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  • Articles  (380)
  • American Association for the Advancement of Science (AAAS)  (380)
  • 2000-2004  (380)
  • 1985-1989
  • 2000  (380)
  • Science. 286(5447): 2051, 2053.  (1)
  • Science. 286(5447): 2087, 2089-90.  (1)
  • Science. 286(5448): 2283-4.  (1)
  • Science. 286(5449): 2452.  (1)
  • Science. 286(5449): 2458-9.  (1)
  • Science. 286(5449): 2468-74.  (1)
  • Science. 286(5449): 2485-8.  (1)
  • Science. 286(5449): 2504-7.  (1)
  • Science. 286(5449): 2511-4.  (1)
  • Science. 286(5449): 2517-20.  (1)
  • Science. 286(5449): 2528-31.  (1)
  • Science. 287(5450): 42.  (1)
  • Science. 287(5451): 237-8.  (1)
  • Science. 287(5451): 306-8.  (1)
  • Science. 287(5451): 308-9.  (1)
  • Science. 287(5452): 428-9.  (1)
  • Science. 287(5452): 435, 437.  (1)
  • Science. 287(5452): 443-9.  (1)
  • Science. 287(5452): 451-2.  (1)
  • Science. 287(5452): 460-2.  (1)
  • 25
  • Natural Sciences in General  (380)
  • Biology  (380)
Collection
  • Articles  (380)
Source
Keywords
Publisher
Years
  • 2000-2004  (380)
  • 1985-1989
Year
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  • 11
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    Historical trends in lake and river ice cover in the northern hemisphere (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-09-08
    Description: Freeze and breakup dates of ice on lakes and rivers provide consistent evidence of later freezing and earlier breakup around the Northern Hemisphere from 1846 to 1995. Over these 150 years, changes in freeze dates averaged 5.8 days per 100 years later, and changes in breakup dates averaged 6.5 days per 100 years earlier; these translate to increasing air temperatures of about 1.2 degrees C per 100 years. Interannual variability in both freeze and breakup dates has increased since 1950. A few longer time series reveal reduced ice cover (a warming trend) beginning as early as the 16th century, with increasing rates of change after about 1850.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Magnuson -- Robertson -- Benson -- Wynne -- Livingstone -- Arai -- Assel -- Barry -- Card V -- Kuusisto -- Granin -- Prowse -- Stewart -- Vuglinski -- New York, N.Y. -- Science. 2000 Sep 8;289(5485):1743-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Limnology, University of Wisconsin-Madison, Madison, WI 53706, USA. U.S. Geological Survey, Water Resources Division, 8505 Research Way, Middleton, WI 53562, USA. Department of Forestry, Virginia Polytechnic Institute and State Unive.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10976066" target="_blank"〉PubMed〈/a〉
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 12
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    Requirement of JNK for stress-induced activation of the cytochrome c-mediated death pathway (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-05-08
    Description: The c-Jun NH2-terminal kinase (JNK) is activated when cells are exposed to ultraviolet (UV) radiation. However, the functional consequence of JNK activation in UV-irradiated cells has not been established. It is shown here that JNK is required for UV-induced apoptosis in primary murine embryonic fibroblasts. Fibroblasts with simultaneous targeted disruptions of all the functional Jnk genes were protected against UV-stimulated apoptosis. The absence of JNK caused a defect in the mitochondrial death signaling pathway, including the failure to release cytochrome c. These data indicate that mitochondria are influenced by proapoptotic signal transduction through the JNK pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tournier, C -- Hess, P -- Yang, D D -- Xu, J -- Turner, T K -- Nimnual, A -- Bar-Sagi, D -- Jones, S N -- Flavell, R A -- Davis, R J -- New York, N.Y. -- Science. 2000 May 5;288(5467):870-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Program in Molecular Medicine, Department of Biochemistry & Molecular Biology, University of Massachusetts Medical School, Worcester, MA 01605, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10797012" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Apoptotic Protease-Activating Factor 1 ; Caspase 3 ; Caspase 9 ; Caspases/metabolism ; Cell Count ; Cell Division ; Cells, Cultured ; Cytochrome c Group/*metabolism ; DNA Fragmentation ; Enzyme Activation ; Fibroblasts ; Gene Targeting ; JNK Mitogen-Activated Protein Kinases ; MAP Kinase Signaling System ; Methyl Methanesulfonate/pharmacology ; Mice ; Mitochondria/metabolism ; Mitogen-Activated Protein Kinases/genetics/*metabolism ; NF-kappa B/metabolism ; *Protein-Serine-Threonine Kinases ; Proteins/metabolism ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-akt ; Proto-Oncogene Proteins c-bcl-2/metabolism ; Tumor Suppressor Protein p53/metabolism ; Ultraviolet Rays
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 13
