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  • 1
    Electronic Resource
    Electronic Resource
    THE RELATION BETWEEN MELATONIN, A PINEAL SUBSTANCE, AND THE EFFECTS OF LIGHT ON THE RAT GONAD (1964)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 117 (1964), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1964.tb48179.x
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  • 2
    Electronic Resource
    Electronic Resource
    Feeding-Associated Alterations in Striatal Neurotransmitter Release (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 575 (1989), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1989.tb53307.x
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  • 3
    Electronic Resource
    Electronic Resource
    Introductory Remarks (1985)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 453 (1985), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1985.tb11792.x
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  • 4
    Electronic Resource
    Electronic Resource
    Possible Behavioral Consequences of Light-Induced Changes in Melatonin Availability (1985)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 453 (1985), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1985.tb11814.x
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  • 5
    Electronic Resource
    Electronic Resource
    Phospholipid and Phospholipid Metabolites in Rat Frontal Cortex Are Decreased following Nucleus Basalis Lesions (1993)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 695 (1993), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Notes: Membrane phospholipid metabolism is abnormal in Alzheimer's disease (AD) brain. Phosphatidylcholine and phosphatidylethanolamine levels are decreased as are choline and ethanolamine, while glycerophosphocholine (GPC) and glycerophosphoethanolamine are increased.1 To develop a rat model for these changes, we examined the effects of unilateral lesion of the cholinergic nucleus basalis (nBM) with ibotenic acid (10 mg/ml in PBS, 0.5 μl) and sham lesion on frontocortical phospholipid, choline and GPC. After one week, choline acetyltransferase activity in frontal cortex was decreased (26%, p 〈 0.005, n = 14) on the nBM ibotenate-lesion side relative to the contralateral side, while there were no differences following the nBM sham-lesion. Levels of membrane phospholipids (nmol/mg protein) in adjacent frontal cortex sections exhibited concomitant decreases (13%, p 〈 0.05, n = 14) on the nBM ibotenate-lesion side, while there were no differences following the nBM sham-lesion. Tissue nBM ibotenate-lesion frontocortical choline and GPC levels were also decreased relative to those in control tissues (choline: 21%, p 〈 0.05, n = 14; GPC: 10%,p 〈 0.05, n = 14), while nBM sham-lesion showed no effect. Muscarinic receptor sensitivity in frontal cortex following nBM ibotenate-lesion was increased, as measured by carbachol-sdmulated inositol phosphate production (p 〈 0.001, n = 12), indicating that increased receptor mediated phospholipid hydrolysis in cortex may occur following nBM ibotenate-lesion. These data suggest that impaired cholinergic transmission alters phospholipid metabolism in cholinergic target regions.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1993.tb23060.x
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  • 6
    Electronic Resource
    Electronic Resource
    Preface (1993)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 695 (1993), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Notes: This volume contains the papers and poster abstracts compiled for the seventh meeting of the International Study Group on the Pharmacology of Memory Disorders Associated with Aging (ISG), that took place in Zürich, Switzerland, on February 12–14, 1993. The ISG was founded 14 years ago in the belief that the development of effective treatments for Alzheimer's disease (AD) and other dementias would be accelerated by periodic meetings of scientists and physicians from around the world who are actively working on issues related to dementia. There have been six previous “Zurich Meetings”—in 1979, 1981, 1984, 1987, 1989, and 1991. The proceedings of the second ISB meeting were published by Raven Press in 1982 (Alzheimer's Disease: A Report of Progress in Research; Corkin, Davis, Growdon, Usdin, and Wurtman, editors); the proceedings of the fourth ISG meeting were published by Springer-Verlag in 1988 as Supplement 24 of the Journal of Neural Transmission (Topics in the Basic and Clinical Science of Dementia; Wurtman, Corkin, and Growdon, editors); the proceedings of the fifth ISB meeting were published by Raven Press in 1990 (Alzheimer's Disease, Advances in Neurology, Volume 51; Wurtman, Corkin, Growdon, and fitter-Walker, editors); and the proceedings of the sixth ISG meeting were published by the New York Academy of Sciences in 1992 (Aging and Alzheimer's Disease, Volume 640; Growdon, Corkin, fitter-Walker, and Wurtman, editors).
