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  • Articles  (182)
  • Male  (93)
  • Cell Line  (92)
  • Cell & Developmental Biology
  • American Association for the Advancement of Science (AAAS)  (182)
  • 1985-1989  (182)
Collection
  • Articles  (182)
Publisher
  • American Association for the Advancement of Science (AAAS)  (182)
  • Wiley-Blackwell  (412)
Years
Year
  • 1
    Publication Date: 1989-05-12
    Description: Methotrexate coupled to maleylated bovine serum albumin was taken up efficiently through the "scavenger" receptors present on macrophages and led to selective killing of intracellular Leishmania mexicana amazonensis amastigotes in cultured hamster peritoneal macrophages. The drug conjugate was nearly 100 times as effective as free methotrexate in eliminating the intracellular parasites. Furthermore, in a model of experimental cutaneous leishmaniasis in hamsters, the drug conjugate brought about more than 90% reduction in the size of footpad lesions within 11 days. In contrast, the free drug at a similar concentration did not significantly affect lesion size. These studies demonstrate the potential of receptor-mediated drug delivery in the therapy of macrophage-associated diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mukhopadhyay, A -- Chaudhuri, G -- Arora, S K -- Sehgal, S -- Basu, S K -- New York, N.Y. -- Science. 1989 May 12;244(4905):705-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Microbial Technology, Chandigarh, India.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2717947" target="_blank"〉PubMed〈/a〉
    Keywords: Albumins/*administration & dosage/metabolism ; Animals ; Cells, Cultured ; Cricetinae ; Female ; Kinetics ; Leishmania mexicana/*drug effects ; Leishmaniasis/*drug therapy ; Macrophages/metabolism/*parasitology ; Male ; *Membrane Proteins ; Mesocricetus ; Methotrexate/*administration & dosage/pharmacology/therapeutic use ; *Receptors, Immunologic/metabolism ; *Receptors, Lipoprotein ; Receptors, Scavenger ; Scavenger Receptors, Class B ; Serum Albumin, Bovine
    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
    Publication Date: 1987-09-11
    Description: The validity of mouse liver tumor end points in assessing the potential hazards of chemical exposure to humans is a controversial but important issue, since liver neoplasia in mice is the most frequent tumor target tissue end point in 2-year carcinogenicity studies. The ability to distinguish between promotion of background tumors versus a genotoxic mechanism of tumor initiation by chemical treatment would aid in the interpretation of rodent carcinogenesis data. Activated oncogenes in chemically induced and spontaneously occurring mouse liver tumors were examined and compared as one approach to determine the mechanism by which chemical treatment caused an increased incidence of mouse liver tumors. Data suggest that furan and furfural caused an increased incidence in mouse liver tumors at least in part by induction of novel weakly activating point mutations in ras genes even though both chemicals did not induce mutations in Salmonella assays. In addition to ras oncogenes, two activated raf genes and four non-ras transforming genes were detected. The B6C3F1 mouse liver may thus provide a sensitive assay system to detect various classes of proto-oncogenes that are susceptible to activation by carcinogenic insult. As illustrated with mouse liver tumors, analysis of activated oncogenes in spontaneously occurring and chemically induced rodent tumors will provide information at a molecular level to aid in the use of rodent carcinogenesis data for risk assessment.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reynolds, S H -- Stowers, S J -- Patterson, R M -- Maronpot, R R -- Aaronson, S A -- Anderson, M W -- New York, N.Y. -- Science. 1987 Sep 11;237(4820):1309-16.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3629242" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; *Cell Transformation, Neoplastic ; Cells, Cultured ; Liver Neoplasms/*genetics ; Mice ; Mutation ; Nucleic Acid Hybridization ; *Oncogenes ; *Proto-Oncogenes ; Risk
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 1985-08-02
    Description: Beta-galactosidase-deficient siblings in two litters of English springer spaniel puppies showed a progressive neurological impairment, dwarfism, orbital hypertelorism, and dysostosis multiplex. An excess of GM1-ganglioside was found in the brain. Three abnormal oligosaccharides were present in samples of urine, brain, liver, and cartilage. Light microscopy of selected tissue specimens revealed cytoplasmic vacuoles in neurons, circulating blood cells, macrophages, and chondrocytes. Ultrastructural studies demonstrated that these membrane-bound vacuoles were of two types--one containing lamellated membranes and the other, finely granular material. These clinical and pathological findings are similar to those observed in human patients affected by the infantile form of GM1-gangliosidosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Alroy, J -- Orgad, U -- Ucci, A A -- Schelling, S H -- Schunk, K L -- Warren, C D -- Raghavan, S S -- Kolodny, E H -- HD 05515/HD/NICHD NIH HHS/ -- HD04147/HD/NICHD NIH HHS/ -- NS 21765/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1985 Aug 2;229(4712):470-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3925555" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Diseases, Metabolic/enzymology/genetics/*veterinary ; Dog Diseases/*enzymology/genetics/pathology ; Dogs ; Female ; G(M1) Ganglioside ; Gangliosidoses/enzymology/genetics/pathology/*veterinary ; Humans ; Lactose Intolerance/genetics/metabolism/*veterinary ; Male ; Neurons/pathology ; Oligosaccharides/metabolism ; Pedigree ; Vacuoles/pathology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1985-11-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Baum, M J -- Carroll, R S -- Erskine, M S -- Tobet, S A -- New York, N.Y. -- Science. 1985 Nov 22;230(4728):960-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2997925" target="_blank"〉PubMed〈/a〉
