AbstractThis paper studies the optimal factor tax incidence in a neoclassical growth model with a given share of government expenditure in output. In the Ramsey planner's optimization, the effect of next period's capital on government expenditure equals the given share of the marginal product of capital. Capital accumulation reduces the discounted net marginal product of next period's capital by way of increasing government expenditure. In order to internalize the distortion, it is optimal to tax capital income in the long run.
Tax Uniformity: A Commitment Device for Restraining Opportunistic Behavior
Authors: DEWIT GERDA , LEAHY DERMOT 
Published: December 2013

AbstractWe show that uniform and differentiated tax systems diverge in their propensity to generate distortionary opportunistic behavior. First, when firms choose investment before the government can commit to its taxes, the tax scheme creates strategic incentives for firms to distort their investment. Second, a system of differentiated taxes has a greater propensity to foster strategic distortions in investment than a uniform tax regime. While the paper makes these points in a set‐up in which polluting firms face an emission tax and invest in abatement, the main message is shown to hold for a wide class of tax policy games.
The Role of Ego Networks in Manufacturing Joint Venture Formations
Authors: Carnovale Steven , Yeniyurt Sengun 
Published: December 2013

This article develops a network theory–based framework of manufacturing joint venture formations and provides an empirical test in the context of the automotive industry. Hypotheses are developed regarding the implications of the network structure for a firm's partner selection in manufacturing joint ventures. The roles of network theory constructs such as ego network size, ego network density, and ego network betweenness centrality on new manufacturing joint venture formations are explored using a dynamic framework. A comprehensive time series panel dataset with 3,247,124 observations containing the joint venture information of 1,158 automotive firms collectively engaging in 589 manufacturing joint ventures over 19 years is utilized to test the hypotheses. Results provide strong empirical support for the role of network structure in equity‐based partnership formation. Specifically, ego network size and ego network betweenness centrality of both the focal manufacturer and potential partner have significant effects on new manufacturing joint venture formations. Findings regarding the role of ego network density are mixed.
Cloning and Activity Analysis of Promoter of RanGTPase Gene from Shrimp, Marsupenaeus japonicus
Authors: Han Fang , Wang Zhi‐Yong 
Published: December 2013

AbstractRanGTPases, one superfamily of small G protein family, have been demonstrated to be involved in the innate immune system and they are up‐regulated after pathogen infection. However, the regulation mechanism of RanGTPases remains unclear. In this study, the 5′ flanking region of shrimp RanGTPase gene was cloned and sequenced. To detect the activity of the promoter, pIZΔIE/EGFP was modified from pIZ/V5‐His by replacing the OPIE2 promoter with this promoter and inserting enhanced green fluorescence protein (EGFP) gene downstream. The promoter can drive the expression of reporter EGFP gene in Hi5 insect cells, indicating the promoter has activity. These results extend our previous findings and provide insights into the molecular regulation of RanGTPase gene expression, which will be helpful for shrimp viral disease control.
Replacement of Fish Meal with Soybean Meal, Alone or in Combination with Distiller's Dried Grains with Solubles in Practical Diets for Pacific White Shrimp, Litopenaeus vannamei, Grown in a Clear‐Water Culture System
Authors: Cummins Vaun C. , Webster Carl D. , Thompson Kenneth R. , Velasquez Alejandro 
Published: December 2013

AbstractThe objective of this study was to evaluate inclusion of distiller's dried grains with solubles (DDGS) as partial replacement of commercial, solvent‐extracted soybean meal (SBM) in fish meal‐free diets for Pacific white shrimp, Litopenaeus vannamei. Aquaria connected to a recirculating biofiltration system were utilized to evaluate growth, survival, and feed conversion of shrimp during the 8‐wk feeding trial. Each 110‐L aquarium was stocked with 15 shrimp (mean individual weight 0.99 g) and fed one of five diets: a diet containing 20% fish meal (FM), which served as the control (Diet 1); a diet containing 0% FM and 52.5% SBM (Diet 2); and diets containing 0% FM and either 10, 20, or 30% DDGS as partial replacement of SBM (Diets 3, 4, and 5, respectively). Shrimp were fed according to a pre‐determined feeding chart five times daily (0730, 1030, 1330, 1630, and 1930 h) and there were three replicates per dietary treatment. The results from the feeding trial demonstrated that final weight, weight gain (g), and percentage weight gain were significantly higher (P < 0.05) for shrimp fed Diet 1 (10.96 g, 10.01 g, and 1051%, respectively) compared to shrimp fed diets containing DDGS; however, shrimp fed diets containing DDGS had similar (P > 0.05) final weight, weight gain (g), and percentage weight gain as shrimp fed a diet containing 0% FM and 52.5% SBM (Diet 2). Feed conversion ratio (FCR) of shrimp fed Diet 1 (2.84) was significantly lower (P < 0.05) compared to shrimp fed any other diet. Survival (%) was not different (P > 0.05) among treatments and averaged 77.3% for the study. This study demonstrated that practical shrimp diets containing no FM had an adverse impact on growth performance of white shrimp when grown in a clear‐water system and that further research is needed to refine diet formulations when culturing shrimp in these systems when attempting to feed a diet without FM.
Possible Roles of Farnesoic Acid O‐Methyltransferase in Regulation of Molting in the Shrimp, Penaeus Chinensis
Authors: Li Zhaoxia , Xu Xiaofei , Wang Jinye , Wang Chunde 
Published: December 2013

