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  • Articles  (3)
  • Male  (3)
  • Cell & Developmental Biology
  • Polymer and Materials Science
  • Science. 234(4777): 728-31.  (1)
  • Science. 252(5011): 1386-9.  (1)
  • Science. 278(5337): 412-9.  (1)
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  • 1
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-10-23
    Description: Neurodegenerative disorders are characterized by extensive neuron death that leads to functional decline, but the neurobiological correlates of functional decline in normal aging are less well defined. For decades, it has been a commonly held notion that widespread neuron death in the neocortex and hippocampus is an inevitable concomitant of brain aging, but recent quantitative studies suggest that neuron death is restricted in normal aging and unlikely to account for age-related impairment of neocortical and hippocampal functions. In this article, the qualitative and quantitative differences between aging and Alzheimer's disease with respect to neuron loss are discussed, and age-related changes in functional and biochemical attributes of hippocampal circuits that might mediate functional decline in the absence of neuron death are explored. When these data are viewed comprehensively, it appears that the primary neurobiological substrates for functional impairment in aging differ in important ways from those in neurodegenerative disorders such as Alzheimer's disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Morrison, J H -- Hof, P R -- AG05138/AG/NIA NIH HHS/ -- AG06647/AG/NIA NIH HHS/ -- MHDA52145/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1997 Oct 17;278(5337):412-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neurobiology of Aging Laboratories, the Fishberg Research Center for Neurobiology, and the Department of Geriatrics and Adult Development, Mount Sinai School of Medicine, New York, NY 10029, USA. morrison@cortex.neuro.mssm.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9334292" target="_blank"〉PubMed〈/a〉
    Keywords: *Aging ; Alzheimer Disease/pathology ; Animals ; Cell Death ; Cell Survival ; Entorhinal Cortex/pathology ; Estrogens/physiology ; Female ; Hippocampus/cytology/pathology/*physiology ; Humans ; Male ; Memory ; Neocortex/cytology/pathology/*physiology ; *Nerve Degeneration ; Neurofibrillary Tangles/pathology ; Neurofilament Proteins/metabolism ; Neurons/cytology/pathology/*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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  • 2
    Publication Date: 1991-06-07
    Description: National, longitudinal surveys from Great Britain and the United States were used to investigate the effects of divorce on children. In both studies, a subsample of children who were in two-parent families during the initial interview (at age 7 in the British data and at ages 7 to 11 in the U.S. data) were followed through the next interview (at age 11 and ages 11 to 16, respectively). At both time points in the British data, parents and teachers independently rated the children's behavior problems, and the children were given reading and mathematics achievement tests. At both time points in the U.S. data, parents rated the children's behavior problems. Children whose parents divorced or separated between the two time points were compared to children whose families remained intact. For boys, the apparent effect of separation or divorce on behavior problems and achievement at the later time point was sharply reduced by considering behavior problems, achievement levels, and family difficulties that were present at the earlier time point, before any of the families had broken up. For girls, the reduction in the apparent effect of divorce occurred to a lesser but still noticeable extent once preexisting conditions were considered.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cherlin, A J -- Furstenberg, F F Jr -- Chase-Lansdale, L -- Kiernan, K E -- Robins, P K -- Morrison, D R -- Teitler, J O -- HD25936/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1991 Jun 7;252(5011):1386-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Sociology, Johns Hopkins University, Baltimore, MD 21218.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2047851" target="_blank"〉PubMed〈/a〉
    Keywords: Achievement ; Adolescent ; Child ; Child Behavior ; Divorce/*psychology ; England ; Female ; Humans ; Longitudinal Studies ; Male ; 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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  • 3
    Publication Date: 1986-11-07
    Description: The current prevalence of the acquired immune deficiency syndrome in humans has provoked renewed interest in methods of protective immunization against retrovirus-induced diseases. In this study, a vaccinia-retrovirus recombinant vector was constructed to study mechanisms of immune protection against Friend virus leukemia in mice. The envelope (env) gene from Friend murine leukemia virus (F-MuLV) was inserted into the genome of a vaccinia virus expression vector. Infected cells synthesized gp85, the glycosylated primary product of the env gene. Processing to gp70 and p15E, and cell surface localization, were similar to that occurring in cells infected with F-MuLV. Mice inoculated with live recombinant vaccinia virus had an envelope-specific T-cell proliferative response and, after challenge with Friend virus complex, developed neutralizing antibody and cytotoxic T cells (CTL) and were protected against leukemia. In contrast, unimmunized and control groups developed a delayed neutralizing antibody response, but no detectable CTL, and succumbed to leukemia. Genes of the major histocompatibility complex influenced protection induced by the vaccinia recombinant but not that induced by attenuated N-tropic Friend virus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Earl, P L -- Moss, B -- Morrison, R P -- Wehrly, K -- Nishio, J -- Chesebro, B -- New York, N.Y. -- Science. 1986 Nov 7;234(4777):728-31.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3490689" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Viral/immunology ; Antigens/*immunology ; DNA, Recombinant ; Female ; Friend murine leukemia virus/genetics/immunology ; *Genes, Viral ; Leukemia, Erythroblastic, Acute/prevention & control ; Leukemia, Experimental/*prevention & control ; Lymphocyte Activation ; Male ; Mice ; Mice, Inbred Strains ; Sex Factors ; Spleen/microbiology ; T-Lymphocytes/*immunology ; T-Lymphocytes, Cytotoxic/immunology ; Vaccines, Synthetic/*immunology ; Vaccinia virus/genetics/immunology ; Viral Envelope Proteins/genetics/*immunology ; Viral Vaccines/*immunology
    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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