bluuebunny/crossref_metadata_2025_split huggingface dataset:
Short-Term Reorganization of Auditory Analysis Induced by Phonetic Experience
Authors: Liebenthal Einat , Binder Jeffrey R. , Piorkowski Rebecca L. , Remez Robert E. 
Published: May 2003

Abstract
Sine wave replicas of spoken words can be perceived both as nonphonetic auditory forms and as words, depending on a listener's experience. In this study, brain areas activated by sine wave words were studied with fMRI in two conditions: when subjects perceived the sounds spontaneously as nonphonetic auditory forms (“naïve condition”) and after instruction and brief practice attending to their phonetic attributes (“informed condition”). The test items were composed such that half replicated natural words (“phonetic items”) and the other half did not, because the tone analogs of the first and third formants had been temporally reversed (“nonphonetic items”). Subjects were asked to decide whether an isolated tone analog of the second formant (T2) presented before the sine wave word (T1234) was included in it. Experience in attending to the phonetic properties of the sinusoids interfered with this auditory matching task and was accompanied by a decrease in auditory cortex activation with word replicas but not with the acoustically matched nonphonetic items. Because the activation patterns elicited by equivalent acoustic test items depended on a listener's awareness of their phonetic potential, this indicates that the analysis of speech sounds in the auditory cortex is distinct from the simple resolution of auditory form, and is not a mere consequence of acoustic complexity. Because arbitrary acoustic patterns did not evoke the response observed for phonetic patterns, these findings suggest that the perception of speech is contingent on the presence of familiar patterns of spectral variation. The results are consistent with a short-term functional reorganization of auditory analysis induced by phonetic experience with sine wave replicas and contingent on the dynamic acoustic structure of speech.
A Cortical Mechanism for Triggering Top-Down Facilitation in Visual Object Recognition
Authors: Bar Moshe 
Published: May 2003

Abstract
The majority of the research related to visual recognition has so far focused on bottom-up analysis, where the input is processed in a cascade of cortical regions that analyze increasingly complex information. Gradually more studies emphasize the role of top-down facilitation in cortical analysis, but it remains something of a mystery how such processing would be initiated. After all, top-down facilitation implies that high-level information is activated earlier than some relevant lower-level information. Building on previous studies, I propose a specific mechanism for the activation of top-down facilitation during visual object recognition. The gist of this hypothesis is that a partially analyzed version of the input image (i.e., a blurred image) is projected rapidly from early visual areas directly to the prefrontal cortex (PFC). This coarse representation activates in the PFC expectations about the most likely interpretations of the input image, which are then back-projected as an “initial guess” to the temporal cortex to be integrated with the bottom-up analysis. The top-down process facilitates recognition by substantially limiting the number of object representations that need to be considered. Furthermore, such a rapid mechanism may provide critical information when a quick response is necessary.
The Children's Treatment of Animals Questionnaire (CTAQ): A Psychometric Investigation
Authors: Thompson Kelly , Gullone Eleonora 
Published: April 2003

AbstractRecognizing the importance of increasing the levels of children's humane behavior toward animals other than humans relates to the developing of valid and reliable measures of such behavior. This study reports the psychometric properties of the Children's Treatment of Animals Questionnaire (CTAQ), which assesses children's humane behavior toward nonhuman animals. The findings, based on self-reports by 61 elementary school children (25 boys; 36 girls), showed that the 13-item scale has adequate internal consistency. In addition, comparing two administrations of the scale over a five-week period demonstrated good test-retest reliability. The scale's convergent validity was demonstrated with significant correlations between responses on the CTAQ and two previously validated measures of empathy. The study concluded that the CTAQ is a valid and reliable measure for assessing the degree to which children's behavior toward nonhuman animals is humane. Determining the sensitivity of the measure to change (following humane education) and the predictive validity of the measure (identification of children who are cruel to animals) will require further research.
Companion Animal Attitude and its Family Pattern in Kuwait
Authors: Al-Fayez Ghenaim , Arikawa Hiroko , Awadalla Abdelwahid , Templer Donald 
Published: April 2003

AbstractThe Pet Attitude Scale (PAS) score of Kuwaiti adolescents correlated more highly with that of their fathers than with the score of their mothers. This contrasts with a similar American study in which the PAS score of adolescents correlated more highly with the score of their mothers. The different pattern seemed to be congruent with the father's more dominant role in Arab families. This study found that Kuwaiti family members had scores on the PAS about a standard deviation lower than that of American family members, a finding viewed as consistent with the less positive attitude toward companion animals in Muslim countries.
"Would You Let Your Child Die Rather than Experiment on Nonhuman Animals?" A Comparative Questions Approach
Authors: Perlo Katherine 
Published: April 2003

