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  • 1
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    Nonproteolytic neuroprotection by human recombinant tissue plasminogen activator (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-24
    Description: Human recombinant tissue plasminogen activator (tPA) may benefit ischemic stroke patients by dissolving clots. However, independent of thrombolysis, tPA may also have deleterious effects on neurons by promoting excitotoxicity. Zinc neurotoxicity has been shown to be an additional key mechanism in brain injuries. Hence, if tPA affects zinc neurotoxicity, this may provide additional insights into its effect on neuronal death. Independent of its proteolytic action, tPA markedly attenuated zinc-induced cell death in cortical culture, and, when injected into cerebrospinal fluid, also reduced kainate seizure-induced hippocampal neuronal death in adult rats.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, Y H -- Park, J H -- Hong, S H -- Koh, J Y -- New York, N.Y. -- Science. 1999 Apr 23;284(5414):647-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Creative Research Initiative Center for the Study of Central Nervous System Zinc and Department of Neurology, University of Ulsan College of Medicine, 388-1 Poongnap-Dong Songpa-Gu, Seoul 138-736, Korea.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10213688" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Death/drug effects ; Cells, Cultured ; Cerebral Cortex/cytology ; *Cytoprotection ; Fibrinolysin/pharmacology ; Hippocampus/pathology ; Humans ; Kainic Acid/pharmacology ; Male ; Mice ; N-Methylaspartate/pharmacology ; Neurons/*cytology/drug effects ; Neuroprotective Agents/*pharmacology ; Oxidative Stress ; Rats ; Rats, Sprague-Dawley ; Recombinant Proteins/cerebrospinal fluid/pharmacology ; Seizures/chemically induced/pathology ; Tissue Plasminogen Activator/cerebrospinal fluid/*pharmacology ; Zinc/metabolism/*toxicity
    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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    Potentiated necrosis of cultured cortical neurons by neurotrophins (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-04-28
    Description: The effects of neurotrophins on several forms of neuronal degeneration in murine cortical cell cultures were examined. Consistent with other studies, brain-derived neurotrophic factor, neurotrophin-3, and neurotrophin-4/5 all attenuated the apoptotic death induced by serum deprivation or exposure to the calcium channel antagonist nimodipine. Unexpectedly, however, 24-hour pretreatment with these same neurotrophins markedly potentiated the necrotic death induced by exposure to oxygen-glucose deprivation or N-methyl-D-aspartate. Thus, certain neurotrophins may have opposing effects on different types of death in the same neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koh, J Y -- Gwag, B J -- Lobner, D -- Choi, D W -- NS 30337/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1995 Apr 28;268(5210):573-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for the Study of Nervous System Injury, Washington University School of Medicine, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7725105" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis/drug effects ; Brain-Derived Neurotrophic Factor ; Calcium/metabolism ; Cell Death/drug effects ; Cells, Cultured ; Cerebral Cortex/cytology ; Dizocilpine Maleate/pharmacology ; Mice ; N-Methylaspartate/pharmacology ; Necrosis ; Nerve Degeneration/*drug effects ; Nerve Growth Factors/*pharmacology ; Nerve Tissue Proteins/pharmacology ; Neurons/*cytology/drug effects/pathology ; Neurotrophin 3 ; Quinoxalines/pharmacology ; Receptors, AMPA/antagonists & inhibitors
    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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  • 3
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    The role of zinc in selective neuronal death after transient global cerebral ischemia (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-05-17
