bluuebunny/crossref_metadata_2025_split huggingface dataset:
RELIABILITY ANALYSIS AND SETTING RELIABILITY REQUIREMENTS BASED ON THE COST OF FAILURE
Authors: TODINOV M. T. 
Published: September 2004

A theoretical framework and models are proposed for reliability analysis and setting reliability requirements based on the cost of failure. It is demonstrated that a high availability target does not necessarily limit the risk of failure or minimize the total losses. The proposed models include: (i) models for determining the value from the reliability investment, (ii) optimization models for minimizing the total losses, (iii) models for limiting the risk of failure below a maximum acceptable level, (iv) a model for guaranteeing an availability target and (v) a model for guaranteeing a minimum failure-free operating interval before each random failure in a finite time interval. The models related to the value from the reliability investment can be used to determine the effect from reducing early-life failures on the financial revenue. On the basis of a counterexample it is demonstrated that altering the hazard rates of the components may lead to decreasing the probability of failure of the system and a simultaneous increase of the risk of failure, which shows that the cost-of-failure reliability analysis requires new reliability tools, different from the conventional tools. A new closed-form relationship has been derived related to reliability associated with an overstress failure mechanism. On its basis, a method for setting reliability requirements has been proposed, which limits the risk of impact failure within a maximum acceptable level. On the basis of counterexamples, it has also been demonstrated that for a load and strength not following a normal distribution, the standard reliability measures "reliability index" and "loading roughness" can be misleading. A new reliability integral has been proposed, based on integration performed only within the region of the upper tail of the load distribution and the lower tail of the strength distribution.
RECOGNITION OF SMILING FACES USING NEURAL NETWORKS AND SPCA
Authors: NAKANO MIYOKO , YASUKATA FUMIKO , FUKUMI MINORU 
Published: September 2004

Research on "man-machine interface" has increased in many fields of engineering and its application to facial expressions recognition is expected. The eigenface method by using the principal component analysis (PCA) is popular in this research field. However, it is not easy to compute eigenvectors with a large matrix if the cost of calculation when applying it for time-varying processing is taken into consideration. In this paper, in order to achieve high-speed PCA, the simple principal component analysis (SPCA) is applied to compress the dimensionality of portions that constitute a face. A value of cos θ is calculated using an eigenvector by SPCA as well as a gray-scale image vector of each picture pattern. By using neural networks (NNs), the difference in the value of cos θ between the true and the false (plastic) smiles is clarified and the true smile is discriminated. Finally, in order to show the effectiveness of the proposed face classification method for true or false smiles, computer simulations are done with real images. Furthermore, an experiment using the self-organisation map (SOM) is also conducted as a comparison.
Increased Expression of the DNA-Binding Cytokine HMGB1 in Human Atherosclerotic Lesions
Authors: Kalinina N. , Agrotis A. , Antropova Y. , DiVitto G. , Kanellakis P. , Kostolias G. , Ilyinskaya O. , Tararak E. , Bobik A. 
Published: September 2004

Objective—Atherosclerosis is a chronic inflammatory response of the arterial wall to injury. High-mobility group box 1 (HMGB1) is a DNA-binding protein, which on release from cells exhibits potent inflammatory actions. We examined its expression in atherosclerotic lesions and regulation by cytokines.Methods and Results—In atherosclerotic lesions, HMGB1 protein is expressed by endothelial cells, some intimal smooth muscle cells, and macrophages. As atherosclerosis develops and progresses from fatty streaks to fibrofatty lesion, the number of HMGB1-producing macrophages increases markedly. Studies using the THP-1 cell line indicated that HMGB1 mRNA expression could be markedly upregulated by inflammatory cytokines, interferon (IFN)-γ, tumor necrosis factor (TNF)-α and also transforming growth factor (TGF)-β. IFN-γ, TNF-α, TWEAK, and TGF-β induced an intracellular redistribution of HMGB1 and stimulated secretion by THP-1 cells and human blood monocytes. Inhibitors of MEK1/MEK2, protein kinase C, and PI-3/Akt, which inhibit lysosomal degranulation and mRNA translation, attenuated cytokine-induced HMGB1 secretion.Conclusions—Macrophage is the major cell type responsible for HMGB1 production in human atherosclerotic lesions. Inflammatory cytokines and TGF-β increase HMGB1 expression and secretion by monocyte/macrophages. HMGB1 appears to be a common mediator of inflammation induced by inflammatory cytokines and is likely to contribute to lesion progression and chronic inflammation.
Cortical Regions for Judgments of Emotions and Personality Traits from Point-light Walkers
Authors: Heberlein Andrea S. , Adolphs Ralph , Tranel Daniel , Damasio Hanna 
Published: September 2004

