bluuebunny/crossref_metadata_2025_split huggingface dataset:
The effect of interpolation methods in surface definition: an experimental study
Authors: Yilmaz H. Murat 
Published: January 2007

AbstractMappings of the earth surface and their representation in 3D (three‐dimensional) models are commonly used in most recent research. Modeling research, which starts with classical surveying methods, acquires new dimensions matching the modern technologies. 3D models of any object or earth surface can be used in much visual and scientific research. A digital model of the landscape is an important part within creation of geo‐information systems used in the public administration and in the commercial sphere. It is an important tool in applications such as geomorphology, hydrology, geology, cartography, ecology, mining etc.Values of volume in terrains that do not have regular geometric structure can be obtained more accurately by using 3D models of surfaces with respect to developing technology. Basic data of 3D models must indicate 3D coordinates of the surveyed object in the reference frame. Distribution and intensity of points are important factors in modeling earth surfaces. A minimum number of points is desired in defining an object in 3D. Interpolation methods employing different mathematical models are used to obtain 3D models of terrain surfaces. In this study, the effect of interpolation methods in defining a terrain surface is investigated. For this purpose, a uniform surface, hill‐shaped artificial object with a known volume is employed. The 3D surface and volume are calculated by using 12 different interpolation methods. Point distribution, point intensity and accuracy of point measurements are not considered. The same data set was used for all the interpolation methods. The interpolation methods are compared and evaluated based on the results. Copyright © 2007 John Wiley & Sons, Ltd.
The contribution of domestic and external factors to emerging market currency crises: an early warning systems approach
Authors: Kamin Steven B. , Schindler John , Samuel Shawna 
Published: January 2007

AbstractIn this paper, a modified ‘early warning system’ (EWS) approach is developed to identify the roles of domestic and external factors in emerging market crises. Several probit models of currency crises were estimated for 26 emerging market countries. These models were used to identify the separate contributions to the probabilities of crisis of domestic and external variables. We found that, relative to domestic factors, adverse external shocks and large external imbalances contributed little to the average estimated probability of crisis in emerging market countries, but accounted for much more of the spikes in the probability of crisis estimated to occur during actual crisis years. We interpret these results to suggest that while, on average over time, domestic factors have tended to contribute to much of the underlying vulnerability of emerging market countries, adverse swings in external factors may have been important in pushing economies ‘over the edge’ and into currency crisis. In consequence, the costs of giving up exchange rate flexibility through adoption of strongly fixed exchange rate regimes—e.g. currency boards or dollarization—may be quite high for some countries. Published in 2007 by John Wiley & Sons, Ltd.
Activating transcription factor 2 controls Bcl‐2 promoter activity in growth plate chondrocytes
Authors: Ma Qin , Li Xinying , Vale‐Cruz Dustin , Brown Mark L. , Beier Frank , LuValle Phyllis 
Published: January 2007

AbstractActivating transcription factor 2 (ATF‐2) is expressed ubiquitously in mammals. Mice deficient in ATF‐2 (ATF‐2 m/m) are slightly smaller than their normal littermates at birth. Approximately 50% of mice born mutant in both alleles die within the first month. Those that survive develop a hypochondroplasia‐like dwarfism, characterized by shortened growth plates and kyphosis. Expression of ATF‐2 within the growth plate is limited to the resting and proliferating zones. We have previously shown that ATF‐2 targets the cyclic AMP response element (CRE) in the promoters of cyclin A and cyclin D1 in growth plate chondrocytes to activate their expression. Here, we demonstrate that Bcl‐2, a cell death inhibitor that regulates apoptosis, is expressed within the growth plate in proliferative and prehypertrophic chondrocytes. However, Bcl‐2 expression declines in hypertrophic chondrocytes. The Bcl‐2 promoter contains a CRE at −1,552 bp upstream of the translation start. Mutations within this CRE cause reduced Bcl‐2 promoter activity. We show here that the absence of ATF‐2 in growth plate chondrocytes corresponds to a decline in Bcl‐2 promoter activity, as well as a reduction in Bcl‐2 protein levels. In addition, we show that ATF‐2 as well as CREB, a transcription factor that can heterodimerize with ATF‐2, bind to the CRE within the Bcl‐2 promoter. These data identify the Bcl‐2 gene as a novel target of ATF‐2 and CREB in growth plate chondrocytes. J. Cell. Biochem. 101: 477–487, 2007. © 2007 Wiley‐Liss, Inc.
Regulation of PDGF‐stimulated SHIP2 tyrosine phosphorylation and association with Shc in 3T3‐L1 preadipocytes
Authors: Artemenko Y. , Gagnon A. , Ibrahim S. , Sorisky A. 
Published: January 2007

