GLORIA

GEOMAR Library Ocean Research Information Access

X
feed icon rss

Ihre E-Mail wurde erfolgreich gesendet. Bitte prüfen Sie Ihren Maileingang.

Leider ist ein Fehler beim E-Mail-Versand aufgetreten. Bitte versuchen Sie es erneut.

Vorgang fortführen?

Exportieren
  • 1
    facet.materialart.
    Unbekannt
    P3N-PIPO, a Frameshift Product from the P3 Gene, Pleiotropically Determines the Virulence of Clover Yellow Vein Virus in both Resistant and Susceptible Peas [Pathogenesis and Immunity] (2016)
    The American Society for Microbiology (ASM)
    Details
    Publikationsdatum: 2016-07-28
    Beschreibung: Peas carrying the cyv1 recessive resistance gene are resistant to clover yellow vein virus (ClYVV) isolates No.30 (Cl-No.30) and 90-1 (Cl-90-1) but can be infected by a derivative of Cl-90-1 (Cl-90-1 Br2). The main determinant for the breaking of cyv1 resistance by Cl-90-1 Br2 is P3N-PIPO produced from the P3 gene via transcriptional slippage, and the higher level of P3N-PIPO produced by Cl-90-1 Br2 than by Cl-No.30 contributes to the breaking of resistance. Here we show that P3N-PIPO is also a major virulence determinant in susceptible peas that possess another resistance gene, Cyn1 , which does not inhibit systemic infection with ClYVV but causes hypersensitive reaction-like lethal systemic cell death. We previously assumed that the susceptible pea cultivar PI 226564 has a weak allele of Cyn1 . Cl-No.30 did not induce cell death, but Cl-90-1 Br2 killed the plants. Our results suggest that P3N-PIPO is recognized by Cyn1 and induces cell death. Unexpectedly, heterologously strongly expressed P3N-PIPO of Cl-No.30 appears to be recognized by Cyn1 in PI 226564. The level of P3N-PIPO accumulation from the P3 gene of Cl-No.30 was significantly lower than that of Cl-90-1 Br2 in a Nicotiana benthamiana transient assay. Therefore, Cyn1 -mediated cell death also appears to be determined by the level of P3N-PIPO. The more efficiently a ClYVV isolate broke cyv1 resistance, the more it induced cell death systemically (resulting in a loss of the environment for virus accumulation) in susceptible peas carrying Cyn1 , suggesting that antagonistic pleiotropy of P3N-PIPO controls the resistance breaking of ClYVV. IMPORTANCE Control of plant viral disease has relied on the use of resistant cultivars; however, emerging mutant viruses have broken many types of resistance. Recently, we revealed that Cl-90-1 Br2 breaks the recessive resistance conferred by cyv1 , mainly by accumulating a higher level of P3N-PIPO than that of the nonbreaking isolate Cl-No.30. Here we show that a susceptible pea line recognized the increased amount of P3N-PIPO produced by Cl-90-1 Br2 and activated the salicylic acid-mediated defense pathway, inducing lethal systemic cell death. We found a gradation of virulence among ClYVV isolates in a cyv1 -carrying pea line and two susceptible pea lines. This study suggests a trade-off between breaking of recessive resistance ( cyv1 ) and host viability; the latter is presumably regulated by the dominant Cyn1 gene, which may impose evolutionary constraints upon P3N-PIPO for overcoming resistance. We propose a working model of the host strategy to sustain the durability of resistance and control fast-evolving viruses.
    Print ISSN: 0022-538X
    Digitale ISSN: 1098-5514
    Thema: Medizin
    Publiziert von The American Society for Microbiology (ASM)
    Standort Signatur Einschränkungen Verfügbarkeit
    BibTip Andere fanden auch interessant ...
    PAPER CURRENT
  • 2
    facet.materialart.
