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  • Female  (247)
  • Organic Chemistry
  • Polymer and Materials Science
  • American Association for the Advancement of Science (AAAS)  (247)
  • 1995-1999  (247)
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Keywords
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  • American Association for the Advancement of Science (AAAS)  (247)
  • Wiley-Blackwell  (2,454)
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Year
  • 1
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    Effectiveness of anthracycline against experimental prion disease in Syrian hamsters (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-05-16
    Description: Prion diseases are transmissible neurodegenerative conditions characterized by the accumulation of protease-resistant forms of the prion protein (PrP), termed PrPres, in the brain. Insoluble PrPres tends to aggregate into amyloid fibrils. The anthracycline 4'-iodo-4'-deoxy-doxorubicin (IDX) binds to amyloid fibrils and induces amyloid resorption in patients with systemic amyloidosis. To test IDX in an experimental model of prion disease, Syrian hamsters were inoculated intracerebrally either with scrapie-infected brain homogenate or with infected homogenate coincubated with IDX. In IDX-treated hamsters, clinical signs of disease were delayed and survival time was prolonged. Neuropathological examination showed a parallel delay in the appearance of brain changes and in the accumulation of PrPres and PrP amyloid.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tagliavini, F -- McArthur, R A -- Canciani, B -- Giaccone, G -- Porro, M -- Bugiani, M -- Lievens, P M -- Bugiani, O -- Peri, E -- Dall'Ara, P -- Rocchi, M -- Poli, G -- Forloni, G -- Bandiera, T -- Varasi, M -- Suarato, A -- Cassutti, P -- Cervini, M A -- Lansen, J -- Salmona, M -- Post, C -- New York, N.Y. -- Science. 1997 May 16;276(5315):1119-22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Istituto Nazionale Neurologico Carlo Besta, via Celoria 11, 20133 Milano, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9148807" target="_blank"〉PubMed〈/a〉
    Keywords: Amyloid/metabolism ; Animals ; Behavior, Animal ; Brain/metabolism/pathology ; Creutzfeldt-Jakob Syndrome/metabolism ; Cricetinae ; Doxorubicin/*analogs & derivatives/metabolism/pharmacology/therapeutic use ; Female ; Humans ; Mesocricetus ; Prions/*metabolism ; RNA, Messenger/genetics/metabolism ; Scrapie/*drug therapy/metabolism/pathology ; Tubulin/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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  • 2
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    Alopecia universalis associated with a mutation in the human hairless gene (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-02-21
    Description: There are several forms of hereditary human hair loss, known collectively as alopecias, the molecular bases of which are entirely unknown. A kindred with a rare, recessively inherited type of alopecia universalis was used to search for a locus by homozygosity mapping, and linkage was established in a 6-centimorgan interval on chromosome 8p12 (the logarithm of the odds favoring linkage score was 6.19). The human homolog of a murine gene, hairless, was localized in this interval by radiation hybrid mapping, and a missense mutation was found in affected individuals. Human hairless encodes a putative single zinc finger transcription factor protein with restricted expression in the brain and skin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ahmad, W -- Faiyaz ul Haque, M -- Brancolini, V -- Tsou, H C -- ul Haque, S -- Lam, H -- Aita, V M -- Owen, J -- deBlaquiere, M -- Frank, J -- Cserhalmi-Friedman, P B -- Leask, A -- McGrath, J A -- Peacocke, M -- Ahmad, M -- Ott, J -- Christiano, A M -- HG-00008/HG/NHGRI NIH HHS/ -- P30AR44535/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 1998 Jan 30;279(5351):720-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Dermatology, Columbia University, 630 West 168 Street, VC-15-526, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9445480" target="_blank"〉PubMed〈/a〉
    Keywords: Alopecia/*genetics ; Amino Acid Sequence ; Animals ; Brain/metabolism ; Chromosome Mapping ; Chromosomes, Human, Pair 8 ; DNA-Binding Proteins/genetics ; Female ; Forkhead Transcription Factors ; Gene Expression ; Genes, Recessive ; Homozygote ; Humans ; Male ; Mice ; Mice, Hairless/genetics ; Microsatellite Repeats ; Molecular Sequence Data ; Mutation ; Pedigree ; Proteins/chemistry/*genetics ; Rats ; Sequence Analysis, DNA ; Sequence Homology, Amino Acid ; Skin/metabolism ; Transcription Factors/genetics ; *Zinc Fingers
