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  • Animals  (739)
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  • thema EDItEUR::N History and Archaeology::NH History
  • thema EDItEUR::N History and Archaeology::NH History::NHD European history
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  • 2010-2014  (785)
  • 1960-1964
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  • 1
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    Anthropology: follow field primatologists (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-03-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nekaris, K Anne-Isola -- Nijman, Vincent -- Godfrey, Laurie R -- England -- Nature. 2011 Mar 24;471(7339):448. doi: 10.1038/471448c.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21430762" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anthropology/*methods ; Culture ; Extinction, Biological ; Humans ; *Interdisciplinary Studies ; *Primates/physiology/psychology ; Tool Use Behavior
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 2
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    Telomere dysfunction induces metabolic and mitochondrial compromise (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-02-11
    Description: Telomere dysfunction activates p53-mediated cellular growth arrest, senescence and apoptosis to drive progressive atrophy and functional decline in high-turnover tissues. The broader adverse impact of telomere dysfunction across many tissues including more quiescent systems prompted transcriptomic network analyses to identify common mechanisms operative in haematopoietic stem cells, heart and liver. These unbiased studies revealed profound repression of peroxisome proliferator-activated receptor gamma, coactivator 1 alpha and beta (PGC-1alpha and PGC-1beta, also known as Ppargc1a and Ppargc1b, respectively) and the downstream network in mice null for either telomerase reverse transcriptase (Tert) or telomerase RNA component (Terc) genes. Consistent with PGCs as master regulators of mitochondrial physiology and metabolism, telomere dysfunction is associated with impaired mitochondrial biogenesis and function, decreased gluconeogenesis, cardiomyopathy, and increased reactive oxygen species. In the setting of telomere dysfunction, enforced Tert or PGC-1alpha expression or germline deletion of p53 (also known as Trp53) substantially restores PGC network expression, mitochondrial respiration, cardiac function and gluconeogenesis. We demonstrate that telomere dysfunction activates p53 which in turn binds and represses PGC-1alpha and PGC-1beta promoters, thereby forging a direct link between telomere and mitochondrial biology. We propose that this telomere-p53-PGC axis contributes to organ and metabolic failure and to diminishing organismal fitness in the setting of telomere dysfunction.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3741661/" 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/PMC3741661/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sahin, Ergun -- Colla, Simona -- Liesa, Marc -- Moslehi, Javid -- Muller, Florian L -- Guo, Mira -- Cooper, Marcus -- Kotton, Darrell -- Fabian, Attila J -- Walkey, Carl -- Maser, Richard S -- Tonon, Giovanni -- Foerster, Friedrich -- Xiong, Robert -- Wang, Y Alan -- Shukla, Sachet A -- Jaskelioff, Mariela -- Martin, Eric S -- Heffernan, Timothy P -- Protopopov, Alexei -- Ivanova, Elena -- Mahoney, John E -- Kost-Alimova, Maria -- Perry, Samuel R -- Bronson, Roderick -- Liao, Ronglih -- Mulligan, Richard -- Shirihai, Orian S -- Chin, Lynda -- DePinho, Ronald A -- P30 DK046200/DK/NIDDK NIH HHS/ -- P30DK079638/DK/NIDDK NIH HHS/ -- R01 CA084628/CA/NCI NIH HHS/ -- R01 DK035914/DK/NIDDK NIH HHS/ -- R01 DK056690/DK/NIDDK NIH HHS/ -- R01 DK063356/DK/NIDDK NIH HHS/ -- R01 DK089185/DK/NIDDK NIH HHS/ -- U24 DK-59635/DK/NIDDK NIH HHS/ -- England -- Nature. 2011 Feb 17;470(7334):359-65. doi: 10.1038/nature09787. Epub 2011 Feb 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Belfer Institute for Applied Cancer Science, Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21307849" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/biosynthesis ; Aging/metabolism/pathology ; Animals ; Cardiomyopathies/chemically induced/metabolism/pathology/physiopathology ; Cell Proliferation ; DNA, Mitochondrial/analysis ; Doxorubicin/toxicity ; Gluconeogenesis ; Hematopoietic Stem Cells/metabolism/pathology ; Liver/cytology/metabolism ; Mice ; Mitochondria/*metabolism/*pathology ; Myocardium/cytology/metabolism ; RNA/genetics ; Reactive Oxygen Species/metabolism ; Telomerase/deficiency/genetics ; Telomere/enzymology/genetics/*metabolism/*pathology ; Transcription Factors/antagonists & inhibitors/metabolism ; Tumor Suppressor Protein p53/deficiency/genetics/metabolism
