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  • 1
    Publication Date: 2012-04-15
    Description: We analysed daily precipitation data at the rain gauge stations in North Korea over a period of 25 years from 1983 to 2007, and in South Korea over a period of 35 years from 1973 and 2007. We found a striking trend of decreasing summer precipitation across North Korea. By contrast, in South Korea, the trend is opposite: there is a major increase in summer precipitation. Also, the number of dry days in summer showed an increasing trend in North Korea and a decreasing trend in South Korea. For the number of days with heavy precipitation (i.e. days with above 50 mm/day daily precipitation) during summer, a decreasing trend was detected in North Korea, but no trend in South Korea. However, in South Korea, there was a significant increase of days with heavy precipitation over the whole year. These opposite trends in summer precipitation between North and South Korea were further confirmed using four global/regional satellite and rain gauge datasets of CPC Merged Analysis of Precipitation (CMAP), the Global Precipitation Climatology Project (GPCP), Precipitation REConstruction over the Land (PREC/L), and the Asian Precipitation-Highly Resolved Observation Data Integration Towards the Evaluation of Water Resources (APHRODITE). Copyright © 2011 Royal Meteorological Society
    Print ISSN: 0899-8418
    Electronic ISSN: 1097-0088
    Topics: Geosciences , Physics
    Published by Wiley
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  • 2
    Publication Date: 2011-11-24
    Description: We analysed daily precipitation data at the rain gauge stations in North Korea over a period of 25 years from 1983 to 2007, and in South Korea over a period of 35 years from 1973 and 2007. We found a striking trend of decreasing summer precipitation across North Korea. By contrast, in South Korea, the trend is opposite: there is a major increase in summer precipitation. Also, the number of dry days in summer showed an increasing trend in North Korea and a decreasing trend in South Korea. For the number of days with heavy precipitation (i.e. days with above 50 mm/day daily precipitation) during summer, a decreasing trend was detected in North Korea, but no trend in South Korea. However, in South Korea, there was a significant increase of days with heavy precipitation over the whole year. These opposite trends in summer precipitation between North and South Korea were further confirmed using four global/regional satellite and rain gauge datasets of CPC Merged Analysis of Precipitation (CMAP), the Global Precipitation Climatology Project (GPCP), Precipitation REConstruction over the Land (PREC/L), and the Asian Precipitation-Highly Resolved Observation Data Integration Towards the Evaluation of Water Resources (APHRODITE). Copyright © 2011 Royal Meteorological Society
    Print ISSN: 0899-8418
    Electronic ISSN: 1097-0088
    Topics: Geosciences , Physics
    Published by Wiley
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  • 3
    Publication Date: 2012-01-14
    Description: Author(s): A. W. Brown and J. M. Adams Models of smectic- C liquid-crystal elastomers predict that they can display soft elasticity, in which the shape of the elastomer changes at no energy cost. The amplitude of the soft mode and the accompanying shears are dependent on the orientation of the layer normal and the director with respect to... [Phys. Rev. E 85, 011703] Published Fri Jan 13, 2012
    Keywords: Liquid crystals
    Print ISSN: 1539-3755
    Electronic ISSN: 1550-2376
    Topics: Physics
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  • 4
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1998-09-12
    Description: Bcl-2 and related cytoplasmic proteins are key regulators of apoptosis, the cell suicide program critical for development, tissue homeostasis, and protection against pathogens. Those most similar to Bcl-2 promote cell survival by inhibiting adapters needed for activation of the proteases (caspases) that dismantle the cell. More distant relatives instead promote apoptosis, apparently through mechanisms that include displacing the adapters from the pro-survival proteins. Thus, for many but not all apoptotic signals, the balance between these competing activities determines cell fate. Bcl-2 family members are essential for maintenance of major organ systems, and mutations affecting them are implicated in cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Adams, J M -- Cory, S -- CA43540/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1998 Aug 28;281(5381):1322-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Walter and Eliza Institute of Medical Research, Post Office Royal Melbourne Hospital, Victoria 3050, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9735050" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Cell Cycle ; *Cell Survival ; Cysteine Endopeptidases/metabolism ; Cytokines/physiology ; Genes, bcl-2 ; Humans ; Neoplasms/etiology/pathology/therapy ; Organelles/physiology ; Proto-Oncogene Proteins c-bcl-2/chemistry/*physiology