AbstractBy placing the title question alongside five comparative questions and offering answers to the whole set as given by seven imaginary respondents, this paper analyzes the question's deceptiveness and the inconsistency of its implied claims. Apart from ambiguities of situation, history, and agency, the question's demand for a choice between "your child" and "nonhuman animals" obscures a field of other values regarding (1) species, (2) family ties, and (3) the wrongness-in-itself (or otherwise) of the experiments envisioned. This paper argues that while a "No" answer to the title question does not, as intended by the questioner, support the experimental status quo, even a "Yes" answer does not reflect a choice between one's own child and animals.
The Labor Process: How the Underdog is Kept Under
Authors: Dickens Peter 
Published: April 2003

Abstract"Marxism and the Underdog" is an impressive paper. It usefully outlines the strengths and weaknesses of the Marxist (what I would prefer to term "historical materialist") perspective on animals. As the paper rightly suggests, much of Marx's own work was predicated on the opposition between humans and animals other than humans. Yet, as the paper also points out, many of his concepts and critiques are useful for addressing contemporary concerns. Among the most important recent examples is Benton's critique of liberal and individualist "animal rights." It is a perspective on Marx and his assertion that much human rights discourse offers little or no fundamental challenge to the patterns of economic, social, and political power that pervade capitalist society. There is little point in allocating rights to humans (and to animals) if the kind of society in which they live systematically denies the realization of these rights. I mention Benton here because his important perspective on animal rights is not fully explained in the paper under review here.
CD2 engagement induces dendritic cell activation: implications for immune surveillance and T-cell activation
Authors: Crawford Keith , Stark Aleksandra , Kitchens Betsy , Sternheim Kerry , Pantazopoulos Vassilios , Triantafellow Ellen , Wang Zhigang , Vasir Baldev , Larsen Charles E. , Gabuzda Dana , Reinherz Ellis , Alper Chester A. 
Published: April 2003

AbstractWe have shown previously that primary dendritic cells and monocytes express equal levels of CD14 but are distinguishable by the presence of CD2 on dendritic cells. CD2 is known to mediate the activation of T and natural killer (NK) cells through its interaction with CD58. CD2 epitopes recognized by anti-T111, -T112, and -T113 monoclonal antibodies (mAbs) are present on dendritic cells. Here we show that CD2 engagement significantly increases class II, costimulatory (CD40, CD80, CD86), adhesion (CD54, CD58), and CCR7 molecule expression on primary dendritic cells. Conversely, minimal or no change in the expression of the above antigens occurs on monocyte-derived dendritic cells, because these molecules are already maximally expressed. However, both kinds of dendritic cells release interleukin-1β (IL-1β) and IL-12 after CD2 engagement. Lastly, interference with dendritic cell CD2–T-cell CD58 engagement decreases naive CD4+CD45RA+ T-cell proliferation. Collectively, our results suggest another role of the CD2-CD58 pathway that allows nonimmune and immune cells to interact directly with dendritic cells and initiate innate and adaptive immune responses.
Ex vivo induction of multiple myeloma–specific cytotoxic T lymphocytes
Authors: Hayashi Toshiaki , Hideshima Teru , Akiyama Masaharu , Raje Noopur , Richardson Paul , Chauhan Dharminder , Anderson Kenneth C. 
Published: April 2003