    Unbekannt
    Direct Binding and Regulation of RhoA by PKGI{alpha} [Molecular Bases of Disease] (2012)
    The American Society for Biochemistry and Molecular Biology (ASBMB)
    Details
    Publikationsdatum: 2012-12-01
    Beschreibung: Vascular smooth muscle cell (VSMC) tone is regulated by the state of myosin light chain (MLC) phosphorylation, which is in turn regulated by the balance between MLC kinase and MLC phosphatase (MLCP) activities. RhoA activates Rho kinase, which phosphorylates the regulatory subunit of MLC phosphatase, thereby inhibiting MLC phosphatase activity and increasing contraction and vascular tone. Nitric oxide is an important mediator of VSMC relaxation and vasodilation, which acts by increasing cyclic GMP (cGMP) levels in VSMC, thereby activating cGMP-dependent protein kinase Iα (PKGIα). PKGI is known to phosphorylate Rho kinase, preventing Rho-mediated inhibition of MLC phosphatase, promoting vasorelaxation, although the molecular mechanisms that mediate this are unclear. Here we identify RhoA as a target of activated PKGIα and show further that PKGIα binds directly to RhoA, inhibiting its activation and translocation. In protein pulldown and immunoprecipitation experiments, binding of RhoA and PKGIα was demonstrated via a direct interaction between the amino terminus of RhoA (residues 1–44), containing the switch I domain of RhoA, and the amino terminus of PKGIα (residues 1–59), which includes a leucine zipper heptad repeat motif. Affinity assays using cGMP-immobilized agarose showed that only activated PKGIα binds RhoA, and a leucine zipper mutant PKGIα was unable to bind RhoA even if activated. Furthermore, a catalytically inactive mutant of PKGIα bound RhoA but did not prevent RhoA activation and translocation. Collectively, these results support that RhoA is a PKGIα target and that direct binding of activated PKGIα to RhoA is central to cGMP-mediated inhibition of the VSMC Rho kinase contractile pathway.
    Print ISSN: 0021-9258
    Digitale ISSN: 1083-351X
    Thema: Biologie , Chemie und Pharmazie
    Publiziert von The American Society for Biochemistry and Molecular Biology (ASBMB)
    Standort Signatur Einschränkungen Verfügbarkeit
    BibTip Andere fanden auch interessant ...
    PAPER CURRENT
  • 3
    facet.materialart.
    Unbekannt
    Fluid shear stress induces differentiation of circulating phenotype endothelial progenitor cells (2012)
    The American Physiological Society (APS)
    Details
    Publikationsdatum: 2012-09-16
    Beschreibung: Endothelial progenitor cells (EPCs) are mobilized from bone marrow to peripheral blood, and contribute to angiogenesis in tissue. In the process, EPCs are exposed to shear stress generated by blood flow and tissue fluid flow. Our previous study showed that shear stress induces differentiation of mature EPCs in adhesive phenotype into mature endothelial cells and, moreover, arterial endothelial cells. In this study we investigated whether immature EPCs in a circulating phenotype differentiate into mature EPCs in response to shear stress. When floating-circulating phenotype EPCs derived from ex vivo expanded human cord blood were exposed to controlled levels of shear stress in a flow-loading device, the bioactivities of adhesion, migration, proliferation, antiapoptosis, tube formation, and differentiated type of EPC colony formation increased. The surface protein expression rate of the endothelial markers VEGF receptor 1 (VEGF-R1) and -2 (VEGF-R2), VE-cadherin, Tie2, VCAM1, integrin α v /β 3 , and E-selectin increased in shear-stressed EPCs. The VEGF-R1, VEGF-R2, VE-cadherin, and Tie2 protein increases were dependent on the magnitude of shear stress. The mRNA levels of VEGF-R1, VEGF-R2, VE-cadherin, Tie2, endothelial nitric oxide synthase, matrix metalloproteinase 9, and VEGF increased in shear-stressed EPCs. Inhibitor analysis showed that the phosphoinositide 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) signal transduction pathway is a potent activator of adhesion, proliferation, tube formation, and differentiation in response to shear stress. Western blot analysis revealed that shear stress activated the VEGF-R2 phosphorylation in a ligand-independent manner. These results indicate that shear stress increases differentiation, adhesion, migration, proliferation, antiapoptosis, and vasculogenesis of circulating phenotype EPCs by activation of VEGF-R2 and the PI3K/Akt/mTOR signal transduction pathway.
    Print ISSN: 0363-6143
    Digitale ISSN: 1522-1563
    Thema: Medizin
    Publiziert von The American Physiological Society (APS)
    Standort Signatur Einschränkungen Verfügbarkeit
    BibTip Andere fanden auch interessant ...