Abstract
Humans are able to use nonverbal behavior to make fast, reliable judgments of both emotional states and personality traits. Whereas a sizeable body of research has identified neural structures critical for emotion recognition, the neural substrates of personality trait attribution have not been explored in detail. In the present study, we investigated the neural systems involved in emotion and personality trait judgments. We used a type of visual stimulus that is known to convey both emotion and personality information, namely, point-light walkers. We compared the emotion and personality trait judgments made by subjects with brain damage to those made by neurologically normal subjects and then conducted a lesion overlap analysis to identify neural regions critical for these two tasks. Impairments on the two tasks dissociated: Some subjects were impaired at emotion recognition, but judged personality normally; other subjects were impaired on the personality task, but normal at emotion recognition. Moreover, these dissociations in performance were associated with damage to specific neural regions: Right somatosensory cortices were a primary focus of lesion overlap in subjects impaired on the emotion task, whereas left frontal opercular cortices were a primary focus of lesion overlap in subjects impaired on the personality task. These findings suggest that attributions of emotional states and personality traits are accomplished by partially dissociable neural systems.
Anticipating Words and Their Gender: An Event-related Brain Potential Study of Semantic Integration, Gender Expectancy, and Gender Agreement in Spanish Sentence Reading
Authors: Wicha Nicole Y. Y. , Moreno Eva M. , Kutas Marta 
Published: September 2004

Abstract
Recent studies indicate that the human brain attends to and uses grammatical gender cues during sentence comprehension. Here, we examine the nature and time course of the effect of gender on word-by-word sentence reading. Event related brain potentials were recorded to an article and noun, while native Spanish speakers read medium to high-constraint Spanish sentences for comprehension. The noun either fit the sentence meaning or not, and matched the preceding article in gender or not; in addition, the preceding article was either expected or unexpected based on prior sentence context. Semantically anomalous nouns elicited an N400. Gender disagreeing nouns elicited a posterior late positivity (P600), replicating previous findings for words. Gender agreement and semantic congruity interacted in both the N400 window—with a larger negativity frontally for double violations—and the P600 window—with a larger positivity for semantic anomalies, relative to the prestimulus baseline. Finally, unexpected articles elicited an enhanced positivity (500–700 msec post onset) relative to expected articles. Overall, our data indicate that readers anticipate and attend to the gender of both articles and nouns, and use gender in real time to maintain agreement and to build sentence meaning.
Deficits for Semantics and the Irregular Past Tense: A Causal Relationship?
Authors: Tyler Lorraine K. , Stamatakis Emmanuel A. , Jones Roy W. , Bright Peter , Acres Kadia , Marslen-Wilson William D. 
Published: September 2004

Abstract
The regular and irregular past tense has become a focus for recent debates about the structure of the language processing system, asking whether language functions are subserved by different neural and functional mechanisms or whether all processes can be accommodated within a single unified system. A critical claim of leading single mechanism accounts is that the relationship between an irregular stem and its past tense form is primarily semantic and not morphological in nature. This predicts an obligatory relationship between semantic performance and access to the irregular past tense, such that a semantic deficit necessarily leads to impairments on the irregulars. We tested this claim in a series of studies probing the comprehension and production of regular and irregular past tense forms in four semantic dementia patients, all of whom had profound semantic deficits. In two elicitation tasks and one auditory priming study, we found that three out of the four patients did not have a deficit for the irregular past tense, in spite of their semantic deficits. This argues against the view that the relationship between irregular past tense forms and their stems is primarily semantic, and more generally against the single system claim that morphological structure can be captured solely based on phonological and semantic relationships.
Competitive clonal hematopoiesis in mouse chimeras explained by a stochastic model of stem cell organization
Authors: Roeder Ingo , Kamminga Leonie M. , Braesel Katrin , Dontje Bert , de Haan Gerald , Loeffler Markus 
Published: September 2004

