bluuebunny/crossref_metadata_2025_split huggingface dataset:
Visyllable Based Speech Animation
Authors: Kshirsagar Sumedha , Magnenat‐Thalmann Nadia 
Published: November 2003

Abstract Visemes are visual counterpart of phonemes. Traditionally, the speech animation of 3D synthetic faces involvesextraction of visemes from input speech followed by the application of co‐articulation rules to generate realisticanimation. In this paper, we take a novel approach for speech animation — using visyllables, the visual counterpartof syllables. The approach results into a concatenative visyllable based speech animation system. The key contributionof this paper lies in two main areas. Firstly, we define a set of visyllable units for spoken English along withthe associated phonological rules for valid syllables. Based on these rules, we have implemented a syllabificationalgorithm that allows segmentation of a given phoneme stream into syllables and subsequently visyllables. Secondly,we have recorded the database of visyllables using a facial motion capture system. The recorded visyllableunits are post‐processed semi‐automatically to ensure continuity at the vowel boundaries of the visyllables. We defineeach visyllable in terms of the Facial Movement Parameters (FMP). The FMPs are obtained as a result of thestatistical analysis of the facial motion capture data. The FMPs allow a compact representation of the visyllables.Further, the FMPs also facilitate the formulation of rules for boundary matching and smoothing after concatenatingthe visyllables units. Ours is the first visyllable based speech animation system. The proposed technique iseasy to implement, effective for real‐time as well as non real‐time applications and results into realistic speechanimation. Categories and Subject Descriptors (according to ACM CCS): 1.3.7 [Computer Graphics]: Three‐Dimensional Graphics and Realism
Narrative Use of Sign Language by a Virtual Character for the Hearing Impaired
Authors: Rieger Thomas , Braun Norbert 
Published: November 2003

Abstract This paper describes the concept and control of a 3d virtual character system with facial expressions and gesturesas a conversational user interface with narrative expressiveness for the hearing impaired. The gestures and facialexpressions are based on morphing techniques. The system allows the generation of sign language and mouthmotion in real time from text at the level of lip reading quality. The concept of Narrative Extended Speech Acts(NESA) is introduced, based on Interactive Storytelling techniques and the concepts of Narrative Conflict andSuspense Progression. We define a choice of annotation tags to be used with NESAs. We use the NESAs to classifyconversation fragments and to enhance computer generated sign language. We note, how the sign language gesturesare generated and show the possibilities for editing sign language gestures. Furthermore, we give details onhow the NESAs are mapped to gestures. We show the possibilities of controlling the virtual character's behaviourand gestures in a human‐oriented way and provide an outlook on future work. Categories and Subject Descriptors (according to ACM CCS): 1.3.6 [Computer Graphics]: Methodology and Techniques
Interactive Cutaway Illustrations
Authors: Diepstraten J. , Weiskopf D. , Ertl T. 
Published: November 2003

Abstract In this paper we discuss different approaches to generate cutaway illustrations. The purpose of such a drawingis to allow the viewer to have a look into an otherwise solid opaque object. Traditional methods to draw thesekinds of illustrations are evaluated to extract a small and effective set of rules for a computer‐based renderingof cutaway illustrations. We show that our approaches are not limited to a specific rendering style but can besuccessfully combined with a great variety of well‐known artistic or technical illustration techniques. All methodsof this paper make use of modern graphics hardware functionality to achieve interactive frame rates.
Vitamin E Supplementation in Patients With Carotid Atherosclerosis
Authors: Micheletta Fausta , Natoli Silvia , Misuraca Maria , Sbarigia Enrico , Diczfalusy Ulf , Iuliano Luigi 
Published: November 2003