    PAPER CURRENT
  • 4
    facet.materialart.
    Unbekannt
    Engulfment of hematopoietic stem cells caused by down-regulation of CD47 is critical in the pathogenesis of hemophagocytic lymphohistiocytosis (2012)
    American Society of Hematology (ASH)
    In: Blood
    Details
    Publikationsdatum: 2012-11-09
    Beschreibung: Hemophagocytic lymphohistiocytosis (HLH) is characterized by deregulated engulfment of hematopoietic stem cells (HSCs) by BM macrophages, which are activated presumably by systemic inflammatory hypercytokinemia. In the present study, we show that the pathogenesis of HLH involves impairment of the antiphagocytic system operated by an interaction between surface CD47 and signal regulatory protein α (SIRPA). In HLH patients, changes in expression levels and HLH-specific polymorphism of SIRPA were not found. In contrast, the expression of surface CD47 was down-regulated specifically in HSCs in association with exacerbation of HLH, but not in healthy subjects. The number of BM HSCs in HLH patients was reduced to approximately 20% of that of healthy controls and macrophages from normal donors aggressively engulfed HSCs purified from HLH patients, but not those from healthy controls in vitro. Furthermore, in response to inflammatory cytokines, normal HSCs, but not progenitors or mature blood cells, down-regulated CD47 sufficiently to be engulfed by macrophages. The expression of prophagocytic calreticulin was kept suppressed at the HSC stage in both HLH patients and healthy controls, even in the presence of inflammatory cytokines. These data suggest that the CD47-SIRPA antiphagocytic system plays a key role in the maintenance of HSCs and that its disruption by HSC-specific CD47 down-regulation might be critical for HLH development.
    Schlagwort(e): Phagocytes, Granulocytes, and Myelopoiesis
    Print ISSN: 0006-4971
    Digitale ISSN: 1528-0020
    Thema: Biologie , Medizin
    Publiziert von American Society of Hematology (ASH)
    Standort Signatur Einschränkungen Verfügbarkeit
    BibTip Andere fanden auch interessant ...
    PAPER CURRENT
  • 5
    facet.materialart.
    Unbekannt
    Antarctica photometry of the Blazhko RR Lyrae star S Arae (2015)
    Oxford University Press
    Details
    Publikationsdatum: 2015-12-16
    Beschreibung: We pursue the study of S Arae, an RRab Lyrae Blazho star, using unique, uninterrupted and accurate optical photometric data acquired from Antarctica at Dome C by PAIX – Photometer AntarctIca eXtraction – during 150 d. The PAIX data were analysed using both Period04 and PDM13. Besides a main pulsation period of 0.452 d and a modulation period of 47.264 d, three other significant frequencies were found. Multiplet patterns, up to the ninth order, were also extracted, showing a clear asymmetric structure. Following these results, a new approximation of the main-frequency harmonics amplitude decrease is suggested, replacing the usual exponential fit by a hyperbolic one. The physical properties of the Blazhko star, namely metallicity, temperature, mass, were obtained using a new approach based on the study of these parameters for each Blazhko phase. Finally, the PAIX data reveal a residual scatter that occurs during a small phase interval, 10 per cent of the pulsation period, corresponding to the phase of the main shock passage across the atmosphere. The position of the so-called main bump, corresponding to the shock resulting from the infalling atmosphere and the expanding photosphere, varies from one cycle to another and, moreover, around this main bump, two other bumps appear and vanish at different phases during a Blazhko cycle. Following these observations, we discuss the relation between the bump topology and the Blazhko period and give new insights for future Blazhko theoretical investigations.
    Print ISSN: 0035-8711
    Digitale ISSN: 1365-2966
    Thema: Physik
    Publiziert von Oxford University Press
    Standort Signatur Einschränkungen Verfügbarkeit
    BibTip Andere fanden auch interessant ...
    PAPER CURRENT
  • 6
    facet.materialart.
