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  • Springer Nature  (487)
  • American Association for the Advancement of Science (AAAS)  (410)
  • 2000-2004
  • 1995-1999  (897)
  • 1980-1984
  • 1940-1944
  • 1999  (897)
Collection
Keywords
Publisher
Years
  • 2000-2004
  • 1995-1999  (897)
  • 1980-1984
  • 1940-1944
Year
  • 1
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    The DNA sequence of human chromosome 22 (1999)
    Springer Nature
    Details
    Publication Date: 1999-12-02
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Springer Nature
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  • 2
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    Sequence and analysis of chromosome 4 of the plant Arabidopsis thaliana (1999)
    Springer Nature
    Details
    Publication Date: 1999-12-01
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Springer Nature
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  • 3
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    The afterglow, redshift and extreme energetics of the γ-ray burst of 23 January 1999 (1999)
    Springer Nature
    Details
    Publication Date: 1999-04-01
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Springer Nature
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  • 4
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    Radar and optical observations of asteroid 1998 KY26 (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-27
    Description: Observations of near-Earth asteroid 1998 KY26 shortly after its discovery reveal a slightly elongated spheroid with a diameter of about 30 meters, a composition analogous to carbonaceous chondritic meteorites, and a rotation period of 10.7 minutes, which is an order of magnitude shorter than that measured for any other solar system object. The rotation is too rapid for 1998 KY26 to consist of multiple components bound together just by their mutual gravitational attraction. This monolithic object probably is a fragment derived from cratering or collisional destruction of a much larger asteroid.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ostro -- Pravec -- Benner -- Hudson -- Sarounova -- Hicks -- Rabinowitz -- Scotti -- Tholen -- Wolf -- Jurgens -- Thomas -- Giorgini -- Chodas -- Yeomans -- Rose -- Frye -- Rosema -- Winkler -- Slade -- New York, N.Y. -- Science. 1999 Jul 23;285(5427):557-60.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Jet Propulsion Laboratory, California Institute of Technology, Pasadena, CA 91109-8099, USA. Astronomical Institute, Academy of Sciences of the Czech Republic, CZ-25165 Ond&rbreve;ejov, Czech Republic. School of Electrical Engineering and.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10417379" target="_blank"〉PubMed〈/a〉
    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)
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  • 5
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    Nonlinear Optics for High-Speed Digital Information Processing (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-11-24
    Description: Recent advances in developing nonlinear optical techniques for processing serial digital information at high speed are reviewed. The field has been transformed by the advent of semiconductor nonlinear devices capable of operation at 100 gigabits per second and higher, well beyond the current speed limits of commercial electronics. These devices are expected to become important in future high-capacity communications networks by allowing digital regeneration and other processing functions to be performed on data signals "on the fly" in the optical domain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cotter -- Manning -- Blow -- Ellis -- Kelly -- Nesset -- Phillips -- Poustie -- Rogers -- New York, N.Y. -- Science. 1999 Nov 19;286(5444):1523-1528.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉BT Advanced Communications Technology Centre, Adastral Park, Martlesham Heath, Ipswich IP5 3RE, United Kingdom. Electronic Engineering, Aston University, Aston Triangle, Birmingham, B4 7ET, United Kingdom.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10567251" target="_blank"〉PubMed〈/a〉
    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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    Peptide antagonists of the human estrogen receptor (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-07-31
