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  • Humans  (1,002)
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  • 1
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    Isolation of sequences that span the fragile X and identification of a fragile X-related CpG island (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-03-08
    Description: Yeast artificial chromosomes (YACs) were obtained from a 550-kilobase region that contains three probes previously mapped as very close to the locus of the fragile X syndrome. These YACs spanned the fragile site in Xq27.3 as shown by fluorescent in situ hybridization. An internal 200-kilobase segment contained four chromosomal breakpoints generated by induction of fragile X expression. A single CpG island was identified in the cloned region between markers DXS463 and DXS465 that appears methylated in mentally retarded fragile X males, but not in nonexpressing male carriers of the mutation nor in normal males. This CpG island may indicate the presence of a gene involved in the clinical phenotype of the syndrome.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Heitz, D -- Rousseau, F -- Devys, D -- Saccone, S -- Abderrahim, H -- Le Paslier, D -- Cohen, D -- Vincent, A -- Toniolo, D -- Della Valle, G -- New York, N.Y. -- Science. 1991 Mar 8;251(4998):1236-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire de Genetique Moleculaire des Eucaryotes du CNRS, Institut de Chimie Biologique, Faculte de Medecine, Strasbourg, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2006411" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Chromosomes, Fungal ; Cloning, Molecular ; DNA Probes ; *Dinucleoside Phosphates ; Fragile X Syndrome/*genetics ; Humans ; Male ; Molecular Sequence Data ; Mutation ; Nucleic Acid Hybridization ; Oligonucleotide Probes ; Polymerase Chain Reaction ; Reference Values ; Restriction Mapping ; Saccharomyces cerevisiae/genetics ; *X Chromosome
    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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    Absence of linkage of chromosome 21q21 markers to familial Alzheimer's disease (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-09-16
    Description: Alzheimer's disease is the most common form of dementia among the elderly population. Although the etiology is unknown, inheritance plays a role in the pathogenesis of the disease. Recent work indicates that an autosomal dominant gene for Alzheimer's disease is located on chromosome 21 at band q21. In the present study of a group of autopsy-documented kindreds, no evidence for linkage was found between familial Alzheimer's disease (FAD) and chromosome 21q21 markers (D21S1/D21S72 and the amyloid beta gene). Linkage to the D21S1/D21S72 locus was excluded at recombination fractions (theta) up to 0.17. Linkage to the amyloid gene was excluded at theta = 0.10. Apparent recombinants were noted in two families for the amyloid gene and in five families for the D21S1/D21S72 locus. These data indicate that FAD is genetically heterogeneous.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schellenberg, G D -- Bird, T D -- Wijsman, E M -- Moore, D K -- Boehnke, M -- Bryant, E M -- Lampe, T H -- Nochlin, D -- Sumi, S M -- Deeb, S S -- AG 00057/AG/NIA NIH HHS/ -- AG 05136/AG/NIA NIH HHS/ -- GM 15253/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1988 Sep 16;241(4872):1507-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neurology, University of Washington, Seattle 98195.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3420406" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/*genetics ; Chromosome Mapping ; *Chromosomes, Human, Pair 21 ; Genetic Linkage ; Humans
    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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    Inhibition of HIV replication in acute and chronic infections in vitro by a Tat antagonist (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-12-20
    Description: The human immunodeficiency virus-1 (HIV-1) trans-activator Tat is an attractive target for the development of antiviral drugs because inhibition of Tat would arrest the virus at an early stage. The drug Ro 5-3335 [7-chloro-5-(2-pyrryl)-3H-1,4-benzodiazepine-2(H)-one], inhibited gene expression by HIV-1 at the level of transcriptional trans-activation by Tat. The compound did not inhibit the basal activity of the promoter. Both Tat and its target sequence TAR were required for the observed inhibitory activity. Ro 5-3335 reduced the amount of cell-associated viral RNA and antigen in acutely, as well as in chronically infected cells in vitro (median inhibition concentration 0.1 to 1 micromolar). Effective inhibition of viral replication was also observed 24 hours after cells were transfected with infectious recombinant HIV-1 DNA. The compound was active against both HIV-1 and HIV-2 and against 3'-azido-3'-deoxythymidine (AZT)-resistant clinical isolates.