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    Evidence for genetic linkage of Alzheimer's disease to chromosome 10q (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-12-23
    Description: Recent studies suggest that insulin-degrading enzyme (IDE) in neurons and microglia degrades Abeta, the principal component of beta-amyloid and one of the neuropathological hallmarks of Alzheimer's disease (AD). We performed parametric and nonparametric linkage analyses of seven genetic markers on chromosome 10q, six of which map near the IDE gene, in 435 multiplex AD families. These analyses revealed significant evidence of linkage for adjacent markers (D10S1671, D10S583, D10S1710, and D10S566), which was most pronounced in late-onset families. Furthermore, we found evidence for allele-specific association between the putative disease locus and marker D10S583, which has recently been located within 195 kilobases of the IDE gene.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bertram, L -- Blacker, D -- Mullin, K -- Keeney, D -- Jones, J -- Basu, S -- Yhu, S -- McInnis, M G -- Go, R C -- Vekrellis, K -- Selkoe, D J -- Saunders, A J -- Tanzi, R E -- New York, N.Y. -- Science. 2000 Dec 22;290(5500):2302-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Genetics and Aging Unit, Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11125142" target="_blank"〉PubMed〈/a〉
    Keywords: Age of Onset ; Aged ; Aged, 80 and over ; Alleles ; Alzheimer Disease/*genetics ; Apolipoproteins E/genetics ; Chromosome Mapping ; Chromosomes, Human, Pair 10/*genetics ; *Genetic Linkage ; Genetic Markers ; Humans ; Insulysin/*genetics ; Linkage Disequilibrium ; Middle Aged
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 14
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    The fall, recovery, orbit, and composition of the Tagish Lake meteorite: a new type of carbonaceous chondrite (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-10-13
    Description: The preatmospheric mass of the Tagish Lake meteoroid was about 200,000 kilograms. Its calculated orbit indicates affinity to the Apollo asteroids with a semimajor axis in the middle of the asteroid belt, consistent with a linkage to low-albedo C, D, and P type asteroids. The mineralogy, oxygen isotope, and bulk chemical composition of recovered samples of the Tagish Lake meteorite are intermediate between CM and CI meteorites. These data suggest that the Tagish Lake meteorite may be one of the most primitive solar system materials yet studied.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brown, P G -- Hildebrand, A R -- Zolensky, M E -- Grady, M -- Clayton, R N -- Mayeda, T K -- Tagliaferri, E -- Spalding, R -- MacRae, N D -- Hoffman, E L -- Mittlefehldt, D W -- Wacker, J F -- Bird, J A -- Campbell, M D -- Carpenter, R -- Gingerich, H -- Glatiotis, M -- Greiner, E -- Mazur, M J -- McCausland, P J -- Plotkin, H -- Rubak Mazur, T -- New York, N.Y. -- Science. 2000 Oct 13;290(5490):320-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physics and Astronomy, University of Western Ontario, London, Ontario N6A 3K7, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11030647" target="_blank"〉PubMed〈/a〉
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 15
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    A whole-genome assembly of Drosophila (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-03-24
    Description: We report on the quality of a whole-genome assembly of Drosophila melanogaster and the nature of the computer algorithms that accomplished it. Three independent external data sources essentially agree with and support the assembly's sequence and ordering of contigs across the euchromatic portion of the genome. In addition, there are isolated contigs that we believe represent nonrepetitive pockets within the heterochromatin of the centromeres. Comparison with a previously sequenced 2.9- megabase region indicates that sequencing accuracy within nonrepetitive segments is greater than 99. 99% without manual curation. As such, this initial reconstruction of the Drosophila sequence should be of substantial value to the scientific community.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Myers, E W -- Sutton, G G -- Delcher, A L -- Dew, I M -- Fasulo, D P -- Flanigan, M J -- Kravitz, S A -- Mobarry, C M -- Reinert, K H -- Remington, K A -- Anson, E L -- Bolanos, R A -- Chou, H H -- Jordan, C M -- Halpern, A L -- Lonardi, S -- Beasley, E M -- Brandon, R C -- Chen, L -- Dunn, P J -- Lai, Z -- Liang, Y -- Nusskern, D R -- Zhan, M -- Zhang, Q -- Zheng, X -- Rubin, G M -- Adams, M D -- Venter, J C -- New York, N.Y. -- Science. 2000 Mar 24;287(5461):2196-204.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Celera Genomics, Inc., 45 West Gude Drive, Rockville, MD 20850, USA. Gene.Myers@celera.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10731133" target="_blank"〉PubMed〈/a〉
