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  • 1
    Publication Date: 1987-05-15
    Description: A new human T-lymphotropic virus (HTLV-4) was recently described in healthy people from Senegal. This virus has many properties in common with members of the human T-lymphotropic viruses, particularly the human immunodeficiency virus or HIV, the etiologic agent of acquired immune deficiency syndrome (AIDS), but does not appear to be associated with immunodeficiency-related disorders. In the present study, serum samples were obtained from 4248 individuals from six West African countries, including Senegal, Guinea, Guinea Bissau, Mauritania, Burkina Faso, and Ivory Coast. These samples, collected during 1985-1987, were from people categorized as healthy control, sexually active risk, and disease populations. All samples were analyzed for reactivity to HTLV-4 and HIV by radioimmunoprecipitation-sodium dodecyl sulfate-polyacrylamide gel electrophoresis and immunoblotting. Evidence for HTLV-4 infection was found in five of the six countries. The seroprevalence varied markedly from country to country. Healthy sexually active individuals in the risk category had the highest levels of HTLV-4 infection compared to individuals in the healthy control category and the disease category, the latter including AIDS patients. The seroprevalence of HIV infection in most of these countries was quite low, although tightly associated with the rare cases of AIDS. The biology of HTLV-4 infection thus differs from that of HIV in Central Africa or the United States and Europe. The presence of these viruses and their different pathogenicities in several countries of West Africa indicate the necessity for serologic assays that will distinguish between them. Further studies of their origin and distribution as well as of their biology will be important in advancing our understanding of AIDS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kanki, P J -- M'Boup, S -- Ricard, D -- Barin, F -- Denis, F -- Boye, C -- Sangare, L -- Travers, K -- Albaum, M -- Marlink, R -- CA 18216/CA/NCI NIH HHS/ -- CA 37466/CA/NCI NIH HHS/ -- FOD 630/OD/NIH HHS/ -- New York, N.Y. -- Science. 1987 May 15;236(4803):827-31.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3033826" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/epidemiology ; Adult ; Africa, Western ; Deltaretrovirus/*isolation & purification ; Demography ; Female ; HIV/*isolation & purification ; Humans ; Inpatients ; Male ; Pregnancy ; Prisoners ; Prostitution ; Reference Values ; Risk
    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: 1987-07-24
    Description: Fragile X syndrome is a common form of mental retardation associated with a fragile site on the human X chromosome. Although fragility at this site is usually evident as a nonstaining chromatid gap, it remains unclear whether or not actual chromosomal breakage occurs. By means of somatic cell hybrids containing either a normal human X or a fragile X chromosome and utilizing two genes that flank the fragile site as markers of chromosome integrity, segregation of these markers was shown to be more frequent if they encompass the fragile site under appropriate culture conditions. Hybrid cells that reveal marker segregation were found to contain rearranged X chromosomes involving the region at or near the fragile site, thus demonstrating true chromosomal breakage within this area. Two independent translocation chromosomes were identified involving a rodent chromosome joined to the human X at the location of the fragile site. DNA analysis of closely linked, flanking loci was consistent with the position of the breakpoint being at or very near the fragile X site. Fragility at the translocation junctions was observed in both hybrids, but at significantly lower frequencies than that seen in the intact X of the parental hybrid. This observation suggests that the human portion of the junctional DNA may contain part of a repeated fragility sequence. Since the translocation junctions join heterologous DNA, the molecular cloning of the fragile X sequence should now be possible.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Warren, S T -- Zhang, F -- Licameli, G R -- Peters, J F -- CA31777/CA/NCI NIH HHS/ -- HD20521/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1987 Jul 24;237(4813):420-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3603029" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Chromosome Banding ; *Cloning, Molecular ; Female ; Fragile X Syndrome/*genetics ; Glucosephosphate Dehydrogenase/genetics ; Humans ; Hybrid Cells/cytology ; Hypoxanthine Phosphoribosyltransferase/genetics ; Male ; Sex Chromosome Aberrations/*genetics ; Translocation, Genetic
