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  • Articles  (334)
  • American Association for the Advancement of Science (AAAS)  (308)
  • Oxford University Press  (21)
  • Wiley  (5)
  • American Chemical Society
  • American Institute of Physics (AIP)
  • 2020-2024
  • 1995-1999  (334)
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  • 1997  (334)
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  • Articles  (334)
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  • 2020-2024
  • 1995-1999  (334)
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  • 1
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    Positional cloning of the gene for multiple endocrine neoplasia-type 1 (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-04-18
    Description: Multiple endocrine neoplasia-type 1 (MEN1) is an autosomal dominant familial cancer syndrome characterized by tumors in parathyroids, enteropancreatic endocrine tissues, and the anterior pituitary. DNA sequencing from a previously identified minimal interval on chromosome 11q13 identified several candidate genes, one of which contained 12 different frameshift, nonsense, missense, and in-frame deletion mutations in 14 probands from 15 families. The MEN1 gene contains 10 exons and encodes a ubiquitously expressed 2.8-kilobase transcript. The predicted 610-amino acid protein product, termed menin, exhibits no apparent similarities to any previously known proteins. The identification of MEN1 will enable improved understanding of the mechanism of endocrine tumorigenesis and should facilitate early diagnosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chandrasekharappa, S C -- Guru, S C -- Manickam, P -- Olufemi, S E -- Collins, F S -- Emmert-Buck, M R -- Debelenko, L V -- Zhuang, Z -- Lubensky, I A -- Liotta, L A -- Crabtree, J S -- Wang, Y -- Roe, B A -- Weisemann, J -- Boguski, M S -- Agarwal, S K -- Kester, M B -- Kim, Y S -- Heppner, C -- Dong, Q -- Spiegel, A M -- Burns, A L -- Marx, S J -- New York, N.Y. -- Science. 1997 Apr 18;276(5311):404-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Gene Transfer, National Human Genome Research Institute (NHGRI), National Institutes of Health (NIH), Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9103196" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Chromosome Mapping ; Chromosomes, Human, Pair 11 ; *Cloning, Molecular ; DNA, Complementary/genetics ; Exons ; Frameshift Mutation ; *Genes, Tumor Suppressor ; Humans ; Molecular Sequence Data ; Multiple Endocrine Neoplasia Type 1/*genetics ; Mutation ; Neoplasm Proteins/chemistry/*genetics ; *Proto-Oncogene 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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  • 2
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    Prevention of mucosal Escherichia coli infection by FimH-adhesin-based systemic vaccination (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-04-25
    Description: Virtually all uropathogenic strains of Escherichia coli, the primary cause of cystitis, assemble adhesive surface organelles called type 1 pili that contain the FimH adhesin. Sera from animals vaccinated with candidate FimH vaccines inhibited uropathogenic E. coli from binding to human bladder cells in vitro. Immunization with FimH reduced in vivo colonization of the bladder mucosa by more than 99 percent in a murine cystitis model, and immunoglobulin G to FimH was detected in urinary samples from protected mice. Furthermore, passive systemic administration of immune sera to FimH also resulted in reduced bladder colonization by uropathogenic E. coli. This approach may represent a means of preventing recurrent and acute infections of the urogenital mucosa.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Langermann, S -- Palaszynski, S -- Barnhart, M -- Auguste, G -- Pinkner, J S -- Burlein, J -- Barren, P -- Koenig, S -- Leath, S -- Jones, C H -- Hultgren, S J -- R01DK51406/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1997 Apr 25;276(5312):607-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉MedImmune, Inc., Gaithersburg, MD 20878, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9110982" target="_blank"〉PubMed〈/a〉
