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  • 1
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    Linkage of plasma Abeta42 to a quantitative locus on chromosome 10 in late-onset Alzheimer's disease pedigrees (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-12-23
    Description: Plasma Abeta42 (amyloid beta42 peptide) is invariably elevated in early-onset familial Alzheimer's disease (AD), and it is also increased in the first-degree relatives of patients with typical late-onset AD (LOAD). To detect LOAD loci that increase Abeta42, we used plasma Abeta42 as a surrogate trait and performed linkage analysis on extended AD pedigrees identified through a LOAD patient with extremely high plasma Abeta. Here, we report linkage to chromosome 10 with a maximal lod score of 3.93 at 81 centimorgans close to D10S1225. Remarkably, linkage to the same region was obtained independently in a genome-wide screen of LOAD sibling pairs. These results provide strong evidence for a novel LOAD locus on chromosome 10 that acts to increase Abeta.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ertekin-Taner, N -- Graff-Radford, N -- Younkin, L H -- Eckman, C -- Baker, M -- Adamson, J -- Ronald, J -- Blangero, J -- Hutton, M -- Younkin, S G -- AG06656/AG/NIA NIH HHS/ -- MH59490/MH/NIMH NIH HHS/ -- P50 AG16574/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2000 Dec 22;290(5500):2303-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Mayo Clinic Jacksonville, Jacksonville, FL 32224, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11125143" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Age of Onset ; Aged ; Aged, 80 and over ; Alzheimer Disease/*blood/*genetics ; Amyloid beta-Peptides/*blood/genetics ; Chromosomes, Human, Pair 10/*genetics ; Female ; *Genetic Linkage ; Genetic Markers ; Genetic Predisposition to Disease ; Humans ; Lod Score ; Male ; Middle Aged ; Pedigree ; Peptide Fragments/*blood/genetics ; Phenotype ; *Quantitative Trait, Heritable
    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
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    Cholinergic enhancement and increased selectivity of perceptual processing during working memory (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-12-23
    Description: Using functional magnetic resonance imaging, we investigated the mechanism by which cholinergic enhancement improves working memory. We studied the effect of the cholinesterase inhibitor physostigmine on subcomponents of this complex function. Cholinergic enhancement increased the selectivity of neural responses in extrastriate cortices during visual working memory, particularly during encoding. It also increased the participation of ventral extrastriate cortex during memory maintenance and decreased the participation of anterior prefrontal cortex. These results indicate that cholinergic enhancement improves memory performance by augmenting the selectivity of perceptual processing during encoding, thereby simplifying processing demands during memory maintenance and reducing the need for prefrontal participation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Furey, M L -- Pietrini, P -- Haxby, J V -- New York, N.Y. -- Science. 2000 Dec 22;290(5500):2315-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Brain and Cognition, National Institute of Mental Health, National Institutes of Health, Bethesda, MD, USA. furey@nih.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11125148" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcholine/*physiology ; Brain Mapping ; Cerebral Cortex/drug effects/*physiology ; Cholinesterase Inhibitors/*pharmacology ; Cross-Over Studies ; Double-Blind Method ; Face ; Female ; Humans ; Male ; Memory, Short-Term/*drug effects/physiology ; Occipital Lobe/drug effects/physiology ; Pattern Recognition, Visual ; Physostigmine/*pharmacology ; Prefrontal Cortex/drug effects/*physiology ; Temporal Lobe/drug effects/physiology ; Visual Cortex/drug effects/physiology ; Visual Perception/drug effects
    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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    Extended life-span conferred by cotransporter gene mutations in Drosophila (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-12-16