    Description: Estrogen receptor alpha transcriptional activity is regulated by distinct conformational states that are the result of ligand binding. Phage display was used to identify peptides that interact specifically with either estradiol- or tamoxifen-activated estrogen receptor alpha. When these peptides were coexpressed with estrogen receptor alpha in cells, they functioned as ligand-specific antagonists, indicating that estradiol-agonist and tamoxifen-partial agonist activities do not occur by the same mechanism. The ability to regulate estrogen receptor alpha transcriptional activity by targeting sites outside of the ligand-binding pocket has implications for the development of estrogen receptor alpha antagonists for the treatment of tamoxifen-refractory breast cancers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Norris, J D -- Paige, L A -- Christensen, D J -- Chang, C Y -- Huacani, M R -- Fan, D -- Hamilton, P T -- Fowlkes, D M -- McDonnell, D P -- DK48807/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1999 Jul 30;285(5428):744-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Duke University Medical Center, Department of Pharmacology and Cancer Biology, Durham, NC 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10426998" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Binding Sites ; Estradiol/metabolism/*pharmacology ; Estrogen Antagonists/*pharmacology ; Estrogen Receptor alpha ; Humans ; Ligands ; Mifepristone/pharmacology ; Molecular Sequence Data ; Peptide Library ; Peptides/metabolism/*pharmacology ; Receptors, Cytoplasmic and Nuclear/metabolism ; Receptors, Estrogen/agonists/*antagonists & inhibitors/chemistry/*metabolism ; Recombinant Fusion Proteins/pharmacology ; Tamoxifen/metabolism/*pharmacology ; Transcription Factor AP-1/genetics/metabolism ; Transcription, Genetic/drug effects
    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
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    Receptor for motilin identified in the human gastrointestinal system (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-06-26
    Description: Motilin is a 22-amino acid peptide hormone expressed throughout the gastrointestinal (GI) tract of humans and other species. It affects gastric motility by stimulating interdigestive antrum and duodenal contractions. A heterotrimeric guanosine triphosphate-binding protein (G protein)-coupled receptor for motilin was isolated from human stomach, and its amino acid sequence was found to be 52 percent identical to the human receptor for growth hormone secretagogues. The macrolide antibiotic erythromycin also interacted with the cloned motilin receptor, providing a molecular basis for its effects on the human GI tract. The motilin receptor is expressed in enteric neurons of the human duodenum and colon. Development of motilin receptor agonists and antagonists may be useful in the treatment of multiple disorders of GI motility.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Feighner, S D -- Tan, C P -- McKee, K K -- Palyha, O C -- Hreniuk, D L -- Pong, S S -- Austin, C P -- Figueroa, D -- MacNeil, D -- Cascieri, M A -- Nargund, R -- Bakshi, R -- Abramovitz, M -- Stocco, R -- Kargman, S -- O'Neill, G -- Van Der Ploeg, L H -- Evans, J -- Patchett, A A -- Smith, R G -- Howard, A D -- New York, N.Y. -- Science. 1999 Jun 25;284(5423):2184-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Metabolic Disorders, Department of Medicinal Chemistry, Merck Research Laboratories, Building RY-80Y-265, 126 East Lincoln Avenue, Rahway, NJ 07065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10381885" target="_blank"〉PubMed〈/a〉
    Keywords: Alternative Splicing ; Amino Acid Sequence ; Base Sequence ; Binding Sites ; Calcium/metabolism ; Cell Line ; Chromosome Mapping ; Chromosomes, Human, Pair 13 ; Cloning, Molecular ; Colon/*metabolism ; Erythromycin/metabolism ; GTP-Binding Proteins/metabolism ; Humans ; In Situ Hybridization ; Intestine, Small/*metabolism ; Ligands ; Molecular Sequence Data ; Motilin/analogs & derivatives/*metabolism ; Receptors, Gastrointestinal Hormone/*chemistry/*genetics/metabolism ; Receptors, Neuropeptide/*chemistry/*genetics/metabolism ; Stomach/*metabolism ; Thyroid Gland/metabolism ; Transfection
    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
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    Functional characterization of the S. cerevisiae genome by gene deletion and parallel analysis (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-08-07
    Description: The functions of many open reading frames (ORFs) identified in genome-sequencing projects are unknown. New, whole-genome approaches are required to systematically determine their function. A total of 6925 Saccharomyces cerevisiae strains were constructed, by a high-throughput strategy, each with a precise deletion of one of 2026 ORFs (more than one-third of the ORFs in the genome). Of the deleted ORFs, 17 percent were essential for viability in rich medium. The phenotypes of more than 500 deletion strains were assayed in parallel. Of the deletion strains, 40 percent showed quantitative growth defects in either rich or minimal medium.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Winzeler, E A -- Shoemaker, D D -- Astromoff, A -- Liang, H -- Anderson, K -- Andre, B -- Bangham, R -- Benito, R -- Boeke, J D -- Bussey, H -- Chu, A M -- Connelly, C -- Davis, K -- Dietrich, F -- Dow, S W -- El Bakkoury, M -- Foury, F -- Friend, S H -- Gentalen, E -- Giaever, G -- Hegemann, J H -- Jones, T -- Laub, M -- Liao, H -- Liebundguth, N -- Lockhart, D J -- Lucau-Danila, A -- Lussier, M -- M'Rabet, N -- Menard, P -- Mittmann, M -- Pai, C -- Rebischung, C -- Revuelta, J L -- Riles, L -- Roberts, C J -- Ross-MacDonald, P -- Scherens, B -- Snyder, M -- Sookhai-Mahadeo, S -- Storms, R K -- Veronneau, S -- Voet, M -- Volckaert, G -- Ward, T R -- Wysocki, R -- Yen, G S -- Yu, K -- Zimmermann, K -- Philippsen, P -- Johnston, M -- Davis, R W -- HG00185-02/HG/NHGRI NIH HHS/ -- HG01627/HG/NHGRI NIH HHS/ -- HG01633/HG/NHGRI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1999 Aug 6;285(5429):901-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, Stanford University School of Medicine, Stanford, CA 94305-5307, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10436161" target="_blank"〉PubMed〈/a〉
