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  • Humans  (472)
  • Amino Acid Sequence  (109)
  • ASTROPHYSICS
  • Life and Medical Sciences
  • American Association for the Advancement of Science (AAAS)  (533)
  • 1985-1989  (533)
Collection
Keywords
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  • American Association for the Advancement of Science (AAAS)  (533)
  • Wiley-Blackwell  (640)
Years
Year
  • 1
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    Neurotoxicity of a fragment of the amyloid precursor associated with Alzheimer's disease (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-07-28
    Description: Amyloid deposition in senile plaques and the cerebral vasculature is a marker of Alzheimer's disease. Whether amyloid itself contributes to the neurodegenerative process or is simply a by-product of that process is unknown. Pheochromocytoma (PC12) and fibroblast (NIH 3T3) cell lines were transfected with portions of the gene for the human amyloid precursor protein. Stable PC12 cell transfectants expressing a specific amyloid-containing fragment of the precursor protein gradually degenerated when induced to differentiate into neuronal cells with nerve growth factor. Conditioned medium from these cells was toxic to neurons in primary hippocampal cultures, and the toxic agent could be removed by immunoabsorption with an antibody directed against the amyloid polypeptide. Thus, a peptide derived from the amyloid precursor may be neurotoxic.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yankner, B A -- Dawes, L R -- Fisher, S -- Villa-Komaroff, L -- Oster-Granite, M L -- Neve, R L -- HD 18655/HD/NICHD NIH HHS/ -- HD 18658/HD/NICHD NIH HHS/ -- NS 01240/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1989 Jul 28;245(4916):417-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, Harvard Medical School, Boston, MA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2474201" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/*etiology/pathology ; Amyloid/genetics/*physiology ; Blotting, Northern ; Cell Line ; Fibroblasts ; Gene Expression Regulation ; Humans ; Immunoblotting ; Neurons/pathology ; Nucleic Acid Hybridization ; Pheochromocytoma ; Protein Precursors/genetics/*physiology ; RNA/analysis/genetics ; Restriction Mapping ; Transfection ; Tumor Cells, Cultured
    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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    Sequence of the immunodominant epitope for the surface protein on sporozoites of Plasmodium vivax (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-12-20
    Description: Plasmodium vivax is one of the four malaria parasites that cause disease in humans. The structure of the immunodominant repeating peptide of the circumsporozoite (CS) protein of P. vivax was determined. A fragment of P. vivax DNA that encodes this tandemly repeating epitope was isolated by use of an oligonucleotide probe whose sequence is thought to be conserved in CS protein genes. DNA sequence analysis of the P. vivax clone indicates that the CS repeat is nine amino acids in length (Gly-Asp-Arg-Ala-Asp-Gly-Gln-Pro-Ala). The structure of the repeating region was confirmed with synthetic peptides and monoclonal antibodies directed against P. vivax sporozoites. This information should allow synthesis of a vaccine for P. vivax that is similar to the one being tested for P. falciparum.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McCutchan, T F -- Lal, A A -- de la Cruz, V F -- Miller, L H -- Maloy, W L -- Charoenvit, Y -- Beaudoin, R L -- Guerry, P -- Wistar, R Jr -- Hoffman, S L -- New York, N.Y. -- Science. 1985 Dec 20;230(4732):1381-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2416057" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antigens, Surface/*genetics ; Base Sequence ; DNA Restriction Enzymes ; Epitopes/*genetics ; *Genes ; Plasmodium vivax/*immunology ; Species Specificity
    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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    Construction of synthetic immunogen: use of new T-helper epitope on malaria circumsporozoite protein (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-02-27
    Description: The circumsporozoite (CS) protein of Plasmodium falciparum is the focus of intense efforts to develop an antisporozoite malaria vaccine. Localization of sites for T-cell recognition on this molecule is critical for vaccine design. By using an algorithm designed to predict T-cell sites and a large panel of H-2 congenic mice, a major nonrepetitive T-cell site was located. When a synthetic peptide corresponding to this site was covalently linked to the major B-cell site on the molecule, an immunogen capable of eliciting a high-titer antibody response was formed. This peptide sequence could prime helper T cells for a secondary response to the intact CS protein. The new helper T-cell site is located outside the repetitive region of the CS protein and appears to be the immunodominant T site on the molecule. This approach should be useful in the rational design and construction of vaccines.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Good, M F -- Maloy, W L -- Lunde, M N -- Margalit, H -- Cornette, J L -- Smith, G L -- Moss, B -- Miller, L H -- Berzofsky, J A -- New York, N.Y. -- Science. 1987 Feb 27;235(4792):1059-62.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2434994" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antibody Formation ; Antigens, Protozoan/immunology ; Antigens, Surface/*immunology ; B-Lymphocytes/immunology ; Epitopes/*immunology ; Mice ; Peptide Fragments/chemical synthesis/*immunology ; Plasmodium falciparum/*immunology ; *Protozoan Proteins ; Receptors, Antigen, B-Cell/immunology ; Receptors, Antigen, T-Cell/immunology ; T-Lymphocytes/immunology ; T-Lymphocytes, Helper-Inducer/*immunology ; Vaccines/immunology