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hsu, M C -- Schutt, A D -- Holly, M -- Slice, L W -- Sherman, M I -- Richman, D D -- Potash, M J -- Volsky, D J -- AI 27397/AI/NIAID NIH HHS/ -- AI 27670/AI/NIAID NIH HHS/ -- AI 29164/AI/NIAID NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1991 Dec 20;254(5039):1799-802.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Virology, Hoffmann-La Roche, Nutley, NJ 07110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1763331" target="_blank"〉PubMed〈/a〉
    Keywords: Antiviral Agents/*pharmacology ; Benzodiazepinones/*pharmacology ; Cell Line ; Gene Products, tat/*antagonists & inhibitors ; HIV Long Terminal Repeat/drug effects ; HIV-1/drug effects/genetics/*physiology ; HIV-2/drug effects/*physiology ; Humans ; Kinetics ; Promoter Regions, Genetic/drug effects ; Pyrroles/*pharmacology ; Virus Replication/*drug effects ; Zidovudine/pharmacology ; tat Gene Products, Human Immunodeficiency Virus
    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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    Mutations in the rod domains of keratins 1 and 10 in epidermolytic hyperkeratosis (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-08-21
    Description: Epidermolytic hyperkeratosis is a hereditary skin disorder characterized by blistering and a marked thickening of the stratum corneum. In one family, affected individuals exhibited a mutation in the highly conserved carboxyl terminal of the rod domain of keratin 1. In two other families, affected individuals had mutations in the highly conserved amino terminal of the rod domain of keratin 10. Structural analysis of these mutations predicts that heterodimer formation would be unaffected, although filament assembly and elongation would be severely compromised. These data imply that an intact keratin intermediate filament network is required for the maintenance of both cellular and tissue integrity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rothnagel, J A -- Dominey, A M -- Dempsey, L D -- Longley, M A -- Greenhalgh, D A -- Gagne, T A -- Huber, M -- Frenk, E -- Hohl, D -- Roop, D R -- HD25479/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1992 Aug 21;257(5073):1128-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Baylor College of Medicine, Houston, TX 77030.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1380725" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; DNA/chemistry ; Humans ; Ichthyosiform Erythroderma, Congenital/*genetics ; Keratins/chemistry/*genetics ; Macromolecular Substances ; Molecular Sequence Data ; *Mutation ; Pedigree ; Polymerase Chain Reaction ; Protein Conformation
    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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  • 5
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    Propolypeptide of von Willebrand factor circulates in blood and is identical to von Willebrand antigen II (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-05-23
    Description: The generally mild bleeding disorder of von Willebrand disease is associated with abnormalities of two distinct plasma proteins, the large multimeric von Willebrand factor (vWF), which mediates platelet adhesion, and von Willebrand antigen II (vW AgII), which is of unknown function. The two proteins were found to have a common biosynthetic origin in endothelial cells and megakaryocytes, which explains their simultaneous absence in the severe form of this hereditary disease. Shared amino acid sequences from a 100-kilodalton plasma glycoprotein and from vW AgII are identical to amino acid sequences predicted from a complementary DNA clone encoding the 5' end of vWF. In addition, these proteins have identical molecular weights and immunologic cross reactivities. Monoclonal antibodies prepared against both proteins recognize epitopes on the pro-vWF subunit and on a 100-kilodalton protein that are not present on the mature vWF subunit in endothelial cell lysates. In contrast, polyclonal antibodies against vWF recognize both pro-vWF and vWF subunits. Thus, the 100-kilodalton plasma glycoprotein and vW AgII are identical proteins and represent an extremely large propolypeptide that is first cleaved from pro-vWF during intracellular processing and then released into plasma.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fay, P J -- Kawai, Y -- Wagner, D D -- Ginsburg, D -- Bonthron, D -- Ohlsson-Wilhelm, B M -- Chavin, S I -- Abraham, G N -- Handin, R I -- Orkin, S H -- HL-30616/HL/NHLBI NIH HHS/ -- HL-34050/HL/NHLBI NIH HHS/ -- HL-34787/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1986 May 23;232(4753):995-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3486471" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Antigens/immunology/*metabolism ; Blood Proteins/immunology/metabolism ; Endothelium/metabolism ; Humans ; Molecular Weight ; Peptide Fragments/analysis ; Protein Precursors/metabolism ; Protein Processing, Post-Translational ; von Willebrand Factor/*metabolism