    Unbekannt
    Circadian rhythms. Atomic-scale origins of slowness in the cyanobacterial circadian clock (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2015-06-27
    Beschreibung: Circadian clocks generate slow and ordered cellular dynamics but consist of fast-moving bio-macromolecules; consequently, the origins of the overall slowness remain unclear. We identified the adenosine triphosphate (ATP) catalytic region [adenosine triphosphatase (ATPase)] in the amino-terminal half of the clock protein KaiC as the minimal pacemaker that controls the in vivo frequency of the cyanobacterial clock. Crystal structures of the ATPase revealed that the slowness of this ATPase arises from sequestration of a lytic water molecule in an unfavorable position and coupling of ATP hydrolysis to a peptide isomerization with high activation energy. The slow ATPase is coupled with another ATPase catalyzing autodephosphorylation in the carboxyl-terminal half of KaiC, yielding the circadian response frequency of intermolecular interactions with other clock-related proteins that influences the transcription and translation cycle.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Abe, Jun -- Hiyama, Takuya B -- Mukaiyama, Atsushi -- Son, Seyoung -- Mori, Toshifumi -- Saito, Shinji -- Osako, Masato -- Wolanin, Julie -- Yamashita, Eiki -- Kondo, Takao -- Akiyama, Shuji -- New York, N.Y. -- Science. 2015 Jul 17;349(6245):312-6. doi: 10.1126/science.1261040. Epub 2015 Jun 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Research Center of Integrative Molecular Systems (CIMoS), Institute for Molecular Science, 38 Nishigo-Naka, Myodaiji, Okazaki 444-8585, Japan. ; Research Center of Integrative Molecular Systems (CIMoS), Institute for Molecular Science, 38 Nishigo-Naka, Myodaiji, Okazaki 444-8585, Japan. Department of Functional Molecular Science, SOKENDAI (The Graduate University for Advanced Studies), 38 Nishigo-Naka, Myodaiji, Okazaki 444-8585, Japan. ; Division of Biological Science, Graduate School of Science, Nagoya University, Furo-cho, Chikusa-ku, Nagoya 464-8602, Japan. ; Department of Functional Molecular Science, SOKENDAI (The Graduate University for Advanced Studies), 38 Nishigo-Naka, Myodaiji, Okazaki 444-8585, Japan. Department of Theoretical and Computational Molecular Science, Institute for Molecular Science, 38 Nishigo-Naka, Myodaiji, Okazaki 444-8585, Japan. ; Research Center of Integrative Molecular Systems (CIMoS), Institute for Molecular Science, 38 Nishigo-Naka, Myodaiji, Okazaki 444-8585, Japan. Department of Functional Molecular Science, SOKENDAI (The Graduate University for Advanced Studies), 38 Nishigo-Naka, Myodaiji, Okazaki 444-8585, Japan. Department of Theoretical and Computational Molecular Science, Institute for Molecular Science, 38 Nishigo-Naka, Myodaiji, Okazaki 444-8585, Japan. ; Research Center of Integrative Molecular Systems (CIMoS), Institute for Molecular Science, 38 Nishigo-Naka, Myodaiji, Okazaki 444-8585, Japan. PSL Research University, Chimie ParisTech, 75005 Paris, France. ; Institute for Protein Research, Osaka University, 3-2 Yamada-oka, Suita 565-0871, Japan. ; Research Center of Integrative Molecular Systems (CIMoS), Institute for Molecular Science, 38 Nishigo-Naka, Myodaiji, Okazaki 444-8585, Japan. Department of Functional Molecular Science, SOKENDAI (The Graduate University for Advanced Studies), 38 Nishigo-Naka, Myodaiji, Okazaki 444-8585, Japan. akiyamas@ims.ac.jp.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26113637" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Adenosine Triphosphatases/*chemistry/genetics ; Adenosine Triphosphate/chemistry ; Bacterial Proteins/*chemistry/genetics ; Catalysis ; *Catalytic Domain ; Circadian Clocks/*physiology ; *Circadian Rhythm ; Circadian Rhythm Signaling Peptides and Proteins/*chemistry/genetics ; Crystallography, X-Ray ; Hydrolysis ; Synechococcus/enzymology/*physiology
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Einschränkungen Verfügbarkeit
    BibTip Andere fanden auch interessant ...
    PAPER CURRENT
  • 7
    facet.materialart.
