bluuebunny/crossref_metadata_2025_split huggingface dataset:
Impact of urbanization on suspended sediment and organic matter fluxes from small catchments in Tahiti
Authors: Wotling G. , Bouvier Ch. 
Published: October 2002

AbstractThis study provides an initial characterization of pollution associated with storm runoff in Tahiti. A thousand floodwater samples were collected from three representative catchments and subsequently analysed. The main pollution parameters chosen were total suspended sediment (TSS), chemical oxygen demand (COD), biochemical oxygen demand (BOD5), total nitrogen (TN) and Total Phosphorus (TP). First, organic pollution appeared to be related closely to sediment, thus TSS could be used as a global indicator. Next, regression models between an event's TSS load and its hydrological characteristics were used to obtain annual load estimates. Great interannual variability was found to be strongly influenced by the few major floods that occur during the rainy season. Our results also emphasize the importance of the impact of urbanization on solid catchment exportation: from 60 TSS t/km2/year in a natural forested catchment, fluxes reached more than 700 TSS t/km2/year during preparatory urbanization earthworks before stabilizing at 140 TSS t/km2/year in a consolidated urbanized area. Clearly, runoff effects need to be taken into consideration for effective urban planning and for the preservation of the coastal environment in Tahiti. Copyright © 2002 John Wiley & Sons, Ltd.
Assessing the uncertainty in distributed model predictions using observed binary pattern information within GLUE
Authors: Aronica G. , Bates P. D. , Horritt M. S. 
Published: October 2002

AbstractIn this paper we extend the generalized likelihood uncertainty estimation (GLUE) technique to estimate spatially distributed uncertainty in models conditioned against binary pattern data contained in flood inundation maps. Untransformed binary pattern data already have been used within GLUE to estimate domain‐averaged (zero‐dimensional) likelihoods, yet the pattern information embedded within such sources has not been used to estimate distributed uncertainty. Where pattern information has been used to map distributed uncertainty it has been transformed into a continuous function prior to use, which may introduce additional errors. To solve this problem we use here ‘raw’ binary pattern data to define a zero‐dimensional global performance measure for each simulation in a Monte Carlo ensemble. Thereafter, for each pixel of the distributed model we evaluate the probability that this pixel was inundated. This probability is then weighted by the measure of global model performance, thus taking into account how well a given parameter set performs overall. The result is a distributed uncertainty measure mapped over real space. The advantage of the approach is that it both captures distributed uncertainty and contains information on global likelihood that can be used to condition predictions of further events for which observed data are not available. The technique is applied to the problem of flood inundation prediction at two test sites representing different hydrodynamic conditions. In both cases, the method reveals the spatial structure in simulation uncertainty and simultaneously enables mapping of flood probability predicted by the model. Spatially distributed uncertainty analysis is shown to contain information over and above that available from global performance measures. Overall, the paper highlights the different types of information that may be obtained from mappings of model uncertainty over real and n‐dimensional parameter spaces. Copyright © 2002 John Wiley & Sons, Ltd.
The zone of vegetation influence on baseflow revealed by diel patterns of streamflow and vegetation water use in a headwater basin
Authors: Bond Barbara J. , Jones Julia A. , Moore Georgianne , Phillips Nathan , Post David , McDonnell Jeffrey J. 
Published: October 2002

