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  • Articles  (90)
  • Female
  • 1985-1989  (90)
  • 1970-1974
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  • Articles  (90)
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Year
  • 1
    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
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  • 2
    Publication Date: 1987-05-29
    Description: Linkage analysis of 15 Utah kindreds demonstrated that a gene responsible for von Recklinghausen neurofibromatosis (NF) is located near the centromere on chromosome 17. The families also gave no evidence for heterogeneity, indicating that a significant proportion of NF cases are due to mutations at a single locus. Further genetic analysis can now refine this localization and may lead to the eventual identification and cloning of the defective gene responsible for this disorder.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barker, D -- Wright, E -- Nguyen, K -- Cannon, L -- Fain, P -- Goldgar, D -- Bishop, D T -- Carey, J -- Baty, B -- Kivlin, J -- CA 28854/CA/NCI NIH HHS/ -- CA 36362/CA/NCI NIH HHS/ -- GM 29090/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1987 May 29;236(4805):1100-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3107130" target="_blank"〉PubMed〈/a〉
    Keywords: Centromere ; Chromosome Mapping ; *Chromosomes, Human, Pair 17/ultrastructure ; DNA, Recombinant ; Female ; *Genes ; Genetic Linkage ; Humans ; Male ; Neurofibromatosis 1/*genetics ; Nucleic Acid Hybridization
    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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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1985-02-22
    Description: Purification of two antigens (48-kilodalton polypeptide and a group with major subunits of 50 and 55 kilodaltons) from the infective larvae of the parasitic nematode Trichinella spiralis was recently reported. Immunization of mice with either of these antigens induces strong resistance to a subsequent challenge infection. In the study reported here the mechanism of this resistance was investigated by monitoring the parasite's life cycle in mice immunized with the antigens. Immunized mice were able to expel intestinal adult worms and to inhibit the fecundity of adult female worms at an accelerated rate compared to control mice. Accelerated expulsion and inhibition of fecundity may account entirely for the level of resistance induced by immunization. Although the effects of the immune response apparently are exerted on adult worms, the target antigens are expressed only by developing larvae. This suggests that immune effector mechanisms act on intestinal larvae in such a way that they develop into defective adults.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Silberstein, D S -- Despommier, D D -- New York, N.Y. -- Science. 1985 Feb 22;227(4689):948-50.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3969571" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Helminth/immunology/*isolation & purification ; Female ; Immunization ; Larva ; Male ; Mice ; Trichinella/growth & development/*immunology ; Trichinellosis/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
    Publication Date: 1988-04-29
    Description: Screening for human T-lymphotropic virus type I (HTLV-I) antibodies was performed on sera from 39,898 blood donors at eight blood centers in geographically distinct areas of the United States. Ten donors (0.025 percent) showed evidence of HTLV-I seropositivity by enzyme immunoassays; this was confirmed by protein immunoblot and radioimmunoprecipitation. Seroprevalence rates ranged from 0 to 0.10 percent at the locations sampled, with HTLV-I antibodies found predominantly in donors from the southeastern and southwestern United States. Matched case-control interviews and laboratory studies were performed on five seropositive women and two seropositive men who participated in an identity-linked collection of sera from a subset of 33,893 donors at six of the eight blood centers. Four of the women and both men are black; one woman is Caucasian. Four of the seven seropositive individuals admitted to prior intravenous drug abuse or sexual contact with an intravenous drug user. Sexual contact with native inhabitants of an HTLV-I endemic area was the only identified risk factor for one male. The distribution of HTLV-I antibodies in this U.S. blood donor sample corroborates the previously reported epidemiology of this agent and suggests that additional donor screening measures, including the testing of donated blood for HTLV-I markers, may be necessary to prevent the spread of HTLV-I to transfusion recipients.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Williams, A E -- Fang, C T -- Slamon, D J -- Poiesz, B J -- Sandler, S G -- Darr, W F 2nd -- Shulman, G -- McGowan, E I -- Douglas, D K -- Bowman, R J -- New York, N.Y. -- Science. 1988 Apr 29;240(4852):643-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉American Red Cross Jerome H. Holland Laboratory, Rockville, MD 20855.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2896386" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Antibodies, Viral/*analysis ; *Blood Donors ; Deltaretrovirus/*immunology/isolation & purification ; Deltaretrovirus Infections/diagnosis/*epidemiology/transmission ; Female ; Humans ; Immunoenzyme Techniques ; Immunosorbent Techniques ; Japan ; Male ; Middle Aged ; Risk Factors ; Sexual Partners ; Substance-Related Disorders ; 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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  • 5
    Publication Date: 1989-08-25
