bluuebunny/crossref_metadata_2025_split huggingface dataset:
Calculating basal temperatures in ice sheets: an Excel spreadsheet method
Authors: Glasser Neil F. , Siegert Martin J. 
Published: October 2002

AbstractThe flow of ice sheets and their geomorphological impact is greatly influenced by their basal thermal regime. Calculations of basal temperatures in ice sheets are therefore fundamental in evaluating glacier dynamics and in determining the spatial distribution of zones of erosion and deposition beneath ice masses. Calculations of basal temperatures are not frequently attempted, however, primarily because of the techniques required to solve the heat conduction equation between the ice surface and the base. This paper describes a new Excel spreadsheet method of solving this equation that can readily be applied to both former and contemporary ice sheets. The application of the spreadsheet is illustrated with two examples. The first provides a calculation of basal thermal regime beneath the north eastern part of the Scottish ice sheet during the last glacial maximum; the second shows how basal ice temperatures can be calculated beneath the modern Antarctic ice sheet. Copyright © 2002 John Wiley & Sons, Ltd.
Missing links: Eugène Dubois and the origins of paleoanthropology
Authors: Shipman Pat , Storm Paul 
Published: October 2002

AbstractExamining the origins of various scientific fields may help to identify particular individuals whose thought, work, and discoveries have had a disproportionately large influence. Such individuals seem to serve as catalysts for a wider set of intellectual reactions, which then give rise to an entire field of study. In this paper, we propose explicit criteria for recognizing the founders of new fields. We contend that Eugène Dubois, best known as the man who found the “missing link” between apes and humans, should be recognized as one of the founding fathers of paleoanthropology.
Wastewater Treatment during Contingency Operations: The Balkans Challenge
Authors: Zettersten Garry C. , Best Raymond K. , Dale Debra A. 
Published: October 2002

AbstractThis article focuses on wastewater treatment during contingency operations at Eagle Base in Bosnia and Camp

Monteith and Camp Bondsteel in Kosovo. Operating in areas with limited regulation, U.S. forces in Europe have again

shown “the ability to demonstrate and incorporate environmental stewardship in all aspects of the

mission.” Over the past four years, environmental protection efforts associated with Balkan contingency

operations have evolved from an “extra duty” to a mission enabler and force protection issue. In the

process, U.S. Army Europe (USAREUR) has established and operates under the following principles:

(1) protect the force; (2) limit U.S. liability against claims; (3) spend

U.S. dollars wisely; and (4) demonstrate and incorporate environmental stewardship in all aspects of

the mission. © 2002 Wiley Periodicals, Inc.*
Hybrid Bioreactors for Decontamination of Water and Air
Authors: Boles Jeffrey L. , Gamble Johnny R. 
Published: October 2002

AbstractThe Tennessee Valley Authority (TVA) has developed and patented innovative Hybrid Bioreactors that

destroy water and air contaminants, with dramatic savings over existing technologies. Hybrid Bioreactors

accomplish single‐step destruction of contaminants without generating contaminated off‐gases or

other secondary waste streams. Contaminants destroyed include a wide variety of volatile organic compounds,

chlorinated solvents, and other compounds. The bioreactors can be used in a variety of applications ranging

from site restoration to industrial compliance. Treatment costs using Hybrid Bioreactors are generally less

than one‐tenth of costs reported at Superfund sites. A gas stream application of the new technology was

field‐demonstrated at Anniston Army Depot in a project funded by the U.S. Army Environmental Center. A

300‐cubic‐foot Hybrid Bioreactor is being demonstrated this year at TVA's Wetlands Complex

in Muscle Shoals, Alabama. Additional information is available at

http://www.tva.gov/environment/envservices/alw_biofilter.htm. © 2002 Wiley

Periodicals, Inc.*
A differential equation for approximate wall distance
Authors: Fares E. , Schröder W. 
Published: October 2002

AbstractA partial differential equation to compute the distance from a surface is derived and solved numerically. The benefit of such a formulation especially in combination with turbulence models is shown. The details of the formulation as well as several examples demonstrating the influence of its parameters are presented. The proposed formulation has computational advantages and can be favourably incorporated into one‐ and two‐equation turbulence models like e.g. the Spalart–Allmaras, the Secundov or Menter's SST model. Copyright © 2002 John Wiley & Sons, Ltd.
Futures price limit moves as options
Authors: Holder Mark E. , Ma Christopher K. , Mallett James E. 
Published: October 2002

