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  • 1
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    Biomedicine. Do G quartets orchestrate fragile X pathology? (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-12-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moine, H -- Mandel, J L -- New York, N.Y. -- Science. 2001 Dec 21;294(5551):2487-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉UPR9002 CNRS, 67084 Strasbourg Cedex, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11752559" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; Brain/metabolism ; Crystallography, X-Ray ; Fragile X Mental Retardation Protein ; Fragile X Syndrome/genetics/*metabolism ; Gene Expression Regulation ; Humans ; Mice ; Nerve Tissue Proteins/chemistry/genetics/*metabolism ; Nucleic Acid Conformation ; Oligonucleotide Array Sequence Analysis ; Protein Biosynthesis ; Protein Structure, Tertiary ; RNA, Messenger/*chemistry/genetics/*metabolism ; *RNA-Binding Proteins ; Synapses/physiology ; Untranslated Regions
    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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    Biomedicine. Huntingtin--profit and loss (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-07-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Trottier, Y -- Mandel, J L -- New York, N.Y. -- Science. 2001 Jul 20;293(5529):445-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉IGBMC-CNRS-INSERM-ULP, Illkirch Cedex 67404, C.U. de Strasbourg, France. yvon@titus.u-strasbg.fr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11463904" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Brain-Derived Neurotrophic Factor/genetics/*metabolism ; CREB-Binding Protein ; Caspases/metabolism ; Cells, Cultured ; Cerebral Cortex/*metabolism/pathology ; Corpus Striatum/*metabolism/pathology ; Gene Expression Regulation ; Humans ; Huntington Disease/genetics/*metabolism/pathology ; Mice ; Mice, Transgenic ; Mutation ; Nerve Tissue Proteins/chemistry/genetics/*physiology ; Neurons/*metabolism/pathology ; Nuclear Proteins/chemistry/genetics/metabolism/*physiology ; Trans-Activators/metabolism ; Transcription Factors/metabolism ; Transcription, Genetic
    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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    Genome analysis and the human X chromosome (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-10-02
    Description: A unified genetic, physical, and functional map of the human X chromosome is being built through a concerted, international effort. About 40 percent of the 160 million base pairs of the X chromosome DNA have been cloned in overlapping, ordered contigs derived from yeast artificial chromosomes. This rapid progress toward a physical map is accelerating the identification of inherited disease genes, 26 of which are already cloned and more than 50 others regionally localized by linkage analysis. This article summarizes the mapping strategies now used and the impact of genome research on the understanding of X chromosome inactivation and X-linked diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mandel, J L -- Monaco, A P -- Nelson, D L -- Schlessinger, D -- Willard, H -- New York, N.Y. -- Science. 1992 Oct 2;258(5079):103-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire de Genetique Moleculaire des Eucaryotes du CNRS, INSERM, Strasbourg, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1439756" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Chromosome Mapping ; Dosage Compensation, Genetic ; Female ; *Genome, Human ; Humans ; Macropodidae ; Male ; Mice ; Mutation ; Sex Chromosome Aberrations ; *X Chromosome
    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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  • 4
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    Exercise and genetic rescue of SCA1 via the transcriptional repressor Capicua (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-11-05
