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  • 2005-2009  (789)
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  • 1
    Publication Date: 2008-02-29
    Description: High-resolution speleothem records from China have provided insights into the factors that control the strength of the East Asian monsoon. Our understanding of these factors remains incomplete, however, owing to gaps in the record of monsoon history over the past two interglacial-glacial cycles. In particular, missing sections have hampered our ability to test ideas about orbital-scale controls on the monsoon, the causes of millennial-scale events and relationships between changes in the monsoon and climate in other regions. Here we present an absolute-dated oxygen isotope record from Sanbao cave, central China, that completes a Chinese-cave-based record of the strength of the East Asian monsoon that covers the past 224,000 years. The record is dominated by 23,000-year-long cycles that are synchronous within dating errors with summer insolation at 65 degrees N (ref. 10), supporting the idea that tropical/subtropical monsoons respond dominantly and directly to changes in Northern Hemisphere summer insolation on orbital timescales. The cycles are punctuated by millennial-scale strong-summer-monsoon events (Chinese interstadials), and the new record allows us to identify the complete series of these events over the past two interglacial-glacial cycles. Their duration decreases and their frequency increases during glacial build-up in both the last and penultimate glacial periods, indicating that ice sheet size affects their character and pacing. The ages of the events are exceptionally well constrained and may thus serve as benchmarks for correlating and calibrating climate records.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Yongjin -- Cheng, Hai -- Edwards, R Lawrence -- Kong, Xinggong -- Shao, Xiaohua -- Chen, Shitao -- Wu, Jiangyin -- Jiang, Xiouyang -- Wang, Xianfeng -- An, Zhisheng -- England -- Nature. 2008 Feb 28;451(7182):1090-3. doi: 10.1038/nature06692.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉College of Geography Science, Nanjing Normal University, Nanjing, Jiangsu 210097, China. yjwang@njnu.edu.cn〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18305541" target="_blank"〉PubMed〈/a〉
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 2
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    Nature Publishing Group (NPG)
    Publication Date: 2008-02-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wu, Ling Juan -- Errington, Jeff -- England -- Nature. 2008 Feb 21;451(7181):900-1. doi: 10.1038/451900a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18288177" target="_blank"〉PubMed〈/a〉
    Keywords: Bacillus subtilis/*cytology/*genetics ; Bacterial Proteins/metabolism ; Biological Transport ; Cell Division ; Cell Membrane/*metabolism ; Chromosomes, Bacterial/genetics/*metabolism ; Spores, Bacterial/cytology/genetics
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  • 3
    Publication Date: 2008-11-21
    Description: Galactic cosmic rays consist of protons, electrons and ions, most of which are believed to be accelerated to relativistic speeds in supernova remnants. All components of the cosmic rays show an intensity that decreases as a power law with increasing energy (for example as E(-2.7)). Electrons in particular lose energy rapidly through synchrotron and inverse Compton processes, resulting in a relatively short lifetime (about 10(5) years) and a rapidly falling intensity, which raises the possibility of seeing the contribution from individual nearby sources (less than one kiloparsec away). Here we report an excess of galactic cosmic-ray electrons at energies of approximately 300-800 GeV, which indicates a nearby source of energetic electrons. Such a source could be an unseen astrophysical object (such as a pulsar or micro-quasar) that accelerates electrons to those energies, or the electrons could arise from the annihilation of dark matter particles (such as a Kaluza-Klein particle with a mass of about 620 GeV).〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chang, J -- Adams, J H -- Ahn, H S -- Bashindzhagyan, G L -- Christl, M -- Ganel, O -- Guzik, T G -- Isbert, J -- Kim, K C -- Kuznetsov, E N -- Panasyuk, M I -- Panov, A D -- Schmidt, W K H -- Seo, E S -- Sokolskaya, N V -- Watts, J W -- Wefel, J P -- Wu, J -- Zatsepin, V I -- England -- Nature. 2008 Nov 20;456(7220):362-5. doi: 10.1038/nature07477.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Purple Mountain Observatory, CAS, 2 West Beijing Road, Nanjing 210008, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19020615" target="_blank"〉PubMed〈/a〉