AbstractMethyl farnesoate (MF) is the crustacean homolog of the insect juvenile hormone and is believed to regulate physiological processes such as molting and reproduction in crustaceans. Farnesoic acid (FA) O‐methyltransferase (FAMeT) is an important enzyme in conversion of FA to MF and may thus play key roles in regulation of growth in crustaceans. In this study, we cloned a full‐length PcFAMeT cDNA sequence consisting of 1319 bp (Genbank: JQ315119) with an open reading frame (ORF) of 840 bp that encodes 280 amino acids from the shrimp, Penaeus chinensis. Comparison of the amino acid sequence revealed that PcFAMeT had an overall similarity of 81.07–96.07% with other penaeid shrimp FAMeT. Quantitative real‐time polymerase chain reaction (PCR) analysis showed that PcFAMeT transcript has a wide tissue distribution pattern in P. chinensis and the highest expression of the transcripts occurred in muscle tissue. Stage‐specific expression profile revealed that the highest expression of FAMeT occurred at the intermolt stage which implied that the conversion of FA to MF may be involved in the onset of molting processes.
Extracellular Ubiquitin Increases Expression of Angiogenic Molecules and Stimulates Angiogenesis in Cardiac Microvascular Endothelial Cells
Authors: Steagall Rebecca J. , Daniels Christopher R. , Dalal Suman , Joyner William L. , Singh Mahipal , Singh Krishna 
Published: December 2013

AbstractExtracellular Ub is an immune modulator that plays a role in suppression of inflammation, organ injury, myocyte apoptosis, and fibrosis. The purpose of this study was to investigate the effects of extracellular Ub on the process of cardiac angiogenesis. CMECs and aortic tissue were isolated from rats to measure changes in angiogenic protein levels and to assess angiogenic responses to extracellular Ub. In CMECs, extracellular Ub increased protein levels of VEGF‐A and MMP‐2, known angiogenesis regulators. CMECs demonstrated enhanced rearrangement of fibrillar actin and migration in response to Ub treatment. Ub‐treated CMECs demonstrated an increase in tube network formation which was inhibited by the CXCR4 receptor antagonist, AMD3100. Methylated Ub, unable to form polyubiquitin chains, enhanced tube network formation. Aortic ring sprouting assays demonstrated that Ub increases microvessel sprouting in the Matrigel. The results of our study suggest a novel role for extracellular Ub in cardiac angiogenesis, providing evidence that extracellular Ub, at least in part acting via the CXCR4 receptor, has the potential to facilitate the process of angiogenesis in myocardial endothelial cells.
The multifunctional role of the pallilysin‐associated Treponema pallidum protein, Tp0750, in promoting fibrinolysis and extracellular matrix component degradation
Authors: Houston Simon , Russell Shannon , Hof Rebecca , Roberts Alanna K. , Cullen Paul , Irvine Kyle , Smith Derek S. , Borchers Christoph H. , Tonkin Michelle L. , Boulanger Martin J. , Cameron Caroline E. 
Published: December 2013

SummaryThe mechanisms that facilitate dissemination of the highly invasive spirochaete, Treponema pallidum, are incompletely understood. Previous studies showed the treponemal metalloprotease pallilysin (Tp0751) possesses fibrin clot degradation capability, suggesting a role in treponemal dissemination. In the current study we report characterization of the functionally linked protein Tp0750. Structural modelling predicts Tp0750 contains a von Willebrand factor type A (vWFA) domain, a protein‐protein interaction domain commonly observed in extracellular matrix (ECM)‐binding proteins. We report Tp0750 is a serine protease that degrades the major clot components fibrinogen and fibronectin. We also demonstrate Tp0750 cleaves a matrix metalloprotease (MMP) peptide substrate that is targeted by several MMPs, enzymes central to ECM remodelling. Through proteomic analyses we show Tp0750 binds the endothelial fibrinolytic receptor, annexin A2, in a specific and dose‐dependent manner. These results suggest Tp0750 constitutes a multifunctional protein that is able to (1) degrade infection‐limiting clots by both inhibiting clot formation through degradation of host coagulation cascade proteins and promoting clot dissolution by complexing with host proteins involved in the fibrinolytic cascade and (2) facilitate ECM degradation via MMP‐like proteolysis of host components. We propose that through these activities Tp0750 functions in concert with pallilysin to enable T. pallidum dissemination.
Genomic resources for breeding crops with enhanced abiotic stress tolerance
Authors: Bansal Kailash C. , Lenka Sangram K. , Mondal Tapan K. 
Published: December 2013