AbstractMany current experimental results show the necessity of new conceptual approaches to understand hematopoietic stem cell organization. Recently, we proposed a novel theoretical concept and a corresponding quantitative model based on microenvironment-dependent stem cell plasticity. The objective of our present work is to subject this model to an experimental test for the situation of chimeric hematopoiesis. Investigating clonal competition processes in DBA/2-C57BL/6 mouse chimeras, we observed biphasic chimerism development with initially increasing but long-term declining DBA/2 contribution. These experimental results were used to select the parameters of the mathematical model. To validate the model beyond this specific situation, we fixed the obtained parameter configuration to simulate further experimental settings comprising variations of transplanted DBA/2-C57BL/6 proportions, secondary transplantations, and perturbation of stabilized chimeras by cytokine and cytotoxic treatment. We show that the proposed model is able to consistently describe the situation of chimeric hematopoiesis. Our results strongly support the view that the relative growth advantage of strain-specific stem cells is not a fixed cellular property but is sensitively dependent on the actual state of the entire system. We conclude that hematopoietic stem cell organization should be understood as a flexible, self-organized rather than a fixed, preprogrammed process.
Circulating endothelial cells, von Willebrand factor, interleukin-6, and prognosis in patients with acute coronary syndromes
Authors: Lee Kaeng W. , Lip Gregory Y. H. , Tayebjee Muzahir , Foster William , Blann Andrew D. 
Published: September 2004

AbstractMarkers of inflammation (eg, interleukin-6 [IL-6]), and endothelial perturbation (von Willebrand factor [VWF], circulating endothelial cells [CECs]) are altered in acute coronary syndromes (ACS). We hypothesized that CECs and IL-6 levels during the first 48 hours of ACS would predict 30-day and 1-year major cardiovascular end points (MACE). A total of 156 patients with ACS were included. Blood was drawn on admission (baseline) and 48 hours later for plasma VWF, IL-6 (both enzyme-linked immunosorbent assay [ELISA]), and CECs (CD146 immunomagnetic separation). CEC phenotyping was performed by indirect immunoperoxidase staining. At 30 days, 48 patients had a MACE, a predicted by baseline and 48-hour CECs and IL-6 levels, 48-hour VWF levels, and by the “admission–48 hour change” (Δ) in CECs, VWF, and IL-6 (all P = .002). On multivariate analysis, 48-hour CECs (P &lt; .001) were the strongest predictor of MACE, followed by ΔIL-6 (P = .01) and ΔVWF (P = .048); 48-hour CECs were the only predictor of death (P = .007). At 1 year, 65 patients had MACE, predicted by 48-hour CECs and ΔIL-6 levels (P &lt; .001); age (P = .046) and 48-hour CECs (P &lt; .001) were the only predictors of death. CECs stained 93% positive for endothelial nitric oxide synthase (eNOS) but were less than 1% positive for CD34, CD36, and CD45 and less than 3% for CD31. Like raised VWF, abnormal CECs and IL-6 levels during the first 48 hours of ACS were strongly associated with 30-day MACE. CECs at 48 hours were the only independent predictor of both death and MACE at 30 days and 1 year, indicating the crucial role of endothelial/vascular damage in ACS pathophysiology.
HCV quasispecies evolution: association with progression to end-stage liver disease in hemophiliacs infected with HCV or HCV/HIV
Authors: Qin Hongxing , Shire Norah J. , Keenan Erica D. , Rouster Susan D. , Eyster M. Elaine , Goedert James J. , Koziel Margaret James , Sherman Kenneth E. ,   and the Multicenter Hemophilia Cohort Study Group
Published: September 2004

AbstractPatients with inherited bleeding disorders who received clotting factor concentrates before 1987 have high rates of hepatitis C virus (HCV) or HCV/HIV infection. We evaluated HCV quasispecies evolution in longitudinally collected specimens comparing those from patients with progression to end-stage liver disease (ESLD; cases) to those with compensated chronic hepatitis (controls). Plasma samples were obtained from the National Cancer Institute Multicenter Hemophilia Cohort Study. Controls were matched for age, sex, infection duration, and presence/absence of HIV. Samples from early infection were compared to those obtained after onset of ESLD in the cases. The first hypervariable (HVR1) and core proteincoding regions were amplified, subcloned, and sequenced. Complexity and diversity were determined. More than 700 sub-clones from 10 pairs of patients (8 with HIV) followed over approximately 9.3 years were evaluated. HVR1 complexity narrowed over time in the cases, whereas it increased in controls (P = .01). Similar trends were observed for diversity within HVR1 and the core region (P = .04). HCV-infected patients with inherited bleeding disorders undergo quasispecies evolution over time. Evolution patterns differ for progressors and nonprogressors. Further understanding of these mechanisms may help identify factors related to progression rate and treatment response.
Human embryonic stem cell–derived CD34+ cells: efficient production in the coculture with OP9 stromal cells and analysis of lymphohematopoietic potential
Authors: Vodyanik Maxim A. , Bork Jack A. , Thomson James A. , Slukvin Igor I. 
Published: September 2004