AbstractWater use by vegetation can be closely linked to streamflow patterns on a variety of time scales. However, many of the details of these linkages are poorly understood. We compared diel (24 h) patterns of transpirational water use with streamflow patterns in a small headwater basin that displays a marked diel variation during summer months. The study site was in western Oregon. Our objectives were to: (1) determine the phase shift, i.e. the time lag between maximum transpiration and minimum streamflow, and the strength of the correlation at that time lag; (2) determine the amount of streamflow that is ‘missing’ during each diel cycle (i.e. the difference between base flow, defined by the daily maxima, and actual flow) and use it to estimate the zone, or area, of vegetation that influences daily streamflow patterns; (3) test and refine a conceptual model of how the coupling between vegetation water use and streamflow changes over the period of summer drought in this basin. We found that vegetation water use in the summer is coupled to streamflow over time scales of 4 to 8 h, and water‐use‐related fluctuations accounted for 1 to 6% of summer base flow. Direct evaporation from the channel was an order of magnitude less than the diel streamflow decrease. Transpiration within only 0·1 to 0·3% of the basin area accounted for the diel variation in streamflow. As the basin drained further through the summer, the coupling between vegetation and streamflow was diminished and occurred at longer time scales, and the zone of vegetation influence became smaller. This pattern is in accordance with our conceptual model, which attributes the summer decline in the strength of the vegetation–streamflow coupling to the increasing depth of plant‐available water in the soil profile. Although this study is preliminary, we believe it is an important first step in describing better the coupling of vegetation water use to streamflow. Copyright © 2002 John Wiley & Sons, Ltd.
Promoting effects of monomethylarsonic acid, dimethylarsinic acid and trimethylarsine oxide on induction of rat liver preneoplastic glutathione S‐transferase placental form positive foci: A possible reactive oxygen species mechanism
Authors: Nishikawa Takayuki , Wanibuchi Hideki , Ogawa Motome , Kinoshita Anna , Morimura Keiichirou , Hiroi Toyoko , Funae Yoshihiko , Kishida Hideki , Nakae Dai , Fukushima Shoji 
Published: October 2002

AbstractDimethylarsinic acid (DMA) is a major metabolite of inorganic arsenicals, which are epidemiologically significant chemicals in relation to liver cancer in mammals. The present study was conducted to determine the promoting effects of organic arsenicals related to DMA [monomethylarsonic acid (MMA) and trimethylarsine oxide (TMAO)] on rat liver carcinogenesis using a liver medium‐term bioassay (the Ito test). Male, 10‐week‐old, F344 rats were given a single i.p. injection of diethylnitrosamine at a dose of 200 mg/kg b.w. as an initiator. Starting 2 weeks thereafter they received 100 ppm of MMA, DMA or TMAO in their drinking water, or no supplement as a control, for 6 weeks. All animals underwent 2/3 partial hepatectomy in week 3 after initiation. Quantification of glutathione S‐transferase placental form (GST‐P)‐positive foci as preneoplastic lesions in liver sections revealed significantly increased numbers and areas in all 3 treated groups compared with controls. Hepatic microsome cytochrome P‐450 content was markedly increased with all 3 arsenic treatments. Markedly elevated CYP 2B1 protein levels and CYP 2B1/2 mRNA levels were thus observed in all cases. The potency of promotion was similar for MMA, DMA and TMAO. Since hydroxyradicals were found to be generated in the relatively early phase while methylated arsenicals were metabolized in liver, the resultant oxidative stress might have promoted lesion development. © 2002 Wiley‐Liss, Inc.
Serum levels of angiogenin, basic fibroblast growth factor and endostatin in patients receiving intensive chemotherapy for acute myelogenous leukemia
Authors: Glenjen Nils , Mosevoll Knut Anders , Bruserud Øystein 
Published: October 2002

