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  • Rats  (4)
  • Mice  (3)
  • American Association for the Advancement of Science (AAAS)  (7)
  • 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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    Activation-induced B cell fates are selected by intracellular stochastic competition (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-01-10
    Description: In response to stimulation, B lymphocytes pursue a large number of distinct fates important for immune regulation. Whether each cell's fate is determined by external direction, internal stochastic processes, or directed asymmetric division is unknown. Measurement of times to isotype switch, to develop into a plasmablast, and to divide or to die for thousands of cells indicated that each fate is pursued autonomously and stochastically. As a consequence of competition between these processes, censorship of alternative outcomes predicts intricate correlations that are observed in the data. Stochastic competition can explain how the allocation of a proportion of B cells to each cell fate is achieved. The B cell may exemplify how other complex cell differentiation systems are controlled.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Duffy, Ken R -- Wellard, Cameron J -- Markham, John F -- Zhou, Jie H S -- Holmberg, Ross -- Hawkins, Edwin D -- Hasbold, Jhagvaral -- Dowling, Mark R -- Hodgkin, Philip D -- New York, N.Y. -- Science. 2012 Jan 20;335(6066):338-41. doi: 10.1126/science.1213230. Epub 2012 Jan 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Hamilton Institute, National University of Ireland, Maynooth, Ireland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22223740" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/*cytology/*immunology ; Cell Death ; Cell Differentiation ; Cell Division ; Female ; Immunoglobulin Class Switching ; *Lymphocyte Activation ; Mice ; Models, Immunological ; Stochastic Processes
    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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    Antibodies to PfSEA-1 block parasite egress from RBCs and protect against malaria infection (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-05-24
    Description: Novel vaccines are urgently needed to reduce the burden of severe malaria. Using a differential whole-proteome screening method, we identified Plasmodium falciparum schizont egress antigen-1 (PfSEA-1), a 244-kilodalton parasite antigen expressed in schizont-infected red blood cells (RBCs). Antibodies to PfSEA-1 decreased parasite replication by arresting schizont rupture, and conditional disruption of PfSEA-1 resulted in a profound parasite replication defect. Vaccination of mice with recombinant Plasmodium berghei PbSEA-1 significantly reduced parasitemia and delayed mortality after lethal challenge with the Plasmodium berghei strain ANKA. Tanzanian children with antibodies to recombinant PfSEA-1A (rPfSEA-1A) did not experience severe malaria, and Kenyan adolescents and adults with antibodies to rPfSEA-1A had significantly lower parasite densities than individuals without these antibodies. By blocking schizont egress, PfSEA-1 may synergize with other vaccines targeting hepatocyte and RBC invasion.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4184151/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4184151/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Raj, Dipak K -- Nixon, Christian P -- Nixon, Christina E -- Dvorin, Jeffrey D -- DiPetrillo, Christen G -- Pond-Tor, Sunthorn -- Wu, Hai-Wei -- Jolly, Grant -- Pischel, Lauren -- Lu, Ailin -- Michelow, Ian C -- Cheng, Ling -- Conteh, Solomon -- McDonald, Emily A -- Absalon, Sabrina -- Holte, Sarah E -- Friedman, Jennifer F -- Fried, Michal -- Duffy, Patrick E -- Kurtis, Jonathan D -- 1K08AI100997-01A1/AI/NIAID NIH HHS/ -- DP2 AI112219/AI/NIAID NIH HHS/ -- DP2-AI112219/AI/NIAID NIH HHS/ -- K08 AI100997/AI/NIAID NIH HHS/ -- P20GM103421/GM/NIGMS NIH HHS/ -- P30 AI042853/AI/NIAID NIH HHS/ -- P30AI042853/AI/NIAID NIH HHS/ -- R01 AI102907/AI/NIAID NIH HHS/ -- R01-AI076353/AI/NIAID NIH HHS/ -- R01-AI102907/AI/NIAID NIH HHS/ -- R01-AI52059/AI/NIAID NIH HHS/ -- T32-DA013911/DA/NIDA NIH HHS/ -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2014 May 23;344(6186):871-7. doi: 10.1126/science.1254417.