ALBERT

All Library Books, journals and Electronic Records Telegrafenberg

feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
Filter
Collection
  • 1
    Publication Date: 2013-09-16
    Description: High-resolution sampling in monogenetic fields has the potential to reveal fine-scale heterogeneity of the mantle, a feature that may be overwhelmed by larger fluxes of magma, or missed by under-sampling. The Quaternary Auckland Volcanic Field (AVF) in northern New Zealand is a basaltic field of 51 small-volume volcanic centres, and is one of the best-sampled examples of a monogenetic volcanic field. We present data for 12 centres in the volcanic field. These show the large compositional variations between volcanoes as well as through single eruptive sequences. Whole-rock compositions range from subalkaline basalt in the larger centres, through alkali basalt to nephelinite in the smallest centres. Fractional crystallization has had a limited effect in many of the centres, but high-pressure clinopyroxene crystallization may have occurred in others. Three end-members are observed in Pb isotope space, indicating that distinct mantle source components are involved in the petrogenesis of the magmas. Whole-rock multi-element patterns show that the larger centres have prominent positive Sr anomalies and lack K anomalies, whereas the smaller centres have prominent negative K anomalies and lack Sr anomalies. The melting parameters and compositions of the sources involved are modelled using trace element ratios and multi-element patterns, and three components are characterized: (1) fertile peridotite with a Pb-isotope composition similar to Pacific mid-ocean ridge basalt; (2) eclogite domains with a HIMU-like isotope composition dispersed within the fertile peridotite; (3) slightly depleted subduction-metasomatized peridotitic lithospheric mantle (containing c . 3% subduction fluids). Modelling shows that melting in the AVF begins in garnet-bearing fertile asthenosphere (with preferential melting of eclogite domains) and that melts are variably diluted by melts of the lithospheric source. The U–Th isotope compositions of the end-members in the AVF show 230 Th excess [( 230 Th/ 232 Th) ratios of 1·11–1·38], with the samples of lower ( 230 Th/ 232 Th) exhibiting higher ( 238 U/ 232 Th), which we attribute to the dilution effect of the melts from the lithospheric mantle source. Modelling reveals a correlation between melting in the asthenosphere, the degree of melting and incorporation of the metasomatized lithospheric mantle source, and the resultant size of the volcanic centre. This suggests that the scale of the eruption may essentially be controlled by asthenospheric mantle dynamics.
    Print ISSN: 0022-3530
    Electronic ISSN: 1460-2415
    Topics: Geosciences
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 2
    Publication Date: 2011-09-14
    Description: Angiogenesis is meticulously controlled by a fine balance between positive and negative regulatory activities. Vascular endothelial growth factor (VEGF) is a predominant angiogenic factor and its dosage is precisely regulated during normal vascular formation. In cancer, VEGF is commonly overproduced, resulting in abnormal neovascularization. VEGF is induced in response to various stimuli including hypoxia; however, very little is known about the mechanisms that confine its induction to ensure proper angiogenesis. Chromatin insulation is a key transcription mechanism that prevents promiscuous gene activation by interfering with the action of enhancers. Here we show that the chromatin insulator-binding factor CTCF binds to the proximal promoter of VEGF. Consistent with the enhancer-blocking mode of chromatin insulators, CTCF has little effect on basal expression of VEGF but specifically affects its activation by enhancers. CTCF knockdown cells are sensitized for induction of VEGF and exhibit elevated proangiogenic potential. Cancer-derived CTCF missense mutants are mostly defective in blocking enhancers at the VEGF locus. Moreover, during mouse retinal development, depletion of CTCF causes excess angiogenesis. Therefore, CTCF-mediated chromatin insulation acts as a crucial safeguard against hyperactivation of angiogenesis.