    Description: Zinc is present in presynaptic nerve terminals throughout the mammalian central nervous system and likely serves as an endogenous signaling substance. However, excessive exposure to extracellular zinc can damage central neurons. After transient forebrain ischemia in rats, chelatable zinc accumulated specifically in degenerating neurons in the hippocampal hilus and CA1, as well as in the cerebral cortex, thalamus, striatum, and amygdala. This accumulation preceded neurodegeneration, which could be prevented by the intraventricular injection of a zinc chelating agent. The toxic influx of zinc may be a key mechanism underlying selective neuronal death after transient global ischemic insults.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koh, J Y -- Suh, S W -- Gwag, B J -- He, Y Y -- Hsu, C Y -- Choi, D W -- NS30337/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1996 May 17;272(5264):1013-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology and Center for the Study of Nervous System Injury, Washington University School of Medicine, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8638123" target="_blank"〉PubMed〈/a〉
    Keywords: Aminoquinolines ; Animals ; Brain/metabolism/*pathology ; Cell Death ; Chelating Agents/pharmacology ; Dithizone/pharmacology ; Edetic Acid/pharmacology ; Fluorescent Dyes ; Hippocampus/metabolism/pathology ; Ischemic Attack, Transient/*metabolism/*pathology ; Microscopy, Fluorescence ; *Nerve Degeneration ; Neurons/metabolism/*pathology ; Presynaptic Terminals/metabolism ; Pyramidal Cells/metabolism/pathology ; Rats ; Tosyl Compounds ; Zinc/*metabolism
    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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  • 4
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    Neurons containing NADPH-diaphorase are selectively resistant to quinolinate toxicity (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-10-03
    Description: Exposure of cultures of cortical cells from mouse to either of the endogenous excitatory neurotoxins quinolinate or glutamate resulted in widespread neuronal destruction; but only in the cultures exposed to quinolinate, an N-methyl-D-aspartate agonist, was there a striking preservation of the subpopulation of neurons containing the enzyme nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d). Further investigation revealed that neurons containing NADPH-d were also resistant to the toxicity of N-methyl-D-aspartate itself but were selectively vulnerable to the toxicity of either kainate or quisqualate. Thus, neurons containing NADPH-d may have an unusual distribution of receptors for excitatory amino acids, with a relative lack of N-methyl-D-aspartate receptors and a relative preponderance of kainate or quisqualate receptors. Since selective sparing of neurons containing NADPH-d is a hallmark of Huntington's disease, the results support the hypothesis that the disease may be caused by excess exposure to quinolinate or some other endogenous N-methyl-D-aspartate agonist.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koh, J Y -- Peters, S -- Choi, D W -- NS21628/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1986 Oct 3;234(4772):73-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2875522" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aspartic Acid/analogs & derivatives/pharmacology ; Glutamates/pharmacology ; Glutamic Acid ; Humans ; Huntington Disease/physiopathology ; Kainic Acid/pharmacology ; Mice ; N-Methylaspartate ; NADH, NADPH Oxidoreductases/*physiology ; NADPH Dehydrogenase/*physiology ; Neurons/*drug effects/physiology ; Oxadiazoles/pharmacology ; Pyridines/*pharmacology ; Quinolinic Acid ; Quinolinic Acids/*pharmacology ; Quisqualic Acid
    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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    Contribution by synaptic zinc to the gender-disparate plaque formation in human Swedish mutant APP transgenic mice (2002)
    National Academy of Sciences
    Details
    Publication Date: 2002-04-30
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 6
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    Activation of the metabotropic glutamate receptor attenuates N-methyl-D-aspartate neurotoxicity in cortical cultures. (1991)
    National Academy of Sciences
    Details
    Publication Date: 1991-11-01
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 7
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    Comparative analyses of plasma amyloid-{beta} levels in heterogeneous and monomerized states by interdigitated microelectrode sensor system (2019)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2019