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  • 3
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    SHARPIN is a component of the NF-kappaB-activating linear ubiquitin chain assembly complex (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-04-02
    Description: Cpdm (chronic proliferative dermatitis) mice develop chronic dermatitis and an immunodeficiency with increased serum IgM, symptoms that resemble those of patients with X-linked hyper-IgM syndrome and hypohydrotic ectodermal dysplasia (XHM-ED), which is caused by mutations in NEMO (NF-kappaB essential modulator; also known as IKBKG). Spontaneous null mutations in the Sharpin (SHANK-associated RH domain interacting protein in postsynaptic density) gene are responsible for the cpdm phenotype in mice. SHARPIN shows significant similarity to HOIL-1L (also known as RBCK1), a component of linear ubiquitin chain assembly complex (LUBAC), which induces NF-kappaB activation through conjugation of linear polyubiquitin chains to NEMO. Here, we identify SHARPIN as an additional component of LUBAC. SHARPIN-containing complexes can linearly ubiquitinate NEMO and activated NF-kappaB. Thus, we re-define LUBAC as a complex containing SHARPIN, HOIL-1L, and HOIP (also known as RNF31). Deletion of SHARPIN drastically reduced the amount of LUBAC, which resulted in attenuated TNF-alpha- and CD40-mediated activation of NF-kappaB in mouse embryonic fibroblasts (MEFs) or B cells from cpdm mice. Considering the pleomorphic phenotype of cpdm mice, these results confirm the predicted role of LUBAC-mediated linear polyubiquitination in NF-kappaB activation induced by various stimuli, and strongly suggest the involvement of LUBAC-induced NF-kappaB activation in various disorders.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tokunaga, Fuminori -- Nakagawa, Tomoko -- Nakahara, Masaki -- Saeki, Yasushi -- Taniguchi, Masami -- Sakata, Shin-ichi -- Tanaka, Keiji -- Nakano, Hiroyasu -- Iwai, Kazuhiro -- England -- Nature. 2011 Mar 31;471(7340):633-6. doi: 10.1038/nature09815.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biophysics and Biochemistry, Graduate School of Medicine, Osaka University, Suita, Osaka 565-0871, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21455180" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CD40 Ligand/metabolism ; Carrier Proteins/metabolism ; Cells, Cultured ; HEK293 Cells ; Humans ; Intracellular Signaling Peptides and Proteins/metabolism ; Mice ; Multiprotein Complexes/*chemistry/*metabolism ; NF-kappa B/*metabolism ; Nerve Tissue Proteins/deficiency/genetics/*metabolism ; Tumor Necrosis Factor-alpha/metabolism ; Ubiquitin/*metabolism ; Ubiquitin-Protein Ligase Complexes/chemistry/metabolism ; Ubiquitin-Protein Ligases/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
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    Structural basis of steroid hormone perception by the receptor kinase BRI1 (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-06-15
    Description: Polyhydroxylated steroids are regulators of body shape and size in higher organisms. In metazoans, intracellular receptors recognize these molecules. Plants, however, perceive steroids at membranes, using the membrane-integral receptor kinase BRASSINOSTEROID INSENSITIVE 1 (BRI1). Here we report the structure of the Arabidopsis thaliana BRI1 ligand-binding domain, determined by X-ray diffraction at 2.5 A resolution. We find a superhelix of 25 twisted leucine-rich repeats (LRRs), an architecture that is strikingly different from the assembly of LRRs in animal Toll-like receptors. A 70-amino-acid island domain between LRRs 21 and 22 folds back into the interior of the superhelix to create a surface pocket for binding the plant hormone brassinolide. Known loss- and gain-of-function mutations map closely to the hormone-binding site. We propose that steroid binding to BRI1 generates a docking platform for a co-receptor that is required for receptor activation. Our findings provide insight into the activation mechanism of this highly expanded family of plant receptors that have essential roles in hormone, developmental and innate immunity signalling.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3280218/" 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/PMC3280218/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hothorn, Michael -- Belkhadir, Youssef -- Dreux, Marlene -- Dabi, Tsegaye -- Noel, Joseph P -- Wilson, Ian A -- Chory, Joanne -- AI042266/AI/NIAID NIH HHS/ -- R01 AI042266/AI/NIAID NIH HHS/ -- R01 AI042266-05/AI/NIAID NIH HHS/ -- R37 AI042266/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2011 Jun 12;474(7352):467-71. doi: 10.1038/nature10153.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Plant Biology Laboratory, The Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, California 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21666665" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Arabidopsis/*chemistry/metabolism ; Arabidopsis Proteins/*chemistry/*metabolism ; Binding Sites ; Brassinosteroids ; Cholestanols/chemistry/*metabolism ; Crystallography, X-Ray ; Enzyme Activation ; Models, Molecular ; Molecular Sequence Data ; Plant Growth Regulators/chemistry/*metabolism ; Protein Binding ; Protein Kinases/*chemistry/*metabolism ; Protein Multimerization ; Protein Structure, Tertiary ; Steroids, Heterocyclic/chemistry/*metabolism ; Structure-Activity Relationship