AbstractTo meet the challenges of climate change, exploring natural diversity in the existing plant genetic resource pool as well as creation of new mutants through chemical mutagenesis and molecular biology is needed for developing climate‐resilient elite genotypes. Ever‐increasing area under existing abiotic stresses as well as emerging abiotic stress factors and their combinations have further added to the problems of the current crop improvement programmes. However, with the advancement in modern techniques such as next‐generation sequencing technologies, it is now possible to generate on a whole‐genome scale, genomic resources for crop species at a much faster pace with considerably less efforts and money. The genomic resources thus generated will be useful for various plant breeding applications such as marker‐assisted breeding for gene introgression, mapping QTLs or identifying new or rare alleles associated with a particular trait. In this article, we discuss various aspects of generation of genomic resources and their utilization for developing abiotic stress‐tolerant crops to ensure sustainable agricultural production and food security in the backdrop of rapid climate change.
The Majority of a Collection of U.S. Endocarditis Enterococcus faecalis Isolates Obtained from 1974 to 2004 Lack Capsular Genes and Belong to Diverse, Non-Hospital-Associated Lineages
Authors: Chowdhury Shahreen A. , Nallapareddy Sreedhar R. , Arias Cesar A. , Murray Barbara E. 
Published: December 2013

ABSTRACT

Eighty-one endocarditis-derived
Enterococcus faecalis
isolates that were collected from individual patients in the United States between 1974 and 2004 were sequence typed and analyzed for the presence of various genes, including some previously associated with virulence. Overall, using our previously described trilocus sequence typing (TLST), 44 different sequence types (STs) were found within this collection; 26 isolates were singletons (a unique TLST sequence type [ST
T
]), some ST
T
s contained multiple isolates (up to 6 isolates), and 16% of the isolates (13 isolates) could be grouped by additional sequence typing into clonal cluster 21 (CC21). Of note, only four isolates (7%) of the 56 whose multilocus sequence types were determined were found to belong to one of the previously described hospital-associated clonal clusters CC2 and CC9, and only 15% and 37% of all isolates had high-level resistance to gentamicin and streptomycin, respectively, including 10% that were resistant to both. We also found that 64% of the isolates lacked the genes for production of capsule polysaccharide, which has been proposed to enhance the pathogenic potential of the hospital-associated clonal clusters. In summary, while our collection is not a random sample of cases of
E. faecalis
endocarditis, these results indicate that nonencapsulated strains belonging to non-hospital-associated lineages were predominant among endocarditis
E. faecalis
isolates recovered during this time period.
H3 Stalk-Based Chimeric Hemagglutinin Influenza Virus Constructs Protect Mice from H7N9 Challenge
Authors: Krammer Florian , Margine Irina , Hai Rong , Flood Alexander , Hirsh Ariana , Tsvetnitsky Vadim , Chen Dexiang , Palese Peter 
Published: December 2013

ABSTRACT
The recent outbreak of H7N9 influenza virus infections in humans in China has raised concerns about the pandemic potential of this strain. Here, we test the efficacy of H3 stalk-based chimeric hemagglutinin universal influenza virus vaccine constructs to protect against H7N9 challenge in mice. Chimeric hemagglutinin constructs protected from viral challenge in the context of different administration routes as well as with a generic oil-in-water adjuvant similar to formulations licensed for use in humans.
High-Multiplicity HIV-1 Infection and Neutralizing Antibody Evasion Mediated by the Macrophage-T Cell Virological Synapse
Authors: Duncan Christopher J. A. , Williams James P. , Schiffner Torben , Gärtner Kathleen , Ochsenbauer Christina , Kappes John , Russell Rebecca A. , Frater John , Sattentau Quentin J. 
Published: December 2013