    Description: Spinocerebellar ataxia type 1 (SCA1) is a fatal neurodegenerative disease caused by expansion of a translated CAG repeat in Ataxin-1 (ATXN1). To determine the long-term effects of exercise, we implemented a mild exercise regimen in a mouse model of SCA1 and found a considerable improvement in survival accompanied by up-regulation of epidermal growth factor and consequential down-regulation of Capicua, which is an ATXN1 interactor. Offspring of Capicua mutant mice bred to SCA1 mice showed significant improvement of all disease phenotypes. Although polyglutamine-expanded Atxn1 caused some loss of Capicua function, further reduction of Capicua levels--either genetically or by exercise--mitigated the disease phenotypes by dampening the toxic gain of function. Thus, exercise might have long-term beneficial effects in other ataxias and neurodegenerative diseases.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3232424/" 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/PMC3232424/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fryer, John D -- Yu, Peng -- Kang, Hyojin -- Mandel-Brehm, Caleigh -- Carter, Angela N -- Crespo-Barreto, Juan -- Gao, Yan -- Flora, Adriano -- Shaw, Chad -- Orr, Harry T -- Zoghbi, Huda Y -- 1F32NS055545/NS/NINDS NIH HHS/ -- HD24064/HD/NICHD NIH HHS/ -- NS022920/NS/NINDS NIH HHS/ -- NS045667/NS/NINDS NIH HHS/ -- NS27699/NS/NINDS NIH HHS/ -- NS27699-20S1/NS/NINDS NIH HHS/ -- P30 HD024064/HD/NICHD NIH HHS/ -- P30 HD024064-22/HD/NICHD NIH HHS/ -- P30 HD024064-23/HD/NICHD NIH HHS/ -- R01 NS027699/NS/NINDS NIH HHS/ -- R01 NS027699-20S1/NS/NINDS NIH HHS/ -- R01 NS027699-21/NS/NINDS NIH HHS/ -- R01 NS027699-22/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 Nov 4;334(6056):690-3. doi: 10.1126/science.1212673.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22053053" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Ataxin-1 ; Ataxins ; Cerebellum/metabolism ; Disease Models, Animal ; *Exercise Therapy ; Gene Knock-In Techniques ; Mice ; Mice, Inbred C57BL ; Mice, Mutant Strains ; Nerve Tissue Proteins/genetics ; Nuclear Proteins/genetics ; Repressor Proteins/genetics/*physiology ; Spinocerebellar Ataxias/genetics/*therapy
    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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  • 5
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    Corepressor-dependent silencing of chromosomal regions encoding neuronal genes (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-10-26
    Description: The molecular mechanisms by which central nervous system-specific genes are expressed only in the nervous system and repressed in other tissues remain a central issue in developmental and regulatory biology. Here, we report that the zinc-finger gene-specific repressor element RE-1 silencing transcription factor/neuronal restricted silencing factor (REST/NRSF) can mediate extraneuronal restriction by imposing either active repression via histone deacetylase recruitment or long-term gene silencing using a distinct functional complex. Silencing of neuronal-specific genes requires the recruitment of an associated corepressor, CoREST, that serves as a functional molecular beacon for the recruitment of molecular machinery that imposes silencing across a chromosomal interval, including transcriptional units that do not themselves contain REST/NRSF response elements.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lunyak, Victoria V -- Burgess, Robert -- Prefontaine, Gratien G -- Nelson, Charles -- Sze, Sing-Hoi -- Chenoweth, Josh -- Schwartz, Phillip -- Pevzner, Pavel A -- Glass, Christopher -- Mandel, Gail -- Rosenfeld, Michael G -- New York, N.Y. -- Science. 2002 Nov 29;298(5599):1747-52. Epub 2002 Oct 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute (HHMI), Department of Computer Science and Engineering, School of Medicine, University of California, San Diego, 9500 Gilman Drive, Room 345, La Jolla, CA 92093-0648, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12399542" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; Carrier Proteins ; Cell Line ; *Chromosomal Proteins, Non-Histone ; Chromosomes/*genetics/metabolism ; Chromosomes, Human/genetics/metabolism ; Co-Repressor Proteins ; Computational Biology ; CpG Islands ; DNA Methylation ; DNA-Binding Proteins/metabolism ; Gene Expression Profiling ; Gene Expression Regulation ; *Gene Silencing ; Histone Deacetylases/metabolism ; Humans ; Intracellular Signaling Peptides and Proteins ; Membrane Proteins ; Methyl-CpG-Binding Protein 2 ; Mice ; Models, Genetic ; NAV1.2 Voltage-Gated Sodium Channel ; Nerve Growth Factors/genetics ; Nerve Tissue Proteins/chemistry/genetics/*metabolism ; Neurons/*metabolism ; Promoter Regions, Genetic ; Protein Structure, Tertiary ; Rats ; Repressor Proteins/chemistry/*metabolism ; Sodium Channels/genetics ; Transcription Factors/chemistry/*metabolism ; Transfection
    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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  • 6
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    A role for glia in the progression of Rett's syndrome (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-07-01