Objective—Oxidative stress is believed to play a pivotal role in the initiation and progression of atherosclerosis. We analyzed whether vitamin E supplementation influences oxidative stress in plasma and atherosclerotic plaques of patients with severe atherosclerosis.Methods and Results—In 16 patients who were candidates for carotid endarterectomy and in 32 age- and sex-matched controls, plasma levels of 7β-hydroxycholesterol, 7-ketocholesterol, cholesterol, and vitamin E were measured. Patients were randomly allocated to standard treatment with or without 900 mg/d vitamin E. After 6 weeks of treatment, the reported variables were measured in plasma and plaques. The plasma vitamin E/cholesterol ratio was significantly lower in patients than in controls (3.05±0.6 versus 6.3±1.7 μmol/mmol cholesterol,P<0.001). Plasma 7β-hydroxycholesterol was significantly higher in patients than in controls (5.0±1.04 versus 4.4±0.6 ng/mL,P<0.05). Patients who were given vitamin E supplementation showed a significant increase of plasma vitamin E with concomitant decrease of 7β-hydroxycholesterol. Conversely, no treatment dependence was observed in oxysterol or vitamin E content of plaques.Conclusions—An imbalance between oxidative stress and antioxidant status is present in patients with advanced atherosclerosis. Vitamin E supplementation improves this imbalance in plasma but not in plaques.
Control of Skin Sympathetic Nerve Activity During Intermittent Static Handgrip Exercise
Authors: Leuenberger Urs A. , Mostoufi-Moab Sogol , Herr Michael , Gray Kristen , Kunselman Allen , Sinoway Lawrence I. 
Published: November 2003

Background—Exercise activates the sympathetic nervous system as a function of the type and intensity of exercise and of the target organ studied. Although central command and activity of metabolically sensitive afferents from exercising muscle are the principal determinants of sympathetic outflow directed to skeletal muscle, the mechanisms that govern sympathetic outflow directed to skin are less clear.Methods and Results—We measured skin sympathetic nerve activity (SSNA) during intermittent static handgrip (SHG; at 45% of maximal voluntary contraction; four 5-second contractions per minute for 3 minutes), during unrestricted forearm perfusion (control), during stimulation of forearm mechanoreceptors with venous congestion, and during ischemia produced by forearm circulatory arrest. Under all 3 conditions, SSNA increased within 1 to 2 seconds of the onset of handgrip. During ischemia but not during venous congestion, SSNA increased more compared with control (P<0.05) and remained elevated when forearm ischemia was maintained after handgrip exercise (posthandgrip circulatory arrest). In addition, simulated handgrip and intermittent forearm compression produced by a pneumatic cuff also evoked brief increases of SSNA.Conclusions—In addition to central neural factors, afferent input from exercising muscle plays an important role in modulating sympathetic outflow directed to skin.
Thrombomodulin mutant mice with a strongly reduced capacity to generate activated protein C have an unaltered pulmonary immune response to respiratory pathogens and lipopolysaccharide
Authors: Rijneveld Anita W. , Weijer Sebastiaan , Florquin Sandrine , Esmon Charles T. , Meijers Joost C. M. , Speelman Peter , Reitsma Pieter H. , Ten Cate Hugo , van der Poll Tom 
Published: November 2003

AbstractThe thrombomodulin–protein C–protein S (TM-PC-PS) pathway exerts anticoagulant and anti-inflammatory effects. We investigated the role of TM in the pulmonary immune response in vivo by the use of mice with a mutation in the TM gene (TMpro/pro) that was earlier found to result in a minimal capacity for activated PC (APC) generation in the circulation. We here demonstrate that TMpro/pro mice also display a strongly reduced capacity to produce APC in the alveolar compartment upon intrapulmonary delivery of PC and thrombin. We monitored procoagulant and inflammatory changes in the lung during Gram-positive (Streptococcus pneumoniae) and Gram-negative (Klebsiella pneumoniae) pneumonia and after local administration of lipopolysaccharide (LPS). Bacterial pneumonia was associated with fibrin(ogen) depositions in the lung that colocalized with inflammatory infiltrates. LPS also induced a rise in thrombin-antithrombin complexes in bronchoalveolar lavage fluid. These pulmonary procoagulant responses were unaltered in TMpro/pro mice, except for enhanced fibrin(ogen) deposition during pneumococcal pneumonia. In addition, TMpro/pro mice displayed unchanged antibacterial defense, neutrophil recruitment, and cytokine/chemokine levels. These data suggest that the capacity of TM to generate APC does not play a role of importance in the pulmonary response to respiratory pathogens or LPS.
The variable number of tandem repeat polymorphism of platelet glycoprotein Ibα and risk of coronary heart disease
Authors: Afshar-Kharghan Vahid , Matijevic-Aleksic Nevenka , Ahn Chul , Boerwinkle Eric , Wu Kenneth K. , López José A. 
Published: November 2003

