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  • Humans  (92)
  • ASTROPHYSICS
  • Life and Medical Sciences
  • American Association for the Advancement of Science (AAAS)  (92)
  • 1985-1989  (92)
  • 1987  (92)
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (92)
  • Wiley-Blackwell  (126)
Years
  • 1985-1989  (92)
Year
  • 1
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    Absence of duplication of chromosome 21 genes in familial and sporadic Alzheimer's disease (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-10-30
    Description: The possibility that Alzheimer's disease (AD) is caused by overexpression or duplication of one or more genes on chromosome 21 has been raised by the observation of AD-like neuropathologic changes in individuals with Down syndrome and by the mapping of both the defect for familial AD and the amyloid beta protein gene to this autosome. Possible duplication on chromosome 21 was investigated in both familial and sporadic AD by means of restriction fragment length polymorphisms for the amyloid and SODI loci, as well as for DNA markers in the vicinity of the familial AD defect and in the critical Down syndrome region of chromosome 21. No evidence of increased DNA dosage was observed in either brain or leukocytes of patients with inherited or sporadic forms of AD. Duplication of these regions is therefore not a frequent event in either form of AD. Furthermore, no significant allelic association was detected between AD and any of the loci, including the amyloid and SODI genes, providing no support for the hypothesis that defects in these specific genes are the primary cause of AD.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉St George-Hyslop, P H -- Tanzi, R E -- Polinsky, R J -- Neve, R L -- Pollen, D -- Drachman, D -- Growdon, J -- Cupples, L A -- Nee, L -- Myers, R H -- ADRC P50 AGO5134-02/AD/ADAMHA HHS/ -- NS20012/NS/NINDS NIH HHS/ -- R01 AGO6865-1/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 1987 Oct 30;238(4827):664-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neurogenetics Laboratory, Massachusetts General Hospital, Boston.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2890206" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Alzheimer Disease/*genetics ; Amyloid/genetics ; *Chromosomes, Human, Pair 21 ; Genes ; Genetic Linkage ; Humans ; Polymorphism, Restriction Fragment Length
    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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    Tissue distribution and developmental expression of the messenger RNA encoding angiogenin (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-07-17
    Description: New blood vessel growth occurs during normal fetal development and in diseases such as cancer and diabetes. The polypeptide angiogenin induces new blood vessel growth in two biological assays and may play a role in the vascular development of the fetus and in the neovascularization that accompanies diseases and wound healing. A complementary DNA probe for human angiogenin was used to examine the tissue distribution of angiogenin messenger RNA (mRNA) in the developing rat and in selected transformed cell lines. Angiogenin mRNA was detected predominantly in adult liver but was also detectable at low levels in other tissues. The expression of the angiogenin gene in rat liver was found to be developmentally regulated; mRNA levels were low in the developing fetus, increased in the neonate, and maximal in the adult. The amount of angiogenin mRNA in human HT-29 colon carcinoma and SK-HEP hepatoma cells was not greater than that in normal rat liver. These results demonstrate that angiogenin is predominantly expressed in adult liver, that the pattern of angiogenin gene expression is not temporally related to vascular development in the rat, and that the transformed cells studied do not contain more angiogenin mRNA than does normal liver. If angiogenin activity is controlled at the transcriptional level, the results of this study suggest that the primary function of angiogenin in vivo may be in processes other than the regulation of vascular growth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weiner, H L -- Weiner, L H -- Swain, J L -- HL26831/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1987 Jul 17;237(4812):280-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2440105" target="_blank"〉PubMed〈/a〉
    Keywords: Age Factors ; Animals ; Cell Line ; Gene Expression Regulation ; Humans ; Liver/physiology ; Neoplasm Proteins/*genetics ; Neovascularization, Pathologic ; RNA, Messenger/genetics ; Rats ; *Ribonuclease, Pancreatic ; Tissue Distribution
    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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    Antidepressant and circadian phase-shifting effects of light (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-01-16
    Description: Bright light can suppress nighttime melatonin production in humans, but ordinary indoor light does not have this effect. This finding suggested that bright light may have other chronobiologic effects in humans as well. Eight patients who regularly became depressed in the winter (as day length shortens) significantly improved after 1 week of exposure to bright light in the morning (but not after 1 week of bright light in the evening). The antidepressant response to morning light was accompanied by an advance (shift to an earlier time) in the onset of nighttime melatonin production. These results suggest that timing may be critical for the antidepressant effects of bright light.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lewy, A J -- Sack, R L -- Miller, L S -- Hoban, T M -- MH40161-01/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1987 Jan 16;235(4786):352-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3798117" target="_blank"〉PubMed〈/a〉
    Keywords: Circadian Rhythm/*radiation effects ; Depression/*therapy ; Humans ; Light ; Melatonin/*blood
