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  • Articles  (17)
  • Female  (17)
  • American Association for the Advancement of Science (AAAS)  (17)
  • American Geophysical Union
  • Blackwell Publishing Ltd
  • 1985-1989  (17)
  • 1980-1984
  • 1970-1974
  • 1986  (17)
Collection
  • Articles  (17)
Source
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (17)
  • American Geophysical Union
  • Blackwell Publishing Ltd
Years
  • 1985-1989  (17)
  • 1980-1984
  • 1970-1974
Year
Journal
Topic
  • 1
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    Atrial natriuretic peptide elevation in congestive heart failure in the human (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-03-07
    Description: A sensitive radioimmunoassay for atrial natriuretic peptide was used to examine the relation between circulating atrial natriuretic peptide and cardiac filling pressure in normal human subjects, in patients with cardiovascular disease and normal cardiac filling pressure, and in patients with cardiovascular disease and elevated cardiac filling pressure with and without congestive heart failure. The present studies establish a normal range for atrial natriuretic peptide in normal human subjects. These studies also establish that elevated cardiac filling pressure is associated with increased circulating concentrations of atrial natriuretic peptide and that congestive heart failure is not characterized by a deficiency in atrial natriuretic peptide, but with its elevation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Burnett, J C Jr -- Kao, P C -- Hu, D C -- Heser, D W -- Heublein, D -- Granger, J P -- Opgenorth, T J -- Reeder, G S -- New York, N.Y. -- Science. 1986 Mar 7;231(4742):1145-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2935937" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; Atrial Natriuretic Factor/*blood ; Cardiovascular Diseases/blood ; Female ; Heart Failure/*blood ; Hemodynamics ; Humans ; Male ; Middle Aged ; Radioimmunoassay
    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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    Lipoprotein mutations in pigs are associated with elevated plasma cholesterol and atherosclerosis (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-12-19
    Description: A strain of pigs bearing three immunogenetically defined lipoprotein-associated markers (allotypes), designated Lpb5, Lpr1, and Lpu1, has marked hypercholesterolemia on a low fat, cholesterol-free diet. Unlike individuals with familial hypercholesterolemia or WHHL rabbits, the affected pigs have normal low density lipoprotein receptor activity. The animals, by 7 months of age, have extensive atherosclerotic lesions in all three coronary arteries. This strain of pig represents an animal model for atherosclerosis and hypercholesterolemia associated with mutations affecting the structures of plasma lipoproteins. One of the variant apolipoproteins, Lpb5, is apolipoprotein-B. A second variant apolipoprotein (Lpr1), termed apo-R, is a 23-kilodalton protein present in both the very low density (d less than 1.006 g/ml) and the very high density (d greater than 1.21 g/ml) fractions of pig plasma. Isoforms of this protein correlate with two Lpr alleles, Lpr1 and Lpr2. The Lpr genes segregate independently of the Lpb5 and Lpu1 alleles. The Lpu1 allotype is a component of low density lipoprotein and is genetically linked to Lpb5.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rapacz, J -- Hasler-Rapacz, J -- Taylor, K M -- Checovich, W J -- Attie, A D -- AG05-856/AG/NIA NIH HHS/ -- HL30594/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1986 Dec 19;234(4783):1573-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3787263" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Apolipoproteins B/genetics ; Arteriosclerosis/blood/*genetics ; Cholesterol/blood ; *Disease Models, Animal ; Female ; Genotype ; Hypercholesterolemia/blood/*genetics ; Immunologic Tests ; Lipoproteins/blood/*genetics ; Lipoproteins, LDL/blood/genetics ; Lipoproteins, VLDL/blood/genetics ; Male ; Mutation ; Receptors, LDL/metabolism ; Swine
    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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    Human multidrug-resistant cell lines: increased mdr1 expression can precede gene amplification (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-05-02
