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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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    Bile acids: natural ligands for an orphan nuclear receptor (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-05-21
    Description: Bile acids regulate the transcription of genes that control cholesterol homeostasis through molecular mechanisms that are poorly understood. Physiological concentrations of free and conjugated chenodeoxycholic acid, lithocholic acid, and deoxycholic acid activated the farnesoid X receptor (FXR; NR1H4), an orphan nuclear receptor. As ligands, these bile acids and their conjugates modulated interaction of FXR with a peptide derived from steroid receptor coactivator 1. These results provide evidence for a nuclear bile acid signaling pathway that may regulate cholesterol homeostasis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Parks, D J -- Blanchard, S G -- Bledsoe, R K -- Chandra, G -- Consler, T G -- Kliewer, S A -- Stimmel, J B -- Willson, T M -- Zavacki, A M -- Moore, D D -- Lehmann, J M -- F32 DK09793/DK/NIDDK NIH HHS/ -- R01 DK53366/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1999 May 21;284(5418):1365-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biochemistry, Glaxo Wellcome Research and Development, Research Triangle Park NC, 27709, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10334993" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bile Acids and Salts/chemistry/*metabolism/pharmacology ; Carrier Proteins/metabolism ; Cell Line ; Chenodeoxycholic Acid/*metabolism/pharmacology ; Cholesterol/metabolism ; DNA-Binding Proteins/chemistry/genetics/*metabolism ; Deoxycholic Acid/metabolism/pharmacology ; Histone Acetyltransferases ; Homeostasis ; Humans ; Ligands ; Lithocholic Acid/metabolism/pharmacology ; Mice ; Nuclear Receptor Coactivator 1 ; *Organic Anion Transporters, Sodium-Dependent ; Protein Conformation ; Receptors, Cytoplasmic and Nuclear/chemistry/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Structure-Activity Relationship ; *Symporters ; Transcription Factors/chemistry/genetics/*metabolism ; Transfection
    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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    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
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  • 4
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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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  • 5
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    Structural convergence in the active sites of a family of catalytic antibodies (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-02-21
    Description: The x-ray structures of three esterase-like catalytic antibodies identified by screening for catalytic activity the entire hybridoma repertoire, elicited in response to a phosphonate transition state analog (TSA) hapten, were analyzed. The high resolution structures account for catalysis by transition state stabilization, and in all three antibodies a tyrosine residue participates in the oxyanion hole. Despite significant conformational differences in their combining sites, the three antibodies, which are the most efficient among those elicited, achieve catalysis in essentially the same mode, suggesting that evolution for binding to a single TSA followed by screening for catalysis lead to antibodies with structural convergence.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Charbonnier, J B -- Golinelli-Pimpaneau, B -- Gigant, B -- Tawfik, D S -- Chap, R -- Schindler, D G -- Kim, S H -- Green, B S -- Eshhar, Z -- Knossow, M -- New York, N.Y. -- Science. 1997 Feb 21;275(5303):1140-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire d'Enzymologie et de Biochimie Structurales, CNRS, 91198 Gif sur Yvette Cedex, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9027317" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Catalytic/*chemistry/metabolism ; Binding Sites ; Catalysis ; Crystallography, X-Ray ; Enzyme-Linked Immunosorbent Assay ; *Evolution, Molecular ; Haptens/chemistry/metabolism ; Hydrogen Bonding ; Immunoglobulin Fab Fragments/chemistry/metabolism ; Mice ; Mice, Inbred BALB C ; Models, Molecular ; Organophosphonates/chemistry/metabolism ; *Protein Conformation ; Tyrosine/chemistry
    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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    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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  • 7
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    Role of mutant CFTR in hypersusceptibility of cystic fibrosis patients to lung infections (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-01-05