    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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    A single ataxia telangiectasia gene with a product similar to PI-3 kinase (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-06-23
    Description: A gene, ATM, that is mutated in the autosomal recessive disorder ataxia telangiectasia (AT) was identified by positional cloning on chromosome 11q22-23. AT is characterized by cerebellar degeneration, immunodeficiency, chromosomal instability, cancer predisposition, radiation sensitivity, and cell cycle abnormalities. The disease is genetically heterogeneous, with four complementation groups that have been suspected to represent different genes. ATM, which has a transcript of 12 kilobases, was found to be mutated in AT patients from all complementation groups, indicating that it is probably the sole gene responsible for this disorder. A partial ATM complementary DNA clone of 5.9 kilobases encoded a putative protein that is similar to several yeast and mammalian phosphatidylinositol-3' kinases that are involved in mitogenic signal transduction, meiotic recombination, and cell cycle control. The discovery of ATM should enhance understanding of AT and related syndromes and may allow the identification of AT heterozygotes, who are at increased risk of cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Savitsky, K -- Bar-Shira, A -- Gilad, S -- Rotman, G -- Ziv, Y -- Vanagaite, L -- Tagle, D A -- Smith, S -- Uziel, T -- Sfez, S -- Ashkenazi, M -- Pecker, I -- Frydman, M -- Harnik, R -- Patanjali, S R -- Simmons, A -- Clines, G A -- Sartiel, A -- Gatti, R A -- Chessa, L -- Sanal, O -- Lavin, M F -- Jaspers, N G -- Taylor, A M -- Arlett, C F -- Miki, T -- Weissman, S M -- Lovett, M -- Collins, F S -- Shiloh, Y -- HG00882/HG/NHGRI NIH HHS/ -- NS31763/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1995 Jun 23;268(5218):1749-53.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Human Genetics, Sackler School of Medicine, Tel Aviv University, Israel.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7792600" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Ataxia Telangiectasia/*genetics ; Ataxia Telangiectasia Mutated Proteins ; Cell Cycle ; Cell Cycle Proteins ; Chromosome Mapping ; Chromosomes, Artificial, Yeast ; *Chromosomes, Human, Pair 11 ; Cloning, Molecular ; DNA, Complementary/genetics ; DNA-Binding Proteins ; Female ; Genetic Complementation Test ; Genetic Predisposition to Disease ; Heterozygote ; Humans ; Male ; Meiosis ; Molecular Sequence Data ; Neoplasms/genetics ; Nucleic Acid Hybridization ; Phosphatidylinositol 3-Kinases ; Phosphotransferases (Alcohol Group Acceptor)/chemistry/*genetics/physiology ; *Protein-Serine-Threonine Kinases ; Proteins/chemistry/*genetics/physiology ; Radiation Tolerance ; Sequence Deletion ; Signal Transduction ; 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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    Distinct mechanism for antidepressant activity by blockade of central substance P receptors (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-09-11
    Description: The localization of substance P in brain regions that coordinate stress responses and receive convergent monoaminergic innervation suggested that substance P antagonists might have psychotherapeutic properties. Like clinically used antidepressant and anxiolytic drugs, substance P antagonists suppressed isolation-induced vocalizations in guinea pigs. In a placebo-controlled trial in patients with moderate to severe major depression, robust antidepressant effects of the substance P antagonist MK-869 were consistently observed. In preclinical studies, substance P antagonists did not interact with monoamine systems in the manner seen with established antidepressant drugs. These findings suggest that substance P may play an important role in psychiatric disorders.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kramer, M S -- Cutler, N -- Feighner, J -- Shrivastava, R -- Carman, J -- Sramek, J J -- Reines, S A -- Liu, G -- Snavely, D -- Wyatt-Knowles, E -- Hale, J J -- Mills, S G -- MacCoss, M -- Swain, C J -- Harrison, T -- Hill, R G -- Hefti, F -- Scolnick, E M -- Cascieri, M A -- Chicchi, G G -- Sadowski, S -- Williams, A R -- Hewson, L -- Smith, D -- Carlson, E J -- Hargreaves, R J -- Rupniak, N M -- New York, N.Y. -- Science. 1998 Sep 11;281(5383):1640-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Merck Research Laboratories, West Point, PA 19456, USA. Mark_Kramer@merck.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9733503" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Aged ; Amygdala/drug effects/metabolism ; Animals ; Antidepressive Agents, Second-Generation/adverse ; effects/metabolism/pharmacology/*therapeutic use ; Behavior, Animal/drug effects ; Brain/drug effects/metabolism ; Depressive Disorder/*drug therapy/etiology/metabolism ; Female ; Gerbillinae ; Guinea Pigs ; Humans ; Male ; Middle Aged ; Morpholines/adverse effects/metabolism/pharmacology/*therapeutic use ; *Neurokinin-1 Receptor Antagonists ; Norepinephrine/physiology ; Paroxetine/therapeutic use ; Receptors, Neurokinin-1/metabolism ; Serotonin/physiology ; Stress, Psychological/drug therapy ; Substance P/*antagonists & inhibitors/metabolism ; Vocalization, Animal/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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  • 5