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  • 4
    Publication Date: 2009-08-21
    Description: Living organisms must acquire new biological functions to adapt to changing and hostile environments. Deepwater rice has evolved and adapted to flooding by acquiring the ability to significantly elongate its internodes, which have hollow structures and function as snorkels to allow gas exchange with the atmosphere, and thus prevent drowning. Many physiological studies have shown that the phytohormones ethylene, gibberellin and abscisic acid are involved in this response, but the gene(s) responsible for this trait has not been identified. Here we show the molecular mechanism of deepwater response through the identification of the genes SNORKEL1 and SNORKEL2, which trigger deepwater response by encoding ethylene response factors involved in ethylene signalling. Under deepwater conditions, ethylene accumulates in the plant and induces expression of these two genes. The products of SNORKEL1 and SNORKEL2 then trigger remarkable internode elongation via gibberellin. We also demonstrate that the introduction of three quantitative trait loci from deepwater rice into non-deepwater rice enabled the latter to become deepwater rice. This discovery will contribute to rice breeding in lowland areas that are frequently flooded during the rainy season.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hattori, Yoko -- Nagai, Keisuke -- Furukawa, Shizuka -- Song, Xian-Jun -- Kawano, Ritsuko -- Sakakibara, Hitoshi -- Wu, Jianzhong -- Matsumoto, Takashi -- Yoshimura, Atsushi -- Kitano, Hidemi -- Matsuoka, Makoto -- Mori, Hitoshi -- Ashikari, Motoyuki -- England -- Nature. 2009 Aug 20;460(7258):1026-30. doi: 10.1038/nature08258.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Bioscience and Biotechnology Center, Nagoya University, Nagoya 464-8601, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19693083" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Physiological/drug effects/genetics/*physiology ; Breeding ; Ethylenes/*metabolism/pharmacology ; *Floods ; Gene Expression Regulation, Plant ; Genes, Plant/genetics/physiology ; Gibberellins/metabolism ; Onions/cytology ; Oryza/drug effects/genetics/*growth & development/*metabolism ; Plant Growth Regulators/*metabolism/pharmacology ; Plant Proteins/genetics/*metabolism ; Quantitative Trait Loci ; Signal Transduction ; Water/metabolism
    Print ISSN: 0028-0836
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
    Publication Date: 2009-01-23
    Description: Host- and pathogen-associated cytoplasmic double-stranded DNA triggers the activation of a NALP3 (also known as cryopyrin and NLRP3)-independent inflammasome, which activates caspase-1 leading to maturation of pro-interleukin-1beta and inflammation. The nature of the cytoplasmic-DNA-sensing inflammasome is currently unknown. Here we show that AIM2 (absent in melanoma 2), an interferon-inducible HIN-200 family member that contains an amino-terminal pyrin domain and a carboxy-terminal oligonucleotide/oligosaccharide-binding domain, senses cytoplasmic DNA by means of its oligonucleotide/oligosaccharide-binding domain and interacts with ASC (apoptosis-associated speck-like protein containing a CARD) through its pyrin domain to activate caspase-1. The interaction of AIM2 with ASC also leads to the formation of the ASC pyroptosome, which induces pyroptotic cell death in cells containing caspase-1. Knockdown of AIM2 by short interfering RNA reduced inflammasome/pyroptosome activation by cytoplasmic DNA in human and mouse macrophages, whereas stable expression of AIM2 in the non-responsive human embryonic kidney 293T cell line conferred responsiveness to cytoplasmic DNA. Our results show that cytoplasmic DNA triggers formation of the AIM2 inflammasome by inducing AIM2 oligomerization. This study identifies AIM2 as an important inflammasome component that senses potentially dangerous cytoplasmic DNA, leading to activation of the ASC pyroptosome and caspase-1.