    Description: Mice fed a chemically defined diet devoid of pyrroloquinoline quinone (PQQ) grew poorly, failed to reproduce, and became osteolathyritic. Moreover, severely affected mice had friable skin, skin collagen that was readily extractable into neutral salt solutions, and decreased lysyl oxidase. The identification of functional defects in connective tissue and the growth retardation associated with PQQ deprivation suggest that PQQ plays a fundamental role as a growth factor or vitamin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Killgore, J -- Smidt, C -- Duich, L -- Romero-Chapman, N -- Tinker, D -- Reiser, K -- Melko, M -- Hyde, D -- Rucker, R B -- AM-35747/AM/NIADDK NIH HHS/ -- HL-15965/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1989 Aug 25;245(4920):850-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Nutrition, School of Agricultural and Environmental Sciences, University of California, Davis 95616.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2549636" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Coenzymes/*physiology ; Collagen/metabolism ; Female ; Growth Substances/physiology ; Mice ; Nutritional Physiological Phenomena ; PQQ Cofactor ; Quinolones/deficiency/*physiology ; Skin/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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  • 6
    Publication Date: 1989-05-26
    Description: Spondyloepiphyseal dysplasias (SED) are a heterogeneous group of inherited disorders characterized by disproportionate short stature and pleiotropic involvement of the skeletal and ocular systems. Evidence has suggested that SED may result from structural defects in type II collagen. To confirm the validity of this hypothesis, the structure of the "candidate" type II collagen gene (COL2A1) has been directly examined in a relatively large SED family. Coarse scanning of the gene by Southern blot hybridization identified an abnormal restriction pattern in one of the affected members of the kindred. Analysis of selected genomic fragments, amplified by the polymerase chain reaction, precisely localized the molecular defect and demonstrated that all affected family members carried the same heterozygous single-exon deletion. As a consequence of the mutation, nearly 90 percent of the assembled type II collagen homotrimers are expected to contain one or more procollagen subunits harboring an interstitial deletion of 36 amino acids in the triple helical domain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, B -- Vissing, H -- Ramirez, F -- Rogers, D -- Rimoin, D -- AR-38648/AR/NIAMS NIH HHS/ -- HD-22657/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1989 May 26;244(4907):978-80.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, State University of New York Health Science Center, Brooklyn 11203.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2543071" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; Child, Preschool ; Chromosome Deletion ; Collagen/*genetics ; DNA Restriction Enzymes ; DNA-Directed DNA Polymerase ; Exons ; Female ; Gene Amplification ; Humans ; Macromolecular Substances ; Male ; Molecular Sequence Data ; Mutation ; Nucleic Acid Hybridization ; Osteochondrodysplasias/*genetics ; Pedigree ; Procollagen/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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  • 7
    Publication Date: 1989-06-16
    Description: Genetic engineering of livestock is expected to have a major effect on the agricultural industry. However, accurate assessment of the consequences of transgene expression is impossible without multigenerational studies. A systematic study of the beneficial and adverse consequences of long-term elevations in the plasma levels of bovine growth hormone (bGH) was conducted on two lines of transgenic pigs. Two successive generations of pigs expressing the bGH gene showed significant improvements in both daily weight gain and feed efficiency and exhibited changes in carcass composition that included a marked reduction in subcutaneous fat. However, long-term elevation of bGH was generally detrimental to health: the pigs had a high incidence of gastric ulcers, arthritis, cardiomegaly, dermatitis, and renal disease. The ability to produce pigs exhibiting only the beneficial, growth-promoting effects of growth hormone by a transgenic approach may require better control of transgene expression, a different genetic background, or a modified husbandry regimen.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pursel, V G -- Pinkert, C A -- Miller, K F -- Bolt, D J -- Campbell, R G -- Palmiter, R D -- Brinster, R L -- Hammer, R E -- HD-09172/HD/NICHD NIH HHS/ -- HD-19018/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1989 Jun 16;244(4910):1281-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉U.S. Department of Agriculture, Beltsville, MD 20705.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2499927" target="_blank"〉PubMed〈/a〉
    Keywords: Agriculture ; Animals ; Animals, Domestic/*genetics/growth & development ; *Animals, Genetically Modified ; Body Weight ; Female ; *Genetic Engineering ; Growth Hormone/genetics ; Growth Hormone-Releasing Hormone/genetics ; Insulin-Like Growth Factor I/genetics ; Mice ; Organ Size ; Swine/genetics/growth & development ; *Transfection
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    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
    Publication Date: 1989-05-12
