ALBERT

All Library Books, journals and Electronic Records Telegrafenberg

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    facet.materialart.
    Unknown
    Mutations in dynein link motor neuron degeneration to defects in retrograde transport (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-05-06
    Description: Degenerative disorders of motor neurons include a range of progressive fatal diseases such as amyotrophic lateral sclerosis (ALS), spinal-bulbar muscular atrophy (SBMA), and spinal muscular atrophy (SMA). Although the causative genetic alterations are known for some cases, the molecular basis of many SMA and SBMA-like syndromes and most ALS cases is unknown. Here we show that missense point mutations in the cytoplasmic dynein heavy chain result in progressive motor neuron degeneration in heterozygous mice, and in homozygotes this is accompanied by the formation of Lewy-like inclusion bodies, thus resembling key features of human pathology. These mutations exclusively perturb neuron-specific functions of dynein.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hafezparast, Majid -- Klocke, Rainer -- Ruhrberg, Christiana -- Marquardt, Andreas -- Ahmad-Annuar, Azlina -- Bowen, Samantha -- Lalli, Giovanna -- Witherden, Abi S -- Hummerich, Holger -- Nicholson, Sharon -- Morgan, P Jeffrey -- Oozageer, Ravi -- Priestley, John V -- Averill, Sharon -- King, Von R -- Ball, Simon -- Peters, Jo -- Toda, Takashi -- Yamamoto, Ayumu -- Hiraoka, Yasushi -- Augustin, Martin -- Korthaus, Dirk -- Wattler, Sigrid -- Wabnitz, Philipp -- Dickneite, Carmen -- Lampel, Stefan -- Boehme, Florian -- Peraus, Gisela -- Popp, Andreas -- Rudelius, Martina -- Schlegel, Juergen -- Fuchs, Helmut -- Hrabe de Angelis, Martin -- Schiavo, Giampietro -- Shima, David T -- Russ, Andreas P -- Stumm, Gabriele -- Martin, Joanne E -- Fisher, Elizabeth M C -- New York, N.Y. -- Science. 2003 May 2;300(5620):808-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurodegenerative Disease, Institute of Neurology, National Hospital for Neurology and Neurosurgery, Queen Square, London WC1N 3BG, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12730604" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anterior Horn Cells/pathology ; Apoptosis ; *Axonal Transport ; Cell Differentiation ; Cell Movement ; Central Nervous System/embryology ; Chromosome Mapping ; Dimerization ; Dyneins/chemistry/*genetics/*physiology ; Female ; Ganglia, Spinal/pathology ; Golgi Apparatus/metabolism/ultrastructure ; Heterozygote ; Homozygote ; Lewy Bodies/pathology ; Male ; Mice ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Motor Neuron Disease/*genetics/pathology/physiopathology ; Motor Neurons/*physiology/ultrastructure ; Mutation ; Mutation, Missense ; *Nerve Degeneration ; Peptide Fragments/metabolism ; Phenotype ; Point Mutation ; Spinal Nerves/growth & development ; Tetanus Toxin/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 2
    facet.materialart.
    Unknown
    Balancing selection at the prion protein gene consistent with prehistoric kurulike epidemics (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-04-12
    Description: Kuru is an acquired prion disease largely restricted to the Fore linguistic group of the Papua New Guinea Highlands, which was transmitted during endocannibalistic feasts. Heterozygosity for a common polymorphism in the human prion protein gene (PRNP) confers relative resistance to prion diseases. Elderly survivors of the kuru epidemic, who had multiple exposures at mortuary feasts, are, in marked contrast to younger unexposed Fore, predominantly PRNP 129 heterozygotes. Kuru imposed strong balancing selection on the Fore, essentially eliminating PRNP 129 homozygotes. Worldwide PRNP haplotype diversity and coding allele frequencies suggest that strong balancing selection at this locus occurred during the evolution of modern humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mead, Simon -- Stumpf, Michael P H -- Whitfield, Jerome -- Beck, Jonathan A -- Poulter, Mark -- Campbell, Tracy -- Uphill, James B -- Goldstein, David -- Alpers, Michael -- Fisher, Elizabeth M C -- Collinge, John -- New York, N.Y. -- Science. 2003 Apr 25;300(5619):640-3. Epub 2003 Apr 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council Prion Unit, and Department of Neurodegenerative Disease, Institute of Neurology, University College, Queen Square, London WC1N 3BG, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12690204" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Animals ; Cannibalism ; Child ; Codon ; Creutzfeldt-Jakob Syndrome/genetics ; Disease Outbreaks/*history ; Ethnic Groups/*genetics ; Female ; Gene Frequency ; Haplotypes ; Heterozygote ; History, 19th Century ; History, 20th Century ; History, Ancient ; Homozygote ; Humans ; Immunity, Innate ; Kuru/epidemiology/genetics/*history/transmission ; Linkage Disequilibrium ; Male ; Methionine/genetics ; Middle Aged ; Mutation ; Papua New Guinea/epidemiology ; *Polymorphism, Genetic ; PrPC Proteins/*genetics ; *Selection, Genetic ; Valine/genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 3
    facet.materialart.