AbstractGlycoprotein (GP) Ib-IX-V complex plays an important role in formation of platelet-fibrin clot at the area of damaged vessel wall. One polymorphism of GP Ibα, the main component of GP Ib-IX-V complex, is due to variable numbers of tandem repeats (VNTRs) in the macroglycopeptide region of this molecule. We studied the association between the presence of different VNTR alleles of GP Ibα and the frequency of coronary heart disease (CHD) among individuals recruited to a large community-based case-cohort study (Atherosclerosis Risk in Communities [ARIC] study). We found that the distribution of VNTR alleles of GP Ibα is different among whites and African Americans. The B allele (with 3 repeats) of GP Ibα is relatively more common among African Americans compared with whites. In African Americans, the CC genotype (homozygous with 2 repeats) is associated with a lower risk of CHD events than all other genotypes. (Blood. 2004;103:963-965)
Cotransplantation of third-party mesenchymal stromal cells can alleviate single-donor predominance and increase engraftment from double cord transplantation
Authors: Kim Dong-Wook , Chung Yang-Jo , Kim Tai-Gyu , Kim Yoo-Li , Oh Il-Hoan 
Published: November 2003

AbstractAlthough the infusion of umbilical cord blood (UCB) from multiple donors can be a strategy to overcome the cell dose limitation frequently encountered in UCB transplantation, clinical trials have revealed that cells from one donor dominate engraftment. To investigate the origin of and the factors influencing this inequality, we performed mixed transplantation of 2 UCB units with varying degrees of HLA disparities into NOD/SCID mice and determined donor origins by polymerase chain reaction–sequence-specific oligonucleotide probe (PCR-SSOP) or real-time quantitative (RQ)–PCR for human short tandem repeats (STRs). When total mononuclear cells from 2 units were transplanted as a mixture, cells from one donor predominated (ratio, 81:19), despite comparable overall engraftment when infused as single units, and no augmentation in overall engraftment was observed when compared with the single-unit controls. However, lineage depletion or cotransplantation of mesenchymal stromal cells (MSCs) expanded from third-party bone marrow resulted in more balanced coengraftment. Direct comparison of double UCB transplantation in the presence or absence of MSCs showed that the reduced deviation in the donor ratio (1.8:1 vs. 2.8:1) correlated with a higher overall level of engraftment with MSC cotransplantation. These results indicate that third-party MSCs can be used to alleviate donor deviation and to facilitate engraftment of multidonor UCB.
Pregnancy induces minor histocompatibility antigen–specific cytotoxic T cells: implications for stem cell transplantation and immunotherapy
Authors: Verdijk Rob M. , Kloosterman Antoinette , Pool Jos , van de Keur Maarten , Naipal Albert M. I. H. , van Halteren Astrid G. S. , Brand Anneke , Mutis Tuna , Goulmy Els 
Published: November 2003

AbstractRecipients of HLA-identical stem cell transplants have a poorer transplant outcome if the donor is female rather than male. We analyzed whether pregnancy primes for minor histocompatibility (H) antigens. Peripheral blood mononuclear cells (PBMCs) from healthy multiparous female blood donors were depleted for CD4+, CD14+, CD16+, and CD19+ cells, stained with minor H antigen–specific HLA-A2 tetramers, sorted by fluorescence-activated cell sorting, and tested for cytotoxic activity. Minor H antigens HY-, HA-1–, and HA-2–specific cytotoxic T cells (CD8+, CD45RA–) were present in PBMCs from 4 of 7 female donors up to 22 years after the last delivery. Interestingly, in 2 of the 4 cases microchimerism of the putative immunizing minor H antigen was observed. Thus, pregnancy can lead to alloimmune responses against the infant's paternal minor H antigens. The minor H antigen immunization status of female donors raises important questions for the clinical practice of stem cell transplantation.
CCL19/CCL21-triggered signal transduction and migration of dendritic cells requires prostaglandin E2
Authors: Scandella Elke , Men Ying , Legler Daniel F. , Gillessen Silke , Prikler Ladislav , Ludewig Burkhard , Groettrup Marcus 
Published: November 2003