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    Mutation of Jak3 in a patient with SCID: essential role of Jak3 in lymphoid development (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-11-03
    Description: Males with X-linked severe combined immunodeficiency (XSCID) have defects in the common cytokine receptor gamma chain (gamma c) gene that encodes a shared, essential component of the receptors of interleukin-2 (IL-2), IL-4, IL-7, IL-9, and IL-15. The Janus family tyrosine kinase Jak3 is the only signaling molecule known to be associated with gamma c, so it was hypothesized that defects in Jak3 might cause an XSCID-like phenotype. A girl with immunological features indistinguishable from those of XSCID was therefore selected for analysis. An Epstein-Barr virus (EBV)-transformed cell line derived from her lymphocytes had normal gamma c expression but lacked Jak3 protein and had greatly diminished Jak3 messenger RNA. Sequencing revealed a different mutation on each allele: a single nucleotide insertion resulting in a frame shift and premature termination in the Jak3 JH4 domain and a nonsense mutation in the Jak3 JH2 domain. The lack of Jak3 expression correlated with impaired B cell signaling, as demonstrated by the inability of IL-4 to activate Stat6 in the EBV-transformed cell line from the patient. These observations indicate that the functions of gamma c are dependent on Jak3 and that Jak3 is essential for lymphoid development and signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Russell, S M -- Tayebi, N -- Nakajima, H -- Riedy, M C -- Roberts, J L -- Aman, M J -- Migone, T S -- Noguchi, M -- Markert, M L -- Buckley, R H -- O'Shea, J J -- Leonard, W J -- M01-RR30/RR/NCRR NIH HHS/ -- R37AI18613-13/AI/NIAID NIH HHS/ -- T32 CA09058/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1995 Nov 3;270(5237):797-800.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Immunology, National Heart, Lung, and Blood Institute (NHLBI), 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/7481768" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; B-Lymphocytes/*immunology ; Base Sequence ; Cell Line, Transformed ; Female ; Frameshift Mutation ; Genetic Linkage ; Humans ; Infant ; Interleukin-4/pharmacology ; Janus Kinase 3 ; Molecular Sequence Data ; Phenotype ; Point Mutation ; Protein-Tyrosine Kinases/deficiency/genetics/*physiology ; RNA, Messenger/genetics/metabolism ; Receptors, Interleukin/physiology ; STAT6 Transcription Factor ; Severe Combined Immunodeficiency/*enzymology/genetics/immunology ; Signal Transduction ; T-Lymphocytes/*immunology ; Trans-Activators/metabolism ; X Chromosome
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 6
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    Regulated delivery of therapeutic proteins after in vivo somatic cell gene transfer (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999
    Description: Stable delivery of a therapeutic protein under pharmacologic control was achieved through in vivo somatic gene transfer. This system was based on the expression of two chimeric, human-derived proteins that were reconstituted by rapamycin into a transcription factor complex. A mixture of two adeno-associated virus vectors, one expressing the transcription factor chimeras and one containing erythropoietin (Epo) under the control of a promoter responsive to the transcription factor, was injected into skeletal muscle of immune-competent mice. Administration of rapamycin resulted in 200-fold induction of plasma Epo. Stable engraftment of this humanized system in immune-competent mice was achieved for 6 months with similar results for at least 3 months in a rhesus monkey.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ye, X -- Rivera, V M -- Zoltick, P -- Cerasoli, F Jr -- Schnell, M A -- Gao, G -- Hughes, J V -- Gilman, M -- Wilson, J M -- P01 AR/NS43648-03/AR/NIAMS NIH HHS/ -- P30 DK47757-05/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1999 Jan 1;283(5398):88-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Human Gene Therapy, University of Pennsylvania, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9872748" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cytomegalovirus/genetics ; Dependovirus/genetics ; Erythropoietin/administration & dosage/blood/*genetics ; Female ; Gene Expression Regulation ; *Gene Transfer Techniques ; Genetic Therapy/*methods ; Genetic Vectors ; Hematocrit ; Injections, Intramuscular ; Macaca mulatta ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Muscle, Skeletal ; Promoter Regions, Genetic ; Recombinant Fusion Proteins ; Recombinant Proteins ; Sirolimus/*pharmacology ; Transcription Factors/*genetics
