bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effects of high‐frequency electromagnetic fields on DNA strand breaks using comet assay method
Authors: Miyakoshi Junji , Yoshida Masami , Tarusawa Yosiaki , Nojima Toshio , Wake Kanako , Taki Masao 
Published: October 2002

AbstractWe investigated whether exposure to high‐frequency electromagnetic fields causes DNA damage in cells, using the alkaline comet assay. The exposure device made for this study used a TE01 circular waveguide operating at a frequency of 2.45 GHz. Cells of the human brain tumor‐derived MO54 cell line were exposed to an electromagnetic field (input power: 7.8 W, average SAR in the middle well of an annular culture plate: CW 50 W/kg) for 2 hours and the tail moments of the cells in the inner, middle, and outer wells of the plate were compared with those of sham‐exposed cells. There was no significant difference between the high‐frequency electromagnetic field‐exposed groups and the sham‐exposed groups. Three studies performed under the same conditions gave similar results. Next, cells were exposed to a stronger electromagnetic field (input power: 13 W, average SAR in the middle well: CW 100 W/kg) for 2 hours and compared with sham‐exposed cells. There was also no significant difference in the tail moments of cells in the inner, middle, and outer wells of the plate in the high‐frequency electromagnetic field‐exposed groups and the sham‐exposed groups. These findings suggest that a high‐frequency electromagnetic field does not cause direct DNA damage, and does not induce DNA strand breaks, even at a SAR of 100 W/kg. © 2002 Wiley Periodicals, Inc. Electr Eng Jpn, 141(4): 9–15, 2002; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/eej.10075
Genotoxic risk and oxidative DNA damage in workers exposed to antimony trioxide
Authors: Cavallo Delia , Iavicoli Ivo , Setini Andrea , Marinaccio Alessandro , Perniconi Barbara , Carelli Giovanni , Iavicoli Sergio 
Published: October 2002

AbstractThe growing use of antimony (Sb) compounds in industry and the consequent increase in the number of exposed workers make it important to carry out a health risk assessment. The main goal of this study was to assess the genotoxicity of Sb2O3 in occupationally exposed workers. Genotoxicity was evaluated by the sister chromatid exchange (SCE) and micronucleus tests, and the enzyme (Fpg)‐modified comet assay. In addition, antimony exposure levels were established by environmental monitoring with personal air samplers. We studied 23 male workers assigned to different fire retardant treatment tasks in the car upholstery industry and a control group of 23 healthy nonexposed males. The exposed workers were divided into two groups on the basis of their tasks and the work cycle: Group A comprised finishing and intermediate inspection operators who directly handled a mixture containing Sb2O3; Group B were jet operators, not directly exposed to the compound. Environmental monitoring detected low Sb exposure levels but significant differences between the two groups, with Group A having the higher exposure level. Cytogenetic analyses showed no difference between exposed workers and controls for micronuclei and SCE. The enzyme‐modified comet assay showed a probable relation between moderate levels of oxidative DNA damage and exposure to antimony, with a significantly higher proportion of workers in Group A having oxidative DNA damage compared to controls. The results support the theory that oxidative DNA damage is involved in the genotoxicity of antimony and indicate the need for further research in this field. Environ. Mol. Mutagen. 40:184–189, 2002. © 2002 Wiley‐Liss, Inc.
Heavy‐ion‐induced mutations in the gpt delta transgenic mouse: Effect of p53 gene knockout
Authors: Yatagai Fumio , Kurobe Toshihiro , Nohmi Takehiko , Masumura Ken‐ichi , Tsukada Teruyo , Yamaguchi Hirotake , Kasai‐Eguchi Kiyomi , Fukunishi Nobuhisa 
Published: October 2002