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
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    Structure of the spliceosomal U4 snRNP core domain and its implication for snRNP biogenesis (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-04-26
    Description: The spliceosome is a dynamic macromolecular machine that assembles on pre-messenger RNA substrates and catalyses the excision of non-coding intervening sequences (introns). Four of the five major components of the spliceosome, U1, U2, U4 and U5 small nuclear ribonucleoproteins (snRNPs), contain seven Sm proteins (SmB/B', SmD1, SmD2, SmD3, SmE, SmF and SmG) in common. Following export of the U1, U2, U4 and U5 snRNAs to the cytoplasm, the seven Sm proteins, chaperoned by the survival of motor neurons (SMN) complex, assemble around a single-stranded, U-rich sequence called the Sm site in each small nuclear RNA (snRNA), to form the core domain of the respective snRNP particle. Core domain formation is a prerequisite for re-import into the nucleus, where these snRNPs mature via addition of their particle-specific proteins. Here we present a crystal structure of the U4 snRNP core domain at 3.6 A resolution, detailing how the Sm site heptad (AUUUUUG) binds inside the central hole of the heptameric ring of Sm proteins, interacting one-to-one with SmE-SmG-SmD3-SmB-SmD1-SmD2-SmF. An irregular backbone conformation of the Sm site sequence combined with the asymmetric structure of the heteromeric protein ring allows each base to interact in a distinct manner with four key residues at equivalent positions in the L3 and L5 loops of the Sm fold. A comparison of this structure with the U1 snRNP at 5.5 A resolution reveals snRNA-dependent structural changes outside the Sm fold, which may facilitate the binding of particle-specific proteins that are crucial to biogenesis of spliceosomal snRNPs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3103711/" 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/PMC3103711/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Leung, Adelaine K W -- Nagai, Kiyoshi -- Li, Jade -- MC_U105184330/Medical Research Council/United Kingdom -- U.1051.04.016(78933)/Medical Research Council/United Kingdom -- Medical Research Council/United Kingdom -- England -- Nature. 2011 May 26;473(7348):536-9. doi: 10.1038/nature09956. Epub 2011 Apr 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉MRC Laboratory of Molecular Biology, Hills Road, Cambridge CB2 0QH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21516107" target="_blank"〉PubMed〈/a〉
    Keywords: Binding Sites ; Crystallography, X-Ray ; Humans ; Models, Molecular ; Nucleotides/chemistry/metabolism ; Protein Folding ; Protein Structure, Tertiary ; RNA/chemistry/metabolism ; Ribonucleoprotein, U1 Small Nuclear/chemistry ; Ribonucleoprotein, U4-U6 Small Nuclear/*biosynthesis/*chemistry/metabolism ; Spliceosomes/chemistry/metabolism ; Structure-Activity Relationship
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  • 6
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    Woody cover and hominin environments in the past 6 million years (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-08-05
    Description: The role of African savannahs in the evolution of early hominins has been debated for nearly a century. Resolution of this issue has been hindered by difficulty in quantifying the fraction of woody cover in the fossil record. Here we show that the fraction of woody cover in tropical ecosystems can be quantified using stable carbon isotopes in soils. Furthermore, we use fossil soils from hominin sites in the Awash and Omo-Turkana basins in eastern Africa to reconstruct the fraction of woody cover since the Late Miocene epoch (about 7 million years ago). (13)C/(12)C ratio data from 1,300 palaeosols at or adjacent to hominin sites dating to at least 6 million years ago show that woody cover was predominantly less than approximately 40% at most sites. These data point to the prevalence of open environments at the majority of hominin fossil sites in eastern Africa over the past 6 million years.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cerling, Thure E -- Wynn, Jonathan G -- Andanje, Samuel A -- Bird, Michael I -- Korir, David Kimutai -- Levin, Naomi E -- Mace, William -- Macharia, Anthony N -- Quade, Jay -- Remien, Christopher H -- England -- Nature. 2011 Aug 3;476(7358):51-6. doi: 10.1038/nature10306.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Utah, Salt Lake City, Utah 84112, USA. thure.cerling@utah.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21814275" target="_blank"〉PubMed〈/a〉
