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  • 1
    Monograph available for loan
    Monograph available for loan
    Canberra : Australian Government. Publ. Service
    Call number: G 8620
    Type of Medium: Monograph available for loan
    Pages: XIV, 160 S. : Ill., graph. Darst.
    ISBN: 0642056951
    Location: Upper compact magazine
    Branch Library: GFZ Library
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  • 2
    Publication Date: 2016-08-02
    Description: Recent warming of the Antarctic Peninsula during austral autumn, winter, and spring has been linked to sea surface temperature (SST) trends in the tropical Pacific and tropical Atlantic, while warming of the northeast Peninsula during summer has been linked to a strengthening of westerly winds traversing the Peninsula associated with a positive trend in the Southern Annular Mode (SAM). Here we demonstrate that circulation changes associated with the SAM dominate interannual temperature variability across the entire Antarctic Peninsula during both summer and autumn, while relationships with tropical Pacific SST variability associated with the El Niño-Southern Oscillation (ENSO) are strongest and statistically significant primarily during winter and spring only. We find the ENSO-Peninsula temperature relationship during autumn to be weak on interannual timescales, and regional circulation anomalies associated with the SAM more important for interannual temperature variability across the Peninsula during autumn. Consistent with previous studies, western Peninsula temperatures during autumn, winter, and spring are closely tied to changes in the Amundsen Sea Low (ASL) and associated meridional wind anomalies. The interannual variability of ASL depth is most strongly correlated with the SAM index during autumn, while the ENSO relationship is strongest during winter and spring. Investigation of western and northeast Peninsula temperatures separately reveals that interannual variability of northeast Peninsula temperatures is primarily sensitive to zonal wind anomalies crossing the Peninsula and resultant lee-side adiabatic warming rather than to meridional wind anomalies, which is closely tied to variability in the zonal portion of the SAM pattern.
    Print ISSN: 0148-0227
    Topics: Geosciences , Physics
    Published by Wiley on behalf of American Geophysical Union (AGU).
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  • 3
    Publication Date: 2016-01-27
    Description: ABSTRACT New insight is provided regarding 21st century projections of synoptic scale atmospheric circulation over the New Zealand region. Daily mean sea level pressure patterns from a number of general circulation models (GCMs) participating in the 5th Coupled Model Intercomparison Project (CMIP5) were analysed through a self-organizing map (SOM) technique. In terms of simulating the synoptic climatology found in reanalyses, an initial model evaluation revealed quite substantial differences in model skill. Generally, those models with relatively high horizontal atmospheric resolution skilfully simulated the historical frequency and mean lifetime of large scale synoptic patterns over this region. Analysing future projections under this smaller subset of better-performing models indicated robust and quite substantial increases in the annual frequency of widespread anticyclonic conditions over New Zealand, accompanied by a general decrease in widespread low pressure. These projected changes in frequency of synoptic occurrences become the most pronounced towards the end of the 21st century and for winter, whereas changes in the average synoptic pattern lifetime remain small. While not robust for all models in this subset, significant 21st century trends in the intensification of geostrophic westerly flow conditions within certain synoptic patterns were also found. Linking synoptic patterns to surface climate variables has also provided evidence that these circulation changes may collectively manifest as a significant non-uniform climatic change across New Zealand. These findings should encourage further focused studies on circulation-relevant applications and impacts in a climate change context.
    Print ISSN: 0899-8418
    Electronic ISSN: 1097-0088
    Topics: Geosciences , Physics
    Published by Wiley
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  • 4
    Publication Date: 2015-12-08
    Description: ABSTRACT We present a 16 000-year vegetation and climate reconstruction from pollen and plant macrofossil records obtained at a small alpine lake in South Island, New Zealand (41°S). The expansion of lowland forest taxa suggests a lifting of the altitudinal forest limits because of a warming pulse between 13 and 10k cal a BP and between 7 and 6k cal a BP, while their decline relative to upland forest taxa indicates cooling phases between 10 and 7k cal a BP and over the last 3000 years. The modern treeline was first established locally by 9.7k cal a BP. Forest persisted at the site until 3k cal a BP then disappeared from the record. Close correspondence between the temperature trends inferred from the pollen and macrofossil records and proxies from Antarctica and the Southern Ocean suggests a strong teleconnection between New Zealand and the Southern Hemisphere high-latitudes between 15 and 6k cal a BP. We note that the breakdown of this coupling, a cooling trend in Adelaide Tarn and the local disappearance of beech forest after 3k cal a BP occur during a period of increased frequency of El Niño events, suggesting an enhanced teleconnection with the low-latitudes during the late Holocene.
