bluuebunny/crossref_metadata_2025_split huggingface dataset:
Locus of the effect of temporal preparation: Evidence from the lateralized readiness potential
Authors: MÜller‐Gethmann Hiltraut , Ulrich Rolf , Rinkenauer Gerhard 
Published: June 2003

AbstractIt is well established that reaction time (RT) is shorter when a response signal is preceded by a warning signal, because the warning signal causes the participant to prepare for the upcoming response. A review of chronometric and psychophysiological studies reveals the prevailing view that this temporal preparation operates mainly at a motor level speeding up rather late processes. To assess the locus of this preparation effect, we conducted two experiments employing the lateralized readiness potential (LRP). Contrary to this prevailing view, the results of both experiments clearly indicate that temporal preparation enhances the processing speed of relatively early processes, because a manipulation of temporal uncertainty affected RT, the P300 latency, and the stimulus‐to‐LRP interval but not the LRP‐to‐keypress interval.
Electrophysiological evidence of visual encoding deficits in a cross‐modal attentional blink paradigm
Authors: Dell'acqua R. , Jolicoeur P. , Pesciarelli F. , Job R. , Palomba D. 
Published: June 2003

AbstractTwo experiments are reported in which two target stimuli, T1 and T2, were presented at variable stimulus onset asynchronies (SOAs). In Experiment 1, T1 and T2 were visual stimuli embedded in a rapid serial visual presentation (RSVP) stream of distractors. Participants were asked to report T1 and T2 at the end of the stream. In Experiment 2, T1 was an auditory stimulus, and T2 a visual stimulus embedded in an RSVP stream. Participants made a speeded discriminative response to T1, and reported T2 at the end of the stream. An attentional blink (AB) effect was observed in both experiments: T2 report suffered at short SOA compared to long SOA. During the AB, the amplitude of the P300 component of the event‐related potential (ERP) locked to T2 onset was sensibly reduced in both experiments. Behavioral and ERP results were very similar across the two experiments. Implications for models of the AB effect are discussed.
Influence of phonological expectations during a phoneme deletion task: Evidence from event‐related brain potentials
Authors: Newman R. L. , Connolly J. F. , Service E. , Mcivor K. 
Published: June 2003

AbstractSeveral studies have identified a negativity [the phonological mismatch negativity (PMN)] preceding the N400 during auditory sentence comprehension. The present study investigated whether the PMN reflects a prelexical or lexical stage of spoken word recognition. Event‐related brain potentials (ERPs) were recorded to investigate phonological processing independently from lexical/semantic influences during a task requiring metalinguistic analysis of speech stimuli. Participants were instructed to omit the initial phoneme from a word (“clap” without the /k/) after which they heard a correct (lap) or incorrect (cap, ap, nose) answer. The PMN (peaking at 270 ms) was largest to incorrect items and did not differentiate between items that shared the same rime and items that were phonologically unrelated to the correct choice. Further, the PMN did not differ between word (cap) and nonword (ap) choices. The P300 was largest to correct items but was also seen to choices that rhymed with the correct answer. It is concluded that the PMN serves as a neural marker for the analysis of acoustic input merging with prelexical phonemic expectations.
Autonomic recovery and habituation in social anxiety
Authors: Mauss Iris B. , Wilhelm Frank H. , Gross James J. 
Published: June 2003

AbstractGrowing evidence suggests that, contrary to expectation, high trait socially anxious (HTSA) and low trait socially anxious (LTSA) individuals show comparable autonomic reactivity during stressful speech tasks. To test the hypothesis that autonomic differences between groups might emerge during recovery or habituation, 35 HTSA and LTSA participants gave two impromptu speeches. Measures of anxiety experience as well as cardiovascular, electrodermal, respiratory, and vagal activation were obtained. Despite greater reports of anxiety experience in the HTSA versus the LTSA participants, autonomic measures showed comparable reactivity, habituation, and recovery in the two anxiety groups. These results suggest minimal autonomic differences between HTSA and LTSA individuals, thus supporting theories of social anxiety that emphasize cognitive factors.
Work Incentives under a New Tax System: The Distribution of Effective Marginal Tax Rates in 2002
Authors: Beer Gillian 
Published: June 2003

