bluuebunny/crossref_metadata_2025_split huggingface dataset:
An autonomous decentralized model with nonlocal interaction: Roles of an extracellular matrix in organization of a multicellular system
Authors: Ogawa Ken‐ichiro , Miyake Yoshihiro 
Published: March 2004

AbstractThe reaction‐diffusion model is one of the theoretical approaches used to realize autonomous decentralized systems. The model conventionally assumes that all components of a system locally interact with each other under ideal conditions, ignoring any effect from the environment. However, it has recently become clear that nonlocal interactions mediated by the environment play an important role in the ontogenesis of multicellular organisms, a typical autonomous decentralized system. In this paper, we discuss the “redifferentiation” phenomenon of cancer cells in which such a nonlocal interaction is considered to play an essential role. Further, we propose a model to reproduce this phenomenon and mathematically analyze our model to construct autonomous decentralized systems with nonlocal interactions mediated by the environment in the future. © 2004 Wiley Periodicals, Inc. Electron Comm Jpn Pt 3, 87(7): 55–65, 2004; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/ ecjc.10101
Fast acquisition methods with code‐orthogonalizing filters in DS/CDMA
Authors: Takahashi Hirokazu , Hamamura Masanori , Tachikawa Shin'ichi 
Published: March 2004

AbstractThis paper presents a new acquisition method achieving reduction of acquisition time by improving the conventional acquisition method using the code‐orthogonalizing filter. In the acquisition method using the code‐orthogonalization filter, most of the acquisition time is spent on the orthogonalization process. Hence, in the proposed method, estimation of synchronous point candidates is performed several times so that the estimation accuracy is improved and the acquisition time is reduced by decreasing the number of orthogonalizations. After the scheme is explained, a performance evaluation of the proposed method is carried out by computer simulation. © 2004 Wiley Periodicals, Inc. Electron Comm Jpn Pt 3, 87(7): 36–44, 2004; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/ecjc.10148
A study of image segmentation based on a robust data clustering method
Authors: Ryu Heeburm , Miyanaga Yoshikazu 
Published: March 2004

AbstractThis paper considers intelligent image clustering and proposes a clustering method based on the self‐organizing mechanism, which is an adaptive and autonomous algorithm. The proposed method solves the problem of initial value setting, which has been a difficulty in the conventional clustering method, and has the feature that the effective clusters are always self‐organized. A method is realized which is robust and does not require empirical setting of the initial value. Thus, the effective initial cluster can always be selected for various kinds of data sets, and an excellent clustering is obtained. A method is proposed in which these features are utilized in image segmentation. © 2004 Wiley Periodicals, Inc. Electron Comm Jpn Pt 3, 87(7): 27–35, 2004; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/ecjc.10154
Iterative inverse filter relaxation algorithm for adaptation to acoustic fluctuation in sound reproduction system
Authors: Nagata Yu , Tatekura Yosuke , Saruwatari Hiroshi , Shikano Kiyohiro 
Published: March 2004

AbstractThis paper proposes a relaxation algorithm for an inverse filter that is adaptive to environmental change in a multichannel sound reproduction system. For a conventional multichannel sound reproduction system, a design method has been proposed for an inverse filter by means of the Moore–Penrose‐type generalized inverse matrix. However, in the inverse filter in the conventional method, background noise and line noise may be enhanced when the room transfer characteristics vary. In order to resolve this problem, an adaptive relaxation method based on the truncated singular value decomposition (TSVD) has been introduced. In the present paper, a microphone for monitoring the noise is placed at a location far from both ears of the listener. Relaxation of the inverse filter is carried out by using the reproduced sound observed by this microphone. From the results of computer simulation, it is found that the proposed method prevents amplification of the noise. Also, as a result of a subjective evaluation experiment on sound reproduction in a real acoustic environment, the sound quality was found to be improved significantly without damaging the sound localization of position. © 2004 Wiley Periodicals, Inc. Electron Comm Jpn Pt 3, 87(7): 15–26, 2004; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/ecjc.10159
Role of inherited defects of MYH in the development of sporadic colorectal cancer
Authors: Kambara Takeshi , Whitehall Vicki L. J. , Spring Kevin J. , Barker Melissa A. , Arnold Sven , Wynter Coral V. A. , Matsubara Nagahide , Tanaka Noriaki , Young Joanne P. , Leggett Barbara A. , Jass Jeremy R. 
Published: March 2004