    Print ISSN: 0267-8179
    Electronic ISSN: 1099-1417
    Topics: Geography , Geosciences
    Published by Wiley
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  • 5
    Publication Date: 2014-02-13
    Description: ABSTRACT A cluster analysis-based synoptic classification scheme, known as the Kidson types, was applied to reanalyses and Coupled Model Inter-comparison Project phase 3 (CMIP3) general circulation model (GCM) output over New Zealand to identify the potential for future changes in regional circulation. Results indicate that a number of GCM 20th century control runs reproduce the type frequencies observed in reanalysis data. Application to future scenario runs for the periods 2046–2065 and 2081–2100 displays little variation in the annual frequency of the synoptic types relative to the 20th century, especially when uncertainty associated with the model ensemble is considered. This is surprising in the context of previous work on possible future movements in jet position and subsequent impacts on weather patterns. A sensitivity analysis that mimics the movement of the jet position was performed, revealing that the annual type frequencies are relatively insensitive to change. To determine whether this is a problem with the synoptic typing scheme, a correlation-based classification technique was also used, but showed similar results. This work highlights issues with applying synoptic classification schemes to GCM output and indicates that if such schemes are to be used they should be designed and tested with this application in mind.
    Print ISSN: 0899-8418
    Electronic ISSN: 1097-0088
    Topics: Geosciences , Physics
    Published by Wiley
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  • 6
    Publication Date: 2014-04-16
    Description: ABSTRACT The focus of this study is the climatological relationship between southwest Pacific Tropical Cyclone (TC) activity and the Madden–Julian Oscillation (MJO) on the interannual time-scale. It investigates TC seasonal characteristics (e.g. cyclogenesis, track morphology, ex-tropical transition, and intensity) as modulated by the phase and intensity of the MJO. The approach is novel as in addition to the focus on the intraseasonal variability of TCs there is also a focus on the interannual variability of TCs even though the MJO is an intraseasonal phenomenon. Links between the MJO, the Southern Annular Mode (SAM) and TC variability are also investigated. Using the MJO phases defined by Wheeler and Hendon ( ), southwest Pacific TC frequency exhibited a statistically significant decrease during MJO phases 2 and 3, and an increase during phases 6 and 7; and during the positive phase of the SAM, an increased frequency of TCs undergoing extratropical transition was observed. In summary, the results show a clear intraseasonal climatological relationship between specific phases of the MJO with respect to a decreased (increased) frequency of TCs during the paired MJO phases 2–3 (6–7); as well as the existence of a statistically significant relationship between the MJO and SAM with respect to the extratropical transition (ETT) of TCs. During positive phases of the SAM, coincident with weak interannual MJO phases 4–5 and 6–7, there are statistically significant greater frequency percentages of TCs undergoing ETT.
    Print ISSN: 0899-8418
    Electronic ISSN: 1097-0088
    Topics: Geosciences , Physics
    Published by Wiley
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  • 7
    Publication Date: 2014-04-08
    Description: ABSTRACT In this study, we focus on possible climatological relationships between southwest Pacific tropical cyclone (TC) activity and the Southern Annular Mode (SAM) and ENSO, at both interannual and synoptic time-scales. The investigation focuses on TC seasonal characteristics (e.g. cyclogenesis, track characteristics, extratropical transition, and intensity) as modulated according to the polarity of the SAM and ENSO. At synoptic time-scales, we also look at possible triggers of TC cyclogenesis in the SAM signal up to 20 days in advance. The physical basis for this relationship is assessed using a number of different gridded data fields. During seasons characterized by positive phases of SAM and both positive and negative Southern Oscillation Index (SOI) values, there is an increased frequency of TCs undergoing extratropical transition near New Zealand. At synoptic time-scales, we found an interesting yet inconclusive relationship between the SAM and tropical cyclogenesis during SOI positive seasons. While statistically significant, there is no clear physical mechanism linking the mid-latitude SAM phenomenon to the genesis of TCs. In summary, the results show a clear interannual climatological relationship between an increased frequency of TCs undergoing extratropical transition near New Zealand and the positive phase of SAM.