    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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    HTLV-V: a new human retrovirus isolated in a Tac-negative T cell lymphoma/leukemia (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-12-11
    Description: A new human retrovirus was isolated from a continuous cell line derived from a patient with CD4+ Tac- cutaneous T cell lymphoma/leukemia. This virus is related to but distinct from human T cell leukemia/lymphoma virus types I and II (HTLV-I and HTLV-II) and human immunodeficiency virus (HIV-1). With the use of a fragment of provirus cloned from one patient with T cell leukemia, closely related sequences were found in DNA of the cell line and of tumor cells from seven other patients with the same disease; these sequences were only distantly related to HTLV-I. The phenotype of the cells and the clinical course of the disease were clearly distinguishable from leukemia associated with HTLV-I. All patients and the wife of one patient showed a weak serological cross-reactivity with both HTLV-I and HIV-1 antigens. None of the patients proved to be at any apparent risk for HIV-1 infection. The name proposed for this virus is HTLV-V, and the date indicate that it may be a primary etiological factor in the major group of cutaneous T cell lymphomas/leukemias, including the sporadic lymphomas known as mycoses fungoides.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Manzari, V -- Gismondi, A -- Barillari, G -- Morrone, S -- Modesti, A -- Albonici, L -- De Marchis, L -- Fazio, V -- Gradilone, A -- Zani, M -- New York, N.Y. -- Science. 1987 Dec 11;238(4833):1581-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Dipartimento di Medicina Sperimentale e Scienze Biochimiche II, Universita di Roma, Tor Vergata, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2825353" target="_blank"〉PubMed〈/a〉
    Keywords: Antigens, Viral/analysis ; Deltaretrovirus/classification/*isolation & purification/ultrastructure ; Female ; Humans ; Leukemia/*microbiology ; Lymphoma/*microbiology ; Male ; Microscopy, Electron ; T-Lymphocytes/cytology
    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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    Smooth muscle-mediated connective tissue remodeling in pulmonary hypertension (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    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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    Lung cancer and indoor air pollution in Xuan Wei, China (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-01-09
    Description: In Xuan Wei County, Yunnan Province, lung cancer mortality is among China's highest and, especially in females, is more closely associated with indoor burning of "smoky" coal, as opposed to wood or "smokeless" coal, than with tobacco smoking. Indoor air samples were collected during the burning of all three fuels. In contrast to wood and smokeless coal emissions, smoky coal emission has high concentrations of submicron particles containing mutagenic organics, especially in aromatic and polar fractions. These studies suggested an etiologic link between domestic smoky coal burning and lung cancer in Xuan Wei.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mumford, J L -- He, X Z -- Chapman, R S -- Cao, S R -- Harris, D B -- Li, X M -- Xian, Y L -- Jiang, W Z -- Xu, C W -- Chuang, J C -- New York, N.Y. -- Science. 1987 Jan 9;235(4785):217-20.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3798109" target="_blank"〉PubMed〈/a〉
    Keywords: China ; *Coal ; Female ; Humans ; Male ; Neoplasms/etiology/*mortality ; Polycyclic Compounds/analysis ; Smoke/*adverse effects/analysis ; Wood
    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
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    Common pathogenetic mechanism for three tumor types in bilateral acoustic neurofibromatosis (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-04-17
    Description: Bilateral acoustic neurofibromatosis (BANF) is a genetic defect associated with multiple tumors of neural crest origin. Specific loss of alleles from chromosome 22 was detected with polymorphic DNA markers in two acoustic neuromas, two neurofibromas, and one meningioma from BANF patients. This indicates a common pathogenetic mechanism for all three tumor types. The two neurofibromas were among three taken from the same patient, and both showed loss of identical alleles demonstrating that the same chromosome suffered deletion in both tumors. The third neurofibroma from this patient showed no detectable loss of heterozygosity, which suggests the possibility of a more subtle mutational event that affects chromosome 22. In the two acoustic neuromas, only a portion of chromosome 22 was deleted, narrowing the possible chromosomal location of the gene that causes BANF to the region distal to the D22S9 locus in band 22q11. The identification of progressively smaller deletions on chromosome 22 in these tumor types may well provide a means to clone and characterize the defect.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Seizinger, B R -- Rouleau, G -- Ozelius, L J -- Lane, A H -- St George-Hyslop, P -- Huson, S -- Gusella, J F -- Martuza, R L -- NS00654/NS/NINDS NIH HHS/ -- NS20025/NS/NINDS NIH HHS/ -- NS22224/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1987 Apr 17;236(4799):317-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3105060" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Chromosome Mapping ; *Chromosomes, Human, Pair 22 ; Heterozygote Detection ; Humans ; Leukocytes/cytology ; Neoplasms/genetics ; Neurofibromatosis 1/*genetics ; Neuroma, Acoustic/*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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  • 8
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    Conservation of brain amyloid proteins in aged mammals and humans with Alzheimer's disease (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-02-20