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 3
    Publication Date: 2009-02-27
    Description: Angiogenesis is controlled by physical interactions between cells and extracellular matrix as well as soluble angiogenic factors, such as VEGF. However, the mechanism by which mechanical signals integrate with other microenvironmental cues to regulate neovascularization remains unknown. Here we show that the Rho inhibitor, p190RhoGAP (also known as GRLF1), controls capillary network formation in vitro in human microvascular endothelial cells and retinal angiogenesis in vivo by modulating the balance of activities between two antagonistic transcription factors, TFII-I (also known as GTF2I) and GATA2, that govern gene expression of the VEGF receptor VEGFR2 (also known as KDR). Moreover, this new angiogenesis signalling pathway is sensitive to extracellular matrix elasticity as well as soluble VEGF. This is, to our knowledge, the first known functional cross-antagonism between transcription factors that controls tissue morphogenesis, and that responds to both mechanical and chemical cues.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2708674/" 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/PMC2708674/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mammoto, Akiko -- Connor, Kip M -- Mammoto, Tadanori -- Yung, Chong Wing -- Huh, Dongeun -- Aderman, Christopher M -- Mostoslavsky, Gustavo -- Smith, Lois E H -- Ingber, Donald E -- P01 CA045548/CA/NCI NIH HHS/ -- P01 CA045548-22/CA/NCI NIH HHS/ -- England -- Nature. 2009 Feb 26;457(7233):1103-8. doi: 10.1038/nature07765.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Vascular Biology Program, Department of Pathology & Surgery, Children's Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19242469" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Cell Line ; Endothelial Cells/metabolism ; Endothelium, Vascular/cytology/growth & development ; Extracellular Matrix/metabolism ; GATA2 Transcription Factor/metabolism ; Gene Knockdown Techniques ; Guanine Nucleotide Exchange Factors/deficiency/genetics/metabolism ; Humans ; Mice ; Mice, Inbred C57BL ; Neovascularization, Physiologic/*genetics/physiology ; Repressor Proteins/genetics/metabolism ; Retinal Vessels/growth & development/metabolism ; Signal Transduction ; Transcription Factors/deficiency/genetics/*metabolism ; Transcription Factors, TFII/metabolism ; *Transcription, Genetic ; Up-Regulation ; Vascular Endothelial Growth Factor A/metabolism ; Vascular Endothelial Growth Factor Receptor-2/biosynthesis/genetics/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 4
    Publication Date: 1997-06-13
    Description: Retinal neovascularization is the major cause of untreatable blindness. The role of growth hormone (GH) in ischemia-associated retinal neovascularization was studied in transgenic mice expressing a GH antagonist gene and in normal mice given an inhibitor of GH secretion (MK678). Retinal neovascularization was inhibited in these mice in inverse proportion to serum levels of GH and a downstream effector, insulin-like growth factor-I (IGF-I). Inhibition was reversed with exogenous IGF-I administration. GH inhibition did not diminish hypoxia-stimulated retinal vascular endothelial growth factor (VEGF) or VEGF receptor expression. These data suggest that systemic inhibition of GH or IGF-I, or both, may have therapeutic potential in preventing some forms of retinopathy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Smith, L E -- Kopchick, J J -- Chen, W -- Knapp, J -- Kinose, F -- Daley, D -- Foley, E -- Smith, R G -- Schaeffer, J M -- EY08670/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 1997 Jun 13;276(5319):1706-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Ophthalmology, Harvard Medical School and Children's Hospital, Boston, MA 02115, USA. smith_lo@a1.tch.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9180082" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Endothelial Growth Factors/genetics/metabolism ; Growth Hormone/agonists/antagonists & inhibitors/blood/pharmacology/*physiology ; Hormone Antagonists/pharmacology ; Insulin-Like Growth Factor I/metabolism/pharmacology ; Ischemia ; Lymphokines/genetics/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Peptides, Cyclic/pharmacology ; Recombinant Proteins/pharmacology ; Retinal Neovascularization/*etiology/metabolism/pathology ; Retinal Vessels ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factors
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 5
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Journal of the American Chemical Society 95 (1973), S. 7497-7500 
    ISSN: 1520-5126
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 6
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Chemical reviews 12 (1912), S. 181-213 
    ISSN: 1520-6890
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 7
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Journal of the American Chemical Society 51 (1929), S. 2574-2581 
    ISSN: 1520-5126
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 8
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Journal of the American Chemical Society 52 (1930), S. 1088-1091 
    ISSN: 1520-5126
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 9
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Journal of the American Chemical Society 53 (1931), S. 4400-4408 
    ISSN: 1520-5126
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 10
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Journal of the American Chemical Society 53 (1931), S. 3072-3077 
    ISSN: 1520-5126
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...