    Description: Rett's syndrome (RTT) is an X-chromosome-linked autism spectrum disorder caused by loss of function of the transcription factor methyl-CpG-binding protein 2 (MeCP2). Although MeCP2 is expressed in most tissues, loss of MeCP2 expression results primarily in neurological symptoms. Earlier studies suggested the idea that RTT is due exclusively to loss of MeCP2 function in neurons. Although defective neurons clearly underlie the aberrant behaviours, we and others showed recently that the loss of MECP2 from glia negatively influences neurons in a non-cell-autonomous fashion. Here we show that in globally MeCP2-deficient mice, re-expression of Mecp2 preferentially in astrocytes significantly improved locomotion and anxiety levels, restored respiratory abnormalities to a normal pattern, and greatly prolonged lifespan compared to globally null mice. Furthermore, restoration of MeCP2 in the mutant astrocytes exerted a non-cell-autonomous positive effect on mutant neurons in vivo, restoring normal dendritic morphology and increasing levels of the excitatory glutamate transporter VGLUT1. Our study shows that glia, like neurons, are integral components of the neuropathology of RTT, and supports the targeting of glia as a strategy for improving the associated symptoms.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3268776/" 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/PMC3268776/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lioy, Daniel T -- Garg, Saurabh K -- Monaghan, Caitlin E -- Raber, Jacob -- Foust, Kevin D -- Kaspar, Brian K -- Hirrlinger, Petra G -- Kirchhoff, Frank -- Bissonnette, John M -- Ballas, Nurit -- Mandel, Gail -- P30 NS061800/NS/NINDS NIH HHS/ -- R01 HD056503/HD/NICHD NIH HHS/ -- R01 HD056503-03/HD/NICHD NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2011 Jun 29;475(7357):497-500. doi: 10.1038/nature10214.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Vollum Institute, Oregon Health and Science University, Portland, Oregon 97239, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21716289" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anxiety/metabolism ; Astrocytes/metabolism ; Behavior, Animal ; Disease Progression ; Female ; Gene Expression Regulation ; Male ; Methyl-CpG-Binding Protein 2/deficiency/genetics/metabolism ; Mice ; Mice, Inbred C57BL ; Motor Activity ; Neuroglia/*metabolism/pathology ; Neurons/metabolism ; Rett Syndrome/*genetics/*metabolism/physiopathology ; Vesicular Glutamate Transport Protein 1/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 7
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    Sensory experience regulates cortical inhibition by inducing IGF1 in VIP neurons (2016)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2016-03-10
    Description: Inhibitory neurons regulate the adaptation of neural circuits to sensory experience, but the molecular mechanisms by which experience controls the connectivity between different types of inhibitory neuron to regulate cortical plasticity are largely unknown. Here we show that exposure of dark-housed mice to light induces a gene program in cortical vasoactive intestinal peptide (VIP)-expressing neurons that is markedly distinct from that induced in excitatory neurons and other subtypes of inhibitory neuron. We identify Igf1 as one of several activity-regulated genes that are specific to VIP neurons, and demonstrate that IGF1 functions cell-autonomously in VIP neurons to increase inhibitory synaptic input onto these neurons. Our findings further suggest that in cortical VIP neurons, experience-dependent gene transcription regulates visual acuity by activating the expression of IGF1, thus promoting the inhibition of disinhibitory neurons and affecting inhibition onto cortical pyramidal neurons.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4823817/" 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/PMC4823817/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mardinly, A R -- Spiegel, I -- Patrizi, A -- Centofante, E -- Bazinet, J E -- Tzeng, C P -- Mandel-Brehm, C -- Harmin, D A -- Adesnik, H -- Fagiolini, M -- Greenberg, M E -- P01 NS047572/NS/NINDS NIH HHS/ -- P30 HD018655/HD/NICHD NIH HHS/ -- R01 NS028829/NS/NINDS NIH HHS/ -- R37 NS028829/NS/NINDS NIH HHS/ -- England -- Nature. 