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  • Female  (16)
  • American Association for the Advancement of Science (AAAS)  (16)
  • 1995-1999  (16)
  • 1950-1954
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  • American Association for the Advancement of Science (AAAS)  (16)
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  • 1
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    Cloned transgenic calves produced from nonquiescent fetal fibroblasts (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-06-20
    Description: An efficient system for genetic modification and large-scale cloning of cattle is of importance for agriculture, biotechnology, and human medicine. Here, actively dividing fetal fibroblasts were genetically modified with a marker gene, a clonal line was selected, and the cells were fused to enucleated mature oocytes. Out of 28 embryos transferred to 11 recipient cows, three healthy, identical, transgenic calves were generated. Furthermore, the life-span of near senescent fibroblasts could be extended by nuclear transfer, as indicated by population doublings in fibroblast lines derived from a 40-day-old fetal clone. With the ability to extend the life-span of these primary cultured cells, this system would be useful for inducing complex genetic modifications in cattle.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cibelli, J B -- Stice, S L -- Golueke, P J -- Kane, J J -- Jerry, J -- Blackwell, C -- Ponce de Leon, F A -- Robl, J M -- New York, N.Y. -- Science. 1998 May 22;280(5367):1256-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Veterinary and Animal Sciences, University of Massachusetts, Amherst, MA 01003, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9596577" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Animals, Genetically Modified ; Blastocyst ; Cattle/embryology/*genetics ; Cell Aging ; Cell Division ; Cell Nucleus/genetics ; Cells, Cultured ; Clone Cells ; *Cloning, Organism ; Embryo Transfer ; Female ; Fetus/cytology ; Fibroblasts/*cytology ; G1 Phase ; Male ; Nuclear Transfer Techniques ; Oocytes/cytology ; Transfection ; Transgenes
    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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    Separate neural bases of two fundamental memory processes in the human medial temporal lobe (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-04-11
    Description: The participation of medial temporal-lobe structures in memory performance was examined by functional magnetic resonance imaging of local blood oxygenation level-dependent signals. Signals were measured during encoding into memory complex scenes or line drawings and during retrieval from memory of previously studied line drawings or words. Encoding tasks yielded increased signals for unfamiliar information in a posterior medial-temporal region that were focused in the parahippocampal cortex. Retrieval tasks yielded increased signals for successfully remembered information in an anterior medial-temporal region that were focused in the subiculum. These results indicate that separate components of the human medial temporal-lobe memory system are active during distinct memory processes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gabrieli, J D -- Brewer, J B -- Desmond, J E -- Glover, G H -- New York, N.Y. -- Science. 1997 Apr 11;276(5310):264-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychology and Neuroscience Program, Stanford University, Stanford, CA 94305, USA. gabrieli@psych.stanford.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9092477" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Brain Mapping ; Female ; Hippocampus/physiology ; Humans ; Magnetic Resonance Imaging ; Male ; Memory/*physiology ; Mental Recall/*physiology ; Temporal Lobe/*physiology
    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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    Preattentive filling-in of visual surfaces in parietal extinction (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-01-31
    Description: Unilateral brain damage frequently produces "extinction," in which patients can detect brief single visual stimuli on either side but are unaware of a contralesional stimulus if presented concurrently with an ipsilesional stimulus. Explanations for extinction have invoked deficits in initial processes that operate before the focusing of visual attention or in later attentive stages of vision. Preattentive vision was preserved in a parietally damaged patient, whose extinction was less severe when bilateral stimuli formed a common surface, even if this required visual filling-in to yield illusory Kanizsa figures or completion of partially occluded figures. These results show that parietal extinction arises only after substantial processing has generated visual surfaces, supporting recent claims that visual attention is surface-based.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mattingley, J B -- Davis, G -- Driver, J -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 1997 Jan 31;275(5300):671-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Experimental Psychology, University of Cambridge, Downing Street, Cambridge CB2 3EB, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9005854" target="_blank"〉PubMed〈/a〉
    Keywords: Aged ; *Attention ; Cerebrovascular Disorders/*physiopathology ; *Extinction, Psychological ; Female ; *Form Perception ; Humans ; Parietal Lobe/*physiopathology ; Psychomotor Performance ; Visual Pathways
    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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    Making memories: brain activity that predicts how well visual experience will be remembered (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-08-26