    Description: 〈p〉Detection of amyloid-β (Aβ) aggregates contributes to the diagnosis of Alzheimer disease (AD). Plasma Aβ is deemed a less invasive and more accessible hallmark of AD, as Aβ can penetrate blood-brain barriers. However, correlations between biofluidic Aβ concentrations and AD progression has been tenuous. Here, we introduce a diagnostic technique that compares the heterogeneous and the monomerized states of Aβ in plasma. We used a small molecule, EPPS [4-(2-hydroxyethyl)-1-piperazinepropanesulfonic acid], to dissociate aggregated Aβ into monomers to enhance quantification accuracy. Subsequently, Aβ levels of EPPS-treated plasma were compared to those of untreated samples to minimize inter- and intraindividual variations. The interdigitated microelectrode sensor system was used to measure plasma Aβ levels on a scale of 0.1 pg/ml. The implementation of this self-standard blood test resulted in substantial distinctions between patients with AD and individuals with normal cognition (NC), with selectivity and sensitivity over 90%.〈/p〉
    Electronic ISSN: 2375-2548
    Topics: Natural Sciences in General
    Published by American Association for the Advancement of Science (AAAS)
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  • 8
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    The principles of cascading power limits in small, fast biological and engineered systems (2018)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2018-04-27
    Description: Mechanical power limitations emerge from the physical trade-off between force and velocity. Many biological systems incorporate power-enhancing mechanisms enabling extraordinary accelerations at small sizes. We establish how power enhancement emerges through the dynamic coupling of motors, springs, and latches and reveal how each displays its own force-velocity behavior. We mathematically demonstrate a tunable performance space for spring-actuated movement that is applicable to biological and synthetic systems. Incorporating nonideal spring behavior and parameterizing latch dynamics allows the identification of critical transitions in mass and trade-offs in spring scaling, both of which offer explanations for long-observed scaling patterns in biological systems. This analysis defines the cascading challenges of power enhancement, explores their emergent effects in biological and engineered systems, and charts a pathway for higher-level analysis and synthesis of power-amplified systems.
    Keywords: Engineering, Online Only
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 9
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    Neuropathogenic role of adenylate kinase-1 in A{beta}-mediated tau phosphorylation via AMPK and GSK3{beta} (2012)
    Oxford University Press
    Details
    Publication Date: 2012-05-25
    Description: Abnormally hyperphosphorylated tau is often caused by tau kinases, such as GSK3β and Cdk5. Such occurrence leads to neurofibrillary tangle formation and neuronal degeneration in tauopathy, including Alzheimer's disease (AD). However, little is known about the signaling cascade underlying the pathologic phosphorylation of tau by Aβ 42 . In this study, we show that adenylate kinase 1 (AK1) is a novel regulator of abnormal tau phosphorylation. AK1 expression is markedly increased in the brains of AD patients and AD model mice and is significantly induced by Aβ 42 in the primary neurons. Ectopic expression of AK1 alone augments the pathologic phosphorylation of tau at PHF1, CP13 and AT180 epitopes and enhances the formation of tau aggregates. Inversely, downregulation of AK1 alleviates Aβ 42 -induced hyperphosphorylation of tau. AK1 plays a role in Aβ 42 -induced impairment of AMPK activity and GSK3β activation in the primary neurons. Pharmacologic studies show that treatment with an AMPK inhibitor activates GSK3β, and a GSK3β inhibitor attenuates AK1-mediated tau phosphorylation. In a Drosophila model of human tauopathy, the retinal expression of human AK1 severely exacerbates rough eye phenotype and increases abnormal tau phosphorylation. Further, neural expression of AK1 reduces the lifespan of tau transgenic files. Taken together, these observations indicate that the neuronal expression of AK1 is induced by Aβ 42 to increase abnormal tau phosphorylation via AMPK-GSK3β and contributes to tau-mediated neurodegeneration, providing a new upstream modulator of GSK3β in the pathologic phosphorylation of tau.
    Print ISSN: 0964-6906
    Electronic ISSN: 1460-2083
    Topics: Biology , Medicine
    Published by Oxford University Press
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  • 10
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    Flow transitions in collisions between vortex-rings and density interfaces (2020)
    Springer
    Details
    Publication Date: 2020-07-07
    Print ISSN: 1343-8875
    Electronic ISSN: 1875-8975
    Topics: Computer Science
    Published by Springer
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