AbstractThe influence of the loss of p53 gene on heavy‐ion‐induced mutations was examined by constructing a new line of transgenic mice, p53 knockout (p53−/−) gpt delta. In this mouse model, deletions in lambda DNA integrated into the mouse genome are preferentially selected as Spi‐ phages, which can then be subjected to molecular analysis. Mice were exposed to 10 Gy of whole‐body carbon‐ion irradiation. The carbon ions were accelerated to 135 MeV/u by the RIKEN Ring Cyclotron. The p53 defect markedly enhanced the Spi‐ mutant frequency (MF) in the kidneys of mice exposed to C‐ion irradiation: the Spi‐ MF increased 4.4‐ and 2.8‐fold over the background level after irradiation in p53−/− and p53+/+ mice, respectively. There was no significant difference in the background Spi‐ MF between p53−/− and p53+/+ mice. Sequence analysis of the Spi‐ mutants indicated that the enhancement of kidney Spi‐ MF in p53−/− mice was primarily due to an increase in complex or rearranged‐type deletions. In contrast to the kidney, the p53 defect had no effect on the Spi‐ MF in liver: Spi‐ MF increased 3.0‐ and 2.7‐fold after the irradiation in p53−/− and p53+/+ mice, respectively. Our results suggest that p53 suppresses deletion mutations induced by heavy‐ion irradiation in an organ‐specific manner. Environ. Mol. Mutagen. 40:216–225, 2002. © 2002 Wiley‐Liss, Inc.
DNA damage in cytologically normal urothelial cells of patients with a history of urothelial cell carcinoma
Authors: de Miranda Cabral Gontijo Álisson Marques , de Castro Marcondes João Paulo , Nunes Elias Flávia , Cotrim Sartor de Oliveira Maria Luiza , Alves de Lima Rodrigo Otávio , Favero Salvadori Daisy Maria , Viana de Camargo João Lauro 
Published: October 2002

AbstractIn order to determine if patients with a history of previous urothelial cell carcinoma (UCC) but with current normal urinary cytology have DNA damage in urothelial cells, the single‐cell gel electrophoresis (comet) assay was conducted with cells obtained by urinary bladder washings from 44 patients (28 with a history of previous UCC). Increased DNA damage was observed in cytologically “normal” urothelial cells of patients with a history of UCC when compared with referents with no similar history and after correcting the data for smoking status and age (P < 0.018). Increased DNA damage also correlated with the highest tumor grade, irrespective of time or course of the disease after clinical intervention (Kendall tau correlation, 0.37, P = 0.016). Moreover, aneuploidy, as assessed by DNA content ratio (DCR; 75th/25th percentile of total DNA fluorescence of 50 comets/patient) was unaltered by smoking status, but increased with UCC grade: 1.39 ± 0.12 (median ± 95% confidence interval; referents); 1.43 ± 0.11 (Grade I UCC; P = 0.264, against referents); 1.49 ± 0.16 (Grade II UCC; P = 0.057); 1.57 ± 0.16 (Grade III UCC; P = 0.003). Micronucleated urothelial cells (MNC) were also scored on Giemsa‐stained routine cytological smears and were found not to correlate with DNA damage or DCR. MNC frequencies were higher for patients with a history of UCC and/or smoking than referents with neither history, but there was no statistical difference between groups. Taken together, these results suggest that the normal‐appearing urothelium of patients resected for UCC still harbor genetically unstable cells. Environ. Mol. Mutagen. 40:190–199, 2002. © 2002 Wiley‐Liss, Inc.
Space–time correlation models and contaminant plumes
Authors: Myers D. E. 
Published: October 2002

AbstractA contaminant plume might be described by a function defined in space–time. Spatial integrals or time derivatives of this function as well as time derivatives of spatial integrals will quantify characteristics such as the total volume of the plume, the total concentration of the contaminant in the plume, rates of change of the volume, and rates of change of concentration.The plume function usually cannot be derived in analytic form but instead must be estimated or approximated. The dual form of the kriging estimator, which is equivalent to the use of radial basis functions, provides a tool for modeling this function in analytic form. The extension of the kriging estimator, in its usual form or in its dual form, to space–time poses no problems since the estimator and the equations are essentially dimension free. The difficulty is an adequate choice of space–time variograms or covariances.The product–sum and integrated product–sum models provide an extensive array of valid models and also lead to a simple process for fitting the models by the use of marginal variograms. Examples are given and an application to air pollution data from the Milan District (Italy) illustrates the method. Copyright © 2002 John Wiley & Sons, Ltd.
The use of distribution mixtures for dose–response modeling in toxicological experiments
Authors: Razzaghi Mehdi 
Published: October 2002

AbstractIn toxicological experiments, animal bioassays are conducted to estimate the risk from exposure to toxic substances. A critical step in the process of risk assessment is the development of a dose–response model which provides a mathematical relationship between the exposure level and the probability of incidence of an adverse effect. Here, we consider the use of mixture models as dose–response functions in animal bioassay experiments. Mixtures of distributions provide a rich and flexible class of models that can be used in a variety of settings and have received a significant amount of attention in recent years. Moreover, because of the existence of susceptibility in toxicological experiments—that is, the fact that some animals appear to be more susceptible to a drug than others—distribution mixtures seem to be a natural choice for dose–response models. Here, we consider various types of toxicological experiments and demonstrate how mixture models can be utilized to describe the relationship between dose and incidence rate. Copyright © 2002 John Wiley & Sons, Ltd.
High‐order algorithms for vascular flow modelling
Authors: Peiró J. , Giordana S. , Griffith C. , Sherwin S. J. 
Published: October 2002