    Keywords: Culture Media ; *Gene Deletion ; Gene Expression Regulation, Fungal ; Gene Targeting ; *Genes, Essential ; Genes, Fungal ; *Genome, Fungal ; *Open Reading Frames ; Phenotype ; Polymerase Chain Reaction ; Recombination, Genetic ; Saccharomyces cerevisiae/*genetics/growth & development
    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
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    Defective angiogenesis in mice lacking endoglin (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-29
    Description: Endoglin is a transforming growth factor-beta (TGF-beta) binding protein expressed on the surface of endothelial cells. Loss-of-function mutations in the human endoglin gene ENG cause hereditary hemorrhagic telangiectasia (HHT1), a disease characterized by vascular malformations. Here it is shown that by gestational day 11.5, mice lacking endoglin die from defective vascular development. However, in contrast to mice lacking TGF-beta, vasculogenesis was unaffected. Loss of endoglin caused poor vascular smooth muscle development and arrested endothelial remodeling. These results demonstrate that endoglin is essential for angiogenesis and suggest a pathogenic mechanism for HHT1.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, D Y -- Sorensen, L K -- Brooke, B S -- Urness, L D -- Davis, E C -- Taylor, D G -- Boak, B B -- Wendel, D P -- K08 HL03490-03/HL/NHLBI NIH HHS/ -- T35 HL07744-06/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1999 May 28;284(5419):1534-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Human Molecular Biology and Genetics, Department of Human Genetics, Howard Hughes Medical Institute, University of Utah, Salt Lake City, UT 84112-5330, USA. dean.li@hci.utah.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10348742" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD ; Antigens, CD31/analysis ; Blood Vessels/cytology/*embryology/metabolism ; Cell Differentiation ; Crosses, Genetic ; Endothelium, Vascular/cytology/*embryology/metabolism ; Female ; Gene Targeting ; In Situ Hybridization ; Male ; Mice ; Mice, Inbred C57BL ; Microscopy, Electron ; Muscle, Smooth, Vascular/cytology/*embryology ; *Neovascularization, Physiologic ; Receptors, Cell Surface ; Signal Transduction ; Transforming Growth Factor beta/metabolism ; Vascular Cell Adhesion Molecule-1/genetics/*physiology ; Yolk Sac/ultrastructure
    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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  • 10
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    The transcriptional program in the response of human fibroblasts to serum (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999
    Description: The temporal program of gene expression during a model physiological response of human cells, the response of fibroblasts to serum, was explored with a complementary DNA microarray representing about 8600 different human genes. Genes could be clustered into groups on the basis of their temporal patterns of expression in this program. Many features of the transcriptional program appeared to be related to the physiology of wound repair, suggesting that fibroblasts play a larger and richer role in this complex multicellular response than had previously been appreciated.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Iyer, V R -- Eisen, M B -- Ross, D T -- Schuler, G -- Moore, T -- Lee, J C -- Trent, J M -- Staudt, L M -- Hudson, J Jr -- Boguski, M S -- Lashkari, D -- Shalon, D -- Botstein, D -- Brown, P O -- CA 77097/CA/NCI NIH HHS/ -- HG00450/HG/NHGRI NIH HHS/ -- T32 HG00450/HG/NHGRI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1999 Jan 1;283(5398):83-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, Stanford University School of Medicine, Stanford CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9872747" target="_blank"〉PubMed〈/a〉
    Keywords: *Blood ; Calcium-Calmodulin-Dependent Protein Kinases/genetics/metabolism ; Cell Cycle/*genetics ; Cell Line ; Cholesterol/biosynthesis ; Culture Media ; Culture Media, Serum-Free ; Expressed Sequence Tags ; Fibroblasts/cytology/*physiology ; Fluorescent Dyes ; *Gene Expression Regulation ; Genes, Immediate-Early ; Humans ; Oligonucleotide Array Sequence Analysis ; Polymerase Chain Reaction/methods ; Software ; Time Factors ; Transcription Factors/genetics ; *Transcription, Genetic ; Wound Healing/*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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