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  • 1
    Publication Date: 2010-09-11
    Description: Millennial-scale cold reversals in the high latitudes of both hemispheres interrupted the last transition from full glacial to interglacial climate conditions. The presence of the Younger Dryas stadial (approximately 12.9 to approximately 11.7 kyr ago) is established throughout much of the Northern Hemisphere, but the global timing, nature and extent of the event are not well established. Evidence in mid to low latitudes of the Southern Hemisphere, in particular, has remained perplexing. The debate has in part focused on the behaviour of mountain glaciers in New Zealand, where previous research has found equivocal evidence for the precise timing of increased or reduced ice extent. The interhemispheric behaviour of the climate system during the Younger Dryas thus remains an open question, fundamentally limiting our ability to formulate realistic models of global climate dynamics for this time period. Here we show that New Zealand's glaciers retreated after approximately 13 kyr bp, at the onset of the Younger Dryas, and in general over the subsequent approximately 1.5-kyr period. Our evidence is based on detailed landform mapping, a high-precision (10)Be chronology and reconstruction of former ice extents and snow lines from well-preserved cirque moraines. Our late-glacial glacier chronology matches climatic trends in Antarctica, Southern Ocean behaviour and variations in atmospheric CO(2). The evidence points to a distinct warming of the southern mid-latitude atmosphere during the Younger Dryas and a close coupling between New Zealand's cryosphere and southern high-latitude climate. These findings support the hypothesis that extensive winter sea ice and curtailed meridional ocean overturning in the North Atlantic led to a strong interhemispheric thermal gradient during late-glacial times, in turn leading to increased upwelling and CO(2) release from the Southern Ocean, thereby triggering Southern Hemisphere warming during the northern Younger Dryas.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaplan, Michael R -- Schaefer, Joerg M -- Denton, George H -- Barrell, David J A -- Chinn, Trevor J H -- Putnam, Aaron E -- Andersen, Bjorn G -- Finkel, Robert C -- Schwartz, Roseanne -- Doughty, Alice M -- England -- Nature. 2010 Sep 9;467(7312):194-7. doi: 10.1038/nature09313.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Lamont-Doherty Earth Observatory, Geochemistry, Palisades, New York 10964, USA. mkaplan@ldeo.columbia.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20829791" target="_blank"〉PubMed〈/a〉
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 2008-05-16
    Description: Understanding the origins and roles of cardiac progenitor cells is important for elucidating the pathogenesis of congenital and acquired heart diseases. Moreover, manipulation of cardiac myocyte progenitors has potential for cell-based repair strategies for various myocardial disorders. Here we report the identification in mouse of a previously unknown cardiac myocyte lineage that derives from the proepicardial organ. These progenitor cells, which express the T-box transcription factor Tbx18, migrate onto the outer cardiac surface to form the epicardium, and then make a substantial contribution to myocytes in the ventricular septum and the atrial and ventricular walls. Tbx18-expressing cardiac progenitors also give rise to cardiac fibroblasts and coronary smooth muscle cells. The pluripotency of Tbx18 proepicardial cells provides a theoretical framework for applying these progenitors to effect cardiac repair and regeneration.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cai, Chen-Leng -- Martin, Jody C -- Sun, Yunfu -- Cui, Li -- Wang, Lianchun -- Ouyang, Kunfu -- Yang, Lei -- Bu, Lei -- Liang, Xingqun -- Zhang, Xiaoxue -- Stallcup, William B -- Denton, Christopher P -- McCulloch, Andrew -- Chen, Ju -- Evans, Sylvia M -- P41 RR005351/RR/NCRR NIH HHS/ -- T32 HL007444/HL/NHLBI NIH HHS/ -- England -- Nature. 2008 Jul 3;454(7200):104-8. doi: 10.1038/nature06969. Epub 2008 May 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Skaggs School of Pharmacy, University of California, San Diego, La Jolla, California 92093, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18480752" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; *Cell Lineage ; Gene Expression Regulation, Developmental ; Heart/growth & development ; Lac Operon/genetics ; Mice ; Myocardium/*cytology/metabolism ; Myocytes, Cardiac/*cytology/metabolism ; Myocytes, Smooth Muscle/metabolism ; Pericardium/*cytology/*metabolism ; Stem Cells/*cytology/metabolism ; T-Box Domain Proteins/genetics/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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