    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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    Altered cochlear fibrocytes in a mouse model of DFN3 nonsyndromic deafness (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-08-28
    Description: DFN3, an X chromosome-linked nonsyndromic mixed deafness, is caused by mutations in the BRN-4 gene, which encodes a POU transcription factor. Brn-4-deficient mice were created and found to exhibit profound deafness. No gross morphological changes were observed in the conductive ossicles or cochlea, although there was a dramatic reduction in endocochlear potential. Electron microscopy revealed severe ultrastructural alterations in cochlear spiral ligament fibrocytes. The findings suggest that these fibrocytes, which are mesenchymal in origin and for which a role in potassium ion homeostasis has been postulated, may play a critical role in auditory function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Minowa, O -- Ikeda, K -- Sugitani, Y -- Oshima, T -- Nakai, S -- Katori, Y -- Suzuki, M -- Furukawa, M -- Kawase, T -- Zheng, Y -- Ogura, M -- Asada, Y -- Watanabe, K -- Yamanaka, H -- Gotoh, S -- Nishi-Takeshima, M -- Sugimoto, T -- Kikuchi, T -- Takasaka, T -- Noda, T -- New York, N.Y. -- Science. 1999 Aug 27;285(5432):1408-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, The Cancer Institute, Japanese Foundation for Cancer Research, 1-37-1 Kami-ikebukuro, Toshima-ku, Tokyo 170-8455, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10464101" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cochlear Duct/*metabolism/pathology ; *DNA-Binding Proteins ; Deafness/genetics/*metabolism/pathology ; Ear, Inner/metabolism/pathology ; Ear, Middle/pathology ; Endolymph/metabolism ; Evoked Potentials, Auditory, Brain Stem ; Female ; Gene Expression ; Gene Targeting ; Genetic Linkage ; In Situ Hybridization ; Ion Transport ; Male ; Membrane Potentials ; Mice ; Mice, Inbred C57BL ; Mutagenesis ; *Nerve Tissue Proteins ; POU Domain Factors ; Potassium/*metabolism ; Transcription Factors/genetics/*metabolism ; X Chromosome
    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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  • 8
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    Mutation of a gene encoding a protein with extracellular matrix motifs in Usher syndrome type IIa (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-06-20
    Description: Usher syndrome type IIa (OMIM 276901), an autosomal recessive disorder characterized by moderate to severe sensorineural hearing loss and progressive retinitis pigmentosa, maps to the long arm of human chromosome 1q41 between markers AFM268ZD1 and AFM144XF2. Three biologically important mutations in Usher syndrome type IIa patients were identified in a gene (USH2A) isolated from this critical region. The USH2A gene encodes a protein with a predicted size of 171.5 kilodaltons that has laminin epidermal growth factor and fibronectin type III motifs; these motifs are most commonly observed in proteins comprising components of the basal lamina and extracellular matrixes and in cell adhesion molecules.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Eudy, J D -- Weston, M D -- Yao, S -- Hoover, D M -- Rehm, H L -- Ma-Edmonds, M -- Yan, D -- Ahmad, I -- Cheng, J J -- Ayuso, C -- Cremers, C -- Davenport, S -- Moller, C -- Talmadge, C B -- Beisel, K W -- Tamayo, M -- Morton, C C -- Swaroop, A -- Kimberling, W J -- Sumegi, J -- 5PO1 DC01813-05/DC/NIDCD NIH HHS/ -- DC03402/DC/NIDCD NIH HHS/ -- EY07003/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 1998 Jun 12;280(5370):1753-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE 68198, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9624053" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Adhesion Molecules/chemistry ; Chromosome Mapping ; Chromosomes, Human, Pair 1 ; Cochlea/chemistry ; Epidermal Growth Factor/chemistry ; Extracellular Matrix Proteins/chemistry/*genetics/physiology ; Female ; Fibronectins/chemistry ; Frameshift Mutation ; Gene Expression ; Genes, Recessive ; Glycosylation ; Hearing Loss, Sensorineural/*genetics ; Humans ; Laminin/chemistry ; Male ; Molecular Sequence Data ; Pedigree ; Retina/chemistry ; Retinitis Pigmentosa/*genetics ; Syndrome ; Tumor Cells, Cultured