AbstractThis note demonstrates that an asset's price in an environment with price limit rules can be replicated by

the price of a portfolio consisting of a riskless asset and two synthetic options. A procedure is developed to

unbundle the unobservable option values imbedded in the actual futures price and impute a theoretical true futures

price. Using this framework, evidence from the Treasury Bond futures market suggests that theoretical true futures

prices diverge from actual futures prices, on average, 3 h prior to the activation of price limit rules,

indicating that price limit moves might be predictable. The reversal of both the actual futures prices and the

theoretical futures prices back within the limit range after a limit move provides support for the possibility

that traders tend to overreact when market prices are near price limits. © 2002 Wiley Periodicals, Inc. Jrl

Fut Mark 22:901–913, 2002
Preferential expression of a mutant allele of the amplified MDR1 (ABCB1) gene in drug‐resistant variants of a human sarcoma
Authors: Chen Kevin G. , Lacayo Norman J. , Durán George E. , Wang Yan , Bangs C. Dana , Rea Susan , Kovacs Mary , Cherry Athena M. , Brown J. Martin , Sikic Branimir I. 
Published: October 2002

AbstractActivation of the MDR1 (ABCB1) gene is a common event conferring multidrug resistance (MDR) in human cancers. We investigated MDR1 activation in MDR variants of a human sarcoma line, some of which express a mutant MDR1, which facilitated the study of allelic gene expression. Structural alterations of MDR1, gene copy numbers, and allelic expression were analyzed by cytogenetic karyotyping, oligonucleotide hybridization, Southern blotting, polymerase chain reaction, and DNA heteroduplex assays. Both chromosome 7 alterations and several cytogenetic changes involving the 7q21 locus are associated with the development of MDR in these sarcoma cells. Multistep‐selected cells and their revertants contain three‐ to six‐fold MDR1 gene amplification compared with that of the drug‐sensitive parental cell line MES‐SA and single‐step doxorubicin‐selected mutants. MDR1 gene amplification precedes the emergence of a mutant allele in cells that were coselected with doxorubicin and a cyclosporin inhibitor of P‐glycoprotein (P‐gp). Allele‐specific oligonucleotide hybridization showed that the endogenous mutant allele was present as a single copy, with multiple copies of the normal allele. Reselection of revertant cells with doxorubicin in either the presence or the absence of the P‐gp inhibitor resulted in exclusive reexpression of the mutant MDR1 allele, regardless of the presence of multiple wild‐type MDR1 alleles. These data provide new insights into how multiple alleles are regulated in the amplicon of drug‐resistant cancer cells and indicate that increased expression of an amplified gene can result from selective transcription of a single mutant allele of the gene. © Wiley‐Liss, Inc.
No evidence for hypermethylation of the hSNF5/INI1 promoter in pediatric rhabdoid tumors
Authors: Zhang Fan , Tan Lu , Wainwright Luanne M. , Bartolomei Marisa S. , Biegel Jaclyn A. 
Published: October 2002

AbstractThe hSNF5/INI1 gene on chromosome 22 has been implicated as a tumor suppressor gene in pediatric rhabdoid tumor, an aggressive malignancy that generally occurs in the first two years of life. The most common sites for tumor development are the brain and kidney. We and other investigators have identified deletions and mutations of the INI1 gene in the majority of rhabdoid tumors of the central nervous system, kidney, and extrarenal tissues. At least 20% of cases do not have genomic alterations of INI1, although expression at the RNA or protein level may be decreased. The aim of this study was to determine whether hypermethylation or mutation of the 5′ promoter region of INI1, or hypermethylation of CpG dinucleotides in a GC‐rich repeat region within the first intron, could account for the decreased expression of INI1 observed in these tumors. We employed bisulfite modification, polymerase chain reaction, and sequence analysis to determine the methylation status of the cytosine nucleotides in the predicted promoter region of the INI1 gene, and two GC repeat regions in intron 1. DNA from 24 tumors with or without coding‐sequence mutations was analyzed. None of the tumors demonstrated methylation of the promoter or intron 1 regions. This mechanism is unlikely to account for the inactivation of INI1 in rhabdoid tumors without coding‐sequence mutations. One tumor demonstrated a potential mutation in the promoter region, but further studies are required for determining its functional significance. © 2002 Wiley‐Liss, Inc.
Comprehensive analysis of genomic alterations in gliosarcoma and its two tissue components
Authors: Actor Bertrand , Cobbers J.M.J. Ludwig , Büschges Rainer , Wolter Marietta , Knobbe Christiane B. , Reifenberger Guido , Weber Ruthild G. 
Published: October 2002