    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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  • 5
    Publication Date: 1999-11-27
    Description: Apoptosis can be triggered by members of the Bcl-2 protein family, such as Bim, that share only the BH3 domain with this family. Gene targeting in mice revealed important physiological roles for Bim. Lymphoid and myeloid cells accumulated, T cell development was perturbed, and most older mice accumulated plasma cells and succumbed to autoimmune kidney disease. Lymphocytes were refractory to apoptotic stimuli such as cytokine deprivation, calcium ion flux, and microtubule perturbation but not to others. Thus, Bim is required for hematopoietic homeostasis and as a barrier to autoimmunity. Moreover, particular death stimuli appear to activate apoptosis through distinct BH3-only proteins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bouillet, P -- Metcalf, D -- Huang, D C -- Tarlinton, D M -- Kay, T W -- Kontgen, F -- Adams, J M -- Strasser, A -- CA43540/CA/NCI NIH HHS/ -- CA80188/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1999 Nov 26;286(5445):1735-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Walter and Eliza Hall Institute of Medical Research, Melbourne, Victoria 3050, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10576740" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Apoptosis Regulatory Proteins ; Autoimmune Diseases/etiology ; *Autoimmunity ; B-Lymphocytes/physiology ; Carrier Proteins/*physiology ; Cells, Cultured ; Crosses, Genetic ; Female ; Gene Targeting ; Glomerulonephritis/etiology ; Hematopoietic Stem Cells/physiology ; Homeostasis ; Leukocyte Count ; Leukocytes/*physiology ; Male ; *Membrane Proteins ; Mice ; Mice, Transgenic ; *Proto-Oncogene Proteins ; Proto-Oncogene Proteins c-bcl-2/physiology ; Signal Transduction ; T-Lymphocyte Subsets/physiology
    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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  • 6
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1991-11-22
    Description: Numerous cancer-prone strains of mice have been created by the introduction of candidate tumor-promoting genes into fertilized eggs. Each transgenic strain is predisposed to develop specific types of tumors, but they usually arise stochastically because of the need for spontaneous mutation of genes that collaborate with the introduced oncogene. These mice are providing insights into the effects of individual oncogenes on cellular proliferation, differentiation, and viability, as well as on oncogene cooperativity. Their predisposed state imposes sensitivity to viral and chemical carcinogenesis, and the mice should prove valuable in tests of potential carcinogens, therapies, and preventive measures.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Adams, J M -- Cory, S -- CA12421/CA/NCI NIH HHS/ -- CA43540/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1991 Nov 22;254(5035):1161-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Walter and Eliza Hall Institute of Medical Research, Melbourne, Victoria, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1957168" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Animals, Genetically Modified ; Genes, Tumor Suppressor ; Leukemia, Experimental/genetics ; Liver Neoplasms/genetics ; Mammary Neoplasms, Experimental/genetics ; Neoplasms, Experimental/*genetics ; Oncogenes ; Pancreatic Neoplasms/genetics ; Precancerous Conditions/genetics
    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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  • 7
    Publication Date: 2007-02-10
    Description: A central issue in the regulation of apoptosis by the Bcl-2 family is whether its BH3-only members initiate apoptosis by directly binding to the essential cell-death mediators Bax and Bak, or whether they can act indirectly, by engaging their pro-survival Bcl-2-like relatives. Contrary to the direct-activation model, we show that Bax and Bak can mediate apoptosis without discernable association with the putative BH3-only activators (Bim, Bid, and Puma), even in cells with no Bim or Bid and reduced Puma. Our results indicate that BH3-only proteins induce apoptosis at least primarily by engaging the multiple pro-survival relatives guarding Bax and Bak.