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  • 1
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    Duplicating a tangled genome (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-09-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cook, P -- New York, N.Y. -- Science. 1998 Sep 4;281(5382):1466-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Sir William Dunn School of Pathology, Oxford OX2 3RE, UK. peter.cook@path.ox.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9750117" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Nucleus/*metabolism ; *DNA Replication ; *Genome ; Genome, Human ; Humans ; Models, Biological ; *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)
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  • 2
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    The organization of replication and transcription (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-06-12
    Description: Models for replication and transcription often display polymerases that track like locomotives along their DNA templates. However, recent evidence supports an alternative model in which DNA and RNA polymerases are immobilized by attachment to larger structures, where they reel in their templates and extrude newly made nucleic acids. These polymerases do not act independently; they are concentrated in discrete "factories," where they work together on many different templates. Evidence for models involving tracking and immobile polymerases is reviewed.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cook, P R -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 1999 Jun 11;284(5421):1790-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Sir William Dunn School of Pathology, University of Oxford, South Parks Road, Oxford OX1 3RE, UK. Peter.Cook@Path.OX.AC.UK〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10364545" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *DNA Replication ; DNA-Directed DNA Polymerase/*metabolism ; DNA-Directed RNA Polymerases/*metabolism ; Humans ; Models, Genetic ; Replication Origin ; Templates, Genetic ; *Transcription, Genetic
    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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  • 3
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    Adipsin and complement factor D activity: an immune-related defect in obesity (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-06-23
    Description: Adipsin is a serine protease that is secreted by adipocytes into the bloodstream; it is deficient in several animal models of obesity, representing a striking example of defective gene expression in this disorder. Recombinant mouse adipsin was purified and its biochemical and enzymatic properties were studied in order to elucidate the function of this protein. Activated adipsin has little or no proteolytic activity toward most substrates but has the same activity as human complement factor D, cleaving complement factor B when it is complexed with activated complement component C3. Like authentic factor D, adipsin can activate the alternative pathway of complement, resulting in red blood cell lysis. Decreased (58 to 80 percent) complement factor D activity, relative to lean controls, was observed as a common feature of several experimental models of obesity, including the ob/ob, db/db, and monosodium glutamate (MSG)-injected mouse and the fa/fa rat. These results suggest that adipsin and the alternative pathway of complement may play an unexpected but important role in the regulation of systemic energy balance in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rosen, B S -- Cook, K S -- Yaglom, J -- Groves, D L -- Volanakis, J E -- Damm, D -- White, T -- Spiegelman, B M -- DK31403/DK/NIDDK NIH HHS/ -- DK34605/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1989 Jun 23;244(4911):1483-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Dana-Farber Cancer Institute, Boston, MA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2734615" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue/metabolism ; Amino Acid Sequence ; Animals ; Cell Line ; Complement Activating Enzymes/*metabolism ; Complement Factor D/*metabolism ; Complement Pathway, Alternative ; Cricetinae ; DNA/genetics ; Gene Expression Regulation ; Humans ; Immunoblotting ; Mice ; Molecular Sequence Data ; Obesity/genetics/*immunology/metabolism ; RNA, Messenger/metabolism ; Recombinant Proteins ; Serine Endopeptidases/genetics/isolation & purification/*metabolism ; Substrate Specificity ; 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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  • 4
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    The molecular basis of muscular dystrophy in the mdx mouse: a point mutation (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-06-30
    Description: The mdx mouse is an X-linked myopathic mutant, an animal model for human Duchenne muscular dystrophy. In both mouse and man the mutations lie within the dystrophin gene, but the phenotypic differences of the disease in the two species confer much interest on the molecular basis of the mdx mutation. The complementary DNA for mouse dystrophin has been cloned, and the sequence has been used in the polymerase chain reaction to amplify normal and mdx dystrophin transcripts in the area of the mdx mutation. Sequence analysis of the amplification products showed that the mdx mouse has a single base substitution within an exon, which causes premature termination of the polypeptide chain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sicinski, P -- Geng, Y -- Ryder-Cook, A S -- Barnard, E A -- Darlison, M G -- Barnard, P J -- New York, N.Y. -- Science. 1989 Jun 30;244(4912):1578-80.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Unit, MRC Centre, Cambridge, United Kingdom.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2662404" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Chromosome Mapping ; Cloning, Molecular ; Codon ; DNA/genetics ; DNA Probes ; DNA-Directed DNA Polymerase ; Dystrophin ; Exons ; Gene Amplification ; Humans ; Mice ; Mice, Mutant Strains ; Molecular Sequence Data ; Muscle Proteins/*genetics ; Muscular Dystrophy, Animal/*genetics ; *Mutation ; Nucleic Acid Hybridization ; Phenotype
    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
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    Meprobamate reduces accuracy of physiological detection of deception (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-04-03
    Description: Normal male subjects attempted to deceive an experimenter recording electrodermal, respiratory, an cardiovascular activity. Those who had ingested a placebo or nothing were detected with statistically significant frequency on the basis of their phasic electrodermal responses, which clearly distinguished them from truthful suspects. That was not the case with deceptive subjects who had ingested 400 milligrams of meprobamate, nor did the examiner detect which subjects had received the drug.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Waid, W M -- Orne, E C -- Cook, M R -- Orne, M T -- New York, N.Y. -- Science. 1981 Apr 3;212(4490):71-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7209522" target="_blank"〉PubMed〈/a〉