    Keywords: Adhesins, Bacterial/*immunology/metabolism ; *Adhesins, Escherichia coli ; Animals ; Antibodies, Bacterial/analysis/immunology ; Bacterial Adhesion ; *Bacterial Vaccines/administration & dosage/immunology ; Child ; Cystitis/immunology/*prevention & control ; Epithelium/microbiology ; Escherichia coli/immunology/metabolism/pathogenicity ; Escherichia coli Infections/immunology/*prevention & control ; Female ; *Fimbriae Proteins ; Fimbriae, Bacterial/immunology ; Humans ; Immunity, Mucosal ; Mice ; Mice, Inbred C3H ; Neutrophils/immunology ; Rabbits ; Urinary Bladder/microbiology ; Vaccination ; *Vaccines, Synthetic/administration & dosage/immunology
    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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  • 3
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    Identification of the tuberous sclerosis gene TSC1 on chromosome 9q34 (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-08-08
    Description: Tuberous sclerosis complex (TSC) is an autosomal dominant disorder characterized by the widespread development of distinctive tumors termed hamartomas. TSC-determining loci have been mapped to chromosomes 9q34 (TSC1) and 16p13 (TSC2). The TSC1 gene was identified from a 900-kilobase region containing at least 30 genes. The 8.6-kilobase TSC1 transcript is widely expressed and encodes a protein of 130 kilodaltons (hamartin) that has homology to a putative yeast protein of unknown function. Thirty-two distinct mutations were identified in TSC1, 30 of which were truncating, and a single mutation (2105delAAAG) was seen in six apparently unrelated patients. In one of these six, a somatic mutation in the wild-type allele was found in a TSC-associated renal carcinoma, which suggests that hamartin acts as a tumor suppressor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉van Slegtenhorst, M -- de Hoogt, R -- Hermans, C -- Nellist, M -- Janssen, B -- Verhoef, S -- Lindhout, D -- van den Ouweland, A -- Halley, D -- Young, J -- Burley, M -- Jeremiah, S -- Woodward, K -- Nahmias, J -- Fox, M -- Ekong, R -- Osborne, J -- Wolfe, J -- Povey, S -- Snell, R G -- Cheadle, J P -- Jones, A C -- Tachataki, M -- Ravine, D -- Sampson, J R -- Reeve, M P -- Richardson, P -- Wilmer, F -- Munro, C -- Hawkins, T L -- Sepp, T -- Ali, J B -- Ward, S -- Green, A J -- Yates, J R -- Kwiatkowska, J -- Henske, E P -- Short, M P -- Haines, J H -- Jozwiak, S -- Kwiatkowski, D J -- New York, N.Y. -- Science. 1997 Aug 8;277(5327):805-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Clinical Genetics, Erasmus University and University Hospital, Rotterdam, Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9242607" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Chromosome Mapping ; Chromosomes, Human, Pair 9/*genetics ; Exons ; *Genes, Tumor Suppressor ; Humans ; Microsatellite Repeats ; Molecular Sequence Data ; Molecular Weight ; Mutation ; Polymerase Chain Reaction ; Proteins/chemistry/*genetics/physiology ; Repressor Proteins/genetics/physiology ; Tuberous Sclerosis/*genetics ; Tumor Suppressor 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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  • 4
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    Mediation of neuronal apoptosis by enhancement of outward potassium current (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-10-06
    Description: Apoptosis of mouse neocortical neurons induced by serum deprivation or by staurosporine was associated with an early enhancement of delayed rectifier (IK) current and loss of total intracellular K+. This IK augmentation was not seen in neurons undergoing excitotoxic necrosis or in older neurons resistant to staurosporine-induced apoptosis. Attenuating outward K+ current with tetraethylammonium or elevated extracellular K+, but not blockers of Ca2+, Cl-, or other K+ channels, reduced apoptosis, even if associated increases in intracellular Ca2+ concentration were prevented. Furthermore, exposure to the K+ ionophore valinomycin or the K+-channel opener cromakalim induced apoptosis. Enhanced K+ efflux may mediate certain forms of neuronal apoptosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yu, S P -- Yeh, C H -- Sensi, S L -- Gwag, B J -- Canzoniero, L M -- Farhangrazi, Z S -- Ying, H S -- Tian, M -- Dugan, L L -- Choi, D W -- 30337/PHS HHS/ -- New York, N.Y. -- Science. 1997 Oct 3;278(5335):114-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for the Study of Nervous System Injury and Department of Neurology, Washington University School of Medicine, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9311914" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Chloromethyl Ketones/pharmacology ; Animals ; *Apoptosis/drug effects ; Benzopyrans/pharmacology ; Calcium/metabolism ; Cerebral Cortex/cytology ; Cromakalim ; Cycloheximide/pharmacology ; Cysteine Proteinase Inhibitors/pharmacology ; Gadolinium/pharmacology ; Mice ; N-Methylaspartate/pharmacology ; Neurons/*cytology/metabolism ; Neuroprotective Agents/pharmacology ; Nifedipine/pharmacology ; Patch-Clamp Techniques ; Potassium/*metabolism ; Potassium Channels/drug effects/*metabolism ; Pyrroles/pharmacology ; Staurosporine/pharmacology ; Tetraethylammonium ; Tetraethylammonium Compounds/pharmacology ; Veratridine/pharmacology