    Print ISSN: 0899-8418
    Electronic ISSN: 1097-0088
    Topics: Geosciences , Physics
    Published by Wiley
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  • 8
    Publication Date: 2015-09-04
    Description: MYC (also known as c-MYC) overexpression or hyperactivation is one of the most common drivers of human cancer. Despite intensive study, the MYC oncogene remains recalcitrant to therapeutic inhibition. MYC is a transcription factor, and many of its pro-tumorigenic functions have been attributed to its ability to regulate gene expression programs. Notably, oncogenic MYC activation has also been shown to increase total RNA and protein production in many tissue and disease contexts. While such increases in RNA and protein production may endow cancer cells with pro-tumour hallmarks, this increase in synthesis may also generate new or heightened burden on MYC-driven cancer cells to process these macromolecules properly. Here we discover that the spliceosome is a new target of oncogenic stress in MYC-driven cancers. We identify BUD31 as a MYC-synthetic lethal gene in human mammary epithelial cells, and demonstrate that BUD31 is a component of the core spliceosome required for its assembly and catalytic activity. Core spliceosomal factors (such as SF3B1 and U2AF1) associated with BUD31 are also required to tolerate oncogenic MYC. Notably, MYC hyperactivation induces an increase in total precursor messenger RNA synthesis, suggesting an increased burden on the core spliceosome to process pre-mRNA. In contrast to normal cells, partial inhibition of the spliceosome in MYC-hyperactivated cells leads to global intron retention, widespread defects in pre-mRNA maturation, and deregulation of many essential cell processes. Notably, genetic or pharmacological inhibition of the spliceosome in vivo impairs survival, tumorigenicity and metastatic proclivity of MYC-dependent breast cancers. Collectively, these data suggest that oncogenic MYC confers a collateral stress on splicing, and that components of the spliceosome may be therapeutic entry points for aggressive MYC-driven cancers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hsu, Tiffany Y-T -- Simon, Lukas M -- Neill, Nicholas J -- Marcotte, Richard -- Sayad, Azin -- Bland, Christopher S -- Echeverria, Gloria V -- Sun, Tingting -- Kurley, Sarah J -- Tyagi, Siddhartha -- Karlin, Kristen L -- Dominguez-Vidana, Rocio -- Hartman, Jessica D -- Renwick, Alexander -- Scorsone, Kathleen -- Bernardi, Ronald J -- Skinner, Samuel O -- Jain, Antrix -- Orellana, Mayra -- Lagisetti, Chandraiah -- Golding, Ido -- Jung, Sung Y -- Neilson, Joel R -- Zhang, Xiang H-F -- Cooper, Thomas A -- Webb, Thomas R -- Neel, Benjamin G -- Shaw, Chad A -- Westbrook, Thomas F -- 1F30CA180447/CA/NCI NIH HHS/ -- 1R01CA178039-01/CA/NCI NIH HHS/ -- P30 AI036211/AI/NIAID NIH HHS/ -- P30CA125123/CA/NCI NIH HHS/ -- R01 AR045653/AR/NIAMS NIH HHS/ -- R01 AR060733/AR/NIAMS NIH HHS/ -- R01 CA140474/CA/NCI NIH HHS/ -- R01 HL045565/HL/NHLBI NIH HHS/ -- S10 RR024574/RR/NCRR NIH HHS/ -- U54-CA149196/CA/NCI NIH HHS/ -- England -- Nature. 