    Keywords: Algorithms ; Animals ; Chromatin/genetics ; *Computational Biology ; Contig Mapping ; Drosophila melanogaster/*genetics ; Euchromatin ; Genes, Insect ; *Genome ; Heterochromatin/genetics ; Molecular Sequence Data ; Physical Chromosome Mapping ; Repetitive Sequences, Nucleic Acid ; *Sequence Analysis, DNA ; Sequence Tagged Sites
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  • 16
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    Interpreting differential temperature trends at the surface and in the lower troposphere (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-02-26
    Description: Estimated global-scale temperature trends at Earth's surface (as recorded by thermometers) and in the lower troposphere (as monitored by satellites) diverge by up to 0.14 degrees C per decade over the period 1979 to 1998. Accounting for differences in the spatial coverage of satellite and surface measurements reduces this differential, but still leaves a statistically significant residual of roughly 0.1 degrees C per decade. Natural internal climate variability alone, as simulated in three state-of-the-art coupled atmosphere-ocean models, cannot completely explain this residual trend difference. A model forced by a combination of anthropogenic factors and volcanic aerosols yields surface-troposphere temperature trend differences closest to those observed.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Santer -- Wigley -- Gaffen -- Bengtsson -- Doutriaux -- Boyle -- Esch -- Hnilo -- Jones -- Meehl -- Roeckner -- Taylor -- Wehner -- New York, N.Y. -- Science. 2000 Feb 18;287(5456):1227-32.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program for Climate Model Diagnosis and Intercomparison, Lawrence Livermore National Laboratory, Livermore, CA 94550, USA. National Center for Atmospheric Research, Boulder, CO 80307, USA. NOAA Air Resources Laboratory, Silver Spring, MD 20910〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10678823" target="_blank"〉PubMed〈/a〉
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 17
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    Ecology. The value of nature and the nature of value (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-08-12
    Description: Ecosystems are capital assets: When properly managed, they yield a flow of vital goods and services. Relative to other forms of capital, however, ecosystems are poorly understood, scarcely monitored, and--in many important cases--undergoing rapid degradation. The process of economic valuation could greatly improve stewardship. This potential is now being realized with innovative financial instruments and institutional arrangements.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Daily, G C -- Soderqvist, T -- Aniyar, S -- Arrow, K -- Dasgupta, P -- Ehrlich, P R -- Folke, C -- Jansson, A -- Jansson, B -- Kautsky, N -- Levin, S -- Lubchenco, J -- Maler, K G -- Simpson, D -- Starrett, D -- Tilman, D -- Walker, B -- New York, N.Y. -- Science. 2000 Jul 21;289(5478):395-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, Stanford University, Stanford, CA 94305, USA. gdaily@leland.stanford.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10939949" target="_blank"〉PubMed〈/a〉
    Keywords: Australia ; Commerce ; Conservation of Natural Resources/*economics ; Costa Rica ; *Ecosystem ; Industry ; Investments
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 18
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    Neurodegeneration prevented by lentiviral vector delivery of GDNF in primate models of Parkinson's disease (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-10-29
    Description: Lentiviral delivery of glial cell line-derived neurotrophic factor (lenti-GDNF) was tested for its trophic effects upon degenerating nigrostriatal neurons in nonhuman primate models of Parkinson's disease (PD). We injected lenti-GDNF into the striatum and substantia nigra of nonlesioned aged rhesus monkeys or young adult rhesus monkeys treated 1 week prior with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Extensive GDNF expression with anterograde and retrograde transport was seen in all animals. In aged monkeys, lenti-GDNF augmented dopaminergic function. In MPTP-treated monkeys, lenti-GDNF reversed functional deficits and completely prevented nigrostriatal degeneration. Additionally, lenti-GDNF injections to intact rhesus monkeys revealed long-term gene expression (8 months). In MPTP-treated monkeys, lenti-GDNF treatment reversed motor deficits in a hand-reach task. These data indicate that GDNF delivery using a lentiviral vector system can prevent nigrostriatal degeneration and induce regeneration in primate models of PD and might be a viable therapeutic strategy for PD patients.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kordower, J H -- Emborg, M E -- Bloch, J -- Ma, S Y -- Chu, Y -- Leventhal, L -- McBride, J -- Chen, E Y -- Palfi, S -- Roitberg, B Z -- Brown, W D -- Holden, J E -- Pyzalski, R -- Taylor, M D -- Carvey, P -- Ling, Z -- Trono, D -- Hantraye, P -- Deglon, N -- Aebischer, P -- NS40578/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2000 Oct 27;290(5492):767-73.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurological Sciences, Rush Presbyterian-St. Luke's Medical Center, Chicago, IL 60612, USA. jkordowe@rush.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11052933" target="_blank"〉PubMed〈/a〉