AbstractThis paper presents the development of spectral/hphigh‐order elements for vascular flows with particular attention to surface reconstruction and high‐order mesh generation. Using ideas from computer visualization we apply a technique of constructing smooth implicit functions to reconstruct incomplete sectional imaging data from magnetic resonance imaging. Using this as a starting point we outline techniques to discretize and computationally solve the Newtonian flow within these geometries using high‐order spectral/hpelement methods. Finally we demonstrate the application of these ideas to anatomically correct and model distal bypass grafts. Copyright © 2002 John Wiley & Sons, Ltd.
An optimal control approach to optical flow computation
Authors: Borzì A. , Ito K. , Kunisch K. 
Published: October 2002

AbstractAn optimal control approach for determining optical flow is presented. The new framework differs from preceding approaches in that it does not require differentiation of the data. A numerical algorithm that solves the optimality system consisting of hyperbolic and elliptic partial differential equations is presented. Copyright © 2002 John Wiley & Sons, Ltd.
A numerical model to track two‐fluid interfaces based on a stabilized finite element method and the level set technique
Authors: Codina R. , Soto O. 
Published: October 2002

AbstractThe objective of this work is to present a stabilized finite element formulation for transient incompressible flows and to apply it to the tracking of two‐fluid interfaces. The stabilization technique employed allows us to use equal velocity–pressure interpolations and to deal with convection–dominated flows. The tracking of the fluid interface is based on the level set technique. A novel smoothing technique of this surface based on ideas of signal processing is presented. Copyright © 2002 John Wiley & Sons, Ltd.
Space‐time residual distribution schemes for hyperbolic conservation laws on unstructured linear finite elements
Authors: Á. Csík  , Deconinck H. 
Published: October 2002

AbstractMultidimensional upwind residual distribution schemes are extended to the context of continuous linear space–time finite elements for the time accurate solution of scalar and hyperbolic systems of conservation laws. The formulation leads to a consistent discretization of the space‐time domain, thus retaining the properties of the underlying basic schemes both in space and time. We propose a particular space–time mesh configuration containing two layers of elements and three levels of nodes in time. This construction leads to unconditionally stable implicit time stepping while retaining second‐order spatial and temporal accuracy in smooth flows and monotone solution across steep gradients. The presented schemes have a strong potential in the field of moving grids, since they allow a dynamic change of the space–time mesh geometry. Numerical results demonstrate the robustness, accuracy and monotonicity of the method. Copyright © 2002 John Wiley & Sons, Ltd.
A note on the valuation of compound options
Authors: Lajeri‐Chaherli Fatma 
Published: October 2002

AbstractThe value of a compound option, an option on an option, has been derived by Geske
(1976) using Fourier integrals. This article presents two alternative proofs to derive the value of a
compound option. One proof is based on the martingale approach, which provides a simple and powerful tool for
valuing contingent claims. The second proof uses the expectation of a truncated bivariate normal variable. These
proofs allow for an intuitive interpretation of the three elements constituting the value of a compound option.
© 2002 Wiley Periodicals, Inc. Jrl Fut Mark 22:1103–1115, 2002
Clinical implications of chromosomal abnormalities in gastric adenocarcinomas
Authors: Wu Chew‐Wun , Chen Gen‐Der , Fann Cathy S.‐J. , Lee Anna F.‐Y. , Chi Chin‐Wen , Liu Jacqueline M. , Weier Ulli , Chen Jeou‐Yuan 
Published: October 2002

