bluuebunny/crossref_metadata_2025_split huggingface dataset:
Talk about texts at the computer: using ICT to develop children's oral and literate abilities
Authors: Mercer Neil , Fernandez Manuel , Dawes Lyn , Wegerif Rupert , Sams Claire 
Published: July 2003

AbstractThis article describes the outcomes of recent research on children's talk while engaged in joint literacy activities in primary school (Year 5). The research is based on a conception of talk as a tool for ‘thinking together’, with computer software being treated as a resource for organising and focusing children's involvement in collaborative activities. The results are used to discuss the value of classroom talk and computer‐based activities for promoting children's literacy development.
The impact of the euro on Europe's financial markets
Authors: Galati Gabriele , Tsatsaronis Kostas 
Published: July 2003

This paper presents an overview of the impact of the introduction of the euro on Europe's financial structure over the first four years since the start of EMU. It analyzes changes in money markets, bond markets, equity markets and foreign exchange markets. Euro's role in originating or catalyzing trends has been uneven across the spectrum of financial markets. From the supply side, banks and investors in fixed income markets have become more focused on the characteristics of individual borrowers rather than the nationality of the issuer and have built up expertise to evaluate credit risk. European equity markets have also been affected by the enhanced ability of investors to build strategies with a pan‐European perspective as prices increasingly reflected risk factors specific to industrial sectors rather than individual countries. On the borrower side, EMU has increased the attractiveness of market‐based financing methods by allowing debt issuers to tap institutional portfolios across the euro area. Lower barriers to cross‐border financial transactions have also increased the contestability of the market for financial services, be it at the wholesale or the retail level.The introduction of the euro has also highlighted the shortcomings of existing institutional structures and areas where excessive focus on narrowly defined interests may stand in the way of realizing the full potential benefits from the new environment. Diverging legal and institutional infrastructures and market practices can impede further financial market development and deepening. Hence, the euro has put a premium on cooperation between national authorities and institution as a means of achieving a more harmonized financial environment.The impact of EMU on depth in foreign exchange markets has been less clear‐cut, as volatility, spreads, trading volumes and liquidity appear not to have changed in a substantial way. Overall, it seems that the new currency has made some progress towards the goal of becoming a currency of international stature that would rival that of the US dollar. However, a number of the necessary next steps towards achieving this goal are also among the trickiest to implement.
From ‘Normal Incidents’ to Political Crises: Understanding the Selective Politicization of Policy Failures
Authors: Brändström Annika , Kuipers Sanneke 
Published: July 2003

AbstractThis article aims to enhance understanding of selective politicization processes in policy failures and examine the attempts of policy-makers to use framing strategies to allocate blame. The policy response to alleged submarine intrusions in Sweden and Dutch military involvement in the fall of Srebrenica are the two case-studies used in this article. These cases will be analysed using three perspectives derived from the literature on framing: depicting events as violations of core public values; depicting events as operational incidents or as symptoms of endemic problems; allocating accountability and blame for the occurrence and/or ‘mismanagement’ of crisis. Finally, we present a conceptual framework of the different shapes that political blaming can take when certain framing strategies are adopted.
Voronoi Diagrams of Moving Points
Authors: Albers Gerhard , Guibas Leonidas J. , Mitchell Joseph S. B. , Roos Thomas 
Published: July 2003

Consider a set of n points in d-dimensional Euclidean space, d ≥ 2, each of which is continuously moving along a given individual trajectory. As the points move, their Voronoi diagram changes continuously, but at certain critical instants in time, topological events occur that cause a change in the Voronoi diagram. In this paper, we present a method of maintaining the Voronoi diagram over time, at a cost of O( log n) per event, while showing that the number of topological events has an upper bound of O(ndλs(n)), where λs(n) is the (nearly linear) maximum length of a (n,s)-Davenport-Schinzel sequence, and s is a constant depending on the motions of the point sites. In addition, we show that if only k points are moving (while leaving the other n - k points fixed), there is an upper bound of O(knd-1λs(n)+(n-k)dλ s(k)) on the number of topological events.
Tumor Necrosis Factor-α Promotes Macrophage-Induced Vascular Smooth Muscle Cell Apoptosis by Direct and Autocrine Mechanisms
Authors: Boyle Joseph J. , Weissberg Peter L. , Bennett Martin R. 
Published: July 2003