    Print ISSN: 0036-8075
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  • 5
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    Structural requirements for glycolipid antigen recognition by CD1b-restricted T cells (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-10-10
    Description: The human CD1b protein presents lipid antigens to T cells, but the molecular mechanism is unknown. Identification of mycobacterial glucose monomycolate (GMM) as a CD1b-presented glycolipid allowed determination of the structural requirements for its recognition by T cells. Presentation of GMM to CD1b-restricted T cells was not affected by substantial variations in its lipid tails, but was extremely sensitive to chemical alterations in its carbohydrate or other polar substituents. These findings support the view that the recently demonstrated hydrophobic CD1 groove binds the acyl chains of lipid antigens relatively nonspecifically, thereby positioning the hydrophilic components for highly specific interactions with T cell antigen receptors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moody, D B -- Reinhold, B B -- Guy, M R -- Beckman, E M -- Frederique, D E -- Furlong, S T -- Ye, S -- Reinhold, V N -- Sieling, P A -- Modlin, R L -- Besra, G S -- Porcelli, S A -- AR01988/AR/NIAMS NIH HHS/ -- GM54045/GM/NIGMS NIH HHS/ -- RR10888/RR/NCRR NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1997 Oct 10;278(5336):283-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Lymphocyte Biology Section, Division of Rheumatology, Immunology, and Allergy, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9323206" target="_blank"〉PubMed〈/a〉
    Keywords: *Antigen Presentation ; Antigens, Bacterial/immunology ; Antigens, CD1/chemistry/*immunology/metabolism ; Epitopes/immunology ; Glycolipids/chemistry/*immunology/metabolism ; Glycosylation ; Humans ; Ligands ; Mass Spectrometry ; Mycobacterium/immunology ; Mycolic Acids/chemistry/immunology ; Receptors, Antigen, T-Cell/immunology/metabolism ; T-Lymphocyte Subsets/*immunology
    Print ISSN: 0036-8075
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  • 6
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    Structure of Bcl-xL-Bak peptide complex: recognition between regulators of apoptosis (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-02-14
    Description: Heterodimerization between members of the Bcl-2 family of proteins is a key event in the regulation of programmed cell death. The molecular basis for heterodimer formation was investigated by determination of the solution structure of a complex between the survival protein Bcl-xL and the death-promoting region of the Bcl-2-related protein Bak. The structure and binding affinities of mutant Bak peptides indicate that the Bak peptide adopts an amphipathic alpha helix that interacts with Bcl-xL through hydrophobic and electrostatic interactions. Mutations in full-length Bak that disrupt either type of interaction inhibit the ability of Bak to heterodimerize with Bcl-xL.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sattler, M -- Liang, H -- Nettesheim, D -- Meadows, R P -- Harlan, J E -- Eberstadt, M -- Yoon, H S -- Shuker, S B -- Chang, B S -- Minn, A J -- Thompson, C B -- Fesik, S W -- P01 A135294/PHS HHS/ -- R37 CA48023/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1997 Feb 14;275(5302):983-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Pharmaceutical Discovery Division, Abbott Laboratories, Abbott Park, IL 60064, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9020082" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Apoptosis ; Crystallography, X-Ray ; Dimerization ; Magnetic Resonance Spectroscopy ; Membrane Proteins/*chemistry/genetics/metabolism ; Models, Molecular ; Molecular Sequence Data ; *Protein Conformation ; Protein Structure, Secondary ; Proto-Oncogene Proteins/*chemistry/metabolism ; *Proto-Oncogene Proteins c-bcl-2 ; Sequence Deletion ; bcl-2 Homologous Antagonist-Killer Protein ; bcl-X Protein