Effective marginal tax rates (EMTRs) provide a way of measuring the balance between targeting of welfare payments and the financial incentive to work. High EMTRs result from income tests for welfare payments overlapping with each other and/or the income tax system.Individuals who face high EMTRs over broad ranges of income have little financial incentive to increase their earned income. This paper examines the distribution of EMTRs across the Australian labour force in 2002. It also looks at how the number of people facing high EMTRs has changed since the introduction of the new tax system.
Public Education or Vouchers? The Importance of Heterogeneous Preferences
Authors: Preston Robb 
Published: June 2003

This paper looks at the impact heterogeneous preferences for education have on education funding under private, public and voucher systems. An overlapping generations model incorporating human capital is used, where parents are the decision‐makers. They determine their labour supply and their child's education – either directly with personal contributions or collectively by voting on taxes.The education systems are compared by their impact on the growth and distribution of human capital. The use of heterogenous preferences proves to be critical, as these comparisons differ markedly from the homogenous case.
Activation of Tumor Antigen-Specific Cytotoxic T Lymphocytes (CTLs) by Human Dendritic Cells Infected with an Attenuated Influenza A Virus Expressing a CTL Epitope Derived from the HER-2/neu Proto-Oncogene
Authors: Efferson Clay L. , Schickli Jeanne , Ko Byung Kyum , Kawano Kouichiro , Mouzi Sara , Palese Peter , García-Sastre Adolfo , Ioannides Constantin G. 
Published: June 2003

ABSTRACTThe development of cancer vaccines requires approaches to induce expansion and functional differentiation of tumor antigen-specific cytotoxic T lymphocyte (CTL) effectors which posses cytolytic capability and produce cytokines. Efficient induction of such cells is hindered by the poor immunogenicity of tumor antigens and by the poor transduction efficiency of dendritic cells (DCs) with current nonreplicating vectors. We have investigated the use of influenza A virus, a potent viral inducer of CTLs, as a vector expressing the immunodominant HER-2 CTL epitope KIF (E75). For this purpose, an attenuated influenza A/PR8/34 virus with a truncated nonstructural (NS1) gene was generated containing the E75 epitope in its neuraminidase protein (KIF-NS virus). Stimulation of peripheral blood mononuclear cells from healthy donors and of tumor-associated lymphocytes from ovarian and breast cancer patients with DCs infected with KIF-NS virus (KIF-NS DC) induced CTLs that specifically recognized the peptide KIF and HER-2-expressing tumors in cytotoxicity assays and secreted gamma interferon (IFN-γ) and interleukin-2 at recall with peptide. Priming with KIF-NS DCs increased the number of E75+CD45RO+cells by more than 10-fold compared to nonstimulated cells. In addition, KIF-NS virus induced high levels of IFN-α in DCs. This is the first report demonstrating induction of human epitope-specific CTLs against a tumor-associated antigen with a live attenuated recombinant influenza virus vector. Such vectors may provide a novel approach for tumor antigen delivery, lymphocyte activation, and differentiation in human cancer vaccine development.
Renoprotective Effects of Omapatrilat Are Mediated Partially by Bradykinin
Authors: Zhou Xiaoyan , Ono Hidehiko , Ono Yuko , Frohlich Edward D. 
Published: June 2003

<i>Aim:</i> To investigate the effects of omapatrilat on systemic and renal hemodynamics, glomerular dynamics, renal function, and histopathological changes as well as the participation of the bradykinin B2 receptor in WKY, SHR, and <i>L</i>-NAME/SHR rats. <i>Methods:</i> Eight groups of 17-week-old rats were examined using renal micropuncture techniques and histopathological analyses after 3 weeks of treatment: group 1, WKY control; group 2, WKY+omapatrilat (40 mg/kg/day); group 3, SHR control; group 4, SHR+omapatrilat; group 5, SHR+<i>L</i>-NAME (50 mg/l); group 6, SHR+<i>L</i>-NAME+omapatrilat; group 7, SHR+<i>L</i>-NAME for 3 weeks followed by omapatrilat for a subsequent 3 weeks, and group 8, SHR+<i>L</i>-NAME+omapatrilat+bradykinin antagonist icatibant (500 µg/kg/day). <i>Results:</i> In WKY and SHR, omapatrilat significantly reduced the mean arterial pressure, increased effective renal blood flow and single nephron plasma flow associated with reduced glomerular arteriolar resistances. Furthermore, omapatrilat prevented and reversed <i>L</i>-NAME induced urinary protein excretion, glomerular and arteriolar injuries, glomerular morphometric alterations, and glomerular apoptosis (at least, p < 0.05). Icatibant partially inhibited these beneficial effects of omapatrilat. <i>Conclusion:</i> Omapatrilat provided potent antihypertensive and renoprotective actions, which were mediated, in part, by bradykinin.
Genetic Background Selectively Influences Innominate Artery Atherosclerosis
Authors: Reardon Catherine A. , Blachowicz Lydia , Lukens John , Nissenbaum Michael , Getz Godfrey S. 
Published: June 2003