2016 Mar 17;531(7594):371-5. doi: 10.1038/nature17187. Epub 2016 Mar 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, University of California Berkeley, 205 Life Sciences Addition, Berkeley, California 94720, USA. ; Department of Neurobiology, Harvard Medical School, 220 Longwood Ave, Boston, Massachusetts 02115, USA. ; FM Kirby Neurobiology Center, Boston Children's Hospital, 3 Blackfan Circle, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26958833" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Female ; Insulin-Like Growth Factor I/*metabolism ; Male ; Mice ; Mice, Inbred C57BL ; *Neural Inhibition ; Neural Pathways ; Neuronal Plasticity ; Neurons/cytology/*metabolism/secretion ; Pyramidal Cells/metabolism ; Synapses/metabolism ; Vasoactive Intestinal Peptide/*metabolism ; Vision, Ocular/physiology ; Visual Cortex/*cytology/*physiology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 8
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    Gonadotroph-specific expression of metallothionein fusion genes in pituitaries of transgenic mice (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-02-28
    Description: Transgenic mice expressing a metallothionein-somatostatin fusion gene contain high concentrations of somatostatin in the anterior pituitary gland, a tissue that does not normally produce somatostatin. Immunoreactive somatostatin within the anterior pituitaries was found exclusively within gonadotrophs. Similarly, a metallothionein-human growth-hormone fusion gene was also expressed selectively in gonadotrophs. It is proposed that sequences common to the two fusion genes are responsible for the gonadotroph-specific expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Low, M J -- Lechan, R M -- Hammer, R E -- Brinster, R L -- Habener, J F -- Mandel, G -- Goodman, R H -- AM 01313/AM/NIADDK NIH HHS/ -- AM 30457/AM/NIADDK NIH HHS/ -- AM 31400/AM/NIADDK NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1986 Feb 28;231(4741):1002-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2868526" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; DNA, Recombinant/metabolism ; Genes ; Genetic Engineering ; Humans ; Immunoenzyme Techniques ; Luteinizing Hormone/metabolism ; Metallothionein/*genetics ; Mice ; Pituitary Gland, Anterior/*metabolism ; Rats ; Somatostatin/*genetics/metabolism
    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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  • 9
    Electronic Resource
    Electronic Resource
    The physical chemistry of polyelectrolyte solutionsPaper presented at the meeting of the GDCh-Fachgruppe “Makromolekulare Chemie” on “Polymers and Water” in Bad Nauheim (W-Germany) on April 2/3 1984. (1984)
    Weinheim : Wiley-Blackwell
    Angewandte Makromolekulare Chemie 123 (1984), S. 63-83 
    Details
    ISSN: 0003-3146
    Keywords: Chemistry ; Polymer and Materials Science
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Chemistry and Pharmacology , Physics
    Notes: Some physical properties of aqueous solutions containing linear, flexible, polyelectrolytes are reviewed in order to emphasize the role of charge interactions in these systems which strongly depend on the charge of the macromolecular chain and the concentration of low molar mass electrolyte in solution. Particular emphasis is put on polyelectrolyte solutions containing an excess of added salt, which from a theoretical point of view are easier to understand. Both the dilute and the semi-dilute case will be discussed. In the former the problem of the electrostatic potential around the macromolecular chain is briefly reviewed as well as the use of a wormlike chain model to derive average dimensions of polyelectrolytes in solutions. In the latter the scaling approach to concentration effects in polyelectrolyte solutions is briefly discussed. The pecularities of the semi-dilute regime in polyelectrolyte solutions is illustrated with the help of results obtained with dynamic light scattering and the time dependent decay of electric birefringence.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/apmc.1984.051230103
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  • 10
    Electronic Resource
    Electronic Resource
    Das Mischzeitverhalten bei sehr geringen Konzentrationen (1993)
    Weinheim : Wiley-Blackwell
    Chemie Ingenieur Technik - CIT 65 (1993), S. 68-70 
    Details
    ISSN: 0009-286X
    Keywords: Chemistry ; Polymer and Materials Science
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Chemistry and Pharmacology , Process Engineering, Biotechnology, Nutrition Technology
    Additional Material: 3 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/cite.330650111
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