AbstractBiallelic germ‐line variants of the 8‐hydroxyguanine repair gene MYH have been associated with multiple colorectal adenomas that display somatic G:C→T:A transversions in APC. However, the effect of single germ‐line variants has not been widely studied. To examine the relationship between monoallelic MYH variants and susceptibility to sporadic colorectal cancer (CRC), 92 cases of sporadic CRC, 19 cases of familial CRC not meeting the Bethesda guidelines, 17 cases with multiple adenomas, and 53 normal blood donors were screened for 8 potentially pathogenic germ‐line MYH variants. Loss of heterozygosity (LOH) at 1p adjacent to the MYH locus, microsatellite instability (MSI) status, and somatic mutations in KRAS2 and APC were analyzed in sporadic cancers. Neither homozygote nor compound heterozygote MYH variants were observed in the germ‐line of any subjects with sporadic CRC. There was no difference in the incidence of monoallelic variants between this group (20 of 92, 22%) and cancer‐free controls (14 of 53, 26%). However, the presence of monoallelic germ‐line MYH variants was negatively associated with an MSI‐high (MSI‐H) tumor phenotype, with an incidence of only 1 of 23 (4%) MSI‐H CRCs as contrasted with 19 of 69 (28%) non‐MSI‐H (P = 0.02). Further, 4 of 5 tumors with 1p LOH contained monoallelic MYH variants compared with 15 of 53 without 1p LOH (P = 0.04) and the normal population (P = 0.03). The presence of G:C→T:A transversions in KRAS2 or APC was significantly more common in single MYH variant tumors (9 of 12) than in MYH wild‐type tumors (11 of 33; P = 0.02). These results suggest that single germ‐line variants of MYH may influence genetic pathways in CRC. © 2004 Wiley‐Liss, Inc.
Method for manufacturing whole‐genome microarrays by rolling circle amplification
Authors: Smirnov Denis A. , Burdick Josh T. , Morley Michael , Cheung Vivian G. 
Published: March 2004

AbstractComparative genomic hybridization (CGH) to metaphase chromosomes is a method for genome‐wide detection of chromosomal aberrations in DNA samples. Recent advances in microarray technology have improved CGH by replacing metaphase chromosomes with a collection of mapped genomic clones placed on glass slides. However, it is quite expensive and labor‐intensive to prepare DNA from the genomic clones for use in constructing genomic microarrays. Here we used strand‐displacement rolling circle amplification (RCA) to manufacture whole‐genome microarrays by using a collection of about 4,500 mapped RPCI‐11 BAC clones that cover the human genome at approximately a 1‐Mb resolution. These genomic microarrays detected all major chromosomal aberrations in cancer cells lines and in cell lines with aneuploidy. In this article, we discuss the advantages of using RCA for the manufacturing of large genomic microarrays. © 2004 Wiley‐Liss, Inc.
Computational BAC clone contig assembly for comprehensive genome analysis
Authors: Lapuk Anna , Volik Stanislav , Vincent Robert , Chin Koei , Kuo Wen‐Lin , de Jong Pieter , Collins Colin , Gray Joe W. 
Published: March 2004

AbstractComparative genomic hybridization (CGH) has proved to be a powerful tool for the detection of genome copy number changes in human cancers and in other diseases caused by segmental aneusomies. Array versions of CGH allow the definition of these aberrations, with resolution determined by the size and distribution of the array elements. Resolution approaching 100 kb can be achieved by use of arrays comprising bacterial artificial chromosomes (BACs) distributed contiguously across regions of interest. We describe here a computer program that automatically assembles contigs of minimally overlapping BAC clones, using information about BAC end‐sequences and the normal genome DNA sequence. We demonstrate the characteristics of contigs assembled and annotated by use of this approach for regions of recurrent abnormality in human ovarian and breast cancers at chromosome bands 3q25–q27 and 8q24 and chromosome arm 20q. We also show illustrative analyses of regions of amplification in these regions in breast and ovarian tumor cell lines by use of array CGH with arrays comprising contiguous BACs. © 2004 Wiley‐Liss, Inc.
Gene copy mapping of the ERBB2/TOP2A region in breast cancer
Authors: Jacobson Kris K. , Morrison Larry E. , Henderson Benita T. , Blondin Beth A. , Wilber Kimberly A. , Legator Mona S. , O'Hare Anna , Van Stedum Susan C. , Proffitt John H. , Seelig Steve A. , Coon John S. 
Published: March 2004