    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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    The neu gene: an erbB-homologous gene distinct from and unlinked to the gene encoding the EGF receptor (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-09-06
    Description: The neu oncogene, identified in ethylnitrosourea-induced rat neuroglioblastomas, had strong homology with the erbB gene that encodes the epidermal growth factor receptor. This homology was limited to the region of erbB encoding the tyrosine kinase domain. It was concluded that the neu gene is a distinct novel gene, as it is not coamplified with sequences encoding the EGF receptor in the genome of the A431 tumor line and it maps to human chromosome 17.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schechter, A L -- Hung, M C -- Vaidyanathan, L -- Weinberg, R A -- Yang-Feng, T L -- Francke, U -- Ullrich, A -- Coussens, L -- CA 39964-01/CA/NCI NIH HHS/ -- GM 26105/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1985 Sep 6;229(4717):976-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2992090" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Neoplasm/*genetics ; Chromosome Mapping ; Chromosomes, Human, 16-18 ; DNA, Neoplasm/*genetics ; Genes ; Genetic Linkage ; Humans ; Neoplasm Proteins/*genetics ; Neuroblastoma/genetics ; Neuroglia ; *Oncogenes ; Rats ; Receptor, Epidermal Growth Factor ; Receptors, Cell Surface/*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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  • 5
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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
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    Congenital poisoning by polychlorinated biphenyls and their contaminants in Taiwan (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-07-15
    Description: In 1979, a mass poisoning occurred in Taiwan from cooking oil contaminated by thermally degraded polychlorinated biphenyls. Because these chemicals persist in human tissue, children born to female patients after the outbreak were exposed in utero. In 1985, 117 children born to affected women and 108 unexposed controls were examined and evaluated. The exposed children were shorter and lighter than controls; they had abnormalities of gingiva, skin, nails, teeth, and lungs more frequently than did controls. The exposed children showed delay of developmental milestones, deficits on formal developmental testing, and abnormalities on behavioral assessment. These findings are most consistent with a generalized disorder of ectodermal tissue. This syndrome is one of very few documented to result from transplacental exposure to pollutant chemicals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rogan, W J -- Gladen, B C -- Hung, K L -- Koong, S L -- Shih, L Y -- Taylor, J S -- Wu, Y C -- Yang, D -- Ragan, N B -- Hsu, C C -- New York, N.Y. -- Science. 1988 Jul 15;241(4863):334-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3133768" target="_blank"〉PubMed〈/a〉
    Keywords: Conjunctivitis/chemically induced/congenital ; Female ; Growth Disorders/chemically induced ; Humans ; Lactation ; Maternal-Fetal Exchange ; Nails, Malformed ; Oils/*adverse effects ; Pigmentation Disorders/chemically induced/congenital ; Polychlorinated Biphenyls/*poisoning ; Pregnancy ; Taiwan
    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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    An assay for circulating antibodies to a major etiologic virus of human non-A, non-B hepatitis (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-04-21
    Description: A specific assay has been developed for a blood-borne non-A, non-B hepatitis (NANBH) virus in which a polypeptide synthesized in recombinant yeast clones of the hepatitis C virus (HCV) is used to capture circulating viral antibodies. HCV antibodies were detected in six of seven human sera that were shown previously to transmit NANBH to chimpanzees. Assays of ten blood transfusions in the United States that resulted in chronic NANBH revealed that there was at least one positive blood donor in nine of these cases and that all ten recipients seroconverted during their illnesses. About 80 percent of chronic, post-transfusion NANBH (PT-NANBH) patients from Italy and Japan had circulating HCV antibody; a much lower frequency (15 percent) was observed in acute, resolving infections. In addition, 58 percent of NANBH patients from the United States with no identifiable source of parenteral exposure to the virus were also positive for HCV antibody. These data indicate that HCV is a major cause of NANBH throughout the world.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kuo, G -- Choo, Q L -- Alter, H J -- Gitnick, G L -- Redeker, A G -- Purcell, R H -- Miyamura, T -- Dienstag, J L -- Alter, M J -- Stevens, C E -- New York, N.Y. -- Science. 1989 Apr 21;244(4902):362-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Chiron Corporation, Emeryville, CA 94608.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2496467" target="_blank"〉PubMed〈/a〉
    Keywords: Antibodies, Viral/*analysis ; Blood Donors ; Blood Transfusion ; Hepatitis C/*immunology/transmission ; Hepatitis Viruses/*immunology ; Hepatitis, Viral, Human/*immunology ; Humans ; Italy ; Japan ; United States