    Unbekannt
    Inclusive fitness theory and eusociality (2011)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2011-03-25
    Beschreibung: Arising from M. A. Nowak, C. E. Tarnita & E. O. Wilson 466, 1057-1062 (2010); Nowak et al. reply. Nowak et al. argue that inclusive fitness theory has been of little value in explaining the natural world, and that it has led to negligible progress in explaining the evolution of eusociality. However, we believe that their arguments are based upon a misunderstanding of evolutionary theory and a misrepresentation of the empirical literature. We will focus our comments on three general issues.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3836173/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3836173/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Abbot, Patrick -- Abe, Jun -- Alcock, John -- Alizon, Samuel -- Alpedrinha, Joao A C -- Andersson, Malte -- Andre, Jean-Baptiste -- van Baalen, Minus -- Balloux, Francois -- Balshine, Sigal -- Barton, Nick -- Beukeboom, Leo W -- Biernaskie, Jay M -- Bilde, Trine -- Borgia, Gerald -- Breed, Michael -- Brown, Sam -- Bshary, Redouan -- Buckling, Angus -- Burley, Nancy T -- Burton-Chellew, Max N -- Cant, Michael A -- Chapuisat, Michel -- Charnov, Eric L -- Clutton-Brock, Tim -- Cockburn, Andrew -- Cole, Blaine J -- Colegrave, Nick -- Cosmides, Leda -- Couzin, Iain D -- Coyne, Jerry A -- Creel, Scott -- Crespi, Bernard -- Curry, Robert L -- Dall, Sasha R X -- Day, Troy -- Dickinson, Janis L -- Dugatkin, Lee Alan -- El Mouden, Claire -- Emlen, Stephen T -- Evans, Jay -- Ferriere, Regis -- Field, Jeremy -- Foitzik, Susanne -- Foster, Kevin -- Foster, William A -- Fox, Charles W -- Gadau, Juergen -- Gandon, Sylvain -- Gardner, Andy -- Gardner, Michael G -- Getty, Thomas -- Goodisman, Michael A D -- Grafen, Alan -- Grosberg, Rick -- Grozinger, Christina M -- Gouyon, Pierre-Henri -- Gwynne, Darryl -- Harvey, Paul H -- Hatchwell, Ben J -- Heinze, Jurgen -- Helantera, Heikki -- Helms, Ken R -- Hill, Kim -- Jiricny, Natalie -- Johnstone, Rufus A -- Kacelnik, Alex -- Kiers, E Toby -- Kokko, Hanna -- Komdeur, Jan -- Korb, Judith -- Kronauer, Daniel -- Kummerli, Rolf -- Lehmann, Laurent -- Linksvayer, Timothy A -- Lion, Sebastien -- Lyon, Bruce -- Marshall, James A R -- McElreath, Richard -- Michalakis, Yannis -- Michod, Richard E -- Mock, Douglas -- Monnin, Thibaud -- Montgomerie, Robert -- Moore, Allen J -- Mueller, Ulrich G -- Noe, Ronald -- Okasha, Samir -- Pamilo, Pekka -- Parker, Geoff A -- Pedersen, Jes S -- Pen, Ido -- Pfennig, David -- Queller, David C -- Rankin, Daniel J -- Reece, Sarah E -- Reeve, Hudson K -- Reuter, Max -- Roberts, Gilbert -- Robson, Simon K A -- Roze, Denis -- Rousset, Francois -- Rueppell, Olav -- Sachs, Joel L -- Santorelli, Lorenzo -- Schmid-Hempel, Paul -- Schwarz, Michael P -- Scott-Phillips, Tom -- Shellmann-Sherman, Janet -- Sherman, Paul W -- Shuker, David M -- Smith, Jeff -- Spagna, Joseph C -- Strassmann, Beverly -- Suarez, Andrew V -- Sundstrom, Liselotte -- Taborsky, Michael -- Taylor, Peter -- Thompson, Graham -- Tooby, John -- Tsutsui, Neil D -- Tsuji, Kazuki -- Turillazzi, Stefano -- Ubeda, Francisco -- Vargo, Edward L -- Voelkl, Bernard -- Wenseleers, Tom -- West, Stuart A -- West-Eberhard, Mary Jane -- Westneat, David F -- Wiernasz, Diane C -- Wild, Geoff -- Wrangham, Richard -- Young, Andrew J -- Zeh, David W -- Zeh, Jeanne A -- Zink, Andrew -- BB/H022716/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- England -- Nature. 2011 Mar 24;471(7339):E1-4; author reply E9-10. doi: 10.1038/nature09831.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21430721" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): *Altruism ; Animals ; *Biological Evolution ; Cooperative Behavior ; Female ; Game Theory ; *Genetic Fitness ; Genetics, Population ; Heredity ; Humans ; Male ; *Models, Biological ; Phenotype ; Reproducibility of Results ; *Selection, Genetic ; Sex Ratio
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
    Standort Signatur Einschränkungen Verfügbarkeit
    BibTip Andere fanden auch interessant ...