AbstractThe control of dendritic cell (DC) migration is pivotal for the initiation of cellular immune responses. When activated with inflammatory stimuli, the chemokine receptor CCR7 is up-regulated on DCs. Activated DCs home to lymphoid organs, where the CCR7 ligands CCL19 and CCL21 are expressed. We previously found that human monocyte-derived DCs (MoDCs) exclusively migrated to CCL19 and CCL21 when matured in the presence of prostaglandin (PG) E2. Because PGE2 did not alter CCR7 cell surface expression, we examined whether PGE2 may exert its effect by coupling CCR7 to signal transduction modules. Indeed, stimulation with CCR7 ligands led to enhanced phosphatidylinositol-3-kinase–mediated phosphorylation of protein kinase B when MoDCs were matured in the presence of PGE2. Moreover, CCL19/CCL21-induced intracellular calcium mobilization in MoDCs occurred only when PGE2 was present during maturation. MoDC migration to CCL19 and CCL21 was dependent on phospholipase C and intracellular calcium flux but not on phosphatidylinositol-3 kinase. Hence, our data provide insight into CCL19/CCL21-triggered signal transduction pathways and identify a novel function for PGE2 in controlling the migration of mature MoDCs by facilitating CCR7 signal transduction.
Adhesion to E-selectin promotes growth inhibition and apoptosis of human and murine hematopoietic progenitor cells independent of PSGL-1
Authors: Winkler Ingrid G. , Snapp Karen R. , Simmons Paul J. , Lévesque Jean-Pierre 
Published: November 2003

AbstractAlthough both P- and E-selectin are constitutively expressed on bone marrow endothelial cells, their role in the regulation of hematopoiesis has only recently been investigated. We have previously shown that P-selectin glycoprotein ligand-l (PSGL-1/CD162) is expressed by primitive human bone marrow CD34+ cells, mediates their adhesion to P-selectin, and, more importantly, inhibits their proliferation. We now demonstrate that adhesion to E-selectin inhibits the proliferation of human CD34+ cells isolated either from human umbilical cord blood, adult mobilized blood, or steady-state bone marrow. Furthermore, a subpopulation, which does not contain the most primitive hematopoietic progenitor cells, undergoes apoptosis following E-selectin–mediated adhesion. The same phenomenon was observed in cells isolated from mouse bone marrow. Using lineage-negative Sca-1+ c-KIT+ bone marrow cells from PSGL-1–/– and wild-type mice, we establish that PSGL-1 is not the ligand involved in E-selectin–mediated growth inhibition and apoptosis. Moreover, stable transfection of the human myeloid cell line K562 (which does not express PSGL-1) with α(1,3) fucosyltransferase VII alone was sufficient to recapitulate the E-selectin–mediated growth inhibition and apoptosis observed in hematopoietic progenitor cells. These data demonstrate that an E-selectin ligand(s) other than PSGL-1 transduces growth inhibitory and proapoptotic signals and requires posttranslational fucosylation to be functional.
Internal tandem duplication mutation of FLT3 blocks myeloid differentiation through suppression of C/EBPα expression
Authors: Zheng Rui , Friedman Alan D. , Levis Mark , Li Li , Weir Edward G. , Small Donald 
Published: November 2003

AbstractConstitutively activating mutations of FMS-like tyrosine kinase 3 (FLT3) occur in approximately one third of patients with acute myeloid leukemia (AML) and are associated with poor prognosis. Altered FLT3 signaling leads to antiapoptotic and proliferative signaling pathways. We recently showed that these mutations can also contribute to the differentiation arrest that characterizes leukemia. In this report we investigated the mechanism by which internal tandem duplication (ITD) mutation of FLT3 signaling blocks differentiation. Normally, myeloid differentiation requires the induction of CCAAT/enhancer-binding protein α (C/EBPα) and PU.1 expression. Expression of both genes was repressed by FLT3/ITD signaling in 32Dcl3 (32D) cells and this repression was overcome by treatment with a FLT3 inhibitor, allowing differentiation to proceed. We also observed increased expression of C/EBPα and PU.1 accompanied by signs of differentiation in 2 of 3 primary AML samples from patients with FLT3/ITD mutations receiving a FLT3 inhibitor, CEP-701, as part of a clinical trial. Forced expression of C/EBPα was also able to overcome FLT3/ITD-mediated differentiation block, further proving the importance of C/EBPα in this process.
Overexpression of IL-7Rα provides a competitive advantage during early T-cell development
Authors: Laouar Yasmina , Crispe I. Nicholas , Flavell Richard A. 
Published: November 2003