2015 Sep 17;525(7569):384-8. doi: 10.1038/nature14985. Epub 2015 Sep 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Verna &Marrs McLean Department of Biochemistry and Molecular Biology, Baylor College of Medicine, Houston, Texas 77030, USA. ; Interdepartmental Program in Molecular and Biomedical Sciences, Baylor College of Medicine, Houston, Texas 77030, USA. ; Medical Scientist Training Program, Baylor College of Medicine, Houston, Texas 77030, USA. ; Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas 77030, USA. ; Princess Margaret Cancer Centre, University Health Network, Toronto M5G 2C4, Canada. ; Department of Molecular Physiology and Biophysics, Baylor College of Medicine, Houston, Texas 77030, USA. ; Department of Pathology and Immunology, Baylor College of Medicine, Houston, Texas 77030, USA. ; Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas 77030, USA. ; Department of Pediatrics, Baylor College of Medicine, Houston, Texas 77030, USA. ; Department of Physics, University of Illinois, Urbana, Illinois 61801, USA. ; Center for Chemical Biology, Bioscience Division, SRI International, Menlo Park, California 94025, USA. ; The Lester and Sue Smith Breast Center, Baylor College of Medicine, Houston, Texas 77030, USA. ; Department of Medical Biophysics, University of Toronto, Toronto M5S 2J7, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26331541" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Breast Neoplasms/*drug therapy/*genetics/pathology ; Cell Line, Tumor ; Cell Survival/drug effects ; Cell Transformation, Neoplastic/drug effects ; Female ; Gene Expression Regulation, Neoplastic/drug effects ; Genes, myc/*genetics ; HeLa Cells ; Humans ; Introns/genetics ; Mice ; Mice, Nude ; Neoplasm Metastasis/drug therapy ; Nuclear Proteins/metabolism ; Phosphoproteins/metabolism ; Proto-Oncogene Proteins c-myc/genetics/metabolism ; RNA Precursors/biosynthesis/genetics ; RNA Splicing/drug effects ; RNA, Messenger/biosynthesis/genetics ; Ribonucleoprotein, U2 Small Nuclear/metabolism ; Ribonucleoproteins/metabolism ; Spliceosomes/*drug effects/*metabolism ; Xenograft Model Antitumor Assays
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 9
    Publication Date: 2012-12-18
    Description: Improved sequencing technologies offer unprecedented opportunities for investigating the role of rare genetic variation in common disease. However, there are considerable challenges with respect to study design, data analysis and replication. Using pooled next-generation sequencing of 507 genes implicated in the repair of DNA in 1,150 samples, an analytical strategy focused on protein-truncating variants (PTVs) and a large-scale sequencing case-control replication experiment in 13,642 individuals, here we show that rare PTVs in the p53-inducible protein phosphatase PPM1D are associated with predisposition to breast cancer and ovarian cancer. PPM1D PTV mutations were present in 25 out of 7,781 cases versus 1 out of 5,861 controls (P = 1.12 x 10(-5)), including 18 mutations in 6,912 individuals with breast cancer (P = 2.42 x 10(-4)) and 12 mutations in 1,121 individuals with ovarian cancer (P = 3.10 x 10(-9)). Notably, all of the identified PPM1D PTVs were mosaic in lymphocyte DNA and clustered within a 370-base-pair region in the final exon of the gene, carboxy-terminal to the phosphatase catalytic domain. Functional studies demonstrate that the mutations result in enhanced suppression of p53 in response to ionizing radiation exposure, suggesting that the mutant alleles encode hyperactive PPM1D isoforms. Thus, although the mutations cause premature protein truncation, they do not result in the simple loss-of-function effect typically associated with this class of variant, but instead probably have a gain-of-function effect. Our results have implications for the detection and management of breast and ovarian cancer risk. More generally, these data provide new insights into the role of rare and of mosaic genetic variants in common conditions, and the use of sequencing in their identification.