AbstractIn 3T3‐L1 and human preadipocytes, insulin results in the isolated rise in phosphatidylinositol (PI)‐3,4,5‐P3, whereas PDGF produces PI(3,4)P2 in addition to PI(3,4,5)P3. SH2 domain‐containing inositol 5‐phosphatase 2 (SHIP2) converts PI(3,4,5)P3 into PI(3,4)P2. PDGF, but not insulin, stimulates SHIP2 tyrosine phosphorylation and its association with Shc in human and 3T3‐L1 preadipocytes. We now demonstrate that SHIP2 tyrosine phosphorylation and association with Shc in PDGF‐treated 3T3‐L1 preadipocytes was reduced by bisindolylmaleimide I (BisI), an inhibitor of conventional/novel protein kinase C (PKC). However, the production of PI(3,4)P2 and PI(3,4,5)P3 by PDGF was unaffected by BisI. Activation of PKC by 12‐O‐tetradecanoylphorbol‐13‐acetate (TPA) was not sufficient to induce SHIP2 tyrosine phosphorylation. Furthermore, we identified threonine 958 (T958) as a novel PDGF‐responsive SHIP2 phosphorylation site. Mutation of T958 to alanine reduced PDGF‐stimulated SHIP2 tyrosine phosphorylation and association with Shc, but did not alter its anti‐proliferative effect on preadipocytes. This study demonstrates that SHIP2 tyrosine phosphorylation and Shc association can be regulated by serine/threonine signaling pathways, either indirectly (via PKC), or directly (via T958). Interestingly, the anti‐proliferative effect of SHIP2 T958A, as well as another SHIP2 mutant (Y986F, Y987F) that also displays defective tyrosine phosphorylation and Shc association, does not depend on these molecular events. J. Cell. Physiol. 211: 598–607, 2007. © 2007 Wiley‐Liss, Inc.
Tiam1 and βPIX mediate Rac‐dependent endothelial barrier protective response to oxidized phospholipids
Authors: Birukova Anna A. , Malyukova Irina , Mikaelyan Arsen , Fu Panfeng , Birukov Konstantin G. 
Published: January 2007

AbstractOxidized 1‐palmitoyl‐2‐arachidonoyl‐sn‐glycero‐3‐phosphorylcholine (OxPAPC) exhibits potent barrier protective effects on pulmonary endothelium, which are mediated by small GTPases Rac and Cdc42. However, upstream mechanisms of OxPAPC‐induced small GTPase activation are not known. We studied involvement of Rac/Cdc42‐specific guanine nucleotide exchange factors (GEFs) Tiam1 and βPIX in OxPAPC‐induced Rac activation, cytoskeletal remodeling, and barrier protective responses in the human pulmonary endothelial cells (EC). OxPAPC induced membrane translocation of Tiam1, βPIX, Cdc42, and Rac, but did not affect intracellular distribution of Rho and Rho‐specific GEF p115‐RhoGEF. Protein depletion of Tiam1 and βPIX using siRNA approach abolished OxPAPC‐induced activation of Rac and its effector PAK1. EC transfection with Tiam1‐, βPIX‐, or PAK1‐specific siRNA dramatically attenuated OxPAPC‐induced barrier enhancement, peripheral actin cytoskeletal enhancement, and translocation of actin‐binding proteins cortactin and Arp3. These results show for the first time that Tiam1 and βPIX mediate OxPAPC‐induced Rac activation, cytoskeletal remodeling, and barrier protective response in pulmonary endothelium. J. Cell. Physiol. 211: 608–617, 2007. © 2007 Wiley‐Liss, Inc.
Interpopulation variation in life‐history traits of Poeciliopsis prolifica: implications for the study of placental evolution
Authors: Pires Marcelo N. , McBride Kevin E. , Reznick David N. 
Published: January 2007