AbstractERBB2 is one of the most important oncogenes in breast cancer, and its disordered expression is commonly associated with gene amplification. Amplification of at least one gene near ERBB2, topoisomerase IIα (TOP2A), has been shown to be clinically significant, but the prevailing patterns of gene amplification in this region of chromosome arm 17q have not been studied systematically in clinical cases of breast cancer. For characterizing this region, a commercial ERBB2‐containing contig probe and 7 probes prepared from single overlapping BAC and P1 clones lying telomeric to ERBB2 and including TOP2A were hybridized to 77 ERBB2‐amplified archival breast tumor specimens from 75 patients. The 7 single‐clone probes covered a region of approximately 650 kb starting 114 kb telomeric to ERBB2. Amplification of the ERBB2 contig target alone was found in 32% of the tumors, whereas all 8 probe targets were amplified in 12% of the tumors, based on an amplification criterion of there being more than or equal to 2 targets per chromosome 17 centromere. When one of the 7 overlapping probes encompassing TOP2A indicated amplification within a specimen, all probes telomeric to that probe usually showed amplification. Only 5 specimens had regions of normal or deleted targets separating 2 amplified targets. Also, tumors that showed deletion of TOP2A usually showed deletion of one or more contiguous targets. The observed patterns of amplification and deletion are consistent with the break–fusion–bridge model for gene amplification. TOP2A was amplified in 25% of all tumor specimens and was deleted in 24%, based on a deletion criterion of there being fewer than or equal to 0.75 targets per chromosome 17 centromere. Considering the relevance of the TOP2A gene product to anthracycline therapy and the wealth of other cancer‐associated genes within the ERBB2/TOP2A region, the pattern of amplification and deletion near ERBB2 and TOP2A may have a dramatic effect on the malignant potential of breast carcinomas and their response to therapy. © 2004 Wiley‐Liss, Inc.
Identification of a novel gene, FGFR1OP2, fused to FGFR1 in 8p11 myeloproliferative syndrome
Authors: Grand Effie K. , Grand Francis H. , Chase Andrew J. , Ross Fiona M. , Corcoran Martin M , Oscier David G. , Cross Nicholas C. P. 
Published: March 2004

AbstractThe 8p11 myeloproliferative syndrome (EMS) is an aggressive hematological malignancy caused by the fusion of diverse partner genes to fibroblast growth factor receptor 1 (FGFR1). The partner proteins promote dimerization and ligand‐independent activation of FGFR1‐encoded tyrosine kinase, deregulating hemopoiesis in a manner analogous to BCR‐ABL in chronic myeloid leukemia. Here, we describe the identification of a new FGFR1 fusion gene in a patient who presented with T‐cell lymphoblastic lymphoma in conjunction with an acquired ins(12;8)(p11;p11p22). Initial FISH analysis and Southern blotting confirmed that FGFR1 was disrupted. Using 5′‐RACE PCR, we identified part of a novel gene, FGFR1OP, at chromosome band 12p11 that was fused to exon 9 of FGFR1.FGFR1OP2 is predicted to be translated into an evolutionarily conserved protein containing coiled‐coil domains but no other recognizable motifs. The presence of the chimeric gene was confirmed by RT‐PCR, genomic DNA PCR, and FISH. These data further support the central role of deregulated FGFR1 in the pathogenesis of EMS. © 2004 Wiley‐Liss, Inc.
Cellular injury induces activation of MAPK via P2Y receptors
Authors: Yang LingLing , Cranson D. , Trinkaus‐Randall V. 
Published: March 2004

AbstractWound healing is a complex process that involves cell communication, migration, proliferation, and changes in gene expression. One of the first events after injury is the rapid release of Ca2+ that propagates as a wave to neighboring cells (Klepeis et al. [2001]: J. Cell. Sci. 114:4185–4195). Our goal was to examine the signaling events induced by cellular injury and identify extracellular molecules that induce the activation of extracellular signal responsive kinase (ERK) (p42/44). In this study we demonstrated that injury induced ERK1/2 activation occurred within 2 min and was negligible by 15 min. Treatment of unwounded cells with wound media caused activation of ERK that could be inhibited by apyrase III. Stimulation with epidermal growth factor (EGF) did not mimic the injury response and it was not detected in the wound media. To identify the active component, size fractionation was performed and factor(s) less than 3 kDa that induced the release of Ca2+ and activation of ERK1/2 were identified. Activity was not altered by heat denaturation, incubation with proteinase K but it was lost by treatment with apyrase. Adenosine triphosphate (ATP), uridine triphosphate (UTP), adenosine diphosphate (ADP), and uridine diphosphate (UDP) promoted activation by 2 min with similar profiles as that generated by injury. Preincubation with phospholipase C inhibitor, U73122, inhibited activation that was induced by injury and/or nucleotides. Lack of activation by alpha‐beta‐methylATP (α, β‐MeATP) and beta‐gamma‐methylATP (β, γ‐MeATP) to purinergic (P)2X receptors further indicated that activation occurs via P2Y and not P2X purinergic receptors. These results indicate that injury‐induced activation of ERK1/2 is mediated by a P2Y signaling pathway. © 2004 Wiley‐Liss, Inc.
BRCA1 interacts with dominant negative SWI/SNF enzymes without affecting homologous recombination or radiation‐induced gene activation of p21 or Mdm2
Authors: Hill David A. , de la Serna Ivana L. , Veal Timothy M. , Imbalzano Anthony N. 
Published: March 2004