AbstractEmbryonic stem (ES) cells have the potential to serve as an alternative source of hematopoietic precursors for transplantation and for the study of hematopoietic cell development. Using coculture of human ES (hES) cells with OP9 bone marrow stromal cells, we were able to obtain up to 20% of CD34+ cells and isolate up to 107 CD34+ cells with more than 95% purity from a similar number of initially plated hES cells after 8 to 9 days of culture. The hES cell–derived CD34+ cells were highly enriched in colony-forming cells, cells expressing hematopoiesis-associated genes GATA-1, GATA-2, SCL/TAL1, and Flk-1, and retained clonogenic potential after in vitro expansion. CD34+ cells displayed the phenotype of primitive hematopoietic progenitors as defined by co-expression of CD90, CD117, and CD164, along with a lack of CD38 expression and contained aldehyde dehydrogenase–positive cells as well as cells with verapamil-sensitive ability to efflux rhodamine 123. When cultured on MS-5 stromal cells in the presence of stem cell factor, Flt3-L, interleukin 7 (IL-7), and IL-3, isolated CD34+ cells differentiated into lymphoid (B and natural killer cells) as well as myeloid (macrophages and granulocytes) lineages. These data indicate that CD34+ cells generated through hES/OP9 coculture display several features of definitive hematopoietic stem cells.
Induction of BCR-ABL–specific immunity following vaccination with chaperone-rich cell lysates derived from BCR-ABL+ tumor cells
Authors: Zeng Yi , Graner Michael W. , Thompson Sylvia , Marron Marilyn , Katsanis Emmanuel 
Published: September 2004

AbstractWe have previously reported that chaperonerich cell lysates (CRCL) derived from the BCR-ABL+ 12B1 leukemia activate dendritic cells (DCs) and stimulate leukemia-specific immune responses. Because CRCL contain a variety of heat shock/chaperone proteins, we theorized that CRCL obtained from BCR-ABL+ leukemias are likely to chaperone BCR-ABL–derived fusion peptides and that DCs pulsed with 12B1 CRCL could cross-present BCR-ABL fusion peptides to T cells. We found that splenocytes from mice vaccinated with BCR-ABL+ leukemia-derived CRCL secreted interferon-γ (IFN-γ) when restimulated with a BCR-ABL peptide, GFKQSSKAL, indicating that BCR-ABL peptides are chaperoned by leukemia-derived CRCL. We next eluted peptides from 12B1 leukemia-derived CRCL and used high-pressure liquid chromatography (HPLC) fractions to restimulate splenocytes harvested from mice vaccinated with DC/GFKQSSKAL or DC/12B1 CRCL. We found that the same peptide fractions derived from 12B1 CRCL and from “refractionated” GFKQSSKAL stimulated IFN-γ production, suggesting the presence of BCR-ABL peptides in the peptide repertoire of 12B1 CRCL. We also demonstrated that immunization with DCs loaded with leukemia-derived CRCL induced BCR-ABL–specific cytotoxic T lymphocytes (CTLs) in vivo. Moreover, mice immunized with DCs pulsed with 12B1-derived CRCL had superior survival (60%) when compared with those immunized with DCs pulsed with BCR-ABL peptide (20%), indicating that CRCL vaccines provide additional immune stimulus over and above individual peptide vaccination.
Donor CD8+ T cells facilitate induction of chimerism and tolerance without GVHD in autoimmune NOD mice conditioned with anti-CD3 mAb
Authors: Liang Yaming , Huang Tammy , Zhang Chunyan , Todorov Ivan , Atkinson Mark , Kandeel Fouad , Forman Stephen , Zeng Defu 
Published: September 2004