Objective—We have previously shown that human macrophages induce human plaque vascular smooth muscle cell (VSMC) apoptosis by cell-cell proximity, Fas-L, and nitric oxide (NO), thereby predisposing to plaque rupture. This study sought to analyze whether tumor necrosis factor-α (TNF-α) contributes additionally to macrophage-induced VSMC apoptosis.Methods and Results—Macrophage-induced VSMC apoptosis was examined in direct coculture. Antagonistic antibodies to TNF-receptor (R1) inhibited VSMC apoptosis, and preincubation of monocytes and VSMCs indicated that TNF-R1 on both cell types contributed to macrophage-induced VSMC apoptosis. Correspondingly, both monocytes and VSMCs expressed TNF-R1, and macrophages expressed cell surface TNF-α. Two NO donors upregulated VSMC surface TNF-R1, and exogenous TNF-α induced VSMC apoptosis synergistically with the NO donor diethylenetriamine/NO, indicating that NO sensitizes VSMCs to TNF-α. Neutralizing anti–TNF-R1 antibodies inhibited macrophage activation assessed by Fas-L expression and NO secretion.Conclusions—TNF-α promotes macrophage-induced VSMC apoptosis by autocrine and direct pathways.
Effect of Glycoprotein IIb/IIIa Antagonist Abciximab on Monocyte-Platelet Aggregates and Tissue Factor Expression
Authors: Steiner Sabine , Seidinger Daniela , Huber Kurt , Kaun Christoph , Minar Erich , Kopp Christoph W. 
Published: July 2003

Objective—Activated platelets rapidly adhere to monocytes and upregulate the expression of tissue factor (TF), the major trigger of the coagulation cascade. In this study, we examined the effect of abciximab, a nonselective glycoprotein IIb/IIIa-receptor antagonist, on monocyte TF expression in thrombin receptor activator–stimulated whole blood in vitro.Methods and Results—Abciximab (50 μg/mL) reduced the mass of platelets attached to monocytes, measured by the mean fluorescence intensity (MFI) of CD42b on CD14+cells, 1 (CD42b, 471±197 versus 1073±217 MFI, mean±SD,P<0.05), 5, and 10 minutes after thrombin receptor activator stimulation of whole blood to the same extent as anti–P-selectin (50 μg/mL; 288±177 MFI,P<0.05) when determined by flow cytometry. In parallel, the expression of the platelet activation marker P-selectin colocalized with CD14+monocytes was reduced up to 25% by abciximab at the same time points. Expression of monocyte TF antigen (CD14+/TF+, 39.9±8.7% versus 66.3±19.9%,P<0.05), chromogenic TF-activity (TF, 8.4±1.9 versus 13.2±2.8 U, arbitrary units,P<0.05), and TF mRNA was suppressed in the presence of abciximab as a consequence of reduced platelet mass attached to monocytes.Conclusions—Our data suggest that heterotypic monocyte-platelet aggregates are a target for abciximab, which suppresses monocyte TF because of a reduction of monocyte-platelet cross talk.
Association between acute and chronic graft-versus-host disease and bronchiolitis obliterans organizing pneumonia in recipients of hematopoietic stem cell transplants
Authors: Freudenberger Todd D. , Madtes David K. , Curtis J. Randall , Cummings Peter , Storer Barry E. , Hackman Robert C. 
Published: July 2003

