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  • 1
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    Ocular dominance column development: analysis and simulation (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-08-11
    Description: The visual cortex of many adult mammals has patches of cells that receive inputs driven by the right eye alternating with patches that receive inputs driven by the left eye. These ocular dominance patches (or "columns") form during early life as a consequence of competition between the activity patterns of the two eyes. A mathematical model of several biological mechanisms that can account for this development is presented. Analysis of this model reveals the conditions under which ocular dominance segregation will occur and determines the resulting patch width. Simulations of the model also exhibit other phenomena associated with early visual development, such as topographic refinement of cortical receptive fields, the confinement of input cell connections to patches, monocular deprivation plasticity including a critical period, and the effect of artificially induced strabismus. The model can be used to predict the results of proposed experiments and to discriminate among various mechanisms of plasticity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miller, K D -- Keller, J B -- Stryker, M P -- New York, N.Y. -- Science. 1989 Aug 11;245(4918):605-15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, University of California, San Francisco 94143-0444.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2762813" target="_blank"〉PubMed〈/a〉
    Keywords: Afferent Pathways/physiology ; Animals ; Cats ; *Computer Simulation ; Eye/growth & development/innervation ; *Functional Laterality ; Geniculate Bodies/physiology ; Mathematics ; *Models, Biological ; *Ocular Physiological Phenomena ; Synapses/physiology ; Vision, Ocular/physiology ; Visual Cortex/growth & development/*physiology
    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
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    Essential fatty acid depletion of renal allografts and prevention of rejection (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-05-20
    Description: A central hypothesis in transplantation biology is that resident leukocytes expressing class II histocompatibility antigens may determine the immunogenicity of an organ. By means of a novel method to deplete the kidney of resident leukocytes, essential fatty acid deficiency (EFAD), this hypothesis was tested in an intact, vascular organ. Kidneys subjected to EFAD and thus depleted of resident Ia-positive macrophages survived and functioned when transplanted across a major histocompatibility antigen barrier in the absence of immunosuppression of the recipient. Control allografts were rejected promptly. Allografts from donors subjected to EFAD normalized their lipid composition and were repopulated with host macrophages by 5 days. Administration of Ia-positive cells at the time of transplantation established that the resident leukocyte depletion induced by EFAD was responsible for the protective effect. These observations may provide insights into the mechanisms underlying tissue immunogenicity and the population of normal tissues with resident leukocytes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schreiner, G F -- Flye, W -- Brunt, E -- Korber, K -- Lefkowith, J B -- New York, N.Y. -- Science. 1988 May 20;240(4855):1032-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3285468" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Fatty Acids, Essential/*physiology ; *Graft Rejection ; Kidney/physiology ; *Kidney Transplantation ; Liver/analysis ; Macrophages/physiology ; Phospholipids/analysis ; Rats ; Rats, Inbred BUF ; Rats, Inbred Lew ; 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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  • 3
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    Identification of specific transducin alpha subunits in retinal rod and cone photoreceptors (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-10-03
    Description: Transducin is a guanyl nucleotide-binding protein that couples rhodopsin photolysis to hydrolysis of guanosine 3',5'-monophosphate in rod photoreceptor cells of vertebrate retinas. Several complementary DNA clones encoding transducin subunits have recently been characterized. One clone, isolated from a bovine retina complementary DNA library, encodes a previously unidentified polypeptide with an amino acid sequence 78% identical to the sequence of the alpha subunit of bovine rod outer segment transducin. Antibodies to a synthetic peptide with amino acid sequence derived specifically from this novel polypeptide recognize a 41-kilodalton polypeptide in homogenates of bovine retina. Localization of this polypeptide in bovine retina by indirect immunofluorescence demonstrates that it is expressed only in cone outer segments. Antibodies to specific sequences found only in the rod transducin alpha subunit recognize a polypeptide localized only in the rod outer segment. Therefore, bovine rod and cone cells each express structurally related yet significantly different forms of transducin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lerea, C L -- Somers, D E -- Hurley, J B -- Klock, I B -- Bunt-Milam, A H -- EYO 1311/EY/NEI NIH HHS/ -- EYO 1730/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 1986 Oct 3;234(4772):77-80.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3529395" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cattle ; DNA/genetics ; Fluorescent Antibody Technique ; Membrane Proteins/genetics/*physiology ; Photoreceptor Cells/*metabolism ; Transducin