    Description: The formation of clusters of altered axons and dendrites surrounding extracellular deposits of amyloid filaments (neuritic plaques) is a major feature of the human brain in both aging and Alzheimer's disease. A panel of antibodies against amyloid filaments and their constituent proteins from humans with Alzheimer's disease cross-reacted with neuritic plaque and cerebrovascular amyloid deposits in five other species of aged mammals, including monkey, orangutan, polar bear, and dog. Antibodies to a 28-amino acid peptide representing the partial protein sequence of the human amyloid filaments recognized the cortical and microvascular amyloid of all of the aged mammals examined. Plaque amyloid, plaque neurites, and neuronal cell bodies in the aged animals showed no reaction with antibodies to human paired helical filaments. Thus, with age, the amyloid proteins associated with progressive cortical degeneration in Alzheimer's disease are also deposited in the brains of other mammals. Aged primates can provide biochemically relevant models for principal features of Alzheimer's disease: cerebrovascular amyloidosis and neuritic plaque formation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Selkoe, D J -- Bell, D S -- Podlisny, M B -- Price, D L -- Cork, L C -- AG05134/AG/NIA NIH HHS/ -- AG06173/AG/NIA NIH HHS/ -- NS23340/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1987 Feb 20;235(4791):873-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3544219" target="_blank"〉PubMed〈/a〉
    Keywords: *Aging ; Alzheimer Disease/pathology/*physiopathology ; Amyloid/immunology/*metabolism ; Amyloidosis/pathology/*physiopathology ; Animals ; Brain/pathology/*physiopathology ; Humans ; Immunoenzyme Techniques ; Macaca mulatta ; Pongo pygmaeus ; Saimiri ; Ursidae
    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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  • 9
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    A DNA segment encoding two genes very tightly linked to Huntington's disease (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-11-13
    Description: The discovery of D4S10, an anonymous DNA marker genetically linked to Huntington's disease (HD), introduced the capacity for limited presymptomatic diagnosis in this late-onset neurodegenerative disorder and raised the hope of cloning and characterizing the defect based on its chromosomal location. Progress on both fronts has been limited by the absence of additional DNA markers closer to the HD gene. An anonymous DNA locus, D4S43, has now been found that shows extremely tight linkage to HD. Like the disease gene, D4S43 is located in the most distal region of the chromosome 4 short arm, flanked by D4S10 and the telomere. In three extended HD kindreds, D4S43 displays no recombination with HD, placing it within 0 to 1.5 centimorgans of the genetic defect. Expansion of the D4S43 region to include 108 kilobases of cloned DNA has allowed identification of eight restriction fragment length polymorphisms and at least two independent coding segments. In the absence of crossovers, these genes must be considered candidates for the site of the HD defect, although the D4S43 restriction fragment length polymorphisms do not display linkage disequilibrium with the disease gene.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gilliam, T C -- Bucan, M -- MacDonald, M E -- Zimmer, M -- Haines, J L -- Cheng, S V -- Pohl, T M -- Meyers, R H -- Whaley, W L -- Allitto, B A -- NS16367/NS/NINDS NIH HHS/ -- NS20012/NS/NINDS NIH HHS/ -- NS22031/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1987 Nov 13;238(4829):950-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neurogenetics Laboratory, Massachusetts General Hospital, Boston.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2890209" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; *Chromosomes, Human, Pair 4 ; Cloning, Molecular ; Cosmids ; *Genes ; *Genetic Linkage ; Humans ; Huntington Disease/*genetics ; Polymorphism, Restriction Fragment Length
    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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  • 10
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    Similarity of synthetic peptide from human tumor to parathyroid hormone in vivo and in vitro (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-12-11
    Description: One mechanism considered responsible for the hypercalcemia that frequently accompanies malignancy is secretion by the tumor of a circulating factor that alters calcium metabolism. The structure of a tumor-secreted peptide was recently determined and found to be partially homologous to parathyroid hormone (PTH). The amino-terminal 1-34 region of the factor was synthesized and evaluated biologically. In vivo it produced hypercalcemia, acted on bone and kidney, and stimulated 1,25-dihydroxy-vitamin D3 formation. In vitro it interacted with PTH receptors and, in some systems, was more potent than PTH. These studies support a long-standing hypothesis regarding pathogenesis of malignancy-associated hypercalcemia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Horiuchi, N -- Caulfield, M P -- Fisher, J E -- Goldman, M E -- McKee, R L -- Reagan, J E -- Levy, J J -- Nutt, R F -- Rodan, S B -- Schofield, T L -- AR 36446/AR/NIAMS NIH HHS/ -- AR 39191/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 1987 Dec 11;238(4833):1566-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Regional Bone Center, Helen Hayes Hospital (New York State Department of Health), West Haverstraw 10993.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3685994" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Calcium/blood ; Humans ; Hypercalcemia/etiology ; Neoplasms/*physiopathology ; Parathyroid Glands/physiology ; Parathyroid Hormone/pharmacology/*physiology ; Peptides/*physiology ; Rats ; Rats, Inbred Strains ; Thyroidectomy
    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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