    Description: Carcinoma of the breast and ovary account for one-third of all cancers occurring in women and together are responsible for approximately one-quarter of cancer-related deaths in females. The HER-2/neu proto-oncogene is amplified in 25 to 30 percent of human primary breast cancers and this alteration is associated with disease behavior. In this report, several similarities were found in the biology of HER-2/neu in breast and ovarian cancer, including a similar incidence of amplification, a direct correlation between amplification and over-expression, evidence of tumors in which overexpression occurs without amplification, and the association between gene alteration and clinical outcome. A comprehensive study of the gene and its products (RNA and protein) was simultaneously performed on a large number of both tumor types. This analysis identified several potential shortcomings of the various methods used to evaluate HER-2/neu in these diseases (Southern, Northern, and Western blots, and immunohistochemistry) and provided information regarding considerations that should be addressed when studying a gene or gene product in human tissue. The data presented further support the concept that the HER-2/neu gene may be involved in the pathogenesis of some human cancers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Slamon, D J -- Godolphin, W -- Jones, L A -- Holt, J A -- Wong, S G -- Keith, D E -- Levin, W J -- Stuart, S G -- Udove, J -- Ullrich, A -- CA 36827/CA/NCI NIH HHS/ -- CA 48780/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1989 May 12;244(4905):707-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, U.C.L.A. School of Medicine 90024.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2470152" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biomarkers, Tumor ; Breast Neoplasms/*genetics ; Cloning, Molecular ; DNA/analysis ; Female ; Gene Amplification ; Gene Expression Regulation ; Humans ; Immunohistochemistry ; Nucleic Acid Hybridization ; Ovarian Neoplasms/*genetics ; Prognosis ; Protein Kinases ; Proto-Oncogene Proteins/*genetics ; *Proto-Oncogenes ; RNA/analysis ; Receptor, ErbB-2
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
    Publication Date: 1989-03-03
    Description: Gap junctions in the early amphibian embryo may play a fundamental role in the regulation of differentiation by mediating the cell-to-cell transfer of chemical signals. A complementary DNA encoding a gap junction present in Xenopus oocytes and early embryos has now been cloned and sequenced. This protein sequence is homologous to the well-characterized gap junction structural proteins rat connexin32 and connexin43. RNA blot analysis of total Xenopus oocyte RNA showed hybridization to a single 1.6-kilobase band. This messenger RNA is abundant in oocytes, decreases to levels below the sensitivity of our assay by stage 15 (18 hours), and is not detectable in RNA from a number of adult organs. To confirm that the oocyte cDNA encodes a gap junction channel, the protein was over expressed in Xenopus oocytes by injection of RNA synthesized in vitro. Pairs of RNA-injected oocytes formed many more time- and voltage-sensitive cell-cell channels than water-injected pairs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ebihara, L -- Beyer, E C -- Swenson, K I -- Paul, D L -- Goodenough, D A -- GM18974/GM/NIGMS NIH HHS/ -- GM37751/GM/NIGMS NIH HHS/ -- HL28958-06/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1989 Mar 3;243(4895):1194-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Columbia University, New York, NY 10032.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2466337" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Communication ; *Cloning, Molecular ; Connexins ; DNA Probes ; Electric Conductivity ; Female ; Gene Expression Regulation ; Intercellular Junctions/physiology ; Membrane Proteins/*genetics/physiology ; Molecular Sequence Data ; Nucleic Acid Hybridization ; Oocytes/analysis/physiology ; RNA/analysis ; RNA, Messenger/analysis ; Rats ; Tissue Distribution ; Xenopus/*embryology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
    Publication Date: 1988-09-30
    Description: Control of growth and differentiation during mammalian embryogenesis may be regulated by growth factors from embryonic or maternal sources. With the use of single-cell messenger RNA phenotyping, the simultaneous expression of growth factor transcripts in single or small numbers of preimplantation mouse embryos was examined. Transcripts for platelet-derived growth factor A chain (PDGF-A), transforming growth factor (TGF)-alpha, and TGF-beta 1, but not for four other growth factors, were found in whole blastocysts. TGF-alpha, TGF-beta 1, and PDGF antigens were detected in blastocysts by immunocytochemistry. Both PDGF-A and TGF-alpha were detected as maternal transcripts in the unfertilized ovulated oocyte, and again in blastocysts. TGF-beta 1 transcripts appeared only after fertilization. The expression of a subset of growth factors in mouse blastocysts suggests a role for these factors in the growth and differentiation of early mammalian embryos.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rappolee, D A -- Brenner, C A -- Schultz, R -- Mark, D -- Werb, Z -- 5T32 ES07106/ES/NIEHS NIH HHS/ -- HD22681/HD/NICHD NIH HHS/ -- HD23539/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1988 Sep 30;241(4874):1823-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Radiobiology and Environmental Health, University of California, San Francisco 94143-0750.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3175624" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blastocyst/*physiology ; Cleavage Stage, Ovum/physiology ; Embryonic Development ; Female ; Gene Expression Regulation ; Growth Substances/*genetics ; Mice ; Oocytes/physiology ; Platelet-Derived Growth Factor/*genetics ; Pregnancy ; RNA, Messenger/genetics ; Transcription, Genetic ; Transforming Growth Factors/*genetics
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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