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  • 3
    Publication Date: 1987-08-07
    Description: Human peripheral blood eosinophils, cells often associated with allergic and parasitic diseases, were maintained in vitro for at least 14 days when they were cocultured with bovine endothelial cells and for at least 7 days when cultured with either bovine or human endothelial cell-derived conditioned medium. The cocultured eosinophils became hypodense and generated about three times as much leukotriene C4 upon activation with calcium ionophore and killed about three times as many antibody-coated larvae of Schistosoma mansoni as freshly isolated normodense eosinophils. That these cells can be maintained in vitro by coculture with endothelial cells, and the surprising finding that the cocultured eosinophils have biochemical, cytotoxic, and density properties similar to those of eosinophils in patients with allergic and other disorders, will facilitate investigation of the regulation and role of these cells in health and disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rothenberg, M E -- Owen, W F Jr -- Silberstein, D S -- Soberman, R J -- Austen, K F -- Stevens, R L -- AI-22531/AI/NIAID NIH HHS/ -- AI-23483/AI/NIAID NIH HHS/ -- AM-01401/AM/NIADDK NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1987 Aug 7;237(4815):645-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3110954" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibody-Dependent Cell Cytotoxicity ; Calcimycin/pharmacology ; Cattle ; *Cell Communication ; Cell Survival ; Cells, Cultured ; Endothelium/*cytology ; Eosinophils/*cytology ; Humans ; SRS-A/biosynthesis ; Schistosoma mansoni/immunology ; Time Factors
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  • 4
    Publication Date: 1987-02-27
    Description: In many genetic disorders, the responsible gene and its protein product are unknown. The technique known as "reverse genetics," in which chromosomal map positions and genetically linked DNA markers are used to identify and clone such genes, is complicated by the fact that the molecular distances from the closest DNA markers to the gene itself are often too large to traverse by standard cloning techniques. To address this situation, a general human chromosome jumping library was constructed that allows the cloning of DNA sequences approximately 100 kilobases away from any starting point in genomic DNA. As an illustration of its usefulness, this library was searched for a jumping clone, starting at the met oncogene, which is a marker tightly linked to the cystic fibrosis gene that is located on human chromosome 7. Mapping of the new genomic fragment by pulsed field gel electrophoresis confirmed that it resides on chromosome 7 within 240 kilobases downstream of the met gene. The use of chromosome jumping should now be applicable to any genetic locus for which a closely linked DNA marker is available.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Collins, F S -- Drumm, M L -- Cole, J L -- Lockwood, W K -- Vande Woude, G F -- Iannuzzi, M C -- GM34960/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1987 Feb 27;235(4792):1046-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2950591" target="_blank"〉PubMed〈/a〉
    Keywords: Bacteriophage lambda/genetics ; *Chromosome Mapping ; Chromosomes, Human, Pair 7 ; *Cloning, Molecular ; Cystic Fibrosis/*genetics ; DNA/*genetics ; Electrophoresis ; Genetic Markers ; Humans ; Nucleic Acid Hybridization ; Oncogenes
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  • 5
    Publication Date: 1987-08-28
    Description: Li-Fraumeni syndrome is manifested in a variety of neoplasms that are transmitted in a dominantly inherited pattern. The noncancerous skin fibroblasts of family members exhibit a unique characteristic of being resistant to the killing effect of ionizing radiation. A three- to eightfold elevation in expression of c-myc and an apparent activation of c-raf-1 gene have been observed in these noncancerous skin fibroblasts. These results may provide insight into the heritable defect underlying the familial predisposition to a variety of cancers.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chang, E H -- Pirollo, K F -- Zou, Z Q -- Cheung, H Y -- Lawler, E L -- Garner, R -- White, E -- Bernstein, W B -- Fraumeni, J W Jr -- Blattner, W A -- CA45158/CA/NCI NIH HHS/ -- CO7488/CO/NCI NIH HHS/ -- New York, N.Y. -- Science. 1987 Aug 28;237(4818):1036-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3616624" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Transformation, Neoplastic/radiation effects ; Cells, Cultured ; Fibroblasts/*radiation effects ; Humans ; Mice ; Mice, Nude ; Neoplastic Syndromes, Hereditary/*genetics ; Oncogenes/*radiation effects ; Pedigree ; *Radiation Tolerance ; Skin/cytology/*radiation effects ; Syndrome