    Description: Aging is genetically determined and environmentally modulated. In a study of longevity in the adult fruit fly, Drosophila melanogaster, we found that five independent P-element insertional mutations in a single gene resulted in a near doubling of the average adult life-span without a decline in fertility or physical activity. Sequence analysis revealed that the product of this gene, named Indy (for I'm not dead yet), is most closely related to a mammalian sodium dicarboxylate cotransporter-a membrane protein that transports Krebs cycle intermediates. Indy was most abundantly expressed in the fat body, midgut, and oenocytes: the principal sites of intermediary metabolism in the fly. Excision of the P element resulted in a reversion to normal life-span. These mutations may create a metabolic state that mimics caloric restriction, which has been shown to extend life-span.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rogina, B -- Reenan, R A -- Nilsen, S P -- Helfand, S L -- AG14532/AG/NIA NIH HHS/ -- AG16667/AG/NIA NIH HHS/ -- R37 AG016667/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2000 Dec 15;290(5499):2137-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics and Developmental Biology, School of Medicine, University of Connecticut Health Center, 263 Farmington Avenue, Farmington CT 06030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11118146" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/*genetics ; Amino Acid Sequence ; Animals ; Behavior, Animal ; Biological Transport ; Carrier Proteins/chemistry/*genetics/metabolism ; Crosses, Genetic ; DNA Transposable Elements ; *Dicarboxylic Acid Transporters ; Digestive System/metabolism ; *Drosophila Proteins ; Drosophila melanogaster/*genetics/metabolism/physiology ; Energy Intake ; Energy Metabolism ; Fat Body/metabolism ; Female ; Fertility ; Gene Expression ; *Genes, Insect ; Longevity/*genetics ; Male ; Membrane Proteins/chemistry/metabolism ; Molecular Sequence Data ; Mutagenesis, Insertional ; Mutagenesis, Site-Directed ; *Organic Anion Transporters, Sodium-Dependent ; Sense Organs/cytology/metabolism ; Sequence Homology, Amino Acid ; *Symporters
    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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    Turning blood into brain: cells bearing neuronal antigens generated in vivo from bone marrow (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-12-02
    Description: Bone marrow stem cells give rise to a variety of hematopoietic lineages and repopulate the blood throughout adult life. We show that, in a strain of mice incapable of developing cells of the myeloid and lymphoid lineages, transplanted adult bone marrow cells migrated into the brain and differentiated into cells that expressed neuron-specific antigens. These findings raise the possibility that bone marrow-derived cells may provide an alternative source of neurons in patients with neurodegenerative diseases or central nervous system injury.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mezey, E -- Chandross, K J -- Harta, G -- Maki, R A -- McKercher, S R -- AI30656/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2000 Dec 1;290(5497):1779-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Basic Neuroscience Program, Laboratory of Developmental Neurogenetics, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA. mezey@codon.nih.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11099419" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens/analysis ; Biomarkers/analysis ; Bone Marrow Cells/*cytology/physiology ; *Bone Marrow Transplantation ; Brain/*cytology ; Cell Differentiation ; Cell Movement ; Female ; Immunoenzyme Techniques ; Intermediate Filament Proteins/analysis ; Male ; Mice ; Mice, Knockout ; Microscopy, Confocal ; Nerve Tissue Proteins/analysis/immunology ; Nestin ; Neurons/chemistry/*cytology/immunology ; Phosphopyruvate Hydratase/analysis ; *Stem Cell Transplantation ; Stem Cells/chemistry/*cytology ; Y Chromosome
    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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    Requirement of the RNA editing deaminase ADAR1 gene for embryonic erythropoiesis (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-12-02
    Description: The members of the ADAR (adenosine deaminase acting on RNA) gene family are involved in site-selective RNA editing that changes adenosine residues of target substrate RNAs to inosine. Analysis of staged chimeric mouse embryos with a high contribution from embryonic stem cells with a functional null allele for ADAR1 revealed a heterozygous embryonic-lethal phenotype. Most ADAR1+/- chimeric embryos died before embryonic day 14 with defects in the hematopoietic system. Our results suggest the importance of regulated levels of ADAR1 expression, which is critical for embryonic erythropoiesis in the liver.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Q -- Khillan, J -- Gadue, P -- Nishikura, K -- New York, N.Y. -- Science. 2000 Dec 1;290(5497):1765-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wistar Institute, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11099415" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Deaminase/*genetics/metabolism ; Alleles ; Animals ; Chimera ; Embryonic and Fetal Development ; Erythroblasts/cytology ; *Erythropoiesis ; Female ; Hematopoietic Stem Cells/*cytology/enzymology ; Hepatocytes/cytology ; Immunoenzyme Techniques ; Liver/cytology/*embryology/enzymology ; Mice ; Mice, Inbred BALB C ; Mice, SCID ; Phenotype ; *RNA Editing ; RNA-Binding Proteins ; Stem Cells/cytology/enzymology ; Teratoma/genetics/pathology