    Unknown
    An aneuploid mouse strain carrying human chromosome 21 with Down syndrome phenotypes (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-09-24
    Description: Aneuploidies are common chromosomal defects that result in growth and developmental deficits and high levels of lethality in humans. To gain insight into the biology of aneuploidies, we manipulated mouse embryonic stem cells and generated a trans-species aneuploid mouse line that stably transmits a freely segregating, almost complete human chromosome 21 (Hsa21). This "transchromosomic" mouse line, Tc1, is a model of trisomy 21, which manifests as Down syndrome (DS) in humans, and has phenotypic alterations in behavior, synaptic plasticity, cerebellar neuronal number, heart development, and mandible size that relate to human DS. Transchromosomic mouse lines such as Tc1 may represent useful genetic tools for dissecting other human aneuploidies.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1378183/" 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/PMC1378183/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉O'Doherty, Aideen -- Ruf, Sandra -- Mulligan, Claire -- Hildreth, Victoria -- Errington, Mick L -- Cooke, Sam -- Sesay, Abdul -- Modino, Sonie -- Vanes, Lesley -- Hernandez, Diana -- Linehan, Jacqueline M -- Sharpe, Paul T -- Brandner, Sebastian -- Bliss, Timothy V P -- Henderson, Deborah J -- Nizetic, Dean -- Tybulewicz, Victor L J -- Fisher, Elizabeth M C -- 076700/Wellcome Trust/United Kingdom -- MC_U117512674/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2005 Sep 23;309(5743):2033-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurodegenerative Disease, 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/16179473" target="_blank"〉PubMed〈/a〉
    Keywords: *Aneuploidy ; Animals ; Behavior, Animal ; Brain/pathology ; Cell Count ; Cell Line ; Chimera ; *Chromosomes, Human, Pair 21 ; *Disease Models, Animal ; *Down Syndrome/genetics/physiopathology ; Embryo, Mammalian/cytology ; Facial Bones/pathology ; Female ; Gene Expression ; *Genetic Engineering ; Genetic Markers ; Heart Defects, Congenital/embryology ; Hippocampus/physiopathology ; Humans ; Long-Term Potentiation ; Lymphocyte Activation ; Male ; Maze Learning ; Memory ; Mice ; Mice, Inbred Strains ; *Mice, Transgenic ; Neurons/cytology ; Oligonucleotide Array Sequence Analysis ; Phenotype ; Skull/pathology ; Stem Cells ; Synaptic Transmission ; T-Lymphocytes/immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 4
    facet.materialart.