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  • 6
    Publication Date: 1987-12-18
    Description: Growth factors and their receptors are involved in the regulation of cell proliferation and also play a key role in oncogenesis. In this study, a novel putative kinase receptor gene, termed eph, has been identified and characterized by molecular cloning. Its primary structure is similar to that of tyrosine kinase receptors thus far cloned and includes a cysteine-rich region in the extracellular domain. However, other features of the sequence distinguish the eph gene product from known receptors with tyrosine kinase activity. Thus the eph protein may define a new class of these molecules. The eph gene is overexpressed in several human carcinomas, suggesting that this gene may be involved in the neoplastic process of some tumors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hirai, H -- Maru, Y -- Hagiwara, K -- Nishida, J -- Takaku, F -- New York, N.Y. -- Science. 1987 Dec 18;238(4834):1717-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Third Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2825356" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Base Sequence ; DNA Restriction Enzymes ; *Genes ; Humans ; Molecular Sequence Data ; Neoplasms/metabolism ; Oncogenes ; Protein-Tyrosine Kinases/metabolism ; Receptor, Epidermal Growth Factor/*genetics ; Transcription, Genetic
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  • 7
    Publication Date: 1987-07-24
    Description: Abnormal accumulation of connective tissue in blood vessels contributes to alterations in vascular physiology associated with disease states such as hypertension and atherosclerosis. Elastin synthesis was studied in blood vessels from newborn calves with severe pulmonary hypertension induced by alveolar hypoxia in order to investigate the cellular stimuli that elicit changes in pulmonary arterial connective tissue production. A two- to fourfold increase in elastin production was observed in pulmonary artery tissue and medial smooth muscle cells from hypertensive calves. This stimulation of elastin production was accompanied by a corresponding increase in elastin messenger RNA consistent with regulation at the transcriptional level. Conditioned serum harvested from cultures of pulmonary artery smooth muscle cells isolated from hypertensive animals contained one or more low molecular weight elastogenic factors that stimulated the production of elastin in both fibroblasts and smooth muscle cells and altered the chemotactic responsiveness of fibroblasts to elastin peptides. These results suggest that connective tissue changes in the pulmonary vasculature in response to pulmonary hypertension are orchestrated by the medial smooth muscle cell through the generation of specific differentiation factors that alter both the secretory phenotype and responsive properties of surrounding cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mecham, R P -- Whitehouse, L A -- Wrenn, D S -- Parks, W C -- Griffin, G L -- Senior, R M -- Crouch, E C -- Stenmark, K R -- Voelkel, N F -- CA31777/CA/NCI NIH HHS/ -- HD20521/HD/NICHD NIH HHS/ -- HL14985/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1987 Jul 24;237(4813):423-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3603030" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anoxia ; Cattle ; Connective Tissue/pathology/*physiopathology ; Disease Models, Animal ; Elastin/genetics/physiology ; Humans ; Hypertension, Pulmonary/pathology/*physiopathology ; Muscle, Smooth, Vascular/pathology/*physiopathology ; RNA, Messenger/genetics ; Transcription, Genetic
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  • 8
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1987-12-11
    Description: Vasoactive intestinal peptide (VIP) is a neuropeptide with broad tissue distribution. Although its precise function is unknown, it is thought to exert its effect, at least in part, by interacting with cell surface receptors. Nuclear receptors for VIP have now been identified by specific binding of 125I-labeled VIP to nuclei of a human colonic adenocarcinoma cell line (HT29) and by cross-linking of 125I-labeled VIP to its receptor on intact nuclei. In contrast, 125I-labeled transferrin shows only background binding to nuclei but significant binding to intact cells. Purity of the isolated nuclei was further substantiated by electron microscopy. The apparent molecular sizes of the VIP--cross-linked nuclear and cell surface receptors are similar but not identical.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Omary, M B -- Kagnoff, M F -- DK07202/DK/NIDDK NIH HHS/ -- DK35108/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1987 Dec 11;238(4833):1578-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department 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/2825352" target="_blank"〉PubMed〈/a〉