    PAPER CURRENT
  • 8
    facet.materialart.
    Unbekannt
    Morphologie et hydrodynamique a l'embouchure du fleuve Bandama. (2006)
    Details
    Publikationsdatum: 2021-05-19
    Beschreibung: Cette étude présente la morphologie récente de l'embouchure du fleuve Bandama à Grand-Lahou. A l'interface eau/sédiment apparaissent des chenaux et des hauts fonds tapissés respectivement par des sables fins à très fins et des sables moyens. Les levés périodiques des contours de la passe effectués jusqu'en 1993 , indiquent une migration significative de l'embouchure vers l'Ouest avec une vitesse de déplacement de l'ordre de 1,1 m/mois....
    Beschreibung: Published
    Schlagwort(e): Coastal morphology ; Sedimentology ; Hydrology ; Hydrology
    Repository-Name: AquaDocs
    Materialart: Journal Contribution
    Format: 478717 bytes
    Format: application/pdf
    Standort Signatur Einschränkungen Verfügbarkeit
    BibTip Andere fanden auch interessant ...
    ARTIKEL (OA)
  • 9
    facet.materialart.
    Unbekannt
    Contribution à l'étude des caractéristiques morphologiques de l'unité littorale de Côte d'Ivoire, Golfe de Guinée: cas du périmètre littoral de Port-Bouet (2021)
    In:  http://aquaticcommons.org/id/eprint/7543 | 424 | 2012-01-31 07:42:19 | 7543 | Centre de Recherches Océanologiques, Côte d'Ivoire
    Details
    Publikationsdatum: 2021-07-04
    Beschreibung: This paper presents a large scale (1/10000) bathymetric chart along with the beach (s.l.) and shoreface schemes of Port-Bouet littoral. All these charts and maps contributed to identify the three morphological sub-areas which characterize the whole littoral area of Port-Bouet.
    Schlagwort(e): Earth Sciences ; Oceanography ; Côte d'Ivoire ; Golf of Guinea ; Port-Bouet ; littorals ; sediment drift ; morphology ; bathymetry
    Repository-Name: AquaDocs
    Materialart: article
    Format: application/pdf
    Format: application/pdf
    Format: 43-52
    Standort Signatur Einschränkungen Verfügbarkeit
    BibTip Andere fanden auch interessant ...
    ARTIKEL (OA)
  • 10
    facet.materialart.
    Unbekannt
    Morphologie et hydrodynamique à l'embouchure du fleuve Bandama (2021)
    In:  http://aquaticcommons.org/id/eprint/7561 | 424 | 2012-01-31 07:36:21 | 7561 | Centre de Recherches Océanologiques, Côte d'Ivoire
    Details
    Publikationsdatum: 2021-07-04
    Beschreibung: This study deals with the present morphology of the Bandama river mouth in Grand-Lahou (Côte d'Ivoire). At the interface water-sediment channels and shallows appear, covered respectively by fine and medium sands. Topographic surveys conducted from 1989 to 1993 show significant migration of the river mouth from east to west. The average migration rate is about 1.1 meter per mouth. Although for the past two years , a rate of about 3.5 meters per month was observed.
    Schlagwort(e): Earth Sciences ; Oceanography ; Côte d'Ivoire ; Bandama river ; morphology ; hydrology ; sedimentology
    Repository-Name: AquaDocs
    Materialart: article
    Format: application/pdf
    Format: application/pdf
    Format: 9-24
    Standort Signatur Einschränkungen Verfügbarkeit
    BibTip Andere fanden auch interessant ...
    ARTIKEL (OA)
Schließen ⊗
Diese Webseite nutzt Cookies und das Analyse-Tool Matomo. Weitere Informationen finden Sie hier...