AbstractAngiogenesis seems to be important both in the pathogenesis of acute myelogenous leukemia (AML) and for the susceptibility of AML blasts to chemotherapy. Recent clinical studies even suggest that antiangiogenic therapy can induce disease control in patients with AML relapse. In this context we have investigated the profile of the systemic component of angiogenic regulation in AML by characterizing the serum levels of (i) the angiogenic regulators angiogenin, basic fibroblast growth factor (bFGF) and endostatin; (ii) the endothelial cell marker soluble (s) E‐selectin. Patients with untreated AML had increased levels of angiogenin, endostatin and sE‐selectin, whereas the levels of bFGF were not significantly altered. The systemic levels of the proangiogenic bFGF, the antiangiogenic endostatin and the endothelial cell marker sE‐selectin showed significant correlations, whereas angiogenin and sE‐selectin levels were not correlated. Furthermore, intensive chemotherapy resulted in decreased systemic levels of the 2 proangiogenic mediators angiogenin and bFGF, whereas endostatin levels remained high after treatment. Although angiogenin normally is a part of the acute phase reaction, its systemic levels were not altered when patients with chemotherapy‐induced cytopenia developed complicating bacterial infections. Our results suggest that intensive chemotherapy can modulate the systemic component of angiogenic regulation in AML patients. © 2002 Wiley‐Liss, Inc.
Characterization of a novel calcium phosphate/sulphate bone cement
Authors: Nilsson M. , Fernández E. , Sarda S. , Lidgren L. , Planell J. A. 
Published: October 2002

AbstractApatitic cements have shown excellent biocompatibility and adequate mechanical properties but have slow resorption in the human body. To assure that new bone tissue grows into the bone defect, a certain porosity is necessary although hard to achieve in injectable cements with suitable mechanical properties. An attempt was made by mixing alpha‐tricalcium phosphate (α‐TCP), calcium sulphate hemihydrate (CSH) and an aqueous solution containing 2.5 wt% of Na2HPO4. The aim was to obtain a material containing two phases: a) one apatitic phase (calcium‐deficient hydroxyapatite; CDHA) and b) one resorbable phase (calcium sulphate dihydrate; CSD). α‐TCP and CSH mixtures were produced at relative intervals of 20 wt%. The liquid‐to−powder (L/P) ratio to obtain a paste was 0.32 mLg−1. The highest compressive strength (34 MPa) was obtained for the pure α‐TCP sample. The strength was, in a first approximation, directly correlated to the weight proportions of the powders. X‐ray diffraction analysis showed that the relative intensity for CDHA increased linearly, and the one for CSD decreased exponentially, when the amount of α‐TCP increased. Thus, CSH ceased to transform to CSD when the amount of α‐TCP increased. Observations in environmental scanning electron microscopy confirmed the X‐ray diffraction results. CSH‐crystals (100 μm) were embedded in the HA‐matrix permitting gradual porosity in the material when resorbed. © 2002 Wiley Periodicals, Inc. J Biomed Mater Res 61: 600–607, 2002
Activation of bone sialoprotein gene transcription by flavonoids is mediated through an inverted CCAAT box in ROS 17/2.8 cells
Authors: Shimizu Emi , Ogata Yorimasa 
Published: October 2002

AbstractBone sialoprotein (BSP) is a major noncollagenous protein of the mineralized bone extracellular matrix that has been implicated in the nucleation of hydroxyapatite. Recent studies have shown that BSP is also expressed by osteotropic cancers suggesting BSP might play a role in the pathogenesis of bone metastases. The present study investigates regulation of BSP transcription in rat osteosarcoma ROS 17/2.8 cells by flavonoids: genistein (an inhibitor of protein tyrosine kinases), daidzein (an inactive compound of genistein), flavone, and flavanone. Genistein, daidzein, and flavone (50 μM) increased steady state levels of BSP mRNA about 1.7‐fold at 12 h. From transient transfection assays using various sized BSP promoter‐luciferase constructs, genistein increased luciferase activities within 12 h. Constructs including the promoter sequence nucleotides (nts) −116 to −43 (pLUC3) were found to enhance transcriptional activity ∼2.6‐fold in ROS 17/2.8 cells treated with genistein (50 μM). Daidzein, flavone, and flavanone (50 μM) also increased luciferase activities. In contrast, the tyrosine kinase inhibitors, herbimycin A and lavendustin A, which do not have a flavonoid structure, did not stimulate BSP transcription. Transcriptional stimulation by genistein was almost completely abrogated in a construct that included 2 bp mutations in the inverted CCAAT box. A monoclonal antibody against NF‐YA, a CCAAT box‐binding transcription factor, inhibited formation of DNA‐NF‐Y protein complex in gel shift assays formed by nuclear extracts of ROS 17/2.8 cells. These data suggest that the inverted CCAAT box is required for flavonoid‐induced BSP expression and that the stimulatory action is dependent on the flavone structure and does not involve an inhibitory action on protein tyrosine kinase. J. Cell. Biochem. 86: 35–44, 2002. © 2002 Wiley‐Liss, Inc.
Regulation of Her2/neu promoter activity by the ETS transcription factor, ER81
Authors: Bosc Denis G. , Janknecht Ralf 
Published: October 2002