    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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    Mutation in transcription factor POU4F3 associated with inherited progressive hearing loss in humans (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-04-16
    Description: The molecular basis for autosomal dominant progressive nonsyndromic hearing loss in an Israeli Jewish family, Family H, has been determined. Linkage analysis placed this deafness locus, DFNA15, on chromosome 5q31. The human homolog of mouse Pou4f3, a member of the POU-domain family of transcription factors whose targeted inactivation causes profound deafness in mice, was physically mapped to the 25-centimorgan DFNA15-linked region. An 8-base pair deletion in the POU homeodomain of human POU4F3 was identified in Family H. A truncated protein presumably impairs high-affinity binding of this transcription factor in a dominant negative fashion, leading to progressive hearing loss.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vahava, O -- Morell, R -- Lynch, E D -- Weiss, S -- Kagan, M E -- Ahituv, N -- Morrow, J E -- Lee, M K -- Skvorak, A B -- Morton, C C -- Blumenfeld, A -- Frydman, M -- Friedman, T B -- King, M C -- Avraham, K B -- R01 DC01076/DC/NIDCD NIH HHS/ -- Z01 DC 00039/DC/NIDCD NIH HHS/ -- New York, N.Y. -- Science. 1998 Mar 20;279(5358):1950-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Human Genetics, Sackler School of Medicine, Tel Aviv University, Tel Aviv 69978, Israel.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9506947" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Animals ; Cell Differentiation ; Chromosome Mapping ; Chromosomes, Human, Pair 5/genetics ; Deafness/*genetics ; Female ; Gene Expression ; Genetic Linkage ; Hair Cells, Auditory/cytology/physiology ; Hearing Loss, Sensorineural/*genetics ; Homeodomain Proteins/*genetics/metabolism ; Humans ; Israel ; Jews/genetics ; Male ; Mice ; Middle Aged ; Molecular Sequence Data ; Pedigree ; Polymerase Chain Reaction ; Protein Structure, Secondary ; Sequence Deletion ; Transcription Factor Brn-3C ; Transcription Factors/*genetics/metabolism/physiology
    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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    Genetic evaluation of suspected cases of transient HIV-1 infection of infants (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-06-06
    Description: Detection of human immunodeficiency virus-type 1 (HIV-1) on only one or a few occasions in infants born to infected mothers has been interpreted to indicate that infection may be transient rather than persistent. Forty-two cases of suspected transient HIV-1 viremia among 1562 perinatally exposed seroreverting infants and one mother were reanalyzed. HIV-1 env sequences were not found in specimens from 20; in specimens from 6, somatic genetic analysis revealed that specimens were mistakenly attributed to an infant; and in specimens from 17, phylogenetic analysis failed to demonstrate the expected linkage between the infant's and the mother's virus. These findings argue that transient HIV-1 infection, if it exists, will only rarely be satisfactorily documented.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Frenkel, L M -- Mullins, J I -- Learn, G H -- Manns-Arcuino, L -- Herring, B L -- Kalish, M L -- Steketee, R W -- Thea, D M -- Nichols, J E -- Liu, S L -- Harmache, A -- He, X -- Muthui, D -- Madan, A -- Hood, L -- Haase, A T -- Zupancic, M -- Staskus, K -- Wolinsky, S -- Krogstad, P -- Zhao, J -- Chen, I -- Koup, R -- Ho, D -- Korber, B -- Apple, R J -- Coombs, R W -- Pahwa, S -- Roberts, N J Jr -- AI27757/AI/NIAID NIH HHS/ -- AI32910/AI/NIAID NIH HHS/ -- UO1-27658/PHS HHS/ -- etc. -- New York, N.Y. -- Science. 1998 May 15;280(5366):1073-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, University of Rochester, Rochester, NY 14642, USA. lfrenkel@u.washington.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9582120" target="_blank"〉PubMed〈/a〉
    Keywords: DNA, Viral/analysis/genetics ; Diagnostic Errors ; Equipment Contamination ; Female ; Genes, env ; HIV Infections/immunology/transmission/*virology ; HIV-1/*genetics/*isolation & purification ; Humans ; Infant ; Infant, Newborn ; Infectious Disease Transmission, Vertical ; Molecular Sequence Data ; Phylogeny ; Polymerase Chain Reaction ; RNA, Viral/analysis ; *Specimen Handling ; T-Lymphocytes, Cytotoxic/immunology ; Viremia/virology
    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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