bluuebunny/crossref_metadata_2025_split huggingface dataset:
Die Aufmerksamkeitsleistungen von 6-10-jährigen Kindern in der TAP
Authors: Földényi Monika , Tagwerker-Neuenschwander Friederike , Giovanoli Anna , Schallberger Urs , Steinhausen Hans-Christoph 
Published: April 2003

Attentional Performance of 6-10-Year-Old Children on the TAP Abstract: The aim of the study was to establish norms for the Attention Test Battery (TAP) for children aged 6 to 10. The effects of the age, gender and computer experience of the children were analyzed and order effects were investigated. The factor structure of the test results was explored. The sample was comprised of 79 girls and 71 boys. In most of the subtests, older children showed a nonspecific reduction of their reaction times and a specific improvement in their controlled information processing abilities compared with the younger children. In some subtests, gender effects were found: Boys had faster reaction times, and made more errors. These results are compatible with the well known differences between boys and girs in the early school years in the development of attention. Therefore, it would make sense to establish separate norms for boys and girls. Computer experience had no effect on the test results of the children. The factore analysis provided evidence that it is possible even in children to differenciate between various aspects of attention. The test results showed order effects. Therefore it would be important to conduct the subtests in a standardized order.
Neutrophils Induce Sequential Focal Changes in Endothelial Adherens Junction Components: Role of Elastase
Authors: Ionescu Carmen V. , Cepinskas Gediminas , Savickiene Jurate , Sandig Martin , Kvietys Peter R. 
Published: April 2003

Objective: In vitro studies have indicated that polymorphonuclear leukocytes (PMNs) traverse endothelial cell monolayers via the paracellular pathway (i.e., through endothelial cell–cell junctions. Herein, we assessed whether the adherens junctions (AJs) are disrupted during PMN transendothelial cell migration.Methods: Human umbilical vein endothelial cells (HUVECs) were grown to confluence on porous membranes and activated with interleukin‐1β, and PMN transendothelial migration was facilitated by formyl‐methionyl‐leucylphenylalanine. Using dual immunofluorescence staining and laser scanning confocal microscopy, we assessed the effects of PMN‐endothelial cell adhesive interactions (i.e., adhesion to and emigration across monolayers) on the AJ components vascular endothelial (VE)‐cadherin, β‐catenin, α‐catenin, and γ‐catenin.Results: In the AJ immediately adjacent to the adherent PMN, there was a loss of staining for some of the AJ components. AJ components further away from HUVEC‐PMN adhesive interactions were unaffected. An iterative approach indicated that the four components were sequentially lost from the AJ. β‐catenin was lost first, followed by VE‐cadherin, α‐catenin, and, finally, γ‐catenin. In the absence of PMNs, the cross‐linking of VE‐cadherin, but not platelet endothelial cell adhesion molecule‐1 or intercellular adhesion molecule‐1, increased the cytoplasmic accumulation of β‐catenin. During PMN transendothelial migration, all of the junctional components under study were lost at the immediate site of monolayer penetration. Again, at regions removed from the actual site of PMN penetration of the monolayers, the AJ components were unaffected. PMN‐induced disorganization of the AJs was partially prevented by an elastase inhibitor.Conclusions: These findings suggest that adherent PMNs induce a localized, sequential disassembly of AJs, which is partially mediated by PMN‐derived elastase and involves the initial loss of an intracellular component of AJs (i.e., β‐catenin).
PARALLEL PREDICTOR-CORRECTOR METHODS FOR THE SOLUTION OF ORDINARY DIFFERENTIAL EQUATIONS II
Authors: MAZZONE A. M. 
Published: April 2003

This work presents parallel multistep methods for the solution of ordinary differential equations. The characteristic of parallel computing is that there is a "front" and the computation at points ahead of the front depends only on information behind it. This requires a resetting of serial algorithms and may also lead to numerical errors and instabilities. The analysis of positive and negative aspects of parallel computing is the subject of this paper. Some of the methods presented below are uncommon in the literature on mathematical computing. Others have been elaborated for this study on the basis of the traditional Adams-Bashforth multistep methods. A performance comparison of the methods is made by numerical testing in molecular dynamics calculations. The increase of the number of processors m appears to seriously deteriorate the stability of the calculations and the use of m larger than 2 seems impractical.
SIMPLE QUEUEING MODEL APPLIED TO THE CITY OF PORTLAND
Authors: SIMON PATRICE M. , ESSER JÖRG , NAGEL KAI 
Published: April 2003