AbstractBRCA1 is a tumor suppressor gene linked to familial breast and ovarian cancer. The BRCA1 protein has been implicated in a diverse set of cellular functions, including activation of gene expression by the p53 tumor suppressor and control of homologous recombination (HR) during DNA repair. Prior reports have demonstrated that BRCA1 can exist in cells in a complex with the BRG1‐based SWI/SNF ATP‐dependent chromatin remodeling enzymes and that SWI/SNF components contribute to p53‐mediated gene activation. To investigate the link between SWI/SNF function and BRCA1 mediated effects on p53‐mediated gene activation and on mechanisms of homologous recombination, we have utilized mammalian cells that inducibly express an ATPase‐deficient, dominant negative SWI/SNF enzymes. Mutant SWI/SNF ATPases retain the ability to interact with BRCA1 in cells. We report that expression of dominant negative SWI/SNF enzymes does not affect p53‐mediated induction of the p21 cyclin dependent kinase inhibitor or the Mdm2 E3 ubiquitin ligase that regulates p53 in cells exposed to UV or gamma irradiation. Similarly, integration of a reporter that monitors homologous recombination by gene conversion into these cells demonstrated no change in the recombination rate in the absence of functional SWI/SNF enzyme. We conclude that the SWI/SNF chromatin remodeling enzymes may contribute to but are not required for these processes. © 2004 Wiley‐Liss, Inc.
Mechanism of taxol‐induced apoptosis in human SKOV3 ovarian carcinoma cells
Authors: Ahn Hak Jun , Kim Yeong Shik , Kim Joung‐Uk , Han Sung Min , Shin Jin Woo , Yang Hyun Ok 
Published: March 2004

AbstractTaxol is extensively used clinically for chemotherapy of patients with ovarian, breast, and lung cancer. Although taxol induces apoptosis of cancer cells, its exact mechanism of action is not yet known. To determine the mechanism of action of taxol in ovarian cancer, we tested the effects of the drug, on the human ovarian carcinoma cell line, SKOV3. We observed that taxol‐induced apoptosis of these cells by phosphatidylserine (PS) externalization and DNA fragmentation. While treatment of cells with taxol resulted in bcl‐2 phosphorylation and mitochondrial depolarization, cytochrome c was not released and pro‐caspase‐3 was not activated. Treatment of SKOV3 cells with taxol, however, resulted in the translocation of AIF from the mitochondria to the nucleus via the cytosol. Taken together, these findings suggest that in SKOV3 cells, taxol induces caspase‐independent AIF‐dependent apoptosis. © 2004 Wiley‐Liss, Inc.
SPARC regulates TGF‐beta1‐dependent signaling in primary glomerular mesangial cells
Authors: Francki Aleksandar , McClure Timothy D. , Brekken Rolf A. , Motamed Kouros , Murri Carrie , Wang Tongwen , Sage E. Helene 
Published: March 2004

AbstractSecreted protein acidic and rich in cysteine (SPARC), a member of the family of matricellular proteins, regulates the interaction of cells with pleiotropic factors and proteins of the extracellular matrix (ECM). Although it has been appreciated that transforming growth factor beta 1 (TGF‐β1) induces SPARC and collagen type I, we have recently shown that SPARC regulates the expression of TGF‐β1 and collagen type I in renal mesangial cells via a TGF‐β1‐dependent pathway, and have proposed a reciprocal, autocrine regulatory feedback loop between SPARC and TGF‐β1. Herein, we sought to determine how SPARC regulates TGF‐β1‐dependent signal transduction. Our data indicate that SPARC modulates the TGF‐β1‐dependent phosphorylation of Smad‐2 in primary mesangial cells derived from wild‐type and SPARC‐null mice. We also show that SPARC regulates the levels and activation of the stress‐activated c‐jun‐N‐terminal kinase (JNK) in mesangial cells by augmentation of the stimulatory effects of TGF‐β1. Furthermore, we found that SPARC increases the levels and the activity of the transcription factor c‐jun. These effects of SPARC on the TGF‐β1 signaling pathway appear to be mediated through an interaction with the TGF‐β1‐receptor complex, but only in the presence of TGF‐β1 bound to its cognate type II receptor. That SPARC is directly involved in the regulation of the TGF‐β1 signaling cascade is consistent with the paradigm that matricellular proteins modulate interactions among cells, growth factors, and their respective receptors. © 2004 Wiley‐Liss, Inc.
Functional role of centrosomes in spindle assembly and organization
Authors: Varmark Hanne 
Published: March 2004