AbstractBronchiolitis obliterans organizing pneumonia (BOOP) has been reported following hematopoietic stem cell (HSC) transplantation, but the clinical features and risk factors for this disorder have not been well characterized. This case-control study of 49 patients with histologic BOOP and 161 control subjects matched by age and year of transplantation describes the clinical features and analyzes the risk factors for BOOP following HSC transplantation. Data on clinical features and outcome were collected by chart review. Odds ratios, estimating the relative risk of BOOP in allogeneic HSC recipients, were calculated by conditional logistic regression with adjustment for potential confounding factors. Clinical features of BOOP in this population were similar to idiopathic BOOP and BOOP occurring in other disease settings. There was an association between acute and chronic graft-versus-host disease (GVHD) and the subsequent development of BOOP (odds ratios, 3.8 [95% CI, 1.2 to 12.3] and 3.1 [95% CI, 1.1 to 9.2], respectively). Patients with BOOP were more likely to have acute GVHD involving the skin (odds ratio, 4.6; P = .005) and chronic GVHD involving the gut (odds ratio, 6.6; P = .018) and oral cavity (odds ratio, 5.9; P = .026). This study shows that histologic BOOP following HSC transplantation has clinical features that resemble idiopathic BOOP and is strongly associated with prior acute and chronic GVHD. These results have important implications for the care of patients who develop respiratory symptoms after HSC transplantation and may help elucidate the pathogenesis of idiopathic BOOP. (Blood. 2003;102:3822-3828)
Late diversification in the clonal composition of human cytomegalovirus-specific CD8+ T cells following allogeneic hemopoietic stem cell transplantation
Authors: Gandhi Maher K. , Wills Mark R. , Okecha Georgina , Day Elizabeth K. , Hicks Ray , Marcus Robert E. , Sissons J. G. Patrick , Carmichael Andrew J. 
Published: July 2003

AbstractTo investigate the mechanisms of human T-cell reconstitution following allogeneic hemopoietic stem cell transplantation (alloSCT), we analyzed the clonal composition of human cytomegalovirus (HCMV)-specific or Epstein-Barr virus (EBV)-specific CD8+ T cells in 10 alloSC transplant recipients and their donors. All virus-specific CD8+ T-cell clones isolated from recipients after alloSCT contained DNA of donor origin. In all 6 D+/R+ sibling alloSCTs from seropositive donors into seropositive recipients, donor virus-specific clones transferred in the allograft underwent early expansion and were maintained long term in the recipient. In contrast, in 2 of 3 HCMV D+/R- alloSC transplant recipients in whom there was no detectable HCMV infection, donor HCMV-specific clones were undetectable, whereas donor EBV-specific clones were maintained in the same EBV-seropositive recipients, suggesting that transferred clones require antigen for their maintenance. Following D-/R+ transplantation from 3 seronegative donors into seropositive recipients, a delayed primary virus-specific CD8+ T-cell response was observed, in which the T cells contained donor DNA, suggesting that new antigen-specific T cells arose in the recipient from donor-derived progenitors. In 2 of 4 HCMV D+/R+ sibling allograft recipients the clonal composition underwent diversification as compared with their donors, with delayed persistent expansion of HCMV-specific clones that were undetectable in the donor or in the recipient during the early months after transplantation; this diversification may represent expansion of new clones generated from donor-derived progenitors. We conclude that, following alloSCT, late diversification of the HCMV-specific CD8+ T-cell clonal repertoire can occur in response to persistent viral antigen.
Attenuated signaling by a phosphotyrosine-null Epo receptor form in primary erythroid progenitor cells
Authors: Li Ke , Menon Madhu P. , Karur Vinit G. , Hegde Shailaja , Wojchowski Don M. 
Published: July 2003