    Unknown
    Tumour angiogenesis is reduced in the Tc1 mouse model of Down's syndrome (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-06-11
    Description: Down's syndrome (DS) is a genetic disorder caused by full or partial trisomy of human chromosome 21 and presents with many clinical phenotypes including a reduced incidence of solid tumours. Recent work with the Ts65Dn model of DS, which has orthologues of about 50% of the genes on chromosome 21 (Hsa21), has indicated that three copies of the ETS2 (ref. 3) or DS candidate region 1 (DSCR1) genes (a previously known suppressor of angiogenesis) is sufficient to inhibit tumour growth. Here we use the Tc1 transchromosomic mouse model of DS to dissect the contribution of extra copies of genes on Hsa21 to tumour angiogenesis. This mouse expresses roughly 81% of Hsa21 genes but not the human DSCR1 region. We transplanted B16F0 and Lewis lung carcinoma tumour cells into Tc1 mice and showed that growth of these tumours was substantially reduced compared with wild-type littermate controls. Furthermore, tumour angiogenesis was significantly repressed in Tc1 mice. In particular, in vitro and in vivo angiogenic responses to vascular endothelial growth factor (VEGF) were inhibited. Examination of the genes on the segment of Hsa21 in Tc1 mice identified putative anti-angiogenic genes (ADAMTS1and ERG) and novel endothelial cell-specific genes, never previously shown to be involved in angiogenesis (JAM-B and PTTG1IP), that, when overexpressed, are responsible for inhibiting angiogenic responses to VEGF. Three copies of these genes within the stromal compartment reduced tumour angiogenesis, explaining the reduced tumour growth in DS. Furthermore, we expect that, in addition to the candidate genes that we show to be involved in the repression of angiogenesis, the Tc1 mouse model of DS will permit the identification of other endothelium-specific anti-angiogenic targets relevant to a broad spectrum of cancer patients.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3479956/" 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/PMC3479956/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reynolds, Louise E -- Watson, Alan R -- Baker, Marianne -- Jones, Tania A -- D'Amico, Gabriela -- Robinson, Stephen D -- Joffre, Carine -- Garrido-Urbani, Sarah -- Rodriguez-Manzaneque, Juan Carlos -- Martino-Echarri, Estefania -- Aurrand-Lions, Michel -- Sheer, Denise -- Dagna-Bricarelli, Franca -- Nizetic, Dean -- McCabe, Christopher J -- Turnell, Andrew S -- Kermorgant, Stephanie -- Imhof, Beat A -- Adams, Ralf -- Fisher, Elizabeth M C -- Tybulewicz, Victor L J -- Hart, Ian R -- Hodivala-Dilke, Kairbaan M -- 080174/Wellcome Trust/United Kingdom -- 12007/Cancer Research UK/United Kingdom -- A12007/Cancer Research UK/United Kingdom -- A3585/Cancer Research UK/United Kingdom -- G0501003/Medical Research Council/United Kingdom -- G0501003(75694)/Medical Research Council/United Kingdom -- G0601056/Medical Research Council/United Kingdom -- G0901609/Medical Research Council/United Kingdom -- MC_U117527252/Medical Research Council/United Kingdom -- U.1175.02.001.00001(60485)/Medical Research Council/United Kingdom -- England -- Nature. 2010 Jun 10;465(7299):813-7. doi: 10.1038/nature09106.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Adhesion and Angiogenesis Laboratory, Barts Institute of Cancer, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, John Vane Science Centre, Charterhouse Square, London EC1M 6BQ, UK. l.reynolds@qmul.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20535211" target="_blank"〉PubMed〈/a〉
    Keywords: ADAM Proteins/genetics/metabolism ; Animals ; Carcinoma, Lewis Lung/*blood supply/complications/genetics/pathology ; Carrier Proteins/genetics/metabolism ; Cell Adhesion Molecules/antagonists & inhibitors/genetics/metabolism ; Chromosomes, Mammalian/genetics ; *Disease Models, Animal ; Down Syndrome/complications/*genetics/physiopathology ; Female ; Gene Dosage/*genetics ; Humans ; Immunoglobulins/genetics/metabolism ; Male ; Melanoma, Experimental/*blood supply/complications/genetics/pathology ; Mice ; Neoplasm Transplantation ; Neovascularization, Pathologic/*genetics/pathology ; Oncogene Proteins/genetics/metabolism ; Proto-Oncogene Protein c-ets-2/genetics/metabolism ; Transcription Factors ; Trisomy/genetics ; Vascular Endothelial Growth Factor A/antagonists & ; inhibitors/metabolism/pharmacology ; Vascular Endothelial Growth Factor Receptor-2/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 5
    facet.materialart.