AbstractOverexpression of the HER2/Neu receptor is correlated to a poor prognosis in tumor patients and leads to stimulation of mitogen‐activated protein kinase (MAPK) signaling pathways, which in turn activate transcription factors, such as the ETS protein ER81. Here, we have analyzed whether, on the other hand, ER81 may regulate the Her2/neu gene. Indeed, ER81, together with its co‐activators, p300 and CBP, activates the Her2/neu promoter, and this activation is enhanced upon stimulation of MAPK pathways as well as by oncogenic HER2/Neu protein. Furthermore, ER81 interacts with one ETS binding site in the Her2/neu promoter, whose mutation decreases ER81‐mediated transcription. Activation of the Her2/neu promoter is also diminished upon mutation of MAPK‐dependent phosphorylation sites in ER81 or upon deletion of ER81 transactivation domains. In addition, the ER81 DNA‐binding domain on its own functions as a dominant‐negative molecule, effectively repressing any stimulation of the Her2/neu promoter. Altogether, our results show that ER81 is a component of a positive regulatory feedback loop, in which the HER2/Neu protein activates ER81, as well as p300/CBP via MAPKs causing the upregulation of the Her2/neu gene. J. Cell. Biochem. 86: 174–183, 2002. © 2002 Wiley‐Liss, Inc.
Characterization of a 1,25(OH)2‐vitamin D3‐responsive capacitative Ca2+ entry pathway in rat osteoblast‐like cells
Authors: Baldi Carolina , Vazquez Guillermo , Boland Ricardo 
Published: October 2002

AbstractWe investigated the existence of a capacitative Ca2+ entry (CCE) pathway in ROS 17/2.8 osteoblast‐like cells and its responsiveness to 1,25‐dihydroxy‐vitamin D3 [1,25(OH)2D3]. Depletion of inner Ca2+ stores with thapsigargin or 1,25(OH)2D3 in the absence of extracellular Ca2+ transiently elevated cytosolic Ca2+ ([Ca2+]i); after recovery of basal values, Ca2+ re‐addition to the medium markedly increased Ca2+ entry, reflecting pre‐activation of a CCE pathway. Recovery of the Ca2+ overshoot that followed the induced CCE was mainly mediated by the plasma membrane Ca2+‐ATPase. Addition of 1,25(OH)2D3 to the declining phase of the thapsigargin‐induced CCE did not modify further [Ca2+]i, indicating that steroid activation of CCE was dependent on store depletion. Pre‐treatment with 1 μM Gd3+ inhibited 30% both thapsigargin‐ and 1,25(OH)2D3‐stimulated CCE, whereas 2.5 μM Gd3+ was required for maximal inhibition (∼ 85%). The activated CCE was permeable to both Mn2+ and Sr2+. Mn2+ entry sensitivity to Gd3+ was the same as that of the CCE. However, 1‐μM Gd3+ completely prevented capacitative Sr2+ influx, whereas subsequent Ca2+ re‐addition was reduced only 30%. These results suggest that in ROS 17/2.8 cells CCE induced by thapsigargin or 1,25(OH)2D3 is contributed by at least two cation entry pathways: a Ca2+/Mn2+ permeable route insensitive to very low micromolar (1 μM) Gd3+ accounting for most of the CCE and a minor Ca2+/Sr2+/Mn2+ permeable route highly sensitive to 1 μM Gd3+. The Ca2+‐mobilizing agonist ATP also stimulated CCE resembling the Ca2+/Sr2+/Mn2+ permeable entry activated by 1,25(OH)2D3. The data demonstrates for the first time, the presence of a hormone‐responsive CCE pathway in an osteoblast cell model, raising the possibility that it could be an alternative Ca2+ influx route through which osteotropic agents influence osteoblast Ca2+ homeostasis. © Wiley‐Liss, Inc.
Theoretical study on the mechanism of the 3CH2 + NO2 reaction
Authors: Liu Jian‐Jun , Ding Yi‐Hong , Tao Yu‐Guo , Feng Ji‐Kang , Sun Chia‐Chung 
Published: October 2002