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1993.tb23017.x
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  • 7
    Electronic Resource
    Electronic Resource
    Regulation of Amyloid Precursor Protein Release By Protein Kinase C in Swiss 3T3 Fibroblasts (1993)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 695 (1993), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Notes: Release of the amyloid precursor protein (APP) of Alzheimer's disease from Swiss 3T3 fibroblasts was stimulated in a concentration-dependent manner by phorbol 12-myristate 13-acetate. In fibroblasts overexpressing protein kinase Co (PKCα), the EC50 for this response was 7 nM, while in control cells the EC50 was 63 nM. The effect of PMA was inhibited by the PKC antagonist H-7 in control cells, but not in cells that overexpressed PKCα. Basal release of APP was higher in cells that overexpressed PKCα, and was not affected by the phosphatase inhibitor okadaic acid, although this compound doubled APP release from control cells. The results suggest that PKCα regulates APP processing in mammalian cells. Alterations in the activity of PKC have been reported to occur in Alzheimer's disease and might potentially contribute to abnormalities of APP metabolism characteristic of this disorder.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1993.tb23040.x
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  • 8
    Electronic Resource
    Electronic Resource
    Receptor-coupled Amyloid Precursor Protein Processing (1993)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 695 (1993), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Notes: The family of β-amyloid protein precursors (APP) can be processed via several alternative proteolytic pathways. Some generate potentially amyloidogenic AFP derivatives, whereas others preclude the formation of such fragments. The cellular mechanisms regulating the relative activities of these pathways are thus important in determining the factors contributing to the formation of amyloidogenic APP derivatives. In order to investigate whether cell-surface receptor activity can regulate APP processing, HEK 293 cell lines stably expressing human muscarinic acetylcholine receptors (mAChR; subtypes m1, m2, m3, m4) were stimulated with the muscarinic agonist carbachol, and the release of APP derivatives was measured. Carbachol increased the release of large amino-terminal APP-fragments 4-to 6-fold in cell lines expressing the m1 or m3 receptors but not in those expressing m2 or m4 subtypes. This increase was blocked by various protein kinase inhibitors and mimicked by phorbol esters, indicating that it is mediated by protein kinase activation, presumably by protein kinase C (PKC). To determine whether additional cell-surface receptor types linked to this signal transduction pathway could also regulate APP processing, we stimulated differentiated PC-12 cells with bradykinin and found that this neuropeptide also increased the secretion of amino-terminal APP derivatives. We next investigated the possibility that neuronal depolarization might affect APP processing in mammalian brain. Electrically stimulated rat hippocampal slices released two times more amino-terminal APP derivatives than unstimulated control slices. This release increased with increasing stimulation frequencies in the physiological firing range of hippocampal pyramidal cells, and was blocked by tetrodotoxin. These results suggest that, in brain, APP processing is regulated by neuronal activity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1993.tb23039.x
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  • 9
    Electronic Resource
    Electronic Resource
    The slowing of treatment discovery, 1965–1995 (1995)
    [s.l.] : Nature Publishing Group
    Nature medicine 1 (1995), S. 1122-1125 
    Details
    ISSN: 1546-170X
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Medicine
    Notes: [Auszug] In the United States, two goals motivate our national effort in biomedical research: The acquisition of knowledge about how the body works, and the discovery of ways to prevent or treat disease. There can be no doubt that this effort — which each year now expends around eleven billion dollars ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/nm1195-1122
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  • 10
    Electronic Resource
    Electronic Resource
    Reply to “A cornucopia of drug discovery?” (1996)
    [s.l.] : Nature Publishing Group
    Nature medicine 2 (1996), S. 6-6 
    Details
    ISSN: 1546-170X
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Medicine
    Notes: [Auszug] Wurtman & Bettiker reply — We appreciate Dr. Gordon's comments and salute his optimism that the fruits of investigator-initiated basic-science research now place us at the “brink of the greatest wave in drug discovery history.” Similar expectations articulated two decades ago ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/nm0196-6b
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