    Description: Experiences are remembered or forgotten, but the neural determinants for the mnemonic fate of experience are unknown. Event-related functional magnetic resonance imaging was used to identify specific brain activations that differentiated between visual experiences that were later remembered well, remembered less well, or forgotten. During scanning of medial temporal lobe and frontal lobe regions, subjects viewed complex, color photographs. Subjects later received a test of memory for the photographs. The magnitudes of focal activations in right prefrontal cortex and in bilateral parahippocampal cortex predicted which photographs were later remembered well, remembered less well, or forgotten.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brewer, J B -- Zhao, Z -- Desmond, J E -- Glover, G H -- Gabrieli, J D -- New York, N.Y. -- Science. 1998 Aug 21;281(5380):1185-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neuroscience Program and School of Medicine, Stanford University, Stanford, CA 94305, USA. brewer@psych.stanford.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9712581" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Brain/physiology ; Brain Mapping ; Female ; Humans ; Magnetic Resonance Imaging ; Male ; Memory/*physiology ; Memory, Short-Term ; Prefrontal Cortex/*physiology ; Temporal Lobe/*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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  • 5
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    Genetic decreases in atrial natriuretic peptide and salt-sensitive hypertension (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-02-03
    Description: To determine if defects in the atrial natriuretic peptide (ANP) system can cause hypertension, mice were generated with a disruption of the proANP gene. Homozygous mutants had no circulating or atrial ANP, and their blood pressures were elevated by 8 to 23 millimeters of mercury when they were fed standard (0.5 percent sodium chloride) and intermediate (2 percent sodium chloride) salt diets. On standard salt diets, heterozygotes had normal amounts of circulating ANP and normal blood pressures. However, on high (8 percent sodium chloride) salt diets they were hypertensive, with blood pressures elevated by 27 millimeters of mercury. These results demonstrate that genetically reduced production of ANP can lead to salt-sensitive hypertension.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉John, S W -- Krege, J H -- Oliver, P M -- Hagaman, J R -- Hodgin, J B -- Pang, S C -- Flynn, T G -- Smithies, O -- GM20069/GM/NIGMS NIH HHS/ -- HL49277/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1995 Feb 3;267(5198):679-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, University of North Carolina, Chapel Hill 27599.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7839143" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Atrial Natriuretic Factor/analysis/blood/*deficiency/*genetics ; *Blood Pressure ; Crosses, Genetic ; Female ; Gene Targeting ; Genotype ; Heart Atria/chemistry/ultrastructure ; Heterozygote ; Homozygote ; Hypertension/genetics/pathology/*physiopathology ; Male ; Mice ; Mice, Inbred C57BL ; Protein Precursors/*genetics ; Sodium, Dietary/*administration & dosage
    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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    Skeletal repair by in situ formation of the mineral phase of bone (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-03-24
    Description: A process has been developed for the in situ formation of the mineral phase of bone. Inorganic calcium and phosphate sources are combined to form a paste that is surgically implanted by injection. Under physiological conditions, the material hardens in minutes concurrent with the formation of dahllite. After 12 hours, dahllite formation was nearly complete, and an ultimate compressive strength of 55 megapascals was achieved. The composition and crystal morphology of the dahllite formed are similar to those of bone. Animal studies provide evidence that the material is remodeled in vivo. A novel approach to skeletal repair is being tested in human trials for various applications; in one of the trials the new biomaterial is being percutaneously placed into acute fractures. After hardening, it serves as internal fixation to maintain proper alignment while healing occurs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Constantz, B R -- Ison, I C -- Fulmer, M T -- Poser, R D -- Smith, S T -- VanWagoner, M -- Ross, J -- Goldstein, S A -- Jupiter, J B -- Rosenthal, D I -- New York, N.Y. -- Science. 1995 Mar 24;267(5205):1796-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Norian Corporation, Cupertino, CA 95014.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7892603" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apatites/*chemistry ; Bone Substitutes/*chemistry ; Calcium Carbonate/*chemistry ; Calcium Phosphates/*chemistry ; Crystallography, X-Ray ; Dogs ; Female ; Fractures, Bone/therapy ; Humans ; Microscopy, Electron ; Middle Aged ; Models, Chemical ; Osseointegration ; Rabbits ; Spectroscopy, Fourier Transform Infrared
    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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    Dosage compensation proteins targeted to X chromosomes by a determinant of hermaphrodite fate (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-06-12
    Description: In many organisms, master control genes coordinately regulate sex-specific aspects of development. SDC-2 was shown to induce hermaphrodite sexual differentiation and activate X chromosome dosage compensation in Caenorhabditis elegans. To control these distinct processes, SDC-2 acts as a strong gene-specific repressor and a weaker chromosome-wide repressor. To initiate hermaphrodite development, SDC-2 associates with the promoter of the male sex-determining gene her-1 to repress its transcription. To activate dosage compensation, SDC-2 triggers assembly of a specialized protein complex exclusively on hermaphrodite X chromosomes to reduce gene expression by half. SDC-2 can localize to X chromosomes without other components of the dosage compensation complex, suggesting that SDC-2 targets dosage compensation machinery to X chromosomes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dawes, H E -- Berlin, D S -- Lapidus, D M -- Nusbaum, C -- Davis, T L -- Meyer, B J -- GM30702/GM/NIGMS NIH HHS/ -- T32 GM07127/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1999 Jun 11;284(5421):1800-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720-3204, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10364546" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caenorhabditis elegans/embryology/*genetics/physiology ; *Caenorhabditis elegans Proteins ; *DNA-Binding Proteins ; Disorders of Sex Development ; *Dosage Compensation, Genetic ; Female ; Gene Expression Regulation, Developmental ; Genes, Helminth ; Helminth Proteins/genetics/*physiology ; Male ; Molecular Sequence Data ; Mutation ; Promoter Regions, Genetic ; Repressor Proteins/genetics/*physiology ; *Sex Determination Processes ; 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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    Postnatal sex reversal of the ovaries in mice lacking estrogen receptors alpha and beta (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-12-22