AbstractThe centrosome is the main MT organizing center in animal cells, and has traditionally been regarded as essential for organization of the bipolar spindle that facilitates chromosome segregation during mitosis. Centrosomes are associated with the poles of the mitotic spindle, and several cell types require these organelles for spindle formation. However, most plant cells and some female meiotic systems get along without this organelle, and centrosome‐independent spindle assembly has now been identified within some centrosome containing cells. How can such observations, which point to mutually incompatible conclusions regarding the requirement of centrosomes in spindle formation, be interpreted? With emphasis on the functional role of centrosomes, this article summarizes the current models of spindle formation, and outlines how observations obtained from spindle assembly assays in vitro may reconcile conflicting opinions about the mechanism of spindle assembly. It is further described how Drosophila mutants are used to address the functional interrelationships between individual centrosomal proteins and spindle formation in vivo. © 2004 Wiley‐Liss, Inc.
Superinduction of IL‐6 by cycloheximide is associated with mRNA stabilization and sustained activation of p38 map kinase and NF‐κB in cultured caco‐2 cells
Authors: Hershko Dan D. , Robb Bruce W. , Wray Curtis J. , Luo Guan‐ju , Hasselgren Per‐Olof 
Published: March 2004

AbstractProtein synthesis inhibitors paradoxically increase the expression of early‐gene products, including various cytokines, through a process known as superinduction. Superinduction is cell‐specific and the mechanisms involved are not fully understood but are usually attributed to decreased mRNA degradation. There is, however, increasing evidence that activation of signaling cascades and increased transcriptional activation may be involved as well. Recent studies suggest that IL‐6 production in the intestinal mucosa is particularly important due to its anti‐inflammatory and protective effects. The effect of protein synthesis inhibitors on IL‐6 production in enterocytes, however, is unknown. Treatment of Caco‐2 cells with cycloheximide (10 μg/ml) increased IL‐6 mRNA and protein levels in IL‐1β‐treated cells and this was associated with increased mRNA stabilization. In addition, cycloheximide suppressed IκBα resynthesis and prolonged p38MAP kinase activation and these changes were associated with sustained activation of the transcription factor NF‐κB. NF‐κB activation, in turn, was prevented by the specific p38MAP kinase inhibitor SB208350. Our results suggest that superinduction of IL‐6 by cycloheximide in enterocytes results from both increased mRNA stabilization and upregulated transcriptional activity mediated by prolonged activation of the p38 MAP kinase and NF‐κB. © 2004 Wiley‐Liss, Inc.
Cell cycle regulatory protein p27KIP1 is a substrate and interacts with the protein kinase CK2
Authors: Tapia Julio C. , Bolanos‐Garcia Victor M. , Sayed Muhammed , Allende Catherine C. , Allende Jorge E. 
Published: March 2004

AbstractThe protein kinase CK2 is constituted by two catalytic (α and/or α′) and two regulatory (β) subunits. CK2 phosphorylates more than 300 proteins with important functions in the cell cycle. This study has looked at the relation between CK2 and p27KIP1, which is a regulator of the cell cycle and a known inhibitor of cyclin‐dependent kinases (Cdk). We demonstrated that in vitro recombinant Xenopus laevis CK2 can phosphorylate recombinant human p27KIP1, but this phosphorylation occurs only in the presence of the regulatory β subunit. The principal site of phosphorylation is serine‐83. Analysis using pull down and surface plasmon resonance (SPR) techniques showed that p27KIP1 interacts with the β subunit through two domains present in the amino and carboxyl ends, while CD spectra showed that p27KIP1 phosphorylation by CK2 affects its secondary structure. Altogether, these results suggest that p27KIP1 phosphorylation by CK2 probably involves a docking event mediated by the CK2β subunit. The phosphorylation of p27KIP1 by CK2 may affect its biological activity. © 2004 Wiley‐Liss, Inc.