    Keywords: 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine ; Aging ; Animals ; Antigens, CD/analysis ; Dihydroxyphenylalanine/*analogs & derivatives/metabolism ; Disease Models, Animal ; Dopamine/*metabolism ; Female ; Gene Expression ; *Genetic Therapy ; Genetic Vectors ; Glial Cell Line-Derived Neurotrophic Factor ; Lentivirus/genetics ; Macaca mulatta ; Neostriatum/metabolism/pathology ; Nerve Degeneration/*prevention & control ; *Nerve Growth Factors ; Nerve Tissue Proteins/*genetics/metabolism/therapeutic use ; Neurons/enzymology ; Parkinson Disease/metabolism/pathology/physiopathology/*therapy ; Parkinsonian Disorders/metabolism/pathology/physiopathology/therapy ; Psychomotor Performance ; Substantia Nigra/metabolism/pathology ; Tyrosine 3-Monooxygenase/metabolism
    Print ISSN: 0036-8075
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  • 19
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    An anti-apoptotic role for the p53 family member, p73, during developmental neuron death (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-07-15
    Description: p53 plays an essential pro-apoptotic role, a function thought to be shared with its family members p73 and p63. Here, we show that p73 is primarily present in developing neurons as a truncated isoform whose levels are dramatically decreased when sympathetic neurons apoptose after nerve growth factor (NGF) withdrawal. Increased expression of truncated p73 rescues these neurons from apoptosis induced by NGF withdrawal or p53 overexpression. In p73-/- mice, all isoforms of p73 are deleted and the apoptosis of developing sympathetic neurons is greatly enhanced. Thus, truncated p73 is an essential anti-apoptotic protein in neurons, serving to counteract the pro-apoptotic function of p53.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pozniak, C D -- Radinovic, S -- Yang, A -- McKeon, F -- Kaplan, D R -- Miller, F D -- New York, N.Y. -- Science. 2000 Jul 14;289(5477):304-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Neuronal Survival, Brain Tumor Research Center, Montreal Neurological Institute, McGill University, Montreal, Canada H3A 2B4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10894779" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoviridae/genetics ; Animals ; Apoptosis/*physiology ; Cells, Cultured ; DNA-Binding Proteins/biosynthesis/chemistry/*physiology ; Escherichia coli ; Genes, Tumor Suppressor ; Humans ; Mice ; Mice, Inbred BALB C ; Nerve Growth Factor/pharmacology ; Neurons/*physiology ; Nuclear Proteins/biosynthesis/chemistry/*physiology ; Protein Isoforms/biosynthesis/chemistry/physiology ; Recombinant Proteins ; Sympathetic Nervous System/cytology/*physiology ; Tumor Suppressor Protein p53/antagonists & inhibitors/*physiology ; Tumor Suppressor Proteins
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 20
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    Signature of superfluid density in the single-particle excitation spectrum of Bi(2)Sr(2)CaCu(2)O(8+delta) (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-07-15
    Description: We report that the doping and temperature dependence of photoemission spectra near the Brillouin zone boundary of Bi(2)Sr(2)CaCu(2)O(8+delta)exhibit unexpected sensitivity to the superfluid density. In the superconducting state, the photoemission peak intensity as a function of doping scales with the superfluid density and the condensation energy. As a function of temperature, the peak intensity shows an abrupt behavior near the superconducting phase transition temperature where phase coherence sets in, rather than near the temperature where the gap opens. This anomalous manifestation of collective effects in single-particle spectroscopy raises important questions concerning the mechanism of high-temperature superconductivity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Feng -- Lu -- Shen -- Kim -- Eisaki -- Damascelli -- Yoshizaki -- Shimoyama -- Kishio -- Gu -- Oh -- Andrus -- O'Donnell -- Eckstein -- New York, N.Y. -- Science. 2000 Jul 14;289(5477):277-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physics, Applied Physics, and Stanford Synchrotron Radiation Laboratory, Stanford University, Stanford, CA 94305, USA. Institute of Applied Physics, University of Tsukuba, Tsukuba, Ibaraki 305, Japan. Department of Applied Chem.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10894771" target="_blank"〉PubMed〈/a〉
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