    Description: The development of simultaneous resistance to multiple structurally unrelated drugs is a major impediment to cancer chemotherapy. Multidrug resistance in human KB carcinoma cells selected in colchicine, vinblastine, or Adriamycin is associated with amplification of specific DNA sequences (the multidrug resistance locus, mdr1). During colchicine selection resistance is initially accompanied by elevated expression of a 4.5-kilobase mdr1 messenger RNA (mRNA) without amplification of the corresponding genomic sequences. During selection for increased levels of resistance, expression of this mRNA is increased simultaneously with amplification of mdr1 DNA. Increased expression and amplification of mdr1 sequences were also found in multidrug-resistant sublines of human leukemia and ovarian carcinoma cells. These results suggest that increased expression of mdr1 mRNA is a common mechanism for multidrug resistance in human cells. Activation of the mdr1 gene by mutations or epigenetic changes may precede its amplification during the development of resistance.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shen, D W -- Fojo, A -- Chin, J E -- Roninson, I B -- Richert, N -- Pastan, I -- Gottesman, M M -- New York, N.Y. -- Science. 1986 May 2;232(4750):643-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3457471" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Colchicine/pharmacology ; Cricetinae ; Cricetulus ; DNA, Neoplasm/genetics ; Doxorubicin/pharmacology ; *Drug Resistance ; Female ; *Gene Amplification ; Humans ; Leukemia, Lymphoid/drug therapy ; Neoplasms/*drug therapy/genetics ; Nucleic Acid Hybridization ; Ovarian Neoplasms/drug therapy ; RNA, Messenger/genetics ; Vinblastine/pharmacology
    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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  • 4
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    Transplantation of fetal hematopoietic stem cells in utero: the creation of hematopoietic chimeras (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-08-15
    Description: Transplantation of normal, immature, fetal hematopoietic cells into a preimmune fetal recipient with a congenital hemoglobinopathy may allow partial reconstitution of normal hemoglobin production without the complications associated with postnatal bone marrow transplantation (immunosuppression and the occurrence of graft versus host disease). In order to test this hypothesis the naturally occurring polymorphism at the beta-hemoglobin locus of the sheep was used as a marker for engraftment and hematopoietic chimerism. Intraperitoneal injection of allogeneic fetal stem cells into normal fetal lambs resulted in hematopoietic chimerism in three of four surviving recipients. This chimerism has been sustained for 6 months after birth and 9 months after engraftment, without evidence of graft versus host disease, and without the use of immunosuppressive therapy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Flake, A W -- Harrison, M R -- Adzick, N S -- Zanjani, E D -- AM-24027/AM/NIADDK NIH HHS/ -- AM-29890/AM/NIADDK NIH HHS/ -- AM-30914/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1986 Aug 15;233(4765):776-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2874611" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Chimera ; Female ; Fetus ; Graft vs Host Disease ; *Hematopoietic Stem Cell Transplantation ; Hemoglobin A/*analysis ; Hemoglobins/*analysis ; Pregnancy ; Sheep ; Transplantation, Homologous
    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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    Anti-idiotypic antibodies bear the internal image of a human tumor antigen (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-04-04
    Description: Goat antibodies to idiotypes (anti-idiotypic antibodies; Ab2) that recognize an idiotype associated with the combining site of a BALB/c mouse IgG2a monoclonal antibody (Ab1) to human gastric carcinoma were used to immunize BALB/c mice and rabbits. A monoclonal anti-anti-idiotypic antibody (Ab3) of IgG1 isotype was obtained after immunization of mice. The Ab3 and the Ab1 showed identical binding specificities and bound with similar avidities to the same tumor antigen. The induction of Ab1-like Ab3 by Ab2 was not restricted to mice, since Ab3 could also be induced in rabbits. Both the mouse- and the rabbit-derived Ab3 bound the same gastrointestinal cancer-associated antigen as Ab1. These findings indicate that Ab2 induced the formation of antigen-specific Ab3, probably because it bears the internal image of the tumor-associated antigen. This Ab2 may therefore have potential for modulating the immune response of cancer patients to their tumors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Herlyn, D -- Ross, A H -- Koprowski, H -- CA-10815/CA/NCI NIH HHS/ -- CA-21124/CA/NCI NIH HHS/ -- CA-33490/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1986 Apr 4;232(4746):100-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3952496" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antibodies ; Antibodies, Monoclonal ; Antigen-Antibody Complex ; Antigens, Neoplasm/*immunology ; Female ; Goats/immunology ; Humans ; Immunoglobulin Idiotypes/*immunology ; Mice ; Mice, Inbred BALB C/immunology ; Neoplasms/immunology ; Rabbits/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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  • 6