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Willis, Simon N -- Fletcher, Jamie I -- Kaufmann, Thomas -- van Delft, Mark F -- Chen, Lin -- Czabotar, Peter E -- Ierino, Helen -- Lee, Erinna F -- Fairlie, W Douglas -- Bouillet, Philippe -- Strasser, Andreas -- Kluck, Ruth M -- Adams, Jerry M -- Huang, David C S -- CA43540/CA/NCI NIH HHS/ -- CA80188/CA/NCI NIH HHS/ -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2007 Feb 9;315(5813):856-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Walter and Eliza Hall Institute of Medical Research, 1G Royal Parade, Parkville, Victoria 3050, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17289999" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Apoptosis Regulatory Proteins/chemistry/genetics/*metabolism ; BH3 Interacting Domain Death Agonist Protein/chemistry/genetics/*metabolism ; Cell Line ; Cells, Cultured ; Humans ; Ligands ; Membrane Proteins/chemistry/genetics/*metabolism ; Mice ; Mice, Knockout ; Models, Biological ; Mutation ; Myeloid Cell Leukemia Sequence 1 Protein ; Neoplasm Proteins/metabolism ; Protein Structure, Tertiary ; Proteins/metabolism ; Proto-Oncogene Proteins/chemistry/genetics/*metabolism ; Proto-Oncogene Proteins c-bcl-2/*metabolism ; Tumor Suppressor Proteins/genetics/metabolism ; bcl-2 Homologous Antagonist-Killer Protein/metabolism ; bcl-2-Associated X Protein/chemistry/*metabolism ; bcl-Associated Death Protein/metabolism ; bcl-X Protein/metabolism
    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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  • 8
    Publication Date: 2003-09-23
    Description: Apoptosis provoked by DNA damage requires the p53 tumor suppressor, but which of the many p53-regulated genes are required has remained unknown. Two genes induced by this transcription factor, noxa and puma (bbc3), stand out, because they encode BH3-only proteins, proapoptotic members of the Bcl-2 family required to initiate apoptosis. In mice with either noxa or puma disrupted, we observed decreased DNA damage-induced apoptosis in fibroblasts, although only loss of Puma protected lymphocytes from cell death. Puma deficiency also protected cells against diverse p53-independent cytotoxic insults, including cytokine deprivation and exposure to glucocorticoids, the kinase inhibitor staurosporine, or phorbol ester. Hence, Puma and Noxa are critical mediators of the apoptotic responses induced by p53 and other agents.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Villunger, Andreas -- Michalak, Ewa M -- Coultas, Leigh -- Mullauer, Franziska -- Bock, Gunther -- Ausserlechner, Michael J -- Adams, Jerry M -- Strasser, Andreas -- New York, N.Y. -- Science. 2003 Nov 7;302(5647):1036-8. Epub 2003 Sep 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Walter and Eliza Hall Institute of Medical Research, Melbourne, Australia. andreas.villunger@uibk.ac.at〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14500851" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Apoptosis Regulatory Proteins ; B-Lymphocytes/drug effects/physiology ; Cell Transformation, Viral ; Cytokines/physiology ; DNA Damage ; Dexamethasone/pharmacology ; Etoposide/pharmacology ; Fibroblasts/drug effects/*physiology ; Gamma Rays ; Gene Targeting ; Ionomycin/pharmacology ; Lymphocytes/drug effects/*physiology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Models, Biological ; Proto-Oncogene Proteins/genetics/*physiology ; Proto-Oncogene Proteins c-bcl-2/genetics/*physiology ; RNA, Messenger/genetics/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; T-Lymphocytes/drug effects/physiology ; Tetradecanoylphorbol Acetate/pharmacology ; Transcription, Genetic ; Tumor Suppressor Protein p53/genetics/*physiology
    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: 2016-03-11
    Description: Critical B-lymphoid cell intrinsic role of endogenous MCL-1 in c-MYC-induced lymphomagenesis Cell Death and Disease 7, e2132 (March 2016). doi:10.1038/cddis.2016.43 Authors: S Grabow, G L Kelly, A R D Delbridge, P N Kelly, P Bouillet, J M Adams & A Strasser
    Electronic ISSN: 2041-4889
    Topics: Biology , Medicine
    Published by Springer Nature
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  • 10
    Publication Date: 2007-07-21
    Description: The cancer stem cell hypothesis postulates that tumor growth is driven by a rare subpopulation of tumor cells. Much of the supporting evidence for this intriguing idea is derived from xenotransplantation experiments in which human leukemia cells are grown in immunocompromised mice. We show that, when lymphomas and leukemias of mouse origin are transplanted into histocompatible mice, a very high frequency (at least 1 in 10) of the tumor cells can seed tumor growth. We suggest that the low frequency of tumor-sustaining cells observed in xenotransplantation studies may reflect the limited ability of human tumor cells to adapt to growth in a foreign (mouse) milieu.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kelly, Priscilla N -- Dakic, Aleksandar -- Adams, Jerry M -- Nutt, Stephen L -- Strasser, Andreas -- New York, N.Y. -- Science. 2007 Jul 20;317(5836):337.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Walter and Eliza Hall Institute of Medical Research, Melbourne 3050, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17641192" target="_blank"〉PubMed〈/a〉
    Keywords: Acute Disease ; Animals ; Humans ; Leukemia, Myeloid/*pathology ; Lymphoma/*pathology ; Lymphoma, B-Cell/*pathology ; Mice ; Mice, Transgenic ; Neoplasm Transplantation ; Neoplastic Stem Cells/pathology/*physiology ; Thymus Neoplasms/*pathology ; Transplantation, Heterologous
    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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