AbstractGastric carcinoma (GC) is one of the most common malignancies worldwide and has a very poor prognosis. Genetic imbalances in 62 primary gastric adenocarcinomas of various histopathologic types and pathologic stages and six gastric cancer–derived cell lines were analyzed by comparative genomic hybridization, and the relationship of genomic abnormalities to clinical features in primary GC was evaluated at a genome‐wide level. Eighty‐four percent of the tumors and all six cell lines showed DNA copy number changes. The recurrent chromosomal abnormalities including gains at 15 regions and losses at 8 regions were identified. Statistical analyses revealed that gains at 17q24‐qter (53%), 20q13‐qter (48%), 1p32–p36 (42%), 22q12‐qter (27%), 17p13‐pter (24%), 16p13‐pter (21%), 6p21‐pter (19%), 20p12‐pter (19%), 7p21‐pter (18%), 3q28‐qter (8%), and 13q13–q14 (8%), and losses at 18q12‐qter (11%), 3p12 (8%), 3p25‐pter (8%), 5q14–q23 (8%), and 9p21‐p23 (5%), are associated with unique patient or tumor‐related features. GCs of differing histopathologic features were shown to be associated with distinct patterns of genetic alterations, supporting the notion that they evolve through distinct genetic pathways. Metastatic tumors were also associated with specific genetic changes. These regions may harbor candidate genes involved in the pathogenesis of this malignancy. © 2002 Wiley‐Liss, Inc.
The SRCR/SID region of DMBT1 defines a complex multi‐allele system representing the major basis for its variability in cancer
Authors: Mollenhauer Jan , Müller Hanna , Kollender Gaby , Lyer Stefan , Diedrichs Laura , Helmke Burkhard , Holmskov Uffe , Ligtenberg Toon , Herbertz Stephan , Krebs Inge , Madsen Jens , Bikker Floris , Schmitt Liane , Wiemann Stefan , Scheurlen Wolfram , Otto Herwart F. , von Deimling Andreas , Poustka Annemarie 
Published: October 2002

AbstractDeleted in malignant brain tumors 1 (DMBT1) at 10q25.3–q26.1 has been proposed as a candidate tumor‐suppressor gene for brain and epithelial cancer. DMBT1 encodes a multifunctional mucin‐like protein presumably involved in epithelial differentiation and protection. The gene consists of highly homologous and repeating exon and intron sequences. This specifically applies to the region coding for the repetitive scavenger receptor cysteine‐rich (SRCR) domains and SRCR‐interspersed domains (SIDs) that constitutes the major part of the gene. This particular structure may previously have interfered with the delineation of DMBT1 alterations in cancer. Uncovering these, however, is of mechanistic importance. By a combined approach, we conducted a detailed mutational analysis, starting from a panel of 51 tumors, including 46 tumor cell lines and five primary tumors. Alterations in the repetitive region were present in 22/31 (71%) tumors that were investigated in detail. Six tumors showed presumably de novo mutations, among these three with point mutations in combination with a loss of heterozygosity. However, none of the alterations unambiguously would be predicted to lead to an inactivation of DMBT1. We define seven distinct DMBT1 alleles based on variable numbers of tandem repeats (VNTRs). At least 11 tumors exclusively harbored these VNTRs. The data suggest that the SRCR/SID region defines a complex multi‐allele system that has escaped previous analyses and that represents the major basis for the variability of DMBT1 in cancer. DMBT1 thus compares to mucins rather than to conventional tumor suppressors. © 2002 Wiley‐Liss, Inc.
Oligodendrocyte and astrocyte development in rodents: An in situ and immunohistological analysis during embryonic development
Authors: Liu Ying , Wu Yuanyuan , Lee Jeffrey C. , Xue Haipeng , Pevny Larysa H. , Kaprielian Zaven , Rao Mahendra S. 
Published: October 2002

AbstractLineally related multipotent neuroepithelial cells (NEP), neuronal restricted precursors (NRP), and glial restricted precursors (GRP) have been identified in the spinal cord. To determine the sequence of differentiation and identify lineage and stage‐specific markers, we have examined the spatiotemporal expression of established glial markers during rodent embryonic development and within fetal cell culture. In this report, we show that proliferating stem cells in the developing neural tube do not express any glial markers at E10.5. By E11, however, glial precursors have begun to differentiate and at least two regions of the ventral neural tube containing glial precursor cells can be distinguished, an Nkx2.2/Neurogenin 3 (Ngn3) domain and a platelet‐derived growth factor receptor alpha (PDGFRα)/Olig2/Sox10 domain. Radial glia, as identified by RC1 immunoreactivity, develop in concert with other glial precursors and can be distinguished by their morphology, spatial distribution, and antigen expression. Astrocytes as assessed by glial fibrillary acidic protein (GFAP) immunoreactivity are first detected at E16. A novel dorsal domain of CD44 immunoreactivity that can be distinguished from the more ventral glial precursor domains can be detected as early as E13.5. GLIA 40:25–43, 2002. Published 2002 Wiley‐Liss, Inc.
Extracellular and intracellular regulation of oligodendrocyte development: Roles of Sonic hedgehog and expression of E proteins
Authors: Sussman Caroline R. , Davies Jeannette E. , Miller Robert H. 
Published: October 2002