    Description: Mice lacking estrogen receptors alpha and beta were generated to clarify the roles of each receptor in the physiology of estrogen target tissues. Both sexes of alphabeta estrogen receptor knockout (alphabetaERKO) mutants exhibit normal reproductive tract development but are infertile. Ovaries of adult alphabetaERKO females exhibit follicle transdifferentiation to structures resembling seminiferous tubules of the testis, including Sertoli-like cells and expression of Mullerian inhibiting substance, sulfated glycoprotein-2, and Sox9. Therefore, loss of both receptors leads to an ovarian phenotype that is distinct from that of the individual ERKO mutants, which indicates that both receptors are required for the maintenance of germ and somatic cells in the postnatal ovary.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Couse, J F -- Hewitt, S C -- Bunch, D O -- Sar, M -- Walker, V R -- Davis, B J -- Korach, K S -- New York, N.Y. -- Science. 1999 Dec 17;286(5448):2328-31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Receptor Biology Section, Laboratory of Reproductive and Developmental Toxicology, Laboratory of Experimental Pathology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10600740" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anti-Mullerian Hormone ; Cell Differentiation ; Clusterin ; *Disorders of Sex Development ; Estradiol/physiology ; Estrogen Receptor alpha ; Estrogen Receptor beta ; Female ; Gene Targeting ; Glycoproteins/analysis ; Growth Inhibitors/analysis ; High Mobility Group Proteins/analysis ; Luteinizing Hormone/blood ; Male ; Mice ; Mice, Knockout ; *Molecular Chaperones ; Ovary/*anatomy & histology/cytology/growth & development/*physiology ; Receptors, Estrogen/genetics/*physiology ; SOX9 Transcription Factor ; Seminiferous Tubules/anatomy & histology/cytology ; Sertoli Cells/cytology ; Signal Transduction ; Testicular Hormones/analysis ; Testis/anatomy & histology/cytology/growth & development/physiology ; Transcription Factors/analysis
    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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    Congenital heart disease caused by mutations in the transcription factor NKX2-5 (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-07-04
    Description: Mutations in the gene encoding the homeobox transcription factor NKX2-5 were found to cause nonsyndromic, human congenital heart disease. A dominant disease locus associated with cardiac malformations and atrioventricular conduction abnormalities was mapped to chromosome 5q35, where NKX2-5, a Drosophila tinman homolog, is located. Three different NKX2-5 mutations were identified. Two are predicted to impair binding of NKX2-5 to target DNA, resulting in haploinsufficiency, and a third potentially augments target-DNA binding. These data indicate that NKX2-5 is important for regulation of septation during cardiac morphogenesis and for maturation and maintenance of atrioventricular node function throughout life.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schott, J J -- Benson, D W -- Basson, C T -- Pease, W -- Silberbach, G M -- Moak, J P -- Maron, B J -- Seidman, C E -- Seidman, J G -- New York, N.Y. -- Science. 1998 Jul 3;281(5373):108-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics and Howard Hughes Medical Institute, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9651244" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Atrioventricular Node/physiopathology ; Chromosome Mapping ; Chromosomes, Human, Pair 5 ; Codon ; Female ; Genes, Dominant ; Genetic Linkage ; Heart Block/*genetics/physiopathology ; Heart Septal Defects, Atrial/*genetics/physiopathology ; Homeodomain Proteins/*genetics/metabolism ; Humans ; Male ; Mice ; Molecular Sequence Data ; Mutation ; Pedigree ; Protein Biosynthesis ; Transcription Factors/*genetics/metabolism ; *Xenopus Proteins
    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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    A p53-dependent mouse spindle checkpoint (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-03-03
    Description: Cell cycle checkpoints enhance genetic fidelity by causing arrest at specific stages of the cell cycle when previous events have not been completed. The tumor suppressor p53 has been implicated in a G1 checkpoint. To investigate whether p53 also participates in a mitotic checkpoint, cultured fibroblasts from p53-deficient mouse embryos were exposed to spindle inhibitors. The fibroblasts underwent multiple rounds of DNA synthesis without completing chromosome segregation, thus forming tetraploid and octaploid cells. Deficiency of p53 was also associated with the development of tetraploidy in vivo. These results suggest that murine p53 is a component of a spindle checkpoint that ensures the maintenance of diploidy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cross, S M -- Sanchez, C A -- Morgan, C A -- Schimke, M K -- Ramel, S -- Idzerda, R L -- Raskind, W H -- Reid, B J -- R01CA55814/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1995 Mar 3;267(5202):1353-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of Washington, Seattle 98195.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7871434" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Cycle ; Cells, Cultured ; DNA/biosynthesis ; Demecolcine/pharmacology ; Diploidy ; Female ; Genes, p53 ; Male ; Mice ; *Mitosis ; Nocodazole/pharmacology ; Ploidies ; Spindle Apparatus/*physiology ; Tumor Suppressor Protein p53/*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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