AbstractPlacental reproduction is widespread across vertebrate taxa, but little is known about its life‐history correlates and putative adaptive value. We studied variation in life‐history traits in two populations of the placental poeciliid fish Poeciliopsis prolifica to determine whether differences in post‐fertilization maternal provisioning to embryos have a genetic basis and how food availability affects reproduction. Life histories were characterized for wild‐caught females and for second‐generation lab‐born females raised under two levels of food availability. We found that the two populations did not differ significantly in the wild for any life‐history traits except for the lipid dry weight in females and in embryos at an advanced stage of development. When environmental effects were experimentally controlled, however, populations exhibited significant differences in several traits, including the degree of maternal provisioning to embryos. Food availability significantly affected female size at first parturition, brood size and offspring dry weight at birth. Altogether, these results demonstrate that population differences in maternal provisioning and other life‐history traits have a genetic basis and show a plastic response to food availability. We infer that phenotypic plasticity may mask population differences in the field. In addition, when comparing life‐history patterns in these two populations with known patterns in placental and non‐placental poeciliids, our results support the hypotheses that placentation is an adaptive reproductive strategy under high‐resource conditions but that it may represent a cost under low‐food conditions. Finally, our results highlight that age at maturity and reproductive allotment may be key life‐history traits accompanying placental evolution. J. Exp. Zool. 307A, 2007. © 2007 Wiley‐Liss, Inc.
Erosion of interaction networks in reduced and degraded genomes
Authors: Ochman Howard , Liu Renyi , Rocha Eduardo P.C. 
Published: January 2007

AbstractUnlike eukaryotes, which often recruit duplicated genes into existing protein–protein interaction (PPI) networks, the low levels of gene duplication coupled with the high probability of lateral transfer of novel genes alters the manner in which PPI networks can evolve in bacteria. By inferring the PPIs present in the ancestor to contemporary Gammaproteobacteria, we were able to trace the changes in gene repertoires, and their consequences on PPI network evolution, in several bacterial lineages that have independently undergone reductions in genome size and genome contents. As genomes degrade, virtually all multi‐partner proteins have lost interactors; however, the overall average number of connections increases due to the preferential elimination of proteins that interact with only one other protein partner. We also studied the effect of lateral gene transfer on PPI network evolution by analyzing the connectivity of genes that have been gained along the Escherichia coli lineage, as well as those acquired genes subsequently silenced in Shigella flexneri, since diverging from the gammaproteobacterial ancestor. The situation in PPI networks, in which newly acquired genes preferentially attach to the hubs of the network, contrasts that observed in metabolic networks, which evolve by the peripheral gain and loss of genes, and in regulatory networks, in which high connectivity increases the propensity of loss. J. Exp. Zool. (Mol. Dev. Evol.) 308B, 2007. © 2007 Wiley‐Liss, Inc.
Explaining the freemartin: Tandler and Keller vs. Lillie and the question of priority
Authors: Freeman Gary 
Published: January 2007