AbstractRecent advances in understanding oligodendrocyte development have revealed the importance of both extra‐ and intracellular molecules in regulating the induction, survival, and proliferation of early oligodendrocyte progenitors. The signaling molecule Sonic hedgehog (Shh) is critical for normal development of oligodendrocytes, although the precise influences of Shh on cells of the oligodendrocyte lineage are unclear. The present study shows that Shh increased the number of oligodendrocyte precursors in both pure cultures of oligodendrocyte precursors and mixed cultures from embryonic rat spinal cord. In pure precursor cultures Shh increased cell survival. In mixed cultures, Shh increased both the survival and proliferation of oligodendrocyte precursors in a concentration dependent manner. One intracellular consequence of exposure to Shh is the activation of transcription factors in oligodendrocyte lineage cells, which are critical for oligodendrocyte development, helix‐loop‐helix (HLH) transcription factors, Olig1 and 2. In many cases, HLH proteins such as Olig1 and Olig2 heterodimerize with other HLH proteins, such as members of the E subfamily, which are critical regulators of cell proliferation and differentiation. Immature (A2B5+) and more mature (O4+) rat oligodendrocyte precursors in dissociated cell culture expressed Olig1 as well as E proteins, HEB and E2A. Similarly, cells bearing the morphology of oligodendrocyte precursors expressed both Olig1 and HEB or E2A. We propose that E2A and/or HEB, possibly in combination with Olig1 and 2, are critical components of oligodendrogenesis and may regulate cell survival, proliferation, and fate decisions in the oligodendrocyte lineage. GLIA 40:55–64, 2002. © 2002 Wiley‐Liss, Inc.
Transforming growth factor β1 prevents IL‐1β–induced microglial activation, whereas TNFα‐ and IL‐6–stimulated activation are not antagonized
Authors: Basu Anirban , Krady J. Kyle , Enterline Jonathan R. , Levison Steven W. 
Published: October 2002

AbstractMicroglia rapidly respond to CNS injury, yet the mechanisms leading to their activation and inactivation remain poorly defined. In particular, few studies have established how interactions between inflammatory mediators affect the innate immune response of microglia. To begin to establish how microglia integrate signals from multiple inflammatory mediators, we examined the effects of interleukin 1β (IL‐1β), interleukin 6 (IL‐6), tumor necrosis factor α (TNFα), interferon γ (IFN‐γ), and transforming growth factor β1 (TGFβ1) on both newborn and bulk‐isolated adult microglia. To assess the functional state of the cells, we assayed the expression of cyclooxygenase 2 (Cox‐2), interleukin 6, and tumor necrosis factor α, and two protein tyrosine kinases that have been implicated in microglial responses to activational stimuli, HCK and FAK. These studies demonstrated that IL‐1β, TNFα, IL‐6, but not IFN‐γ increase the expression of Cox‐2, whereas they all increase the expression of HCK and FAK. In these studies, TGFβ1 either had no effect, or it decreased basal levels of these proteins. TGFβ1 blocked activation by IL‐1β when given prior to, or simultaneously with, IL‐1β. TGFβ1 blocked the induction of the tyrosine kinases, Cox‐2, and the induction of IL‐6 and TNFα mRNAs. However, TGFβ1 was ineffective in antagonizing the induction of Cox‐2 by either IL‐6 or TNFα. We conclude that the TGFβ receptor signaling cascades intersect with IL‐1, but they may not interact with IL‐6 or TNFα signaling pathways that lead to activation. GLIA 40:109–120, 2002. © 2002 Wiley‐Liss, Inc.
Apolipoprotein E ε4 and testosterone interact in the risk of Alzheimer's disease in men
Authors: Hogervorst E. , Lehmann D. J. , Warden D. R. , McBroom J. , Smith A. D. 
Published: October 2002

AbstractObjectivesTo assess the association between testosterone levels and APOEε4 in cases with AD and controls.MethodWe included 61 men with definite or probable Alzheimer's disease (AD) and 55 elderly male controls from the Oxford Project to Investigate Memory and Ageing (OPTIMA). Testosterone was measured using a competitive enzyme immunoassay (Bayer®).ResultsWe found that both low serum testosterone and the interaction between testosterone and APOEε4 were associated with AD. Furthermore, testosterone levels were lower in APOEε4‐positive controls (mean: 11.3 nmol/L) than in controls without the allele (19.1 nmol/L).ConclusionsLow testosterone is potentially a modifiable risk factor, which may prove relevant to APOEε4 carriers who are at risk of AD. Copyright © 2002 John Wiley & Sons, Ltd.