We use a simple traffic micro-simulation model based on queueing dynamics as introduced by Gawron [IJMPC, 9(3):393, 1998] in order to simulate traffic in Portland/Oregon. Links have a flow capacity, that is, they do not release more vehicles per second than is possible according to their capacity. This leads to queue built-up if demand exceeds capacity. Links also have a storage capacity, which means that once a link is full, vehicles that want to enter the link need to wait. This leads to queue spill-back through the network. The model is compatible with route-plan-based approaches such as TRANSIMS, where each vehicle attempts to follow its pre-computed path. Yet, both the data requirements and the computational requirements are considerably lower than for the full TRANSIMS microsimulation. Indeed, the model uses standard emme/2 network data, and runs about eight times faster than real time with more than 100 000 vehicles simultaneously in the simulation on a single Pentium-type CPU. We derive the model's fundamental diagrams and explain it. The simulation is used to simulate traffic on the emme/2 network of the Portland (Oregon) metropolitan region (20 000 links). Demand is generated by a simplified home-to-work destination assignment which generates about half a million trips for the morning peak. Route assignment is done by iterative feedback between micro-simulation and router. An iterative solution of the route assignment for the above problem can be achieved within about half a day of computing time on a desktop workstation. We compare results with field data and with results of traditional assignment runs by the Portland Metropolitan Planning Organization. Thus, with a model such as this one, it is possible to use a dynamic, activities-based approach to transportation simulation (such as in TRANSIMS) with affordable data and hardware. This should enable systematic research about the coupling of demand generation, route assignment, and micro-simulation output.
VISUALIZING ANIMATION DATABASES
Authors: AKANKSHA  , HUANG Z. , PRABHAKARAN B. , RUIZ C. R. 
Published: April 2003

We consider a repository of animation models and motions that can be reused to generate new animation sequences. For instance, a user can retrieve an animation of a dog kicking its leg (in air) and manipulate the result to generate a new animation where the dog is kicking a ball. In this particular example, inverse kinematics technique can be used to retarget the kicking motion of a dog to a ball. This approach of reusing models and motions to generate new animation sequences can be facilitated by operations such as querying of animation databases for required models and motions, and manipulation of the query results to meet new constraints. However, manipulation operations such as motion retargeting are quite complex in nature. Hence, there is a need for visualizing the queries on animation databases as well as the manipulation operations on the query results. In this paper, we propose a visually interactive method for reusing motions and models, by adjusting the query results from animation databases for new situations while at the same time, keeping the desired properties of the original models and motions. Here, a user first queries for animation objects, i.e., geometric models and motions. Then, the user interactively makes new animations by visually manipulating the query results. Depending on the orders in which the GUIs (Graphical User Interfaces) are invoked and the parameters are changed, the system automatically generates a sequence of operations, a list of SQL-like syntax commands, and applies it to the query results of motions and models. With the help of visualization tools, the user can view the changes before accepting them.
Reaction Stereochemistry of 2-Deoxy-scyllo-inosose Synthase, the Key Enzyme in the Biosynthesis of 2-Deoxystreptamine
Authors: Nango Eriko , Kudo Fumitaka , Eguchi Tadashi , Kakinuma Katsumi 
Published: April 2003

Abstract
The reaction stereochemistry of 2-deoxy-scyllo-inosose (DOI) synthase (DOIS) derived from butirosin-producing Bacillus circulans, the key starter enzyme of 2-deoxystreptamine biosynthesis, was closely analyzed by use of the purified recombinant DOIS. The stereochemical pathway of the DOIS reaction is common in the aminoglycoside-producing Bacillus and Streptomyces, but is distinct from a related dehydroquinate synthase reaction in the shikimate pathway. Evolutionary relationship between these enzymes is also discussed.
Prevalence of birth defects among infants of Gulf War veterans in Arkansas, Arizona, California, Georgia, Hawaii, and Iowa, 1989–1993
Authors: G. Araneta Maria Rosario , Schlangen Karen M. , Edmonds Larry D. , Destiche Daniel A. , Merz Ruth D. , Hobbs Charlotte A. , Flood Timothy J. , Harris John A. , Krishnamurti Diane , Gray Gregory C. 
Published: April 2003