    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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    Gamma oscillations and object processing in the infant brain (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-11-25
    Description: An enduring controversy in neuroscience concerns how the brain "binds" together separately coded stimulus features to form unitary representations of objects. Recent evidence has indicated a close link between this binding process and 40-hertz (gamma-band) oscillations generated by localized neural circuits. In a separate line of research, the ability of young infants to perceive objects as unitary and bounded has become a central focus for debates about the mechanisms of perceptual development. Here we demonstrate that binding-related 40-hertz oscillations are evident in the infant brain around 8 months of age, which is the same age at which behavioral and event-related potential evidence indicates the onset of perceptual binding of spatially separated static visual features.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Csibra, G -- Davis, G -- Spratling, M W -- Johnson, M H -- New York, N.Y. -- Science. 2000 Nov 24;290(5496):1582-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for Brain and Cognitive Development, School of Psychology, Birkbeck College, University of London, Malet Street, London WC1E 7HX, UK. g.csibra@bbk.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11090357" target="_blank"〉PubMed〈/a〉
    Keywords: *Electroencephalography ; Evoked Potentials, Visual ; Female ; *Form Perception ; Frontal Lobe/*physiology ; Humans ; Infant ; Male ; Occipital Lobe/physiology ; Parietal Lobe/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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  • 7
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    X-Chromosome inactivation in cloned mouse embryos (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-11-25
    Description: To study whether cloning resets the epigenetic differences between the two X chromosomes of a somatic female nucleus, we monitored X inactivation in cloned mouse embryos. Both X chromosomes were active during cleavage of cloned embryos, followed by random X inactivation in the embryo proper. In the trophectoderm (TE), X inactivation was nonrandom with the inactivated X of the somatic donor being chosen for inactivation. When female embryonic stem cells with two active X chromosomes were used as donors, random X inactivation was seen in the TE and embryo. These results demonstrate that epigenetic marks can be removed and reestablished on either X chromosome during cloning. Our results also suggest that the epigenetic marks imposed on the X chromosomes during gametogenesis, responsible for normal imprinted X inactivation in the TE, are functionally equivalent to the marks imposed on the chromosomes during somatic X inactivation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Eggan, K -- Akutsu, H -- Hochedlinger, K -- Rideout, W 3rd -- Yanagimachi, R -- Jaenisch, R -- 5-R35-CA44339/CA/NCI NIH HHS/ -- R01-CA84198/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2000 Nov 24;290(5496):1578-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research and Department of Biology, Massachusetts Institute of Technology, 9 Cambridge Center, Cambridge, MA 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11090356" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Cell Differentiation ; *Cloning, Organism ; *Dosage Compensation, Genetic ; Embryo, Mammalian/cytology/*metabolism ; Embryonic and Fetal Development ; Female ; Gene Silencing ; Genes, Reporter ; Genomic Imprinting ; Green Fluorescent Proteins ; Luminescent Proteins/genetics ; Male ; Mice ; Muridae ; Nuclear Transfer Techniques ; Oocytes ; Placenta/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Stem Cell Transplantation ; Stem Cells/metabolism ; Transgenes ; X Chromosome/*genetics/metabolism
    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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  • 8
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    Protection against cutaneous leishmaniasis resulting from bites of uninfected sand flies (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-11-18