    Keywords: Estrogens, Conjugated (USP)/*pharmacology ; Female ; *Homosexuality ; Humans ; Luteinizing Hormone/*secretion ; Male
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  • 5
    Publication Date: 1985-05-17
    Description: Clones of complementary DNA encoding the human lymphokine known as granulocyte-macrophage colony-stimulating factor (GM-CSF) were isolated by means of a mammalian cell (monkey COS cell) expression screening system. One of these clones was used to produce recombinant GM-CSF in mammalian cells. The recombinant hematopoietin was similar to the natural product that was purified to apparent homogeneity from medium conditioned by a human T-cell line. The human T-cell GM-CSF was found to be 60 percent homologous with the GM-CSF recently cloned from murine lung messenger RNA.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wong, G G -- Witek, J S -- Temple, P A -- Wilkens, K M -- Leary, A C -- Luxenberg, D P -- Jones, S S -- Brown, E L -- Kay, R M -- Orr, E C -- New York, N.Y. -- Science. 1985 May 17;228(4701):810-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3923623" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cell Line ; *Cloning, Molecular ; Colony-Stimulating Factors/biosynthesis/*genetics/isolation & purification ; *Dna ; DNA, Recombinant ; *Granulocytes ; Haplorhini ; Humans ; *Macrophages ; RNA, Messenger/genetics ; T-Lymphocytes ; Transfection
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
    Publication Date: 1986-10-31
    Description: A novel human B-lymphotropic virus (HBLV) was isolated from the peripheral blood leukocytes of six individuals: two HTLV-III seropositive patients from the United States (one with AIDS-related lymphoma and one with dermatopathic lymphadenopathy), three HTLV-III seronegative patients from the United States (one with angioimmunoblastic lymphadenopathy, one with cutaneous T-cell lymphoma, and one with immunoblastic lymphoma), and one HTLV-III seronegative patient with acute lymphocytic leukemia from Jamaica. All six isolates were closely related by antigenic analysis, and sera from all six virus-positive patients reacted immunologically with each virus isolate. In contrast, only four sera from 220 randomly selected healthy donors and none from 12 AIDS patients without associated lymphoma were seropositive. The virus selectively infected freshly isolated human B cells and converted them into large, refractile mono- or binucleated cells with nuclear and cytoplasmic inclusion bodies. HBLV is morphologically similar to viruses of the herpesvirus family but is readily distinguishable from the known human and nonhuman primate herpesviruses by host range, in vitro biological effects, and antigenic features.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Salahuddin, S Z -- Ablashi, D V -- Markham, P D -- Josephs, S F -- Sturzenegger, S -- Kaplan, M -- Halligan, G -- Biberfeld, P -- Wong-Staal, F -- Kramarsky, B -- New York, N.Y. -- Science. 1986 Oct 31;234(4776):596-601.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2876520" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/microbiology ; Cell Line ; Deltaretrovirus Infections/microbiology ; Fluorescent Antibody Technique ; Haplorhini ; Herpesviridae/*isolation & purification ; Herpesviridae Infections/*microbiology ; Humans ; Lymphoproliferative Disorders/*microbiology ; Microscopy, Electron ; T-Lymphocytes/microbiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
    Publication Date: 1987-01-30
    Description: In seven right-handed adults, the brain electrical patterns before accurate performance differed from the patterns before inaccurate performance. Activity overlying the left frontal cortex and the motor and parietal cortices contralateral to the performing hand preceded accurate left- or right-hand performance. Additional strong activity overlying midline motor and premotor cortices preceded left-hand performance. These measurements suggest that brief, spatially distributed neural activity patterns, or "preparatory sets," in distinct cognitive, somesthetic-motor, and integrative motor areas of the human brain may be essential precursors of accurate visuomotor performance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gevins, A S -- Morgan, N H -- Bressler, S L -- Cutillo, B A -- White, R M -- Illes, J -- Greer, D S -- Doyle, J C -- Zeitlin, G M -- New York, N.Y. -- Science. 1987 Jan 30;235(4788):580-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3810158" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Cerebral Cortex/*physiology ; Cognition/physiology ; Electroencephalography ; Electrophysiology ; Functional Laterality ; Humans ; Male ; Motor Activity/physiology ; Time Factors ; Visual Perception/physiology
