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  • Rats  (4)
  • Models, Biological  (2)
  • American Association for the Advancement of Science (AAAS)  (6)
  • 1
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    Neurotrophic and neurotoxic effects of amyloid beta protein: reversal by tachykinin neuropeptides (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-10-12
    Description: The amyloid beta protein is deposited in the brains of patients with Alzheimer's disease but its pathogenic role is unknown. In culture, the amyloid beta protein was neurotrophic to undifferentiated hippocampal neurons at low concentrations and neurotoxic to mature neurons at higher concentrations. In differentiated neurons, amyloid beta protein caused dendritic and axonal retraction followed by neuronal death. A portion of the amyloid beta protein (amino acids 25 to 35) mediated both the trophic and toxic effects and was homologous to the tachykinin neuropeptide family. The effects of the amyloid beta protein were mimicked by tachykinin antagonists and completely reversed by specific tachykinin agonists. Thus, the amyloid beta protein could function as a neurotrophic factor for differentiating neurons, but at high concentrations in mature neurons, as in Alzheimer's disease, could cause neuronal degeneration.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yankner, B A -- Duffy, L K -- Kirschner, D A -- AG08572/AG/NIA NIH HHS/ -- NS01240/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1990 Oct 12;250(4978):279-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, Harvard Medical School, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2218531" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Amyloid beta-Peptides/antagonists & inhibitors/*pharmacology ; Animals ; Cells, Cultured ; Embryo, Mammalian ; Hippocampus/cytology ; Molecular Sequence Data ; Neurons/*cytology/drug effects ; *Neurotoxins ; Peptide Fragments/pharmacology ; Rats ; Tachykinins/*pharmacology
    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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    Ecological context influences epidemic size and parasite-driven evolution (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-03-31
    Description: The occurrence and magnitude of disease outbreaks can strongly influence host evolution. In particular, when hosts face a resistance-fecundity trade-off, they might evolve increased resistance to infection during larger epidemics but increased susceptibility during smaller ones. We tested this theoretical prediction by using a zooplankton-yeast host-parasite system in which ecological factors determine epidemic size. Lakes with high productivity and low predation pressure had large yeast epidemics; during these outbreaks, hosts became more resistant to infection. However, with low productivity and high predation, epidemics remained small and hosts evolved increased susceptibility. Thus, by modulating disease outbreaks, ecological context (productivity and predation) shaped host evolution during epidemics. Consequently, anthropogenic alteration of productivity and predation might strongly influence both ecological and evolutionary outcomes of disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Duffy, Meghan A -- Ochs, Jessica Housley -- Penczykowski, Rachel M -- Civitello, David J -- Klausmeier, Christopher A -- Hall, Spencer R -- New York, N.Y. -- Science. 2012 Mar 30;335(6076):1636-8. doi: 10.1126/science.1215429.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Biology, Georgia Institute of Technology, Atlanta, GA 30332-0230, USA. duffy@gatech.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22461614" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Daphnia/*microbiology/*physiology ; *Ecosystem ; Female ; Fishes ; *Host-Pathogen Interactions ; Indiana ; *Lakes ; Male ; Metschnikowia/*pathogenicity ; Models, Biological ; Population Dynamics ; Predatory Behavior ; Reproduction ; Zooplankton/microbiology/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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  • 3
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    Bright light induction of strong (type 0) resetting of the human circadian pacemaker (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-06-16
    Description: The response of the human circadian pacemaker to light was measured in 45 resetting trials. Each trial consisted of an initial endogenous circadian phase assessment, a three-cycle stimulus which included 5 hours of bright light per cycle, and a final phase assessment. The stimulus induced strong (type 0) resetting, with responses highly dependent on the initial circadian phase of light exposure. The magnitude and direction of the phase shifts were modulated by the timing of exposure to ordinary room light, previously thought to be undetectable by the human pacemaker. The data indicate that the sensitivity of the human circadian pacemaker to light is far greater than previously recognized and have important implications for the therapeutic use of light in the management of disorders of circadian regulation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Czeisler, C A -- Kronauer, R E -- Allan, J S -- Duffy, J F -- Jewett, M E -- Brown, E N -- Ronda, J M -- 1-RO1-AG06072/AG/NIA NIH HHS/ -- 2-S07-RR-05950/RR/NCRR NIH HHS/ -- 5-M01-RR00888/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1989 Jun 16;244(4910):1328-33.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Harvard Medical School, Brigham and Women's Hospital, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2734611" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; *Circadian Rhythm ; Humans ; Male ; Models, Biological ; *Phototherapy ; Time Factors