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2862225/" 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/PMC2862225/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fernandes-Alnemri, Teresa -- Yu, Je-Wook -- Datta, Pinaki -- Wu, Jianghong -- Alnemri, Emad S -- AG14357/AG/NIA NIH HHS/ -- AR055398/AR/NIAMS NIH HHS/ -- R01 AG014357/AG/NIA NIH HHS/ -- R01 AG014357-11/AG/NIA NIH HHS/ -- R01 AR055398/AR/NIAMS NIH HHS/ -- R01 AR055398-11A2/AR/NIAMS NIH HHS/ -- England -- Nature. 2009 Mar 26;458(7237):509-13. doi: 10.1038/nature07710. Epub 2009 Jan 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biology, Center for Apoptosis Research, Kimmel Cancer Institute, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19158676" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis Regulatory Proteins ; Caspase 1/metabolism ; Cell Death ; Cell Line ; Cytoplasm/*genetics ; Cytoskeletal Proteins/metabolism ; DNA/immunology/*metabolism ; DNA-Binding Proteins ; Enzyme Activation ; Humans ; Inflammation/*metabolism/*pathology ; Mice ; Nuclear Proteins/chemistry/deficiency/genetics/*metabolism ; Protein Binding
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  • 6
    Publication Date: 2009-06-26
    Description: Genome-wide copy number analyses of human cancers identified a frequent 5p13 amplification in several solid tumour types, including lung (56%), ovarian (38%), breast (32%), prostate (37%) and melanoma (32%). Here, using integrative analysis of a genomic profile of the region, we identify a Golgi protein, GOLPH3, as a candidate targeted for amplification. Gain- and loss-of-function studies in vitro and in vivo validated GOLPH3 as a potent oncogene. Physically, GOLPH3 localizes to the trans-Golgi network and interacts with components of the retromer complex, which in yeast has been linked to target of rapamycin (TOR) signalling. Mechanistically, GOLPH3 regulates cell size, enhances growth-factor-induced mTOR (also known as FRAP1) signalling in human cancer cells, and alters the response to an mTOR inhibitor in vivo. Thus, genomic and genetic, biological, functional and biochemical data in yeast and humans establishes GOLPH3 as a new oncogene that is commonly targeted for amplification in human cancer, and is capable of modulating the response to rapamycin, a cancer drug in clinical use.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2753613/" 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/PMC2753613/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Scott, Kenneth L -- Kabbarah, Omar -- Liang, Mei-Chih -- Ivanova, Elena -- Anagnostou, Valsamo -- Wu, Joyce -- Dhakal, Sabin -- Wu, Min -- Chen, Shujuan -- Feinberg, Tamar -- Huang, Joseph -- Saci, Abdel -- Widlund, Hans R -- Fisher, David E -- Xiao, Yonghong -- Rimm, David L -- Protopopov, Alexei -- Wong, Kwok-Kin -- Chin, Lynda -- 5-T32-AR07098-31/AR/NIAMS NIH HHS/ -- P50 CA090578/CA/NCI NIH HHS/ -- P50 CA093683/CA/NCI NIH HHS/ -- P50 CA093683-06A20011/CA/NCI NIH HHS/ -- P50 CA93683/CA/NCI NIH HHS/ -- R0-1 CA 114277/CA/NCI NIH HHS/ -- R01 AG2400401/AG/NIA NIH HHS/ -- R01 CA093947/CA/NCI NIH HHS/ -- R01 CA093947-08/CA/NCI NIH HHS/ -- R01 CA114277/CA/NCI NIH HHS/ -- R01 CA114277-04/CA/NCI NIH HHS/ -- R01 CA122794/CA/NCI NIH HHS/ -- R01 CA122794-03/CA/NCI NIH HHS/ -- R01 CA93947/CA/NCI NIH HHS/ -- T32 AR007098/AR/NIAMS NIH HHS/ -- T32 AR007098-32/AR/NIAMS NIH HHS/ -- England -- Nature. 2009 Jun 25;459(7250):1085-90. doi: 10.1038/nature08109.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19553991" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibiotics, Antineoplastic/*pharmacology ; Cell Line, Tumor/drug effects ; DNA-Binding Proteins/genetics ; Female ; Gene Knockdown Techniques ; Humans ; Membrane Proteins/genetics/*metabolism ; Mice ; Mice, Nude ; Neoplasms/*physiopathology ; Protein Kinases/genetics/*metabolism ; Saccharomyces cerevisiae/genetics ; *Signal Transduction ; Sirolimus/*pharmacology ; TOR Serine-Threonine Kinases ; Transcription Factors/genetics