Objective—We sought to examine whether there is a site-specific effect on atherosclerosis of the absence of mature T and B cells caused by a recombination activating-gene deficiency in LDL receptor-deficient mice and whether this effect is influence by the extent of backcrossing to C57BL/6 mice.Methods and Results—Male mice were fed atherogenic diets for 3 months. In strain 1 mice, in which ≈93% of the genes were from C57BL/6 mice, the absence of mature T and B cells led to a significant reduction in atherosclerosis in both the aortic sinus and the innominate artery. In strain 2 mice, in which ≈99+% of the genes were from C57BL/6 mice, immune system deficiency led to a site-specific effect on atherosclerosis, with a reduction in atherosclerosis in the aortic sinus but not in the innominate artery, similar to previous results obtained with apolipoprotein E−/− mice. All of the immune system-incompetent mice had lower plasma total and VLDL cholesterol levels regardless of strain or diet, indicating that differences in lipid levels were unlikely to be responsible for these site-specific effects of immune system deficiency.Conclusions—These results suggest that immune system deficiency has a site-specific effect on atherosclerosis that is sensitive to the genetic background of the mice.
CD8+ T cells that express CD4 on their surface (CD4dimCD8bright T cells) recognize an antigen-specific target, are detected in vivo, and can be productively infected by T-tropic HIV
Authors: Zloza Andrew , Sullivan Yvonne B. , Connick Elizabeth , Landay Alan L. , Al-Harthi Lena 
Published: June 2003

AbstractCD4 can be up-regulated on CD8+ T cells generating a CD4dimCD8bright phenotype. We previously demonstrated that the CD4dimCD8bright phenotype constitutes an activated phenotype of CD8+ T cells. We demonstrate here that the activated CD4dimCD8bright T cells are not undergoing apoptosis and do not produce significant intracellular levels of interferon γ (IFNγ), interleukin 2 (IL-2), or IL-10 but express elevated levels of intracellular IL-4 in comparison to CD8+CD4– and CD4+ T cells. In response to cytomegalovirus (CMV) peptide (pp65) priming, CD4dimCD8bright cells recognized CMV pp65 tetramer approximately 19-fold higher than CD4–CD8+ T cells, indicating that these cells are capable of antigen-specific recognition to a far greater extent than CD4–CD8+ T cells. CD4dimCD8bright T cells also express both CXCR4 and CCR5 but are susceptible to T-tropic and not M-tropic HIV infection. A soluble factor believed to be β-chemokine is responsible for the inhibition of M-tropic HIV infection in CD4dimCD8bright T cells. CD8+ T cells from HIV+ patients were capable of up-regulating CD4 on CD8+ T cells. We also provide evidence of the presence of peripheral blood CD4dimCD8bright T cells in HIV+ patients, albeit at low frequency. Collectively, these data suggest a role of CD4dimCD8bright T cells in both normal T-cell biology and HIV pathogenesis.
A new xenograft model for graft-versus-host disease by intravenous transfer of human peripheral blood mononuclear cells in RAG2-/- γc-/- double-mutant mice
Authors: van Rijn Rozemarijn S. , Simonetti Elles R. , Hagenbeek Anton , Hogenes Marieke C. H. , de Weger Roel A. , Canninga-van Dijk Marijke R. , Weijer Kees , Spits Hergen , Storm Gert , van Bloois Louis , Rijkers Ger , Martens Anton C. M. , Ebeling Saskia B. 
Published: June 2003