    Keywords: Blood Pressure/drug effects ; Double-Blind Method ; Galvanic Skin Response/drug effects ; Humans ; *Lie Detection ; Male ; Meprobamate/*pharmacology ; Overlearning ; Respiration/drug effects ; Stress, Psychological/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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    Benzodiazepine receptor-mediated experimental "anxiety" in primates (1982)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1982-12-24
    Description: The ethyl ester of beta-carboline-3-carboxylic acid has a high affinity for benzodiazepine receptors in the brain. In the rhesus monkey this substance produces an acute behavioral syndrome characterized by dramatic elevations in heart rate, blood pressure, plasma cortisol, and catecholamines. The effects are blocked by benzodiazepines and the specific benzodiazepine receptor antagonist Ro 15-1788. The benzodiazepine receptor may consist of several subsites or functional domains that independently recognize agonist, antagonists, or "active" antagonists such as beta-carboline-3-carboxylic acid ethyl ester. These results suggest that the benzodiazepine receptor is involved in both the affective and physiological manifestations of anxiety, and that the administration of beta-carboxylic acid ethyl ester to monkeys may provide a reliable and reproducible animal model of human anxiety.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ninan, P T -- Insel, T M -- Cohen, R M -- Cook, J M -- Skolnick, P -- Paul, S M -- New York, N.Y. -- Science. 1982 Dec 24;218(4579):1332-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6293059" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anxiety/*etiology ; Benzodiazepinones ; Blood Pressure/drug effects ; Carbolines/pharmacology ; *Disease Models, Animal ; Epinephrine/pharmacology ; Flumazenil ; Heart Rate/*drug effects ; Humans ; Hydrocortisone/blood ; Macaca mulatta ; Male ; Norepinephrine/pharmacology ; Receptors, Drug/*physiology ; Receptors, GABA-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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  • 7
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    Differential NK cell and macrophage killing of hamster cells infected with nononcogenic or oncogenic adenovirus (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-05-11
    Description: Hamster cells infected with highly oncogenic human adenovirus type 12 (Ad12) were resistant to lysis by natural killer cells and macrophages, compared to cells infected with nononcogenic adenovirus type 2 (Ad2). The data suggest that early adenovirus gene expression in hamster cells results in preferential survival of Ad12, compared to Ad2, infected cells in vivo, thus providing an explanation for the differences in the oncogenicities of these two transforming viruses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cook, J L -- Lewis, A M Jr -- CA 31732/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1984 May 11;224(4649):612-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6710160" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoviruses, Human/*immunology ; Animals ; Cell Transformation, Neoplastic/metabolism ; Cell Transformation, Viral ; Cricetinae ; Humans ; Immunity, Cellular ; Killer Cells, Natural/*physiology ; Macrophages/*physiology ; Mesocricetus ; Oncogenic Viruses/*immunology ; Rats
    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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    The origins of U.S. safety standards for microwave radiation (1980)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1980-06-13
    Description: An analysis is made of the scientific research and values influencing the policy decisions that led to the adoption of the 1966 U.S. standard for exposure to microwave radiation. This analysis is used as a tool for understanding the problems faced by those who set standards. An effort is made to unravel the complex motivations that lay behind the adoption of the microwave standard. Based on the past record, it is suggested that standard setting remain distinct from basic scientific research and that adversary procedures be used only as a last resort in seeking consensus over a proposed standard.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Steneck, N H -- Cook, H J -- Vander, A J -- Kane, G L -- New York, N.Y. -- Science. 1980 Jun 13;208(4449):1230-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6990492" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Dose-Response Relationship, Radiation ; History, 20th Century ; Humans ; Information Services ; *Microwaves/adverse effects ; Military Medicine/history ; Radar ; Radiation Injuries/*prevention & control ; Radiation Monitoring/*standards ; United States
    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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    Gamma interferon synthesis by human thymocytes and T lymphocytes inhibited by cyclosporin A (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-07-01
    Description: Cyclosporin A depresses the synthesis of gamma interferon by human thymocytes and T lymphocytes in vitro. This observation is of potential clinical significance because the long-term treatment of transplant patients with cyclosporin A, a widely used immunosuppressive agent, can give rise to B-cell lymphoma resulting from Epstein-Barr virus activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reem, G H -- Cook, L A -- Vilcek, J -- A1-07055/PHS HHS/ -- A1-12948/PHS HHS/ -- New York, N.Y. -- Science. 1983 Jul 1;221(4605):63-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6407112" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Division/drug effects ; Child, Preschool ; Cyclosporins/*pharmacology ; Humans ; Infant ; Interferon-gamma/*biosynthesis ; T-Lymphocytes/*drug effects/metabolism ; Thymus Gland/*cytology/drug effects/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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  • 10
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    Human brain tumor--derived cell lines: growth rate reduced by human fibroblast interferon (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-02-18
    Description: The biological response modifier human beta-interferon had pronounced antigrowth effects on various histologic types of human brain tumor cells but no effects on a nontransformed cell line, MRC-5. The cultures of brain tumor cells showed severe alterations indicative of cell injury and death after exposure to beta-interferon for 2 to 6 days. Similar results were obtained with cells freshly explanted from human brain tumors. The results indicate that it may be possible to use fresh, explanted tumor tissue to identify patients who might benefit from therapy with beta-interferon.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cook, A W -- Carter, W A -- Nidzgorski, F -- Akhtar, L -- New York, N.Y. -- Science. 1983 Feb 18;219(4586):881-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6401866" target="_blank"〉PubMed〈/a〉
    Keywords: Brain Neoplasms/pathology/*therapy ; Cell Division ; Cells, Cultured ; Humans ; Interferon-gamma/pharmacology/*therapeutic use
    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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