AbstractGliosarcoma is a variant of glioblastoma multiforme characterized by two components displaying gliomatous or sarcomatous differentiation. We investigated 38 gliosarcomas for aberrations of tumor‐suppressor genes and proto‐oncogenes that are commonly altered in glioblastomas. Amplification of CDK4, MDM2, EGFR, and PDGFRA were found in 11% (4/35), 8% (3/38), 8% (3/38), and 3% (1/35) of the tumors, respectively. Nine of 38 gliosarcomas (24%) carried TP53 mutations. PTEN mutations were identified in 45% (9/20) of the investigated tumors. Twenty gliosarcomas were analyzed by comparative genomic hybridization (CGH). Chromosomal imbalances commonly detected were gains on chromosomes 7 (15/20; 75%), X (4/20; 20%), 9q, and 20q (3/20, 15% each); and losses on chromosomes 10 and 9p (7/20, 35% each), and 13q (3/20, 15%). Five different high‐level amplifications were mapped to 4q12–q21 (1 case), 6p21 (1 case), 7p12 (2 cases), proximal 12q (4 cases), and 14q32 (1 case) by CGH. Southern blot and/or differential PCR analyses identified amplification of PDGFRA (4q12), CCND3 (6p21), EGFR (7p12), CDK4 (12q14) and/or MDM2 (12q14.3–q15), and AKT1 (14q32.3) in the respective tumors. Separate analysis of the gliomatous and sarcomatous components of eight gliosarcomas by CGH after microdissection and universal DNA amplification revealed that both components shared 57% of the chromosomal imbalances detected. Taken together, our data indicate that the genomic changes in gliosarcomas closely resemble those found in glioblastomas. However, the number of chromosomes involved in imbalances in gliosarcomas was significantly lower than that in glioblastomas, indicating a higher genomic stability in gliosarcomas. In addition, we provide further support for the hypothesis that the gliomatous and sarcomatous components are derived from a single precursor cell clone, which progressed into subclones with distinct morphological features during tumor evolution. According to our data, gain/amplification of genes on proximal 12q may facilitate the development of a sarcomatous phenotype. © 2002 Wiley‐Liss, Inc.
Differential expression of multiple isoforms of the ELKS mRNAs involved in a papillary thyroid carcinoma
Authors: Nakata Tomoko , Yokota Takashi , Emi Mitsuru , Minami Shiro 
Published: October 2002

AbstractA novel gene, ELKS, whose 5′ portion was fused to the RET gene, was found in a papillary thyroid carcinoma. A cDNA of this gene obtained from a human‐brain cDNA library revealed that it encoded a peptide of 948 amino acids, termed ELKSα. We identified four other isoforms, which encoded ELKSβ, ELKSγ, ELKSδ, and ELKSϵ proteins consisting, respectively, of 992, 720, 1088, and 1116 amino acid residues. Analysis of the gene structure revealed that the isoforms were generated by alternative splicing. Isoforms β, γ, δ, and ϵ all contain an optional exon (exon14a), but ELKSγ, ‐δ, and ‐ϵ lack exon 1b. ELKSγ lacks exons 3 to 6. ELKSδ and ‐ϵ lack exons 12 and 17; ELKSϵ contains an optional exon (exon 6a). Analysis by RT‐PCR suggested that ELKSα and ELKSβ mRNAs are abundant in the brain, ELKSδ and ELKSϵ mRNAs predominate in testis and thyroid, and ELKSϵ mRNA predominates in other tissues. To prove whether the fusion of different ELKS isoforms to RET (between ELKS coiled‐coil domains and the RET kinase domain) could produce chimeric proteins that could be autophosphorylated, we synthesized ELKSγ‐RET, ELKSδ‐RET, and ELKSϵ‐RET fusion proteins in vitro. Immunoblotting with anti‐ELKS, anti‐RET, and anti‐phosphotyrosine antibodies demonstrated that the chimeric proteins were constitutively phosphorylated at tyrosine residues, whereas native RET protein was not. These results indicate that the ELKS gene is alternatively spliced, and that every type of ELKS‐RET chimeric protein having oligomerization domains can activate RET's cytoplasmic tyrosine kinase. © 2002 Wiley‐Liss, Inc.
Axes establishment during eye morphogenesis in Xenopus by coordinate and antagonistic actions of BMP4, Shh, and RA
Authors: Sasagawa Satoru , Takabatake Takashi , Takabatake Yuka , Muramatsu Tatsuo , Takeshima Kazuhito 
Published: October 2002