AbstractBACKGROUNDEpidemiologic studies of birth defects among infants of Gulf War veterans (GWV) have been limited to military hospitals, anomalies diagnosed among newborns, or self‐reported data. This study was conducted to measure the prevalence of birth defects among infants of GWVs and nondeployed veterans (NDV) in states that conducted active case ascertainment of birth defects between 1989–93.METHODSMilitary records of 684,645 GWVs and 1,587,102 NDVs were electronically linked with 2,314,908 birth certificates from Arizona, Hawaii, Iowa, and selected counties of Arkansas, California, and Georgia; 11,961 GWV infants and 33,052 NDV infants were identified. Of these, 450 infants had mothers who served in the Gulf War, and 3966 had NDV mothers.RESULTSInfants conceived postwar to male GWVs had significantly higher prevalence of tricuspid valve insufficiency (relative risk [RR], 2.7; 95% confidence interval [CI], 1.1–6.6; p = 0.039) and aortic valve stenosis (RR, 6.0; 95% CI, 1.2–31.0; p = 0.026) compared to infants conceived postwar to NDV males. Among infants of male GWVs, aortic valve stenosis (RR, 16.3; 95% CI, 0.09–294; p = 0.011) and renal agenesis or hypoplasia (RR, 16.3; 95% CI, 0.09–294; p = 0.011) were significantly higher among infants conceived postwar than prewar. Hypospadias was significantly higher among infant sons conceived postwar to GWV women compared to NDV women (RR, 6.3; 95% CI, 1.5–26.3; p = 0.015).CONCLUSIONWe observed a higher prevalence of tricuspid valve insufficiency, aortic valve stenosis, and renal agenesis or hypoplasia among infants conceived postwar to GWV men, and a higher prevalence of hypospadias among infants conceived postwar to female GWVs. We did not have the ability to determine if the excess was caused by inherited or environmental factors, or was due to chance because of myriad reasons, including multiple comparisons. Although the statistical power was sufficient to compare the combined birth defects prevalence, larger sample sizes were needed for less frequent individual component defects. Birth Defects Research (Part A) 67:246–260, 2003. Published 2003 Wiley‐Liss, Inc.
Zinc treatment prevents lipopolysaccharide‐induced teratogenicity in mice
Authors: Carey Luke C. , Berbée Paulien L. , Coyle Peter , Philcox Jeffrey C. , Rofe Allan M. 
Published: April 2003

AbstractBackgroundDuring pregnancy, exposure to lipopolysaccharide (LPS) can lead to abortion, preterm delivery, and teratogenicity. The mechanisms underlying these effects are unclear. Both LPS and ethanol are potent inducers of liver metallothionein (MT), a key Zn binding protein. The teratogenic effects of ethanol have been linked to MT‐induced changes in maternal‐fetal Zn homeostasis, leading to fetal deficiency. This study was designed to assess whether the teratogenic effects of LPS are also related to MT induction and changes in Zn homeostasis.METHODSNon‐pregnant normal (MT+/+) and MT‐null (MT−/−) mice were injected subcutaneously with 0.5 μg/gm LPS and killed over 48 hr. In MT+/+ mice, liver MT concentrations were elevated from 6 hr, and were maximal at 24 hr (30‐fold basal), whereas liver Zn levels were also increased from 6 hr. Plasma Zn concentrations decreased by 80% at 6 hr, and were below normal between 6 and 24 hr. In MT−/− mice, plasma Zn levels were increased from basal between 6 and 16 hr. Dams were injected with LPS, saline, or LPS and ZnSO4 (2 μg/gm, MT+/+ only) on Day 8 of gestation (GD8), killed on GD18, and the fetuses examined for malformations.RESULTSExternal abnormalities were most prevalent in fetuses from MT+/+ dams exposed to LPS, where 34% of fetuses in each litter were affected. MT+/+ dams treated with LPS and ZnSO4, and MT−/− dams treated with LPS had litters in which 5.4 and 4.8% of fetuses were abnormal respectively.CONCLUSIONSThe findings of this study strongly support the hypothesis that LPS teratogenicity is mediated at least in part by MT‐induced changes in maternal Zn homeostasis, which compromises fetal Zn supply. Birth Defects Research (Part A) 67:240–245, 2003. © 2003 Wiley‐Liss, Inc.
Population‐based study of congenital diaphragmatic hernia: Risk factors and survival in metropolitan Atlanta, 1968–1999
Authors: Dott Mary M. , Wong Lee‐Yang C. , Rasmussen Sonja A. 
Published: April 2003