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 4
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    Facial recognition cells and autism (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-12-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fotheringham, J B -- New York, N.Y. -- Science. 1987 Dec 11;238(4833):1496-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3685989" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autistic Disorder/etiology/*physiopathology ; Brain/*physiopathology ; Face ; *Form Perception ; Humans ; Infant
    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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    Reduced numbers of somatostatin receptors in the cerebral cortex in Alzheimer's disease (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-07-19
    Description: Somatostatin receptor concentrations were measured in patients with Alzheimer's disease and controls. In the frontal cortex (Brodmann areas 6, 9, and 10) and temporal cortex (Brodmann area 21), the concentrations of somatostatin in receptors in the patients were reduced to approximately 50 percent of control values. A 40 percent reduction was seen in the hippocampus, while no significant changes were found in the cingulate cortex, postcentral gyrus, temporal pole, and superior temporal gyrus. Scatchard analysis showed a reduction in receptor number rather than a change in affinity. Somatostatin-like immunoreactivity was significantly reduced in both the frontal and temporal cortex. Somatostatin-like immunoreactivity was linearly related to somatostatin-receptor binding in the cortices of Alzheimer's patients. These findings may reflect degeneration of postsynaptic neurons or cortical afferents in the patients' cerebral cortices. Alternatively, decreased somatostatin-like immunoreactivity in Alzheimer's disease might indicate increased release of somatostatin and down regulation of postsynaptic receptors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Beal, M F -- Mazurek, M F -- Tran, V T -- Chattha, G -- Bird, E D -- Martin, J B -- 1P50AG05134/AG/NIA NIH HHS/ -- IR23NS19867-1/NS/NINDS NIH HHS/ -- MN/NS31862/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1985 Jul 19;229(4710):289-91.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2861661" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; Alzheimer Disease/*metabolism ; Cerebral Cortex/*analysis ; Chromatography, High Pressure Liquid ; Female ; Frontal Lobe/analysis ; Humans ; Male ; Middle Aged ; Neurons/metabolism/physiology ; Radioimmunoassay ; Receptors, Cell Surface/*analysis ; Receptors, Somatostatin ; Somatostatin/metabolism/physiology ; Temporal Lobe/analysis
    Print ISSN: 0036-8075
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  • 6
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    Biosynthesis and secretion of proatrial natriuretic factor by cultured rat cardiocytes (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-12-06
    Description: Rat atrial natriuretic factor (ANF) is translated as a 152-amino acid precursor preproANF. PreproANF is converted to the 126-amino acid proANF, the storage form of ANF in the atria. ANF isolated from the blood is approximately 25 amino acids long. It is demonstrated here that rat cardiocytes in culture store and secrete proANF. Incubation of proANF with serum produced a smaller ANF peptide. PreproANF seems to be processed to proANF in the atria, and proANF appears to be released into the blood, where it is converted by a protease to a smaller peptide.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bloch, K D -- Scott, J A -- Zisfein, J B -- Fallon, J T -- Margolies, M N -- Seidman, C E -- Matsueda, G R -- Homcy, C J -- Graham, R M -- Seidman, J G -- 1R23CA33570/CA/NCI NIH HHS/ -- HL07208/HL/NHLBI NIH HHS/ -- HL26215/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1985 Dec 6;230(4730):1168-71.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2933808" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Atrial Natriuretic Factor/*biosynthesis/genetics/secretion ; Autoradiography ; Cells, Cultured ; Electrophoresis, Polyacrylamide Gel ; Heart/physiology ; Immune Sera/immunology ; Myocardium/*cytology/metabolism ; Protein Precursors/*biosynthesis/genetics/secretion ; RNA, Messenger/genetics ; Rabbits/immunology ; Rats
    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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  • 7
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    Endogenous anticonvulsant substance in rat cerebrospinal fluid after a generalized seizure (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-05-31
    Description: Cerebrospinal fluid taken from rats subjected to electroshock-induced seizures and injected into the cerebral ventricles of rats that had not been shocked increased the seizure threshold of the recipients. The anticonvulsant activity of the donor cerebrospinal fluid was antagonized by opioid antagonists and enhanced by peptidase inhibitors. These results suggest the existence of an endogenous anticonvulsant substance in rat cerebrospinal fluid, possibly opioid in nature, which is activated as a consequence of a seizure and which may play a critical role in postseizure inhibition.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tortella, F C -- Long, J B -- New York, N.Y. -- Science. 1985 May 31;228(4703):1106-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2986292" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anticonvulsants/*cerebrospinal fluid ; Electroshock ; Enkephalin, Leucine/analogs & derivatives/pharmacology ; Male ; Naloxone/pharmacology ; Narcotic Antagonists/pharmacology ; Peptide Hydrolases ; Rats ; Rats, Inbred Strains ; Receptors, Opioid/drug effects ; Receptors, Opioid, delta ; Seizures/*cerebrospinal fluid