AbstractThe complex doublet potential energy surface of the CH2NO2 system is investigated at the B3LYP/6‐31G(d,p) and QCISD(T)/6‐311G(d,p) (single‐point) levels to explore the possible reaction mechanism of the triplet CH2 radical with NO2. Forty minimum isomers and 92 transition states are located. For the most relevant reaction pathways, the high‐level QCISD(T)/6‐311 + G(2df,2p) calculations are performed at the B3LYP/6‐31G(d,p) geometries to accurately determine the energetics. It is found that the top attack of the 3CH2 radical at the N‐atom of NO2 first forms the branched open‐chain H2CNO2 a with no barrier followed by ring closure to give the three‐membered ring isomer cC(H2)ON—O b that will almost barrierlessly dissociate to product P1 H2CO + NO. The lesser followed competitive channel is the 1,3‐H‐shift of a to isomer HCN(O)OH c, which will take subsequent cis‐trans conversion and dissociation to P2 OH + HCNO. The direct O‐extrusion of a to product P3 3O + H2CNO is even much less feasible. Because the intermediates and transition states involved in the above three channels are all lower than the reactants in energy, the title reaction is expected to be rapid, as is consistent with the measured large rate constant at room temperature. Formation of the other very low‐lying dissociation products such as NH2 + CO2, OH + HNCO and H2O + NCO seems unlikely due to kinetic hindrance. Moreover, the 3CH2 attack at the end‐O of NO2 is a barrier‐consumed process, and thus may only be of significance at very high temperatures. The reaction of the singlet CH2 with NO2 is also briefly discussed. Our calculated results may assist in future laboratory identification of the products of the title reaction. © 2002 Wiley Periodicals, Inc. J Comput Chem 23: 1031–1044, 2002
Plasmin activates pro‐matrix metalloproteinase‐2 with a membrane‐type 1 matrix metalloproteinase‐dependent mechanism
Authors: Monea Sara , Lehti Kaisa , Keski‐Oja Jorma , Mignatti Paolo 
Published: October 2002

AbstractMembrane‐type 1 matrix metalloproteinase (MT1‐MMP) has been implicated as a physiological activator of progelatinase A (MMP‐2). We previously reported that plasmin treatment of cells results in proMMP‐2 activation and increased type IV collagen degradation. Here, we analyzed the role of MT1‐MMP in plasmin activation of MMP‐2 using HT‐1080 cells transfected with MT1‐MMP sense or antisense cDNA. Control, vector‐transfected cells that expressed endogenous MT1‐MMP, and antisense cDNA transfectants with very low levels of MT1‐MMP did not activate proMMP‐2. Conversely, cells transfected with sense MT1‐MMP cDNA expressed high MT1‐MMP levels and processed proMMP‐2 to 68/66‐kDa intermediate activation products. Control cells and MT1‐MMP transfectants had much higher levels of cell‐associated MMP‐2 than antisense cDNA transfectants. Addition of plasmin(ogen) to control or MT1‐MMP‐transfected cells generated active, 62‐kDa MMP‐2, but was ineffective with antisense cDNA transfectants. The effect of plasmin(ogen) was prevented by inhibitors of plasmin, but not by metalloproteinase inhibitors, implicating plasmin as a mechanism for proMMP‐2 activation independent of the activity of MT1‐MMP or other MMPs. Plasmin‐mediated activation of proMMP‐2 did not result from processing of proMT1‐MMP and did not correlate with αvβ3 integrin or TIMP‐2 levels. Thus, plasmin can activate proMMP‐2 only in the presence of MT1‐MMP; however, this process does not require the catalytic activity of MT1‐MMP. © 2002 Wiley‐Liss, Inc.
Physiological functions of imprinted genes
Authors: Tycko Benjamin , Morison Ian M. 
Published: October 2002