    Description: Cystic fibrosis (CF) patients are hypersusceptible to chronic Pseudomonas aeruginosa lung infections. Cultured human airway epithelial cells expressing the delta F508 allele of the cystic fibrosis transmembrane conductance regulator (CFTR) were defective in uptake of P. aeruginosa compared with cells expressing the wild-type allele. Pseudomonas aeruginosa lipopolysaccharide (LPS)-core oligosaccharide was identified as the bacterial ligand for epithelial cell ingestion; exogenous oligosaccharide inhibited bacterial ingestion in a neonatal mouse model, resulting in increased amounts of bacteria in the lungs. CFTR may contribute to a host-defense mechanism that is important for clearance of P. aeruginosa from the respiratory tract.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3677515/" 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/PMC3677515/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pier, G B -- Grout, M -- Zaidi, T S -- Olsen, J C -- Johnson, L G -- Yankaskas, J R -- Goldberg, J B -- AI22806/AI/NIAID NIH HHS/ -- AI35674/AI/NIAID NIH HHS/ -- HL42384/HL/NHLBI NIH HHS/ -- R01 HL058398/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1996 Jan 5;271(5245):64-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Channing Laboratory, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115-5899, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8539601" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Cell Line, Transformed ; Cystic Fibrosis/*complications/genetics/microbiology ; Cystic Fibrosis Transmembrane Conductance Regulator/genetics/*physiology ; Disease Susceptibility ; Epithelium/microbiology ; Humans ; Lipopolysaccharides/pharmacology ; Lung/microbiology ; Mice ; Mice, Inbred BALB C ; Pseudomonas Infections/*etiology/microbiology ; Pseudomonas aeruginosa/*physiology ; Respiratory System/*microbiology ; Respiratory Tract Infections/*etiology/microbiology
    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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    Inhibition of adipogenesis through MAP kinase-mediated phosphorylation of PPARgamma (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-12-20
    Description: Adipocyte differentiation is an important component of obesity and other metabolic diseases. This process is strongly inhibited by many mitogens and oncogenes. Several growth factors that inhibit fat cell differentiation caused mitogen-activated protein (MAP) kinase-mediated phosphorylation of the dominant adipogenic transcription factor peroxisome proliferator-activated receptor gamma (PPARgamma) and reduction of its transcriptional activity. Expression of PPARgamma with a nonphosphorylatable mutation at this site (serine-112) yielded cells with increased sensitivity to ligand-induced adipogenesis and resistance to inhibition of differentiation by mitogens. These results indicate that covalent modification of PPARgamma by serum and growth factors is a major regulator of the balance between cell growth and differentiation in the adipose cell lineage.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hu, E -- Kim, J B -- Sarraf, P -- Spiegelman, B M -- R37DK31405/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1996 Dec 20;274(5295):2100-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Dana-Farber Cancer Institute and Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8953045" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Adipocytes/*cytology/metabolism ; Animals ; Blood ; Calcium-Calmodulin-Dependent Protein Kinases/antagonists & inhibitors/*metabolism ; Cell Differentiation ; Cell Line ; Enzyme Inhibitors/pharmacology ; Epidermal Growth Factor/pharmacology ; Flavonoids/pharmacology ; Insulin/pharmacology ; Ligands ; Mice ; Mitogens/pharmacology ; Mutation ; Phosphorylation ; Rats ; Receptors, Cytoplasmic and Nuclear/chemistry/genetics/*metabolism ; Tetradecanoylphorbol Acetate/pharmacology ; Transcription Factors/chemistry/genetics/*metabolism ; Transcription, Genetic/drug effects ; Transfection
    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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    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
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
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    Prevention of atherosclerosis in apolipoprotein E-deficient mice by bone marrow transplantation (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-02-17
    Description: Apolipoprotein E (apoE) deficiency causes severe hyperlipidemia and atherosclerosis in humans and in gene-targeted mice. Although the majority of apoE in plasma is of hepatic origin, apoE is synthesized by a variety of cell types, including macrophages. Because macrophages derive from hematopoietic cells, bone marrow transplantation was used to examine the potential of apoE synthesized by bone marrow-derived cells to correct the hyperlipidemia and atherosclerosis caused by apoE deficiency. After transplantation of bone marrow from mice with the normal apoE gene into apoE-deficient mice, apoE was detected in serum and promoted clearance of lipoproteins and normalization of serum cholesterol levels. ApoE-deficient mice given transplants of normal bone marrow showed virtually complete protection from diet-induced atherosclerosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Linton, M F -- Atkinson, J B -- Fazio, S -- DK-26657-15/DK/NIDDK NIH HHS/ -- HL-02925/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1995 Feb 17;267(5200):1034-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN 37232-2250.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7863332" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aortic Diseases/prevention & control ; Apolipoproteins E/blood/*deficiency/genetics ; Arteriosclerosis/*prevention & control ; *Bone Marrow Transplantation ; Cholesterol/*blood ; Coronary Artery Disease/prevention & control ; Lipoproteins/*blood ; Lipoproteins, IDL ; Lipoproteins, LDL/blood ; Lipoproteins, VLDL/blood ; Macrophages/metabolism ; Mice ; Mice, Inbred C57BL
    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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