    Print ISSN: 0036-8075
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  • 8
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    Gene interaction at HLA-DQ enhances autoantibody production in primary Sjogren's syndrome (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-05-30
    Description: Primary Sjogren's syndrome is an autoimmune disorder characterized by dryness of the mouth and eyes. The human leukocyte antigen (HLA) locus DQ is related to the primary Sjogren's syndrome autoantibodies that bind the RNA proteins Ro/SSA and La/SSB. Both DQ1 and DQ2 alleles are associated with high concentrations of these autoantibodies. An analysis of all possible combinations at DQ has shown that the entire effect was due to heterozygotes expressing the DQ1 and DQ2 alleles. These data suggest that gene interaction between DQ1 and DQ2 (or alleles at associated loci), possibly from gene complementation of trans-associated surface molecules, influences the autoimmune response in primary Sjogren's syndrome.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Harley, J B -- Reichlin, M -- Arnett, F C -- Alexander, E L -- Bias, W B -- Provost, T T -- AM 31133/AM/NIADDK NIH HHS/ -- AM 34159/AM/NIADDK NIH HHS/ -- HL 30748/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1986 May 30;232(4754):1145-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3458307" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Autoantibodies/*biosynthesis/genetics ; HLA-DQ Antigens ; HLA-DR Antigens ; Histocompatibility Antigens Class II/*genetics/immunology ; Mice ; Sjogren's Syndrome/*genetics/immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 9
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    The NOD mouse: recessive diabetogenic gene in the major histocompatibility complex (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-02-14
    Description: Examination of the histocompatibility region of the nonobese diabetic (NOD) mouse with antibodies against class II glycoproteins (products of immune response genes of the major histocompatibility complex I-A and I-E), hybrid T-cell clones, and mixed-lymphocyte cultures and analysis of restriction fragment length polymorphisms indicate that the NOD mouse has a unique class II major histocompatibility complex with no expression of surface I-E, no messenger RNA for I-E alpha, and an I-A not recognized by any monoclonal antibodies or hybrid T-cell clones studied. In crosses of NOD mice with control C3H mice, the development of diabetes was dependent on homozygosity for the NOD mouse's unique major histocompatibility region.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hattori, M -- Buse, J B -- Jackson, R A -- Glimcher, L -- Dorf, M E -- Minami, M -- Makino, S -- Moriwaki, K -- Kuzuya, H -- Imura, H -- AM07009-01/AM/NIADDK NIH HHS/ -- AM32083-03/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1986 Feb 14;231(4739):733-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3003909" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosome Mapping ; DNA Restriction Enzymes/metabolism ; Diabetes Mellitus, Type 1/*genetics ; Genes, Recessive ; Genetic Linkage ; Genotype ; H-2 Antigens/genetics ; Histocompatibility Antigens Class II/*genetics ; Interleukin-2/biosynthesis ; *Major Histocompatibility Complex ; Mice ; Mice, Mutant Strains/*genetics ; Spleen/physiology
    Print ISSN: 0036-8075
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  • 10
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    Iron-responsive elements: regulatory RNA sequences that control mRNA levels and translation (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-05-13
    Description: The biosynthetic rates for both the transferrin receptor (TfR) and ferritin are regulated by iron. An iron-responsive element (IRE) in the 5' untranslated portion of the ferritin messenger RNA (mRNA) mediates iron-dependent control of its translation. In this report the 3' untranslated region of the mRNA for the human TfR was shown to be necessary and sufficient for iron-dependent control of mRNA levels. Deletion studies identified a 678-nucleotide fragment of the TfR complementary DNA that is critical for this iron regulation. Five potential stem-loops that resemble the ferritin IRE are contained within the region critical for TfR regulation. Each of two of the five TfR elements was independently inserted into the 5' untranslated region of an indicator gene transcript. In this location they conferred iron regulation of translation. Thus, an mRNA element has been implicated in the mediation of distinct regulatory phenomena dependent on the context of the element within the transcript.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Casey, J L -- Hentze, M W -- Koeller, D M -- Caughman, S W -- Rouault, T A -- Klausner, R D -- Harford, J B -- New York, N.Y. -- Science. 1988 May 13;240(4854):924-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cell Biology and Metabolism Branch, National Institute of Child Health and Human Development, Bethesda, MD 20892.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2452485" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; DNA/genetics ; DNA, Recombinant ; Ferritins/biosynthesis/*genetics ; Growth Hormone/genetics ; Humans ; Iron/*pharmacology ; Mice ; Plasmids ; Protein Biosynthesis/*drug effects ; RNA/*genetics ; RNA, Messenger/*genetics ; Receptors, Transferrin/biosynthesis/*genetics ; *Regulatory Sequences, Nucleic Acid ; Transcription, Genetic ; Transfection ; Transformation, Genetic
    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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