    Print ISSN: 0036-8075
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  • 7
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    Angiopoietin-2, a natural antagonist for Tie2 that disrupts in vivo angiogenesis (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-07-04
    Description: Angiogenesis is thought to depend on a precise balance of positive and negative regulation. Angiopoietin-1 (Ang1) is an angiogenic factor that signals through the endothelial cell-specific Tie2 receptor tyrosine kinase. Like vascular endothelial growth factor, Ang1 is essential for normal vascular development in the mouse. An Ang1 relative, termed angiopoietin-2 (Ang2), was identified by homology screening and shown to be a naturally occurring antagonist for Ang1 and Tie2. Transgenic overexpression of Ang2 disrupts blood vessel formation in the mouse embryo. In adult mice and humans, Ang2 is expressed only at sites of vascular remodeling. Natural antagonists for vertebrate receptor tyrosine kinases are atypical; thus, the discovery of a negative regulator acting on Tie2 emphasizes the need for exquisite regulation of this angiogenic receptor system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Maisonpierre, P C -- Suri, C -- Jones, P F -- Bartunkova, S -- Wiegand, S J -- Radziejewski, C -- Compton, D -- McClain, J -- Aldrich, T H -- Papadopoulos, N -- Daly, T J -- Davis, S -- Sato, T N -- Yancopoulos, G D -- New York, N.Y. -- Science. 1997 Jul 4;277(5322):55-60.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Regeneron Pharmaceuticals Inc., 777 Old Saw Mill River Road, Tarrytown, NY 10591, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9204896" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Angiopoietin-1 ; Angiopoietin-2 ; Animals ; Blood Vessels/embryology/*metabolism ; Cells, Cultured ; Cloning, Molecular ; Embryo, Mammalian/metabolism ; Endothelial Growth Factors/genetics/metabolism ; Endothelium, Vascular/*cytology/metabolism ; Female ; Humans ; Ligands ; Lymphokines/genetics/metabolism ; Membrane Glycoproteins/antagonists & inhibitors/metabolism ; Mice ; Mice, Transgenic ; Molecular Sequence Data ; *Neovascularization, Physiologic ; Phosphorylation ; Proteins/chemistry/*metabolism ; Rats ; Rats, Sprague-Dawley ; Receptor Protein-Tyrosine Kinases/*antagonists & inhibitors/metabolism ; Receptor, TIE-2 ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factors
    Print ISSN: 0036-8075
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  • 8
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    Circadian rhythms in rapidly dividing cyanobacteria (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-01-10
    Description: The long-standing supposition that the biological clock cannot function in cells that divide more rapidly than the circadian cycle was investigated. During exponential growth in which the generation time was 10 hours, the profile of bioluminescence from a reporter strain of the cyanobacterium Synechococcus (species PCC 7942) matched a model based on the assumption that cells proliferate exponentially and the bioluminescence of each cell oscillates in a cosine fashion. Some messenger RNAs showed a circadian rhythm in abundance during continuous exponential growth with a doubling time of 5 to 6 hours. Thus, the cyanobacterial circadian clock functions in cells that divide three or more times during one circadian cycle.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kondo, T -- Mori, T -- Lebedeva, N V -- Aoki, S -- Ishiura, M -- Golden, S S -- New York, N.Y. -- Science. 1997 Jan 10;275(5297):224-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biological Science, Graduate School of Science, Nagoya University, Chikusa, Nagoya, 464-01 Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8985018" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Division ; *Circadian Rhythm ; Cyanobacteria/cytology/genetics/growth & development/*physiology ; Genes, Reporter ; Luciferases/genetics/metabolism ; Luminescence ; Mutation ; Photosynthetic Reaction Center Complex Proteins/genetics ; Photosystem II Protein Complex ; RNA, Bacterial/genetics/metabolism ; RNA, Messenger/genetics/metabolism ; Transformation, Bacterial
    Print ISSN: 0036-8075
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  • 9
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    V(D)J recombinase activity in a subset of germinal center B lymphocytes (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-10-10