AbstractThe correct explanation for the freemartin phenotype in the female twin of a female–male pair in cattle was first reported by Tandler and Keller (1911. Deutsche Tierärzt Wochenschr 19:148–149). This same explanation for the freemartin was independently discovered by Lillie (1916. Science 43:611–613). Today both set of scientists are given credit for this discovery; it is the basis for much of the subsequent work on the developmental basis for sex differentiation in vertebrates. Even though Lillie published after Keller and Tandler, he gets credit for this discovery because: (1) Keller and Tandler published in a veterinary journal and as a consequence their work was not disseminated as broadly throughout the larger scientific community; this problem was compounded by the fact that their definitive 1916 paper was published under wartime conditions during World War I, and (2) Lillie was an influential scientist with a group of graduate students who could elaborate on and extend his work; they published a number of papers on the freemartin. At some point while Lillie was doing his initial work on the freemartin he may have become aware that Keller and Tandler were also working on the freemartin problem; this information may have shaped his decision on when to publish. J. Exp. Zool. (Mol. Dev. Eiol.) 308B, 2007. © 2007 Wiley‐Liss, Inc.
Maternal control of pattern formation in Xenopus laevis
Authors: White Jody A. , Heasman Janet 
Published: January 2007

AbstractWe review the essential role of maternal factors in pattern formation for Xenopus laevis, focusing on VegT, Vg1, and Wnt11. Results from loss of function experiments demonstrate a clear requirement for these genes in germ layer specification, dorsal–ventral axis formation, and convergence extension. We also discuss these genes in the broader context of metazoan development, exploring whether and how their functions in the X. laevis model organism may or may not be conserved in other species. Wnt11 signaling in particular provides a classic example where understanding context in development is crucial to understanding function. Genomic sequencing, gene expression, and functional screening data that are becoming available in more species are providing invaluable aid to decoding and modeling signaling pathways. More work is needed to develop a comprehensive catalog of the Wnt signaling, T‐box, and TGF‐β genes in metazoans both near and far in evolutionary distance. We finally discuss some specific experimental and modeling efforts that will be needed to understand the behavior of these signaling networks in vivo so that we can interpret these critical pathways in an evolutionary framework. J. Exp. Zool. (Mol. Dev. Evol.) 310B:73–84, 2008. © 2007 Wiley‐Liss, Inc.
Serum cytokine levels in response to hepatic cryoablation
Authors: Osada Shinji , Imai Hisashi , Tomita Hiroyuki , Tokuyama Yasuharu , Okumura Naoki , Matsuhashi Nobuhisa , Sakashita Fumio , Nonaka Kenichi 
Published: January 2007

AbstractBackground and ObjectivesCryogenic treatment sometimes stimulates the immune system by releasing intracellular antigens. We evaluated anti‐tumor immune response by analyzing alterations in serum cytokine levels.MethodsPercutaneous cryosurgery was performed in 13 patients with unresectable tumors. Serum levels of interleukin (IL) ‐4, ‐6, and ‐10, tumor necrosis factor (TNF)‐alpha, and interferon (IFN)‐gamma were measured by enzyme‐linked immunosorbent assay (ELISA). The Th1/Th2 ratio was estimated from the IFN‐gamma/IL‐4 ratio.ResultsLevels of serum factors in the immune reaction (IR) group, in which tumor necrosis was identified not only in the treated area but also away from the treated area, were compared with those in the local effect (LE) group. Serum amyloid A (SAA), C‐reactive protein (CRP), and IL‐6 levels were increased in both groups after three treatments. The serum IL‐10 level tended to increase with the number of treatments. Pretreatment IL‐10 levels in the LE group were significantly greater than those in the IR group, and the maximum value in the LE group (59.5 ± 13.2 pg/ml) was greater than that in the IR group (47.0 ± 15.0 pg/ml). The TNF‐alpha level was increased in the IR group. Pretreatment TNF‐alpha levels and maximum levels in response to treatment were significantly greater in the IR group than in the LE group (P = 0.0313). The Th1/Th2 ratio was increased in the IR group, and the maximum ratio was significantly greater in the IR group than in the LE group.ConclusionIt might be possible to evaluate the appearance of immune responses to cryosurgery by monitoring serum cytokine levels. J. Surg. Oncol. 2007; 95: 491–498. © 2007 Wiley‐Liss, Inc.
Germline MYH mutations in a clinic‐based series of Canadian multiple colorectal adenoma patients
Authors: Croitoru Marina E. , Cleary Sean P. , Berk Terri , Di Nicola Nando , Kopolovic Ilana , Bapat Bharati , Gallinger Steven 
Published: January 2007