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  • 7
    Publication Date: 2009-09-11
    Description: Rapid release of prepublication data has served the field of genomics well. Attendees at a workshop in Toronto recommend extending the practice to other biological data sets.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3073843/" 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/PMC3073843/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Toronto International Data Release Workshop Authors -- Birney, Ewan -- Hudson, Thomas J -- Green, Eric D -- Gunter, Chris -- Eddy, Sean -- Rogers, Jane -- Harris, Jennifer R -- Ehrlich, S Dusko -- Apweiler, Rolf -- Austin, Christopher P -- Berglund, Lisa -- Bobrow, Martin -- Bountra, Chas -- Brookes, Anthony J -- Cambon-Thomsen, Anne -- Carter, Nigel P -- Chisholm, Rex L -- Contreras, Jorge L -- Cooke, Robert M -- Crosby, William L -- Dewar, Ken -- Durbin, Richard -- Dyke, Stephanie O M -- Ecker, Joseph R -- El Emam, Khaled -- Feuk, Lars -- Gabriel, Stacey B -- Gallacher, John -- Gelbart, William M -- Granell, Antoni -- Guarner, Francisco -- Hubbard, Tim -- Jackson, Scott A -- Jennings, Jennifer L -- Joly, Yann -- Jones, Steven M -- Kaye, Jane -- Kennedy, Karen L -- Knoppers, Bartha Maria -- Kyrpides, Nikos C -- Lowrance, William W -- Luo, Jingchu -- MacKay, John J -- Martin-Rivera, Luis -- McCombie, W Richard -- McPherson, John D -- Miller, Linda -- Miller, Webb -- Moerman, Don -- Mooser, Vincent -- Morton, Cynthia C -- Ostell, James M -- Ouellette, B F Francis -- Parkhill, Julian -- Raina, Parminder S -- Rawlings, Christopher -- Scherer, Steven E -- Scherer, Stephen W -- Schofield, Paul N -- Sensen, Christoph W -- Stodden, Victoria C -- Sussman, Michael R -- Tanaka, Toshihiro -- Thornton, Janet -- Tsunoda, Tatsuhiko -- Valle, David -- Vuorio, Eero I -- Walker, Neil M -- Wallace, Susan -- Weinstock, George -- Whitman, William B -- Worley, Kim C -- Wu, Cathy -- Wu, Jiayan -- Yu, Jun -- 062023/Wellcome Trust/United Kingdom -- 077198/Wellcome Trust/United Kingdom -- U54 HG003273/HG/NHGRI NIH HHS/ -- U54 HG003273-04/HG/NHGRI NIH HHS/ -- U54 HG003273-04S1/HG/NHGRI NIH HHS/ -- U54 HG003273-05/HG/NHGRI NIH HHS/ -- U54 HG003273-05S1/HG/NHGRI NIH HHS/ -- U54 HG003273-05S2/HG/NHGRI NIH HHS/ -- U54 HG003273-06/HG/NHGRI NIH HHS/ -- U54 HG003273-06S1/HG/NHGRI NIH HHS/ -- U54 HG003273-06S2/HG/NHGRI NIH HHS/ -- U54 HG003273-07/HG/NHGRI NIH HHS/ -- U54 HG003273-08/HG/NHGRI NIH HHS/ -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- England -- Nature. 2009 Sep 10;461(7261):168-70. doi: 10.1038/461168a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19741685" target="_blank"〉PubMed〈/a〉
    Keywords: *Access to Information ; Cooperative Behavior ; *Guidelines as Topic ; Human Genome Project ; Humans ; Ontario ; *Publishing/ethics/standards ; *Research/standards ; Research Personnel/ethics/standards
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  • 8
    Publication Date: 2006-06-17
    Description: In developing embryos of some extant spiralian animals, polar lobe formation is one of the symmetry-breaking mechanisms for segregation of maternal cytoplasmic substances to certain blastomeres and not others. Polar lobe formation leads to unique early cleavage morphologies that include trilobed, J-shaped, and five-lobed structures. Fossil embryos similar to modern lobeforming embryos are recognized from the Precambrian Doushantuo Formation phosphates, Weng'an, Guizhou Province, China. These embryos are abundant and form a developmental sequence comparable to different developing stages observed in lobe-forming embryos of extant spiralians. These data imply that lobe formation is an evolutionarily ancient process of embryonic specification.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Jun-Yuan -- Bottjer, David J -- Davidson, Eric H -- Dornbos, Stephen Q -- Gao, Xiang -- Yang, Yong-Hua -- Li, Chia-Wei -- Li, Gang -- Wang, Xiu-Qiang -- Xian, Ding-Chang -- Wu, Hung-Jen -- Hwu, Yeu-Kuang -- Tafforeau, Paul -- New York, N.Y. -- Science. 2006 Jun 16;312(5780):1644-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Nanjing Institute of Geology and Paleontology, Institute of Evo/Developmental Biology, and State Key Laboratory of Pharmaceutical Biotechnology, Nanjing University, Nanjing 210093, China. chenjy@nju.edu.cn〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16778054" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Annelida/embryology ; Biological Evolution ; Blastomeres/cytology ; China ; Embryo, Nonmammalian/*anatomy & histology/cytology ; *Embryonic Development ; *Fossils ; Geologic Sediments ; Invertebrates/*embryology ; Mollusca/embryology ; Phosphates ; Platyhelminths/embryology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