    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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  • 6
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    A larger spectrum of severe HIV-1--related disease in intravenous drug users in New York City (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-11-11
    Description: Increasing mortality in intravenous (IV) drug users not reported to surveillance as acquired immunodeficiency syndrome (AIDS) has occurred in New York City coincident with the AIDS epidemic. From 1981 to 1986, narcotics-related deaths increased on average 32% per year from 492 in 1981 to 1996 in 1986. This increase included deaths from AIDS increasing from 0 to 905 and deaths from other causes, many of which were infectious diseases, increasing from 492 to 1091. Investigations of these deaths suggest a causal association with human immunodeficiency virus (HIV) infection. These deaths may represent a spectrum of HIV-related disease that has not been identified through AIDS surveillance and has resulted in a large underestimation of the impact of AIDS on IV drug users and blacks and Hispanics.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stoneburner, R L -- Des Jarlais, D C -- Benezra, D -- Gorelkin, L -- Sotheran, J L -- Friedman, S R -- Schultz, S -- Marmor, M -- Mildvan, D -- Maslansky, R -- New York, N.Y. -- Science. 1988 Nov 11;242(4880):916-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉AIDS Research Unit, New York City Department of Health, NY 10013.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3187532" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/complications/*epidemiology/microbiology ; Cause of Death ; Endocarditis/complications ; Hiv ; HIV Seropositivity ; Homosexuality ; Humans ; Male ; New York City ; Pneumonia/complications ; Substance-Related Disorders/*complications/epidemiology/mortality ; Tuberculosis/complications
    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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  • 7
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    The MHC-binding and gp120-binding functions of CD4 are separable (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-08-18
    Description: CD4 is a cell surface glycoprotein that is thought to interact with nonpolymorphic determinants of class II major histocompatibility (MHC) molecules. CD4 is also the receptor for the human immunodeficiency virus (HIV), binding with high affinity to the HIV-1 envelope glycoprotein, gp120. Homolog-scanning mutagenesis was used to identify CD4 regions that are important in class II MHC binding and to determine whether the gp120 and class II MHC binding sites of CD4 are related. Class II MHC binding was abolished by mutations in each of the first three immunoglobulin-like domains of CD4. The gp120 binding could be abolished without affecting class II MHC binding and vice versa, although at least one mutation examined reduced both functions significantly. These findings indicate that, while there may be overlap between the gp120 and class II MHC binding sites of CD4, these sites are distinct and can be separated. Thus it should be possible to design CD4 analogs that can block HIV infectivity but intrinsically lack the ability to affect the normal immune response by binding to class II MHC molecules.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lamarre, D -- Ashkenazi, A -- Fleury, S -- Smith, D H -- Sekaly, R P -- Capon, D J -- New York, N.Y. -- Science. 1989 Aug 18;245(4919):743-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire d'Immunologie, Institut de Recherches Cliniques de Montreal, Quebec, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2549633" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigens, Surface ; Binding Sites ; DNA, Recombinant ; HIV/*metabolism ; HIV Envelope Protein gp120 ; HLA-DP Antigens/immunology ; Histocompatibility Antigens Class II/*immunology ; Humans ; Hybridomas ; Mice ; Molecular Sequence Data ; Mutation ; Receptors, HIV ; Receptors, Virus/genetics/immunology/*metabolism ; Retroviridae Proteins/immunology/*metabolism ; Rosette Formation ; Structure-Activity Relationship ; T-Lymphocytes/immunology/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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  • 8