AbstractObjectivesMYH is a member of the DNA base excision repair (BER) pathway and mutations of this gene predispose to the development of colorectal neoplasia in an autosomal recessive transmission pattern. Our objective was to determine the significance of MYH mutations in a series of Canadian patients with multiple adenomas.MethodsWe screened for germline MYH mutations (by dHPLCO) in 20 clinic‐based multiple adenoma patients who were adenomatous polyposis coli (APC) mutation‐negative. Suspected mutations were confirmed by sequence analysis.ResultsSix of 20 (30%) patients carried pathogenic biallelic MYH mutations, 1 Y165C homozygote and 5 compound heterozygotes of other sequence variants. We identified three novel variants, Q377X, 1314delA, and P281L, which are likely pathogenic. Twenty‐nine relatives of the Y90X/1103delC compound heterozygous carrier were also screened for germline MYH mutations, and 1 homozygous and 14 heterozygous carriers were identified.ConclusionsAmong patients with multiple adenomas, biallelic MYH mutations account for approximately 30% of APC mutation negative cases and two thirds of these carry mutations other than the “common” Y165C and G382D variants. Clinical screening algorithms which focus only on the Y165C and G382D alleles are inadequate since additional pathogenic mutations may be identified by screening the entire gene. J. Surg. Oncol. 2007; 95: 499–506. © 2007 Wiley‐Liss, Inc.
Cyclooxygenase‐2 expression is critical for chronic UV‐induced murine skin carcinogenesis
Authors: Fischer Susan M. , Pavone Amy , Mikulec Carol , Langenbach Robert , Rundhaug Joyce E. 
Published: January 2007

AbstractWhile it has been established that both the constitutive and inducible forms of cyclooxygenase (COX‐1 and COX‐2, respectively) play important roles in chemical initiation‐promotion protocols with phorbol ester tumor promoters, the contribution of these two enzymes to ultraviolet (UV) light‐induced skin tumors has not been fully assessed. To better understand the contribution of COX‐1 and COX‐2 to UV carcinogenesis, we transferred the null allele for each isoform onto the SKH‐1 hairless strain of mouse. Due to low viability on this background with complete knockout of COX‐2, heterozygous mice were used in UV carcinogenesis experiments. While the lack of one allele of COX‐1 had no effect on tumor outcome, the lack of one allele of COX‐2 resulted in a 50–65% reduction in tumor multiplicity and a marked decrease in tumor size. Additionally, transgenic SKH‐1 mice that overexpress COX‐2 under the control of a keratin 14 promoter developed 70% more tumors than wild‐type SKH‐1 mice. The lack of one allele of either COX‐1 or COX‐2 reduced prostaglandin (PG) E2 levels in response to a single UV treatment. The proliferative response to UV was significantly reduced in COX‐2, but not COX‐1, heterozygous mice. UV‐induced apoptosis, however, was greater in COX‐2 heterozygous mice. Collectively, these results clearly establish the requirement for COX‐2 in the development of skin tumors. © 2007 Wiley‐Liss, Inc.
Mouse skin chemical carcinogenesis is inhibited by antizyme in promotion‐sensitive and promotion‐resistant genetic backgrounds
Authors: Feith David J. , Shantz Lisa M. , Shoop Paula L. , Keefer Kerry A. , Prakashagowda Chethana , Pegg Anthony E. 
Published: January 2007