    Description: Reexpression of the V(D)J recombinase-activating genes RAG1 and RAG2 in germinal center B cells creates the potential for immunoglobulin gene rearrangement and the generation of new antigen receptor specificities. Intermediate products of V(D)J recombination are abundant in a subset of germinal center B cells, demonstrating that the kappa immunoglobulin light-chain locus becomes a substrate for renewed V(D)J recombinase activity. This recombinationally active cell compartment contains many heavy-chain VDJ rearrangements that encode low-affinity or nonfunctional antibody. In germinal centers, secondary V(D)J recombination may be induced by diminished binding to antigen ligands, thereby limiting abrupt changes in receptor specificity to B cells that are usually eliminated from the germinal center reaction. This restriction preserves efficient antigen-driven selection in germinal centers while allowing for saltations in the somatic evolution of B cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Han, S -- Dillon, S R -- Zheng, B -- Shimoda, M -- Schlissel, M S -- Kelsoe, G -- AI24335/AI/NIAID NIH HHS/ -- AI40227/AI/NIAID NIH HHS/ -- HL48722/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1997 Oct 10;278(5336):301-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology and Program in Molecular and Cell Biology, University of Maryland School of Medicine, 655 West Baltimore Street, Baltimore, MD 21201, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9323211" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibody Diversity ; B-Lymphocytes/*enzymology/immunology ; DNA Nucleotidyltransferases/*metabolism ; DNA-Binding Proteins/genetics ; *Gene Rearrangement, B-Lymphocyte ; *Genes, Immunoglobulin ; Genes, RAG-1 ; Germinal Center/cytology/*immunology ; Immunization ; Immunoglobulin Joining Region/genetics ; Immunoglobulin Variable Region/genetics ; Immunoglobulin kappa-Chains/genetics ; Lymphocyte Activation ; Mice ; Mice, Inbred C57BL ; *Recombination, Genetic ; VDJ Recombinases
    Print ISSN: 0036-8075
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  • 10
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    Diameter-Selective Raman Scattering from Vibrational Modes in Carbon Nanotubes (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-01-10
    Description: Single wall carbon nanotubes (SWNTs) that are found as close-packed arrays in crystalline ropes have been studied by using Raman scattering techniques with laser excitation wavelengths in the range from 514.5 to 1320 nanometers. Numerous Raman peaks were observed and identified with vibrational modes of armchair symmetry (n, n) SWNTs. The Raman spectra are in good agreement with lattice dynamics calculations based on C-C force constants used to fit the two-dimensional, experimental phonon dispersion of a single graphene sheet. Calculated intensities from a nonresonant, bond polarizability model optimized for sp2 carbon are also in qualitative agreement with the Raman data, although a resonant Raman scattering process is also taking place. This resonance results from the one-dimensional quantum confinement of the electrons in the nanotube.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rao -- Richter -- Bandow -- Chase -- Eklund -- Williams -- Fang -- Subbaswamy -- Menon -- Thess -- Smalley -- Dresselhaus -- New York, N.Y. -- Science. 1997 Jan 10;275(5297):187-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉A. M. Rao and P. C. Eklund, Department of Physics and Astronomy and Center for Applied Energy Research, University of Kentucky, Lexington, KY 40506-0055, USA. E. Richter, K. A. Williams, S. Fang, K. R. Subbaswamy, Department of Physics and Astronomy, University of Kentucky, Lexington, KY 40506-0055, USA. S. Bandow, Instrument Center, Institute for Molecular Science, Myodaiji, Okazaki 444, Japan. B. Chase, Dupont Experimental Station, E328163, P.O. Box 80328, Wilmington, DE 19880-0328, USA. M. Menon, Department of Physics and Astronomy and Center for Computational Sciences, University of Kentucky, Lexington, KY 40506-0055, USA. A. Thess and R. E. Smalley, Department of Chemistry, Rice University, Houston, TX 77005, USA. G. Dresselhaus, Francis Bitter Magnet Laboratory, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. M. S. Dresselhaus, Department of Physics and Department of Electrical Engineering and Computer Science, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8985007" target="_blank"〉PubMed〈/a〉
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