AbstractSignals provided by the erythropoieitin receptor (EpoR) are required for erythroid development beyond the erythroid colony-forming unit (CFU-e) stage and are propagated via the EpoR-tethered Janus kinase, JAK2. JAK2 functions, in part, to phosphorylate 8 conserved EpoR phosphotyrosine (PY) sites for the binding of a diverse set of signaling factors. However, recent studies in transgenic and knock-in mice have demonstrated substantial bioactivity for PY-null EpoR forms. Presently, the activities of a PY-null EpoR-HM form in primary progenitor cells from knock-in mice were further assessed using optimized Epo dose-dependent proliferation, survival, and differentiation assays. As compared with the wild-type (wt)–EpoR, EpoR-HM activity was compromised several-fold in each context when Epo was limited to physiologic concentrations. Possible compensatory increases in serum growth factor levels also were investigated, and as assayed using embryonic stem (ES) cell–derived erythroid G1E2 cells, activities in serum from EpoR-HM mice were substantially elevated. In addition, when challenged with phenylhydrazine-induced anemia, EpoR-HM mice failed to respond with efficient splenic stress erythropoiesis. Thus, the function of this JAK2-coupled but minimal PY-null EpoR-HM form appears to be attenuated in several contexts and to be assisted in vivo by compensatory mechanisms. Roles normally played by EpoR PY sites and distal domains therefore should receive continued attention.
Antiphospholipid/antiprotein antibodies, hemostasis-related autoantibodies, and plasma homocysteine as risk factors for a first early pregnancy loss: a matched case-control study
Authors: Gris Jean-Christophe , Perneger Thomas V. , Quéré Isabelle , Mercier Eric , Fabbro-Peray Pascale , Lavigne-Lissalde Géraldine , Hoffet Médéric , Déchaud Hervé , Boyer Jean-Christophe , Ripart-Neveu Sylvie , Tailland Marie-Laure , Daurès Jean-Pierre , Marès Pierre , Dauzat Michel 
Published: July 2003

AbstractMaternal hypercoagulability is a possible cause of miscarriage during the eighth and ninth weeks of pregnancy, when the placenta replaces the yolk sac. We thus examined associations between putative markers of an acquired hypercoagulable state and the risk of first miscarriage. We conducted a case-control study comparing 743 women who miscarried in weeks 8 and 9 with 743 women who underwent a first provoked abortion, matched for age, number of pregnancies, and time elapsed since abortion. Levels of plasma homocysteine and of various antiphospholipid/antiprotein and hemostasis-related autoantibodies were categorized in 4 strata (percentiles 1-80, 81-95, 96-99, 100 among control patients) and analyzed in conditional logistic regression models. Pregnancy loss was independently associated with positive lupus anticoagulant (matched odds ratio [OR], 2.6; 95% confidence interval [CI], 1.1-6.0), high levels of immunoglobulin M (IgM) antibodies against cardiolipin (OR for percentile 100 versus 0-80, 3.5; CI, 1.2-10.1) and against phosphatidylethanolamine (OR, 4.7; CI, 1.9-12.1), high levels of IgG antibodies against annexin V (OR, 3.2; CI, 1.1-9.1) and against tissue-type plasminogen activator (OR, 19.5; CI, 7.9-48.0), and high homocystinemia (OR, 4.1; CI, 1.3-12.5). A first early pregnancy loss is associated with increased levels of several autoantibodies and of homocysteine. (Blood. 2003;102:3504-3513)
Human dendritic cell subsets in NOD/SCID mice engrafted with CD34+ hematopoietic progenitors
Authors: Palucka A. Karolina , Gatlin Joel , Blanck Jean Philippe , Melkus Michael W. , Clayton Sandra , Ueno Hideki , Kraus Elizabeth T. , Cravens Petra , Bennett Lynda , Padgett-Thomas Angela , Marches Florentina , Islas-Ohlmayer Miguel , Garcia J. Victor , Banchereau Jacques 
Published: July 2003