    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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    Long-term potentiation in the hippocampal slice: evidence for stimulated secretion of newly synthesized proteins (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-06-05
    Description: Long-term potentiation of the hippocampal slice preparation results in an increase in the incorporation of labeled valine into the proteins destined for secretion into the extracellular medium. Double-labeling methods established that the increased secretion of the labeled proteins was limited to the potentiated region of a slice; incorporation of labeled valine was increased in the hippocampus if potentiation was through the Schaffer collaterals and in the dentate if potentiation was through the perforant path. Controls for nonspecific stimulation showed no changes. There appears to be a link between long-term potentiation and the metabolic processes that lead to protein synthesis in the hippocampal slice system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Duffy, C -- Teyler, T J -- Shashoua, V E -- New York, N.Y. -- Science. 1981 Jun 5;212(4499):1148-51.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7233208" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carbon Radioisotopes ; Electric Stimulation ; Hippocampus/*metabolism/physiology ; In Vitro Techniques ; Kinetics ; Nerve Tissue Proteins/*biosynthesis/secretion ; Rats ; Tritium ; Valine
    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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    Local cerebral glucose metabolism during controlled hypoxemia in rats (1979)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1979-05-11
    Description: 2-Deoxy-[14C]glucose metabolism was examined in brains of hypoxic, normotensive rats by autoradiography, which revealed alternating cortical columns of high and low metabolism. Activity in white matter was increased severalfold over that in adjacent gray matter. The columns were anatomically related to penetrating cortical arteries with areas between arteries demonstrating higher rates of metabolism. The results suggest the presence of interarterial tissue oxygen gradients that influence regional glucose metabolism. The relatively greater sensitivity of white matter metabolism to hypoxia may lead to an understanding of white matter damage in postanoxic leukoencephalopathy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pulsinelli, W A -- Duffy, T E -- New York, N.Y. -- Science. 1979 May 11;204(4393):626-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/432667" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anoxia/*metabolism/physiopathology ; Brain/*metabolism ; Cerebral Cortex/metabolism ; Cerebrovascular Circulation ; Deoxyglucose/metabolism ; Glucose/*metabolism ; Male ; Phosphorylation ; Rats
    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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  • 6
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    Neuronal supersensitivity to acetylcholine induced by kindling in the rat hippocampus (1979)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1979-06-08
    Description: Kindling is an experimental model of epilepsy in which periodic brain stimulation induces the progressive development of electrical and behavioral seizures. A kindling-induced electrical seizure (afterdischarge) in the rat hippocampus produces prolonged neuronal supersensitivity to microiontophoretically applied acetylcholine after a latency of 40 to 60 minutes. Neuronal acetylcholine supersensitivity is correlated with the further progression of kindling. A larger hippocampal after-discharge is elicited by a subsequent kindling stimulus delivered in the presence of acetylcholine supersensitivity, but not by one delivered before the onset of the supersensitivity. The results suggest that alteration of synaptic sensitivity to acetylcholine may contribute to kindling and epileptogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Burchfiel, J L -- Duchowny, M S -- Duffy, F H -- New York, N.Y. -- Science. 1979 Jun 8;204(4397):1096-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/36660" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcholine/*pharmacology ; Animals ; Electric Stimulation ; Epilepsy/physiopathology ; Glutamates/pharmacology ; Hippocampus/drug effects/*physiology ; Neurotransmitter Agents/pharmacology ; Rats ; Synaptic Transmission ; Time Factors ; gamma-Aminobutyric Acid/pharmacology
    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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