    Keywords: Africa, Eastern ; Animals ; *Biological Evolution ; Calibration ; Carbon Isotopes/analysis ; *Ecosystem ; Fossils ; Gait/physiology ; Hominidae/anatomy & histology/*physiology ; Paleontology ; Plant Leaves/growth & development ; Poaceae/growth & development ; Population Dynamics ; Soil/chemistry ; *Trees/growth & development ; Tropical Climate ; Wilderness ; Wood
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  • 7
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    Induction of functional hepatocyte-like cells from mouse fibroblasts by defined factors (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-05-13
    Description: The generation of functional hepatocytes independent of donor liver organs is of great therapeutic interest with regard to regenerative medicine and possible cures for liver disease. Induced hepatic differentiation has been achieved previously using embryonic stem cells or induced pluripotent stem cells. Particularly, hepatocytes generated from a patient's own induced pluripotent stem cells could theoretically avoid immunological rejection. However, the induction of hepatocytes from induced pluripotent stem cells is a complicated process that would probably be replaced with the arrival of improved technology. Overexpression of lineage-specific transcription factors directly converts terminally differentiated cells into some other lineages, including neurons, cardiomyocytes and blood progenitors; however, it remains unclear whether these lineage-converted cells could repair damaged tissues in vivo. Here we demonstrate the direct induction of functional hepatocyte-like (iHep) cells from mouse tail-tip fibroblasts by transduction of Gata4, Hnf1alpha and Foxa3, and inactivation of p19(Arf). iHep cells show typical epithelial morphology, express hepatic genes and acquire hepatocyte functions. Notably, transplanted iHep cells repopulate the livers of fumarylacetoacetate-hydrolase-deficient (Fah(-/-)) mice and rescue almost half of recipients from death by restoring liver functions. Our study provides a novel strategy to generate functional hepatocyte-like cells for the purpose of liver engineering and regenerative medicine.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huang, Pengyu -- He, Zhiying -- Ji, Shuyi -- Sun, Huawang -- Xiang, Dao -- Liu, Changcheng -- Hu, Yiping -- Wang, Xin -- Hui, Lijian -- England -- Nature. 2011 May 11;475(7356):386-9. doi: 10.1038/nature10116.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Cell Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy for Sciences, Yueyang Road 320, 200031 Shanghai, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21562492" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Differentiation/genetics ; Cell Lineage ; Cells, Cultured ; Cyclin-Dependent Kinase Inhibitor p16/deficiency/genetics ; DNA-Binding Proteins/deficiency ; Fibroblasts/*cytology/*metabolism ; GATA4 Transcription Factor/genetics/metabolism ; Gene Expression Profiling ; Hepatocyte Nuclear Factor 1-alpha/genetics/metabolism ; Hepatocyte Nuclear Factor 3-gamma/genetics/metabolism ; Hepatocytes/*cytology/*metabolism/physiology/transplantation ; Hydrolases/deficiency/genetics ; Liver/cytology/enzymology/physiology/physiopathology ; Liver Diseases/enzymology/pathology/physiopathology/therapy ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Regenerative Medicine/methods ; Survival Rate ; Tail/cytology ; Tissue Engineering/methods ; Transduction, Genetic
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  • 8
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    Prion propagation and toxicity in vivo occur in two distinct mechanistic phases (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-02-26