    Keywords: Adenocarcinoma/*metabolism/ultrastructure ; Cell Line ; Cell Nucleus/*metabolism/ultrastructure ; Colonic Neoplasms/*metabolism/ultrastructure ; Humans ; Kinetics ; Microscopy, Electron ; Receptors, Gastrointestinal Hormone/*metabolism ; Receptors, Vasoactive Intestinal Peptide ; Vasoactive Intestinal Peptide/*metabolism
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  • 9
    Publication Date: 1987-07-10
    Description: Inhibin is a gonadal glycoprotein hormone that regulates the production of follicle-stimulating hormone (FSH) by the anterior pituitary gland and exhibits intragonadal actions as well. The present study shows that inhibin-like immunoreactivity (inhibin-LI) is present in cells of the cytotrophoblast layer of human placenta at term and in primary cultures of human trophoblasts. Human chorionic gonadotropin (hCG) stimulated secretion of inhibin-LI from these cultured placental cells. This effect was mimicked by 8-bromo-cyclic adenosine monophosphate (8-bromo-cAMP), forskolin, and cholera toxin, suggesting that the mechanism of hCG induction of placental inhibin-LI secretion is cAMP-dependent. Incubation with an antiserum that binds the alpha-subunit of human inhibin increased the secretion of hCG and gonadotropin-releasing hormone-like immunoreactivity (GnRH-LI) from trophoblast cells in culture, suggesting a local tonic inhibitory action of endogenous inhibin on hCG and GnRH-LI release. The action of inhibin on hCG secretion may partially require the presence of placental GnRH, as suggested by evidence that a synthetic GnRH antagonist partially reverses the hCG increase induced by inhibin immunoneutralization. Results suggest paracrine roles for both inhibin and GnRH in the regulation of placental hCG production.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Petraglia, F -- Sawchenko, P -- Lim, A T -- Rivier, J -- Vale, W -- AM26741/AM/NIADDK NIH HHS/ -- HD13527/HD/NICHD NIH HHS/ -- NS21182/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1987 Jul 10;237(4811):187-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3299703" target="_blank"〉PubMed〈/a〉
    Keywords: 8-Bromo Cyclic Adenosine Monophosphate/pharmacology ; Cells, Cultured ; Cholera Toxin/pharmacology ; Chorionic Gonadotropin/pharmacology/*secretion ; Chorionic Villi/analysis ; Colforsin/pharmacology ; Feedback ; Female ; Gonadotropin-Releasing Hormone/antagonists & inhibitors/pharmacology/secretion ; Humans ; Infant, Newborn ; Inhibins/analysis/*physiology ; Male ; Pregnancy ; Secretory Rate/drug effects ; Trophoblasts/analysis/drug effects/*secretion
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  • 10
    Publication Date: 1987-10-23
    Description: The fluorescence anisotropy of 1,6-diphenyl-1,3,5-hexatriene in labeled platelet membranes, an index of membrane fluidity, identifies a prominent subgroup of patients with Alzheimer's disease who manifest distinct clinical features. In a family study, the prevalence of this platelet membrane abnormality was 3.2 to 11.5 times higher in asymptomatic, first-degree relatives of probands with Alzheimer's disease than in neurologically healthy control subjects chosen without regard to family history of dementia. The pattern of the platelet membrane abnormality within families was consistent with that of a fully penetrant autosomal dominant trait. Thus, this abnormality of platelet membranes may be an inherited factor that is related to the development of Alzheimer's disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zubenko, G S -- Wusylko, M -- Cohen, B M -- Boller, F -- Teply, I -- AG03705/AG/NIA NIH HHS/ -- AG05133/AG/NIA NIH HHS/ -- MH30915/MH/NIMH NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1987 Oct 23;238(4826):539-42.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry, University of Pittsburgh, Western Psychiatric Institute and Clinic, PA 15213.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3659926" target="_blank"〉PubMed〈/a〉
    Keywords: Aged ; Alzheimer Disease/blood/*genetics ; Blood Platelets/*ultrastructure ; Cell Membrane/physiology ; Diphenylhexatriene ; Female ; Fluorescence Polarization ; Humans ; Male ; *Membrane Fluidity ; Middle Aged ; Risk Factors
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