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  • 1
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    Clues to the pathogenesis of familial colorectal cancer (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-05-07
    Description: A predisposition to colorectal cancer is shown to be linked to markers on chromosome 2 in some families. Molecular features of "familial" cancers were compared with those of sporadic colon cancers. Neither the familial nor sporadic cancers showed loss of heterozygosity for chromosome 2 markers, and the incidence of mutations in KRAS, P53, and APC was similar in the two groups of tumors. Most of the familial cancers, however, had widespread alterations in short repeated DNA sequences, suggesting that numerous replication errors had occurred during tumor development. Thirteen percent of sporadic cancers had identical abnormalities and these cancers shared biologic properties with the familial cases. These data suggest a mechanism for familial tumorigenesis different from that mediated by classic tumor suppressor genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Aaltonen, L A -- Peltomaki, P -- Leach, F S -- Sistonen, P -- Pylkkanen, L -- Mecklin, J P -- Jarvinen, H -- Powell, S M -- Jen, J -- Hamilton, S R -- CA 35494/CA/NCI NIH HHS/ -- CA 47527/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1993 May 7;260(5109):812-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Genetics, University of Helsinki, Finland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8484121" target="_blank"〉PubMed〈/a〉
    Keywords: Chromosome Mapping ; *Chromosomes, Human, Pair 2 ; Colonic Neoplasms/*genetics ; Colorectal Neoplasms/*genetics ; DNA, Satellite/genetics ; Female ; Genetic Markers ; Humans ; Lod Score ; Male ; Mutation ; Pedigree ; Polymorphism, Genetic ; Rectal Neoplasms/genetics ; Repetitive Sequences, Nucleic Acid
    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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    Genetic mapping of a locus predisposing to human colorectal cancer (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-05-07
    Description: Genetic linkage analysis was used to determine whether a specific chromosomal locus could be implicated in families with a history of early onset cancer but with no other unique features. Close linkage of disease to anonymous microsatellite markers on chromosome 2 was demonstrated in two large kindreds. The pairwise lod scores for linkage to marker D2S123 in these kindreds were 6.39 and 1.45 at zero recombination, and multipoint linkage with flanking markers resulted in lod scores of 6.47 and 6.01. These results prove the existence of a genetically determined predisposition to colorectal cancer that has important ramifications for understanding and preventing this disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Peltomaki, P -- Aaltonen, L A -- Sistonen, P -- Pylkkanen, L -- Mecklin, J P -- Jarvinen, H -- Green, J S -- Jass, J R -- Weber, J L -- Leach, F S -- CA 35494/CA/NCI NIH HHS/ -- CA 47527/CA/NCI NIH HHS/ -- HG 00248/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 1993 May 7;260(5109):810-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Genetics, University of Helsinki, Finland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8484120" target="_blank"〉PubMed〈/a〉
    Keywords: *Chromosome Mapping ; *Chromosomes, Human, Pair 2 ; Colonic Neoplasms/*genetics ; Colorectal Neoplasms/*genetics ; DNA, Satellite/genetics ; Disease Susceptibility ; Female ; *Genes ; Genetic Markers ; Humans ; Male ; Pedigree ; Rectal Neoplasms/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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  • 3
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    Linkage on chromosome 3 of autoimmune diabetes and defective Fc receptor for IgG in NOD mice (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-04-30
    Description: A congenic, non-obese diabetic (NOD) mouse strain that contains a segment of chromosome 3 from the diabetes-resistant mouse strain B6.PL-Thy-1a was less susceptible to diabetes than NOD mice. A fully penetrant immunological defect also mapped to this segment, which encodes the high-affinity Fc receptor for immunoglobulin G (IgG), Fc gamma RI. The NOD Fcgr1 allele, which results in a deletion of the cytoplasmic tail, caused a 73 percent reduction in the turnover of cell surface receptor-antibody complexes. The development of congenic strains and the characterization of Mendelian traits that are specific to the disease phenotype demonstrate the feasibility of dissecting the pathophysiology of complex, non-Mendelian diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Prins, J B -- Todd, J A -- Rodrigues, N R -- Ghosh, S -- Hogarth, P M -- Wicker, L S -- Gaffney, E -- Podolin, P L -- Fischer, P A -- Sirotina, A -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 1993 Apr 30;260(5108):695-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Nuffield Department of Surgery, University of Oxford, John Radcliffe Hospital, Headington, United Kingdom.