    Publication Date: 2007-10-13
    Description: The catalytic (C) subunit of cyclic adenosine monophosphate (cAMP)-dependent protein kinase (PKA) is inhibited by two classes of regulatory subunits, RI and RII. The RII subunits are substrates as well as inhibitors and do not require adenosine triphosphate (ATP) to form holoenzyme, which distinguishes them from RI subunits. To understand the molecular basis for isoform diversity, we solved the crystal structure of an RIIalpha holoenzyme and compared it to the RIalpha holoenzyme. Unphosphorylated RIIalpha(90-400), a deletion mutant, undergoes major conformational changes as both of the cAMP-binding domains wrap around the C subunit's large lobe. The hallmark of this conformational reorganization is the helix switch in domain A. The C subunit is in an open conformation, and its carboxyl-terminal tail is disordered. This structure demonstrates the conserved and isoform-specific features of RI and RII and the importance of ATP, and also provides a new paradigm for designing isoform-specific activators or antagonists for PKA.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4036697/" 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/PMC4036697/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wu, Jian -- Brown, Simon H J -- von Daake, Sventja -- Taylor, Susan S -- GM34921/GM/NIGMS NIH HHS/ -- R01 GM034921/GM/NIGMS NIH HHS/ -- R01 GM034921-23/GM/NIGMS NIH HHS/ -- T32-CA009524/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2007 Oct 12;318(5848):274-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry and Biochemistry, University of California, San Diego, La Jolla, CA 92093, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17932298" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Amino Acid Motifs ; Animals ; Binding Sites ; Catalytic Domain ; Crystallography, X-Ray ; Cyclic AMP/metabolism ; Cyclic AMP-Dependent Protein Kinase RIIalpha Subunit ; Cyclic AMP-Dependent Protein Kinase RIalpha Subunit ; Cyclic AMP-Dependent Protein Kinases/*chemistry/genetics/metabolism ; Holoenzymes/chemistry ; Hydrophobic and Hydrophilic Interactions ; Isoenzymes/chemistry ; Mice ; Models, Molecular ; Protein Conformation ; Protein Structure, Secondary ; Protein Structure, Tertiary
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  • 10
    Publication Date: 2005-05-10
    Description: A 5-year-resolution absolute-dated oxygen isotope record from Dongge Cave, southern China, provides a continuous history of the Asian monsoon over the past 9000 years. Although the record broadly follows summer insolation, it is punctuated by eight weak monsoon events lasting approximately 1 to 5 centuries. One correlates with the "8200-year" event, another with the collapse of the Chinese Neolithic culture, and most with North Atlantic ice-rafting events. Cross-correlation of the decadal- to centennial-scale monsoon record with the atmospheric carbon-14 record shows that some, but not all, of the monsoon variability at these frequencies results from changes in solar output.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Yongjin -- Cheng, Hai -- Edwards, R Lawrence -- He, Yaoqi -- Kong, Xinggong -- An, Zhisheng -- Wu, Jiangying -- Kelly, Megan J -- Dykoski, Carolyn A -- Li, Xiangdong -- New York, N.Y. -- Science. 2005 May 6;308(5723):854-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉College of Geography Science, Nanjing Normal University, Nanjing 210097, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15879216" target="_blank"〉PubMed〈/a〉
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