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    Adrenal-mediated endogenous metabolites inhibit puberty in female mice (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-02-14
    Description: While assessing a potential role of adrenal glands in the production of the hitherto unidentified puberty-delaying pheromone of female mice, the urinary volatile profiles of normal and adrenalectomized animals were quantitatively compared. Six components, whose concentrations were depressed after adrenalectomy, were identified: 2-heptanone, trans-5-hepten-2-one, trans-4-hepten-2-one, n-pentyl acetate, cis-2-penten-1-yl acetate, and 2,5-dimethylpyrazine. When these laboratory-synthesized chemicals were added (in their natural concentrations) to either previously inactive urine from adrenalectomized females or plain water, the biological activity was fully restored.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Novotny, M -- Jemiolo, B -- Harvey, S -- Wiesler, D -- Marchlewska-Koj, A -- New York, N.Y. -- Science. 1986 Feb 14;231(4739):722-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3945805" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenal Glands/*physiology ; Animals ; Female ; Ketones/urine ; Mice ; Ovary/physiology ; Pentanols/urine ; Pheromones/physiology/urine ; Pyrazines/urine ; *Sexual Maturation
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 7
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    Shock and tissue injury induced by recombinant human cachectin (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-10-24
    Description: Cachectin (tumor necrosis factor), a protein produced in large quantities by endotoxin-activated macrophages, has been implicated as an important mediator of the lethal effect of endotoxin. Recombinant human cachectin was infused into rats in an effort to determine whether cachectin, by itself, can elicit the derangements of host physiology caused by administration of endotoxin. When administered in quantities similar to those produced endogenously in response to endotoxin, cachectin causes hypotension, metabolic acidosis, hemoconcentration, and death within minutes to hours, as a result of respiratory arrest. Hyperglycemia and hyperkalemia were also observed after infusion. At necropsy, diffuse pulmonary inflammation and hemorrhage were apparent on gross and histopathologic examination, along with ischemic and hemorrhagic lesions of the gastrointestinal tract, and acute renal tubular necrosis. Thus, it appears that a single protein mediator (cachectin) is capable of inducing many of the deleterious effects of endotoxin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tracey, K J -- Beutler, B -- Lowry, S F -- Merryweather, J -- Wolpe, S -- Milsark, I W -- Hariri, R J -- Fahey, T J 3rd -- Zentella, A -- Albert, J D -- New York, N.Y. -- Science. 1986 Oct 24;234(4775):470-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3764421" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Glucose/metabolism ; Endotoxins/toxicity ; Female ; Glycoproteins/*toxicity ; Humans ; Potassium/blood ; Rats ; Recombinant Proteins ; Shock/*chemically induced/pathology/physiopathology ; Sodium/blood ; Tumor Necrosis Factor-alpha
    Print ISSN: 0036-8075
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  • 8
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    Induction of suppressor cells specific for AChR in experimental autoimmune myasthenia gravis (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-04-18
    Description: Suppressor cells specific for acetylcholine receptor (AChR) were induced in a population of lymphocytes previously sensitized to AChR, obtained from rats with experimental autoimmune myasthenia gravis (EAMG). The lymphocytes were cultured with the immunosuppressive drug cyclosporin A plus purified AChR for 7 days. These cells, when mixed with lymphocytes from rats with EAMG in vitro, strongly suppressed the antibody response to AChR. They did not inhibit antibody responses to an unrelated antigen, an indication that suppression was specific for AChR. This approach should be a useful way to induce specific suppressor cells from sensitized populations of lymphocytes and may be applicable in the treatment of autoimmune diseases such as myasthenia gravis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McIntosh, K R -- Drachman, D B -- 5RO1 HD04817-16/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1986 Apr 18;232(4748):401-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2938256" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cyclosporins/pharmacology ; Female ; Lymph Nodes/cytology ; Lymphocytes/drug effects ; Myasthenia Gravis/*immunology ; Rats ; Rats, Inbred Lew ; Receptors, Cholinergic/*immunology ; Spleen/cytology ; T-Lymphocytes, Regulatory/*immunology