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8480181" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autoimmune Diseases/*genetics ; Base Sequence ; Crosses, Genetic ; Diabetes Mellitus, Type 1/*genetics ; Endocytosis ; Female ; Gene Deletion ; *Genetic Linkage ; Genetic Markers ; Immunoglobulin G/metabolism ; Male ; Mice ; Mice, Inbred NOD ; Molecular Sequence Data ; Mutation ; Phenotype ; Receptors, IgG/*genetics/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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  • 4
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    Abnormal development of peripheral lymphoid organs in mice deficient in lymphotoxin (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-04-29
    Description: Mice rendered deficient in lymphotoxin (LT) by gene targeting in embryonic stem cells have no morphologically detectable lymph nodes or Peyer's patches, although development of the thymus appears normal. Within the white pulp of the spleen, there is failure of normal segregation of B and T cells. Spleen and peripheral blood contain CD4+CD8- and CD4-CD8+ T cells in a normal ratio, and both T cells subsets have an apparently normal lytic function. Lymphocytes positive for immunoglobulin M are present in increased numbers in both the spleen and peripheral blood. These data suggest an essential role for LT in the normal development of peripheral lymphoid organs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉De Togni, P -- Goellner, J -- Ruddle, N H -- Streeter, P R -- Fick, A -- Mariathasan, S -- Smith, S C -- Carlson, R -- Shornick, L P -- Strauss-Schoenberger, J -- CA 16885/CA/NCI NIH HHS/ -- CA 28533/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1994 Apr 29;264(5159):703-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Internal Medicine, Washington University School of Medicine, St. Louis, MO 63110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8171322" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/immunology ; Blastocyst ; Cytotoxicity, Immunologic ; Female ; Leukocyte Count ; Lymph Nodes/cytology/*growth & development/immunology ; Lymphoid Tissue/cytology/*growth & development/immunology ; Lymphotoxin-alpha/genetics/*physiology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Peyer's Patches/cytology/growth & development/immunology ; Receptors, Tumor Necrosis Factor/physiology ; Spleen/cytology/immunology ; T-Lymphocyte Subsets/immunology ; T-Lymphocytes/immunology ; Thymus Gland/cytology/immunology ; Tumor Necrosis Factor-alpha/genetics/physiology
    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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    Myoblast therapy (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-08-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Epstein, H F -- Fischman, D A -- Bader, D -- Changeux, J P -- Buckhold, K -- Ordahl, C P -- Hoffman, E -- Kedes, L H -- Konieczny, S -- Leinwand, L A -- New York, N.Y. -- Science. 1992 Aug 7;257(5071):738.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1496388" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Child ; Humans ; Male ; Muscles/*transplantation ; Muscular Dystrophies/*surgery ; Transplantation/adverse 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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  • 6
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    Suppression of tumorigenicity of human prostate carcinoma cells by replacing a mutated RB gene (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-02-09
    Description: Introduction of a normal retinoblastoma gene (RB) into retinoblastoma cells was previously shown to suppress several aspects of their neoplastic phenotype, including tumorigenicity in nude mice, thereby directly demonstrating a cancer suppression function of RB. To explore the possibility of a similar activity in a common adult tumor, RB expression was examined in three human prostate carcinoma cell lines. One of these, DU145, contained an abnormally small protein translated from an RB messenger RNA transcript that lacked 105 nucleotides encoded by exon 21. To assess the functional consequences of this mutation, normal RB expression was restored in DU145 cells by retrovirus-mediated gene transfer. Cells that maintained stable exogenous RB expression lost their ability to form tumors in nude mice, although their growth rate in culture was apparently unaltered. These results suggest that RB inactivation can play a significant role in the genesis of a common adult neoplasm and that restoration of normal RB-encoded protein in tumors could have clinical utility.