AbstractSummary: We have examined the roles of BMP4, Shh, and retinoic acid in establishing the proximal‐distal and dorsal‐ventral axes in the developing Xenopus eye. Misexpression of BMP4 caused the absence of an optic stalk and the expansion of dorsal and distal markers, tbx2/3/5, and pax6, at the expense of ventral and proximal markers vax2 and pax2. When Shh or Noggin, an antagonist of BMPs, was misexpressed, the reverse expression patterns of these marker genes were observed. These results suggest that BMP4 is involved in the specification of not only dorsal in the optic cup but also distal in the optic vesicle. Because Shh did not suppress bmp4 expression, unlike Noggin, Shh and BMP4 may antagonistically regulate common downstream genes in developing eye. We also found the difference between the effects of Shh and retinoic acid, another possible ventralizing factor, suggesting that Shh could promote ventralization independently of retinoic acid. These findings provide important clues to the coordinate and antagonistic actions of BMP4, Shh, and retinoic acid in axes specifications of Xenopus eyes. genesis 33:86–96, 2002. © 2002 Wiley‐Liss, Inc.
A human CD2 minigene directs CRE‐mediated recombination in T cells in vivo
Authors: Wilson Trevor J. , Cowdery Helen E. , Xu Dakang , Kola Ismail , Hertzog Paul J. 
Published: October 2002

AbstractSummary: We have produced a mouse line that expresses the Cre recombinase under the regulation of a human CD2 minigene to facilitate Cre‐specific recombination in T lymphocytes. These mice express Cre in thymocytes and T cells and are capable of efficient site‐specific recombination as shown in the spleen and thymus, but not other tissues. These mice thus provide an excellent resource for the study of gene function during thymocyte development and in mature T cells. genesis 33:181–184, 2002. © 2002 Wiley‐Liss, Inc.
Mantel statistics to correlate gene expression levels from microarrays with clinical covariates
Authors: Shannon William D. , Watson Mark A. , Perry Arie , Rich Keith 
Published: October 2002

AbstractMantel statistics provide an additional step to standard approaches in the analysis of gene expression and covariate data, allow the calculation of standard statistics such as correlation, partial correlation, and regression coefficients, and, with permutation tests, provide P values for these statistics to relate the sample covariates to the expression levels. In this article we describe the Mantel statistics and illustrate their use and interpretation with data from a study of seven human oligodendrogliomas (brain tumors) where expression levels of 1,013 genes and five covariates were previously analyzed using standard approaches. In the previous analysis of these data, qualitative relationships were found between gene expressions and two of the clinical covariates. We show in this article how the Mantel statistics are able to formally quantify and provide P values to determine statistical significance of these relationships. We also show how the Mantel statistics can be used to rank subsets of genes, found using standard clustering methods, in terms of differential expression across samples. Genet. Epidemiol. 23:87–96, 2002. © 2002 Wiley‐Liss, Inc.
Role of gene expression microarray analysis in finding complex disease genes
Authors: Gu Chi C. , Rao D.C. , Stormo Gary , Hicks Chindo , Province Michael A. 
Published: October 2002