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    Human immunodeficiency virus infection of human-PBL-SCID mice (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-02-15
    Description: Severe combined immunodeficient (SCID) mice reconstituted with human peripheral blood leukocytes (hu-PBL-SCID mice) have inducible human immune function and may be useful as a small animal model for acquired immunodeficiency syndrome (AIDS) research. Hu-PBL-SCID mice infected with human immunodeficiency virus-1 (HIV-1) contained virus that was recoverable by culture from the peritoneal cavity, spleen, peripheral blood, and lymph nodes for up to 16 weeks after infection; viral sequences were also detected by in situ hybridization and by amplification with the polymerase chain reaction (PCR). Mice could be infected with multiple strains of HIV-1, including LAV-1/Bru, IIIB, MN, SF2, and SF13. HIV-1 infection affected the concentration of human immunoglobulin and the number of CD4+ T cells in the mice. These results support the use of the hu-PBL-SCID mouse for studies of the pathogenesis and treatment of AIDS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mosier, D E -- Gulizia, R J -- Baird, S M -- Wilson, D B -- Spector, D H -- Spector, S A -- AI-27703/AI/NIAID NIH HHS/ -- AI-29182/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1991 Feb 15;251(4995):791-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Immunology, Medical Biology Institute, La Jolla, CA 92037.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1990441" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Transfusion ; Chimera/*immunology ; *Disease Models, Animal ; *HIV Infections/immunology ; *HIV-1/isolation & purification ; Humans ; Immunologic Deficiency Syndromes/genetics/*immunology ; Lymphocyte Transfusion ; Mice ; Mice, Mutant Strains/*immunology ; Spleen/microbiology
    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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  • 9
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    Structurally homologous ligand binding of integrin Mac-1 and viral glycoprotein C receptors (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-11-22
    Description: Three spatially distant surface loops were found to mediate the interaction of the coagulation protein factor X with the leukocyte integrin Mac-1. This interacting region, which by computational modeling defines a three-dimensional macromotif in the catalytic domain, was also recognized by glycoprotein C (gC), a factor X receptor expressed on herpes simplex virus (HSV)-infected endothelial cells. Peptidyl mimicry of each loop inhibited factor X binding to Mac-1 and gC, blocked monocyte generation of thrombin, and prevented monocyte adhesion to HSV-infected endothelium. These data link the ligand recognition of Mac-1 to established mechanisms of receptor-mediated vascular injury.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Altieri, D C -- Etingin, O R -- Fair, D S -- Brunck, T K -- Geltosky, J E -- Hajjar, D P -- Edgington, T S -- HL 46408/HL/NHLBI NIH HHS/ -- P01 HL 16411/HL/NHLBI NIH HHS/ -- R01 HL 43773/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1991 Nov 22;254(5035):1200-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Scripps Research Institute, La Jolla, CA 92037.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1957171" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Binding, Competitive ; Cell Line ; Factor X/*metabolism/ultrastructure ; Humans ; In Vitro Techniques ; Ligands ; Macrophage-1 Antigen/*metabolism ; Models, Molecular ; Molecular Sequence Data ; Peptides/chemistry/metabolism ; Protein Conformation ; Viral Envelope Proteins/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
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    Genome maps 1991 [wall chart] (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-10-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chipperfield, M -- Maidek, M -- Pearson, P -- Ashburner, M -- Glover, D M -- Saunders, R D -- Duncan, I -- Hartl, D -- Merriam, J -- Lee, G -- New York, N.Y. -- Science. 1991 Oct 11;254(5029):247-62.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1925580" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Chromosome Mapping ; Chromosomes ; Drosophila melanogaster/*genetics ; Genes ; *Genome ; *Genome, Human ; Humans
    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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