AbstractBACKGROUNDCongenital diaphragmatic hernia affects about 1000 United States infants a year. In most cases, the etiology of this condition is unknown. Treatment strategies have changed in recent years. We sought to calculate the birth prevalence, determine risk factors, examine associated defects, and assess trends in survival.METHODSWe conducted a population‐based cohort study of all infants born during 1968–99 whose mothers resided in the five‐county metropolitan Atlanta area (n = 1,029,143). Infants with congenital diaphragmatic hernia were identified using the Metropolitan Atlanta Congenital Defects Program. To document vital status, we used data from hospital records, Georgia vital records, and the National Death Index.RESULTSThe birth prevalence of congenital diaphragmatic hernia was 2.4 per 10,000 births. Infants with isolated congenital diaphragmatic hernia were more likely to be premature, macrosomic, and male than their birth cohort. About one‐third of affected infants had additional major defects. Of infants with congenital diaphragmatic hernia, 8% had known syndromes, most commonly chromosomal abnormalities. During the study period, the percentage of infants with congenital diaphragmatic hernia who survived to 1 year of age increased from 19% (1968–71) to about 54% (1996–99). During the last 10 years of the study, infants who were of low birth weight, had a syndrome, or were prenatally diagnosed were more likely to die than other infants with congenital diaphragmatic hernia.CONCLUSIONSDespite new treatments, the death rate from congenital diaphragmatic hernia remains substantial, highlighting the need to identify mechanisms for primary prevention. Birth Defects Research (Part A) 67:261–267, 2003. Published 2003 Wiley‐Liss, Inc.
Asymmetry in first‐price auctions with affiliated private values
Authors: Campo Sandra , Perrigne Isabelle , Vuong Quang 
Published: April 2003

AbstractCollusion and heterogeneity across firms may introduce asymmetry in bidding games. A major difficulty in asymmetric auctions is that the Bayesian Nash equilibrium strategies are solutions of an intractable system of differential equations. We propose a simple method for estimating asymmetric first‐price auctions with affiliated private values. Considering two types of bidders, we show that these differential equations can be rewritten using the observed bid distribution. We establish the identification of the model, characterize its theoretical restrictions, and propose a two‐step non‐parametric estimation procedure for estimating the private value distributions. An empirical analysis of joint bidding in OCS auctions is provided. Copyright © 2003 John Wiley & Sons, Ltd.
Why “auditing” is a dirty word
Authors: Noland Thomas G. 
Published: April 2003

AbstractBecause of recent corporate scandals, “auditing” is held in low esteem by the public. However,
auditing has also become a “dirty word” for large accounting firms—who are offering profitable
new services at the expense of quality audits. But are there other reasons audit quality has plummeted?
© 2003 Wiley Periodicals, Inc.
Dual effect of lysine‐rich polypeptides on the activity of protein kinase CK2
Authors: Romero‐Oliva Francisco , Jacob Germaine , Allende Jorge E. 
Published: April 2003

AbstractProtein kinase CK2 (casein kinase II) is normally a heterotetramer composed of catalytic (α, α′) and regulatory subunits (β). CK2 is able to phosphorylate a large number of protein substrates but the physiological mechanisms of its regulation are still unresolved. Lysine‐rich peptides such as polylysine and histone H1 are known to stimulate the catalytic activity of the holoenzyme. This activation is mediated through the CK2β regulatory subunit. In this communication, we report that the same concentrations of lysine‐rich peptides or proteins that activate the holoenzyme cause strong inhibition of the phosphorylation of proteins catalyzed by the free catalytic CK2α subunit. The inhibitory effect of polylysine and histone H1 is observed with several protein substrates of CK2α (casein, adeno E1A, transcription factor II A, and CK2β itself). With calmodulin, however, the inhibition of CK2α phosphorylation caused by polylysine is much lower while with a model peptide substrate of CK2 the inhibition caused by this polycation is negligible. The inhibition of CK2α by polylysine is observed only at limiting concentrations of the target substrate proteins. The dual effect of polylysine and of histone H1, which results in the inhibition of CK2α and stimulation of the CK2 α2β2 tetrameric holoenzyme, has the consequence that the addition of the CK2β, in the presence of polylysine and low concentrations of substrate protein, can cause a 242‐fold stimulation of the activity of CK2α. Other polycationic compounds such as polyarginine and spermine do not inhibit the phosphorylation of casein by CK2α, indicating that the effect is specific for lysine‐rich peptides. Since there is evidence that there may be free CK2α subunits in the nuclei of cells, where there is abundant histone H1, the inhibition of CK2α by this lysine‐rich protein may have physiological relevance. J. Cell. Biochem. 89: 348–355, 2003. © 2003 Wiley‐Liss, Inc.
Mitochondrial and microsomal derived reactive oxygen species mediate apoptosis induced by transforming growth factor‐β1 in immortalized rat hepatocytes
Authors: Albright Craig D. , Salganik Rudolf I. , Craciunescu Corneliu N. , Mar Mei‐Heng , Zeisel Steven H. 
Published: April 2003