AbstractMultiple myeloma (MM) is an incurable plasma cell malignancy characterized by immunosuppression. In this study, we identified factors in patients' bone marrow (BM) sera inhibiting autologous anti-MM immunity and developed an ex vivo strategy for inducing MM-specific cytotoxic T lymphocytes (CTLs). We found that sera from BM of MM patients inhibited induction of dendritic cells (DCs), evidenced by both phenotype and only weak stimulation of T-cell proliferation. Anti–vascular endothelial growth factor (anti-VEGF) and/or anti–interleukin 6 (anti–IL-6) antibodies neutralized this inhibitory effect, confirming that VEGF and IL-6, at least in part, mediate immunosuppression in MM patients. To induce MM-specific CTLs ex vivo, immature DCs were generated by culture of adherent mononuclear cells in medium containing granulocyte-macrophage colony-stimulating factor (GM-CSF) and IL-4 for 5 days and then cocultured with apoptotic MM bodies in the presence of tumor necrosis factor α (TNF-α) for 3 days to induce their maturation. Autologous BM or peripheral blood mononuclear cells were stimulated weekly with these DCs, and cytotoxicity was examined against the MM cells used to pulse DCs. DCs cultured with apoptotic bodies stimulated significantly greater T-cell proliferation (stimulation index [SI] = 23.2 at a T-DC ratio of 360:1) than T cells stimulated by MM cells only (SI = 5.6), DCs only (SI = 9.3), or MM lysate–pulsed DCs (SI = 13.5). These CTLs from MM patients demonstrated specific cytotoxicity (24.7% at the effector-target [E/T] ratio of 40:1) against autologous primary MM cells. These studies therefore show that CTLs from MM patients can recognize and lyse autologous tumor cells and provide the framework for novel immunotherapy to improve patient outcome in MM.
Placenta growth factor activates monocytes and correlates with sickle cell disease severity
Authors: Perelman Natalya , Selvaraj Suresh K. , Batra Sandeep , Luck Lori R. , Erdreich-Epstein Anat , Coates Thomas D. , Kalra Vijay K. , Malik Punam 
Published: April 2003

AbstractSickle cell disease (SCD) results in chronic hypoxia and secondarily increased erythropoietin concentrations. Leukocytosis and activated monocytes are also observed in SCD in absence of infection or vaso-occlusion (steady state), the reasons for which are unknown. We found that erythroid cells produced placenta growth factor (PlGF), an angiogenic growth factor belonging to the vascular endothelial growth factor (VEGF) family, and its expression was induced in bone marrow CD34+ progenitor cells in the presence of erythropoietin. Furthermore, the steady state circulating PlGF levels in subjects with severe SCD (at least 3 vaso-occlusive crises [VOCs] per year) were 18.5 ± 1.2 pg/mL (n = 9) compared with 15.5 ± 1.2 pg/mL (n = 13) in those with mild SCD (fewer than 3 VOCs per year) and 11.3 ± 0.7 pg/mL (n = 9) in healthy controls (P &lt; .05), suggesting a correlation between PlGF levels and SCD severity. In addition, PlGF significantly increased mRNA levels of the proinflammatory cytochemokines interleukin-1β, interleukin-8, monocyte chemoattractant protein-1, and VEGF in peripheral blood mononuclear cells (MNCs) of healthy subjects (n = 4; P &lt; .05). Expression of these same cytochemokines was significantly increased in MNCs from subjects with SCD at steady state (n = 14), compared with healthy controls. Of the leukocyte subfractions, PlGF stimulated monocyte chemotaxis (P &lt; .05, n = 3). Taken together, these data show for the first time that erythroid cells intrinsically release a factor that can directly activate monocytes to increase inflammation. The baseline inflammation seen in SCD has always been attributed to sequelae secondary to the sickling phenomenon. We show that PlGF contributes to the inflammation observed in SCD and increases the incidence of vaso-occlusive events.
Induction of FucT-VII by the Ras/MAP kinase cascade in Jurkat T cells
Authors: Barry Sheila M. , Zisoulis Dimitrios G. , Neal Joel W. , Clipstone Neil A. , Kansas Geoffrey S. 
Published: May 2003

AbstractInduction of the α1,3-fucosyltransferase FucT-VII in T lymphocytes is crucial for selectin ligand formation, but the signaling and transcriptional pathways that govern FucT-VII expression are unknown. Here, using a novel, highly phorbol myristate acetate (PMA)–responsive variant of the Jurkat T-cell line, we identify Ras and downstream mitogen-activated protein (MAP) kinase pathways as essential mediators of FucT-VII gene expression. PMA induced FucT-VII in only a subset of treated cells, similar to expression of FucT-VII in normal activated CD4 T cells. Introduction of constitutively active Ras or Raf by recombinant retroviruses induced FucT-VII expression only in that subset of cells expressing the highest levels of Ras, suggesting that induction of FucT-VII required a critical threshhold of Ras signaling. Both PMA treatment and introduction of active Ras led to rolling on E-selectin. Pharmacologic inhibition studies confirmed the involvement of the classic Ras-Raf-MEK–extracellular signal-regulated kinase (Ras-Raf-MEK-ERK) pathway in FucT-VII induction by PMA, Ras, and Raf. These studies also revealed a second, Ras-induced, Raf-1–independent pathway that participated in induction of FucT-VII. Strong activation of Ras represents a major pathway for induction of FucT-VII gene expression in T cells.
TGFβ inhibits LPS-induced chemokine mRNA stabilization
Authors: Dai Yalei , Datta Shyamsree , Novotny Michael , Hamilton Thomas A. 
Published: April 2003