    Unknown
    Species-specific transcription in mice carrying human chromosome 21 (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-09-13
    Description: Homologous sets of transcription factors direct conserved tissue-specific gene expression, yet transcription factor-binding events diverge rapidly between closely related species. We used hepatocytes from an aneuploid mouse strain carrying human chromosome 21 to determine, on a chromosomal scale, whether interspecies differences in transcriptional regulation are primarily directed by human genetic sequence or mouse nuclear environment. Virtually all transcription factor-binding locations, landmarks of transcription initiation, and the resulting gene expression observed in human hepatocytes were recapitulated across the entire human chromosome 21 in the mouse hepatocyte nucleus. Thus, in homologous tissues, genetic sequence is largely responsible for directing transcriptional programs; interspecies differences in epigenetic machinery, cellular environment, and transcription factors themselves play secondary roles.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3717767/" 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/PMC3717767/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wilson, Michael D -- Barbosa-Morais, Nuno L -- Schmidt, Dominic -- Conboy, Caitlin M -- Vanes, Lesley -- Tybulewicz, Victor L J -- Fisher, Elizabeth M C -- Tavare, Simon -- Odom, Duncan T -- 080174/Wellcome Trust/United Kingdom -- 15603/Cancer Research UK/United Kingdom -- 202218/European Research Council/International -- A15603/Cancer Research UK/United Kingdom -- G0601056/Medical Research Council/United Kingdom -- MC_U117527252/Medical Research Council/United Kingdom -- Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2008 Oct 17;322(5900):434-8. doi: 10.1126/science.1160930. Epub 2008 Sep 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Research UK, Cambridge Research Institute, Li Ka Shing Centre, Robinson Way, Cambridge CB2 0RE, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18787134" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Nucleus/metabolism ; Chromatin Assembly and Disassembly ; Chromatin Immunoprecipitation ; Chromosomes, Human, Pair 21/*genetics/metabolism ; Disease Models, Animal ; Down Syndrome/genetics ; *Gene Expression Regulation ; Hepatocyte Nuclear Factors/*metabolism ; Hepatocytes/*metabolism ; Histones/metabolism ; Humans ; Methylation ; Mice ; Oligonucleotide Array Sequence Analysis ; *Regulatory Sequences, Nucleic Acid ; Species Specificity ; Transcription Initiation Site ; *Transcription, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 6
    facet.materialart.
    Unknown
    C9orf72 repeat expansions cause neurodegeneration in Drosophila through arginine-rich proteins (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-08-12
    Description: An expanded GGGGCC repeat in C9orf72 is the most common genetic cause of frontotemporal dementia and amyotrophic lateral sclerosis. A fundamental question is whether toxicity is driven by the repeat RNA itself and/or by dipeptide repeat proteins generated by repeat-associated, non-ATG translation. To address this question, we developed in vitro and in vivo models to dissect repeat RNA and dipeptide repeat protein toxicity. Expression of pure repeats, but not stop codon-interrupted "RNA-only" repeats in Drosophila caused adult-onset neurodegeneration. Thus, expanded repeats promoted neurodegeneration through dipeptide repeat proteins. Expression of individual dipeptide repeat proteins with a non-GGGGCC RNA sequence revealed that both poly-(glycine-arginine) and poly-(proline-arginine) proteins caused neurodegeneration. These findings are consistent with a dual toxicity mechanism, whereby both arginine-rich proteins and repeat RNA contribute to C9orf72-mediated neurodegeneration.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mizielinska, Sarah -- Gronke, Sebastian -- Niccoli, Teresa -- Ridler, Charlotte E -- Clayton, Emma L -- Devoy, Anny -- Moens, Thomas -- Norona, Frances E -- Woollacott, Ione O C -- Pietrzyk, Julian -- Cleverley, Karen -- Nicoll, Andrew J -- Pickering-Brown, Stuart -- Dols, Jacqueline -- Cabecinha, Melissa -- Hendrich, Oliver -- Fratta, Pietro -- Fisher, Elizabeth M C -- Partridge, Linda -- Isaacs, Adrian M -- 089701/Wellcome Trust/United Kingdom -- 098565/Wellcome Trust/United Kingdom -- G0701441/Medical Research Council/United Kingdom -- G1000287/Medical Research Council/United Kingdom -- MR/J004022/1/Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2014 Sep 5;345(6201):1192-4. doi: 10.1126/science.1256800. Epub 2014 Aug 7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurodegenerative Disease, UCL Institute of Neurology, London WC1N 3BG, UK. ; Max Planck Institute for Biology of Ageing, 50931 Cologne, Germany. ; Max Planck Institute for Biology of Ageing, 50931 Cologne, Germany. Department of Genetics, Evolution and Environment, Institute of Healthy Ageing, University College London, London WC1E 6BT, UK. ; Department of Neurodegenerative Disease, UCL Institute of Neurology, London WC1N 3BG, UK. Department of Genetics, Evolution and Environment, Institute of Healthy Ageing, University College London, London WC1E 6BT, UK. ; Department of Neurodegenerative Disease, UCL Institute of Neurology, London WC1N 3BG, UK. MRC Prion Unit, UCL Institute of Neurology, London WC1N 3BG, UK. ; Institute of Brain, Behaviour and Mental Health, Faculty of Human and Medical Sciences, University of Manchester, Manchester M13 9PT, UK. ; Department of Genetics, Evolution and Environment, Institute of Healthy Ageing, University College London, London WC1E 6BT, UK. ; Department of Neurodegenerative Disease, UCL Institute of Neurology, London WC1N 3BG, UK. MRC Centre for Neuromuscular Disease, UCL Institute of Neurology, London WC1N 3BG, UK. ; Max Planck Institute for Biology of Ageing, 50931 Cologne, Germany. Department of Genetics, Evolution and Environment, Institute of Healthy Ageing, University College London, London WC1E 6BT, UK. a.isaacs@prion.ucl.ac.uk l.partridge@ucl.ac.uk. ; Department of Neurodegenerative Disease, UCL Institute of Neurology, London WC1N 3BG, UK. a.isaacs@prion.ucl.ac.uk l.partridge@ucl.ac.uk.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25103406" target="_blank"〉PubMed〈/a〉
    Keywords: Amyotrophic Lateral Sclerosis/*genetics/pathology ; Animals ; Cell Line, Tumor ; DNA Repeat Expansion/*genetics ; Dipeptides/metabolism ; Disease Models, Animal ; Drosophila melanogaster/*genetics ; Escherichia coli ; Frontotemporal Dementia/*genetics/pathology ; Humans ; Neurons/metabolism/pathology ; Proteins/*genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 7
    Electronic Resource
    Electronic Resource
    Observations on Lake Sediments using Fallout 137 Cs as a Tracer (1973)
    [s.l.] : Nature Publishing Group
    Nature 242 (1973), S. 324-326 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Cores were taken from the deepest part of each lake with aim Mackereth corer2, diameter 5.3 cm. Three replicate cores were extruded into 0.5 cm or 1.0 cm slices and combined. Samples were dried and analysed for 137Cs by gamma ray spectrometry3 using germanium (lithium) detectors. Generally each ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/242324a0
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 8
    Electronic Resource
    Electronic Resource
    The mapping of a cDNA from the human X-linked Duchenne muscular dystrophy gene to the mouse X chromosome (1987)
    [s.l.] : Nature Publishing Group
    Nature 328 (1987), S. 166-168 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] An interspecific Mus domesticus/ Mus spretus cross was initiated for the mapping of molecular markers to the mouse X chromosome (Fig. 1). A female M. domesticus mouse carrying the X-linked coat-texture mutations Harlequin (Hq), Tabby (Ta) and Lined (Li) was crossed to a male M. spretus. Four female ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/328166a0
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 9
    Electronic Resource
    Electronic Resource
    Weathering of Cæsium-137 in Soil (1964)
    [s.l.] : Nature Publishing Group
    Nature 201 (1964), S. 257-261 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] THERE is continual interest in the radiological dose to persons due to the deposition on the Earth's surface of fission products from nuclear test explosions. In considering the long-term hazard of whole-body y-irradiation caesium-137 is a major contributor. Calculations of the dose due to a ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/201257a0
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 10
    Electronic Resource
    Electronic Resource
    Radioactivity of the Atmosphere due to Distant Nuclear Test Explosions (1960)
    [s.l.] : Nature Publishing Group
    Nature 186 (1960), S. 224-225 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] The dust samples are collected in filters of esparto fibre mounted in holders such that forward movement of the aircraft forces air through the filter. Measurements have been made of the concentration in air of fission-product activities at an altitude of 47,000 ft. in the lower stratosphere and in ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/186224a0
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...