    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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    Molecular cloning of the chicken progesterone receptor (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-08-15
    Description: To define the functional domains of the progesterone receptor required for gene regulation, complementary DNA (cDNA) clones encoding the chicken progesterone receptor have been isolated from a chicken oviduct lambda gt11 cDNA expression library. Positive clones expressed antigenic determinants that cross-reacted with six monospecific antibodies derived from two independent sources. A 36-amino acid peptide sequence obtained by microsequencing of purified progesterone receptor was encoded by nucleotide sequences in the longest cDNA clone. Analysis of the amino acid sequence of the progesterone receptor deduced from the cDNA clones revealed a cysteine-rich region that was homologous to a region found in the estrogen and glucocorticoid receptors and to the avian erythroblastosis virus gag-erb-A fusion protein. Northern blot analysis with chicken progesterone receptor cDNA's indicated the existence of at least three messenger RNA species. These messages were found only in oviduct and could be induced by estrogens.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Conneely, O M -- Sullivan, W P -- Toft, D O -- Birnbaumer, M -- Cook, R G -- Maxwell, B L -- Zarucki-Schulz, T -- Greene, G L -- Schrader, W T -- O'Malley, B W -- New York, N.Y. -- Science. 1986 Aug 15;233(4765):767-70.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2426779" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Antibodies, Monoclonal ; Base Sequence ; Chickens ; *Cloning, Molecular ; Cross Reactions ; DNA/*metabolism ; Epitopes/analysis ; Female ; *Genes ; Humans ; Nucleic Acid Hybridization ; Oviducts/metabolism ; RNA, Messenger/genetics ; Receptors, Progesterone/*genetics ; Species Specificity
    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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    Bright light resets the human circadian pacemaker independent of the timing of the sleep-wake cycle (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-08-08
    Description: Human circadian rhythms were once thought to be insensitive to light, with synchronization to the 24-hour day accomplished either through social contacts or the sleep-wake schedule. Yet the demonstration of an intensity-dependent neuroendocrine response to bright light has led to renewed consideration of light as a possible synchronizer of the human circadian pacemaker. In a laboratory study, the output of the circadian pacemaker of an elderly woman was monitored before and after exposure to 4 hours of bright light for seven consecutive evenings, and before and after a control study in ordinary room light while her sleep-wake schedule and social contacts remained unchanged. The exposure to bright light in the evening induced a 6-hour delay shift of her circadian pacemaker, as indicated by recordings of body temperature and cortisol secretion. The unexpected magnitude, rapidity, and stability of the shift challenge existing concepts regarding circadian phase-resetting capacity in man and suggest that exposure to bright light can indeed reset the human circadian pacemaker, which controls daily variations in physiologic, behavioral, and cognitive function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Czeisler, C A -- Allan, J S -- Strogatz, S H -- Ronda, J M -- Sanchez, R -- Rios, C D -- Freitag, W O -- Richardson, G S -- Kronauer, R E -- 1 R01-AG-04912-02/AG/NIA NIH HHS/ -- 1 R01-HD-20174-01/HD/NICHD NIH HHS/ -- AFOSR-83-0309/PHS HHS/ -- etc. -- New York, N.Y. -- Science. 1986 Aug 8;233(4764):667-71.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3726555" target="_blank"〉PubMed〈/a〉
    Keywords: Aged ; Body Temperature ; *Circadian Rhythm ; Female ; Humans ; Hydrocortisone/blood ; *Light ; Sleep/*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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