AbstractThe safe application of new strategies for the treatment of graft-versus-host disease (GVHD) is hampered by the lack of a clinically relevant model for preclinical testing. Current models are based on intraperitoneal transfer of human peripheral blood mononuclear cells (huPBMCs) into NOD-SCID (nonobese diabetic-severe combined immunodeficient)/SCID mice. Intravenous transfer would be preferred but this has always been ineffective. We developed a new model for xenogeneic GVHD (X-GVHD) by intravenous transfer of huPBMCs into RAG2-/- γc-/-mice. Our results show a high human T-cell chimerism of more than 20% (up to 98%) in more than 90% of mice, associated with a consistent development of XGVHD within 14 to 28 days and a total mortality rate of 85% shorter than 2 months. After murine macrophage depletion, engraftment was earlier and equally high with lower doses of huPBMCs. Human macrophages were also absent in these mice. Purified huCD3+ cells showed a similar X-GVH effect with contribution of both CD4 and CD8 phenotypes. Human immunoglobulins and cytokines were produced in diseased mice. One of 30 mice developed chronic X-GVHD with skin histology similar to human GVHD. In conclusion, we present a new model for X-GVHD by intravenous transfer of huPBMCs in RAG2-/- γc-/- mice. Murine and human macrophages do not seem to be necessary for acute X-GVHD in this model. (Blood. 2003;102:2522-2531)
Angiogenic effects of prostaglandin E2 are mediated by up-regulation of CXCR4 on human microvascular endothelial cells
Authors: Salcedo Rosalba , Zhang Xia , Young Howard A. , Michael Nelson , Wasserman Ken , Ma Wei-Hong , Martins-Green Manuela , Murphy William J. , Oppenheim Joost J. 
Published: June 2003

AbstractStimulation of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) increases the expression of CXCR4 on endothelial cells, rendering these cells more responsive to stromal-derived factor 1 (SDF-1), an angiogenic CXC chemokine and unique ligand for CXCR4. Here, we show that prostaglandin E2 (PGE2) mediates the effects of bFGF and VEGF in up-regulating CXCR4 expression on human microvascular endothelial cells (HMECs). Forskolin or 3-isobutyl-1-methyl xanthine (IBMX), 2 inducers of adenylate cyclase, markedly enhanced, whereas cyclooxygenase (COX) inhibitors including aspirin, piroxicam, and NS398 markedly inhibited CXCR4 expression on HMECs. Furthermore, the ability of PGE2 to augment in vitro tubular formation in SDF-1α containing matrigel was inhibited completely by blocking CXCR4. Treatment of bFGF- or VEGF-stimulated HMECs with COX inhibitors blocked tubular formation by about 50% to 70%. Prostaglandin-induced human endothelial cell organization and subsequent vascularization can be inhibited to a greater extent by a neutralizing antibody to human CXCR4 in severe combined immunodeficient mice. Additionally, VEGF- and bFGF-induced angiogenesis in vivo was also inhibited by about 50% by NS-398 or piroxicam, and this inhibitory effect was accompanied by decreased expression of CXCR4 on murine endothelial cells. Consequently, by inducing CXCR4 expression, prostaglandin accounts for about 50% of the tubular formation in vitro and in vivo angiogenic effects of VEGF and bFGF. Moreover, augmentation of CXCR4 expression by VEGF, bFGF, and PGE2 involves stimulation of transcription factors binding to the Sp1-binding sites within the promoter region of the CXCR4 gene. These findings indicate that PGE2 is a mediator of VEGF- and bFGF-induced CXCR4-dependent neovessel assembly in vivo and show that angiogenic effects of PGE2 require CXCR4 expression.
T-cell developmental blockage by tachykinin antagonists and the role of hemokinin 1 in T lymphopoiesis
Authors: Zhang Yu , Paige Christopher J. 
Published: June 2003

AbstractHemokinin 1 (HK-1) is a new member of the tachykinin peptide family that is expressed in hematopoietic cells. Recent reports studying mouse, rat, and human orthologs of HK-1 demonstrate a broader distribution than originally reported. Our previous studies demonstrated that HK-1, by promoting proliferation, survival, and possibly maturation of B-cell precursors, plays an important role in B lymphopoiesis. Here we present data showing that HK-1 also influences T-cell development at a similar stage of differentiation. This peptide enhanced the proliferation of T-cell precursors and increased the number of thymocytes in fetal thymus organ cultures (FTOCs). Tachykinin antagonists, on the other hand, greatly reduced the cellularity of thymi both in vivo and in vitro. The major reduction occurred in the CD4/CD8 double-positive (DP) cells and the CD44–CD25+ subset of the CD4/CD8 double-negative (DN) cells. Of note, these populations also express HK-1, raising the possibility of autocrine or paracrine pathways influencing T-cell development as we previously reported for B-cell development. Consistent with this, the detrimental effect of tachykinin antagonists could be partially overcome with exogenous HK-1 peptide.
Filamin A binding to the cytoplasmic tail of glycoprotein Ibα regulates von Willebrand factor–induced platelet activation
Authors: Feng Shuju , Reséndiz Julio C. , Lu Xin , Kroll Michael H. 
Published: June 2003