AbstractPrevention of autoimmune diabetes and induction of islet transplantation tolerance in nonobese diabetic (NOD) mice can be reached by induction of mixed chimerism via bone marrow transplantation (BMT), but this procedure requires total body irradiation (TBI) conditioning of the recipients. The toxicity of radiation and potential for graft-versus-host disease (GVHD) prevents its clinical application. Donor CD8+ T cells play a critical role in facilitation of engraftment but also contribute to induction of GVHD in TBI-conditioned recipients. Here, we showed that high doses of donor CD8+ T cells in combination with bone marrow (BM) cells induced mixed chimerism without GVHD in NOD recipients conditioned with anti-CD3 monoclonal antibody (mAb). The prevention of GVHD in those recipients was associated with low-level production of inflammatory cytokines (ie, tumor necrosis factor α [TNF-α]), high-level production of anti-inflammatory cytokines (ie, interleukin 4 [IL-4] and IL-10), and confining of the donor CD8+ T-cell expansion to lymphohematopoietic tissues. The chimeric NOD recipients showed donor-specific tolerance and reversal of insulitis. These results demonstrate that donor CD8+ T-cell–mediated facilitation of engraftment can be separated from GVHD in nonirradiated recipients. This regimen may have potential application in the treatment of autoimmune disorders as well as induction of transplantation tolerance.
High-resolution tracking of cell division demonstrates differential effects of TH1 and TH2 cytokines on SCF-dependent human mast cell production in vitro:correlation with apoptosis and Kit expression
Authors: Kulka Marianna , Metcalfe Dean D. 
Published: September 2004

AbstractT-helper 1 (TH1) (interferon-γ [IFN-γ]) and TH2 (interleukin-4 [IL-4] and IL-5) cytokines have been variably reported to alter human mast cell numbers in complex culture systems. The effects of these cytokines on the kinetics of cell division and cell death are unknown, and their effect on mast cell behavior is relevant to anticipate the consequences of in vivo strategies that alter cytokine levels. To determine the effect of these cytokines on stem cell factor (SCF)–dependent human mast cell production, we used highresolution tracking of cell division and correlated the results with cell apoptosis, expression of Kit, and mast cell degranulation. When IFN-γ, IL-5, or IL-4 was administered over 8 weeks, we found each cytokine decreased the mast number through a different mechanism. IFN-γ inhibited early progenitor cell division, IL-4 down-regulated early Kit expression, and IL-5 blocked later cell division. Further, IL-4 and IFN-γ had the greatest suppressive effect on degranulation and FcϵRI expression. When these cytokines were administered to mature mast cells, IFN-γ and IL-5 had no effect on degranulation and cell division, but IL-4 induced division and potentiated FcϵRI-mediated degranulation. Thus, exposure of human mast cells to IL-4, IL-5, and IFN-γ during growth and differentiation generally down-regulated mast cell number and function, whereas IL-4 increased mature mast cell division and degranulation.
Proinflammatory role of inducible nitric oxide synthase in acute hyperoxic lung injury
Authors: Hesse Anne-Karin , Dörger Martina , Kupatt Christian , Krombach Fritz 
Published: September 2004

Abstract
Background
Hyperoxic exposures are often found in clinical settings of respiratory insufficient patients, although oxygen therapy (>50% O2) can result in the development of acute hyperoxic lung injury within a few days. Upon hyperoxic exposure, the inducible nitric oxide synthase (iNOS) is activated by a variety of proinflammatory cytokines both in vitro and in vivo. In the present study, we used a murine hyperoxic model to evaluate the effects of iNOS deficiency on the inflammatory response.

Methods
Wild-type and iNOS-deficient mice were exposed to normoxia, 60% O2 or >95% O2 for 72 h.

Results
Exposure to >95% O2 resulted in an increased iNOS mRNA and protein expression in the lungs from wild-type mice. No significant effects of iNOS deficiency on cell differential in bronchoalveolar lavage fluid were observed. However, hyperoxia induced a significant increase in total cell count, protein concentration, LDH activity, lipid peroxidation, and TNF-α concentration in the bronchoalveolar lavage fluid compared to iNOS knockout mice. Moreover, binding activity of NF-κB and AP-1 appeared to be higher in wild-type than in iNOS-deficient mice.

Conclusion
Taken together, our results provide evidence to suggest that iNOS plays a proinflammatory role in acute hyperoxic lung injury.