AbstractThe mechanisms involved in anti-inflammatory action of transforming growth factor β (TGFβ) have been examined by evaluating its effect on chemokine gene expression in mouse macrophages. Lipopolysaccharide (LPS)–stimulated expression of the CXC chemokines KC and MIP-2 was selectively reduced by TGFβ in a time- and protein synthesis–dependent process. While TGFβ had a modest effect on transcription of the KC and MIP-2 mRNAs as measured by nuclear run-on, it had no effect on LPS-stimulated luciferase expression driven by the KC promoter nor on the activation of nuclear factor κB (NFκB) DNA-binding activity and transactivation function. Interestingly, KC mRNA levels were markedly reduced by TGFβ treatment in cells transfected with KC genomic or cDNA constructs driven from either the KC or cytomegalovirus (CMV) promoters, demonstrating the importance of sequences within the mature mRNA and suggesting that suppression may involve a posttranscriptional mechanism. In support of this possibility, LPS stimulation prolonged the half-life of KC mRNA and this stabilization response was blocked in cells treated with TGFβ. Examination of KC mRNA expressed under control of a tetracycline-responsive promoter demonstrated that TGFβ prevented stabilization of KC mRNA, in response to LPS but did not alter KC mRNA half-life directly. KC mRNA stabilization by LPS was dependent on activation of p38 mitogen-activated protein kinase (MAPK) activity, and TGFβ treatment inhibited p38 MAPK activation. These findings support the hypothesis that TGFβ-mediated suppression of chemokine gene expression involves antagonism of LPS-stimulated KC mRNA stabilization via inhibition of p38 MAPK.
Antiapoptotic effect of coagulation factor VIIa
Authors: Sorensen Brit B. , Vijaya Mohan Rao L. , Tornehave Ditte , Gammeltoft Steen , Petersen Lars C. 
Published: May 2003

AbstractBinding of factor VIIa (FVIIa) to its cellular receptor tissue factor (TF) was previously shown to induce various intracellular signaling events, which were thought to be responsible for TF-mediated biologic effects, including angiogenesis, tumor metastasis, and restenosis. To understand the mechanisms behind these processes, we have examined the effect of FVIIa on apoptosis. Serum deprivation–induced apoptosis of BHK(+TF) cells was characterized by apoptotic blebs, nuclei with chromatin-condensed bodies, DNA degradation, and activation of caspase 3. FVIIa markedly decreased the number of cells with apoptotic morphology and prevented the DNA degradation as measured by means of TdT-mediated dUTP nick end labeling (TUNEL). The antiapoptotic effect of FVIIa was confirmed by the observation that FVIIa attenuated caspase 3 activation. FVIIa-induced antiapoptotic effect was dependent on its proteolytic activity and TF but independent of factor Xa and thrombin. FVIIa-induced cell survival correlated with the activation of Akt and was inhibited markedly by the specific PI3-kinase inhibitor, LY294002. Blocking the activation of p44/42 mitogen-activated protein kinase (MAPK) by the specific mitogen-induced extracellular kinase (MEK) inhibitor, U0126, impaired modestly the ability of FVIIa to promote cell survival. In conclusion, FVIIa binding to TF provided protection against apoptosis induced by growth factor deprivation, primarily through activation of PI3-kinase/Akt pathway, and to a lesser extent, p44/42 MAPK pathway.
Hematopoietic stimulation by a dipeptidyl peptidase inhibitor reveals a novel regulatory mechanism and therapeutic treatment for blood cell deficiencies
Authors: Jones Barry , Adams Sharlene , Miller Glenn T. , Jesson Michael I. , Watanabe Takeshi , Wallner Barbara P. 
Published: May 2003