AbstractDistinct human dendritic cell (DC) subsets differentially control immunity. Thus, insights into their in vivo functions are important to understand the launching and modulation of immune responses. We show that nonobese diabetic/LtSz-scid/scid (NOD/SCID) mice engrafted with human CD34+ hematopoietic progenitors develop human myeloid and plasmacytoid DCs. The skin displays immature DCs expressing Langerin, while other tissues display interstitial DCs. Myeloid DCs from these mice induce proliferation of allogeneic CD4 T cells in vitro, and bone marrow human cells containing plasmacytoid DCs release interferon-α (IFN-α) upon influenza virus exposure. Injection of influenza virus into reconstituted mice triggers IFN-α release and maturation of mDCs. Thus, these mice may provide a model to study the pathophysiology of human DC subsets.
G-protein-coupled receptor S1P1 acts within endothelial cells to regulate vascular maturation
Authors: Allende Maria L. , Yamashita Tadashi , Proia Richard L. 
Published: July 2003

AbstractSphingosine-1-phosphate (S1P) stimulates signaling pathways via G-protein-coupled receptors and triggers diverse cellular processes, including growth, survival, and migration. In S1P1 receptor-deficient embryos, blood vessels were incompletely covered by vascular smooth muscle cells (VSMCs), indicating the S1P1 receptor regulates vascular maturation. Because S1P1 receptor expression is not restricted to a particular cell type, it was not known whether the S1P1 receptor controlled VSMC coverage of vessels in a cell-autonomous fashion by functioning directly in VSMCs or indirectly through its activity in endothelial cells (ECs). By using the Cre/loxP system, we disrupted the S1P1 gene solely in ECs. The phenotype of the conditional mutant embryos mimicked the one obtained in the embryos globally deficient in S1P1. Thus, vessel coverage by VSMCs is directed by the activity of the S1P1 receptor in ECs. (Blood. 2003;102:3665-3667)
Cooperative signaling between cytokine receptors and the glucocorticoid receptor in the expansion of erythroid progenitors: molecular analysis by expression profiling
Authors: Kolbus Andrea , Blázquez-Domingo Montserrat , Carotta Sebastian , Bakker Walbert , Luedemann Susanna , von Lindern Marieke , Steinlein Peter , Beug Hartmut 
Published: July 2003

AbstractErythroid progenitors undergo renewal (proliferation without apparent differentiation) in response to erythropoietin (Epo), stem cell factor (SCF), and glucocorticoids (dexamethasone) (Dex). SCF and Dex cooperate with Epo to promote proliferation and inhibit differentiation of erythroid progenitors, while Epo alone is required to protect erythroid cells from apoptosis during terminal red cell maturation. To examine the mechanism of the synergistic interactions of Epo, SCF, and Dex, we analyzed gene expression patterns using DNA chip–based large-scale comparative gene profiling using microarrays enriched in hematopoietic transcripts or containing randomly selected genes. Differentially regulated genes were validated by real-time reverse transcription–polymerase chain reaction (RT-PCR). The results reveal cooperative regulation of gene expression by glucocorticoids and Epo/SCF on a number of genes, such as CIS, BTG1, VDUP1, CXCR4, GILZ, and RIKEN29300106B05. While Epo and SCF never showed opposite effects on gene expression, Dex either enhanced or attenuated the effect of Epo and/or SCF. Several glucocorticoid receptor (GR)–target genes were regulated by Dex only in the presence of Epo and/or SCF, suggesting that the GR functions in the context of a larger transactivation complex to regulate these genes. The data also suggest that modulation of cytokine-induced signals by the GR is an important mechanism in erythroid progenitor renewal.
Improved hemostasis with superactive analogs of factor VIIa in a mouse model of hemophilia A
Authors: Tranholm Mikael , Kristensen Kim , Kristensen Annemarie T. , Pyke Charles , Røjkjær Rasmus , Persson Egon 
Published: July 2003