AbstractElevated polyamine content and increased ornithine decarboxylase (ODC) activity have been associated with neoplastic growth in numerous animal models and human tissues. Antizyme (AZ) is a negative regulator of polyamine metabolism that inhibits ODC activity, stimulates ODC degradation, and suppresses polyamine uptake. Preliminary evidence, obtained from transgenic mice with tissue specific overexpression of AZ indicates that tumor development can be suppressed by AZ. To extend these studies, we have examined the effect of keratin 5 (K5)‐ or K6‐driven AZ transgenes on 7,12‐dimethylbenz[a]anthracene (DMBA)/12‐O‐tetradecanoylphorbol‐13‐acetate (TPA) chemical carcinogenesis of the skin, in promotion‐resistant C57BL/6 and promotion‐sensitive DBA/2 mice. On both genetic backgrounds, K6‐AZ mice showed a reduction in tumor multiplicity, with 85% fewer tumors than wild‐type controls on the C57BL/6 background and 50% fewer tumors on the DBA/2 background. K5‐AZ mice developed 50% fewer tumors than controls on both backgrounds. The percent of mice with tumors and tumor size were also reduced in the K5‐AZ and K6‐AZ groups. Tumor and TPA‐treated skin sections from K6‐AZ mice exhibited the strongest AZ expression, with localization mainly in suprabasal keratinocytes. K6‐AZ mice also had slightly reduced cell proliferation rates in tumors and TPA‐treated skin. The lack of a more pronounced effect on cell proliferation is probably explained by the observation that AZ staining did not colocalize with proliferating cell nuclear antigen (PCNA), a marker for the proliferative compartment. These studies demonstrate a tumor‐suppressive effect of AZ in C57BL/6 and DBA/2 mice, and confirm the importance of ODC and polyamines in tumor development. © 2007 Wiley‐Liss, Inc.
Potentiation of chemotherapeutics by the Hsp90 antagonist geldanamycin requires a steady serum condition
Authors: Burkitt Michael , Magee Conor , O'Connor David , Campbell Fiona , Cornford Philip , Greenhalf William 
Published: January 2007

AbstractInhibition of Hsp90 potentiates diverse chemotherapeutics, but it is not clear if this applies only to specific agents, tumor types or conditions. The aim of this report is to determine the effect of serum starvation (SS) on potentiation. SUIT2 cells were cultured with and without the presence of serum and 3‐[4,5‐dimethylthiazol‐2‐yl]‐2,5‐diphenyltetrazolium bromide (MTT) assays were carried out at time intervals. Cytotoxic agents were added individually or in combination. Immunohistochemistry of tumor samples and immunofluorescence of cultured cells were used to examine Hsp90 localization. In the presence of serum an at least additive effect of combining the Hsp90 inhibitor geldanamycin (GA) with 5‐fluorouracil (5FU) was demonstrated. Following pretreatment with GA, 5FU and GA were synergistic. However, during SS GA was protective against 5FU. Geldanamycin also protected cells from 12‐O‐tetradecanoylphorbol‐13‐acetate (TPA) during SS. Protection of cells is transitory, as after 24 h of SS GA again has an at least additive negative effect on vitality with 5FU or TPA. Serum starvation of pancreatic cancer cell lines causes normally largely cytoplasmic Hsp90 to become predominantly nuclear localized. Hsp90 nuclear localization was observed in pancreatic and prostate tumors. Hsp90 binding to a pro‐apoptotic client could explain the transitory protection of cells by Hsp90 inhibition during SS. Although potentiation of chemotherapeutics by Hsp90 inhibition is probably a general phenomenon, design of clinical trials should take into account that continuous co‐administration may be ineffective because of a balance of synergy of the drugs in some cells and mutual inhibition of the two drug activities in other cells. © 2007 Wiley‐Liss, Inc.