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bookstein, R -- Shew, J Y -- Chen, P L -- Scully, P -- Lee, W H -- 5758/PHS HHS/ -- New York, N.Y. -- Science. 1990 Feb 9;247(4943):712-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, School of Medicine, University of California, San Diego, La Jolla 92093.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2300823" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; DNA/genetics ; Gene Amplification ; Gene Expression ; Humans ; Male ; Mice ; Mice, Nude ; Molecular Sequence Data ; Mutation ; Nucleic Acid Hybridization ; Prostatic Neoplasms/*genetics/pathology ; RNA, Messenger/genetics ; Retinoblastoma/*genetics ; *Suppression, Genetic ; Transfection ; Tumor Cells, Cultured
    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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    LAV revisited: origins of the early HIV-1 isolates from Institut Pasteur (1991)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1991-05-17
    Description: Two of the first human immunodeficiency virus type-1 (HIV-1) strains isolated were authenticated by reanalyzing original cultured samples stored at the Collection Nationale de Culture des Microorganismes as well as uncultured primary material. Cloned polymerase chain reaction products were used to analyze coding sequences of the V3 loop in the gp120 glycoprotein. The original isolate HIV-1 Bru, formerly called LAV, was derived from patient BRU. HIV-1 Lai was derived from patient LAI and contaminated a HIV-1 Bru culture between 20 July and 3 August 1983. The culture became, in effect, HIV-1 Lai, identifiable by a unique motif in the V3 loop. Because of this contamination two, rather than one, HIV-1 isolates were sent to the Laboratory of Tumor Cell Biology at the National Cancer Institute on 23 September 1983. Original HIV-1 Bru was indeed present in the sample marked JBB/LAV. However the M2T-/B sample harbored HIV-1 Lai, a strain capable of growing on established cell lines. The striking similarity between HIV-1 Lai (formerly LAV-Bru) and HTLV-3B sequences remains.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wain-Hobson, S -- Vartanian, J P -- Henry, M -- Chenciner, N -- Cheynier, R -- Delassus, S -- Martins, L P -- Sala, M -- Nugeyre, M T -- Guetard, D -- New York, N.Y. -- Science. 1991 May 17;252(5008):961-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratoire de Retrovirologie Moleculaire, Institut Pasteur, Paris.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2035026" target="_blank"〉PubMed〈/a〉
    Keywords: Academies and Institutes ; Acquired Immunodeficiency Syndrome/*microbiology/pathology ; Amino Acid Sequence ; Base Sequence ; Biopsy ; Cell Line ; Cloning, Molecular ; DNA, Viral/genetics/isolation & purification ; France ; HIV Envelope Protein gp120/*genetics ; HIV-1/classification/genetics/growth & development/*isolation & purification ; Humans ; Lymph Nodes/microbiology/pathology ; Male ; Molecular Sequence Data ; National Institutes of Health (U.S.) ; Oligonucleotide Probes ; Polymerase Chain Reaction/methods ; Sequence Homology, Nucleic Acid ; United States ; Virology/methods
    Print ISSN: 0036-8075
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  • 8
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    Structure and function of lipopolysaccharide binding protein (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-09-21
    Description: The primary structure of lipopolysaccharide binding protein (LBP), a trace plasma protein that binds to the lipid A moiety of bacterial lipopolysaccharides (LPSs), was deduced by sequencing cloned complementary DNA. LBP shares sequence identity with another LPS binding protein found in granulocytes, bactericidal/permeability-increasing protein, and with cholesterol ester transport protein of the plasma. LBP may control the response to LPS under physiologic conditions by forming high-affinity complexes with LPS that bind to monocytes and macrophages, which then secrete tumor necrosis factor. The identification of this pathway for LPS-induced monocyte stimulation may aid in the development of treatments for diseases in which Gram-negative sepsis or endotoxemia are involved.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schumann, R R -- Leong, S R -- Flaggs, G W -- Gray, P W -- Wright, S D -- Mathison, J C -- Tobias, P S -- Ulevitch, R J -- AI 15136/AI/NIAID NIH HHS/ -- AI 25563/AI/NIAID NIH HHS/ -- GM 28485/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1990 Sep 21;249(4975):1429-31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Research Institute of Scripps Clinic, La Jolla, CA 92037.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2402637" target="_blank"〉PubMed〈/a〉