AbstractIt is currently debated whether the mechanism of action of therapeutic doses of recombinant factor VIIa (rFVIIa, Novo-Seven) relies on the tissue factor (TF)-independent activity of the enzyme. The present study was conducted to investigate the in vivo hemostatic effects of rFVIIa and 3 analogs thereof with superior intrinsic activity (FVIIaIIa, K337A-FVIIaIia, and M298Q-FVIIa) in mice with antibody-induced hemophilia A. A highly significant dose response was observed for the bleeding time and blood loss for each of the rFVIIa variants. The bleeding time and blood loss were normalized after administration of 10 mg/kg rFVIIa, 3 mg/kg K337A-FVIIaIia, and 3 mg/kg M298Q-FVIIa, indicating a potency of these FVIIa analogs 3-4 times above that of rFVIIa in FVIII-depleted mice. The different in vivo potencies of the various forms of FVIIa could not be explained by the pharmacokinetics. Histopathological evaluation of kidneys revealed no signs of treatment-related pathological changes even after treatment with the superactive variants. The fact that FVIIa analogs with enhanced intrinsic activity are more efficacious in the murine hemophilia A model strongly suggests that the TF-independent procoagulant activity of FVIIa contributes to its clinical hemostatic effect. (Blood. 2003; 102:3615-3620)
Generation of an erythrocyte vesicle transport system by Plasmodium falciparum malaria parasites
Authors: Taraschi Theodore F. , O'Donnell Megan , Martinez Sandra , Schneider Timothy , Trelka Darin , Fowler Velia M. , Tilley Leann , Moriyama Yoshinori 
Published: July 2003

AbstractThe asexual maturation of Plasmodium falciparum is accompanied by the transport of parasite-encoded proteins to the erythrocyte plasma membrane. Activation of G proteins by treatment with aluminum fluoride produced an accumulation within the erythrocyte cytosol of vesicles coated with Plasmodium homologues of COPII and N-ethylmaleimide-sensitive factor, proteins involved in intracellular transport between the Golgi apparatus and the endoplasmic reticulum. These vesicles contain malarial proteins that appear on the erythrocyte plasma membrane, as well as actin and myosin. It is proposed that the parasite adapted a process well established for intracellular transport to mediate the extracellular movement of its proteins through the erythrocyte cytosol to the surface membrane.
Survival advantage associated with heterozygous factor V Leiden mutation in patients with severe sepsis and in mouse endotoxemia
Authors: Kerlin Bryce A. , Yan S. Betty , Isermann Berend H. , Brandt John T. , Sood Rashmi , Basson Bruce R. , Joyce David E. , Weiler Hartmut , Dhainaut Jean-Francois 
Published: July 2003

AbstractSepsis is associated with systemic inflammation, coagulopathy, and disrupted protein C (PC) pathway function. The effect of prothrombotic polymorphism, factor V Leiden (Arg506Gln; FV Leiden), was examined in a large clinical trial (PROWESS) of severe sepsis and a mouse endotoxemia model. In PROWESS, 4.1% (n = 65) of patients were heterozygous FV Leiden (VL+/–) carriers. The 28-day mortality was lower in VL+/– (13.9%) than in non-FV Leiden (VL–/–; 27.9%) patients (P = .013). The mortality benefit of recombinant human activated PC (rhAPC) treatment was similar in VL+/– (placebo, 15.6%; rhAPC,12.1%) and VL–/– patients (placebo, 31.0%; rhAPC, 24.7%; interaction P = .981). VL+/– status did not appear to influence baseline biomarkers of coagulopathy and inflammation or disease severity, with the exception that vasopressor usage was less in VL+/– patients (46.2% versus 63.0%; P = .009). In a median lethal dose (40 mg/kg) endotoxin mouse model, VL+/– mice had lower mortality than wild-type mice (19% versus 57%; P = .008), whereas the mortality of homozygous (VL+/+) mice was almost identical to that of wild-type mice (65% versus 57%; P = .76). The findings suggest that FV Leiden constitutes a rare example of a balanced gene polymorphism that maintains the FV Leiden mutation in the general gene pool due to a survival advantage of VL+/– in severe sepsis.