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for International Health Research, Rhode Island Hospital, The Warren Alpert Medical School of Brown University, Providence, RI 02903, USA. ; Division of Infectious Diseases, Boston Children's Hospital and Harvard Medical School, Boston, MA 02115, USA. ; Center for International Health Research, Rhode Island Hospital, The Warren Alpert Medical School of Brown University, Providence, RI 02903, USA. Department of Pediatrics, Rhode Island Hospital, The Warren Alpert Medical School of Brown University, Providence, RI 02903, USA. ; Department of Pathology and Laboratory Medicine, Rhode Island Hospital, The Warren Alpert Medical School of Brown University, Providence, RI 02906, USA. ; Laboratory of Malaria Immunology and Vaccinology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD 20892, USA. ; Fred Hutchinson Cancer Research Center Program in Biostatistics and Biomathematics, Department of Biostatistics and Global Health, University of Washington, Seattle, WA 98109, USA. ; Center for International Health Research, Rhode Island Hospital, The Warren Alpert Medical School of Brown University, Providence, RI 02903, USA. Department of Pathology and Laboratory Medicine, Rhode Island Hospital, The Warren Alpert Medical School of Brown University, Providence, RI 02906, USA. jonathan_kurtis@brown.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24855263" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Animals ; Antibodies, Protozoan/blood/*immunology ; Antigens, Protozoan/*immunology ; Child ; Erythrocytes/*parasitology ; Hepatocytes/immunology/parasitology ; Humans ; Immunoglobulin G/blood/immunology ; Kenya ; Malaria/prevention & control ; Malaria Vaccines/*immunology ; Malaria, Falciparum/*prevention & control ; Mice ; Plasmodium berghei/immunology ; Plasmodium falciparum/*growth & development/immunology ; Protozoan Proteins/*immunology ; Recombinant Proteins/immunology ; Schizonts/*growth & development ; Young Adult
    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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    T cell signaling. Antigen affinity, costimulation, and cytokine inputs sum linearly to amplify T cell expansion (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-11-29
    Description: T cell responses are initiated by antigen and promoted by a range of costimulatory signals. Understanding how T cells integrate alternative signal combinations and make decisions affecting immune response strength or tolerance poses a considerable theoretical challenge. Here, we report that T cell receptor (TCR) and costimulatory signals imprint an early, cell-intrinsic, division fate, whereby cells effectively count through generations before returning automatically to a quiescent state. This autonomous program can be extended by cytokines. Signals from the TCR, costimulatory receptors, and cytokines add together using a linear division calculus, allowing the strength of a T cell response to be predicted from the sum of the underlying signal components. These data resolve a long-standing costimulation paradox and provide a quantitative paradigm for therapeutically manipulating immune response strength.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marchingo, Julia M -- Kan, Andrey -- Sutherland, Robyn M -- Duffy, Ken R -- Wellard, Cameron J -- Belz, Gabrielle T -- Lew, Andrew M -- Dowling, Mark R -- Heinzel, Susanne -- Hodgkin, Philip D -- New York, N.Y. -- Science. 2014 Nov 28;346(6213):1123-7. doi: 10.1126/science.1260044.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Immunology, The Walter and Eliza Hall Institute of Medical Research, Parkville, VIC, Australia. Department of Medical Biology, The University of Melbourne, Parkville, VIC, Australia. ; Hamilton Institute, National University of Ireland, Maynooth, Ireland. ; Division of Immunology, The Walter and Eliza Hall Institute of Medical Research, Parkville, VIC, Australia. Department of Medical Biology, The University of Melbourne, Parkville, VIC, Australia. The Royal Melbourne Hospital, Parkville, VIC, Australia. ; Division of Immunology, The Walter and Eliza Hall Institute of Medical Research, Parkville, VIC, Australia. Department of Medical Biology, The University of Melbourne, Parkville, VIC, Australia. hodgkin@wehi.edu.au.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25430770" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens/*immunology ; CD8-Positive T-Lymphocytes/cytology/*immunology ; Cell Division ; Cell Proliferation ; Cytokines/*immunology ; *Immune Tolerance ; Lymphocyte Activation ; Mice ; Receptors, Antigen, T-Cell/*immunology ; Signal Transduction
    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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    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
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  • 6
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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
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  • 7
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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
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