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  • 8
    Publication Date: 1987-05-29
    Description: Preneoplastic and neoplastic liver nodules and hepatocytes isolated from regenerating rat liver have been shown to be resistant to a broad range of carcinogenic agents. This phenomenon was studied by measuring the expression of the multidrug-resistant (mdr) gene in normal liver cells and in preneoplastic and neoplastic nodules and regenerating liver. Levels of messenger RNA for the mdr gene, which encodes P-glycoprotein, were elevated in both preneoplastic and neoplastic lesions. Expression of the mdr gene also reached high levels in regenerating rat liver 24 to 72 hours after partial hepatectomy. These results show that the expression of the mdr gene can be regulated in liver and is likely to be responsible for part of the multidrug-resistance phenotype of carcinogen-initiated hepatocytes and regenerating liver cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thorgeirsson, S S -- Huber, B E -- Sorrell, S -- Fojo, A -- Pastan, I -- Gottesman, M M -- New York, N.Y. -- Science. 1987 May 29;236(4805):1120-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3576227" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carcinogens/*pharmacology ; Drug Resistance/*genetics ; *Genes ; Humans ; Liver/drug effects ; Liver Neoplasms, Experimental/chemically induced ; Liver Regeneration/*drug effects ; Male ; Precancerous Conditions/chemically induced ; RNA, Messenger/genetics ; Rats
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  • 9
    Publication Date: 1986-01-24
    Description: Human T-lymphotropic virus type III (HTLV-III) or lymphadenopathy-associated virus (LAV) is tropic for human T cells with the helper-inducer phenotype, as defined by reactivity with monoclonal antibodies specific for the T4 molecule. Treatment of T4+ T cells with monoclonal antibodies to T4 antigen blocks HTLV-III/LAV binding, syncytia formation, and infectivity. Thus, it has been inferred that the T4 molecule itself is a virus receptor. In the present studies, the surfaces of T4+ T cells were labeled radioactively, and then the cells were exposed to virus. After the cells were lysed, HTLV-III/LAV antibodies were found to precipitate a surface protein with a molecular weight of 58,000 (58K). By blocking and absorption experiments, this 58K protein was identified as the T4 molecule. No cell-surface structures other than the T4 molecule were involved in the antibody-antigen complex formation. Two monoclonal antibodies, each reactive with a separate epitope of the T4 molecule, were tested for their binding capacities in the presence of HTLV-III/LAV. When HTLV-III/LAV was bound to T4+ T cells, the virus blocked the binding of one of the monoclonal antibodies, T4A (OKT4A), but not of the other, T4 (OKT4). When HTLV-III/LAV was internally radiolabeled and bound to T4+ T cells which were then lysed, a viral glycoprotein of 110K (gp110) coprecipitated with the T4 molecule. The binding of gp110 to the T4 molecule may thus be a major factor in HTLV-III/LAV tropism and may prove useful in developing therapeutic or preventive measures for the acquired immune deficiency syndrome.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McDougal, J S -- Kennedy, M S -- Sligh, J M -- Cort, S P -- Mawle, A -- Nicholson, J K -- New York, N.Y. -- Science. 1986 Jan 24;231(4736):382-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3001934" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/microbiology ; Antibodies, Monoclonal ; Cell Line ; Deltaretrovirus/*metabolism ; Humans ; T-Lymphocytes/metabolism/*microbiology ; Viral Proteins/*metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
    Publication Date: 1988-06-10
    Description: The human platelet-derived growth factor (PDGF) receptor complementary DNA was cloned and expressed by transfection of Chinese hamster ovary (CHO) fibroblasts. The ability of CHO cells expressing the human receptor complementary DNA (CHO-HR5) to interact with different recombinant forms of PDGF (AA and BB homodimers) was tested. Both forms of PDGF bind to the transfected receptor, stimulate the receptor tyrosine kinase activity, and elicit a mitogenic response in a manner that was indistinguishable from the responses of Balb/c 3T3 cells to AA and BB forms of PDGF can be attributed to a single type of receptor and show that the AA form, like the BB form, is a true mitogen.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Escobedo, J A -- Navankasatussas, S -- Cousens, L S -- Coughlin, S R -- Bell, G I -- Williams, L T -- HL-32898/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1988 Jun 10;240(4858):1532-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of California, San Francisco.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2836953" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Division/drug effects ; Cell Line ; Cells, Cultured ; DNA Replication/drug effects ; Enzyme Activation ; Humans ; Kinetics ; Macromolecular Substances ; Mice ; Phosphorylation ; Platelet-Derived Growth Factor/genetics/*metabolism/pharmacology ; Protein-Tyrosine Kinases/*metabolism ; Receptors, Cell Surface/genetics/*metabolism ; Receptors, Platelet-Derived Growth Factor ; Recombinant Proteins/pharmacology ; Transfection
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