AbstractIn hematopoiesis, cytokine levels modulate blood cell replacement, self-renewal of stem cells, and responses to disease. Feedback pathways regulating cytokine levels and targets for therapeutic intervention remain to be determined. Amino boronic dipeptides are orally bioavailable inhibitors of dipeptidyl peptidases. Here we show that the high-affinity inhibitor Val-boro-Pro (PT-100) can stimulate the growth of hematopoietic progenitor cells in vivo and can accelerate neutrophil and erythrocyte regeneration in mouse models of neutropenia and acute anemia. Hematopoietic stimulation by PT-100 correlated with increased cytokine levels in vivo. In vitro, PT-100 promoted the growth of primitive hematopoietic progenitor cells by increasing granulocyte–colony-stimulating factor (G-CSF), interleukin-6 (IL-6), and IL-11 production by bone marrow stromal cells. Two molecular targets of PT-100 are expressed by stromal cells— CD26/DPP-IV and the closely related fibroblast activation protein (FAP). Because PT-100 was active in the absence of CD26, FAP appears to be the hematopoietic target for PT-100. Interaction of PT-100 with the catalytic site seems to be required because amino-terminal acetylation of PT-100 abrogated enzyme inhibition and hematopoietic stimulation. PT-100 is a therapeutic candidate for the treatment of neutropenia and anemia. The data support increasing evidence that dipeptidyl peptidases can regulate complex biologic systems by the proteolysis of signaling peptides.
Bacterial lipopolysaccharide directly induces angiogenesis through TRAF6-mediated activation of NF-κB and c-Jun N-terminal kinase
Authors: Pollet Ingrid , Opina Christy J. , Zimmerman Carla , Leong Kevin G. , Wong Fred , Karsan Aly 
Published: April 2003

AbstractThe intracellular pathways by which inflammatory mediators transmit their angiogenic signals is not well studied. The effects of a potent inflammatory mediator, bacterial lipopolysaccharide (LPS), are transmitted through Toll-like receptors (TLRs). A major, although not exclusive, LPS/TLR intracellular signaling pathway is routed through TNF (tumor necrosis factor) receptor associated factor 6 (TRAF6). In this report we demonstrate that LPS directly stimulates endothelial sprouting in vitro. By blocking TRAF6 activity using retroviral expression of a dominant-negative TRAF6 in endothelial cells, we show that TRAF6 is absolutely required for the LPS-initiated angiogenic response in vitro and in vivo. Inhibition of either c-Jun N-terminal kinase (JNK) activity or nuclear factor κB (NF-κB) activity, downstream of TRAF6, is sufficient to inhibit LPS-induced endothelial sprouting. In contrast, only inhibition of NF-κB, but not JNK, activity blocks basic fibroblast growth factor (bFGF)–induced angiogenesis. Our findings thus demonstrate a direct endothelial-stimulatory role of LPS in initiating angiogenesis through activation of TRAF6-dependent signaling pathways.
Autologous transplantation of granulocyte colony-stimulating factor–primed bone marrow is effective in supporting myeloablative chemotherapy in patients with hematologic malignancies and poor peripheral blood stem cell mobilization
Authors: Lemoli Roberto M. , de Vivo Antonio , Damiani Daniela , Isidori Alessandro , Tani Monica , Bonini Alessandro , Cellini Claudia , Curti Antonio , Gugliotta Luigi , Visani Giuseppe , Fanin Renato , Baccarani Michele 
Published: April 2003

AbstractWe assessed the hematopoietic recovery and transplantation-related mortality (TRM) of patients who had failed peripheral blood stem cell mobilization and subsequently received high-dose chemotherapy supported by granulocyte colony-stimulating factor (G-CSF)–primed bone marrow (BM). Studied were 86 heavily pretreated consecutive patients with acute leukemia (n = 21), refractory/relapsed non-Hodgkin lymphoma (n = 41) and Hodgkin disease (n = 17), and multiple myeloma (n = 7). There were 78 patients who showed insufficient mobilization of CD34+ cells (&lt; 10 cells/μL), whereas 8 patients collected less than 1 × 106 CD34+ cells/kg. BM was primed in vivo for 3 days with 15 to 16 μg/kg of subcutaneous G-CSF. Median numbers of nucleated cells, colony-forming unit cells (CFU-Cs), and CD34+ cells per kilogram harvested were 3.5 × 108, 3.72 × 104, and 0.82 × 106, respectively. Following myeloablative chemotherapy, median times to achieve a granulocyte count higher than 0.5 × 109/L and an unsupported platelet count higher than 20 and 50 × 109/L were 13 (range, 8-24), 15 (range, 12-75), and 22 (range, 12-180) days, respectively, for lymphoma/myeloma patients and 23 (range, 13-53), 52 (range, 40-120), and 90 (range, 46-207) days, respectively, for leukemia patients. Median times to hospital discharge after transplantation were 17 (range, 12-40) and 27 (range, 14-39) days for lymphoma/myeloma and acute leukemia patients, respectively. TRM was 4.6%, whereas 15 patients died of disease. G-CSF–primed BM induces effective multilineage hematopoietic recovery after high-dose chemotherapy and can be safely used in patients with poor stem cell mobilization.