    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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    Purification and complementary DNA cloning of a receptor for basic fibroblast growth factor (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-07-07
    Description: Basic fibroblast growth factor (bFGF) participates in many processes including early developmental events, angiogenesis, wound healing, and maintenance of neuronal cell viability. A 130-kilodalton protein was isolated on the basis of its ability to specifically bind to bFGF. A complementary DNA clone was isolated with an oligonucleotide probe corresponding to determined amino acid sequences of tryptic peptide fragments of the purified protein. The putative bFGF receptor encoded by this complementary DNA is a transmembrane protein that contains three extracellular immunoglobulin-like domains, an unusual acidic region, and an intracellular tyrosine kinase domain. These domains are arranged in a pattern that is different from that of any growth factor receptor described.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, P L -- Johnson, D E -- Cousens, L S -- Fried, V A -- Williams, L T -- CA 21765/CA/NCI NIH HHS/ -- R01 HL32898/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1989 Jul 7;245(4913):57-60.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Medicine, University of California, San Francisco 94143.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2544996" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cells, Cultured ; Chick Embryo ; *Cloning, Molecular ; DNA/*genetics ; Fibroblast Growth Factors/*genetics ; Kinetics ; Mice ; Molecular Sequence Data ; Peptide Fragments/analysis ; Receptors, Cell Surface/*genetics/metabolism ; Receptors, Fibroblast Growth Factor ; Recombinant 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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  • 9
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    Purification, cloning, and expression of ciliary neurotrophic factor (CNTF) (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-11-24
    Description: Ciliary neurotrophic factor (CNTF) is one of a small number of proteins with neurotrophic activities distinct from nerve growth factor (NGF). CNTF has now been purified and cloned and the primary structure of CNTF from rabbit sciatic nerve has been determined. Biologically active CNTF has been transiently expressed from a rabbit complementary DNA clone. CNTF is a neural effector without significant sequence homologies to any previously reported protein.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lin, L F -- Mismer, D -- Lile, J D -- Armes, L G -- Butler, E T 3rd -- Vannice, J L -- Collins, F -- New York, N.Y. -- Science. 1989 Nov 24;246(4933):1023-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Protein Chemistry Group, Synergen, Inc., Boulder, CO 80301.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2587985" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Line ; Ciliary Neurotrophic Factor ; Cloning, Molecular ; DNA/genetics ; Molecular Sequence Data ; Nerve Growth Factors/*genetics ; Nerve Tissue Proteins/biosynthesis/*genetics/isolation & purification ; Rabbits ; Recombinant Proteins/biosynthesis ; Sciatic Nerve/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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  • 10
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    Absence of duplication of chromosome 21 genes in familial and sporadic Alzheimer's disease (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-10-30
    Description: The possibility that Alzheimer's disease (AD) is caused by overexpression or duplication of one or more genes on chromosome 21 has been raised by the observation of AD-like neuropathologic changes in individuals with Down syndrome and by the mapping of both the defect for familial AD and the amyloid beta protein gene to this autosome. Possible duplication on chromosome 21 was investigated in both familial and sporadic AD by means of restriction fragment length polymorphisms for the amyloid and SODI loci, as well as for DNA markers in the vicinity of the familial AD defect and in the critical Down syndrome region of chromosome 21. No evidence of increased DNA dosage was observed in either brain or leukocytes of patients with inherited or sporadic forms of AD. Duplication of these regions is therefore not a frequent event in either form of AD. Furthermore, no significant allelic association was detected between AD and any of the loci, including the amyloid and SODI genes, providing no support for the hypothesis that defects in these specific genes are the primary cause of AD.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉St George-Hyslop, P H -- Tanzi, R E -- Polinsky, R J -- Neve, R L -- Pollen, D -- Drachman, D -- Growdon, J -- Cupples, L A -- Nee, L -- Myers, R H -- ADRC P50 AGO5134-02/AD/ADAMHA HHS/ -- NS20012/NS/NINDS NIH HHS/ -- R01 AGO6865-1/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 1987 Oct 30;238(4827):664-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neurogenetics Laboratory, Massachusetts General Hospital, Boston.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2890206" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Alzheimer Disease/*genetics ; Amyloid/genetics ; *Chromosomes, Human, Pair 21 ; Genes ; Genetic Linkage ; Humans ; Polymorphism, Restriction Fragment Length
    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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