ABSTRACTMacrophage infection is considered to play an important role in HIV-1 pathogenesis and persistence. Using a primary cell-based coculture model, we show that monocyte-derived macrophages (MDM) efficiently transmit a high-multiplicity HIV-1 infection to autologous CD4+T cells through a viral envelope glycoprotein (Env) receptor- and actin-dependent virological synapse (VS), facilitated by interactions between ICAM-1 and LFA-1. Virological synapse (VS)-mediated transmission by MDM results in high levels of T cell HIV-1 integration and is 1 to 2 orders of magnitude more efficient than cell-free infection. This mode of cell-to-cell transmission is broadly susceptible to the activity of CD4 binding site (CD4bs) and glycan or glycopeptide epitope-specific broadly neutralizing monoclonal antibodies (bNMAbs) but shows resistance to bNMAbs targeting the Env gp41 subunit membrane-proximal external region (MPER). These data define for the first time the structure and function of the macrophage-to-T cell VS and have important implications for bNMAb activity in HIV-1 prophylaxis and therapy.IMPORTANCEThe ability of HIV-1 to move directly between contacting immune cells allows efficient viral dissemination with the potential to evade antibody attack. Here, we show that HIV-1 spreads from infected macrophages to T cells via a structure called a virological synapse that maintains extended contact between the two cell types, allowing transfer of multiple infectious events to the T cell. This process allows the virus to avoid neutralization by a class of antibody targeting the gp41 subunit of the envelope glycoproteins. These results have implications for viral spreadin vivoand the specificities of neutralizing antibody elicited by antibody-based vaccines.
Management of children in the deployed intensive care unit at Camp Bastion, Afghanistan
Authors: Inwald David P , Arul G S , Montgomery M , Henning J , McNicholas J , Bree S 
Published: December 2013

BackgroundThe deployed Intensive Therapy Unit (ITU) in the British military field hospital in Camp Bastion, Afghanistan, admits both adults and children. The purpose of this paper is to review the paediatric workload in the deployed ITU and to describe how the unit copes with the challenge of looking after critically injured and ill children.MethodsRetrospective review of patients <16 years of age admitted to the ITU in the British military field hospital in Camp Bastion, Afghanistan, over a 1-year period from April 2011 to April 2012.Results112/811 (14%) admissions to the ITU were paediatric (median age 8 years, IQR 6–12, range 1–16). 80/112 were trauma admissions, 13 were burns, four were non-trauma admissions and 15 were readmissions. Mechanism of injury in trauma was blunt in 12, blast (improvised explosive device) in 45, blast (indirect fire) in seven and gunshot wound in 16. Median length of stay was 0.92 days (IQR 0.45–2.65). 82/112 admissions (73%) were mechanically ventilated, 16/112 (14%) required inotropic support. 12/112 (11%) died before unit discharge. Trauma scoring was available in 65 of the 80 trauma admissions. Eight had Injury Severity Score or New Injury Severity Score >60, none of whom survived. However, of the 16 patients with predicted mortality >50% by Trauma Injury Severity Score, seven survived. Seven cases required specialist advice and were discussed with the Birmingham Children's Hospital paediatric intensive care retrieval service. The mechanisms by which the Defence Medical Services support children admitted to the deployed adult ITU are described, including staff training in clinical, ethical and child protection issues, equipment, guidelines and clinical governance and rapid access to specialist advice in the UK.ConclusionsWith appropriate support, it is possible to provide intensive care to children in a deployed military ITU.
FGFR1–WNT–TGF-β Signaling in Prostate Cancer Mouse Models Recapitulates Human Reactive Stroma
Authors: Carstens Julienne L. , Shahi Payam , Van Tsang Susan , Smith Billie , Creighton Chad J. , Zhang Yiqun , Seamans Amber , Seethammagari Mamatha , Vedula Indira , Levitt Jonathan M. , Ittmann Michael M. , Rowley David R. , Spencer David M. 
Published: December 2013

Abstract
The reactive stroma surrounding tumor lesions performs critical roles ranging from supporting tumor cell proliferation to inducing tumorigenesis and metastasis. Therefore, it is critical to understand the cellular components and signaling control mechanisms that underlie the etiology of reactive stroma. Previous studies have individually implicated fibroblast growth factor receptor 1 (FGFR1) and canonical WNT/β-catenin signaling in prostate cancer progression and the initiation and maintenance of a reactive stroma; however, both pathways are frequently found to be coactivated in cancer tissue. Using autochthonous transgenic mouse models for inducible FGFR1 (JOCK1) and prostate-specific and ubiquitously expressed inducible β-catenin (Pro-Cat and Ubi-Cat, respectively) and bigenic crosses between these lines (Pro-Cat × JOCK1 and Ubi-Cat × JOCK1), we describe WNT-induced synergistic acceleration of FGFR1-driven adenocarcinoma, associated with a pronounced fibroblastic reactive stroma activation surrounding prostatic intraepithelial neoplasia (mPIN) lesions found both in in situ and reconstitution assays. Both mouse and human reactive stroma exhibited increased transforming growth factor-β (TGF-β) signaling adjacent to pathologic lesions likely contributing to invasion. Furthermore, elevated stromal TGF-β signaling was associated with higher Gleason scores in archived human biopsies, mirroring murine patterns. Our findings establish the importance of the FGFR1–WNT–TGF-β signaling axes as driving forces behind reactive stroma in aggressive prostate adenocarcinomas, deepening their relevance as therapeutic targets. Cancer Res; 74(2); 609–20. ©2013 AACR.