    Description: Despite the fact that Leishmania are transmitted exclusively by sand flies, none of the experimental models of leishmaniasis have established infection via sand fly bites. Here we describe a reproducible murine model of Leishmania major infection transmitted by Phlebotomus papatasi. Prior exposure of mice to bites of uninfected sand flies conferred powerful protection against Leishmania major that was associated with a strong delayed-type hypersensitivity response and with interferon-gamma production at the site of parasite delivery. These results have important implications for the epidemiology of cutaneous leishmaniasis and suggest a vaccination strategy against this and possibly other vector-borne diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kamhawi, S -- Belkaid, Y -- Modi, G -- Rowton, E -- Sacks, D -- New York, N.Y. -- Science. 2000 Nov 17;290(5495):1351-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11082061" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Dermis/immunology/parasitology ; Disease Models, Animal ; Ear ; Epidermis/immunology/parasitology ; Female ; Humans ; Hypersensitivity, Delayed ; *Insect Bites and Stings ; *Insect Vectors/parasitology ; Interferon-gamma/biosynthesis ; Interleukins/biosynthesis ; *Leishmania major/physiology ; Leishmaniasis, Cutaneous/*immunology/parasitology/*transmission ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; *Phlebotomus/parasitology ; Saliva/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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  • 9
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    Early development of ocular dominance columns (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-11-18
    Description: The segregation of lateral geniculate nucleus (LGN) axons into ocular dominance columns is believed to involve a prolonged, activity-dependent sorting process. However, visualization of early postnatal ferret LGN axons by direct LGN tracer injections revealed segregated ocular dominance columns 〈7 days after innervation of layer 4. These early columns were unaffected by experimentally induced imbalances in retinal activity, implying that different mechanisms govern initial column formation and their modification during the subsequent critical period. Instead of activity-dependent plasticity, we propose that ocular dominance column formation relies on the targeting of distinct axonal populations to defined locales in cortical layer 4.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Crowley, J C -- Katz, L C -- EY07690/EY/NEI NIH HHS/ -- MH12359/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2000 Nov 17;290(5495):1321-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Neurobiology, Duke University Medical Center, Durham, NC 27710, USA. jcrowley@neuro.duke.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11082053" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Axons/*physiology ; Female ; Ferrets ; Geniculate Bodies/cytology/*physiology ; Male ; Neurons, Afferent/physiology ; Photic Stimulation ; Retina/physiology ; Sensory Deprivation ; Vision, Ocular ; Visual Cortex/cytology/*growth & development/physiology ; Visual Pathways/growth & development/*physiology ; *Visual Perception
    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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  • 10
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    Promiscuity and the primate immune system (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-11-10
    Description: The behavioral and ecological factors involved in immune system evolution remain poorly explored. We present a phylogenetic analysis of white blood cell counts in primates to test three hypotheses related to disease risk: increases in risk are expected with group size or population density, exposure to soil-borne pathogens, and mating promiscuity. White blood cell counts were significantly greater in species where females have more mating partners, indicating that the risk of sexually transmitted disease is likely to be a major factor leading to systematic differences in the primate immune system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nunn, C L -- Gittleman, J L -- Antonovics, J -- GM60766-01/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2000 Nov 10;290(5494):1168-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Gilmer Hall, University of Virginia, Charlottesville, VA 22904-4328, USA. charlie.nunn@virginia.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11073457" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Zoo ; Biological Evolution ; Body Weight ; Female ; Haplorhini/blood/*immunology ; Immune System/*physiology ; *Leukocyte Count ; Male ; Population Density ; Primate Diseases/epidemiology/immunology ; Risk Factors ; *Sexual Behavior, Animal ; Sexually Transmitted Diseases/epidemiology/immunology/veterinary ; Species Specificity
    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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