    Keywords: *Acute-Phase Proteins ; Amino Acid Sequence ; Animals ; Base Sequence ; Blood Proteins/*genetics ; Carrier Proteins/*genetics/metabolism ; Gene Library ; Humans ; Kinetics ; Lipid A/metabolism ; Lipopolysaccharides/*metabolism/pharmacology ; Male ; *Membrane Glycoproteins ; Molecular Sequence Data ; Oligonucleotide Probes ; Rabbits ; Sequence Homology, Nucleic Acid ; Sheep ; Staphylococcus aureus ; Tumor Necrosis Factor-alpha/biosynthesis
    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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    DNA binding activity of recombinant SRY from normal males and XY females (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-01-24
    Description: The protein encoded by the human testis determining gene, SRY, contains a high mobility group (HMG) box related to that present in the T cell-specific, DNA-binding protein TCF-1. Recombinant SRY protein was able to bind to the same core sequence AACAAAG recognized by TCF-1 in a sequence dependent manner. In five XY females point mutations were found in the region encoding the HMG box. In four cases DNA binding activity of mutant SRY protein was negligible; in the fifth case DNA binding was reduced. These results imply that the DNA binding activity of SRY is required for sex determination.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Harley, V R -- Jackson, D I -- Hextall, P J -- Hawkins, J R -- Berkovitz, G D -- Sockanathan, S -- Lovell-Badge, R -- Goodfellow, P N -- MC_U117562207/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 1992 Jan 24;255(5043):453-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Human Molecular Genetics Laboratory, Imperial Cancer Research Fund, London, United Kingdom.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1734522" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; DNA-Binding Proteins/*metabolism ; Female ; Gene Expression Regulation ; Humans ; In Vitro Techniques ; Male ; Mice ; Molecular Sequence Data ; *Nuclear Proteins ; Oligonucleotide Probes ; Recombinant Proteins/metabolism ; Sequence Alignment ; Sex-Determining Region Y Protein ; Transcription Factors/metabolism
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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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    A mechanism for virilization of female spotted hyenas in utero (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-06-25
    Description: Female spotted hyenas exhibit male-like genitalia and dominance over males. Hyena ovarian tissues incubated in vitro produced large quantities of the steroid hormone precursor androstenedione. The activity of aromatase, which converts androstenedione to estrogen, was one-twentieth as great in hyena versus human placental homogenates. In comparison, the activity of 17 beta-hydroxysteroid dehydrogenase, which converts androstenedione to testosterone, was equal in the two homogenates. The limited aromatase activity may allow the hyena placenta to convert high circulating concentrations of androstenedione to testosterone, which results in virilization of the fetal external genitalia and possibly destruction of fetal ovarian follicles. Androstenedione production by residual ovarian stromal cells during reproductive life accounts for the epigenetic transmission of virilization in female spotted hyenas.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yalcinkaya, T M -- Siiteri, P K -- Vigne, J L -- Licht, P -- Pavgi, S -- Frank, L G -- Glickman, S E -- CA-39825/CA/NCI NIH HHS/ -- MH-39917/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1993 Jun 25;260(5116):1929-31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Obstetrics, Gynecology, University of California School of Medicine, San Francisco 94143.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8391165" target="_blank"〉PubMed〈/a〉
    Keywords: 17-Hydroxysteroid Dehydrogenases/metabolism ; Animals ; Aromatase/*metabolism ; Carnivora/embryology/*metabolism ; Corpus Luteum/metabolism ; Estradiol/biosynthesis ; Female ; Humans ; In Vitro Techniques ; Luteinizing Hormone/pharmacology ; Male ; Ovary/*metabolism ; Placenta/enzymology/*metabolism ; Pregnancy ; Progesterone/biosynthesis ; *Sex Differentiation ; Testosterone/*biosynthesis
    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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