AbstractTransforming growth factor‐β1 (TGFβ1) is a multifunctional cytokine that is over expressed during liver hepatocytes injury and regeneration. SV40‐transformed CWSV‐1 rat hepatocytes that are p53‐defective undergo apoptosis in response to choline deficiency (CD) or TGFβ1, which mediates CD‐apoptosis. Reactive oxygen species (ROS) are essential mediators of apoptosis. We have shown that apoptosis induced by TGFβ1 is accompanied by ROS generation and the ROS‐trapping agent N‐acetylcysteine (NAC) inhibits TGFβ1‐induced apoptosis. While persistent induction of ROS contributes to this form of apoptosis, the source of ROS generated downstream of TGFβ1 is not clear. The mitochondria and the endoplasmic reticulum both harbor potent electron transfer chains that might be the source of ROS essential for completion of TGFβ1‐apoptosis. Here we show that CWSV‐1 cells treated with cyclosporine A, which prevents opening of mitochondrial membrane pores required for ROS generation, inhibits TGFβ1‐induced apoptosis. A similar effect was obtained by treating these cells with rotenone, an inhibitor of complex 1 of the mitochondrial electron transfer chain. However, we demonstrate that TGFβ1 induces cytochrome P450 1A1 and that metyrapone, a potent inhibitor of cytochrome P450 1A1, inhibits TGFβ1‐induced apoptosis. Therefore, our studies indicate that concurrent with promoting generation of ROS from mitochondria, TGFβ1 also promotes generation of ROS from the cytochrome P450 electron transfer chain. Since inhibition of either of these two sources of ROS interferes with apoptosis, it is reasonable to conclude that the combined involvement of both pathways is essential for completion of TGFβ1‐induced apoptosis. J. Cell. Biochem. 89: 254–261, 2003. © 2003 Wiley‐Liss, Inc.
Interferon‐γ induces reactive oxygen species and endoplasmic reticulum stress at the hepatic apoptosis
Authors: Watanabe Yoshifumi , Suzuki Osamu , Haruyama Takahiro , Akaike Toshihiro 
Published: April 2003

AbstractInterferon‐γ (IFN‐γ) induces cell‐cycle arrest and p53‐independent apoptosis in primary cultured hepatocytes. However, the detailed mechanism, including regulating molecules, is still unclear. In this study, we found that IFN‐γ induced generation of reactive oxygen species (ROS) in primary hepatocytes and that pyrrolidinedithiocarbamate (PDTC), an anti‐oxidant reagent, completely suppressed IFN‐γ‐induced hepatic apoptosis. PDTC blocked apoptosis downstream from IRF‐1 and upstream from caspase activation, suggesting that the generation of ROS occurred between these stages. However, IFN‐γ also induced the generation of ROS in IRF‐1‐deficient hepatocytes, cells insensitive to IFN‐γ‐induced apoptosis. Moreover, a general cyclooxygenase (COX) inhibitor, indomethacin (but not the cyclooxygenase 2‐specific inhibitor, NS‐398) also inhibited the apoptosis without blocking the generation of ROS. Both PDTC and indomethacin also blocked IFN‐γ‐induced release of cytochrome c from mitochondria. These results suggest that ROS are not the only or sufficient mediators of IFN‐γ‐induced hepatic apoptosis. In contrast, we also found that IFN‐γ induced endoplasmic reticulum (ER) stress proteins, CHOP/GADD153 and caspase 12, in wild‐type primary hepatocytes, but induced only caspase 12 and not CHOP/GADD153 protein in IRF‐1‐deficient hepatocytes. These results suggest that IFN‐γ induces ER stress in primary hepatocytes. Both the ROS and ER stress induced by IFN‐γ may be complementary mediators that induce apoptosis in primary hepatocytes. J. Cell. Biochem. 89: 244–253, 2003. © 2003 Wiley‐Liss, Inc.