AbstractGenomic imprinting in gametogenesis marks a subset of mammalian genes for parent‐of‐origin‐dependent monoallelic expression in the offspring. Embryological and classical genetic experiments in mice that uncovered the existence of genomic imprinting nearly two decades ago produced abnormalities of growth or behavior, without severe developmental malformations. Since then, the identification and manipulation of individual imprinted genes has continued to suggest that the diverse products of these genes are largely devoted to controlling pre‐ and post‐natal growth, as well as brain function and behavior. Here, we review this evidence, and link our discussion to a website (http://www.otago.ac.nz/IGC) containing a comprehensive database of imprinted genes. Ultimately, these data will answer the long‐debated question of whether there is a coherent biological rationale for imprinting. © 2002 Wiley‐Liss, Inc.
Role of leukemia inhibitory factor in the regulation of the proliferation and differentiation of neonatal mouse epidermal melanocytes in culture
Authors: Hirobe Tomohisa 
Published: October 2002

AbstractMouse epidermal melanoblasts/melanocytes preferentially proliferated from disaggregated epidermal cell suspensions derived from newborn mouse skin in a serum‐free melanoblast/melanocyte‐proliferation medium supplemented with dibutyryl adenosine 3′:5′‐cyclic monophosphate (DBcAMP) and/or basic fibroblast growth factor (bFGF). Leukemia inhibitory factor (LIF) supplemented to the medium from initiation of primary culture increased the proliferation of melanoblasts or melanocytes as well as the differentiation of melanocytes. Pure cultured primary melanoblasts or melanocytes were further cultured with the medium supplemented with LIF from 14 days (keratinocyte depletion). LIF stimulated the proliferation of melanoblasts or melanocytes as well as the differentiation of melanocytes in the absence of keratinocytes. Moreover, anti‐LIF antibody supplemented to the medium from initiation of primary culture inhibited the proliferation of melanoblasts or melanocytes as well as the differentiation of melanocytes. These results suggest that LIF is one of the keratinocyte‐derived factors involved in regulating the proliferation and differentiation of neonatal mouse epidermal melanocytes in culture in cooperation with cAMP elevator and bFGF. © 2002 Wiley‐Liss, Inc.
New insights into the role of extracellular matrix during tumor onset and progression
Authors: Pupa Serenella M. , Ménard Sylvie , Forti Stefania , Tagliabue Elda 
Published: October 2002

AbstractRecently, a view of the tumor as a functional tissue interconnected with the microenvironment has recently been described. For many years, the stroma has been studied in the context of the malignant lesion, and only rarely has its role been considered before carcinogenic lesions appear. Recent studies have provided evidence that stromal cells and their products can cause the transformation of adjacent cells through transient signaling that leads to the disruption of homeostatic regulation, including control of tissue architecture, adhesion, cell death, and proliferation. It is now well established that tumor progression requires a continually evolving network of interactions between neoplastic cells and extracellular matrix. A relevant step of this process is the remodeling of microenvironment which surrounds tumors leading to the release of ECM‐associated growth factors which can then stimulate tumor and/or endothelial cells. Finally, tumor cells reorganizing the extracellular matrix to facilitate communications and escape the homeostatic control exerted by the microenvironment modify response to cytotoxic treatments. © 2002 Wiley‐Liss, Inc.