AbstractCritical checkpoints controlling early thymic T-cell development and homeostasis are set by the proper signaling function of the interleukin 7 receptor (IL-7R) and the pre–T-cell antigen receptor. Although αβ T-cell development is observed in IL-7– and IL-7Rα–deficient mice, the number of thymocytes is significantly reduced, implying a role for the IL-7R in controlling the size of the thymic T-cell compartment. Here, we report the overexpression of IL-7Rα that occurs in the early T-cell compartment from AKR/J mice, animals that are highly susceptible to the spontaneous development of thymoma. Increased IL-7Rα was revealed by surface staining, and increased IL-7Rα mRNA was documented by using reverse transcriptase–polymerase chain reaction (RT-PCR). This resulted in increased survival of AKR/J early thymocytes, shown by the decreased frequency of TUNEL+ (terminal deoxynucleotidyl transferase mediated deoxyuridine triphosphate [dUTP]–fluorescein nick end labeling) cells. In an in vivo thymocyte repopulation model, AKR/J thymocytes had a selective advantage over healthy thymocytes. This advantage occurred at early stages of T-cell development. Our findings support the model that overexpression of growth factor receptors can contribute to proliferation and malignancy.
Receptor synergy of interleukin-6 (IL-6) and insulin-like growth factor-I in myeloma cells that highly express IL-6 receptor α
Authors: Abroun Saeid , Ishikawa Hideaki , Tsuyama Naohiro , Liu Shangqin , Li Fu-Jun , Otsuyama Ken-ichiro , Zheng Xu , Obata Masanori , Kawano Michio M. 
Published: November 2003

AbstractInterleukin-6 (IL-6) is a growth and antiapoptotic factor for human myeloma cells. The autocrine loop and increased expression of the growth factor receptors have been postulated as the mechanisms of tumorigenesis. Here we show that IL-6 stimulation induced the phosphorylation of insulin-like growth factor-I (IGF-I) receptors in a human myeloma cell line, NOP2, highly expressing IL-6 receptor α (IL-6Rα) and in the IL-6Rα–transfected U266 cell line. IL-6–dependent complex formation of IL-6Rα with IGF-I receptor β was found in NOP2 where IL-6Rα colocalized with IGF-I receptors at lipid rafts. Moreover, the IL-6–induced phosphorylation of IGF-I receptor β was not blocked by a Janus kinase 2 (Jak2) inhibitor. In addition to the activation of the signal transducer and activator of transcription 3 and extracellular signal-regulated kinase 1/2, IL-6 stimulation led to the activation of Akt, presumably following the phosphorylation of IGF-I receptors. Thus, our results suggest that in NOP2, IL-6Rα and IGF-I receptors exist on the plasma membrane in close proximity, facilitating the efficient assembly of 2 receptors in response to IL-6. The synergistic effects of highly expressed IL-6Rα on IGF-I receptor–mediated signals provide a novel insight into the Jak-independent IL-6 signaling mechanism of receptor cross-talk in human myeloma cells.
Recombinant factor VIIa restores aggregation of αIIbβ3-deficient platelets via tissue factor–independent fibrin generation
Authors: Lisman Ton , Adelmeijer Jelle , Heijnen Harry F. G. , de Groot Philip G. 
Published: November 2003

AbstractRecombinant factor VIIa (rFVIIa) is a safe and effective prohemostatic drug for patients with Glanzmann thrombasthenia (GT). However, the mechanism of action of rFVIIa in these patients is still unclear. Although patients with GT are characterized by a complete absence of platelet aggregation to a variety of agonists, it has been shown that GT platelets are able to form aggregates, provided polymerizing fibrin is present. We studied the effect of rFVIIa-mediated fibrin formation on aggregation of αIIbβ3-deficient platelets. When washed platelets from GT patients or platelets from healthy volunteers treated with an arginyl-glycyl-aspartyl–containing peptide were activated with collagen in the presence of rFVIIa and purified coagulation factors X, II, and fibrinogen, complete aggregation occurred after a lag phase. Fibrin generation proceeded via rFVIIa-mediated thrombin generation on the activated platelet surface independently of tissue factor. Electron microscopic analysis of αIIbβ3-independent platelet aggregates showed a densely packed structure suggestive of a true platelet-fibrin interaction and not via trapping of platelets into a fibrin network. Also, rFVIIa-mediated αIIbβ3-independent aggregation was demonstrated under conditions of flow using a collagen-coated surface. In conclusion, the efficacy of rFVIIa in GT patients might be explained by induction of αIIbβ3-independent platelet aggregation, which compensates the lack of αIIbβ3-dependent aggregation.