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3759028/" 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/PMC3759028/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ruark, Elise -- Snape, Katie -- Humburg, Peter -- Loveday, Chey -- Bajrami, Ilirjana -- Brough, Rachel -- Rodrigues, Daniel Nava -- Renwick, Anthony -- Seal, Sheila -- Ramsay, Emma -- Duarte, Silvana Del Vecchio -- Rivas, Manuel A -- Warren-Perry, Margaret -- Zachariou, Anna -- Campion-Flora, Adriana -- Hanks, Sandra -- Murray, Anne -- Ansari Pour, Naser -- Douglas, Jenny -- Gregory, Lorna -- Rimmer, Andrew -- Walker, Neil M -- Yang, Tsun-Po -- Adlard, Julian W -- Barwell, Julian -- Berg, Jonathan -- Brady, Angela F -- Brewer, Carole -- Brice, Glen -- Chapman, Cyril -- Cook, Jackie -- Davidson, Rosemarie -- Donaldson, Alan -- Douglas, Fiona -- Eccles, Diana -- Evans, D Gareth -- Greenhalgh, Lynn -- Henderson, Alex -- Izatt, Louise -- Kumar, Ajith -- Lalloo, Fiona -- Miedzybrodzka, Zosia -- Morrison, Patrick J -- Paterson, Joan -- Porteous, Mary -- Rogers, Mark T -- Shanley, Susan -- Walker, Lisa -- Gore, Martin -- Houlston, Richard -- Brown, Matthew A -- Caufield, Mark J -- Deloukas, Panagiotis -- McCarthy, Mark I -- Todd, John A -- Breast and Ovarian Cancer Susceptibility Collaboration -- Wellcome Trust Case Control Consortium -- Turnbull, Clare -- Reis-Filho, Jorge S -- Ashworth, Alan -- Antoniou, Antonis C -- Lord, Christopher J -- Donnelly, Peter -- Rahman, Nazneen -- 068545/Z/02/Wellcome Trust/United Kingdom -- 083948/Wellcome Trust/United Kingdom -- 090532/Wellcome Trust/United Kingdom -- 090532/Z/09/Z/Wellcome Trust/United Kingdom -- 091157/Wellcome Trust/United Kingdom -- 095552/Wellcome Trust/United Kingdom -- 098051/Wellcome Trust/United Kingdom -- 100140/Wellcome Trust/United Kingdom -- 11174/Cancer Research UK/United Kingdom -- C12292/A11174/Cancer Research UK/United Kingdom -- CZB/4/540/Chief Scientist Office/United Kingdom -- ETM/137/Chief Scientist Office/United Kingdom -- ETM/75/Chief Scientist Office/United Kingdom -- G0000934/Medical Research Council/United Kingdom -- G0600329/Medical Research Council/United Kingdom -- G0800759/Medical Research Council/United Kingdom -- G0900747 91070/Medical Research Council/United Kingdom -- G9521010/Medical Research Council/United Kingdom -- MR/K006584/1/Medical Research Council/United Kingdom -- England -- Nature. 2013 Jan 17;493(7432):406-10. doi: 10.1038/nature11725. Epub 2012 Dec 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Genetics & Epidemiology, The Institute of Cancer Research, Sutton SM2 5NG, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23242139" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Breast Neoplasms/*genetics ; Cluster Analysis ; Exons ; Female ; Genetic Predisposition to Disease/*genetics ; Humans ; Isoenzymes/genetics ; Lymphocytes/metabolism ; *Mosaicism ; *Mutation ; Ovarian Neoplasms/*genetics ; Phosphoprotein Phosphatases/*genetics ; Sequence Analysis, DNA ; Tumor Suppressor Protein p53/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 10
    Publication Date: 2016-09-29
    Description: Antarctic climate trends observed in the satellite record are compared with a two hundred year paleoclimate record. The satellite record is found to be too short to attribute changes to anthropogenic forcing, with natural variability overwhelming the forced signal. Nature Climate Change 6 917 doi: 10.1038/nclimate3103
    Print ISSN: 1758-678X
    Electronic ISSN: 1758-6798
    Topics: Geosciences
    Published by Springer Nature
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