AbstractThe promise of gene expression studies using microarray technology has inspired much new hope for finding complex diseases genes. It has become clear that complex diseases result from collective actions of many genetic and nongenetic factors. Therefore, genetic dissection of complex diseases should be carried out in a global context. The technology of gene expression microarray analysis (GEMA) can provide such global information on transcription activities of essentially all genes simultaneously. It is hoped that this promising technology can be applied to samples drawn from large‐scale, well‐defined genetic epidemiological studies and help us untangle the web of pathways leading to complex diseases. However, extremely noisy GEMA data pose serious challenges in terms of the statistical methodologies needed. Extensive work is needed in order to respond to the challenges before one can fully utilize the potential power provided by GEMA. We begin in this paper by identifying several statistical problems related to the application of GEMA to genetic epidemiological analysis, and consider study designs that might benefit from this promising new technology. While it is still too early to tell how much of the enormous potential of GEMA will be realized ultimately, its success will probably depend most critically on the ability of statistical genetics to rise to the challenge of mining information from a sea of noise. Genet. Epidemiol. 23:37–56, 2002. © 2002 Wiley‐Liss, Inc.
Depositional environment and sequence architecture of the Silurian Coralliferous Group, Southern Pembrokeshire, UK
Authors: Hillier Robert D. 
Published: October 2002

AbstractThe Lower Silurian siliciclastic Coralliferous Group is shown to have been deposited in an intra‐shelf position 10–15 km south of the palaeogeographic shelf‐break of the Welsh Basin. After a phase of thermal subsidence related to the development of the predominantly Llandovery Skomer Volcanic Group, the shelf basin was transgressed. This transgression was punctuated by an episode of tectonic uplift in southern Pembrokeshire, resulting in subaerial exposure of the shelf and a significant basinward shift in sedimentary environments. Erosion and sediment bypass ensued, with coarse‐grained low‐sinuosity fluvial channels transporting sediment to the northerly Welsh Basin, where significant submarine fans developed. During the early Telychian, renewed transgression took place, with lowstand gravels being ravined and reworked into parasequences of the transgressive systems tract. These thin, coarse‐grained parasequences record deposition within high‐energy wave‐dominated shoreface/inner shelf environments. Further coastal onlap resulted in the closing down of significant coarse‐grained sediment supply, with the remaining Coralliferous Group being dominated by wave‐influenced silts, mud‐shales and thin sandstones comprising the highstand systems tract. Copyright © 2002 John Wiley & Sons, Ltd.
Glial induction of blood‐brain barrier‐Like L‐system amino acid transport in the ECV304 cell line
Authors: Chishty M. , Reichel A. , Begley D.J. , Abbott N.J. 
Published: October 2002

AbstractThe blood‐brain barrier (BBB) is formed by the presence of tight junction complexes between brain endothelial cells that restrict paracellular permeability. As a consequence, a number of transport proteins are expressed on cerebral endothelial cells to facilitate the transport of nutrients into the brain. Although the modulation of barrier tight junction properties by glial‐conditioned medium and by second messengers is well established, little is known about the effects of these factors on carrier‐mediated BBB transport processes. The ECV304 cell line shows an endothelial phenotype and can be induced to upregulate certain BBB features in the presence of glial factors. In the present study, we have examined the effect of conditioned medium derived from rat C6‐glioma cells (C6CM) on the function of the L‐system amino acid transporter in ECV304 cells, using L‐leucine as the model substrate, and have determined whether the changes observed can be mimicked by modulating intracellular cAMP levels. ECV304 cells exposed to C6CM exhibited a significant increase in both the affinity of leucine transport and the diffusional constant (Michaelis‐Menten), while the maximal transport capacity remained unchanged. Conversely, acute exposure to modulators of the PKA and PKC second messenger pathways was found to reduce significantly the maximal transport capacity and diffusion constants, while transport affinity remained unchanged. In both cases, the maximal flux of leucine was increased, indicating transport of greater efficiency. This study indicates that exposure of ECV304 cells to C6CM provides an influence inducing L‐system transport properties characteristic of brain endothelial cells. Furthermore, it appears that L‐system‐mediated transport of amino acids can be modulated by several distinct pathways. GLIA 39:99–104, 2002. © 2002 Wiley‐Liss, Inc.