AbstractWe examined the hypothesis that filamin A binding to the cytoplasmic tail of platelet glycoprotein Ibα (GpIbα) is regulated by pathologic shear stress and modulates von Willebrand factor (VWF)–induced platelet activation. To begin, we examined filamin binding to GpIbα in Chinese hamster ovary cells coexpressing mutant human GpIb-IX and wild-type human filamin A. We observed that many different deletions and truncations N-terminal to GpIbα's cytoplasmic domain residue 594 disrupted filamin A binding, but that binding was unaffected by 14 different point mutations in hydrophilic residues between amino acids 557 and 593. To try to narrow GpIbα's filamin A–binding domain, we next measured the effect of several cytoplasmic domain peptides on human filamin A binding to a GST-GpIbα cytoplasmic domain fusion protein. One peptide (residues 557-575; designated “A4 peptide”) inhibited filamin A binding to the GST-GpIbα cytoplasmic domain fusion protein and competed with GpIbα for binding to filamin A. When the A4 peptide was delivered to intact human platelets using a carrier peptide, we observed the dose-dependent inhibition of VWF-induced platelet aggregation in response to both ristocetin and shear stress. The effect of the A4 peptide on shear-induced platelet aggregation was accompanied by the attenuation of shear-induced filamin A binding to GpIbα and diminished shear-dependent protein tyrosine phosphorylation. These results suggest that shear-dependent VWF-induced platelet activation affects filamin A binding to GpIb-IX-V, and that filamin A binding to the cytoplasmic tail of GpIbα regulates proaggregatory tyrosine kinase signaling.
A novel strategy using single-chain antibody to show the importance of Bcl-2 in mast cell survival
Authors: Cohen-Saidon Cellina , Nechushtan Hovav , Kahlon Shira , Livni Nadav , Nissim Ahuva , Razin Ehud 
Published: June 2003

Abstract
Apoptosis or programmed cell death plays an important role in a wide variety of physiologic processes and is regulated by proteins of the Bcl-2 family consisting of both antiapoptotic and proapoptotic factors. The direct involvement of the Bcl-2 protein family in the process of mast cell apoptosis has not been clarified. In the present work we have used a single-chain antibody (scFv) raised against Bcl-2 derived from a semisynthetic human phage-display antibody library. The addition of TAT sequence, which is responsible for translocation through the membrane, endows the anti-Bcl-2-scFv with the ability to penetrate living cells. Moreover, it specifically neutralizes Bcl-2 intracellularly by binding to the BH1 domain and eradicates its antiapoptotic activity in 2 types of mast cells and in a human breast cancer cell line. (Blood. 2003;102:2506-2512)
FLT3 and MLL intragenic abnormalities in AML reflect a common category of genotoxic stress
Authors: Libura Marta , Asnafi Vahid , Tu Angela , Delabesse Eric , Tigaud Isabelle , Cymbalista Florence , Bennaceur-Griscelli Annelise , Villarese Patrick , Solbu Gabriel , Hagemeijer Anne , Beldjord Kheira , Hermine Olivier , Macintyre Elizabeth 
Published: June 2003

AbstractMLL rearrangements in acute myeloid leukemia (AML) include translocations and intragenic abnormalities such as internal duplication and breakage induced by topoisomerase II inhibitors. In adult AML, FLT3 internal tandem duplications (ITDs) are more common in cases with MLL intragenic abnormalities (33%) than those with MLL translocation (8%). Mutation/deletion involving FLT3 D835 are found in more than 20% of cases with MLL intragenic abnormalities compared with 10% of AML with MLL translocation and 5% of adult AML with normal MLL status. Real-time quantification of FLT3 in 141 cases of AML showed that all cases with FLT3 D835 express high level transcripts, whereas FLT3-ITD AML can be divided into cases with high-level FLT3 expression, which belong essentially to the monocytic lineage, and those with relatively low-level expression, which predominantly demonstrate PML-RARA and DEK-CAN. FLT3 abnormalities in CBF leukemias with AML1-ETO or CBFβ-MYH11 were virtually restricted to cases with variant CBFβ-MYH11 fusion transcripts and/or atypical morphology. These data suggest that the FLT3 and MLL loci demonstrate similar susceptibility to agents that modify chromatin configuration, including topoisomerase II inhibitors and abnormalities involving PML and DEK, with consequent errors in DNA repair. Variant CBFβ-MYH11 fusions and bcr3 PML-RARA may also be initiated by similar mechanisms.