    Description: Mammalian prions cause fatal neurodegenerative conditions including Creutzfeldt-Jakob disease in humans and scrapie and bovine spongiform encephalopathy in animals. Prion infections are typically associated with remarkably prolonged but highly consistent incubation periods followed by a rapid clinical phase. The relationship between prion propagation, generation of neurotoxic species and clinical onset has remained obscure. Prion incubation periods in experimental animals are known to vary inversely with expression level of cellular prion protein. Here we demonstrate that prion propagation in brain proceeds via two distinct phases: a clinically silent exponential phase not rate-limited by prion protein concentration which rapidly reaches a maximal prion titre, followed by a distinct switch to a plateau phase. The latter determines time to clinical onset in a manner inversely proportional to prion protein concentration. These findings demonstrate an uncoupling of infectivity and toxicity. We suggest that prions themselves are not neurotoxic but catalyse the formation of such species from PrP(C). Production of neurotoxic species is triggered when prion propagation saturates, leading to a switch from autocatalytic production of infectivity (phase 1) to a toxic (phase 2) pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sandberg, Malin K -- Al-Doujaily, Huda -- Sharps, Bernadette -- Clarke, Anthony R -- Collinge, John -- MC_U123160656/Medical Research Council/United Kingdom -- MC_U123192748/Medical Research Council/United Kingdom -- Medical Research Council/United Kingdom -- England -- Nature. 2011 Feb 24;470(7335):540-2. doi: 10.1038/nature09768.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉MRC Prion Unit and Department of Neurodegenerative Disease, UCL Institute of Neurology, Queen Square, London WC1N 3BG, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21350487" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biocatalysis ; Biological Assay ; Disease Models, Animal ; Gene Expression ; Kinetics ; Mice ; Mice, Transgenic ; Models, Biological ; PrPC Proteins/analysis/biosynthesis/genetics/metabolism ; PrPSc Proteins/biosynthesis/*metabolism/*pathogenicity/toxicity ; Prion Diseases/*metabolism/*pathology/physiopathology/transmission ; Survival Rate ; Time Factors ; Toxicity Tests
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  • 9
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    Lowland-upland migration of sauropod dinosaurs during the Late Jurassic epoch (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-10-28
    Description: Sauropod dinosaurs were the largest vertebrates ever to walk the Earth, and as mega-herbivores they were important parts of terrestrial ecosystems. In the Late Jurassic-aged Morrison depositional basin of western North America, these animals occupied lowland river-floodplain settings characterized by a seasonally dry climate. Massive herbivores with high nutritional and water needs could periodically experience nutritional and water stress under these conditions, and thus the common occurrence of sauropods in this basin has remained a paradox. Energetic arguments and mammalian analogues have been used to suggest that migration allowed sauropods access to food and water resources over a wide region or during times of drought or both, but there has been no direct support for these hypotheses. Here we compare oxygen isotope ratios (delta(18)O) of tooth-enamel carbonate from the sauropod Camarasaurus with those of ancient soil, lake and wetland (that is, 'authigenic') carbonates that formed in lowland settings. We demonstrate that certain populations of these animals did in fact undertake seasonal migrations of several hundred kilometres from lowland to upland environments. This ability to describe patterns of sauropod movement will help to elucidate the role that migration played in the ecology and evolution of gigantism of these and associated dinosaurs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fricke, Henry C -- Hencecroth, Justin -- Hoerner, Marie E -- England -- Nature. 2011 Oct 26;480(7378):513-5. doi: 10.1038/nature10570.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Geology, Colorado College, Colorado Springs, Colorado 80903, USA. hfricke@coloradocollege.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22031326" target="_blank"〉PubMed〈/a〉
    Keywords: *Animal Migration ; Animals ; Dental Enamel/chemistry ; Dinosaurs/*physiology ; Oxygen Isotopes/analysis ; Seasons ; Soil/analysis
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  • 10
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    Stem cells: iPS cells under attack (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-06-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Apostolou, Effie -- Hochedlinger, Konrad -- England -- Nature. 2011 Jun 8;474(7350):165-6. doi: 10.1038/474165a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21654792" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cellular Reprogramming/genetics/immunology ; Graft Rejection/*genetics/*immunology ; Induced Pluripotent Stem Cells/cytology/*immunology/metabolism/*transplantation ; Mice ; Teratoma/genetics/immunology ; Transplantation, Homologous/immunology ; Transplantation, Isogeneic/immunology ; Up-Regulation/genetics/immunology
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